Short-Term Mechanical

Circulatory Support
for Cardiogenic Shock
EDITORS

Adhir R. Shroff, MD, MPH, FSCAI

Alexander G. Truesdell, MD, FSCAI

Duane S. Pinto, MD, MPH, FSCAI

PUBLISHED BY

The Society for Cardiovascular Angiography & Interventions (SCAI)

1100 17th ST NW, Suite 400

Washington, DC, 20036

UNITED STATES | [Link]

Copyright © 2024 by The Society for Cardiovascular Angiography & Interventions.

All rights reserved. This book is protected by copyright. No part of this book or its supplemental videos and graphics may be reproduced or modified in any form,
including photocopying, recording, or utilized by any information storage and retrieval system, without permission in writing from the publisher. This book is for
individual personal use only and may not be used for commercial purposes.

Care has been taken to confirm the accuracy of information presented and to describe generally accepted interventional practices. However, the authors, editors,
and publisher are not responsible for errors or omissions or for any consequences from the application of the information in this book and make no warranty,
expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular
situation remains the professional responsibility of the practitioner. Some medical devices presented in the book may have Food and Drug Administration (FDA)
clearance for limited use in restricted research settings at the time of publication. It is the responsibility of the health care provider to ascertain the current status
of each device planned for use in clinical practice.

This project is supported through funding by Abiomed.

 Introduction

Introduction
The incidence of cardiogenic shock is growing year by year and becoming an increasingly important
part of cardiovascular care. Treatment options, notably temporary and durable mechanical circulatory
support, are diversifying in variety and utility. Clinical data is expanding and outcomes are slowly
improving. Cardiogenic shock management is increasingly becoming a multidisciplinary and multispecialty
collaborative team sport. The authors of this work and intended audience of this eBook are similarly
varied, and include interventional cardiology, cardiac surgery, advanced heart failure, cardiac critical care
specialists, and other professionals involved in the care of shock patients. Together, we have developed a
contemporary, practical, and highly visual reference to assist practicing physicians, health care providers,
trainees, and students—in the emergency department, cardiac catheterization laboratory, cardiac intensive
care unit, and operating room—to better care for our shock patients.

This eBook is divided into 5 sections:

• Section 1. Introduction to Cardiogenic Shock and Therapies
• Section 2. Basics of Mechanical Circulatory Support
• Section 3. In-Depth Review of Devices
• Section 4. Selecting Devices and Device Combinations Based on Clinical Need
• Section 5. Future Innovations

Each section contains brief, highly visual, and easy-to-read chapters with references to more definitive
works. Photos, illustrations, and embedded videos enhance the content of this digital eBook. Our
clinically focused authors share their best practices throughout. While the development of this
educational product was supported by a grant from industry, none of the authors or editors received
payment or honoraria for their work. The work’s organization, authors, and topics were selected entirely
by the editors without industry influence.

We are excited to offer this valuable and practical resource to fellows in training, early career physicians, and
experienced physicians of all specialties. Given the electronic format, we look forward to providing periodic
updates as new innovations, clinical guidelines, and trials continue to inform clinical practice.

Special thanks to all of the authors, and most importantly to our patients – to whom we dedicate this work.

Adhir R. Shroff, MD, MPH, FSCAI Alexander G. Truesdell, MD, FSCAI Duane S. Pinto, MD, MPH, FSCAI
Professor of Medicine Virginia Heart / Inova Schar Heart and Associate Professor of Medicine
Associate Chief of Cardiology Section Vascular Harvard Medical School
Falls Church, Virginia dpinto@[Link]
University of Illinois - Chicago
agtruesdell@[Link] @duanepinto
arshroff@[Link]
@AdhirShroff @agtruesdell

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Foreword

Foreword
I am honored to provide a foreword to this eBook on mechanical circulatory support (MCS) therapy
for cardiogenic shock, including acute myocardial infarction cardiogenic shock (AMICS) and acute
worsening of chronic heart failure. These chapters from esteemed colleagues are dedicated to
understanding the new era of MCS therapy.

In the 1950s, the Western world was recovering from the aftermath of World War II and two healthcare
epidemics were plaguing society. Acute poliomyelitis afflicted young and old alike. As a kid, I remember
the late summers in Ann Arbor, Michigan as a time of angst, with our parents keeping us indoors for
fear of mosquito-borne infection. Meanwhile, heavy smoking and close quarters had led to a sharp
increase in pulmonary tuberculosis (TB) among soldiers. Thus, hospitals had polio wards with iron lungs
and sanitoria for convalescence of TB. Miraculously, by the mid-1950s isoniazid was discovered to treat
TB and the Salk and Sabin vaccines were discovered to treat polio, and these 2 epidemics receded.

The next lethal risk to society came from smoking, uncontrolled hypertension, and lack of effective
therapies for hypercholesterolemia, ushering in a new epidemic of cardiovascular and cerebrovascular
disease. Myocardial infarction (MI) and stroke became the number 1 and 2 killers in the United States
with over a million people succumbing each year. To meet this challenge, coronary care units emerged
for intensive monitoring of cardiac rhythms. Bernard Lown, MD, developed electrical cardioversion to
treat ventricular fibrillation in acute MI. In 1967, Thomas Killip, MD, published his classification of acute
MI outcomes. Patients in the highest classification experienced an increased likelihood of developing
cardiogenic shock, had a 50% mortality rate within 12 hours of symptom onset, and 90% mortality at 1
week after presentation.

Unlike TB and polio, no real therapies for MI were developed except for defibrillation. Nothing in my
medical career was as psychologically demoralizing as watching a young, otherwise healthy man or
woman being admitted to our cardiac unit with a large MI and knowing we could only provide morphine,
bedrest, and hope. These patients would often slowly slide into heart failure or shock, or suffer acute
cardiac rupture or fatal refractory arrhythmias.

In the 1970s, three major discoveries provided the foundation for the reperfusion era.
• Keith Reimer, MD, and Robert Jennings, MD, demonstrated that timely reperfusion could limit the
size of infarction in a canine occlusion-reperfusion model. Myocardial salvage was feasible when
occlusion was less than 3 hours in duration.
• Marcus DeWood, MD, and colleagues performed emergency coronary angiography on STEMI
patients about to undergo emergency coronary bypass. He found that when patients presented
within 4 hours of symptom onset, they had a greater than 90% prevalence of thrombotic occlusion.
When presenting after 12 hours, they had undergone spontaneous thrombolysis in about 30% of
cases. Thus, it was assumed that coronary thrombotic occlusion was the inciting event in acute MI
and a rationale now existed to use thrombolytic therapy to enhance thrombolysis.
• Professor Michael Davies performed elegant histologic evaluation of coronary arteries in patients
dying of acute MI and clearly demonstrated that acute plaque rupture occurred in culprit lesions.
Furthermore, he described that inflammation at the site of rupture caused the occlusion.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Foreword

These concepts and discoveries led to the rationale for timely revascularization therapy to provide
myocardial salvage. Emergency bypass was effective, but logistically impractical. An alternate
reperfusion modality—intracoronary streptokinase infusion—was studied in the late 1970s. This
therapy required emergency coronary angiography. The angiograms provided proof that occlusion was
reversed with infusion of thrombolytic agents. J. Ward Kennedy, MD, and colleagues performed the
western Washington randomized trial of intracoronary streptokinase in acute MI and found that 1-year
survival was improved with this therapy. Soon after publication of that trial, intravenous streptokinase
therapy was demonstrated to improve survival in the Italian GISSI trial.

As thrombolytic therapy became widely used in the mid-1980s, coronary angioplasty was also being
developed. At first this therapy was considered dangerous and impractical. Over a 15-year period,
and 27 randomized trials of percutaneous transluminal coronary angioplasty (PTCA) vs thrombolytic
therapy, it was finally concluded that PTCA was superior to thrombolytic therapy, with emergency PTCA
reducing death, reinfarction, and intracranial hemorrhage.

Primary percutaneous coronary intervention (PCI) therapy has been the most impactful cardiac
therapy of the last 50 years. Mortality has dropped from 13% to 2% with primary PCI. Perhaps the
biggest impact on survival has been seen in the most hemodynamically compromised patients, those
in cardiogenic shock. We published the first report of primary PCI therapy in 1987. We found that
mortality improved from 90%, as described in the 1967 Killip study, to 50%. Judith Hochman, MD,
confirmed these findings in the first randomized trial in cardiogenic shock in 1999. Survival was
significantly better at 6 months for patients randomized to PCI therapy. Unfortunately, no further
advancement in improving survival to more than 50% was demonstrated until 2023.

Now with the publication of the randomized, controlled DanGer Shock trial, a new era for treatment
of cardiogenic shock is upon us. DanGer Shock demonstrated a significant reduction in mortality at 6
months in patients who received mechanical support with a microaxial flow pump as an adjunct to PCI.

The pages of this eBook describe best practices, elucidate the hemodynamic underpinnings, and discuss
the use of right heart catheter-derived hemodynamic measures. I hope that understanding this data and
implementing these practices will significantly improve outcomes at your institution.

William W. O’Neill, MD, FACC, MSCAI

Medical Doctor Emeritus
Henry Ford Health

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Acknowledgments

Acknowledgments
Acknowledgments from the Editors
Collaboration And Dedication to this project have made this journey possible. I must thank all of the authors for sharing
their expertise with us, my co-editors (Alex and Duane) for their creativity and persistence throughout this process, our
sponsors for trusting us to create a fair and comprehensive book, and most of all our amazing project manager, Jennifer
Melton, who has kept us all on task for the past several years. Finally, I want to thank my family for their support and
encouragement through the many ups and downs of this effort. - Adhir R. Shroff, MD, MPH, FSCAI

Acknowledgments from Society for Cardiovascular Angiography and Interventions (SCAI)

The completion of this book would not have been possible without the dedicated efforts of the executive editors and
authors listed in this book. The Society for Cardiovascular Angiography & Interventions also extends its gratitude to all of
the peer-reviewers, whose insightful comments and valuable assistance helped shape this book.

Peer reviewers:

• Yousif Ahmad MD, PhD, FSCAI, Director of Complex Coronary Intervention, University of California, San Francisco
• Lawrence Ang, MD, FACC, FSCAI, Associate Professor of Medicine, Interventional Cardiology, University of
California, San Diego
• Said Ashraf MD, FSCAI, Interventional Cardiologist, Assistant Professor, Department of Medicine, Rowan-Virtua
School of Medicine, AtlantiCare Regional Medical Center
• James C. Blankenship, MD, MHCM, MACC, MSCAI, Professor of Medicine and Flinn Chair of Cardiology, University
of New Mexico, Albuquerque, NM
• Arka Chatterjee, MD, FACC, FSCAI, Associate Professor of Medicine; Director, Structural Heart & Valve Disease
Program, BUMC Tucson / Univ of AZ COM, Tucson
• Saurav Chatterjee MD, FACC, FSCAI, FSVM, FAHA, Staff Interventional Cardiologist and Faculty, NYU Grossman
School of Medicine, Clinical Assistant Professor of Medicine, Zucker School of Medicine, Hempstead, NY
• Rhian E. Davies, DO, MS, FACC, FSCAI, Director of Complex Coronary Interventional Cardiology, WellSpan Health,
York, PA
• Alison Dupont, MD, FSCAI, Interventional Cardiologist, Medical Director CCU and ECMO Program, Northside
Hospital Heart Institute, Atlanta, GA
• Dean Ferrera, DO, FACC, FSCAI, Powers Health, Munster, IN
• Nkechinyere N. Ijioma, MBBS, FSCAI, Clinical Assistant Professor, Division of Cardiovascular Medicine, Department
of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH
• Anand Irimpen, MD, FACC, FSCAI, Professor of Medicine, Director of Interventional Cardiology, Tulane University;
Chief of Cardiology, VA, New Orleans
• Manju Bengaluru Jayanna MD, MS, Interventional Cardiologist, Bryn Mawr Medical Specialists Association,
Lankenau Institute for Medical Research
• Arun Kalyanasundaram, MD, FSCAI
• Subrata Kar, DO, RPVI, FACC, FSCAI, Interventional Cardiologist and Structural Heart Disease, Peripheral and
Endovascular Interventionalist, Advanced Heart Failure and Transplant Cardiologist, Associate Professor of Medicine,
Virginia Commonwealth University School of Medicine/VAMC, Division of Cardiology
• Neelima Katukuri, MD, FSCAI, Associate Professor, University of Central Florida, Orlando VA Medical Center, FL
• Jimmy Kerrigan, MD, FACC, FSCAI, FASNC, RPVI, Assistant Professor, University of Tennessee Health Science
Center; Section of Interventional Cardiology, Division of Cardiology, Department of Cardiac Sciences, Ascension Saint
Thomas Heart at Ascension Saint Thomas West
• Ajar Kochar, MD, MHS, FSCAI, FACC, Program Director, Interventional Cardiology Fellowship Training Program,
Brigham and Women’s Hospital, Harvard Medical School
• Priya Rao Kothapalli, MD, FACC, FSCAI, Interventional/Structural Cardiology

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Acknowledgments

• Parasuram Krishnamoorthy, MD, FACC, FSCAI, Associate Director, Structural Heart Program, Assistant Professor
of Medicine, Icahn School of Medicine at Mount Sinai; Associate Director, Mount Sinai Brooklyn Cardiology Fellowship;
Medical Director, Cardiac Cath Lab, Mount Sinai Brooklyn Hospital
• Sibi Krishnamurthy, MD, FSCAI, Clinical Instructor, Interventional and Structural Cardiology, NYU Langone
• Sabina Kumar, DO, MS, McLaren Macomb/Oakland-Michigan State University
• Issa Kutkut, MD, FACP, FACC, FSCAI, Interventional Cardiology, Lutheran Hospital; Adjunct Clinical Assistant
Professor IU School of Medicine, Fort Wayne, IN
• Hady Lichaa, MD, FSVM, FACC, FSCAI, RPVI, Assistant Professor of Medicine, University of Tennessee Health
Science Center, Ascension Saint Thomas Heart Rutherford, Murfreesboro and Nashville, TN
• Arthur H. Loussararian, MD, FACC, FSCAI, Providence Mission Hospital Regional Medical Center
• Ramesh Mazhari, MD, MBA, Professor of Medicine, George Washington University
• Mark A. Menegus, MD, FACC, FSCAI, Director, Cardiac Catheterization Laboratory, Montefiore Medical Center-
Einstein Division; Professor of Medicine, Albert Einstein College of Medicine, New York
• Christopher Michaeles, MD, FACC, FSCAI, Clinical Assistant Professor of Medicine, University at Buffalo, Jacobs
School of Medicine and Biomedical Sciences
• Chad V. Morreale, DO, Interventional Cardiology Fellow, Aurora St Luke’s Medical Center
• Sandeep Nathan, MD, MSc, FACC, FSCAI, Professor of Medicine, Medical Director, Cardiac Intensive Care Unit;
Director, Interventional Cardiology Fellowship Program; Co-Director, Cardiac Catheterization Laboratory,
The University of Chicago Medicine; Heart and Vascular Center, Chicago, IL
• Mitul P. Patel, MD, FACC, FSCAI, Directory of High-Risk PCI, Intermountain Heart Institute, Intermountain Health,
Salt Lake City, UT
• Rajan A.G. Patel, MD, FACC, FAHA, FSCAI, Professor of Medicine, Cardiology Division, Department of Medicine,
University of Virginia
• Timir K. Paul, MD, PhD, MPH, FACC, FSCAI, FAHA, Professor of Medicine, Program Director, Cardiovascular
Disease Fellowship, University of Tennessee Health Science Center at Nashville; Interventional Cardiologist,
Department of Cardiac Sciences, St. Thomas Heart Institute / Ascension St. Thomas Hospital, Nashville, TN
• Vinoy S. Prasad, MD, FACC, FSCAI, Associate Professor of Medicine, Director of Interventional Cardiology, Loma
Linda University Health
• Louai Razzouk, MD MPH, Assistant Professor of Medicine, Program Director, Interventional Cardiology Fellowship,
Associate Director (Quality), Cardiac Catheterization Lab (Tisch / Kimmel), Department of Medicine, Division of
Cardiology, NYU Langone Health, NYU School of Medicine
• Sumon Roy, MD, FACC, FSCAI, Interventional & Structural Cardiologist, Boston Medical Center Health System
• Aisha Siraj, MD, FACC, FSCAI, Interventional Cardiologist, MetroHealth, Medical Center, Cleveland, OH
• Prashanth D. Thakker, MD, MHPE, FACC, FSCAI, Assistant Professor of Medicine, Interventional Cardiology Director,
Cardiovascular Diseases Fellowship Associate Director, Interventional Cardiology Fellowship, Cardiovascular Division,
John T. Milliken Department of Internal Medicine, Washington University School of Medicine; Barnes-Jewish Hospital
• Saraschandra Vallabhajosyula, MD, MSc, FACP, FCCP, FCCM, FAHA, FACC, FSCAI, Assistant Professor of
Medicine; Director, Coronary Care Unit, Brown University Health Cardiovascular Institute, Division of Cardiology,
Department of Medicine, Warren Alpert Medical School of Brown University, Providence, RI
• Poonam Velagapudi, MD, MS, FSCAI, Structural and Interventional Cardiologist, Demarest, NJ
• Adam Vohra, MD, MBA, Assistant Professor of Medicine, The University of Chicago Medicine, Department of
Medicine, Section of Cardiology
• Raymond Yau MD, FSCAI, Chief of Advanced Heart Failure and Mechanical Support, Heart Hospital of New Mexico

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Table of Contents

Table of Contents
SECTION 1 Introduction to Cardiogenic Shock and Therapies 1 10.5 Manual Compression and Assisted Manual Compression for Large
Bore Access and Closure....................................................................... 98
1 Cardiogenic Shock Overview............................................................................ 2 Madhan Shanmugasundaram, MD, FACC, FSCAI
Mir Babar Basir, DO, FACC, FSCAI 10.6 Cross-over Balloon Occlusion “Dry Closure” Technique for Large
Bore Femoral Access............................................................................104
William W. O’Neill, MD, FACC, MSCAI
Alexander G. Truesdell, MD, FSCAI
2 Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction:
Unraveling the Differences Between the Phenotypes ................................ 8 Nadim A. Geloo, MD, FSCAI
Ilan Vavilin, MD Behnam Tehrani, MD, FSCAI
Ran Lee, MD 10.7 Large Bore Arterial Post-Closure Hemostasis.................................112
Ahmad A. Abdul-Aziz, MD Mark J. Ricciardi, MD, FSCAI
3 Understanding Intracardiac Hemodynamics: A Refresher on Interpreting Luis H. Paz Rios, MD, FSCAI
PV Loops............................................................................................................ 13 10.8 Access Strategies for Monitoring or Prolonged MCS Use.............119
Michael I. Brener, MD Amer K. Ardati, MD, MSC, FACC, FSCAI
Daniel Burkhoff MD, PhD Jonathan Meyer, MD
4 Cardiogenic Shock Terminology and Metrics Explained............................ 19 10.9 Delayed Closure Techniques...............................................................125
Jaya Mallidi, MD, MHS, FSCAI Kusum Lata, MD, FACC, FSCAI
5 Hemodynamic Assessment: Right Heart Catheterization......................... 27 Anshita Kumari, MBBS
Michael Sumner, DO Avijit Bagga
Robert J. Widmer, MD, PhD 10.10 Percutaneous Axillary Artery Access Best Practices...................130
Ahmed Ghoneem, MD, MSc James M. McCabe, MD, FSCAI
Jaime Hernandez-Montfort, MD, MPH, MSc Kathleen Kearney, MD, FSCAI
6 Pharmacotherapy Overview: Inotropes, Vasopressors, 10.11 Distal Limb Perfusion Strategies.....................................................136
and Vasodilators............................................................................................... 34
Chirdeep Patel, MD, FSCAI
Ankit Kumar, MBBS MRCP, FRCA, FFICM
Pooja Swamy, MD
Alastair Proudfoot, MBChB, PhD
Amir Kaki, MD, FACC, FSCAI
7 Treatment Escalation Guidelines.................................................................... 41
11 Anticoagulation Strategies and Patient Considerations
Mir B. Basir, DO, FACC, FSCAI When Using MCS..........................................................................................149
Alejandro Lemor, MD, MS, FSCAI Manoj Ambalavanan, MD
Katherine J. Kunkel, MD, MSEd, FSCAI Anish Shah, MD, MS
8 Systems of Care: Shock Protocols, Teams, Centers, and Networks......... 49 Helena Dickens, BS
Alexander G. Truesdell, MD, FSCAI Stephanie Dwyer Kaluzna, PharmD, BCCP
Wayne B. Batchelor, MD, FSCAI Adhir R. Shroff, MD, MPH, FSCAI
Erik A. Osborn, MD 12 Vasoinotropic Considerations with Short-Term MCS............................161
Carolyn S. Rosner, NP Michael J. Lim, MD, FSCAI, FACC, FAHA
Ramesh Singh, MD
Shashank S. Sinha, MD
SECTION 3 In-Depth Review of Devices 174
Behnam N. Tehrani, MD
13 Pulsatile Devices...........................................................................................175
SECTION 2 Basics of Mechanical Circulatory Support 58 13.1 IABP and iVAC2L Mechanism of Action & Clinical Data................176
Paul Brocklebank, BS
9 Patient Identification and Device Selection.................................................. 59
Maxwell Kilcoyne, DO
Leah B. Kosyakovsky, MD
Arman Kilic, MD, FACS, FACC
Haval Chweich, MD
13.2 Pulsatile Devices: Troubleshooting Complications.........................183
Navin K. Kapur, MD, FSCAI
Matthew C. Evans, MD
Jeffrey A. Marbach, MBBS, MS, FRCPC, FSCAI
Anbukarasi Maran, MD
10 Access and Closure Techniques in MCS...................................................... 70
13.3 Axillary-Subclavian Intra-aortic Balloon Pump Insertion.............187
10.1 Best Practice Algorithm for Large Bore Femoral Artery Access.... 71
Neha Yadav, MD
Marie-France Poulin, MD, FACC, FSCAI
Kameel Kassab, MD, FSCAI
Ashvarya Mangla, MD, FSCAI
14 Impella® Family of MCS Axial Flow Pumps..............................................192
10.2 Large Bore Femoral Venous Access and Closure.............................. 79
14.1 Impella® Mechanism of Action............................................................193
Ashish Pershad, MD, FSCAI
Francesco Burzotta, MD, PhD
Vamshidhara Gade, MD, FSCAI
Cristina Aurigemma, MD, PhD
Philipp Wiesner, MD
Carlo Trani, MD
10.3 Suture-based Closure Devices for Large Bore Access..................... 85
14.2 Troubleshooting Complications for Impella Left-sided Devices...202
Thomas M. Todoran, MD, MSC, FSCAI
Miguel Martillo, MD
Jeffrey P. Yourshaw, MD, FSCAI
Tawseef Dar, MD
10.4 Closure Devices: Plugs, Patches, Hybrid............................................ 92
Mauricio G. Cohen, MD, FACC, FSCAI
John Blair, MD, FACC
14.3 Impella RP® Insertion, Tips & Tricks, and Challenges ....................213
Sandeep Nathan, MD, MSC, FACC, FSCAI
Joaquim Spadoni Barboza, MD, FSCAI, FACC
Kent Brummel, MD, FACC
Khalil Ibrahim, MD, FSCAI, FACC

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Table of Contents

14.4 Transcaval Access for Mechanical Circulatory Support.................219 19 ECMO Patient Management, Weaning, Troubleshooting,
Toby Rogers, MD, PhD LV Unloading, and Closure..........................................................................353
Robert J. Lederman, MD, FSCAI 19.1 Managing VA ECMO in the ICU..........................................................354
Adam B. Greenbaum, MD Kari Gorder, MD
14.5 Single Access Technique for Impella Assisted High-risk PCI.......228 Timothy D. Smith, MD, FSCAI
Jason Wollmuth, MD, FACC, FSCAI 19.2 Anticoagulation & Transfusion Strategies in ECMO ......................361
14.6 Initial Management of the Impella in the ICU.................................235
® Emily Larnard, MD
Kari Gorder, MD Bharath G. Rathakrishnan, MD, FSCAI
Timothy D. Smith, MD, FSCAI Jeffrey A. Marbach, MBBS, MS, FRCPC, FSCAI

15 TandemHeart® Device..................................................................................240 19.3 ECMO Complications............................................................................370

James Lantry III, MD
15.1 TandemHeart: Clinical Data and Mechanism of Action..................241
Mehul Desai, MD
Katherine J. Kunkel, MD, MSEd, FSCAI
Erik Osborn, MD
Hussayn J. Alrayes, DO
Christopher A. King, MD, FSCAI
Brian O’Neill, MD
Khaldoon Alaswad, MD, FSCAI 19.4 Unloading the LV When Using ECMO...............................................381
Allison G. Dupont, MD, FACC, FSCAI
15.2 Transseptal Access...............................................................................248
Jason J. Grady, NRP
Elliott M. Groves, MD, MEng, FACC, FSCAI
Charlie Nix, RN
15.3 Troubleshooting TandemHeart® Complications..............................255
19.5 Weaning and Decannulation of VV and VA ECMO.........................387
Katrine A. Zhiroff, MD, FSCAI
Ginger Jiang, MD
16 ECMO Overview............................................................................................262
A. Reshad Garan, MD, MS
16.1 ECMO Program Development.............................................................263 19.6 ECMO Access Site Closure: OR, Cath Lab, Bedside........................395
Eric M. Gnall, DO, FACC Araba Ofosu-Somuah, MD
16.2 ECMO Approved Devices.....................................................................270 Mehul Desai, MD
Donald Quimby Jr., MD Ramesh Singh, MD
Nick Martini, CCP
Hiram Grando Bezerra, MD, PhD SECTION 4 Selecting Devices and Device Combinations
16.3 VA vs VV ECMO: Why, When and How?..........................................275 Based on Clinical Need 406
Christopher M. Fernandez, MD, MHS
20 AMICS/Post PCI Shock.................................................................................407
Sandeep Nathan, MD, MSc
Manu Kaushik, MD
17 VA ECMO........................................................................................................287
21 Isolated RV Support: Impella RP® and TandemHeart®..........................417
17.1 Introduction to VA ECMO................................................................... 288
Mario Gramegna, MD
Siddharth Sarangi, MD
Alessandro Beneduce, MD
John M. Lasala, MD, PhD, FACC, FSCAI
Anna Mara Scandroglio, MD
Akinobu Itoh, MD, PhD
Alaide Chieffo, MD
17.2 Common Access Strategies for VA ECMO.......................................297
22 Biventricular Support Without ECMO .....................................................425
Rami Zein, DO
Kathryn Dawson, MD
Chirdeep Patel, MD, FSCAI
Kathleen Kearney, MD, FSCAI
Theodore L. Schreiber, MD, FSCAI
23 Weaning of Mechanical Circulatory Support...........................................431
Amir Kaki, MD, FACC, FSCAI
Waqas Ghumman, MD
17.3 LAVA ECMO...........................................................................................307
24 MCS Considerations in Acute Myocarditis, Chronic Decompensated HF,
Marvin Eng, MD, FACC, FSCAI
and AMI Cardiogenic Shock
17.4 Common VA ECMO Management Issues..........................................314 Nathan W. Kong, MD
Ranya Sweis, MD, MS, FACC, FSCAI Viktoriya Kagan, APN-BC
Duc Thinh Pham, MD, FACS John E. A. Blair, MD
18 VV ECMO........................................................................................................324
18.1 Introduction to VV ECMO....................................................................325 SECTION 5 Future Innovations 444
Anthony J. Faugno, MD
Haval Chweich, MD 25 Mechanical Circulatory Support Innovations and
Future Directions...........................................................................................445
Navin K. Kapur, MD, FSCAI
Morgan H. Randall, MD, FSCAI
18.2 Common Access Strategies: 2-site vs 1-site Peripheral Access..330
Ki Park, MD, MS, FSCAI
Rajiv Tayal MD, MPH, FSCAI
Duane S. Pinto, MD, MPH, FSCAI
Jagpreet Grewal, MD
18.3 ECMO Daily Management....................................................................336
James Lantry III, MD
Mehul Desai, MD
Erik Osborn, MD
Araba Ofosu-Somuah, MD
Theresa Ganoe, ACNP-BC

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 SECTION 1: Introduction to Cardiogenic Shock and Therapies NEXT SECTION

SECTION 1

Introduction
to Cardiogenic
Shock and
Therapies

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

1
Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

Cardiogenic
Shock Overview
Mir Babar Basir, DO, FACC, FSCAI
Director of Acute Mechanical Circulatory Support
Henry Ford Hospital, Division of Cardiology
Detroit, MI
mbasir1@[Link]
@Babar_Basir

William W. O’Neill, MD, FACC, MSCAI

Director of Center for Structural Heart Disease
Henry Ford Hospital, Division of Cardiology
Detroit, MI
woneill1@[Link]
@BillOneillMD

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

 Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

Definition and etiologies

Cardiogenic shock (CS) is a state of low cardiac output failure which can result in end-organ hypoperfusion
and hypoxia. Table 1 lists the most common etiologies and phenotypes of cardiogenic shock.

Table 1. Etiology of Cardiogenic Shock and Common Shock Phenotypes

COMMON SHOCK ETIOLOGIES SHOCK PHENOTYPES

Decompensated heart failure Acute vs chronic

Acute myocardial infarction Univentricular vs biventricular

Valvular disease Congested vs uncongested

Myocarditis

Pulmonary embolism

Pericardial disease

Arrhythmia

Cardiomyopathies

Iatrogenic

Once pump failure ensues, a cascade of neurohormonal and inflammatory changes occurs, often
resulting in systemic inflammatory response syndrome (SIRS). If cardiogenic shock progresses into
metabolic shock, it often becomes challenging to treat despite aggressive therapies. Therefore, prompt
recognition and treatment are paramount (Table 2).

Table 2. Diagnosis of Cardiogenic Shock

PHYSICAL EXAMINATION DIAGNOSTIC & LABORATORY HEMODYNAMICS

• Altered mentation • Lactate • Bradycardia, tachycardia

• Oliguria / anuria • Cardiac markers • Hypotension, severe hypertension

• Decreased breath sounds / • Renal function / electrolytes / liver • Cardiac power output / index
crackles function
• Cardiac output / index
• Delayed capillary refill / cool • Complete blood count /
extremities coagulation / type and cross • Filling pressures

• Orthopnea • LDH / haptoglobin / fibrinogen • Right atrial to pulmonary capillary

wedge ratio
• Elevated jugular venous pressure • Electrocardiogram
• Pulmonary pulsatility index
• Murmur • Echocardiogram
• Right ventricular stroke work
• Edema • Invasive testing / monitoring index

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 3

 Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

Cardiogenic shock has historically been defined as the presence of sustained hypotension, often
requiring the use of vasopressors and inotropes, along with clinical manifestations of end organ
hypoperfusion. More recently the SCAI Shock Classification1 (Figure 1) has been adopted as a simple
and predictive classification system which can be easily utilized clinically and academically.

STAGE E: A patient with refractory shock or actual/impending

E
circulatory collapse.
EXTREMIS
STAGE D: A patient who has clinical evidence of shock that

D
worsens or fails to improve despite escalation of therapy.
DETERIORATING
STAGE C: A patient who has clinical evidence of

C
hypoperfusion that initially requires pharmacologic or
CLASSIC mechanical support. Hypotension is usually present.

STAGE B: A patient who has clinical evidence of

B
hemodynamic instability (including hypotension,
BEGINNING tachycardia, or abnormal systemic
hemodynamics) without hypoperfusion.

STAGE A: A patient who is hemodynamically

A
stable and is NOT experiencing signs or
AT RISK symptoms of cardiogenic shock, but is at
risk for its development (ie, large AMI or
decompensated heart failure).

STAGE
Figure 1. SCAI Shock Classification1

Pathophysiology
Left ventricular (LV) failure is commonly caused by decreasing LV compliance, increasing LV end
diastolic pressure, LV dilatation, and reduced systolic function. Commonly, there is development of
compensatory tachycardia in an effort to maintain cardiac output, as well as activation of the renin
angiotensin system and release of catecholamines, which results in sodium retention and peripheral
vasoconstriction. These changes help to improve cardiac output temporarily but often lead to coronary
and peripheral hypoperfusion, resulting in worsening cardiogenic shock.

Similarly, right ventricular (RV) failure is commonly caused by decreasing RV compliance that results in
RV dilatation and peripheral congestion. RV dilatation results in bowing of the interventricular septum,
decreasing LV compliance and function. RV failure also leads to inadequate filling of the LV resulting in a
reduced cardiac output (Figure 2).

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 4

 Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

Acute cardiac event

or
Decompensation of
LV dysfunction prior heart failure RV dysfunction

LV compliance RV compliance
Contractility RV dilatation
Septal shift
LV preload

Stroke volume
Cardiac output Congestion

RAAS activation
Neurohormonal cascade Systemic
Catecholamine SIRS inflammation
release
Pathologic
Vasoconstriction vasodilatation
Sodium
retention

End-organ failure
Death

Figure 2. Pathophysiology of Cardiogenic Shock

Incidence
CS secondary to AMI complicates 5-10% of AMI cases and is more common in patients presenting with
STEMI, women, and those ≥75 years old. Isolated RV infarction leading to CS is rare and occurs in 3-5%
of patients, while biventricular shock occurs in 30-50% of patient in CS.

There is an increased incidence of CS that is likely due to a combination of effects including improved access
to healthcare, greater recognition of CS, and an increasingly elderly patient population (Figure 3). Patients are
more likely to present with comorbid conditions and with higher acuity. These patients have longer hospital
length of stays, increased resource utilization, and higher readmission rates. These factors have led to the
growing incidence of CS secondary to etiologies other than acute myocardial infarction (AMI).

500
CARDIOGENIC SHOCK PER 100,000 HOSPITALIZATIONS

400 CS

300
CS (non-AMI)

200

100 CS (AMI)

0
2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018
YEAR

Figure 3. Incidence of Cardiogenic Shock (adapted from Osman et al.2)

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 5

 Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

Morbidity and mortality

CS has been associated with significant morbidity and mortality and despite advances in treatment strategies,
CS remains a significant priority for cardiovascular clinicians. Prior to the advent of early revascularization using
percutaneous coronary intervention (PCI), mortality rates for CS secondary to an AMI were 70-80%. With
the development of STEMI systems of care, mortality has decreased to 40-50% (Figure 4). CS secondary to
decompensated chronic heart failure portends a better prognosis (mortality ~20%). Numerous studies have
validated the increasing mortality associated with increasing SCAI shock stage.

100%

80%

60%

40%

20%

0%
1970 1980 1990 2000 2010 2020

Figure 4. Mortality in Acute Myocardial Infarction and Cardiogenic Shock

The future of cardiogenic shock care

Given the high morbidity and mortality associated with CS, an emphasis on understanding the pathophysiology
and development of new treatment protocols has led to an evolution in the care for this high-risk group of
patients. There has been great growth and uptake in the use of advanced mechanical circulatory support
devices within the past decade (Figure 5). In the past, use of these devices was limited by paucity of data,
limited by the types of available devices, andesd largely delegated to surgeons. Recently, however, there has
been a diffusion of shock care to a multidisciplinary team approach, involving interventional, heart failure, and
critical care cardiologists. Accessibility to smaller, more mobile percutaneous ventricular assist devices (pVAD)
has allowed for shock care to be less confined to academic centers and more accessible to community-based
programs throughout the country.

16 pVAD (ICM)

14

12
% UTILIZATION

10
pVAD (NICM)
8

4
ECMO (ICM)
2 ECMO (NICM)

0
2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018
YEAR
ECMO=extracorporeal membrane oxygenation; ICM=ischemic cardiomyopathy; NICM=nonischemic cardiomyopathy; pVAD=percutaneous ventricular assist device

Figure 5. Utilization of Mechanical Circulatory Support in Cardiogenic Shock (adapted from Lemor et al.3)

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 6

 Chapter 1: Cardiogenic Shock Overview NEXT CHAPTER

There remain, however, challenges ahead. Enrolling patients into CS randomized control trials has
been challenging as patients typically present critically ill, requiring rapid delivery of care, and are
often incapacitated and unable to consent for studies. In the past 15 years only ~2000 patients have
been enrolled into CS trials. As more clinicians and hospitals treat CS, we must prioritize research and
standardize quality of care in an effort to improve outcomes.

References
1. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update: a review
and incorporation of validation studies. Journal of the Society for Cardiovascular Angiography & Interventions.
2022;1(1):100008. [Link]

2. Osman M, Syed M, Patibandla S, et al. Fifteen-year trends in incidence of cardiogenic shock hospitalization and in-
hospital mortality in the United States. J Am Heart Assoc. 2021;10(15):e021061. doi: 10.1161/JAHA.121.021061.
Epub 2021 Jul 28. PMID: 34315234; PMCID: PMC8475696.

3. Lemor A, Hosseini Dehkordi SH, Alrayes H, et al. Outcomes, temporal trends, and resource utilization in ischemic
versus nonischemic cardiogenic shock. Crit Pathw Cardiol. 2022;21(1):11-7. doi: 10.1097/HPC.0000000000000272.
PMID: 34907938.

4. Megaly M, Buda K, Alaswad K, et al. Comparative analysis of patient characteristics in cardiogenic shock
studies: differences between trials and registries. JACC Cardiovasc Interv. 2022;15(3):297-304. doi: 10.1016/j.
jcin.2021.11.036. PMID: 35144785.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 7

2
PREVIOUS CHAPTER Chapter 2: Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction: NEXT CHAPTER
Unraveling the Differences Between the Phenotypes

Cardiogenic Shock in
Heart Failure versus
Acute Myocardial
Infarction: Unraveling
the Differences Between
the Phenotypes
Ilan Vavilin, MD Ahmad A. Abdul-Aziz, MD
Chief Cardiovascular Disease Fellow Advanced Heart Failure/Transplant
Inova Schar Heart and Vascular and Critical Care Cardiologist
Inova Fairfax Medical Campus Inova Schar Heart and Vascular
Falls Church, VA Inova Fairfax Medical Campus
[Link]@[Link] Falls Church, VA
[Link]-Aziz@[Link]
Ran Lee, MD
Advanced Heart Failure/Transplant and
Critical Care Cardiologist
Heart and Vascular and Thoracic Institute
Cleveland Clinic Foundation
Cleveland, OH
LeeR2@[Link]

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

PREVIOUS CHAPTER Chapter 2: Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction: NEXT CHAPTER
Unraveling the Differences Between the Phenotypes

Introduction
Cardiogenic shock is a clinical condition that despite medical advances continues to carry approximately
40-60% associated morbidity and mortality. It is a complex and heterogenous clinical syndrome with
multiple etiologies. Consequently, proper identification of the etiology and phenotype is critical to tailor
the management for each patient with cardiogenic shock. In this chapter, we focus on the most common
etiologies of cardiogenic shock, acute decompensated heart failure (HF-CS) and acute myocardial
infarction (AMI-CS).

ACUTE MYOCARDIAL HEART FAILURE

INFARCTION CARDIOGENIC SHOCK
CARDIOGENIC SHOCK

• Older age • Younger age

• More comorbid conditions • Larger LV cavity size
• Normal LV cavity size • Hypotension • Lower LV ejection fraction
• Higher LV ejection fraction • Hypoperfusion • Pre-emptively prescribed heart
• Higher cardiac output and failure guideline directed
• High readmission medical therapy
index rates
• Higher use of temporary • Lower cardiac output and index
• High risk of
mechanical circulatory MACCE • Higher use of durable
support mechanical circulatory support
• Higher 1-year mortality • Higher rates of cardiac
transplantation
• Longer lengths of stay
• Lower 1-year mortality

Figure 1. AMI-CS and HF-CS

Cardiogenic shock due to acute decompensated heart failure

The classic trial definition of cardiogenic shock includes a systolic blood pressure (SBP) <90 mmHg
for ≥30 minutes, a cardiac index (CI) ≤2.2 L/min/m2, pulmonary capillary wedge pressure (PCWP)
≥15 mmHg, and markers of end-organ hypoperfusion. This definition has been used in clinical trials
associated with AMI-CS. The clinical assessment of HF-CS may be challenging. Patients with HF-
CS typically present with abnormalities representing congestion rather than hypotension. As such,
hypotension may be absent in patients with HF-CS who may have the ability to compensate with higher
vascular resistance. In an International Society for Heart and Lung Transplantation (ISHLT) consensus
statement,1 HF-CS was defined as circulatory failure attributable to cardiac dysfunction that results in
abnormal tissue perfusion.

In a large single center study,2 in-hospital and 1-year outcomes were compared among patients
presenting with HF-CS and AMI-CS. There were several substantial differences in the age, clinical
presentation, hemodynamics, vasopressor requirements, MCS choices, and clinical course. Patients with
HF-CS were younger with lower rates of cardiac arrest, lower ejection fraction on presentation, higher
PCWP, and a lower cardiac power output (CPO). Rates of vasopressor use were lower in the HF-CS
population. However, patients with HF-CS had higher utilization of durable mechanical circulatory
support (MCS), heart transplantation, and longer lengths of stay.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 9

PREVIOUS CHAPTER Chapter 2: Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction: NEXT CHAPTER
Unraveling the Differences Between the Phenotypes

Patients presenting with HF-CS should have early assessment of invasive hemodynamics with
pulmonary artery catheters to guide therapy. Inotropic and vasopressor support remain the first
line therapy options for the initial management of HF-CS. For patients presenting with advanced
stages of CS (SCAI C-E), temporary MCS should be considered early. Furthermore, any reversible
conditions contributing to the shock state (eg, tachyarrhythmias, acute valvular pathology) should be
identified and addressed as early as possible. Many patients with HF-CS have a longstanding history
of cardiomyopathies with a low likelihood of recovery; therefore, candidacy for advanced heart failure
therapies should be considered early to help guide the appropriateness of temporary MCS. If advanced
heart failure therapies are not available at the treating institution, early referral to a ventricular assist
device (VAD) or transplant capable hospital should be pursued.

There is a paucity of data for management of HF-CS. As such, most treatment algorithms reflect current
best practices (Figure 2). The choice of therapies should be tailored to the etiology and degree of CS as
well as the availability of therapeutic options at the treating facility.

Figure 2. HF-Cardiogenic Shock Management

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 10

PREVIOUS CHAPTER Chapter 2: Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction: NEXT CHAPTER
Unraveling the Differences Between the Phenotypes

Cardiogenic shock in the setting of acute myocardial infarction

AMI-CS is triggered by an acute epicardial coronary artery obstruction due to plaque rupture and ensuing
thrombosis, spontaneous coronary artery dissection, and less commonly embolization resulting in
ischemia. This abrupt cessation of blood flow leads to infarction of myocardium which results in multiple
hemodynamic derangements including reduction in cardiac output, elevation of intracardiac filling
pressures, and reflex sympathetic activation resulting in systemic vasoconstriction and increased afterload.

Patients with AMI-CS are older and have more comorbid conditions. LV cavity size tends to be normal,
and these patients have higher ejection fractions at presentation. There is also a greater use of
temporary MCS in the AMI-CS population (Figure 3).

The fundamental treatment approach to AMI-CS is early revascularization. The SHOCK trial in addition
to multiple other studies demonstrated that early revascularization leads in a reduction in all-cause
mortality. Studies suggest that early stabilization with temporary mechanical support within the first
1.25 hours of shock onset yields greater survival rates. Up to 80% of patients with AMI-CS will present
with multivessel coronary artery disease. The CULPRIT-SHOCK trial demonstrated a 17% absolute
reduction in the primary endpoint of 30-day death or renal replacement therapy with culprit-vessel
percutaneous coronary intervention (PCI). Considering this trial, both the US and European guidelines
have given a class III recommendation for the practice of ad-hoc multivessel PCI in AMI-CS. Patients
with AMI-CS have a greater likelihood of presenting with univentricular failure. The DanGer Shock trial3
demonstrated that the routine use of a microaxial flow pump in a carefully selected patient population
with ST-elevation MI (STEMI) led to a lower risk of death from any cause at 180 days compared to
standard care alone. Biventricular support should be strongly considered for AMI-CS presenting with
severe biventricular failure or SCAI stage E cardiogenic shock.

Figure 3. AMI-Cardiogenic Shock Management

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 11

PREVIOUS CHAPTER Chapter 2: Cardiogenic Shock in Heart Failure versus Acute Myocardial Infarction: NEXT CHAPTER
Unraveling the Differences Between the Phenotypes

Summary
• Morbidity and mortality from CS remain high. CS is most associated with acute decompensated
heart failure (HF-CS) or acute myocardial infarction (AMI-CS).
• There are several substantial differences in the age, clinical presentation, hemodynamics,
temporary vasopressor and MCS requirements, and clinical course of AMI-CS versus HF-CS.
• The choice of therapies should be tailored to the etiology and degree of CS as well as the
availability of therapeutic options at the treating facility.

References
1. Kanwar MK, Billia F, Randhawa V, et al. Heart failure related cardiogenic shock: An ISHLT consensus conference
content summary. J Heart Lung Transplant. 2024;43(2):189-203. doi: 10.1016/[Link].2023.09.014. Epub 2023 Dec
8. PMID: 38069920.

2. Sinha SS, Rosner CM, Tehrani BN, et al. Cardiogenic shock from heart failure versus acute myocardial infarction:
clinical characteristics, hospital course, and 1-year outcomes. Circ Heart Fail. 2022;15(6):e009279. doi: 10.1161/
CIRCHEARTFAILURE.121.009279. Epub 2022 May 5. PMID: 35510546; PMCID: PMC9286066.

3. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock. N
Engl J Med. 2024;390(15):1382-93. doi: 10.1056/NEJMoa2312572. Epub 2024 Apr 7. PMID: 38587239.

4. Zweck E, Thayer KL, Helgestad OKL, et al. Phenotyping cardiogenic shock. J Am Heart Assoc. 2021;10(14):e020085.
doi: 10.1161/JAHA.120.020085. Epub 2021 Jul 6. PMID: 34227396; PMCID: PMC8483502.

5. Abraham J, Blumer V, Burkhoff D, et al. Heart failure-related cardiogenic shock: pathophysiology, evaluation and
management considerations: review of heart failure-related cardiogenic shock. J Card Fail. 2021;27(10):1126-40. doi:
10.1016/[Link].2021.08.010. PMID: 34625131.

6. Mehta A, Vavilin I, Nguyen AH, et al. Contemporary approach to cardiogenic shock care: a state-of-the-art
review. Front Cardiovasc Med. 2024;11:1354158. doi: 10.3389/fcvm.2024.1354158. PMID: 38545346; PMCID:
PMC10965643.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 12

3
PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

Understanding
Intracardiac
Hemodynamics:
A Refresher on
Interpreting PV
Loops
Michael I. Brener, MD Daniel Burkhoff MD, PhD
Fellow, Cardiovascular Medicine Director, Heart Failure, Hemodynamics,
Division of Cardiology and Circulatory Support Research
Columbia University Medical Center Cardiovascular Research Foundation
New York Presbyterian Hospital Adjunct Associate Professor of Medicine
New York, NY Division of Cardiology
@BrenerMickey Columbia University Medical Center
New York Presbyterian Hospital
New York, NY
@BurkhoffMd

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

Introduction
The events occurring during a single cardiac cycle are portrayed by ventricular pressure-volume (PV)
loops (Figure 1A). Under normal conditions, the PV loop is trapezoidal with a rounded top. The four
sides of the loop denote the cardiac cycles’ four phases:
• Isovolumic contraction
• Ejection
• Isovolumic relaxation
• Filling
The width of the loop represents the stroke volume (SV), while the height of the loop represents the
systolic blood pressure. The area inside the loop is the stroke work (SW) (Figure 1B).

A Normal LV PV Loop
B Increased
125 Ejection 125 Contractility Decreased
Contractility

Ea
100 100
(Ves, Pes)
LV PRESSURE (mmHg)

Systolic
Blood LV PRESSURE (mmHg)
75 Pressure 75 ESPVR
SW
Isovolumetric Isovolumetric
Relaxation Contraction
50 Stroke Volume 50 Increased
Decreased Afterload
Afterload

Ees
EDPVR
25 25

Filling
V0
0 0
0 50 100 150 0 50 100 150
LV VOLUME (mL) LV VOLUME (mL)

C D
125 Baseline 125 Acute HF
Acute HF Chronic HF

100 100
LV PRESSURE (mmHg)

LV PRESSURE (mmHg)

75 75

SVahf SVchf

50 Ees
50
Ees-aHF

25 25

0 0
0 50 100 150 50 100 150 200
LV VOLUME (mL) LV VOLUME (mL)

Figure 1. Pressure-Volume Loops in Normal and Diseased Left Ventricles

(A,B) Aspects of the normal left ventricular (LV) pressure-volume (PV). Note that the PV loop is bound by the end-systolic PV relationship
(ESPVR) and the end-diastolic PV relationship (EDPVR). The ESPVR is reasonably linear, and characterized by the slope Ees, or end-systolic
elastance, and Vo, the unstressed LV volume. In contrast, the EDPVR is non-linear. Afterload is characterized by the effective arterial elastance
line, with slope Ea. (C) Changes in the PV loop with acute heart failure. (D) Consequences of chronic heart failure and ventricular remodeling; while
stroke volume (SV) returns closer to pre-insult ranges, it comes at the expense of marked ventricular dilation.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 14

PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

The loop falls within the boundaries of the end-systolic pressure-volume relationship (ESPVR) and the
end-diastolic pressure-volume relationship (EDPVR). The ESPVR is reasonably linear, with slope Ees
and volume-axis intercept Vo such that ESP = Ees (ESV-Vo) (Figure 1B; ESP = end-systolic pressure, ESV
= end-systolic volume). Vo represents the unstressed volume, which is the volume required to fill the
ventricle before pressure rises. Shifts of the ESPVR occur with changes in ventricular contractility such
that increases in contractility are associated with upward/leftward shifts of the ESPVR (Figure 1B).1, 2

The EDPVR indexes the extent of relaxation and indicates the passive ventricular properties when all
actin-myosin bonds are uncoupled and myocytes are completely relaxed. The EDPVR (Figure 1B) is
nonlinear and can be described by simple equations such as P=β(eα(V-Vo)-1) or P=βVα, where constants
like α and β relate to mechanical properties and structural features of the ventricle and myocardial and
extracellular matrix mechanical properties. Shifts of the EDPVR can occur in pathological states such as
hypertrophic cardiomyopathy and infiltrative diseases (leftward shifts indicative of diastolic dysfunction)
or in all forms of dilated cardiomyopathy (rightward shifts indicative of remodeling).

Ventricular preload, at the organ level, can be defined as either the end-diastolic pressure (EDP) or the
end-diastolic volume (EDV), which relate to average sarcomere stretch throughout the myocardium.

Ventricular afterload is determined by the hemodynamic properties of the vascular system against
which the ventricle contracts and is commonly indexed by total peripheral resistance (TPR). Afterload
can also be depicted on the pressure-volume diagram by the “effective arterial elastance” (Ea) line
(Figure 1B).3 The Ea line starts on the volume axis at the EDV and intersects the ESPVR at the
ventricular end-systolic pressure-volume point of the PV loop. When TPR, HR, or preload change, the
Ea line rotates and/or shifts so that its intersection with the ESPVR occurs at a different point, thus
indicating how pressure generation and stroke volume will vary in response to such changes.

In addition to providing a platform for explaining ventricular mechanics, the pressure-volume diagram
also provides a construct for understanding the determinants of myocardial oxygen consumption
(MVO2).4 MVO2 per beat is linearly related to the ventricular pressure-volume area (PVA), which is the
sum of the SW and the potential energy (PE). PE is the area bound by the ESPVR, the EDPVR, and the
diastolic portion of the PV loop and represents the residual energy stored in the myofilaments at the end
of systole that was not converted to external work.

PV loop derangements
The PV loop can be particularly helpful for depicting and characterizing the pathophysiology of various
cardiovascular pathologies. Compared to normal, in the immediate aftermath of a myocardial infarction,
for example, the ESPVR shifts downward and rightward, signifying the abrupt reduction of ventricular
contractility (Figure 1C). This reduction is accompanied by a decline in systolic blood pressure (indexed
by the height of the PV loop), SV, and cardiac output (CO), while small elevations of LVEDP and
pulmonary capillary wedge pressure (PCWP) may also be seen.

Over time, the LV remodels and undergoes a geometric transformation as a consequence of physical
forces exerted by elevated LV end-diastolic pressures and constantly heightened adrenergic tone
and other neurohormonal derangements occurring after the acute insult. These mechanisms result in
rightward shifts of the EDPVR toward larger volumes as surviving myocytes hypertrophy (elongate and
widen) and as extracellular matrix turnover increases, allowing reorganization of myocytes. Shifts of the
EDPVR also result in concomitant rightward shifts of the ESPVR, signifying worsening of LV systolic
function (Figure 1D).

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 15

PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

PV loops with inotropes

Dobutamine and milrinone, the two most
frequently used inodilators, increase LV contractility
(signaled on the PV diagram by a leftward shift
of the ESPVR), reduce arterial resistance, and
increased HR. Collectively, these measures increase
SV, causing the PV loop to become wider, and
also increase SW, as the area encapsulated by
the PV loop expands (Figure 2). However, the net
effect on blood pressure (ie, the height of the PV
loop) is difficult to predict since this will depend
on the balance between increases in contractility
and decreases in TPR. The LV is also typically
unloaded to some degree with inotropes, reflected
Figure 2. PV Loops with inotropes
by a leftward shift of the PV loop along the EDPVR
(Click image to see animation)
toward lower EDP and EDV.

PV loops with IABP

The intra-aortic balloon pump (IABP) remains
the most commonly used form of percutaneous
mechanical circulatory support. The device features
a balloon-tipped catheter that inflates during diastole
and deflates during systole to promote coronary
blood flow during diastole and reduce afterload
such that resistance to systemic blood flow during
systole is minimized. These effects, particularly the
latter aspect of counterpulsation, drive the PV loop
leftwards along the EDPVR (Figure 3). SV increases
slightly while peak systolic pressure falls. However,
the overall PV loop does not change dramatically,
especially when the pumping ratio falls below 1:1.
Figure 3. PV Loops with IABP
That being said, the effect on coronary perfusion may (Click image to see animation)
be the key factor driving its hemodynamic benefits
and perceived clinical benefits, which cannot be
readily depicted in the PV diagram.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 16

PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

PV loops with Impella®

The impact of LV-to-aorta pumping on the PV loop
is illustrated in Figure 4 with different Impella flow
rates. Since these devices pump blood continuously
out of the LV into the aorta independent of the
phase of the cardiac cycle, there is loss of isovolumic
contraction and isovolumic relaxation phases; the
loop transforms from a more or less rectangular
shape shown in Figure 1 toward a more triangular
shape, with the degree of triangulation dependent
on Impella flow rate. Also, as pumping speed is
increased, there is a progressively greater leftward
shift of the loop toward lower ventricular EDV and
EDP, corresponding with progressively smaller
PVA and, therefore, progressively lower levels of
Figure 4. PV Loops with Impella®
myocardial oxygen demand.
(Click image to see animation)

PV loops with TandemHeart®

Temporary left atrial (LA)-to-arterial mechanical
circulatory support (MCS) can be achieved with
extracorporeal devices such as TandemHeart,
which has a flow capacity up to ~5 L/min. The site
of blood return is typically one or both femoral
arteries for the percutaneous approach. Given
that blood is withdrawn directly from the LA,
PCWP and LVEDP decrease dramatically. The LV
is progressively unloaded as blood is withdrawn
from the LA, but the concomitant increase in
arterial blood pressure that occurs with arterial
re-infusion results in a narrow SV (Figure 5). PVA
and MVO2 both decline, albeit to variable degrees, Figure 5. PV Loops with TandemHeart®
with increasing levels of flow through the LA-to- (Click image to see animation)
arterial pump.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 17

PREVIOUS CHAPTER Chapter 3: Understanding Intracardiac Hemodynamics: A Refresher on Interpreting PV Loops NEXT CHAPTER

PV loops with ECMO

Extracorporeal membrane oxygenation (ECMO)
utilizes a pump that has the capacity to assume
responsibility for the entire CO and a gas exchange
unit for normalizing arterial gas composition and pH.
However, strictly on a hemodynamic basis, the use
of this configuration, which pumps blood from the
right atrium (or central vein) to the arterial system,
increases arterial pressure and can, consequently,
cause significant increases in LF preload. This effect
is illustrated in Figure 6, which depicts changes in
the PV loop at different ECMO flow rates. The PV
loop shifts rightward and upward along the EDPVR.
Consequently, LVEDP, LA pressure, and PCWP Figure 6. PV Loops with ECMO
can increase. Since the EDPVR is nonlinear, large (Click image to see animation)
increases in LVEDP may cause only subtle (clinically
undetectable) increases in LV dimensions and
volumes. These increases in LV preload and PCWP
can be detrimental to blood oxygen saturation and
markedly increase myocardial oxygen demand as
indexed by the increase in PVA. These factors can
paradoxically worsen LV function, especially in the
setting of acute myocardial ischemia or infarction.

References
1. Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties via pressure-volume analysis:
a guide for clinical, translational, and basic researchers. Am J Physiol Heart Circ Physiol. 2005;289(2):H501-12.

2. Sagawa K. The end-systolic pressure-volume relation of the ventricle: definition, modifications and clinical use.
Circulation. 1981;63(6):1223-7.

3. Brener MI, Burkhoff D, Sunagawa K. Effective arterial elastance in the pulmonary arterial circulation: derivation,
assumptions, and clinical applications. Circ Heart Fail. 2020;13(3):e006591.

4. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support. J Am Coll Cardiol.
2015;66(23):2663-74.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 18

4
3
PREVIOUS CHAPTER Chapter 4: Cardiogenic Shock Terminology and Metrics Explained NEXT CHAPTER

Cardiogenic
Shock
Terminology and
Metrics Explained
Jaya Mallidi, MD, MHS, FSCAI
Interventional Cardiologist
St. Joseph Cardiology Medical Group
Santa Rosa, CA
[Link]@[Link]
@JayaMallidi

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

PREVIOUS CHAPTER Chapter 4: Cardiogenic Shock Terminology and Metrics Explained NEXT CHAPTER

Introduction
A generally accepted definition of cardiogenic shock (CS) is a state of reduced cardiac output (CO) due
to a primary cardiac pathology resulting in clinical and biochemical manifestations of inadequate end-
organ perfusion.1 In clinical practice, patients with CS have a heterogenous presentation. Hence, to date,
the definitions used in various clinical trials and registries are varied to include different combinations
of clinical, hemodynamic, and metabolic profiles. The keys to early identification and subsequent
management strategies lie in understanding this heterogeneity as a continuum in the spectrum of CS.
Having a common shared language to describe this heterogeneity helps us communicate the clinical status
of our patients in everyday practice without ambiguity. This chapter describes the terminology and metrics
used to define and describe this heterogeneity among CS patients as well as proposed process-driven
metrics to help in implementation of standardized quality initiatives to improve outcomes.

Stages and classification of cardiogenic shock

The SCAI and CSWG Expert Clinical Consensus Statement on Classification of Cardiogenic Shock2
describes 5 stages—A through E—of cardiogenic shock. The Cardiogenic Shock Working Group
(CSWG) provides additional insights on classifying shock.3 Figure 1 combines both the SCAI and CSWG
shock descriptions.

EXTREMIS E
STAGE E: Circulatory collapse with ongoing CPR, including ECMO assisted CPR
Metrics: Imminent death with zero SBP, no CO without ongoing aggressive interventions

D
STAGE D: Failure to stabilize despite treatment

DETERIORATING Metrics: Persistently low SBP / MAP, worsening lactate, renal function, and CI
despite treatment, often needing escalation of support with 2-5 devices or drugs

C
STAGE C: Hypotension + hypoperfusion

CLASSIC Metrics: SBP <90 mmHg or MAP <60 mmHg, needing intervention
with 1 drug or device to maintain above this target, elevated lactate,
BNP, creatinine, PCWP >15 mmHg, and CI <2.2 L/min/m2

STAGE B: Hypoperfusion OR hypotension

BEGINNING B Metrics: Marker of hypoperfusion – elevated lactate,

impaired renal function, elevated BNP, PCWP >15 mmHg OR
Marker of hypotension – SBP <90 mmHg or >30 mmHg drop
from baseline

A
STAGE A: Hemodynamically stable, with no

AT RISK hypotension or hypoperfusion

Metrics: Normal vital signs, hemodynamics, and labs

STAG E
Figure 1. SCAI Cardiogenic Shock Classification Pyramid (adapted from SCAI Consensus Document on
Classification of Cardiogenic Shock2 and Cardiogenic Shock Working Group8)
Abbreviations: CPR–cardiopulmonary resuscitation; ECMO–extracorporeal membrane oxygenation; SBP–systolic blood pressure; MAP–mean
arterial pressure; CI–cardiac index; PCWP–pulmonary capillary wedge pressure; BNP–brain natriuretic peptide

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Hemodynamic phenotypes
Based on invasive hemodynamic measurements — cardiac output (CO), cardiac index (CI), systemic
vascular resistance (SVR), and pulmonary capillary wedge pressure (PCWP) representing volume status
(wet vs. dry) and peripheral perfusion (cold vs. warm) — Table 1 describes the different phenotypes of
CS.1 In all phenotypes, CO and CI are reduced. Additionally, in right ventricular (RV) shock, the central
venous pressure (CVP) or right atrial pressure (RAP) is significantly elevated, with the ratio of CVP
to PCWP≥0.8.1 Pulmonary artery pulsatility index (PAPi) <0.9, also correlates highly with severe RV
dysfunction or RV shock in acute myocardial infarction.4 Table 2 explains calculation of PAPi.

Table 1. Hemodynamic Phenotypes of Cardiogenic Shock

HEMODYNAMIC TYPE CO SVR PCWP

Classic CS:
Cold and Wet
ò ñ ñ
Euvolemic CS:
Cold and Dry
ò ñ ó
Vasodilatory CS / Mixed shock:
Warm and Wet
ò ó ñ
Right ventricular (RV) shock ò ó ó
Abbreviations: CO–cardiac output; SVR–systemic vascular resistance; PCWP–pulmonary capillary wedge pressure. Definitions and normal values
of these metrics explained in Table 2.

Patient-related metrics in cardiogenic shock

There are several patient-related metrics or measurements that should be monitored either continuously
or at specific frequency intervals in CS patients to enable the clinician to determine the clinical stage of
CS1 and hemodynamic phenotype, as well as tailor treatment by escalation or de-escalation of inotropic
and vasopressor agents and mechanical circulatory support. Table 2 explains these patient-related
metrics.

All patients with CS—stages A through E—require continuous measurement of noninvasive metrics.
Invasive metrics obtained through right heart catheterization can be reserved for patients in stages C
and D, as can more frequent checking of laboratory parameters such as lactate to assess hypoperfusion.
Careful monitoring and interpretation of noninvasive and invasive laboratory metrics during stages C
and D is critical to avoid deterioration to stage E of CS.

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Table 2. Patient-related Metrics in Cardiogenic Shock

MONITORING
METRIC CARDIOGENIC SHOCK CONSIDERATIONS
FREQUENCY

NON-INVASIVE METRICS

Continuous • Continuous monitoring needed in

Telemetry
intensive care unit given the high risk of
Pulse oximetry life-threatening arrhythmias, respiratory
Respiratory rate failure with pulmonary edema, and end
Urine output organ failure manifested early on as renal
dysfunction with reduced urine output

INVASIVE HEMODYNAMIC METRICS

Mean arterial blood pressure (MAP) Continuous • Continuous monitoring with invasive
with invasive arterial line is needed until patient weaned
• MAP = [systolic blood pressure + (2 x diastolic arterial line from all pharmacologic and mechanical
blood pressure)] /3 support

• In CS, inotropes, vasopressors, and/or

mechanical circulatory support (MCS)
devices are needed to maintain a MAP>60-
65 mmHg

Continuous • Significantly elevated in right ventricular

Central venous pressure (CVP)
shock

METRICS FROM RIGHT HEART CATHETERIZATION / INDWELLING SWAN-GANZ CATHETER

Pulmonary capillary wedge pressure (PCWP) Selectively as • In CS patients, PCWP is elevated at

needed >18 mmHg
• Indirect measure of left atrial pressure

• Measured by inserting a catheter into a small

pulmonary artery branch and wedging the catheter
by inflating the balloon at its tip

• Normal PCWP = 6-12 mmHg

Cardiac output (CO) Every 4-6 • Reduced CO is the hallmark of CS

hours
• Amount of blood ejected from the ventricle in
1 minute

• CO = heart rate x stroke volume

• Normal CO = 4-8 liters/minute

Cardiac index (CI) Every 4-6 • CS is defined as CI < 2.2 L/min/m2

hours
• CI = CO / BSA

• Normal CI = 2.5-4 L/min/m2

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MONITORING
METRIC CARDIOGENIC SHOCK CONSIDERATIONS
FREQUENCY

Cardiac power output (CPO) Every 4-6 • In CS, CPO is less than 0.6 watts
hours
• Pumping ability or hydraulic energy of the heart to
maintain circulation5

• CPO = [MAP (pressure) x CO (flow)] / 451 (in watts)

• Normal CPO at rest = 1 watt

Cardiac power index (CPI) Every 4-6 • In CS, CPI is less than 0.33 watts/m2
hours
• Pumping ability, or hydraulic energy, of the heart to
maintain circulation indexed to body surface area5

• CPI = [MAP (pressure) x CI (flow)] / 451 (in watts/m2)

• Normal CPI = 0.5-0.7 watts/m2

Pulmonary artery pulsatility index (PAPi) Every 4-6 In cardiogenic shock:

hours • If CPO>0.6 and PAPi>0.9, consider
• Hemodynamic metric that evaluates right
ventricular function weaning support6

• PAPi = (pulmonary artery systolic pressure – • If CPO<0.6 and PAPi>0.9, consider

pulmonary artery diastolic pressure) / right atrial escalation of hemodynamic support6
pressure4 • If CPO< 0.6 and PAPi <0.9, consider right
sided hemodynamic support6

Systemic vascular resistance (SVR) Every 4-6 • In CS, SVR is usually increased
hours
• Quantitative value for left ventricular afterload • When vasoplegia sets in, SVR can
normalize or become low
• SVR = (MAP – RAP) / CO

• SVR (in Woods units) x 80 = SVR in dynes/sec/cm-5

• Normal SVR values: 900-1400 dynes/sec/cm-5

LABORATORY METRICS

Lactate Every 4-6 • Elevated lactate >3.1 mmol/L after 8

hours hours or lack of lactate clearance on serial
• Elevated serum lactate is a marker of tissue measurements is strongly associated with
hypoperfusion mortality in CS patients7

At index • Elevated BNP is a marker of heart failure in

evaluation CS
Brain natriuretic peptide (BNP)
• Normal or low BNP argues against CS in
the presence of hypotension

Every 12-24 • Together with reduced urine output,

hours elevated serum creatinine is a marker of
Serum creatinine
renal hypoperfusion or acute kidney injury
in CS patients

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MONITORING
METRIC CARDIOGENIC SHOCK CONSIDERATIONS
FREQUENCY

Every 24 • Liver function tests are elevated in

Liver function tests hours CS patients as result of congestive
hepatopathy or hypoperfusion

Every 12-24 • CS patients on MCS, anticoagulation,

hours antiplatelet agents post revascularization
Complete blood count
are at high risk of bleeding; consider more
frequent monitoring if required

Every 12-24 • CS patients are prone to arrhythmias

hours
Serum electrolytes • Frequently check serum electrolytes,
specifically potassium and magnesium, and
replace as necessary

Process-related metrics in CS
To date there are no standardized, society endorsed, or widely adopted system level process metrics
for management of CS, like that of AHA Mission Lifeline STEMI Regional systems of care. Given the
heterogeneity of clinical presentations in CS, and variation in institutional capabilities (eg, non-PCI
capable facility vs. PCI capable facility with no expertise in MCS vs. tertiary shock center), developing
and implementing standardized quality process metrics is a daunting task. Nevertheless, efforts
are being made on various fronts in this direction.1,5,6,8 Figure 2 depicts proposed quality metrics in
CS that could potentially serve as benchmarks for identifying and improving areas of performance.
The proposed metrics shown in Figure 2 are for a tertiary shock center. Depending on the facility’s
capabilities, the metrics may need to be modified to reflect time to identify shock, reperfusion, and
transfer to a tertiary hub.

EMERGENCY ROOM CARDIAC CATH LAB CARDIAC INTENSIVE CARE UNIT

GOAL FOR Coronary angiogram Weaning from pharmacologic
CS PATIENT agents followed by MCS
Reduce 3 Ms: Assess & Classify PCI
Continue to assess for bleeding
• Mortality
MCS (pre /post PCI as needed) complications
• Morbidity Activate multidisciplinary
• Multiorgan shock team RHC (pre /post MCS as needed) TTM in OHCA
dysfunction
Palliative care consultation

CLASSIFICATION DIAGNOSTIC EVALUATION TREATMENT OUTCOMES

Door to identify / classify

Clinically meaningful metrics
across continuum of care:
METRICS

Door to activation of shock team • Survival rate

• Length of hospitalization
Door to reperfusion and unload time with MCS • Morbidity associated with
bleeding complications /
Door to start of TTM in OHCA patients readmission rates

Figure 2. Proposed Process-related Metrics at a Tertiary Shock Hub Center

Abbreviations: PCI–percutaneous coronary intervention; MCS–mechanical circulatory support; RHC–right heart catheterization; TTM–targeted
temperature management; OHCA–outside hospital cardiac arrest

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CLINICAL VIGNETTE
63-year-old male, smoker, with no other known history, brought in by ambulance with
outside hospital cardiac arrest. Patient had a V-fib arrest while driving his car, shocked 3x
in the field. Total code time in the field – 15 minutes. Post return of spontaneous circulation
(ROSC) EKG showed inferior-posterior STEMI.

Emergency room:
• Assess and classify: Patient tachycardic at 110 beats/min, hypotensive with
SBP 60 mmHg without improvement after a bolus. Extensive rales on auscultation
of lung – cardiogenic shock class C
• Activate shock team and cath lab as per institution protocols
• Advanced airway management, start inotropic support and get basic laboratory
metrics; lactate elevated at 5 mmHg

Cath lab:
• Coronary angiogram: LM–normal, LAD–chronic total occlusion, LCX–100%
occlusion, RCA–mid 99%; LVEDP–26 mmHg
• Mechanical circulatory support with Impella CP® via femoral route
• PCI of LCX and RCA performed
• Right heart cath post revascularization; with Impella–CPO>0.6, PAPi>0.9

Cardiac intensive care unit:

• Targeted temperature management (TTM) initiated
• Monitored noninvasive, invasive, and laboratory metrics as described in Table 2
• No bleeding complications
• Weaned off pressors followed by MCS on day 2; good neurological recovery
• Echocardiogram showed EF of 45% on day 5 (improved from 20% on day of
admission)
• Discharged home on day 6

QUICK READ SUMMARY

✓ Accurate clinical assessment, early identification, and classification (A–E) are important
to tailor subsequent management strategy in CS patients.

✓ Several patient-related metrics are measured at initial presentation and at frequent

intervals along the continuum of care in CS to escalate or deescalate therapy as needed.

✓ Process-related metrics in CS are not yet universally standardized.

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References
1. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from
the American Heart Association. Circulation. 2017;136(16):e232-68.

2. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic
shock: this document was endorsed by the American College of Cardiology (ACC), the American Heart Association
(AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019.
Catheter Cardiovasc Interv. 2019;94(1):29-37.

3. Kapur NK, Kanwar M, Sinha SS, et al. Criteria for defining stages of cardiogenic shock severity. J Am Coll Cardiol.
2022;80(3):185-98.

4. Korabathina R, Heffernan KS, Paruchuri V, et al. The pulmonary artery pulsatility index identifies severe right
ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80(4):593-600.

5. Jones TL, Nakamura K, McCabe JM. Cardiogenic shock: evolving definitions and future directions in management.
Open Heart. 2019;6(1):e000960.

6. Basir MB, Kapur NK, Patel K, et al. Improved outcomes associated with the use of shock protocols: updates from the
National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):1173-83.

7. Fuernau G, Desch S, de Waha-Thiele S, et al. Arterial lactate in cardiogenic shock: prognostic value of clearance
versus single values. JACC Cardiovasc Interv. 2020;13(19):2208-16.

8. Henry TD, Tomey MI, Tamis-Holland JE, et al. Invasive management of acute myocardial infarction complicated by
cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2021;143(15):e815-29.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 26

5
PREVIOUS CHAPTER Chapter 5: Hemodynamic Assessment: Right Heart Catheterization NEXT CHAPTER

Hemodynamic
Assessment:
Right Heart
Catheterization
Michael Sumner, DO Ahmed Ghoneem, MD, MSc
Cardiovascular Disease Fellowship Program Cardiovascular Disease Fellowship Program
Baylor Scott and White Health University of Pittsburgh Medical Center
Temple, TX (Harrisburg)
[Link]@[Link] Harrisburg, Pennsylvania
ghoneema@[Link]
Robert J. Widmer, MD, PhD
Director of Cardiac Catheterization Jaime Hernandez-Montfort, MD, MPH, MSc
Laboratory Advanced Heart Disease, Recovery and
Baylor Scott and White Health Replacement Program
Temple, TX Baylor Scott and White Health
[Link]@[Link] Temple, TX
[Link]@[Link]

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

PREVIOUS CHAPTER Chapter 5: Hemodynamic Assessment: Right Heart Catheterization NEXT CHAPTER

Introduction
Cardiogenic shock is a complex and heterogenous disease state. To better differentiate and clearly
communicate, the Society for Cardiovascular Angiography & Interventions (SCAI) developed a classification
of cardiogenic shock incorporating clinical bedside findings, biochemical markers, and hemodynamics.1,2
Both bedside findings and biomarkers are readily available when assessing a patient. Certain hemodynamic
parameters are not readily available without further invasive procedures.3 These parameters are attainable
with a right heart catheterization (RHC) allowing for complete assessment of a patient’s hemodynamics to
further characterize the patient’s cardiogenic shock phenotype and tailor management.4

Contraindications to RHC include infection at the insertion site and presence of temporary or surgical
right ventricular assist device. Potential complications include those related to insertion, maintenance
and (mis-)interpretation of invasive hemodynamic data.5

Structural abnormalities, such as severe RV dilation or severe tricuspid regurgitation (TR), as well as
device leads and artificial valves, can increase the difficulty of RHC. Use of fluoroscopy or a wire can help
navigate the cardiac chambers to overcome these impediments. Right heart catheterization is generally
considered a low-risk procedure, but complications, such as valve and heart wall injury, can occur.

Right heart catheterization basics

When performing a RHC, clinicians obtain access via the internal jugular, subclavian, or femoral vein and
insert a Swan-Ganz catheter through the right atrium, right ventricle, and into the pulmonary artery. Once
in the pulmonary artery, the catheter is advanced until the balloon is “wedged,” creating a closed system
from the pulmonary artery to the left atrium. Different access sites are chosen depending on the clinical
circumstances. The internal jugular vein is considered when patients are in the intensive care unit or
when there is limited access to fluoroscopy; femoral access is considered when patients are in the cardiac
catheterization laboratory and femoral procedures are being concomitantly considered. Access via the
antecubital vein has also been implemented ipsilateral to right radial procedures.6

Fluoroscopy, pressure waveform analysis (Figure 1), or pulmonary capillary wedge saturation is used to
confirm that the catheter is navigated into correct position.7

Figure 1. Pressure Waveform Analysis for RHC

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Hemodynamic data is obtained with multiple methods including direct measurement and serum labs
obtained from the catheter. The catheter is connected to a transducer that measures cardiac chamber
pressures including right atrial pressure (RAP), pulmonary artery systolic pressure (PASP), pulmonary
artery diastolic pressure (PADP), as well as pulmonary capillary wedge pressure (PCWP), which is an
estimate of left atrial pressure. Cardiac output can be obtained with thermodilution or Fick calculation.
Thermodilution entails injecting cold saline into the proximal port of the catheter and measuring the
temperature difference with a thermistor to determine cardiac output. Fick method uses the difference
in the oxygen saturation of the mixed venous oxygen saturation (PA) and arterial oxygen saturation to
determine cardiac output.

Right heart catheterization utility

A right heart catheter does not provide any therapeutic effect; it is a tool that provides hemodynamic
data to complete a hemodynamic assessment including evaluation of loading conditions and right and
left myocardial/valvular performance and interdependence. What is crucial is how the information it
provides is interpreted and used to impact the patient’s outcome. RHC use decreased in the early 2000s
after trials showed no difference in mortality regardless of whether RHCs were used.8 These trials
evaluated heart failure and excluded the cardiogenic shock population. Recent studies have evaluated
registries and assessed patient outcomes utilizing RHCs in cardiogenic shock.9,10

The primary objective of the Pulmonary Artery Catheter in Cardiogenic Shock (PACCS) trial is to
evaluate if early invasive hemodynamic assessment and ongoing management with a RHC in patients
with cardiogenic shock due to acutely decompensated heart failure (ADHF-CS) is associated with lower
mortality risk compared to the current standard of care with no or delayed RHC assessment.11

Cardiogenic shock phenotypes

Cardiogenic shock is fundamentally a term used to describe the heart’s inability to provide adequate
cardiac output to perfuse organs. Cardiogenic shock is heterogeneous and has many different
phenotypes and classifications which makes its evaluation very complex.

Classical description phenotype

The classic description of cardiogenic shock has 2 main axes, congestion and perfusion, with decreased
cardiac output ubiquitous among all types of cardiogenic shock. This allows for creating a 2x2 table to
describe cardiogenic shock phenotypes (Table 1). The first phenotype is characterized as “cold and wet”
with decreased perfusion and congestion. The second phenotype is characterized “cold and dry” with
decreased perfusion without congestion. The third phenotype is “warm and wet” or “mixed” shock with
evidence of relative perfusion with congestion. Differentiating these hemodynamic states with physical
exam and laboratory data alone can be challenging. Right heart catheterization enables differentiation
by assessing cardiac output and right- and left-sided filling pressures, confirming the presence or
absence of congestion, and assessing systemic vascular resistance.

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Table 1. Classic Shock Phenotypes

VOLUME STATUS

WET DRY
PERIPHERAL CIRCULATION

Classic cardiogenic shock Euvolemic cardiogenic shock

COLD

(âCI; áSVRI; áPCWP) (âCI; áSVRI; ßàPCWP)

Vasodilatory cardiogenic shock Vasodilatory shock

WARM

or Mixed shock (Not cardiogenic shock)

(âCI; â/ßàSVRI; áPCWP) (áCI; âSVRI; âPCWP)
CI-cardiac index; PCWP-pulmonary capillary wedge pressure; SVRI-systemic vascular resistance index

Structural phenotypes
Dysfunction of one or both of the heart’s ventricles can dramatically impact cardiac output leading
to cardiogenic shock. Cardiogenic shock can be described as right ventricular, left ventricular, or
biventricular depending on which ventricle(s) are inadequately performing. Many RHC-derived
hemodynamic variables have emerged as strong predictors to help discriminate between right, left, and
biventricular failure. Cardiac power output (CPO) is the pumping ability of the heart and decreased CPO
was shown to be the strongest predictor of mortality in cardiogenic shock (SHOCK Trial). Pulmonary
artery pulsatility index (PAPi) is a composite measure of right ventricular (RV) function and reduced
PAPi is a strong predictor of RV dysfunction.3 Disproportionate elevation in right-sided filling pressures
compared to the left-sided filling pressures (RAP/PCWP) suggests RV dysfunction. Assessment of
ventricular dysfunction using these RHC-derived variables is summarized in Table 2.

Table 2. Using RHC-derived Variables to Assess Ventricular Function and Differentiate Types of Shock12

RV-DOMINANT LV-DOMINANT BIVENTRICULAR

CARDIOGENIC SHOCK CARDIOGENIC SHOCK CARDIOGENIC SHOCK

CPO < 0.6W CPO < 0.6W CPO < 0.6W

PAPi < 1.0 PAPi > 1.0 PAPi < 1.0
RA > 15 mmHg RA < 15 mmHg RA > 15 mmHg
PCWP < 15 mmHg PCWP > 15 mmHg PCWP > 15 mmHg

Table 3. Using RHC-derived Variables to Assess Pulmonary Hypertension (PH)14

PRECAPILLARY PH ISOLATED POSTCAPILLARY PH PRE- AND POSTCAPILLARY PH

mPAP >20 mmHg mPAP >20 mmHg mPAP >20 mmHg

PCWP ≤15 mmHg PCWP >15 mmHg PCWP >15 mmHg
PVR >2 WU PVR ≤2 WU PVR >2 WU

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CARDIAC POWER OUTPUT (CPO)

= (MAP x CO)/451
RA/PCWP RATIO
(N: <0.5) • Reflects hydraulic energy
delivered by the LV
• RA/PCWP > 0.5 à RV • CPO of < 0.6 watt à severe LV
dysfunction in the setting of dysfunction
elevated wedge pressure
• CPO was the strongest
independent hemodynamic
correlate in the SHOCK trial
registry for in-hospital mortality in
patients with cardiogenic shock

PULMONARY ARTERY
PULSATILITY INDEX (PAPi)
SYSTEMIC VASCULAR
= (sPAP – dPAP)/RA
RESISTANCE (SVR)
• PAPi < 0.9 predicts RV failure (N: 800-1200 dynes-sec/cm5)*
and in-hospital mortality in = [(MAP – RAP)/CO] x 80
inferior MI; may consider RV
hemodynamic support • áSVR à cardiogenic shock**,
• PAPi < 1.85 predicts RV failure hypovolemic shock
in patients with LVAD; may • âSVR à distributive shock,
consider RVAD neurogenic shock

* 1 WU = 80 dynes-sec/cm5
** Cardiogenic shock can sometimes have
normal or even low SVR (“warm and
wet” profile)

CARDIAC OUTPUT (CO) (N: 4-8 L/MIN)

THERMODILUTION (TD) FICK
Principle: Washout of a temperature change induced by Principle: Blood flow is proportional to the difference in the
injection of a defined fluid volume cooler than the body concentration of oxygen between arterial and venous blood
temperature. The faster the circulation or flow (ie, cardiac and the rate of oxygen uptake in the lungs.
output), the quicker the neutralization of the temperature
change.

GOLD STANDARD FOR

EASY TO USE MEASURING CO

BUT BUT
• Less accurate in patients with inracardiac shunts • Direct Fick requires specialized equipment to measure
(overestimates CO) or irregular rhythms. oxygen consumption, which is generally not feasible in
Was previously thought to be less accurate in severe TR and
most catheterization laboratories.
extremes of CO. However, several studies have shown good • Indirect Fick (using nomogram-based estimates of oxygen
correlation between TD and direct Fick in severe TR and extremes consumption) can lead to large errors, as much as 40% in
of CO, and TD should be favored in clinical practice (except in cardiac output estimates, compared with the direct Fick.
patients with intracardiac shunts).
• Accuracy also affected by intracardiac shunts.

Both methods are based on the assumption that pulmonary blood flow (PBF) is equal to systemic blood flow (SBF) in the absence of an intracardiac shunt.

CARDIAC INDEX (Cl) (N: 2.5-4 L/min/m2) = CO/BSA

• Cardiogenic shock + Cl < 2.2 usually indicates “cold” profile.
• Bedside clue to a low Cl: the proportional pulse pressure ((SBP-DBP)/SBP)
of less than 25% suggests a cardiac index of less than 2.2 L/min/m².

Figure 2. Right Heart Catheterization: Pressure, Gradient, and Index Basics

(adapted with permission from CardioNerds13)

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QUICK READ SUMMARY

✓ Right heart catheterization enables complete assessment of a patient’s hemodynamics to
further characterize cardiogenic shock phenotype and tailor management.

✓ Recent retrospective observational studies have demonstrated improved survival with RHC use.

✓ RHC data assists in determining shock phenotype by assessing cardiac output and right- and
left-sided filling pressures, confirming the presence or absence of congestion, and assessing
systemic vascular resistance.

✓ RHC data can also help differentiate between LV-dominant, RV-dominant, and Bi-V failure
in cardiogenic shock.

✓ Cardiac power output (CPO) is a strong predictor of mortality in cardiogenic shock.

✓ Pulmonary artery pulsatility index (PAPi) is a strong predictor of RV dysfunction.

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References
1. Jentzer JC, van Diepen S, Barsness GW, et al. Cardiogenic shock classification to predict mortality in the cardiac intensive
care unit. J Am Coll Cardiol. 2019;74(17):2117-28. doi: 10.1016/[Link].2019.07.077. Epub 2019 Sep 20. PMID: 31548097.

2. Thayer KL, Zweck E, Ayouty M, et al. Invasive hemodynamic assessment and classification of in-hospital
mortality risk among patients with cardiogenic shock. Circ Heart Fail. 2020;13(9): e007099. doi: 10.1161/
CIRCHEARTFAILURE.120.007099. Epub 2020 Sep 9. PMID: 32900234.

3. Jain P, Thayer KL, Abraham J, et al. Right ventricular dysfunction is common and identifies patients at risk of dying in
cardiogenic shock. J Card Fail. 2021;27(10):1061-72. doi: 10.1016/[Link].2021.07.013. PMID: 34625126.

4. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with pulmonary artery catheters in
cardiogenic shock is associated with lower in-hospital mortality. JACC Heart Fail. 2020;8(11):903-13. doi: 10.1016/j.
jchf.2020.08.012. PMID: 33121702.

5. Coulter TD, Wiedemann HP. Complications of hemodynamic monitoring. Clin Chest Med. 1999;20(2):249-67.

6. Waheed O, Sharma A, Singh M, Kaluski E. Antecubital fossa venous access for right heart catheterization. J Invasive
Cardiol. 2017;29(5):169-74. PMID: 28441639.

7. Hsu S, Fang JC, Borlaug BA. Hemodynamics for the heart failure clinician: a state-of-the-art review. J Card Fail. 2021
Aug 10: S1071-9164(21)00306-7. doi: 10.1016/[Link].2021.07.012. Epub ahead of print. PMID: 34389460.

8. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization
effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-33. doi: 10.1001/jama.294.13.1625. PMID: 16204662.

9. Ranka S, Mastoris I, Kapur NK, et al. Right heart catheterization in cardiogenic shock is associated with improved
outcomes: insights from the Nationwide Readmissions Database. J Am Heart Assoc. 2021;10(17): e019843. doi:
10.1161/JAHA.120.019843. Epub 2021 Aug 21. PMID: 34423652

10. Chow JY, Vadakken ME, Whitlock RP, et al. Pulmonary artery catheterization in patients with cardiogenic shock: a
systematic review and meta-analysis. Can J Anaesth. 2021;68(11):1611-29. English. doi: 10.1007/s12630-021-
02083-2. Epub 2021 Aug 17. PMID: 34405356.

11. Pulmonary Artery Catheter in Cardiogenic Shock (PACCS) trial. [Link]. Accessed 9/3/24 at https://
[Link]/study/NCT05485376.

12. Abraham J, Blumer V, Burkhoff D, et al. Heart failure-related cardiogenic shock: pathophysiology, evaluation and
management considerations: review of heart failure-related cardiogenic shock. J Card Fail. 2021;27(10):1126-40. doi:
10.1016/[Link].2021.08.010. PMID: 34625131.

13. Right Heart Catheterization. Available at: [Link] Accessed 31

December 2021.

14. Rajagopal S, Ruetzler K, Ghadimi K, et al. Evaluation and management of pulmonary hypertension in noncardiac
surgery: a scientific statement from the American Heart Association. Circulation. 2023;147(17):1317-43.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 33

6
PREVIOUS CHAPTER Chapter 6: Pharmacotherapy Overview: Inotropes, Vasopressors, and Vasodilators NEXT CHAPTER

Pharmacotherapy
Overview:
Inotropes,
Vasopressors, and
Vasodilators
Ankit Kumar, MBBS MRCP, FRCA, FFICM Alastair Proudfoot, MBChB, PhD
ST5 Anaesthesia and Intensive Care Consultant Intensivist and Lead for
North East Thames London School of Cardiogenic Shock
Anaesthesia and Intensive Care Medicine Barts Heart Centre
London, UK
Alastair.proudfoot1@[Link]
@ICUDocAP

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Introduction
Many of the drugs available to treat cardiogenic shock have both inotropic and vasoactive effects. Most
vasoactive drugs have distinct "inotrope" or "vasopressor" actions, although certain agents, such as
epinephrine and norepinephrine, may have dual actions.
• An inotrope increases myocardial contractility and in many cases heart rate
• A vasopressor increases systemic vascular resistance and therefore mean arterial pressure
In contrast, a vasodilator reduces vascular tone and systemic afterload. Figure 1 illustrates these distinctions.

DIRECT INOTROPIC EFFECTS

YES (INOTROPES) NO
VASOCONSTRICTION
(VASOPRESSORS)

VASOCONSTRICTORS
INOCONSTRICTORS
PERIPHERAL VASCULAR EFFECTS

metaraminol
epinephrine
vasopressin
norepinephrine
phenylephrine
VASODILATION

INODILATORS VASODILATORS
milrinone nitroglycerin
dobutamine sodium nitroprusside
isoproterenol labetalol
levosimendan hydralazine

Figure 1. Classification of Agents by Inotropic and Vasoactive Effects

Trials of vasoactive agents in shock have largely focussed on septic shock, hence there are limited
robust randomized data that demonstrate mortality benefit of one agent over another in cardiogenic
shock. This uncertainty is reflected in societal guidelines. The aim of vasoactive drugs is to restore organ
perfusion through optimization of cardiac output and blood (perfusion) pressure. Regardless of the
choice of agent(s), efforts should be made to minimize dose and duration of support to offset any side
effects. Multiple agents at lower doses may be preferable to single agents at high doses. To ensure both
efficacy and safety, agent choice should reflect local guidance and familiarity.

Inotropes
Inotropes, including epinephrine, dobutamine, and isoprenaline, increase myocardial contractility (inotropy).
Most act via a final common pathway to increase the availability of calcium within the myocyte. The
activation of adenylyl cyclase in turn increases the production of cAMP from ATP and a rise in calcium flux
produces increased myocardial contractile force. Inodilators have inotropic effects but also cause arterial
vasodilation, reducing systemic vascular resistance (SVR) and/or pulmonary vascular resistance (PVR).

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Examples of these drugs include milrinone and levosimendan. Inotropes should usually be commenced
when there is a low cardiac output state with preserved blood pressure. Dobutamine or milrinone can
be considered as first-line with a preference for dobutamine in the context of severe renal impairment.
Epinephrine should be restricted to patients with persistent hypotension despite adequate cardiac filling
pressures as it has not been shown to be superior to alternatives, and compared to norepinephrine
is associated with lactic acidosis, no clear hemodynamic benefit, increased oxygen consumption, and
increased mortality.

Table 1. Inotropic Agents

DURATION
DRUG CLASSIFICATION MODE OF ACTION DOSE RANGE COMMENTS
OF ACTION
Epinephrine Endogenous β receptor activity Minutes Peripherally • Increases cardiac output, heart
catecholamine predominates at low administered: 1 mg rate, and myocardial oxygen
doses bolus in cardiac arrest consumption
α receptor activity Centrally • Peripheral vasodilation at
predominates at high administered: low doses, where β effects
doses (>0.2mcg/ infusion is used for predominate
kg/min) where management of shock
it becomes an at a rate of 0.01 to 1 • Use may be limited by arrhythmia,
inocostrictor mcg/kg/min increased myocardial oxygen
consumption, increased lactate,
refractory cardiogenic shock, and
higher mortality

Dobutamine Synthetic Mixed β1 and β2 Minutes Centrally • β1 effects increase cardiac output
catecholamine activity administered: 2.5 to by means of increased contractility
20 mcg/kg/min and heart rate
• Increases myocardial oxygen
demand
• ẞ2 effects cause decreased SVR
and potentially hypotension, thus
may need to add a vasopressor

Isoprenaline Synthetic β1 and β2 activity Minutes Peripherally • β1 effects increase cardiac output
catecholamine administered: 0.5 to by means of increased contractility,
10 mcg/min automaticity, and heart rate
• β2 effects cause decreased SVR
and potentially cause hypotension

Milrinone Phosphodiesterase-3 Inhibition of Minutes to Peripherally • Increases contractility and

inhibitor (PDE 3) phosphodiesterase in hours administered: 50 mcg/ improves relaxation (lusitropy)
cardiac and vascular kg IV bolus over 10
smooth muscle • Vasodilation of systemic and
minutes followed by
results in increased pulmonary circulation leading to
infusion of 0.1 to 0.75
hypotension
intracellular cAMP mcg/kg/min for up to
72 hours • Used primarily in cardiac surgery
May take up to 30 to facilitate weaning from
minutes to take effect cardiopulomonary bypass
• Effective for RV failure and
pulmonary hypertension

Levosimendan Calcium sensitizer Binds to troponin C, Hours to days Peripherally • Increases cardiac output without
blocking interaction administered: loading increase in myocardial oxygen
with inhibitory dose 6 to12 mcg/kg demand
troponin I. over 10 mins; infusion
Prolongs actin-myosin of 0.05 to 0.2 mcg/kg/ • Improves coronary blood flow
crossbridge formation min over 24 hours • Improves myocardial relaxation
(lusitropy)
• Vasodilation of systemic and
pulmonary circulation (inodilator),
leading to reduction in afterload
• One dose per week due to long
duration of action

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Vasopressors
Vasopressors, such as norepinephrine, dopamine, and vasopressin, cause vasoconstriction leading
to increased systemic and/or pulmonary vascular resistance. High dose catecholamines, in particular
norepinephrine, are potent vasoconstrictors. Norepinephrine should be regarded as the first-line vasopressor
in the context of cardiogenic shock with hypotension as it is noninferior to dopamine and dopamine is
associated with arrhythmias and possibly worse outcomes. Dopamine, which is not recommended in
guidelines, has differential effects on D1 and serotonin receptors depending on dosing, with a weak inotropic
effect at intermediate doses (eg, 3–5 mcg/kg/min) and a vasopressor effect at higher doses (>10 mcg/kg/
min). Vasopressin is increasingly deployed as a norepinephrine sparing vasopressor and in the context of
right heart failure owing to its pulmonary vasodilatory properties.

Table 2. Vasopressor Agents

DURATION
DRUG CLASSIFICATION MODE OF ACTION DOSE RANGE COMMENTS
OF ACTION
Norepinephrine Endogenous Primarily α1 agonist Minutes Centrally • Limited inotropic effect
catecholamine administered: 0.01 to
Minimal β activity 1 mcg/kg/min, titrated • May increase cardiac output
to effect without significantly increasing
heart rate
• Peripheral and pulmonary
vasoconstriction
• Venoconstriction leading to
increased venous return
• Increases systolic and diastolic
pressures
• First-line vasopressor
• High doses can lead to ischemia
and gangrene of extremities
• Tissue necrosis if extravasates

Vasopressin Endogenous Vasoconstricts via Minutes Centrally • Increases SVR and PVR
hormone V1 receptors and administered: 0.01 to
increase in water 0.04 units/hour • High doses can lead to ischemia
retention via V2 and gangrene of extremities
receptors • Resultant increase in blood
pressure seen in the shock state
may in part be due to a relative
insufficiency of vasopressin in
critical illness

Metaraminol Synthetic amine Primarily α1 agonist Minutes Peripherally • Cardiac output typically drops on
administered: 0.5 to 1 administration due to an increase
mg boluses in afterload
• May result in reflex bradycardia
• Increases SVR and PVR

Phenylephrine Synthetic amine α1 agonist Minutes Peripherally • Cardiac output typically drops on
administered: 50 to administration due to an increase
100 mcg boluses in afterload
• May result in reflex bradycardia
• Increases SVR and PVR

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Vasodilators
Vasodilators, such as glyceryl trinitrate (GTN), sodium nitroprusside (SNP), and hydralazine, reduce
systemic and/or pulmonary vascular resistance. Dilating the vascular system reduces afterload and cardiac
work leading to improved cardiac output. The increase in venous capacitance will tend to reduce venous
return and some agents such as hydralazine may cause profound falls in blood pressure at low dose.
In practice, a balance must be sought to optimize cardiac output while maintaining adequate perfusion
pressure, so these agents should be limited to those patients with normotensive cardiogenic shock.

Table 3. Vasodilator Agents

DURATION
DRUG CLASSIFICATION MODE OF ACTION DOSE RANGE COMMENTS
OF ACTION
Sodium Inorganic prodrug Prodrug facilitating Minutes Peripherally • Very potent and fast acting
nitroprusside nitric oxide production administered: 0.5 to 6
(SNP) leading to increased mcg/kg/min • Reduces both SVR and preload
cGMP which results • Cardiac output is maintained by
in arterial and venous reflex tachycardia
dilation
• Cyanide is a byproduct of SNP
metabolism and can accumulate
under certain circumstances
causing unexplained high lactate
• Protecting the infusion from light
reduces liberation of cyanide ions

Hydralazine Hydrazinophthalazine Activates guanylate Minutes Peripherally • Reduces arteriolar tone and SVR
cyclase leading to administered: initially
increased intracellular 200 to 300 mcg/min • Capacitance vessels are less
cGMP affected, thus less postural
Maintenance infusion hypotension
50 to 150 mcg/min
• Causes reflex tachycardia and an
increase in cardiac output
• Cerebral blood flow increases due
to cerebral vasodilation
• Nausea and vomiting are common

Glyceryl Organic nitrite Forms nitric oxide Seconds to Peripherally • Vasodilation predominantly in
trinitrate (GTN) causing vascular minutes administered: 0.1 to the capacitance vessels (veins)
relaxation similar to 10 mg/hr causing reduced preload, venous
SNP return, end diastolic pressure, and
wall tension
Causes venodilation
more than arterial • Vasodilation leads to reduced
dilation oxygen demand and increased
coronary blood flow
• Rapid onset
• May cause headache secondary to
cerebral vasodilation
• Tachyphylaxis develops over the
first 48 hours

Labetalol Combined α1 and Specific α1 blockade Minutes Peripherally • Can be administered orally or
β antagonist with leads to vasodilation administered: 20 mg/ intravenously
around 1:3 ratio of hour titrated to effect
α:β effect Non-specific β up to 160 mg/hour • Can lead to bradycardia
blockade inhibits
reflex tachycardia and
reduces shear forces
on the aorta

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Selection of therapies
The interaction between the heart and vasculature means that neither should be considered in isolation
when selecting therapy. The combined goal is adequate/optimal perfusion and organ function. Table 4,
which is based on the French recommendations for management of cardiogenic shock, outlines a possible
hierarchy of therapies depending on severity.

Table 4. Recommended Treatments by Patient Condition

PATIENT CONDITION RECOMMENDED TREATMENT 7

Hemodynamic collapse (SCAI stage E) Norepinephrine + dobutamine/milrinone + vasopressin +/- MCS

Refractory shock (SCAI stage D) Norepinephrine + dobutamine/milrinone +/- MCS

Overt shock (SCAI stage C) Norepinephrine + dobutamine/milrinone +/- MCS

Decompensated heart failure Inotropes not recommended without cardiogenic shock

As previously mentioned, to offset side effects, minimize both the dose and duration of these agents.

Titration of therapies
Assessment of clinical response to all interventions should occur serially through a combination of
clinical assessment, biochemical assessment (lactate, liver and renal function tests, central venous
oxygen saturations), and hemodynamic assessment (echocardiography, CO, cardiac index, and
pulmonary capillary wedge pressure). Continuous hemodynamic monitoring with invasive (mean)
arterial blood pressure and central venous access to both safely administer vasoactive drugs and
measure right ventricular preload is essential for early identification of changes in clinical condition
and titration of therapies, although consensus on the optimal method is lacking. Pulmonary artery
catheterization is advocated in the management of cardiogenic shock to aid diagnosis and monitor
response to interventions. If a commensurate physiologic response is not being achieved despite
escalating pharmacotherapy, consider the addition of mechanical circulatory support and consequent
weaning of vasoactive drugs.

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QUICK READ SUMMARY

✓ Inotropes increase myocardial contractility.

✓ Vasopressors increase vascular tone.

✓ Vasodilators reduce vascular tone and systemic afterload.

✓ Minimize dose and duration of support of these agents to offset side effects; avoid
epinephrine where possible and consider transition to MCS to avoid prolonged and
high-dose inopressor use.

✓ Norepinephrine should be considered first-line for hypotensive cardiogenic shock while

dobutamine or milrinone should be considered the first-line inotrope in normotensive
patients.

✓ Consider mechanical circulatory support early when escalating pharmacotherapy does

not achieve desired physiologic response.

References
1. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force
of the European Society of Intensive Care Medicine. Intensive Care Med. 2014;40(12):1795-815.

2. Bloom JE, Chan W, Kaye DM, Stubb D. State of shock: contemporary vasopressor and inotrope use in cardiogenic
shock. J Am Heart Assoc. 2023;12:e029787.

3. Bruno L, Clere-Jehl R, Legras A, et al. Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial
infarction. J Am Coll Cardiol. 2018;10(72):173-82.

4. Henry TD, Tomey MI, Tamis-Holland JE, et al. Invasive management of acute myocardial infarction complicated by
cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2021;143(15):e815–e829.

5. De Backer D, Biston P, Devriendt J, et al. for the SOAP II Investigators. Comparison of dopamine and norepinephrine
in the treatment of shock. N Engl J Med. 2010;362:779-89.

6. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from
the American Heart Association. Circulation. 2017;136(16):e232-e268.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 40

7
PREVIOUS CHAPTER Chapter 7: Treatment Escalation Guidelines NEXT CHAPTER

Treatment
Escalation
Guidelines
Mir B. Basir, DO, FACC, FSCAI
Director, Acute Mechanical Circulatory Support
Henry Ford Hospital
Detroit, MI
Mbasir1@[Link]

Alejandro Lemor, MD, MS, FSCAI

Interventional Cardiology
University of Mississippi Medical Center
Jackson, MS
alemor@[Link]

Katherine J. Kunkel, MD, MSEd, FSCAI

Interventional Cardiologist
Piedmont Heart Institute
Atlanta, GA
[Link]@[Link]
@kjkunkelmd

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Introduction
Early identification and intervention in cardiogenic shock are critical first steps in improving survival.
After a management strategy is initiated, ongoing monitoring and serial evaluations are vital in
recognizing dynamic changes in response to initial therapeutic interventions, shock progression, and the
need for early mechanical circulatory support (MCS) escalation.

Recognizing undertreated shock

Knowing when to escalate MCS begins with identifying worsening or undertreated cardiogenic shock.
Serial assessment of patients should occur using a combination of clinical (Table 1) and invasive
hemodynamic (Table 2) parameters. Early escalation may be required in the presence of hypoperfusion
or hemodynamic deterioration. It is important to evaluate for worsening trends but also plateauing
values.

Consideration to escalate MCS should take into account the patient's overall clinical picture. Based upon
a patient's cardiac function and the etiology of shock, MCS escalation may serve as a bridge to recovery
or a bridge to advanced heart failure therapies such as durable LVAD and transplant. In some patients,
however, MCS escalation may be futile. These determinations are made based on a constellation of
medical comorbidities, patient age, candidacy for advanced therapies, multiorgan failure, and patient/
family wishes.

Table 1. Clinical Parameters of Worsening Hypoperfusion

PARAMETERS FINDINGS OF WORSENING HYPOPERFUSION

Vasopressors and inotropes • Increasing vasopressor/inotrope requirements or need for additional agents to
maintain a mean arterial pressure (MAP) of >65 mmHg

End organ damage • Increasing creatinine (>0.3 mg/dL within 24 hours)

• Decreasing urine output (<0.5 mL/kg/hour for 6 hours)

• Increasing lactate or lactate clearance <50% within 6-24 hours

• Rising liver function (>25 x normal) and INR (>1.5)

• Neurological injury

Respiratory status • Increase in oxygen requirements, tachypnea

• Chest x-ray with worsening pulmonary edema

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Table 2. Parameters Indicating Worsening Hemodynamics

FINDINGS OF WORSENING
PARAMETERS
HEMODYNAMICS

Cardiac output deficit (COD)

dysfunction

COD = Target CO – current CO COD > 2.0 L/min

Cardiac

Target CO = BSA x 2.2 L/min/m2

Cardiac power output (CPO)

CPO < 0.6 W
CPO = MAP x CO / 451

Central venous pressure (CVP) CVP > 12 mmHg

CVP / PCWP CVP/PCWP > 0.8

Right ventricular
dysfunction

Pulmonary artery pulsatility index (PAPi)

PAPi < 1.0
PAPi = (Systolic PA pressure – diastolic PA pressure) / CVP

Right ventricular stroke work index (RVSWI)

RVSWI < 300 g-m/m2
RVSWI = (Mean PA pressure − CVP) × Stroke volume index (SVI)

Escalation options with mechanical circulatory support

Once the decision to escalate MCS has been made, prompt evaluation for large bore MCS candidacy
should take into account the following factors:
• Presence of peripheral arterial disease that will require alterative access
• Presence of valvular lesions
• Presence of intracardiac thrombi

Multiple devices can be considered based on the level of hemodynamic support required and whether
hemodynamic parameters indicate predominantly right, left, or biventricular failure (Table 3). Isolated
left-sided support can be considered in patients with normal PAPi and CVP in the setting of elevated
left-sided filling pressures and reduced CPO. In patients with poor right-sided hemodynamics (low PAPi,
elevated CVP, low CVP/PCWP and RVSWI) in the setting of relatively normal left-sided filling pressures,
isolated right-sided support may be adequate. Abnormal right- and left-sided parameters favor a
biventicular support strategy. Escalation or de-escalation decisions are based on multiple hemodynamic
parameters (Figure 1).

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Table 3. MCS Device Options for Uni- and Biventricular Support

FLOW
DEVICE ACCESS
(L/MIN)

Left Univentricular Support IABP 0.5 – 1 7-8 Fr femoral or axillary artery

Impella CP® 3.5 14 Fr femoral or axillary artery

21-23 Fr surgical arterial access or transcaval via

Impella 5.0® 5.0
the femoral vein

Impella 5.5® 5.5 23 Fr surgical arterial access

21 Fr venous access
TandemHeart® 3.5 – 4.5
15-19 Fr femoral artery

Right Univentricular Support

Protek Duo 2–4 29 – 31 Fr right internal jugular vein

Impella RP® 2-4 22 Fr femoral vein

Biventricular Support 21-29 Fr femoral vein

VA ECMO 3-6
15-19 Fr femoral artery

24 Fr femoral vein (with fenestrated cannula

LA-VA ECMO 3–6 through the interatrial septum)
15-19 Fr femoral artery

21-29 Fr femoral vein

ECpella ™
3–6 15-19 Fr femoral artery (ECMO outflow access)
14 Fr femoral artery (Impella access)

21-29 Fr femoral vein

ECMO-IABP 3–6 15-19 Fr femoral artery (ECMO outflow access)
7-8 Fr femoral artery (IABP access)
IABP: Intra-aortic balloon pump; ECMO: Extracorporeal membrane oxygenation; Fr: French

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CONSIDER ESCALATING SUPPORT

Increasing requirement of Elevated PCWP

pressors or inotropes

PAPi < 1.0 Unable to clear lactate

N
O
MAPs < 65 CPO < 0.6

TI
A LA
ESC Cardiac index < 2.2

MCS
DE- Cardiac index > 2.2
ES
CA
CPO > 0.6
Stable MAPs LA
T IO
Normal lactate
PAPi > 1.0
N
No pressors or inotropes Stable PCWP
and CVP

CONSIDER WEANING SUPPORT

Figure 1. MCS Escalation and De-escalation

Decision making in MCS escalation

When deciding what the next step should be in MCS escalation, use of a shock team to reach
consensus based on local experience and expertise is recommended. When possible, isolating where
and how much support is needed is critical. While placing ECMO stabilizes nearly all hemodynamic
lesions in cardiogenic shock, placing more selective MCS, when appropriate, can help avoid the risk of
stroke and vascular access site complications and spare patients significant risk of complications. Limb
ischemia, in particular, is a significant limiting factor in the use of large bore devices among patients
with small habitus and/or peripheral arterial disease, particularly when multiple simultaneous devices
are being considered (ie, ECpella™). Potential complications associated with various MCS devices are
discussed in later chapters in this eBook. Overall, deciding which device to escalate to is a complex
decision, and until more data is available to support one strategy over another, operators should use
devices that they have expertise with placing and managing.

A future direction in the field of cardiogenic shock is the development of shock centers of excellence
that offer expertise and a full array of MCS devices for centralized care of patients with cardiogenic
shock, particularly among those requiring escalating support.

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Case examples
Case 1

PRE-ECMO POST-ECMO
HEMODYNAMICS
PLACEMENT PLACEMENT

Systemic blood pressure 64/44 85/81

(mmHg)

Central venous pressure 21 7

(mmHg)

Pulmonary artery 36/26 (31) 11/9 (10)

Initial coronary angiography
pressure (mmHg)

PCWP (mmHg) 29 n/a

Cardiac output (L/min) 3.1 11.6

Impella
Cardiac index (L/min/m2) 1.54 5.8
ECMO
venous CPO (Watts) 0.35 2.1
cannula

PAPi 0.48 0.3

Post-PCI of LAD Post-ECpella

Figure 2. Patient Case 1

A 50-year-old man with a history of diabetes presented to the emergency department with chest
pain and suffered VT/VF cardiac arrest shortly after arrival. After 15 minutes of ACLS, he had return
of spontaneous circulation, and initial EKG showed an anterior STEMI. On arrival to the cardiac
catheterization lab, the patient had a heart rate of 126 bpm and blood pressure of 72/28 mmHg. A
transfemoral Impella CP was urgently placed, and the patient underwent primary PCI to the LAD.
At the conclusion of the procedure, hemodynamics showed biventricular failure despite Impella CP
support (CPO 0.35W, PAPi 0.48) (Figure 2). Given inadequate biventricular support, the patient was
upgraded to VA ECMO with the Impella CP for LV venting. In the ICU, hemodynamics were markedly
improved. All pressors were weaned off within 18 hours, and lactate, which had been 14.0 mmol/L
on arrival to the cardiac catheterization lab, normalized to 1.6 mmol/L in 24 hours. The patient was
ultimately discharged following a prolonged hospitalization.

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Case 2

Impella RP

Impella CP

Initial coronary angiography

DAY 1 ON DAY 2 ON
AT IMMEDIATELY 45 MINUTE
PARAMETER BIVENTRICULAR BIVENTRICULAR
PRESENTATION POST-IMPELLA CP POST-IMPELLA CP
IMPELLA IMPELLA

Heart rate (bpm) 104 149 140 121 92

Systemic blood pressure 80/41 (61) 115/84 (94) 73/53 (60) 77/70 (72) 94/71 (78)
(mmHg)

Central venous pressure 15 12 15 10 7

Pulmonary artery 34/26 (30) 24/16 (20) 23/19 (20) 27/19 (22) 25/14 (18)
pressure (mmHg)

PCWP (mmHg) 26 16 n/a n/a n/a

Cardiac output (L/min) 3.38 4.18 3.1 3.7 5.7

Cardiac index (L/min/m2) 1.94 2.4 1.7 2.1 3.3

CPO (Watts) 0.52 0.9 0.4 0.59 0.99

PAPi 0.73 0.8 0.27 0.8 1.6

RVSWI 281 161 61 209 395

Figure 3. Patient Case 2

A 65-year-old woman with a history of hypertension presented with 2 days of chest pain and was found
to have anterior Q waves and inferior ST depressions as well as a severely depressed left ventricular
ejection fraction (LVEF) of 15% with moderately reduced RV function and severe mitral regurgitation.
The patient developed hypoxemic respiratory failure and was emergently intubated. Urgent coronary
angiography revealed 3 vessel CAD for which an IABP as placed. On transfer to a tertiary medical center,
the patient was hypotensive and tachycardic. Hemodynamics were notable for cardiogenic shock due
to biventricular failure (Figure 3). A transfemoral Impella CP was placed. After observation in the cardiac
catheterization laboratory for 45 minutes, the patient’s cardiac power output continued to fall with right-
sided hemodynamic parameters showing worsening congestion and failure. Right-sided hemodynamic
support with an Impella RP was placed, and the patient was transferred to the ICU where hemodynamics
normalized over 48 hours. She ultimately underwent multivessel PCI, and MCS was successful weaned.
She was successfully discharged after a prolonged hospital course.

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QUICK READ SUMMARY

✓ Knowing when to escalate MCS entails serial assessment of a patient’s clinical and
hemodynamic parameters to identify worsening or undertreated cardiogenic shock.

✓ Consider the decision to escalate MCS in the context of the patient’s overall clinical
picture.

✓ When deciding next steps in MCS escalation, a shock team can help reach consensus
based on local experience and expertise.

✓ When possible, isolating where and how much support is needed is critical.

✓ MCS options for left univentricular support include IABP, Impella CP, Impella
5.0, Impella 5.5 and TandemHeart, each of which has its own flow and access
considerations.

✓ MCS options for right univentricular support include Protek Duo and Impella RP.

✓ MCS options for biventricular support include VA ECMO, LA-VA ECMO, ECpella, and
ECMO-IABP.

✓ Until more data is available to support one escalation strategy over another, operators
should use devices that they have expertise with placing and managing.

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PREVIOUS CHAPTER Chapter 8: Systems of Care: Shock Protocols, Teams, Centers, and Networks NEXT CHAPTER

Systems of Care:
Shock Protocols,
Teams, Centers,
and Networks
Alexander G. Truesdell, MD, FSCAI
Virginia Heart / Inova Schar Heart and Vascular
Falls Church, Virginia
agtruesdell@[Link]
@agtruesdell

Wayne B. Batchelor, MD, FSCAI

Erik A. Osborn, MD
Carolyn S. Rosner, NP
Ramesh Singh, MD
Shashank S. Sinha, MD
Behnam N. Tehrani, MD
Inova Schar Heart and Vascular
Falls Church, Virginia

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Introduction
“Coming together is a beginning, staying together is progress, and working together is success.”
- Henry Ford

Following the adoption of early revascularization for acute myocardial infarction (AMI) and
improvements in pharmacotherapy for acute decompensated heart failure (ADHF), cardiogenic shock
(CS) survival rates increased from only 10% in the 1960s to 50% by the 1990s.1,2 In decades since,
in-hospital survival plateaued while the incidence of both AMI and ADHF CS continue to increase,
despite improvements in medical therapies, percutaneous and surgical coronary revascularization
tools and techniques, temporary mechanical circulatory support (MCS) options, and durable left
ventricular assist device (VAD) technology.3,4 Delays in CS recognition, barriers to access to disease-
modifying interventions, and undesired heterogeneities of care within and between medical facilities
likely contribute in part to the persistent lethality of CS.5-10 More recently, multidisciplinary team-based
protocol-driven CS care has demonstrated promising potential to improve clinical outcomes beyond the
50% glass ceiling.11, 25

Teams and protocols

Patients in CS often deteriorate rapidly, and as shock persists, end-organ hypoperfusion, ischemia,
and acidosis worsen, often irreversibly. Successful diagnostic and therapeutic decision making must
therefore be both timely and rapidly effective. Use of newer advanced therapies and various forms
of mechanical circulatory support often require the coordinated efforts of multiple medical experts
including interventional cardiologists, cardiothoracic surgeons, advanced heart failure specialists, cardiac
intensivists, and others, as shown in Figure 1.
NURSING
NE

S
ST
PH

NI
RO

IO
LO

US

OC PH
GY

CU YSI
RF

TH PA CA AL
PE

ER TIO L & TUR

C T
AP N
Y AL RU AR
ST HE

CRITICAL CARE
ELECTROP
HYSIOLOG ADVANCED RESPIRA
TORY
Y
HEART FAILURE THER PY
A

CARDIAC SURGERY
INT
ERV
EC
AR
E INTERVENTIONAL RAD ENTIO
IV IOLO NAL
LIA
T CARDIOLOGY GY
PAL
ER R

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RG ULA
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AR
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SU SC

M
EMER CINE
IOLO

AC
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GENC
THES
ANES

Figure 1. Multidisciplinary Shock Team

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 50

PREVIOUS CHAPTER Chapter 8: Systems of Care: Shock Protocols, Teams, Centers, and Networks NEXT CHAPTER

Defined protocols are important to guide initial and ongoing patient management. Multidisciplinary teams
are designed to enhance the individual strengths of component team members and streamline care
delivery to optimize patient outcomes in complex and resource-intensive CS patients.12 It is likewise critical
to leverage multidisciplinary team expertise to achieve consensus regarding patient selection, futility, and
individual short- and long-term goals of care, and to embed these multiple considerations into institutional
care pathways and decision-making processes such as those shown in Figures 2-5.

Cardiogenic Shock Team Activation XXX-XXX-XXXX

WHY is there a Shock Team? WHEN is the Team Activated?
Early identification and treatment Call the Shock Team as soon as Cardiogenic Shock is suspected
improves survival in Cardiogenic Shock
Clinical Criteria
• SBP < 90mmHg (for 30 min) or use of vasopressors/inotropes
WHAT is the Cardiogenic Shock Team? • Lactate > 2 mmol/L
A multidisciplinary team dedicated to • Evidence of end-organ (eg, renal, hepatic, cerebral) hypoperfusion
optimizing the care of Cardiogenic Shock • ACS or Heart Failure
patients via: Hemodynamic Criteria (if known)
• Rapid identification • CI < 1.8 (or 2.2 L/min/m2 with inotropes or vasopressors)
• Coordinated consultation • CPO < 0.6
• Early transfer/admission to Cardiac • PAPi < 1.0
ICU, Cath Lab or Operating Room • PCWP ≥ 15 mmHg

Contraindications*
WHO is on the Shock Team? • DNAR
• Interventional Cardiologist • Terminal Illness
• Cardiac Surgeon
• Advanced Heart Failure » Note: for STEMI, follow STEMI pathway
• Cardiac Critical Care *If any questions, contact Shock Team

HOW is the Shock Team activated? AFTER the team has been activated
Inova Transfer Center: XXX-XXX-XXXX • Obtain ongoing Vital Signs, ECG, Labs (eg, BNP, Tn I, Lactate, CBC, CMP)
• Maintain 2 large bore IVs (consider central line as needed)
WHO activates the Shock Team? • Minimize vasopressors/inotropes to maintain MAP of ≥ 60 mmHg
• Emergency Department • Preferential use of norepinephrine for vasopressor support
• Other units in the hospital (eg, Cath Lab or • Avoid use of phenylephrine
ICUs) • Preferential use of amiodarone for control of VT or AF
• Other hospitals • Avoid negative inotropes (eg, β-blockers, Ca++ channel blockers)
Revised May 3, 2022 • Consider airway stabilization

Figure 2. Shock Team Activation

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Cardiogenic Shock Team Coordination

Cardiogenic Shock Team Activation
Heart Team Goals • Call XXX-XXX-XXXX for any patient with criteria for Cardiogenic Shock
• Early identification of CS patients • Obtain ongoing Vital Signs, ECG, Labs
• Early CS phenotyping
• Selective and tailored PMCS HF-CS AMI-CS
• Optimize hemodynamics • Echocardiography • Coronary angiography with LVEDP
• Native heart recovery • Right Heart Catheterization • Right Heart Catheterization

*Clinical Considerations for PMCS Are Criteria for Cardiogenic Shock Met?
• Shock phenotype (AMI-CS vs HF-CS) • SBP < 90mmHg or use of vasopressors/inotropes AND:
• Shock severity (SCAI Classification)
• Lactate > 2 mmol/L
• CI < 1.8 (or < 2.2 L/min/m2 with inotropes/vasopressors)
• Shock profile (LV, RV, Bi-V) • PCWP ≥ 15 mmHg and/or LVEDP ≥ 15 mmHg • Evidence of end-organ
• Lactate level • CPO < 0.6 hypoperfusion
• Severity of end-organ dysfunction • PAPi < 1.0
• Amount of vasopressor/inotropic support
• Presence of hypoxia
• Presence of arrhythmias YES NO
• Consider Percutaneous • Coronary revascularization as
Mechanical Circulatory Support needed
Relative PMCS Contraindications (PMCS) based on Clinical
• DNAR Considerations for PMCS* • Swan-Ganz Catheter left in place
• Terminal illness • Coronary revascularization prn
• Unable to anticoagulate (consider IV antiplatelet agent)
• Cardiac arrest with neurocatastrophe
• Advanced multi-system organ failure
• LA or LV thrombus Cardiac Intensive Care Unit for ongoing CS Management
• Serial reassessment of hemodynamics & end-organ perfusion
CPO = MAP x CO/451 • Optimize Preload, Afterload, and Contractility
PAPi = (sPAP-dPAP)/RA • Timely, tailored escalation of treatment for Worsening Shock
• Assess for ability to wean PMCS
Revised April 24, 2022

Figure 3. Shock Team Coordination and Initial Patient Management

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AMI-Cardiogenic Shock Management

Call XXX-XXX-XXXX to activate Cardiogenic Shock Team
CS Management Goals
Treatment Considerations for AMI-CS
• Serial reassessment (≤ q 6hr) of • Shock severity (SCAI stage) • Presence of hypoxia
hemodynamics & end-organ perfusion
• Shock profile (LV, RV or Bi-V) • Presence of arrhythmias
• Lactate
• Renal, hepatic function • Revascularization status (mode and completeness) • Contraindications to PMCS
• Continuous hemodynamics • Presence of mechanical complications (eg, VSD, MR) • Use of IV antiplatelet agent
• CPO & PAPi
• Optimize Preload, Afterload and
Contractility
• Volume or diuresis SCAI B CS SCAI C CS SCAI D CS SCAI E CS
• Vasodilators or Vasopressors
• Inotropes Beginning Classic Deteriorating Extremis
• Timely, tailored treatment escalation Hypoperfusion: Hypoperfusion: Hypoperfusion: Hypoperfusion:
for Worsening Shock: Lactate < 2 mmol/L Lactate ≥ 2 mmol/L Lactate ≥ 4 mmol/L Lactate ≥ 8 mmol/L
• Rising Lactate Minor renal & hepatic Alteration of renal & Worsening renal & Severe acidosis & end-
• Increasing pressor requirement dysfunction hepatic function hepatic function organ failure
• Worsening end-organ function +/- + + +
• CPO < 0.6 and/or PAPi < 1 Hypotension: Hypotension: Hypotension: Hypotension:
• RA > 15 and/or PCWP > 15 SBP < 90 mmHg SBP < 90 mmHg Escalating pressors Refractory
• Assess for LV and RV recovery
OR OR OR
• Wean PMCS, vasopressors and
inotropes Current Treatment: Current Treatment: Current Treatment: Current Treatment:
No drugs or devices 1 drug OR device 2 drugs OR devices ≥ 3 drugs OR devices

CS Hemodynamic Profile
LV- RV- Bi-V LV, RV LV-dominant: RV-dominant LV-dominant: RV-dominant LV, RV
or Bi-V: or Bi-V: or Bi-V: or Bi-V:
dominant dominant
RA < 15 > 15 > 15 IABP IABP Pro-Tek Duo Impella 5.5 VA-ECMO VA-ECMO
PCWP > 15 < 15 > 15 (and/or trial of or +/- or +/- +/-
vasopressors) Impella CP Impella CP VA-ECMO LV vent LV vent
CPO < 0.6 < 0.6 < 0.6
+/-
PAPi > 1.0 < 1.0 < 1.0 LV vent
CPO = MAP x CO/451
PAPi = (sPAP-dPAP)/RA
Revised May 10, 2022

Figure 4. Shock Team Management, Escalation, and Weaning—Acute Myocardial Infarction Cardiogenic Shock

HF-Cardiogenic Shock Management

Call XXX-XXX-XXXX to activate Cardiogenic Shock Team
CS Management Goals
• Serial reassessment (≤ q 6hr) of Treatment Considerations for Heart Failure-CS
hemodynamics & end-organ perfusion • Shock severity (SCAI stage) • Presence of arrhythmias
• Lactate • Shock profile (LV, RV or Bi-V) • Anticipated duration of support
• Renal, hepatic function • Anticipated exit strategy (BTT or BTR) • Ability to ambulate
• Continuous hemodynamics • Presence of hypoxia • Contraindications to PMCS
• CPO & PAPi
• Optimize Preload, Afterload and
Contractility
• Volume or diuresis SCAI B CS SCAI C CS SCAI D CS SCAI E CS
• Vasodilators or Vasopressors
• Inotropes Beginning Classic Deteriorating Extremis
• Timely, tailored treatment escalation Hypoperfusion: Hypoperfusion: Hypoperfusion: Hypoperfusion:
for Worsening Shock: Lactate < 2 mmol/L Lactate ≥ 2 mmol/L Lactate ≥ 4 mmol/L Lactate ≥ 8 mmol/L
• Rising Lactate Minor renal & hepatic Major renal & hepatic Worsening renal & Severe acidosis & end-
• Increasing pressor requirement dysfunction dysfunction hepatic function organ failure
• Worsening end-organ function +/- + + +
• CPO < 0.6 and/or PAPi < 1 Hypotension: Hypotension: Hypotension: Hypotension:
• RA > 15 and/or PCWP > 15 SBP < 90 mmHg SBP < 90 mmHg Escalating pressors Refractory
• Assess for LV and RV recovery
OR OR OR
• Wean PMCS, vasopressors and
inotropes Current Treatment: Current Treatment: Current Treatment: Current Treatment:
No drugs or devices 1 drug OR device 2 drugs OR devices ≥3 drugs OR devices

CS Hemodynamic Profile
LV- RV- Bi-V LV, RV LV-dominant: RV-dominant LV-dominant: RV-dominant LV, RV
or Bi-V: or Bi-V: or Bi-V: or Bi-V:
dominant dominant Impella 5.5
RA < 15 > 15 > 15 IABP IABP Pro-Tek Duo or VA-ECMO VA-ECMO
(and/or trial of or +/- Trans-apical +/- +/-
PCWP > 15 < 15 > 15
vasopressors, or LV vent
CPO < 0.6 < 0.6 < 0.6 Impella 5.5 Impella 5.5 LV vent
Trans-septal
inotropes or
PAPi > 1.0 < 1.0 < 1.0 temporary
vasodilators) LVAD
CPO = MAP x CO/451
PAPi = (sPAP-dPAP)/RA Revised May 3, 2022

Figure 5. Shock Team Management, Escalation, and Weaning—Heart Failure Cardiogenic Shock

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Most medical facilities do not employ the full complement of medical and surgical specialists and
therapies and thus team composition and capabilities will vary across institutions. “Level I” centers,
however, should offer full-spectrum short-term and definitive medical and surgical therapies (which
may include durable left ventricular assist devices and orthotopic heart transplantation), as shown
in Figure 6.13,14 All centers of all “levels” should furthermore partner with their local and regional
counterparts to establish formal or informal networks of care.

Advanced MCS LEVEL Dedicated Cardiac Shock Care Center

I

Culprit PCI LEVEL LEVEL STEMI Receiving and PCI Capable

II II Hospital Without Advanced MCS

Triage and Transfer LEVEL LEVEL LEVEL Non-PCI Capable Hospital

III III III (Generally Rural Hospital)

Figure 6. Cardiogenic Shock Centers and Networks (adapted from Tchantchaleishvili et al.13)

Suggested keys to successful shock team implementation include:

• An institutional commitment
• Multidisciplinary leadership with supported time
• Key personnel with continuous involvement in CS patient management
• Ongoing sustainment training
• A consultative service to evaluate and manage CS patients
• Protocols for diagnosis and management
• An infrastructure for data collection
• A system for case review and quality assurance
• Liaison services with other local and regional medical centers

The team “lead” may differ depending on institutional capabilities and culture, although each discipline
should have a designated “champion” and all team members should actively participate in decision making.

Several groups in the United States and Canada have demonstrated that the implementation of a shock
team utilizing a multidisciplinary standardized team-based approach emphasizing timely diagnosis,
mandatory invasive hemodynamics, and appropriate use of MCS is not only feasible but may result
in improved survival in all-comer patients with CS.15-18 Despite limited randomized control trial data,
these registry reports have demonstrated the highest survival ever reported in AMI CS and ADHF CS
populations.19 One contemporary registry further demonstrates equivalent survival among both “hub”
and “spoke” patients treated within an established shock network (unpublished data Inova-Shock
Registry NCT03378739).26 Together, these reports suggest that this shock management model is
reproducible in both academic and community facilities. The sustainability of the CS team in clinical
practice also appears feasible as evidenced by several institutions now 5-6 years or more into their CS
team process.15-18

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Shock centers and shock networks

Contemporary CS management in tertiary care centers presently requires expertise with multiple
pharmacologic and device technologies. Various intracorporeal, extracorporeal, catheter- and cannula-
based devices, including intra-aortic balloon pump (IABP), Impella (2.5®, CP®, RP®, 5.0®, and 5.5®),
extracorporeal membrane oxygenation (ECMO), TandemHeart, Centrimag, Rotaflow, and Protek
Duo, may often be used in different “plug-and-play” configurations. Device selection will vary based
on CS etiology and stage, presence or absence of accompanying cardiac arrest, respiratory failure,
vasodilatory shock, and/or extra-cardiac organ compromise, vascular access considerations, technology-
specific contraindications, and institution-specific preference and expertise.27 Selection requires a clear
understanding of goals of support and goals of care, as well as whether it be bridge to decision-making,
bridge to recovery, bridge to transplantation, or bridge to durable VAD.

Availability of emergency percutaneous coronary intervention (PCI), hemodynamic support devices,

and advanced heart failure therapies may be limited to specialized referral centers. Thus, a regional
referral network for CS care is advised. Utilizing a “spoke-and-hub” model, referring centers may
provide varying degrees of on-site medical stabilization, revascularization, and mechanical support prior
to transport for a higher level of comprehensive CS care as necessary. Although institutional volume
has been demonstrated to impact survival in both AMI and ADHF CS, the vast majority of patients do
not currently present to high-volume full-spectrum cardiac care centers with 24/7 on-site critical care,
interventional cardiology, cardiac surgery, and advanced heart failure specialists and technology.7,20,21
Thus it is critical that large and small academic and community medical centers and health systems
collaborate for early identification and stabilization of CS patients with expedited follow-on consultation
and/or transfer for definitive management.

Case Study
Inova Schar Heart and Vascular

Since 2017, the shock team at the at Inova Schar Heart and Vascular may be activated 24 hours
per day, 7 days per week, via a “one-call” process to a central operator who gathers the core
multidisciplinary team members (interventional cardiology, critical care, cardiac surgery, and advanced
heart failure) for urgent telephone consultation.

When activated, the shock team develops an initial consensus plan of care based on the specific clinical
scenario according to the institutional protocol. Follow-on decisions regarding adequacy of support
and need for escalation or modification of support are subsequently made via group decision making
based on serial clinical, laboratory, imaging, and hemodynamic reassessments. This pattern of recurring
assessment, adjustment, reassessment, and readjustment forms the “unblinking eye” of shock team
management.

Between shock team activities, team members engage in their usual daily activities in the clinics,
hospital wards, intensive care units, cardiac catheterization labs, and operating rooms. Every 2 weeks,
the Inova shock team conducts brief cross-discipline meetings, which build esprit de corps, assess
compliance to protocols, evaluate the effectiveness of interventions, and facilitate regular incremental
changes in care pathways as part of a continuous quality improvement program.22

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Future directions
Although limited by small samples sizes and lack of long-term outcomes data, current registries and
single center and multicenter reports suggest that standardized team-based multidisciplinary care, early
initiation of MCS, and hemodynamic guidance of therapies may significantly improve outcomes in both
AMI and ADHF CS.23 Looking ahead, it will be important to further validate and implement treatment
protocols and coordinated regionalized systems of care to identify and optimize best practices, reduce
practice variation, improve access to high-quality and high-value care, and possibly centralize the
sickest of CS patients to high-volume full-spectrum specialty care CS “centers of excellence.”24, 28

QUICK READ SUMMARY

✓ Successful diagnostic and therapeutic decision making for patients in CS often requires the
coordinated efforts of a multidisciplinary shock team.

✓ Defined protocols are important to guide initial and ongoing patient management.

✓ Keys to successful shock team implementation include key personnel with continuous
involvement in CS patient management, an infrastructure for data collection, and a system for
case review and quality assurance.

✓ A regional referral network for CS care is advised since emergency PCI, hemodynamic support
devices, and advanced heart failure therapies may be limited to specialized referral centers.

✓ Current registries and single center and multicenter reports suggest that standardized team-
based multidisciplinary care, early initiation of MCS, and hemodynamic guidance of therapies
may significantly improve outcomes in both AMI and ADHF CS.

References
1. Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250
patients. Am J Cardiol. 1967;20(4):457-64.

2. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by
cardiogenic shock. SHOCK Investigators. Should we emergently revascularize occluded coronaries for cardiogenic
shock. N Engl J Med. 1999;341(9):625-34.

3. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from
the American Heart Association. Circulation. 2017;136(16):e232-e268.

4. Thiele H, Ohman EM, de Waha-Thiele, et al. Management of cardiogenic shock complicating myocardial infarction: an
update 2019. Eur Heart J. 2019;40(32):2671-83.

5. Harhash AA, Kennedy KF, Fendler TJ, et al. Comparison of outcomes among patients with cardiogenic shock admitted
on weekends versus weekdays. Am J Cardiol. 2021;144:20-5.

6. Ya’qoub L, Lemor A, Dabbagh M, et al. Racial, ethnic, and sex disparities in patients with STEMI and cardiogenic
shock. JACC Cardiovasc Interv. 2021;14(6):653-60.

7. Wang JI, Lu DY, Mhs, et al. Outcomes of hospitalizations for cardiogenic shock at left ventricular assist device versus
non-left ventricular assist device centers. J Am Heart Assoc. 2020;9(23):e017326.

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8. Vallabhajosyula S, Dunlay SM, Barsness GW, et al. Hospital-level disparities in the outcomes of acute myocardial
infarction with cardiogenic shock. Am J Cardiol. 2019;124(4):491-8.

9. Lattuca B, Kerneis M, Saib A, et al. On- versus off-hours presentation and mortality of ST-segment elevation
myocardial infarction patients treated with primary percutaneous coronary intervention. JACC Cardiovasc Interv.
2019;12(22):2260-8.

10. Strom JB, Zhao Y, Shen C, et al. Hospital variation in the utilization of short-term nondurable mechanical circulatory
support in myocardial infarction complicated by cardiogenic shock. Circ Cardiovasc Interv. 2019;12(1):e007270.

11. Tehrani BN, Truesdell AG, Psotka MA, et al. A standardized and comprehensive approach to the management of
cardiogenic shock. JACC Heart Fail. 2020;8(11):879-91.

12. Truesdell AG, Tehrani B, Singh R, et al. ‘Combat’ approach to cardiogenic shock. Interv Cardiol. 2018;13(2):81-6.

13. Tchantchaleishvili V, Hallinan W, Massey HT. Call for organized statewide networks for management of acute
myocardial infarction-related cardiogenic shock. JAMA Surg. 2015;150(11):1025-6.

14. Rab T, Ratanapo S, Kern KB, et al. Cardiac shock care centers: JACC review topic of the week. J Am Coll Cardiol.
2018;72(16):1972-80.

15. Basir MB, Kapur NK, Patel K, et al. Improved outcomes associated with the use of shock protocols: updates from the
National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7): p. 1173-1183.

16. Tehrani, B.N., et al., Standardized team-based care for cardiogenic shock. J Am Coll Cardiol. 2019. 73(13):1659-69.

17. Taleb I, Koliopoulou AG, Tandar A, et al. Shock team approach in refractory cardiogenic shock requiring short-term
mechanical circulatory support: a proof of concept. Circulation. 2019;140(1):98-100.

18. Lee F, Hutson JH, Boodhwani M, et al. Multidisciplinary code shock team in cardiogenic shock: a Canadian centre
experience. CJC Open. 2020;2(4):249-57.

19. Moghaddam N, van Diepen S, So D, et al. Cardiogenic shock teams and centres: a contemporary review of
multidisciplinary care for cardiogenic shock. ESC Heart Fail. 2021;8(2):988-98.

20. Shaefi S, O’Gara B, Kociol RD, et al. Effect of cardiogenic shock hospital volume on mortality in patients with
cardiogenic shock. J Am Heart Assoc. 2015;4(1):e001462.

21. Wayangankar SA, Bangalore S, McCoy LA, et al. Temporal trends and outcomes of patients undergoing percutaneous
coronary interventions for cardiogenic shock in the setting of acute myocardial infarction: a report from the CathPCI
Registry. JACC Cardiovasc Interv. 2016;9(4):341-51.

22. Truesdell AG, Tehrani B, Rosner C, et al. After action reviews. J Invasive Cardiol. 2019;31(11):E341.

23. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with pulmonary artery catheters in
cardiogenic shock is associated with lower in-hospital mortality. JACC Heart Fail. 2020;8(11):903-13.

24. Samsky M, Krucoff M, Althouse AD, et al. Clinical and regulatory landscape for cardiogenic shock: a report from the
Cardiac Safety Research Consortium ThinkTank on cardiogenic shock. Am Heart J. 2020;219:1-8.

25. Papolos AI, Kenigsberg BB, Berg DD, et al. Management and outcomes of cardiogenic shock in cardiac ICUs with
versus without shock teams. J Am Coll Cardiol. 2021; 78(13):1309-17.

26. Tehrani BN, Sherwood MW, Rosner C, et al. A standardized and regionalized network of care for cardiogenic shock. J
Am Coll Cardiol HF. 2022. Epublished DOI: 10.1016/[Link].2022.04.004.

27. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update: a review
and incorporation of validation studies. Journal of the Society for Cardiovascular Angiography & Interventions.
2022;1(1):100008. [Link]

28. Mehta A, Vavilin I, Nguyen AH, et al. Contemporary approach to cardiogenic shock care: a state-of-the-art review.
Front Cardiovasc Med. 2024;11:1354158.

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SECTION 2

Basics of
Mechanical
Circulatory
Support

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

9
PREVIOUS CHAPTER Chapter 9: Patient Identification and Device Selection NEXT CHAPTER

Patient
Identification and
Device Selection
Leah B. Kosyakovsky, MD Navin K. Kapur, MD, FSCAI
Cardiology Fellow Associate Professor
Division of Cardiovascular Medicine The Cardiogenic Shock Working Group
Beth Israel Deaconess Medical Center The Cardiovascular Center
Boston, MA Tufts Medical Center and Tufts University
School of Medicine
Haval Chweich, MD Boston, MA
Assistant Professor
Division of Pulmonary, Critical Care and Jeffrey A. Marbach, MBBS, MS,
Sleep Medicine FRCPC, FSCAI
The Cardiogenic Shock Working Group Interventional Cardiologist & Cardiac
The Cardiovascular Center Intensivist
Tufts Medical Center and Tufts University Division of Cardiology, Knight
School of Medicine Cardiovascular Institute
Boston, MA Assistant Professor
Oregon Health & Sciences University
marbach@[Link]
@JAMarbach

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Introduction
The management of patients with cardiogenic shock (CS) has evolved considerably over the past two
decades as technological advances have led to the development of numerous mechanical circulatory
support (MCS) devices. Today, temporary MCS platforms—capable of providing left ventricular (LV),
right ventricular (RV), and biventricular (BiV) support—can be initiated in a matter of minutes through
percutaneous arterial and venous access.1-3 In concert with these advances there has been significant
progress in our understanding of risk stratification in CS, which has enabled better identification of
patients unlikely to respond to conventional medical therapy, and who therefore may benefit from
invasive support. While randomized clinical trial evidence supporting the use of MCS is limited, recent
CS management algorithms focused on early identification and management of high-risk patients
(within a multidisciplinary team at dedicated CS centers) have shown significant improvements in
clinical outcomes.4,5 In this chapter, we summarize the indications for temporary MCS, discuss the
advantages and disadvantages of key MCS platforms, and provide a contemporary decision-making
algorithm for device selection in CS based on the most recent clinical evidence.

Indications for mechanical circulatory support

Numerous clinical parameters serve as markers of severity and poor prognosis in CS. While no
individual parameter in and of itself may necessarily dictate the use of advanced therapies, the presence
of several clinical, hemodynamic, and laboratory indices taken together may identify patients who
require temporary mechanical circulatory support (Table 1).

Table 1. Indications for MCS

LABORATORY INDICES OF POOR

HEMODYNAMIC INDICES CLINICAL INDICES
PERFUSION

• Lactate elevation or absence of • Reduced CI (<2.2) or CPO <0.6 W • Hypotension with escalating
lactate clearance pressor requirement
• Severe LV congestion (elevated
• Elevated transaminases PCWP or LVEDP) • Cardiac arrest

• Hypoglycemia • RV dysfunction (depressed PAPi, • Refractory ventricular arrythmia

elevated RAP/PCWP, reduced
• Renal dysfunction RVSWI, RV congestion)

All of the following have been shown to predict short-term mortality in both CS secondary to acute
decompensated heart failure (ADHF-CS) and acute myocardial infarction (AMI-CS):6–9
• Hemodynamic assessments of LV dysfunction (LV congestion, reduced ejection fraction)
• RV dysfunction (increased RAP/PCWP, reduced PAPi, and RVSWI, RV congestion)
• Reduced cardiac output (cardiac output [CO], cardiac index [CI], cardiac power output [CPO])
• Other systemic measures (reduced MAP, increased HR, and vasopressor requirement)
Similarly, lab-based biomarkers including reduced lactate clearance, elevated transaminases,
hyperglycemia, and worsening renal function portend worse clinical outcomes.6,10,11 More broadly,
integrated clinical classification systems such as the Society for Cardiovascular Angiography &
Interventions (SCAI) stages of cardiogenic shock have been used to predict both short- and long-term
mortality; generally, patients in SCAI stages C-E are potential candidates for MCS.12–15

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The use of temporary MCS should be considered in patients with evidence of ongoing severe (or
“refractory”) CS despite medical therapy. While specific definitions may vary, this is typically evidenced
by severely reduced cardiac function (CI <2.2 L/min, CPO <0.6 W) as well as evidence of hypoperfusion
(eg, reduced urine output, altered mental status, increasing lactate). Other urgent indications for MCS
include persistent unstable ventricular arrhythmia and refractory cardiac arrest. Guided selection of
specific device therapy based on hemodynamic patterns is detailed further below.

Contemporary mechanical circulatory support devices

The fundamental features of typical contemporary MCS devices are summarized in Table 2.4,16,17
Currently available MCS devices can be implemented alone or in varying combinations to provide LV,
RV, or BiV hemodynamic support depending on individual patient requirements (Figure 1).

Table 2. Characteristics of Contemporary MCS Devices

DEVICE FLOW INSERTION HEMODYNAMICS CONTRAINDICATIONS

LEFT VENTRICULAR SUPPORT

IABP Pulsatile Femoral - 7–8 Fr Reduced afterload, Aortic dissection,

(0.5 L/min) increased MAP, mod-severe aortic
increased coronary regurgitation, severe PAD
perfusion

Impella 2.5, CP, Axial Femoral -13 Fr (2.5), 14 Fr LV unloading, Mechanical aortic valve,
5.0, 5.5 (2.5–6 L/min) (CP), 22 Fr (5.0) increased cardiac LV thrombus, VSD
Axillary - 21 Fr (5.5) power, decreased
A B afterload

TandemHeart Centrifugal Femoral venous - 21 Fr LV unloading, VSD, mod-severe aortic

(3.5–4 L/min) Arterial - 15 or 17 Fr increased cardiac regurgitation, severe PAD
power
RIGHT VENTRICULAR SUPPORT

Impella RP Axial Femoral venous - 23 Fr RV unloading Severe tricuspid/pulmonic

(2–4 L/min) stenosis, severe tricuspid/
pulmonic regurgitation,
mechanical tricuspid/
pulmonic valve, RA or IVC
thrombus, IVC filter

ProtekDuo Centrifugal Right internal jugular vein RV unloading, Severe tricuspid/pulmonic

(4–5 L/min) - 29 or 31 Fr +/- improved stenosis, mechanical
oxygenation tricuspid/pulmonic valve,
(with additional RA thrombus
oxygenator)
BIVENTRICULAR SUPPORT

VA ECMO Centrifugal Femoral venous - 21–25 Fr Increased cardiac Severe aortic regurgitation,
(4–7 L/min) Arterial - 15–19 Fr power, increased LV aortic dissection, severe
afterload, decreased PAD
LV preload, variable
effects on LV
unloading

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Figure 1. Contemporary Mechanical Circulatory Support Platforms

Options for LV support include intra-aortic balloon pump (IABP), TandemHeart® (LivaNova; London,
UK), and the Impella® (Abiomed; Danvers, MA).
• The IABP is a catheter-mounted aortic counterpulsation device that is positioned in the
descending aorta. Through diastolic inflation blood volume is displaced to the proximal aorta,
thereby increasing MAP and coronary perfusion. The balloon subsequently deflates during systole
to reduce afterload and further augment pulsatile blood flow.18
• TandemHeart is an extracorporeal, centrifugal continuous flow device that provides direct left
atrial to arterial bypass through venous and arterial catheters positioned across the interatrial
septum and femoral artery, respectively.
• Impella LV support devices are microaxial flow pumps that can be inserted percutaneously
(Impella 2.5®, Impella CP®) or through a surgical cutdown (Impella 5.0®, Impella 5.5®) and are
positioned across the aortic valve where they provide direct unloading of the LV.

With mechanisms similar to their LV counterparts, RV support devices include the Impella RP®
(Abiomed; Danvers, MA) and ProtekDuo® (LivaNova; London, UK).
• Impella RP is a transaxial flow pump that provides direct RV bypass to the pulmonary artery
• ProtekDuo is a centrifugal pump providing right atrial to pulmonary bypass

Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is another centrifugal system providing
BiV support as well as both oxygenation and ventilation.

Table 2 provides details regarding mechanism of support, flow capacity, hemodynamic effects, and
contraindications for each device.

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Device selection in cardiogenic shock

Numerous algorithms for specific MCS device selection in CS have been published.4,19–21 Here, we
provide the Tufts Medical Center Cardiogenic Shock algorithm, which consolidates available evidence
and represents a pragmatic approach to the initial evaluation and management of patients with
suspected CS. Importantly, this approach considers the differences in phenotype and clinical trajectory
for patients with AMI-CS and ADHF-CS.

Eligible patients with suspected cardiogenic shock with emergent indications for MCS (ie, cardiac arrest,
VT storm, or refractory hypoxemia) should be considered for upfront biventricular support with VA
ECMO (Figure 2).22 In absence of these emergent MCS indications, patients with shock can be assessed
depending on etiology as per an AMI-CS (Figure 3) or ADHF-CS algorithm (Figure 4).

SUSPECTED CARDIOGENIC SHOCK

BP <90/60 mmHg for ≥20 min, or 1 vasopressor/inotrope, or lactate ≥3 mmol/L

Cardiac arrest, or YES

VT storm, or
refractory hypoxemia?

VA ECMO

Known or suspected
acute myocardial
infarction?

YES NO

Acute Myocardial Infarction Acute Decompensated Heart

Shock Pathway Failure Shock Pathway
(see Figure 3) (see Figure 4)

Figure 2. Tufts Cardiogenic Shock Evaluation & Management Algorithm

AMI-CS
An initial left ventricular end-diastolic pressure (LVEDP) measurement enables rapid decision making
at the time of revascularization in AMI-CS. Elevated LV filling pressures in patients with AMI have
been consistently correlated with increased short- and long-term mortality23,24; therefore, in patients
with an initial LVEDP ≥20 mmHg, it is reasonable to consider initiating LV unloading with Impella CP.
Patients receiving upfront LV unloading with Impella may then undergo right heart catherization (RHC)
to determine whether additional RV support is necessary (as evidenced by RA/PCWP >0.86 or PAPi
<1).4,25–27 If RV dysfunction is present, further support may be achieved with inotropy, a right-sided device
(Impella RP / ProtekDuo), or advancement to VA ECMO. In the absence of significant RV dysfunction,
patients with Impella unloading may still need to be considered for further inotropic agents or more
advanced LV support (ie, ECMO) should they continue to deteriorate despite initial LV support measures.

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Similarly, patients without an initial indication for Impella at the time of revascularization may still be
considered for LV unloading should their subsequent RHC demonstrate a reduced CI in conjunction with
elevated filling pressures (PCWP >20), with additional RV support added in the setting of concomitant
RV dysfunction. In the absence of any of these indications, patients may be transferred to the ward/CCU
and treated with medical therapy, with frequent evaluation for deteriorating clinical or hemodynamic
status which would suggest a reassessment of MCS (Figure 3).

ACUTE MYOCARDIAL (AMI)

SHOCK PATHWAY

Obtain femoral artery access and measure LVEDP

Left heart cath ± PCI NO YES Initiate left

and then LVEDP ≥20 mmHg? ventricular unloading
Right heart cath with Impella CP

NO Cardiac index ≤2.2 Left heart cath ± PCI

L/min/m2? and then
Right heart cath
YES

YES Cardiac index ≤2.2 NO

PCWP ≥20 mmHg? Unload LV with Impella CP
L/min/m2?
NO
YES

Assess need for RV YES YES Assess need for RV

support support
(RA/PCWP >0.86 or PAPi <1) (RA/PCWP >0.86 or PAPi <1)

NO NO

Consider IV fluid Initiate RV support Consider additional

challenge and reassess Inotropes OR Impella OR LV support
hemodynamics Protek Duo OR VA ECMO† Inotropes or VA ECMO†

Transfer to ward/CCU

†Consider VA ECMO in patients with advanced hemo-metabolic shock

(ie, lactate >5 mmol/L, refractory hypoxemia = PA02/FiO2 <80 on PEEP ≥10 mmHg)

Figure 3. Tufts AMI-CS Management Algorithm

ADHF-CS
Indications for MCS consideration in patients with ADHF-CS (Figure 4) may include either:
• Escalation of vasoactive medication requirement, or
• Lactate elevation >3 mmol/L, lack of lactate clearance, or other signs of persistent poor end-organ
perfusion11,28
Patients not responding to initial medical therapy may proceed to RHC (with or without concomitant
LVEDP assessment). Hemodynamically unstable patients with depressed CI should have LV support with
Impella initiated; escalation to VA ECMO or additional insertion of RV support may be necessary with
evidence of RV congestion (RA >16 mmHg, RA/PCWP >0.63) or poor RV function (PAPi <1.85).6,29,30

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In contrast, hemodynamically stable ADHF-CS patients with depressed CI may only require the lesser
support of an IABP, or potentially simply escalation of existing inotrope/vasodilator therapy provided BP
tolerance as well as further room for medical afterload reduction (MAP >60 mmHg and SVR >1500).
Frequent reassessment of clinical and hemodynamic status is imperative to determine efficacy of therapy
and need for potential escalation.

ACUTE DECOMPENSATED HEART FAILURE (ADHF)

SHOCK PATHWAY

Assess clinical &

hemodynamic stability
(HR, BP, urine output, lactate)

Escalating vasoactive medications,

OR
Lactate ≥3 mmol/L,
OR
Failure to clear lactate with initial therapy?

HEMODYNAMICALLY STABLE HEMODYNAMICALLY UNSTABLE

URGENT EMERGENT
Right heart cath ± Left heart cath Right heart cath ± Left heart cath

YES
NO
Cardiac index ≤2.2 L/min/m ? 2
Cardiac index ≤2.2 L/min/m2?
YES

Can patient tolerate Initiate LV support NO

vasodilators/inotropes? (Impella CP / 5.0 / 5.5 or VA ECMO†)
(MAP ≥60 mmHg, SVR ≥1500)

YES RA ≥16 mmHg and PCWP >0.63 NO

OR
NO
PAPi <1.85?
YES

Initiate/increase vasodilators Protek Duo

Insert IABP OR OR
inotropes VA ECMO†

Transfer to CCU with continuous

hemodynamic monitoring

†Consider VA ECMO in patients with advanced hemo-metabolic shock

(ie, lactate >5 mmol/L, refractory hypoxemia = PA02/FiO2 <80 on PEEP ≥10 mmHg)

Figure 4. Tufts ADHF-CS Management Algorithm

While there is a dearth of high-quality randomized evidence examining and comparing MCS devices
in specific populations of CS, a selected summary of available evidence for IABP, Impella, and
TandemHeart is provided in Table 3.

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Table 3. Trial Summary to Date of MCS Use in Cardiogenic Shock

TRIAL YEAR POPULATION (N) ARMS OUTCOMES RESULTS

IABP

TACTICS31 2005 AMI-CS (57) IABP vs All-cause No significant

fibrinolysis alone mortality difference

IABP-SHOCK32 2010 AMI-CS (45) IABP vs APACHE score No significant

PCI alone (30-day) difference

IABP-SHOCK II33 2012 AMI-CS (600) IABP vs All-cause No significant

PCI alone mortality difference

IMPELLA

ISAR-Shock34 2008 AMI-CS (25) IABP vs All-cause No significant

Impella 2.5 mortality difference
in mortality;
improved CI/CP
with Impella

IMPRESS35 2017 AMI-CS (48) IABP vs All-cause No significant

Impella CP mortality difference

DanGer Shock39 2024 AMI-CS (360) Impella-CP vs All-cause Impella reduced

Standard Care mortality mortality, but
(180 Days) also increased
composite
adverse events
TANDEMHEART

Burkhoff et al., 2006 Refractory CS IABP vs All-cause No significant

200636 TandemHeart mortality, severe difference in
adverse events, survival/adverse
hemodynamics events; improved
MAP, CI, and
PCWP with
TandemHeart

VA ECMO

ECLS Shock37 2023 AMI-CS (420) VA ECMO vs All-cause No significant

Standard Care mortality differences
(30 Days) in mortality;
ECMO resulted
in increased
bleeding and
ischemic
complications

ECMO CS38 2022 Refractory CS VA ECMO vs Composite No significant

(122) Standard Care of all-cause difference
mortality,
resuscitated
arrest, use of
other MCS
(30 days)

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QUICK READ SUMMARY

✓ Inadequate tissue perfusion can be ascertained through a combination of clinical, laboratory,

and hemodynamic parameters.

✓ The presence of several markers of hypoperfusion may identify patients who require
temporary MCS.

✓ Beyond initial risk stratification for MCS therapy, the decision-making process for MCS
consideration and specific device selection in cardiogenic shock should be a dynamic process
with continuous reassessment of clinical and hemodynamic status along the course of the
patient’s illness.

✓ As we develop a greater understanding of the distinct hemodynamic and clinical phenotypes

of cardiogenic shock and accumulate more high-quality randomized evidence in specific
etiologies of shock, we will move toward increasingly personalized, nuanced MCS selection
across the spectrum of cardiac critical illness.

References
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hospital mortality in the United States. J Am Heart Assoc. 2021;10(15):e021061.

2. Lang CN, Kaier K, Zotzmann V, et al. Cardiogenic shock: incidence, survival and mechanical circulatory support usage
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3. Dhruva SS, Ross JS, Mortazavi BJ, et al. Use of mechanical circulatory support devices among patients with acute
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4. Tehrani BN, Truesdell AG, Psotka MA, et al. A standardized and comprehensive approach to the management of
cardiogenic shock. JACC Heart Fail. 2020;8(11):879–91.

5. Nagpal AD, Singal RK, Arora RC, Lamarche Y. Temporary mechanical circulatory support in cardiac critical care: a
state of the art review and algorithm for device selection. Can J Cardiol. 2017;33(1):110–8.

6. Hernandez-Montfort J, Sinha SS, Thayer KL, et al. Clinical outcomes associated with acute mechanical circulatory
support utilization in heart failure related cardiogenic shock. Circ Heart Fail. 2021;14(5):542-52.

7. Thayer KL, Zweck E, Ayouty M, et al. Invasive hemodynamic assessment and classification of in-hospital mortality risk
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8. Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in
cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340–8.

9. Parlow S, Di Santo P, Mathew R, et al. The association between mean arterial pressure and outcomes in patients with
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10. Pöss J, Köster J, Fuernau G, et al. Risk stratification for patients in cardiogenic shock after acute myocardial infarction. J
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11. Marbach JA, Stone S, Schwartz B, et al. Lactate clearance is associated with improved survival in cardiogenic shock: a
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12. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic
shock: this document was endorsed by the American College of Cardiology (ACC), the American Heart Association
(AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019.
Catheter Cardiovasc Interv. 2019;94(1):29–37.

13. Jentzer JC, Burstein B, van Diepen S, et al. Defining shock and preshock for mortality risk stratification in cardiac
intensive care unit patients. Circ Heart Fail. 2021;14(1):e007678.

14. Jentzer JC, van Diepen S, Barsness GW, et al. Cardiogenic shock classification to predict mortality in the cardiac
intensive care unit. J Am Coll Cardiol. 2019;74(17):2117–28.

15. Schrage B, Dabboura S, Yan I, et al. Application of the SCAI classification in a cohort of patients with cardiogenic
shock. Catheter Cardiovasc Interv. 2020;96(3):E213–E219.

16. Mandawat A, Rao SV. Percutaneous mechanical circulatory support devices in cardiogenic shock. Circ Cardiovasc
Interv. 2017;10(5). Available from: [Link]

17. Atkinson TM, Ohman EM, O’Neill WW, et al. A practical approach to mechanical circulatory support in patients
undergoing percutaneous coronary intervention: an interventional perspective. JACC Cardiovasc Interv.
2016;9(9):871–83.

18. Marbach JA, Chweich H, Miyashita S, Kapur NK. Temporary mechanical circulatory support devices: updates from
recent studies. Curr Opin Cardiol. 2021;36(4):375–83.

19. Rab T, Ratanapo S, Kern KB, et al. Cardiac shock care centers: JACC review topic of the week. J Am Coll Cardiol.
2018;72(16):1972–80.

20. Basir MB, Schreiber T, Dixon S, et al. Feasibility of early mechanical circulatory support in acute myocardial
infarction complicated by cardiogenic shock: the Detroit cardiogenic shock initiative. Catheter Cardiovasc Interv.
2018;91(3):454–61.

21. Garan AR, Takeda K, Salna M, et al. Prospective comparison of a percutaneous ventricular assist device and
venoarterial extracorporeal membrane oxygenation for patients with cardiogenic shock following acute myocardial
infarction. J Am Heart Assoc. 2019;8(9):e012171.

22. Yannopoulos D, Bartos J, Raveendran G, et al. Advanced reperfusion strategies for patients with out-of-hospital
cardiac arrest and refractory ventricular fibrillation (ARREST): a phase 2, single centre, open-label, randomised
controlled trial. Lancet. 2020;396(10265):1807–16.

23. Planer D, Mehran R, Witzenbichler B, et al. Prognostic utility of left ventricular end-diastolic pressure in patients with
ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Am J Cardiol.
2011;108(8):1068-74.

24. Kirtane AJ, Bui A, Murphy SA, et al. Association of epicardial and tissue-level reperfusion with left ventricular end-
diastolic pressures in ST-elevation myocardial infarction. J Thromb Thrombolysis. 2004;17(3):177-84.

25. Cohen A, Guyon P, Johnson N, et al. Hemodynamic criteria for diagnosis of right ventricular ischemia associated with
inferior wall left ventricular acute myocardial infarction. Am J Cardiol. 1995;76(4):220–5.

26. Korabathina R, Heffernan KS, Paruchuri V, et al. The pulmonary artery pulsatility index identifies severe right
ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80(4):593–600.

27. Lim HS, Howell N. Cardiogenic shock due to end-stage heart failure and acute myocardial infarction: characteristics
and outcome of temporary mechanical circulatory support. Shock. 2018;50(2):167–72.

28. Fuernau G, Desch S, de Waha-Thiele S, et al. Arterial lactate in cardiogenic shock: prognostic value of clearance
versus single values. JACC Cardiovasc Interv. 2020;13(19):2208–16.

29. Morine KJ, Kiernan MS, Pham DT, et al. Pulmonary artery pulsatility index is associated with right ventricular failure
after left ventricular assist device surgery. J Card Fail. 2016;22(2):110–6.

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30. Kochav SM, Flores RJ, Truby LK, Topkara VK. Prognostic impact of pulmonary artery pulsatility index (PAPi) in patients
with advanced heart failure: insights from the ESCAPE Trial. J Card Fail. 2018;24(7):453–9.

31. Ohman EM, Nanas J, Stomel RJ, [Link]. Thrombolysis and counterpulsation to improve survival in myocardial infarction
complicated by hypotension and suspected cardiogenic shock or heart failure: results of the TACTICS Trial. J Thromb
Thrombolysis. 2005;19(1):33–9.

32. Prondzinsky R, Lemm H, Swyter M, et al. Intra-aortic balloon counterpulsation in patients with acute myocardial
infarction complicated by cardiogenic shock: the prospective, randomized IABP SHOCK Trial for attenuation of
multiorgan dysfunction syndrome. Crit Care Med. 2010;38(1):152–60.

33. Thiele H, Schuler G, Neumann F-J, et al. Intraaortic balloon counterpulsation in acute myocardial infarction
complicated by cardiogenic shock: design and rationale of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-
SHOCK II) trial. Am Heart J. 2012;163(6):938–45.

34. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous
left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by
myocardial infarction. J Am Coll Cardiol. 2008;52(19):1584–8.

35. Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous mechanical circulatory support versus intra-aortic balloon
pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69(3):278–87.

36. Burkhoff D, Cohen H, Brunckhorst C, O’Neill WW, TandemHeart Investigators Group. A randomized multicenter
clinical study to evaluate the safety and efficacy of the TandemHeart percutaneous ventricular assist device
versus conventional therapy with intraaortic balloon pumping for treatment of cardiogenic shock. Am Heart J.
2006;152(3):469.e1–8.

37. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock. N Engl J Med.
2023;389(14):1286-97.

38. Ostadal P, Rokyta R, Karasek J, et al. Extracorporeal membrane oxygenation in the therapy of cardiogenic shock:
results of the ECMO-CS randomized clinical trial. Circulation. 2023;147(6):454-64.

39. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl J Med. 2024;390(15):1382-93.

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10
PREVIOUS CHAPTER Chapter 10: Access and Closure Techniques in MCS NEXT CHAPTER

Access and
Closure
Techniques in
MCS

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10.1
Best Practice
Algorithm for
Large Bore
Femoral Artery
Access
Marie-France Poulin, MD, FACC, FSCAI
Beth Israel Deaconess Medical Center
Associate Director, Structural Heart Clinical Services
Assistant Professor of Medicine, Harvard Medical School
Boston, MA
mpoulin@[Link]

Ashvarya Mangla, MD, FSCAI

OSF Saint Francis Medical Center
Peoria, IL

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Overview
With recent advancements in interventional cardiology techniques, more complex procedures are being
performed percutaneously. Several procedures—such as transcatheter aortic valve replacement (TAVR),
transcatheter endovascular aortic repair (TEVAR), and placement of percutaneous hemodynamic
support devices such as Impella® and venoarterial extracorporeal membrane oxygenation (VA ECMO)—
require large bore femoral arterial access (sheath size ≥12 Fr). The success of these procedures relies
heavily on good femoral arterial access techniques. This section provides a brief overview of strategies
to achieve optimal femoral arterial access and sustained hemostasis.

Strategic planning, equipment, and procedural consideration

Successful femoral large bore access requires entering the artery with a single antegrade puncture
(modified Seldinger technique), avoiding areas of calcification in the vessel, and entering at least 1 cm
above the femoral bifurcation (to minimize the risk of pseudoaneurysm and hematoma and allow for the
safe placement of a covered stent) and below the inferior reflection of the inferior epigastric artery (to
minimize the risk of retroperitoneal bleeding).

Anatomic landmarks, such as skin crease, anterior superior iliac spine, and pubic symphysis, are unreliable
for predicting the entry site into the common femoral artery and should not be used to guide access.
Combining fluoroscopy and ultrasonography is the safest and most reliable technique to obtain access,
as shown in Figure 1. The optimal femoral artery entry site is just below the center of the femoral head,
at least 1 cm above the bifurcation. Fluoroscopy or vascular ultrasound can be used to identify the inferior
border of the femoral head and help avoid a high puncture. The femoral head can be seen on ultrasound
by sliding the probe laterally and can be used as a landmark. Vascular ultrasonography should be used to
identify the femoral artery bifurcation, areas of calcification, and significant plaque in the common femoral
artery. Operators should optimize the vessel entry site based on these findings. To ensure that the arterial
access is in the desired location and to avoid hemostasis-related complications, direct visualization of
the tip of the needle entering the anterior wall of the femoral artery is critical. A side puncture will often
result in failed closure device hemostasis. A final fluoroscopy of the needle through the skin, just prior to
puncturing the vessel, can also avoid a high puncture.

The micropuncture needle and wire should also be evaluated in a longitudinal view of the vessel to
confirm entry point is >1 cm above the bifurcation (to allow for a covered stent placement in case of a
complication), and over the femoral head.

Using ultrasound has been shown to improve first pass success rate, reduce the number of attempts,
reduce the rate of venipuncture, reduce vascular complications, and increase the rate of sheath insertion
into the common femoral artery in patients with a high common femoral artery bifurcation. Thus,
ultrasound can help to identify the “ideal” puncture location. Other resources, such as prior femoral
angiography and CT angiography (CTA), when available, should also be reviewed to understand the
vessel’s anatomy.

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Figure 1. Fluoroscopic and Ultrasound Techniques for Femoral Access

(A) Hemostat to identify lower edge of femoral head. (B) Confirm position of hemostat with fluoroscopy. (C) Ultrasound positioned to visualize
common femoral artery (f.a.). (D) Ultrasound visualization of common femoral artery (left) and bifurcation into superficial and profunda (right).
(E, F) Triangulation for needle entry. (G) Needle entry position (arrow) and guidewire advancement assessed using fluoroscopy. (H) Femoral
angiography. From: Sandoval, Y. et al. J Am Coll Cardiol Intv. 2017;10(22):2233-41.

CTA is an essential part of procedural planning for patients undergoing structural and vascular
procedures. CTA analysis and reconstructions are very informative regarding femoral, iliac, and aortic
anatomy. The analysis provides information about the femoral artery bifurcation height, the extent and
location of calcifications, vessel diameters, tortuosity, and the presence of intravascular pathologies
such
A as hematoma, dissection, pseudoaneurysm, or B atheroma (Figure 2). To minimize vessel injury and
ensure proper distal perfusion while the large sheath is in place, the ideal sheath to femoral arterial ratio
(SFAR) should be <1.05.

A B

C D

Figure 2. CTA Analysis

(A) CT angiographic reconstruction of iliofemoral vessels. (B) Severely calcified iliofemoral vessels (blue arrows). (C) Severe anterior calcification in
the common femoral artery with very narrow target zone. (D) Bilateral high common femoral artery bifurcation. FH=femoral head

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Micropuncture technique is the preferred method for large bore common femoral artery access. The
micropuncture needle is an 21G needle, as opposed to a traditional 18G Cook needle. It reduces vessel
trauma and blood loss and facilitates hemostasis in case of inadequate vessel entry site.

For this technique, advance a 0.018″ guidewire through the needle into the artery, remove the needle, and
advance a micropuncture sheath (usually 4 Fr) into the femoral artery and withdraw the guidewire. At this
point, perform a femoral angiogram, with ipsilateral 30° angulation, through the sheath to confirm a safe
entry point into femoral artery (Figure 3). If inadequate, remove the micropuncture sheath, apply manual
pressure, and obtain new access. Once satisfied with the puncture location, upsize the micropuncture
sheath to a 5-8 Fr sheath over a 0.035″ wire. The wire should then be exchanged for a stiff wire, such as
an Amplatz Super Stiff ™ wire, to avoid vessel injury when advancing large bore sheaths.

Figure 3. Femoral Angiogram Through Micropuncture

Sheath
Angiogram shows satisfactory femoral artery entry point above the
bifurcation and below the lower part of the inferior epigastric artery.
FH=femoral head

Successful hemostasis and lack of high-grade stenosis should be confirmed in the room with an
angiography from the contralateral access site, radial access, or Doppler ultrasound. In case of a
vascular complication such as a flow limiting dissection, significant residual bleeding, or stenosis, the
other access site can be used to cross over and treat that condition.

Large bore closure devices currently available in the United States include the Perclose ProGlide® Suture
(up to 8 Fr sheath with a single device and 21 Fr with 2 devices), the Prostar XL® Percutaneous Vascular
Surgical System (8.5–10 Fr sheaths), and the Manta Vascular Closure Device (10–20 Fr sheaths). The
Vivasure PerQseal closure device system, a sutureless fully absorbable synthetic implant, is currently
being studied in the PATCH clinical trial (for arteriotomy of 14-24 Fr).

Our preferred closure device for large bore access closure is the Perclose ProGlide. Using this device
with sheaths larger than 8 Fr, we “pre-close” the vessel with 2 Perclose devices. After dilating the
access site with a 6 Fr sheath over an 0.035″ guidewire, both Perclose devices are sequentially
deployed upright (facing 12 o’clock). An 8 Fr sheath is then inserted, and the soft wire exchanged for
a stiff guidewire prior to inserting the large bore sheath. The sutures are tightened at the end of the
procedure, after removal of the large bore sheath.

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After successful deployment of the sutures, angiography from the contralateral access or vascular
ultrasound should be done to confirm hemostasis and the absence of flow-limiting dissection or
significant vessel stenosis. In case of significant bleeding, an appropriately sized peripheral balloon (6-8
x 40 mm) can be inflated in the femoral artery from the contralateral arterial access using the cross-over
technique to temporarily stabilize the patient. Operators should also be familiar with the Coda® balloon,
which can be inflated in the aorta in case of an iliac perforation. If hemostasis cannot be achieved with
prolonged balloon inflations and manual pressure, consider deployment of a covered stent from the
contralateral side or radial artery. Limitations of covered stents in the common femoral artery include
risk of losing a branch (superficial femoral artery or profunda) and risk of stent fracture from repetitive
hip flexion. A covered stent should only be placed if it can end above the bifurcation, ensuring that flow
down the profunda artery does not get compromised. If hemostasis cannot be achieved, or the injury
is not amenable to percutaneous repair, assistance from peripheral IC colleagues or vascular surgery
should be obtained prior to considering a surgical repair. Significant vessel stenosis after deployment of
the Perclose can usually be treated with low pressure balloon inflation across the lesion.

Once the large bore sheath is inserted, anticoagulation should be initiated immediately with heparin
(ACT goal >250) to avoid thrombus formation. Additional considerations include having a valid type and
screen prior to starting the case. This ensures that blood is readily available for transfusion and saves
precious time in the event of hemorrhage. Operators should also be familiar with devices and techniques
needed in case of complications (Table 1).

Table 1. Potential Complications and Management

COMPLICATION PREVENTION AND MANAGEMENT

• Minimize the number of puncture attempts

• Use vascular ultrasound and fluoroscopy to gain access; avoid areas of calcification
General precautions and high puncture and ensure vessel entry point is at least 1 cm above the bifurcation
whenever possible
• Ensure proper deployment of closure device

• Prolonged manual pressure usually leads to hemostasis

• Use protamine to reverse anticoagulation
Bleeding / Hematoma • If bleeding is more severe, use balloon tamponade from the contralateral side
• Consider covered stent placement
• Consult peripheral IC colleagues or vascular surgery if percutaneous management fails or
is not feasible

• Obtain angiogram to confirm diagnosis through contralateral or radial access

• Apply manual pressure
Pseudoaneurysm • Pseudoaneurysms can be treated with ultrasound-guided compression and thrombin
injection.
• Consult vascular surgery if percutaneous management fails or is not feasible

• Obtain angiogram through contralateral access

Dissection • Use balloon tamponade and consider stent placement if balloon tamponade fails
• Consult vascular surgery if needed

• Use balloon tamponade in proximal vessel through contralateral access; if iliac ruptures,
Vessel place Coda balloon in the distal aorta
avulsion / rupture • Employ aggressive volume resuscitation
• Consult vascular surgery if needed

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When placing large sheaths (14 Fr or larger) that will remain in place for >12-24h, operators should ensure
adequate distal perfusion of that leg. There should be a low threshold to place an ipsilateral antegrade
cannula to avoid acute limb ischemia from an occlusive large bore sheath (for more information, see Chapter
10.11 Distal Limb Perfusion Strategies). Best practice for the placement of that antegrade canula includes
sheath placement in the distal common femoral artery whenever possible, or in the very proximal superficial
common femoral artery above the femoral head to minimize the risk of pseudoaneurysm and bleeding. It is
technically much easier to obtain antegrade access first using a micropuncture needle, before the large bore
retrograde sheath is in place over the distal vessel. A 6 Fr kink-resistant sheath, such as a BRITE TIP® sheath,
works best for the antegrade access.

Case example
A 59-year-old male with diabetes mellitus, hypertension, severe peripheral arterial disease with
prior bilateral femoral popliteal bypass surgery, right external iliac artery stenting, and left common
femoral artery endarterectomy with patch repair presented with non-ST elevation acute coronary
syndrome. His coronary angiogram revealed severe distal left main disease extending into LAD with
total occlusion of RCA and LCX, which were filled by collaterals. He had small radial arteries, disease
in bilateral subclavian arteries, and his saphenous veins had been previously harvested for fem-pop
bypass grafting. He was deemed not to be a surgical candidate and underwent successful percutaneous
coronary intervention to his unprotected left main into LAD with Impella® support. Ultrasound was used
to obtain access into left femoral bypass graft and helped identify an area free of calcium and plaque.
Hemostasis was successfully obtained with 2 Perclose devices (see Figure 4).

A B C

D E

Figure 4. Case Example Images

(A) Severe distal left main disease extending into the proximal LAD. (B) Diseased right common femoral artery used for the PCI. (C) Left common
femoral artery with prior endarterectomy and patch repair DSA angiography prior to the case. This side was used for Impella CP support during
the PCI. (D) Post successful left main into LAD placement of drug-eluting stent. (E) Completion left common femoral artery angiography with
successful hemostasis.

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QUICK READ SUMMARY

Pre-procedure
• Review prior femoral angiogram (if available).
• Review prior CTA (if available) to assess level of femoral bifurcation, calcification,
femoral and iliac vessel size, prior stents.

Day of procedure
• Identify the lower border of femoral head with hemostat under fluoroscopy.
• Use ultrasound to delineate femoral bifurcation, identify femoral head and femoral
arterial calcification or plaque.
• Use micropuncture needle and ultrasound guidance to obtain access into common
femoral artery with single anterior wall stick.
• Advance the 0.018″ micropuncture wire under fluoroscopic guidance into the common
iliac artery.
• Insert the micropuncture sheath into the femoral artery.
• Remove the 0.018″ wire and perform angiogram with ipsilateral 30° angulation to
confirm that the femoral puncture is above femoral bifurcation and below inferior
epigastric artery.
• Pre-close the vessel with 2 Perclose ProGlide sutures both deployed facing up
(at 12 o’clock).
• Over an Amplatz super stiff wire, serially dilate the arteriotomy and insert large bore
sheath required for the procedure.
• At the end of the case, remove the sheath but leave a long 0.035″ wire in the artery.
• Tighten the Perclose sutures in the order they were deployed. If near hemostasis is
seen, remove the wire and tighten the sutures again. Lock the knot by pulling on the
short thread of each Perclose. Some operators may deploy additional closure devices in
cases of significant residual bleeding (before the wire is removed), although there is no
data to support this practice.
• Confirm hemostasis and normal flow distal to the access site. This can be done
through an angiogram from a contralateral/radial access, or using completion vascular
ultrasound showing complete hemostasis, no stenosis at the access site, and normal
flow down the leg.

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References
1. Seto AH, Abu-Fadel MS, Sparling JM, et al. Real-time ultrasound guidance facilitates femoral arterial access and
reduces vascular complications: FAUST (Femoral Arterial Access With Ultrasound Trial). JACC Cardiovasc Interv.
2010;3(7):751–8. doi: 10.1016/[Link].2010.04.015.

2. Mangla A, Gupta S. Vascular complications post transcatheter aortic valve procedures. Indian Heart J. 2016;68(5):24–
731.

3. Lee MS, Applegate B, Rao SV, et al. Minimizing femoral artery access complications during percutaneous coronary
intervention: a comprehensive review. Catheter Cardiovasc Interv. 2014;84(1):62–9.

4. Rao SV, Stone GW. Arterial access and arteriotomy site closure devices. Nat Rev Cardiol. 2016;13(11):641–50.

5. McGraw CJ, Gandhi RT, Vatakencherry G, et al. Percutaneous large arterial access closure techniques. Tech Vasc
Interv Radiol. 2015;18(2):122–6.

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10.2
Large Bore
Femoral Venous
Access and
Closure
Ashish Pershad, MD, FSCAI
Dignity Health, Arizona
asper1971@[Link]

Vamshidhara Gade, MD, FSCAI

The Heart Group
Fresno, California

Philipp Wiesner, MD
Banner University Medical Center Phoenix
University of Arizona

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Overview
With increasing use of percutaneous mechanical circulatory support (MCS) devices and structural
heart procedures, large bore venous access via the femoral vein has become mainstream. Access size
required for current procedures can be as large as 24 Fr [for the MitraClip® device (Abbott)]. Despite low
pressure in the venous circulation, large access site size carries substantial bleeding risk. To mitigate this
bleeding risk, alternatives to manual hemostasis for access site management have gained traction.

Traditionally, manual pressure with bedrest has been the standard of care for venous access hemostasis
whereas vascular closure devices (VCDs) have become the default for large bore arterial access.
Currently, two methods are in vogue for managing venous access sites:
• The “Z” stitch (also known as the “Figure of 8” suture)
• Pre-closure with a suture-mediated vascular closure with the ProGlide® device (Abbott Vascular,
Menlo Park, CA)
The “Z” stitch is safe, efficient, and cost-effective.1 It leads to faster hemostasis, earlier ambulation, and
fewer access site complications when compared to manual compression alone.2 Long-term patency of
the femoral vein is not negatively impacted by this method.2 Alternatively, pre-closure with a suture-
mediated closure device like Perclose is also effective and safe, but adds to the cost of the procedure.3,4

Access site complications such as bleeding, deep vein thrombosis, AV fistulae, and pseudoaneurysm
formation following large bore venous access can lead to disability and prolonged hospital stay, as well
as adversely affect outcomes including survival. In this chapter we outline the techniques for large bore
femoral venous access and closure.

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Access
In our opinion, one fundamental difference between a routine right heart catheterization and large bore
femoral venous access is that we advocate using ultrasound guidance for every large bore procedure,
even when performed urgently (such as for Impella RP® (Abiomed) or ECMO). This minimizes
inadvertent arterial puncture or entering the vein from an unfavorable angle. However, this is only our
opinion, and no data currently support this recommendation.

A standard 18-gauge needle or a 21-gauge micropuncture needle can be utilized. Whether use of the
micropuncture technique confers any advantage over standard technique when accessing a vein is a
matter of debate.5
1. Using fluoroscopy, identify the bottom of the femoral head with the help of a Kelly clamp or other
radiopaque sterile surgical tool. This will help approximate the level of needle entry. The femoral vein
is located 1 cm medial to the femoral artery. The skin entry site should be approximately 0.5–1 cm
medial and caudal to arterial pulse.
2. Prepare ultrasound by placing the probe in a sterile sheath cover and applying gel. Set depth on the
ultrasound to 3–4 cm (may vary based on patient body habitus).
3. Hold the ultrasound perpendicular to the course of the femoral vein in axial view. The femoral vein
will be medial, larger, and easily compressible. Align the target in the center of the ultrasound screen
to ensure that the target vessel is directly beneath the center of the probe.
4. Inject lidocaine under the center of probe with direct visualization under ultrasound. This guarantees
proper delivery of anesthetic along the entry path.
5. Using an 18-gauge Seldinger needle on a slip tip 10 mL syringe with 3–5 mL of saline, enter the
A skin at an approximately 45 degree angle withBnegative pressure toward the vessel as seen on
ultrasound.
6. When the vein is entered, dark, non-pulsatile blood should fill the syringe. Remove the syringe
with one hand while tightly holding the needle with the other hand to ensure the tip of the needle
remains within the vessel.
7. Smoothly advance a 0.038 cm J wire into the IVC. No resistance should be met. Otherwise we
recommend the use of fluoroscopy to confirm the intravascular course of the J wire (IVC should be to
the right of the spine).
8. The appropriate sheath may be advanced over the 0.038 wire or serial dilatation can be performed
as needed to insert the desired sheath size. If use of a closure device is being planned, use a 6 Fr
dilator to dilate the tract and perform the following steps.

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Closure with a suture-mediated closure device

1. After obtaining access to the vein, advance a 6 Fr dilator over the wire to pre-dilate the track and
assure smooth transition of the closure device. We recommend using a long (150 or 180 cm) 0.038
wire for this.
2. After removal of the dilator, advance the Perclose over the wire into the venotomy. Remove the wire
and advance the Perclose into the vein until blood return confirms proper intravenous position of the
device. Due to the low pressure of the venous system, return of blood can be hard to see or even
absent. In this case, exert manual pressure on the patient’s abdomen to return blood and help with
device positioning.
3. Deploy the Perclose according to the IFU with the top of the device at the 2 o’clock position. Partially
remove the device and reinsert the J-wire. Harvest the sutures and secure with a Kelly clamp. Safely
position the sutures in a wet gauze to the right of the venotomy. Fully remove the Perclose. For
proper closure of large bore accesses, we recommend using 2 Perclose devices. Advance the second
Perclose over the wire into the venotomy and deploy 90 degrees rotated from the first Perclose
at a 10 o’clock position. Partially remove the device again, rewire with a 0.038 J wire, harvest the
sutures, secure with a Kelly clamp, and position to the left of the access site. Remove the second
Perclose and insert the large bore access sheath for the procedure over a stiff wire.
4. At the end of the case, insert the J wire through the sheath. Remove the sheath and cinch the
sutures with the 0.038 J wire left in the vein. Tighten the earlier deployed suture (2 o’clock position)
first. Before removing the wire, confirm proper hemostasis. If proper hemostasis is not achieved,
place a third Perclose over the wire. Remove the wire and tighten the two Perclose sutures.
Hemostasis is usually achieved.

Figure 1 (video). Closure With

Perclose ProGlide Suture-
Mediated Closure Device

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Closure with a “Z” stitch (Figure of 8)

1. At the end of the procedure, partially retract the large bore access sheath, but leave it within the
vein. For proper placement of the suture we recommend a size #1 non-absorbable silk surgical
suture or larger with a curved needle and a needle driver.
2. Place a suture loop underneath the skin below the sheath by staying 0.5 to 1 cm caudal to the
access site. Place the loop by entering the skin to the right of the access site and exiting the skin on
the left. The depth of entry should be about 1–2 cm and about 2–4 cm wide (depending on the size
of the patient) to allow for grasp of a large piece of soft tissue. Particularly in thin patients, ensure
that the needle and suture do not accidentally “catch” the sheath, artery, or vein below the skin.
3. After exiting the skin, place a second loop underneath the skin cranial to the insertion of sheath
in the same fashion as the first loop described above. Bring the ends of the sutures together and
tighten with a knot.
4. Remove the sheath and tighten the suture. Hemostasis is usually achieved at this point. If there
is inadequate closure or oozing, apply manual pressure or a second suture at the access site
perpendicular to the first suture. Be sure to remove the suture after at least 4 hours to ensure
adequate hemostasis, and be sure the suture gets removed before discharge.
A 3-way stopcock (Figure 2) is an alternative to securing the suture with a knot. Feed the end of the
sutures exiting the skin into the stopcock. After the loop is tightened at the level of the skin, turn the
valve of the stopcock 90 degrees and the suture is secured. After hemostasis is achieved, remove
the stopcock and suture. An advantage of this technique is the ability to remove the suture without
additional tools (eg, scissors or scalpel). The suture can also easily be tightened again if hemostasis
is not yet achieved.

A B

Figure 2. Three-way Stopcock Alternative

(A) Sutures fed through stopcock. (B) Valve turned 90 degrees to secure sutures.

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Figure 3 (video). Closure With

“Z” Stitch (Figure of 8)

QUICK READ SUMMARY

✓ With the advent of new applications for hemodynamic support and structural heart disease
interventions, the safe management of large bore venous access becomes just as important
as arterial access.

✓ This section provided step-by-step instructions to safely access the venous system in
preparation for large bore access and described two standard closure techniques—suture-
mediated closure device and “Z” stitch (Figure of 8)—to limit procedural complications.

References
1. Seth A, Modi R. Venous access closure: from A to Z. Catheter Cardiovasc Interv. 2018;91(1):113-4.

2. Pracon R, Bangalore S, Henzel J, et al. A randomized comparison of modified subcutaneous “Z”-stitch versus manual
compression to achieve hemostasis after large caliber femoral venous sheath removal. Catheter Cardiovasc Interv.
2018;91(1):105-12.

3. Hamid T, Rajagopal R, Pius, C, et al. Preclosure of large-sized venous access sites in adults undergoing transcatheter
structural interventions. Catheter Cardiovasc Interv. 2012;81(4):586-90.

4. Geis NA, Pleger ST, Chorianopoulos E, et al. Feasibility and clinical benefit of a suture-mediated closure device for
femoral vein access after percutaneous edge-to-edge mitral valve repair. EuroIntervention. 2015;10(11):1346-53.

5. Ben-Dor I, Maluenda G, Mahmoudi M, et al. A novel, minimally invasive access technique versus standard 18-gauge
needle set for femoral access. Catheter Cardiovasc Interv. 79(7):1180-85.

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10.3
Suture-based
Closure Devices
for Large Bore
Access
Thomas M. Todoran, MD, MSC, FSCAI
Division of Cardiology
Medical University of South Carolina
Charleston, SC
todoran@[Link]

Jeffrey P. Yourshaw, MD, FSCAI

Division of Cardiology
Medical University of South Carolina
Charleston, SC

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Introduction
While radial artery access is being widely adopted in cardiac catheterization labs throughout the
world, large bore percutaneous femoral access is becoming more prevalent with increasing numbers of
procedures for thoracic aortic aneurysms (TEVAR), abdominal aortic aneurysms (EVAR), cardiogenic
shock (ECMO, Impella®), and cardiac valves (TAVR). With this increase in novel procedures comes an
increase in the use of suture-mediated closure devices to close the large arteriotomies. Use of these
devices has been shown to reduce infection, mortality, and the need for blood transfusions and is
associated with shorter lengths of stay following procedures compared to surgical cutdown.1 This
chapter describes the proper patient selection and technique for percutaneous suture-based closure of
femoral arteries and veins.

Overview of approved devices

Current FDA-approved suture-mediated closure devices for large bore femoral access include:
• Perclose ProGlide® (Abbott Vascular)
• Prostar® XL Percutaneous Vascular Surgery System (Abbott Vascular)
The Perclose ProGlide is a 6 Fr system that is indicated for femoral access sizes ranging from 5 Fr to 21
Fr (Max OD 26 Fr) and venous access sizes from 5 Fr to 24 Fr (Max OD 29 Fr). The Perclose ProGlide
system utilizes a pair of polypropylene monofilament-loaded suture needles for arteriotomy closure. For
arterial or venous sheaths greater than 8 Fr, 2 Perclose ProGlide systems must be used to “pre-close”
the arteriotomy site. The Prostar XL Percutaneous Vascular Surgery System is a 10 Fr system that can
be used for femoral access sizes ranging from 8.5 Fr to 10 Fr. The Prostar XL system uses 2 braided
polyester sutures and 4 nitinol needles for closure.

The Perclose ProGlide is widely used in cardiac catheterization laboratories and its use will be the focus
of this chapter. The use of Perclose ProGlide has been shown to effectively achieve rapid hemostasis
in the presence of anticoagulation in femoral vein punctures with ≥10 Fr sheaths.2 Large bore venous
access closure can also be achieved utilizing a figure of eight stitch3 or purse-string suture technique
(see Figures 1 and 2). Closure of arterial ECMO cannulas has also been described utilizing a direct
puncture of the arterial cannula and 2 Perclose ProGlide devices. This method was feasible and safe for
closure following decannulation.4

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Figure 1. Purse-string Suture Technique

A B
(1) Load 2-0 Vicryl suture onto a needle driver. Starting at the far end, insert needle approximately 5 mm above the cannula. (2) Insert needle at
a 90 degree angle to the previous suture immediately below where the suture exits the skin. (3,4) Repeat; the final suture exits next to where the
first suture entered the skin.

Figure 2 (video). Purse-string

Suture
After the purse-string suture is
complete, pull the suture taut. Place
a half throw of a hand tied knot. As
the catheter or cannula is pulled, hold
constant pressure on the knot. Allow
a small amount of blood to bleed
back before pulling the knot taut and
completing the full knot. Hold pressure
for complete hemostasis.

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Patient selection
The patient and femoral artery must be suitable for percutaneous closure. Box 1 describes
contraindications for using the Perclose ProGlide system.5

Imaging is important to ensure correct location of puncture in the common femoral artery. The vessel
should be imaged with either computed tomography angiography (CTA) or ultrasound prior to
arteriotomy and imaged with angiography after arteriotomy.

BOX 1. CONTRAINDICATIONS FOR USING THE PERCLOSE

PROGLIDE SYSTEM
• Common femoral artery anterior wall calcification
• Circumferential common femoral artery calcification
• Common femoral artery aneurysm
• Arteriotomy outside of the common femoral artery (high or low sticks)
• Obesity (relative)6
• Access vessel diameters <5 mm have also been associated with device failure7

Preclosure with 2 Perclose ProGlide systems

1. Obtain access under ultrasound guidance utilizing a 21-gauge, 7 inch Micropuncture® Access Set
(Cook Medical, Indiana) and 0.018″ 40 cm wire.
2. Create a nick over the micropuncture needle with a scalpel to avoid cutting the wire.
3. Exchange the needle for a 4 Fr 10 cm micropuncture catheter.
4. With the catheter in place, perform a femoral angiogram to ensure puncture of the common femoral
artery.
5. Place a 0.035″ J-wire through the micropuncture catheter and exchange it for a 10 cm 6 Fr sheath.
6. Remove the 6 Fr sheath over the 0.035″ J-wire and exchange it for the first Perclose ProGlide system.
7. Advance the Perclose ProGlide system over the wire into the vessel. Remove the J-wire.
8. Advance the device into the vessel without the wire at a 45-degree angle to the skin until pulsatile
flow is seen from the marker lumen. Rotate the device to the 10 o’clock position from the midline
and deploy (Figure 3A).
9. After deployment, reinsert the 0.035″ J-wire into the Perclose ProGlide and remove the device.
10. Secure the sutures using a sterile towel clip, knot pusher, or hemostats and place to the side the
device was deployed. The sutures are typically covered with wet Telfa to keep them clean as well as
ensure they remain wet to prevent suture breakage (Figure 3C).
11. Repeat this procedure with the second Perclose ProGlide system at the 2 o’clock position (Figure 3B).

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A B

Figure 3. Perclose ProGlide Positioning and Hemostats

(A) First Perclose ProGlide system at 10 o’clock position. (B) Second
Perclose ProGlide system at 2 o’clock position. (C) Hemostats holding
the tails of both sets of Perclose ProGlide sutures and a femoral arterial
sheath present.

Following removal of the second Perclose ProGlide system over the 0.035″ J-wire, an 8 Fr sheath is
typically placed back into the vessel. Through the 8 Fr sheath, place a stiff guidewire and serially dilate
the vessel to the adequate diameter. Following the procedure, a stiff guidewire is typically placed
through the sheath and utilizing the included knot pushers, the knots are advanced sequentially as
the sheath is removed. The stiff guidewire ensures that a large sheath may be advanced easily should
control of the vessel be lost. Once hemostasis is achieved, remove the guidewire and lock the sutures by
pulling the white sutures and cut using the knot pusher. Hold pressure at the arteriotomy site as long as
protamine is being administered (Figure 4).

Complications
Bleeding is the most common complication following use of the pre-close device. If significant bleeding
is observed prior to the guidewire being pulled, deploy another device to attempt hemostasis. If a large
amount of bleeding remains, place the large bore sheath for hemostasis and consider open vessel
repair with vascular surgery consultation. Oozing at the site may be controlled by manual pressure
and reversal of anticoagulation. Investigate hematoma formation, auscultated bruit, or tenderness
at the site of arteriotomy with arterial duplex ultrasound to rule out arteriovenous fistula, aneurysm,
or pseudoaneurysm formation. Vascular surgery consultation may be needed if these findings are
discovered. Other complications that may occur include vascular occlusion and lymphoceles.8

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A B

Figure 4. Locking Down

Sutures and Complete
Hemostasis
(A) Lock down the 10 o’clock
Perclose ProGlide sutures. (B)
Lock down the 2 o’clock Perclose
ProGlide sutures. (C) Complete
hemostasis of bifemoral arterial
preclosure.

QUICK READ SUMMARY

✓ Perclose ProGlide and purse-string sutures can be used for closure of large bore venous
access.

✓ Perclose ProGlide systems can be used for closure of large-bore vascular access up to 24 Fr.

✓ Use of ultrasound guidance, micropuncture sheaths, and re-sticking if necessary ensures

accurate placement.

✓ Appropriate patient selection and femoral artery anatomy is important for successful
deployment and closure.

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References
1. Schneider DB. Perclose ProGlide versus surgical closure outcomes – real world evidence. Presented at: The Leipzig
Interventional Course (LINC) 2018; January 30, 2018–February 2, 2018; Leipzig, Germany.

2. Mahadevan VS, Jimeno S, Benson LN, et al., Pre-closure of femoral venous access sites used for large-sized sheath
insertion with the Perclose device in adults undergoing cardiac intervention. Heart. 2008;94(5):571-2. Epub 2006
Nov 3.

3. Bagai J, Zhao D. Subcutaneous “figure-of-eight” stitch to achieve hemostasis after removal of large-caliber femoral
venous sheaths. Cardiac Interventions Today. July/August 2008.

4. Hwang JW, Yang JH, Sung K, et al. Percutaneous removal using Perclose ProGlide closure devices versus surgical
removal for weaning after percutaneous cannulation for venoarterial extracorporeal membrane oxygenation. Journal
of Vascular Surgery. 2016;63(4):998-1003.

5. McGraw CJ, Gandhi RT, Vatakencherry G, et al. Percutaneous large arterial access closure techniques. Techniques in
Vascular and Interventional Radiology. 2015;18(2):122-6.

6. Smith ST, Timaran CH, Valentine RJ, et al. Percutaneous access for endovascular abdominal aortic aneurysm repair:
can selection criteria be expanded? Annals of Vascular Surgery. 2009;23(5):621-6.

7. Bensley RP, Hurks R, Huang Z, et al. Ultrasound-guided percutaneous endovascular aneurysm repair success is
predicted by access vessel diameter. Journal of Vascular Surgery. 2012;55(6):1554-61.

8. Torsello GB, Kasprzak B, Klenk E, et al. Endovascular suture versus cutdown for endovascular aneurysm repair: a
prospective randomized pilot study. Journal of Vascular Surgery. 2003;38(1):78-82.

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10.4
Closure Devices:
Plugs, Patches,
Hybrid
John Blair, MD, FACC
Associate Professor of Clinical Medicine
University of Washington Hospitals
Seattle, WA
jblair1@[Link]

Sandeep Nathan, MD, MSC, FACC, FSCAI

Associate Professor of Medicine
Medical Director, Cardiac Intensive Care Unit
Director, Interventional Cardiology Fellowship Program
Co-Director, Cardiac Catheterization Laboratory
The University of Chicago Medicine
Chicago, IL

Kent Brummel, MD, FACC

Assistant Professor of Medicine
Department of Medicine, Division of Cardiovascular Medicine
University of Michigan
Ann Arbor, MI

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Overview
This section is devoted to techniques of large-bore arterial access closure not related to suture-based
techniques, which are discussed elsewhere. The most popular and widely-available technique for large-
bore arterial or venous access closure is use of 2 Perclose ProGlide® suture-mediated closure (SMC)
devices (Abbott Vascular, Santa Clara, CA) placed in an “X” configuration to close arteriotomies up to 26
Fr outer diameter (OD) and venotomies up to 29 Fr OD. This technique has a steep learning curve, requires
placement of the device prior to large bore sheath insertion, is challenging in calcified arterial access
segments, and occasionally results in one or both sutures breaking during the closure procedure. If pre-
close is not performed prior to large-bore sheath placement, it can be done after the sheath is removed,
but may not result in optimal approximation of the vascular tissue and therefore not attain hemostasis as
well as the pre-close technique. For these reasons, newer approaches have been designed.

The collagen-based Manta™ closure system (Essential Medical, Exton, PA) was FDA approved in
2019 and is growing in popularity. The nitinol patch-based InClosure VCD system (InSeal Medical
Ltd, Caesarea, Israel) is still under development. Existing plug-based closure devices can be used in
combination with a single Perclose ProGlide SMC in a “hybrid technique.” Finally, off-label use of two
Angio-Seal™ (Terumo Corporation, Tokyo, Japan) plug-based closure devices has been described.

As with closure of all arteriotomies, it is important to enter the common femoral artery, avoiding the
bifurcation and staying within the borders of the femoral head and below the inguinal ligament. Access
techniques are outlined in another section.

Manta closure
The Manta system is a plug-based device designed specifically to close arteriotomy sites up to 25 Fr. There are
2 Manta devices:
• A 14 Fr device designed for 10-14 Fr devices or sheaths with a maximum OD of 18 Fr
• An 18 Fr device designed for 15-18 Fr devices or sheaths with a maximum OD of 25 Fr
The Manta has a puncture locator dilator with a centimeter scale imprinted proximal to a side hole that
connects to the sidearm of the sheath to help operators determine initial puncture depth and to aid in
deployment after the procedure. Operators advance this puncture locator dilator and once blood flow
begins, puncture depth is noted and confirmed for device deployment.

After the large-bore procedure is completed, operators exchange the procedure sheath for the Manta
sheath over a 0.035″ guidewire, which remains in place throughout the closure procedure. The Manta
dilator is removed and replaced with the Manta device that locks into the Manta sheath. The operator
retracts the assembled device to the noted deployment depth plus 1 cm at an angle of 45°. The operator
then pulls the lever on the Manta device to deploy the toggle / footplate and gently retracts the device,
allowing the toggle to engage the anterior luminal surface of the vessel and deploy the collagen-based
closure material on the exterior surface of the vessel. An indicator on the handle of the device signals
adequate tension. While maintaining tension, the operator advances the lock advancer tube until an
audible click signifies full deployment of the device. This tube positions the radiopaque lock atop the
collagen to secure the collagen and ensures hemostasis. After retracting the lock advancer tube to
confirm hemostasis, the operator removes the guidewire and trims the suture material. The toggle is
slowly resorbed over 6 months allowing for re-access if needed, and a radiographically visible stainless-
steel lock remains visible to guide future access.1

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A large, multicenter study demonstrated rapid hemostasis with few complications using the Manta
device.2 The device achieved hemostasis in 257 out of 263 patients in the primary analysis cohort.
Eleven patients had VARC-2 major vascular complications with 4 receiving a covered stent, 3 with
access site bleeding, 2 required surgical repair, and 2 required balloon inflation. A study comparing
suture or plug-based closure with the Manta device after TAVR demonstrated no statistically significant
difference in access site complications or bleeding. There were numerically more covered stents and
surgical bailouts with Manta, but bailout was required less often with Manta (20%) than with suture-
based closure (40%).6

In addition to not requiring pre-closure, the Manta device has the advantage of maintaining access to
the vessel with a 0.035″ wire throughout the entire deployment, in case hemostasis is not maintained.
In this case, a smaller sheath may be placed for later removal once anticoagulation is reversed or has
worn off, or another smaller closure device may be placed.

Even before receiving FDA approval in the US in 2019, the Manta system received the European CE
Mark in July 2016 with over 3,000 commercial cases performed in Europe.

A B

Figure 1. Manta Closure

(A) Manta puncture locator inserted over guidewire. (B) Dilator is removed. (C) Manta device placed. (D) Manta device locked into sheath. (E) Lever
on Manta deployed. (F) Footplate deployed and device retracted. (G) Collagen-based closure material released. (H) Indicator on device demonstrated
adequate tension. (I) Lock advancer tube is advanced to secure collagen. (J) Lock advancer tube removed and hemostasis is confirmed.

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InClosure VCD
The InClosure VCD (InSeal Medical Ltd, Caesarea, Israel) is a patch-based closure device designed to
close 14 to 21 Fr access sites. It features a biodegradable membrane mounted on a self-expanding nitinol
frame designed to conform to the shape of the vessel after luminal deployment. Following completion of
the procedure, the procedure sheath is left in place and the InClosure VCD delivery handle is inserted into
the delivery sheath, exposing the vascular closure device in the vessel. Retracting the sheath automatically
aligns the closure device with the vessel, releasing the device with only a tethering wire attaching the
sheath to the device. The tethering wire is fixed to the skin and cut once hemostasis is confirmed.

Preliminary data demonstrated good early and late hemostasis with no complications in the initial
InClosure VCD validation study.3 The InClosure VCD received the European CE mark in August, 2016.
The primary advantages to this device are its simplicity and compatibility. It requires no pre-closure
procedure, does not require a specialized sheath, and is compatible with a wide range of sheath and
vessel sizes from 14 to 21 Fr. In addition, the device provides radial support to the accessed vessel,
uses the blood pressure within the vessel to facilitate hemostasis, and can be re-accessed in future
procedures. Currently, there is no pending FDA application for this device, but this device provides a
framework for future device designs in that it does not use sutures or plugs.

Hybrid closure
The hybrid closure technique uses both Perclose ProGlide SMC and plug-based closure devices. Initially
described with the use of a microaxial flow pump percutaneous ventricular assist device, the authors
describe obtaining access and pre-closing with a Perclose ProGlide SMC device, followed by sheath
and device insertion. Following completion of the case, the microaxial flow pump was removed and
the sheath accessed with a 0.035″ guidewire. The Perclose ProGlide SMC device was deployed as the
sheath was removed, leaving a smaller arteriotomy. A 6–8 Fr sheath was then advanced over the wire
and used to deploy a 6–8 Fr plug-based closure device.3

This technique is versatile and may be used with multiple commercially-available plug-based devices
such as the 6–8 Fr Angio-Seal device, the 5 or 6/7 Fr Vascade® VCS (Cardiva Medical Inc, Santa Rosa,
CA), or the 5/6/7 Fr MYNX ACE® or 5 or 6/7 Fr MYNXGRIP® devices (CardinalHealth, Dublin, OH). It
may be used as an upfront closure strategy or as a bailout strategy for the double if 1 of the 2 original
Perclose ProGlide SMC devices fails upon completion of the procedure. To use this as a bailout strategy,
it is important to maintain access to the vessel with a 0.035″ guidewire when tightening the 2 Perclose
ProGlide SMC devices. If one of the sutures fails, the wire may be used to insert a sheath to facilitate
deployment of a plug-based device. Another important step in the bailout hybrid approach is to remove
the broken suture by pulling the suture with the white markings until all suture material is removed.

Figure 2 depicts the hybrid approach used in a right transfemoral transcatheter aortic valve replacement
(TAVR) in a 74-year-old man with severe symptomatic aortic stenosis.

Following pre-closure with 2 Perclose ProGlide devices, TAVR was performed using a 29 mm SAPIEN 3
(Edwards Lifesciences, Irvine, CA).

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Some operators advocate an upfront double-wire, double-Angio-Seal.5 We do not recommend this due
to lack of available evidence and the potential for mismatch of the device footplate/plug and arteriotomy.
This may be used as a bailout strategy if both Perclose ProGlide sutures break.

As seen in Figure 3, following pre-closure with 1 Perclose ProGlide device, a left transfemoral TAVR
was performed using the 29 mm CoreValve™ Elolut™ R (Medtronic, Minneapolis, MN) in a 90-year-old
man with severe symptomatic aortic stenosis. Due to extensive calcium, only 1 Perclose ProGlide device
could be deployed, with the second device failing, so a hybrid approach was planned.

Figure 2. Hybrid Approach Figure 3. Double Angio-Seal Approach

(A) Device and sheath removed over J-tipped 0.035″ Amplatz extra-stiff (A) Perclose ProGlide tightened, however suture came out of the
wire (Cook Medical, Bloomington, IN) used for the procedure and Perclose defect, indicating misplaced device. (B) TAVR device removed over
ProGlide sutures tightened. (B) Excessive bleeding noted at access site. the 0.035″ Lunderquist extra-stiff wire (Cook Medical, Bloomington,
(C) 8 Fr Angio-Seal locator sheath placed, and (D) Angio-Seal VIP device IN) used for device deployment, and (C) 14 Fr sheath placed. (D) Two
deployed using standard techniques. (E) Two Perclose ProGlide sutures 0.035″ J-tipped wires inserted into the sheath, and (E) 6 Fr and
trimmed using trimming device. (F) Hemostasis achieved. 8 Fr Angio-Seal locator sheaths placed into the lumen of the vessel.
(F) Angio-Seal VIP devices deployed, (G) with standard procedures,
resulting in (H) hemostasis.

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PRO TIPS
• As with closure of all arteriotomies, it is important to enter the common femoral artery
avoiding the bifurcation, and to stay within the borders of the femoral head and below
the inguinal ligament.
• Newer-generation plug- and patch-based closure devices are being developed and may
reach the United States market soon.
• Off-label plug-based closure devices may be used in conjunction with a Perclose
ProGlide SMC pre-closure using the hybrid technique as an upfront or bailout strategy.
• For bailout use of the hybrid technique, maintain wire access for every double Perclose
ProGlide SCM closure until hemostasis is confirmed. Failure to do this will make it
impossible to use the hybrid technique as a bailout if one or both sutures fail.
• For bailout use of the hybrid technique, remove the failed suture from the arteriotomy
by pulling on the white-marked suture until all attached suture is removed from the
arteriotomy.
• We recommend the upfront hybrid technique only in patients with heavily-calcified
vessels or in cases when a second Perclose ProGlide SMC pre-close cannot be deployed.
• We do not recommend the double-wire double-plug technique as an upfront technique,
but it may be used in cases where both Perclose ProGlide SMC pre-closure sutures fail.

References
1. De Palma R, Settergren M, Rück A, et al. Impact of percutaneous femoral arteriotomy closure using the MANTA™
device on vascular and bleeding complications after transcatheter aortic valve replacement. Catheter Cardiovasc
Interven. 2018;Mar 25; ePub

2. Wood D, Krajcer Z, Sathananthan J, et al. Pivotal clinical study to evaluate the safety and effectiveness of the MANTA
percutaneous closure device. Circ Cardiovasc Interven. 2019;12(7):e007258

3. Kambara AM, Bastos M, Ribamar Costa J Jr, et al. First-in-man assessment of the InSeal VCD, a novel closure device
for large puncture accesses. EuroIntervention. 2015;10(12):1391-5.

4. Amponsah MK, Tayal R, Khakwani Z, et al. Safety and efficacy of a novel “hybrid closure” technique in large-bore
arteriotomies. Int J Angiol. 2017;26(2):116-120.

5. Abi Rafeh N, Quevedo HC, DeAndrade KB, et al. The double angio-seal technique for arterial closure following large-
bore access. J Invasive Cardiol. 2013;25(8):412-4.

6. van Wiechen M, Tchetche D, Ooms J, et al. Suture- or plug-based large-bore arteriotomy closure: a pilot randomized
controlled trial. JACC Intervention. 2021;14(2):149-57.

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10.5
Manual
Compression and
Assisted Manual
Compression for
Large Bore Access
and Closure
Madhan Shanmugasundaram, MD, FACC, FSCAI
The University of Arizona College of Medicine
Banner University Medical Center
Tucson, AZ
msundaram@[Link]

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Overview
Large bore arterial access has become increasingly common with rapidly expanding structural heart
disease interventions and the use of percutaneous hemodynamic support devices. Not surprisingly,
large bore arterial access procedures are associated with a higher risk of access site complications,
including bleeding. Widespread adoption of large bore access procedures was initially limited by access
complications as these procedures required vascular surgeons to perform arterial cutdowns; albeit
closure was relatively straightforward with surgical techniques. Today, however, these procedures are
being performed percutaneously, obviating the need for surgery. Thus, arterial hemostasis at the end of
the procedure now has to be achieved by non-surgical techniques.

Careful patient selection, consideration of peripheral arterial anatomy, and safe access techniques are key
to avoiding vascular complications in patients undergoing large bore access procedures. Vascular closure
devices, specifically suture-mediated devices (Perclose ProGlide® and Prostar XL®) have been used to
achieve hemostasis after large bore arterial access with good technical success. However, there is still a
significant failure rate with these devices resulting in high vascular complication rates.1 This chapter focuses
on manual compression and assisted manual compression as alternatives to vascular closure devices.

Manual compression
Manual compression has long been the gold standard technique for achieving hemostasis following arterial
access. After large bore arterial access, however, manual compression becomes more challenging, as it is
harder to control access site bleeding. Nevertheless, it is a useful skill to possess in case the closure devices fail.

Although manual compression is simple, it is essential to apply good technique to achieve hemostasis
and to prevent complications. Good manual compression technique entails the following:
• Ensure ACT is less than 180 seconds before sheath pull (general recommendation), and in
patients with significantly elevated blood pressure, lower blood pressure modestly before
sheath removal to ensure that adequate pressure can be applied above that level for successful
hemostasis. Be careful to avoid significant BP lowering or using long-acting BP lowering drugs in
case the patient has a vagal reaction or bleeding during the manual compression process.
• Continuously monitor patient’s vital signs during manual compression.
• Flush the sheath before pulling it to ensure there is no thrombus that could embolize when it is
withdrawn.
• Administer adequate analgesia to ensure the patient is comfortable.
• Place fingers about an inch above the sheath (arteriotomy site) and apply firm manual pressure.
Standing on a short bedside stool permits upper body weight to be used for pressure application.
• After achieving adequate control of the artery (identified by the pulse), remove the sheath taking
care not to crush or shear the sheath.
• Allow a small spurt of blood to dislodge any clot in the arteriotomy track.

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Figure 1. Manual Compression

Monitor distal pedal pulses every 2 to 3 minutes during manual compression. Although a diminished
pulse is acceptable during brief full-pressure application, distal pulses should not be obliterated
completely. If the pedal pulse is absent during compression, periodically decrease the pressure over the
artery to allow distal circulation. Complete artery occlusion prevents mobilization of clotting factors and
platelets at the arterial wall puncture site, prolonging the time to hemostasis.

Every institution has a protocol for manual hemostasis, but manual compression has to be applied
directly over the arteriotomy site until complete hemostasis is achieved. A general recommendation is 3
minutes of pressure per French size, which means it could take up to 45 minutes of pressure for a 14 Fr
sheath; hence more than one operator may be needed to achieve effective manual hemostasis for large
A arteriotomy access. Following hemostasis, prolonged
bore B bed rest is indicated for these patients.

GENERAL RECOMMENDATION
3 minutes of manual compression pressure per French size (eg, up to 45 minutes for a 14 Fr sheath)

Assisted manual compression

In some situations, hemostasis is best achieved by assisted manual compression—use of an extrinsic
compression device or topical hemostasis patch to help with hemostasis. FDA-approved and
commercially available devices for extrinsic compression include:
• FemoStop™ Gold (St. Jude Medical)
• C-Clamp devices such as CompressAR®, ClampEase®, Compass™, PressureMate™ and
ComfortPress™ (Advanced Vascular Dynamics), Assiut Femoral Compression Device
• Hemostasis pads such as Clo-Sur P.A.D.™ (Scion Cardiovascular), D-Stat® Dry (Vascular
Solutions), and Neptune Pad (TZ Medical)

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FemoStop
FemoStop Gold (Figure 2) is the most commonly used assisted manual compression device. It consists
of a rigid frame and a pneumatic dome that can be inflated once positioned on top of the femoral artery.
A belt that goes across the patient’s hip holds the frame and the dome in place. The dome is attached
to a manometer. Once the belt is secure at the hip, the dome is positioned on top of the femoral artery
and inflated to 60-80 mmHg. The sheath can then be removed, and the dome inflated to supra-systolic
pressure. After 3-5 minutes, the cuff is gradually deflated until distal pedal pulses are restored; the
cuff remains inflated at that pressure for the duration of the procedure. It is critical to closely monitor
the device and patient during this process. The device is not approved for unsupervised use. Once a
hematoma forms, it is likely that the dome is no longer above the arteriotomy site.

Figure 2. FemoStop

C-Clamp devices
Assisted manual compression can also be accomplished with one of several currently available C-Clamp
devices—a stand with an arm that exerts direct pressure on the arteriotomy site after sheath pull—
such as CompressAR® System (Figure 3). While these devices reduce the need for manual pressure
and standardize arteriotomy compression, they require close patient monitoring to avoid hematoma or
limb ischemia. A study comparing manual to mechanical compression demonstrated no difference in
bleeding but a significant reduction in hematoma formation with mechanical compression device use.2

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Figure 3. CompressAR System

Hemostasis pads
Hemostasis pads contain procoagulant coating to accelerate coagulation and hemostasis. Numerous
products are available, and these devices result in shorter compression times and lower incidence of
bleeding. A large study comparing hemostasis pads to manual compression demonstrated a significant
reduction in bleeding or vascular complications with hemostasis pads.3

QUICK READ SUMMARY

✓ Manual compression is feasible and effective if done correctly, but associated with a higher
incidence of hematoma and bleeding following large bore arterial access.

✓ A variety of mechanical compression devices and hemostasis pads are available to assist
in achieving manual hemostasis by potentially reducing compression times and access site
bleeding.

✓ When using compression devices, closely monitor patients to prevent bleeding or limb ischemia.

✓ Hemostasis pads contain procoagulants that accelerate hemostasis.

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References
1. Barbash
 IM, Barbanti M, Webb J, et al. Comparison of vascular closure devices for access site closure after
transfemoral aortic valve implantation. Eur Heart J. 2015;36(47):3370-9. Epub 2015/09/01. doi: 10.1093/eurheartj/
ehv417. PubMed PMID: 26314688.

2. J ones T, McCutcheon H. Effectiveness of mechanical compression devices in attaining hemostasis after femoral
sheath removal. Am J Crit Care. 2002;11(2):155-62. Epub 2002/03/13. PubMed PMID: 11888128.

3. T
 avris DR, Wang Y, Jacobs S, et al. Bleeding and vascular complications at the femoral access site following
percutaneous coronary intervention (PCI): an evaluation of hemostasis strategies. J Invasive Cardiol. 2012;24(7):328-
34. Epub 2012/07/12. PubMed PMID: 22781471.

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10.6
Cross-over Balloon
Occlusion “Dry
Closure” Technique
for Large Bore
Femoral Access
Alexander G. Truesdell, MD, FSCAI
Virginia Heart
Inova Schar Heart and Vascular
Falls Church, VA
agtruesdell@[Link]

Nadim A. Geloo, MD, FSCAI

Senior Medical Director, Abbott Structural Heart
Chicago, IL

Behnam Tehrani, MD, FSCAI

Inova Schar Heart and Vascular
Falls Church, VA

Special thanks to the RCIS and RN staff at the INOVA Heart and Vascular Institute Cardiac
Catheterization Labs

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Overview
Safe vascular closure, like safe vascular access, is a cornerstone of percutaneous coronary, cardiac,
and vascular intervention and should be given the same attention as the primary procedure. Vascular
complications occur more frequently than procedural complications, are associated with significantly
increased patient morbidity and mortality, and typically occur during insertion and removal of sheaths.

With growing utilization of radial artery access for percutaneous interventions, femoral access is
increasingly reserved for more complex procedures (eg, TAVR, EVAR, and mechanical circulatory
support [MCS]) necessitating larger-bore 13 –18 Fr sheaths. In addition to utilizing best practices for
femoral vascular access, operators should employ safe closure protocols such as the contralateral
femoral crossover (or ipsilateral femoral or transradial) balloon occlusion “dry closure” technique
(CBOT). CBOT is a simple, reliable, convenient, and reproducible procedure with high success rates,
demonstrated reductions in major vascular and bleeding complications, and potential benefits of
reduced nuisance oozing, earlier mobilization, decreased length of stay, and cost savings.1,2,3,7

Strategic planning
For elective femoral cases, perform pre-procedural aorto-iliac and common femoral CT angiography
or duplex arterial ultrasound to assess vascular anatomy and individual vessel internal diameters.
For urgent cases, utilize intraprocedural aorto-iliac angiography instead. Note that in the case of
percutaneous transfemoral (or transaxillary or transcaval) MCS insertion for cardiogenic shock, sheath
and device explantation (utilizing CBOT) often may be performed several days (or more) following the
index procedure.4

CBOT equipment and procedural considerations

Step 1: Perform ultrasound-guided common femoral artery (CFA) micropuncture access and single or
dual Perclose vascular closure device (VCD) pre-closure (Figure 1) utilizing current best practices for
either same-sitting or delayed large bore sheath removal (Figure 2).

Figure 1 (video). Perclose Deployment in CFA Prior to

Large-bore Sheath Insertion

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Figure 2. Repositioning Sheath in CFA With Perclose

Sutures in Position at 10 o’clock and 2 o’clock

Step 2: Insert large bore sheath, anticoagulate patient, and perform index coronary, cardiac, or vascular
procedure.

Step 3: Advance crossover catheter (UF, Omni™ Flush, or similar) via contralateral CFA access to the
ipsilateral common iliac artery (CIA) over a 260 cm 0.035" Glidewire Advantage (or similar soft tip-stiff
shaft wire) positioned in the ipsilateral superficial femoral artery (SFA) distal to the large bore access
sheath (Figures 3, 4). If ipsilateral or contralateral radial or ulnar access is utilized instead, advance a
125 cm multipurpose or vertebral catheter over a wire into the iliac artery ipsilateral to the large bore
sheath. Alternatively, ipsilateral femoral dry closure techniques may also be used.5 These ipsilateral
A
femoral and radial techniques importantly reduce the B risks of bleeding complications related to a second
femoral access site.

Figure 3 (video). Wire Advanced Through Crossover

Catheter Into EIA

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Figure 4 (video). Wire Advanced Beyond Sheath in

CFA and Into SFA

Step 4: Position appropriately sized over-the-wire vascular balloon (typically 8–10 mm diameter x
20–40 mm length) in the very proximal external iliac artery (EIA), either sheathless or via an appropriate
length 6 or 7 Fr vascular sheath. Optional: 0.035" wire within the crossover peripheral balloon may be
replaced with a 0.018" wire advanced into the SFA.

Step 5: Retract large bore sheath to the CFA / EIA junction. Optional: Inject contrast via the large bore
sheath prior to removal to identify any major iliac vascular injury.

Step 6: Inflate contralateral crossover, ipsilateral femoral, or radial balloon at non-traumatic low
pressure in the EIA to occlude distal flow (Figures 5, 6). Optional: Pressure may be transduced from the
occlusion balloon or the large bore sheath after balloon inflation to confirm EIA occlusion (via a flatline
pressure tracing).

Figure 5. “Dry closure” Occlusion Balloon

Inflated in EIA

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Figure 6. Crossover Balloon Inflated in EIA to Occlude

Distal Flow

Step 7: Remove large bore sheath over a wire under bloodless “dry-closure” conditions.

Step 8: Sequentially secure Perclose VCD, placed previously via pre-close technique (Figure 7).
Optional: If Perclose VCD not inserted pre-procedurally via pre-close technique, an alternative dual
Perclose “parallel suture technique” (author personal experience) may instead be utilized for “post-
closure” of large bore femoral access.6

Figure 7 (video). Secure Perclose Sutures Following

Sheath Removal

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Step 9: Perform selective femoral angiography via the inflated (and occlusive) EIA balloon to ensure no
vascular injury, effective hemostasis, and good distal flow (Figure 8). Optional: With 0.018" wire (within
the 0.035" wire compatible balloon) in the SFA, place a 3-way stopcock or Tuohy Borst adapter on the
end of the balloon and perform contrast injection to facilitate angiography without surrendering distal
wire position (Figure 9).

Figure 8 (video). Selective Femoral Angiography

Performed Through EIA Occlusion Balloon

Figure 9 (video). Selective Femoral Angiography

Performed Through Inflated 0.035" Occlusion Balloon
in EIA With 0.018" Wire in SFA

Step 10: In the event of inadequate hemostasis, contrast extravasation, or flow-limiting “pinching” of
the femoral artery by the Perclose sutures, advance the vascular balloon over a wire across the CFA
arteriotomy (Figure 10) and perform additional sequential 5 minute inflations (limited in duration to
minimize the risk of thrombosis and distal embolization) with adjunctive manual compression until
hemostasis is achieved.

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Figure 10. Transradial Vascular Balloon Inflated Across CFA Arteriotomy to Resolve Perclose “Pinch,” Address
Flow Impairment, and Achieve Hemostasis

Step 11: Remove crossover occlusion balloon. Optional: In extreme circumstances of major vascular
injury unsuccessfully managed with sequential balloon occlusion, a covered stent can be delivered and
deployed across the common femoral arteriotomy site as a final bailout strategy (Note: If a sheathless
strategy [Step 4] is employed, a new femoral or radial sheath may need to be utilized to deliver a
covered stent).

Step 12: Apply light external manual pressure for 5 minutes (or longer) to complete hemostasis.

Step 13: Once final hemostasis of the large bore access site is achieved, remove the contralateral
femoral (or radial) sheath and perform non-large bore access site closure and hemostasis utilizing
current best practices.

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QUICK READ SUMMARY

✓ Safe vascular closure deserves as much attention as safe vascular access, particularly when
using large bore sheaths.

✓ Crossover balloon occlusion technique (CBOT) is simple, reliable, convenient, and

reproducible.

✓ Balloon occlusion provides a “dry” environment for controlled vascular closure and
hemostasis of large bore sheaths.

✓ Angiography via the occlusion balloon effectively assesses for vascular injury, adequate
hemostasis, and preserved distal flow before, during, and after sheath removal.

✓ Catheter access to the large bore sheath site (and wire access more distally) permits
immediate rescue treatment of Perclose “pinches,” major vascular injury, bleeding, and distal
flow compromise.

✓ CBOT safely facilitates percutaneous mechanical circulatory support (MCS) explantation

several days (or more) following device insertion.

✓ CBOT should be in the arsenal of all operators employing large bore sheaths.

✓ Current alternatives to CBOT are ipsilateral femoral and transradial balloon occlusion
(although full-spectrum follow-on management options, while increasing, are not currently
available via radial access).

References
1. S
 harp AS, Michev I, Maisano F, et al. A new technique for vascular access management in transcatheter aortic valve
implantation. Catheter Cardiovasc Interv. 2010;75(5):784-793.

2. G
 enereux P, Kodali S, Leon MB, et al. Clinical outcomes using a new crossover balloon occlusion technique for
percutaneous closure after transfemoral aortic valve implantation. JACC Cardiovasc Interv. 2011;4(8):861-867.

3. B
 uchanan GL, Chieffo A, Montorfano M, et al. A “modified crossover technique” for vascular access management
in high-risk patients undergoing transfemoral transcatheter aortic valve implantation. Catheter Cardiovasc Interv.
2013;81:579-583.

4. L
 ata K, Kaki A, Grines C, et al. Pre-close technique of percutaneous closure for delayed hemostasis of large-bore
femoral sheaths. J Interv Cardiol. 2018;31(4):504-510. doi: 10.1111/joic.12490. Epub 2018 Feb 5.

5. Lichaa H, Wollmuth J, Tayal R. Dry field closure of large-bore access with iliac artery angioplasty through the
ipsilateral sheath: the single-access dry-closure technique. J Invasiv Cardiol. 2021;33(7):E516-21.

6. O
 tt I, Shivaraju A, Schäffer NR, et al. Parallel suture technique with ProGlide: a novel method for management of
vascular access during transcatheter valve implantation. EuroIntervention. 2017;13(8):928-934.

7. Sandoval Y, Basir MB, Lemor A, et al. Optimal large-bore femoral access, indwelling device management, and vascular
closure for percutaneous mechanical circulatory support. Am J Cardiol. 2023;206:262-76.

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10.7
Large Bore Arterial
Post-Closure
Hemostasis
Mark J. Ricciardi, MD, FSCAI
Section Chief, Interventional Cardiology and Structural Heart Disease
Mr. and Mrs. Charles R. Walgreen Jr. Chair of Cardiology
Endeavor Health NorthShore Cardiovascular Institute
Clinical Professor of Medicine
University of Chicago Pritzer School of Medicine
mricciardi@[Link]

Luis H. Paz Rios, MD, FSCAI

Cardiovascular Department
Rooney Heart Institute
Naples Community Hospital

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Overview
Achieving large bore arterial access (LBA) and managing the access site are now mandatory skills for
the interventional cardiologist and many cardiac and vascular surgeons. Without a methodical approach,
we can expect increased morbidity and associated costs.1 Elective or semi-elective procedures like
transcatheter aortic valve implantation (TAVI) and percutaneous coronary interventions (PCI) with
percutaneous mechanical circulatory support (MCS) often allow for careful pre-procedure imaging of the
pelvic vasculature and usually result in prompt removal of the LBA device and immediate hemostasis
with a preclosure technique. For other situations, such as the patient in cardiogenic shock requiring
percutaneous MCS, the luxury of detailed pre-procedure imaging is absent and LBA device placement
often demands prolonged dwell times (days), both of which increase the risk for vascular complications.
For such patients, sheath removal at the bedside using manual compression for hemostasis is frequently
associated with bleeding and incomplete hemostasis.2 In this chapter we describe techniques to achieve
hemostasis for indwelling large bore sheaths, also called “post-closure hemostasis.”

Strategic planning and procedural considerations

Manual compression at the patient bedside has been the gold standard for hemostasis in standard
arteriotomies with indwelling catheters. However, when dealing with LBA (>8 Fr outer diameter)
regardless of the chosen hemostatic method, we recommend performing LBA sheath removal in the
cardiac catheterization laboratory. This provides a controlled environment with the necessary tools for
technique escalation when required.

As part of the planning for LBA post-closure hemostasis, heparin discontinuation in advance and
verification of an activated clotting time (ACT) of <180 seconds is recommended prior to sheath
removal. If ACT remains above the goal and LBA sheath removal cannot be delayed, protamine sulfate
can be used immediately following device removal to reverse anticoagulation (1 mg protamine for
every 100 units of heparin administered in the previous 2 to 3 hours, max dose 50 mg). Prior to LBA
sheath removal, and especially in cases when the risk of bleeding is high, we recommend obtaining
contralateral femoral or radial access for dry field closure.

If manual compression is attempted, apply firm pressure (occlusive pressure while removing sheath)
on the vessel 2-3 cm proximal to the skin entry site for about 10 minutes, followed by moderate
pressure, and finally mild pressure for a total pressure time equivalent to 3 minutes per French size (3
x Fr size). Alternatively, assisted manual compression is possible with extrinsic devices (FemoStop™,
C-Clamp devices) under direct supervision to rapidly identify complications. However, it is currently
considered best practice to achieve hemostasis with fully percutaneous dedicated closure techniques
and devices that are reliable, safe, and reproducible. As such, manual compression is largely considered
an adjunctive technique used to maximize hemostasis and to bail out device failures.

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Post-closure techniques
Oftentimes, it is possible to pre-close the access site prior to sheath upsizing. In this setting, the use
of orthogonal Perclose systems (Abbott) is widely accepted. Anticipating prolonged dwell times, the
Perclose sutures should be clamped with hemostats or stopcocks, then wrapped under sterile towels,
covered with sterile Tegaderm™ patches, and finally fixed to the abdominal wall. Special precautions to
maintain sterility are vital to avoid infectious complications. Before removing the sheath, it is necessary
to prepare the skin and sutures with a chlorhexidine-based solution.

For situations when pre-closure is not possible, the following “post-closure” techniques are useful and
can be safely applied.

Double wire double sheath post-closure technique

The author's preferred technique is a variation of a previously described Perclose-based post-closure
technique.3 The first step for the double wire technique is arterial re-access. If the device is a microaxial
flow pump, re-access can be achieved through the rewiring port inlet on the repositioning sheath
(older generation devices devoid of rewiring ports required salvage techniques not discussed here). If
removing an extracorporeal membrane oxygenation (ECMO) cannula, the non-braided portion of the
cannula can be punctured with an 18-gauge needle for re-access.

A 0.035" guidewire is advanced to the proximal thoracic aorta and the large bore sheath removed over
the wire (OTW). A new sheath is then inserted (elastic arterial recoil often provides enough hemostasis
even when the replacement sheath is up to 3 Fr smaller than arteriotomy). Often an assistant is needed
to apply moderate manual pressure over the arteriotomy during this step.
A B
A second 0.035" guidewire is then advanced to the proximal thoracic aorta through the hemostatic
valve and the new sheath removed. Two separate 6-8 Fr sheaths over each wire side by side are then
inserted. This will result in a combined sheath perimeter similar to the arteriotomy.

One of the sheaths is then removed OTW and a Perclose device deployed at the 10 o’clock position. The
operator can then use either an 8 Fr Angio-Seal device (Terumo Interventional Systems) in a “Hybrid
approach” or an additional Perclose suture device (our preferred technique). If a second Perclose is used,
the second sheath is removed OTW and the second Perclose device deployed at the 2 o’clock position.

Once the second device is deployed, a contralateral angiogram is performed to confirm hemostasis and
artery patency.3 This access site could then be using to perform balloon tamponade and our covered
stent placement if needed. An alternative to using a contralateral access side for angiography is to
maintain wire position over which a microcatheter is placed to perform ipsilateral femoral angiography.
The wire is then removed and the second Perclose is fully deployed. This approach to completion
angiography allows for continued wire access and the option for placement of a third closure device
when needed. In such instances, the wire is re-inserted and a third Perclose is deployed in an alternative
angle (12 o’clock). This is now our preferred technique for completion angiography unless the patient is
at very high risk for incomplete hemostasis or vascular injury requiring balloon tamponade or stenting.
The primary disadvantage of the ipsilateral angiography technique is the potential to miss iliac and
aorto-iliac vascular injury that would otherwise be easier to identify with a more complete abdominal
aortogram from a contralateral artery.

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Figure 1. Double Wire Double Sheath Post-Closure Technique

(A) Insert two 0.035" guidewires together followed by two 8 Fr sheaths side-by-side for perimeter coverage of the arteriotomy and successful
Perclose deployment. (B) Deploy the first Perclose and assess for hemostasis. (C) Deploy second Perclose and remove wire if adequate
hemostasis achieved.

A recently described “sideclose technique” performed at the time of microaxial flow pump placement is
a promising technique that would allow for simpler post closure.4 With this technique, the arteriotomy
is made smaller by placing a Perclose alongside the repositioning sheath. At the time of the microaxial
flow pump removal, only a single vascular closure device would be needed.

Double Angio-Seal™ post-closure technique

The Angio-Seal device is a suture-tethered extravascular collagen plug with a low-profile intravascular
anchoring polymer that dissolves in approximately 90 days. The plug is pushed to cover the arterial
puncture creating an anchor-arteriotomy-collagen plug sandwich. Currently available in 6 Fr and
8 Fr, the double wire double Angio-Seal technique5 has been effectively employed for closure of
arteriotomies up to 16 Fr outer diameter.4 We recommend using the 8 Fr Angio-Seal vascular closure
device (VCD) first and if residual bleeding is observed, deploy an additional 6 Fr or 8 Fr Angio-Seal VCD
(considering oozing vs. brisk flow).

As previously described in the double Perclose technique, once the two 0.035" guidewires are in
position in the proximal thoracic aorta, the large bore sheath is removed OTW. The 8 Fr Angio-Seal
insertion sheath is loaded onto the first wire and the collagen plug deployed using the standard
technique.

If hemostasis is achieved with the first VCD, the stiff 0.035" wire is withdrawn while maintaining
simultaneous traction on the Angio-Seal suture. If hemostasis is not achieved, a second Angio-Seal VCD
insertion sheath is placed over the wire and deployed.

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Figure 2. Double wire Double Angio-Seal Post-

Closure Technique
(A) Insert two 0.035″ wires in parallel and remove procedure
sheath followed by deployment of first Angio-Seal collagen plug.
(B) Load and deploy second Angio-Seal over parallel 0.035″ wire
as back-up if hemostasis is not achieved with first one.

Post hoc LBA closure with MANTA device

The plug-based VCD MANTA™ (Teleflex, Wayne, PA) was designed for closure of LBA up to 22 Fr outer
diameter. Although “skin to arterial wall” depth measurement is considered critical prior to sheath upsizing,
the following post hoc method to obtain deployment depth and effective closure has been employed
with success in a case series of a 14 Fr microaxial flow pump and is a plausible postclosure alternative for
hemostasis.6
1. Advance a 0.035″ J-wire to the descending aorta and remove LBA sheath OTW applying manual
compression, all under fluoroscopic guidance.
2. Place an 11-14 Fr introducer sheath for transitory hemostasis.
3. Through the introducer sheath, advance a marker pigtail catheter (1 cm markers, Angiodynamics),
then place a hemostat at the skin puncture site to allow measurement with angiography.
4. Using lateral projection (LAO or RAO at 90º) perform angiography to obtain the “skin to arterial
wall” measurement from the hemostat to arteriotomy site.
5. Deploy MANTA VCD at the measured depth plus 0.5-1 cm (recommended when using standard
depth locator tool).
6. Confirm ipsilateral hemostasis from the contralateral access.

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Figure 3. Post Hoc Large Bore Closure with MANTA Device

(A) Place an 11-14 Fr introducer sheath over 0.035″ wire for transient hemostasis and advance marker pigtail to measure “skin to arterial wall”
distance. (B) Insert MANTA sheath fully into puncture. (C) Withdraw handle to measured depth and deploy feet. (D) Deploy MANTA vascular plug
to seal arteriotomy.

Bail-out considerations
Hemostasis may be incomplete despite a methodical approach to arteriotomy closure. In this setting,
and using the contralateral access, prolonged balloon occlusion (15-60 minutes) over the arteriotomy
site may suffice with careful management of anticoagulation to avoid thrombosis due to stasis.
With persistent bleeding or in cases of vascular injury, covered stents are of particular utility and usually
a last resource for hemostasis. It is advantageous to keep the vascular surgical team aware while
escalating hemostatic techniques as surgical vessel cut-down may be ultimately required.

Conclusions
Post closure techniques for large bore access site management are now well established. A methodical
approach is especially important for these patients who are at highest risk for bleeding. The techniques
described above are proven and effective in most situations. The techniques that are most attractive are
those that are reproducible but also allow for bail-out strategies when persistent bleeding or vascular
injury are identified.

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References
1. Redfors B, Watson BM, McAndrew T, et al. Mortality, length of stay, and cost implications of procedural bleeding after
percutaneous interventions using large-bore catheters. JAMA Cardiol. 2017;2(7):798-802.

2. Jones T, McCutcheon H. Effectiveness of mechanical compression devices in attaining hemostasis after femoral
sheath removal. Am J Crit Care. 2002;11(2):155-62.

3. Thawabi M, Cohen M, Wasty N. Post-close technique for arteriotomy hemostasis after Impella removal. J Invasive
Cardiol. 2019;31(6):E159.

4. Korngold E, Wollmuth J. The sideclose technique: a novel method for achieving hemostasis with an indwelling Impella
CP. JSCAI. In press: [Link]://[Link]/10.1016/[Link].2024.102141

5. Chaudhuri A. Femoral arterial haemostasis using an anchored collagen plug after percutaneous EVAR with
an ultra-low profile device: prospective audit of an evolving “post-close” technique. Eur J Vasc Endovasc Surg.
2017;54(2):241-6.

6. Sharma RK, Poulin MF, Tamez-Aguilar H, Pinto DS. Post hoc closure of large bore vascular access using the MANTA
closure device. Catheter Cardiovasc Interv. 2020.

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10.8
Access Strategies
for Monitoring
or Prolonged
MCS Use
Amer K. Ardati, MD, MSC, FACC, FSCAI
Interventional Cardiologist
University of Illinois-Chicago
Chicago, IL
aardati@[Link]
@Spiritus_Bah

Jonathan Meyer, MD
Cardiology Fellow
University of Illinois-Chicago
Chicago, IL
Jmeyer32@[Link]
@JonathanDMeyer

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Introduction
In contrast to early studies suggesting no rationale for the routine use of pulmonary artery catheters (PAC)
in decompensated heart failure,1 contemporary data have shown that PAC use is associated with improved
survival in cardiogenic shock (CS)2 and improved outcomes in patients in CS requiring mechanical circulatory
support.3 Long-term hemodynamic monitoring in the intensive care unit (ICU) requires careful planning at
the time of catheter insertion to select the optimal access point and consistent high-quality nursing care to
ensure that data veracity is maintained outside of the cardiac catherization laboratory. In addition to PAC
use, arterial pressure monitoring via the radial artery is often needed to complement data available from the
mechanical circulatory support (MCS) device and can facilitate frequent arterial blood sampling. This chapter
focuses on access site selection and optimal practices for hemodynamic monitoring in the ICU.

Access for invasive hemodynamic monitoring

PAC placement
Jugular venous access, preferably right sided, is ideal for long-term hemodynamic monitoring in the ICU.
Neck access is superior to femoral access due to the lower rate of infection and the ability to deliver the
device without fluoroscopic guidance in the ICU.

Brachial venous access is typically reserved for single assessment (“in-and-out”) right heart
catheterization due to potential kinking of the catheter and potential decrease in long-term patency
of the smaller caliber veins (especially important in patients with chronic kidney disease). If long-term
use is not necessary, or femoral/jugular anatomy is unsuitable, brachial venous access can be obtained
rapidly via direct ultrasound-guided venipuncture of the brachial or by exchanging a previously placed
20-guage intravenous catheter for an introducer sheath over a wire.

Femoral venous (FV) access for PAC can be obtained quickly via ultrasound-guided venipuncture and
if done at the time of femoral arterial access for placement of MCS does not require additional site
preparation. FV access requires strict bedrest and, therefore, is not recommended if long-term use of
MCS is to be utilized from an alternative site (eg, transaxillary). While femoral venous access is more
expedient than jugular access during initial management of cardiogenic shock, care should be taken to
balance early convenience against longer-term patient-centered benefits of jugular access.

Regardless of access site selected, use of direct sonographic guidance at the time of insertion can help
reduce bleeding complications. In the case of jugular vein access, sonographic guidance also helps to
avoid pneumothorax.

There is no widely accepted recommendation regarding the duration of use of a PAC to prevent
catheter-related infections. Overall, PACs have similar infection rates as other central venous catheters,
and do not need to be routinely replaced at an additional site more frequently than every 7-14 days.

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Arterial line placement

Arterial lines for monitoring can be placed at bedside or during MCS placement. The radial arteries are
preferred due to low complication rate, even with prolonged monitoring. Radial and ulnar arteries can be
accessed by palpation or with ultrasound guidance if needed. Case reports have described converting
radial angiography access to an arterial monitoring line over a wire. Standard radial artery band
facilitated patent hemostasis techniques can be used over the monitoring line. Radial hemostasis is then
applied with a wrist band which can be removed 2 hours later leaving the arterial monitoring line intact.4

The femoral artery is a common access site for hemodynamic monitoring. There is a theoretical risk
of increased infection due to proximity of the perineum, however, this has not been demonstrated in
practice. Common femoral artery cannulation has a higher rate of hematoma than the superficial femoral
artery; however, superficial femoral artery access has a higher rate of pseudoaneurysm formation.

Brachial and axillary artery access have been used for prolonged pressure monitoring. These access
points are traditionally avoided because they are subject to inconsistent hemostasis and access site
complications can lead to limb ischemia.

Proper calibration of the hemodynamic monitoring lines is critical for reliable clinical information. Prior
to obtaining hemodynamic parameters, all lines should be flushed and cleared of any microbubbles to
avoid damping of the system. The transducer should be calibrated to the mid-axillary line using a ruler
while the patient is laid flat in a supine position. All measurements should be taken at end-expiration,
particularly in patients with mechanical positive pressure ventilation. Positive end-expiratory pressure
(PEEP) should be considered when documenting hemodynamic parameters.

A B
Data interpretation
PAC measurements
Cardiogenic shock is defined as systolic blood pressure (SBP) less than 90 mmHg or the requirement
of inotropes/vasopressors to maintain SBP greater than 90 mmHg with reduced cardiac output in the
setting of normal or elevated ventricular filling pressures. Invasive hemodynamic measurements can
inform every phase of clinical care in patients with known or suspected cardiogenic shock (Table 1).

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Table 1. Invasive Hemodynamic Parameters

HEMODYNAMIC PARAMETERS NORMAL RANGE UNITS EQUATION

MEASURED

Central venous pressure (CVP) 2-6 mmHg —

Pulmonary capillary wedge pressure
6-12 mmHg —
(PCWP)
PA systolic pressure (PASP) 15-30 mmHg —

PA diastolic pressure (PADP) 8-15 mmHg —

Mean PA pressure (MPAP) 8-20 mmHg —

Mixed venous oxygen saturation (SvO2) 60-80 % —

Cardiac output (CO) 4-8 L/min —

Cardiac index (CI) 2.2-4 L/min/m2 —

DERIVED

Systemic vascular resistance (SVR) 700-1500 dynes/sec/cm-5 80 (MAP - CVP)/CO

Pulmonary vascular resistance (PVR) < 250 dynes/sec/cm-5 80 (MPAP - PCWP)/CO

LV stroke work index (LVSWI) 2.4-4.2 mmHg.L/beat/m2 (MAP-PCWP) x (CI/HR)/BSA

RV stroke work index (RVSWI) 0.1-0.25 mmHg.L//beat/m2 (MPAP-CVP) x (CI/HR)/BSA

Cardiac power output (CPO) >1 Watts MAP x CO / 451

Pulmonary artery pulsatility index (PAPi) >0.6 Watts/m2 (PASP - PADP) / CVP

CVP/PCWP ratio 0.3-0.5 unitless CVP/PCWP

PAC measurements can inform the diagnosis of cardiogenic shock by demonstrating a low cardiac
output (CO), elevated filling pressures, and elevated systemic vascular resistance (SVR). Further invasive
hemodynamic data enable classification of the predominant form of cardiogenic shock: left ventricular,
right ventricular, or biventricular shock (Table 2).
• In RV predominant shock, the low cardiac output and hypotension are driven by the failure of
the RV to adequately fill the LV. Hemodynamics of RV predominant shock show an elevated CVP
(>14 mmHg), low pulmonary artery pulsatility index (PAPi <1.5), and low PCWP (<18 mmHg).
• In LV predominant shock, there is typically a low CVP (<14 mmHg), normal PAPi (>1.5), and
elevated PCWP (>18 mmHg).
• Biventricular (BiV) shock can be challenging to diagnose due to the attribution of elevated
right-sided filling pressures to sole LV dysfunction. BiV CS typically becomes apparent once LV
support is optimized. With reduction of LV filling pressures (possibly due to LV unloading), there is
progressive increase in the RV filling pressures while cardiac index remains low.

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PRE-IMPELLA
RA a/v/m PCW a/v/m Ao s/d/m LV s/d/ed
22 / 18 / 17 50 / 49 / 42 124 / 68 / 91 120 / 26 / 36

s
s
s
25 A
A
A
50 v
A
v
v v 100 100

D
D

ED
ED
ED

D
D

0 0 0 0

POST-IMPELLA
RA a/v/m PCW a/v/m Ao s/d/m
15 / 7 / 7 19 / 18 / 17 97 / 68 / 77
100
s

25 25

A D D

A
A 50

v v

0 0 0

Figure 1. Hemodynamic Tracings Pre- and Post-Impella Support

Impella placed for left main PCI in the setting of severe volume overload and reduced cardiac output; note the significant unloading of the bilateral
ventricular filling pressures post-Impella support.

Table 2. Hemodynamics of Right, Left, and Biventricular Shock

HEMODYNAMIC PARAMETER RV PREDOMINANT SHOCK LV PREDOMINANT SHOCK BIV SHOCK

CVP >14 mmHg <14 mmHg >14 mmHg

PCWP <18 mmHg >18 mmHg Variable

CVP/PCWP >0.86 <0.86 >0.86

PAPi <1.5 >1.5 <1.5

As the patient becomes refractory to vasoactive medications, hemodynamic measurements and

classification of shock can aid in determining which MCS device is appropriate. With elevated LV filling
pressures in the setting of low cardiac output, LV unloading is necessary (Impella® or TandemHeart®).
Isolated VA ECMO without LV venting can lead to increased afterload and failure to relieve the ventricle.

Once MCS is placed, PACs can allow optimization of biventricular filling pressures and guide fluid,
diuretic, or renal replacement therapy as needed. Precise measurements of SVR can substantially guide
optimal use of inotropes and vasoactive medications.

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Finally, PACs are vital during weaning of MCS or escalation to durable ventricular support or heart
transplantation. Once the patient is able to be weaned from high-dose/multiple vasoactive medications,
PAC and arterial monitoring in combination allow for calculation of cardiac power output (CPO=MAP x
CO/451) which, when less than 0.8, has been associated with poorer survival.5

Arterial monitoring
Similar to the PAC, the arterial line must be flushed and balanced as outlined above. In addition to
arterial pressure monitoring, real-time cardiac output estimation is possible using an arterial line. The
general principle is pulse contour analysis, which estimates stroke volume based on the time-pressure
curve during systole compared to diastole, measuring the area under the curve in systole. The utility of
such analysis in patients on mechanical circulatory support is unknown and may be compromised by
continuous flow of the support device.

QUICK READ SUMMARY

✓ Contemporary data have shown that PAC use is associated with improved survival in
cardiogenic shock (CS)2 and improved outcomes in patients in CS requiring mechanical
circulatory support.3

✓ Right-sided jugular venous access is ideal for long-term hemodynamic monitoring with a
PAC in the ICU. Other access options include femoral venous access and brachial venous
access for “in-and-out” assessment.

✓ Arterial pressure monitoring via the radial artery is often needed to complement data
available from the MCS device and can facilitate frequent arterial blood sampling.

✓ Invasive hemodynamic measurements can inform every phase of clinical care in patients with
known or suspected cardiogenic shock and can help differentiate LV, RV, and BiV shock.

References
1. The ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation Study of Congestive Heart Failure and
Pulmonary Artery Catheterization Effectiveness: The ESCAPE Trial. JAMA. 2005;294(13):1625-33. doi:10.1001/
jama.294.13.1625.

2. Hernandez GA, Lemor A, Blumer V, et al. Trends in utilization and outcomes of pulmonary artery catheterization in
heart failure with and without cardiogenic shock. J Card Fail. 2019;25(5):364-71. doi:10.1016/[Link].2019.03.004.

3. O’Neill WW, Grines C, Schreiber T, et al. Analysis of outcomes for 15,259 US patients with acute myocardial
infarction cardiogenic shock (AMICS) supported with the Impella device. Am Heart J. 2018;202:33-8. doi:10.1016/j.
ahj.2018.03.024.

4. Truesdell A. [@agtruesdell]. (2018, June 7). 4/4 Right #radialfirst sheath (used for LM PCI) switched out
for my own favorite “A-Line” prior to CICU admission…. [Tweet]. Twitter. [Link]
status/1004948331179790338.

5. Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in
cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340-8. doi:10.1016/j.
jacc.2004.03.060.

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10.9
Delayed Closure
Techniques
Kusum Lata, MD, FACC, FSCAI
Interventional Cardiology
Cardiology & Vascular Disease
Sutter Gould Medical Group
Vice Chair, Board of Directors
Sutter Gould Medical Group
Board of Trustees, Society of Cardiovascular & Angiography
Tracy, CA
[Link]@[Link]

Anshita Kumari, MBBS

Kasturba Medical College, Manipal, India
Research Associate
Sutter Health
Tracy, CA
anshitakumari0@[Link]

Avijit Bagga
Research Associate
Sutter Health
Tracy, CA
avijitbagga@[Link]

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Introduction
Successful hemostasis is vital for all percutaneous procedures. Risk of bleeding and subsequent
complications rises as arteriotomy size increases. The traditional method of hemostasis with manual
compression is challenging following large bore access procedures. Surgical cutdown and closure for
large bore access carries higher risk than percutaneous access and closure. Recent advancements
in technology and percutaneous procedures, increased usage of hemodynamic support devices, and
innovative endovascular treatments require a new look at hemostasis, especially if the device with large
bore sheath is left in place and not immediately removed.1,2 In this section, we discuss delayed arterial
closure using Perclose sutures placed during a prior procedure.

Pre-close technique
Delayed closure in large bore sheath procedures is feasible and can be safely performed. The “pre-
close technique,” utilizing two Perclose ProGlide® suture mediated closure systems (Abbott Vascular),
is safer than postprocedural closure because we place the sutures during initial access before any
anticoagulation.3 The details of the pre-close technique are discussed elsewhere.

Large bore sheath maintenance

Securing pre-close sutures
Once the large bore sheath is pre-closed and the decision is made to leave the hemodynamic support
device in place, the physician should wrap and secure the pre-close sutures.
1. Wrap the Perclose sutures in sterile towels and gauze to keep the entire length of the sutures, all the
way to the skin, sterile. The wrapping process can be done in various ways. The pre-close sutures can
be wrapped separately in a sterile towel and covered with gauze close to the sheath (near skin), or the
sutures can be placed inside a hollow syringe and then covered with sterile towels.
2. Use large breathable, sterile, clear, waterproof, adhesive dressings (eg, Tegaderm™) to wrap the
sterile towels and secure them to the abdomen. Use meticulous care to ensure that during this
process the towels and gauze covering the sutures are not pulled up, leaving the pre-close sutures
exposed to a length of skin and at risk for infection.

Figure 1. Two Pre-close Sutures at Right

Angle to Each Other with Sheath in Center

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Figure 2. Pre-close Sutures Wrapped in Sterile Towels and

Secured with Tegaderms

3. Once the sutures are secured, ensure that the large bore device has not moved and is correctly
positioned. If needed, adjust the device and note the marker length for follow up during ICU stay.
4. Make a loop of the external length of the device around the lateral side of the thigh and suture the
large bore sheath to the skin to prevent it from being pulled off inadvertently. This provides ample
length for maneuvering and adjusting the device and prevents dislodgment of device if pulled back.
5. Always maintain a clear view of the sheath site and outside device length so that you can monitor
A device position and watch for bleeding, hematoma,
B or potential external sheath fracture. Do NOT
place too much gauze or place the towels on the top of sheath or device length outside the body.
6. Cover entire area with large, clear, sterile, waterproof, adhesive dressing.
7. Place leg immobilization brace prior to transfer from the cath lab to prevent excessive leg movement
and potential device dislodgment.

Adjusting sheath or device position or performing other procedures

If the large bore sheath or device needs to be repositioned, adjustments should be performed in a
systematic manner by an experienced clinician. When possible, intravenous (arterial or venous) access
and Foley catheter placement should be done prior to placement of the large bore sheath.
1. We do not clean the sutures on regular basis. No need for prophylactic antibiotics.
2. Remove superficial Tegaderm and sutures as needed.
3. Adjust the device using either hemodynamic waveform monitoring or echocardiographic guidance.
Note: Perform device adjustment only if hemodynamic or clinical criteria necessitate, and not on the
sole basis of echocardiographic criteria.
4. Avoid excessive patient movement and/or cleaning. Perform any out of bed maneuvers under direct
supervision.
5. Perform only necessary procedures and imaging. Any procedures on fully anticoagulated patients
can be traumatic. A minor trauma from a catheter can lead to bleeding, hematoma, and serious
complications. If the patient requires any additional procedures, such as intravenous arterial access,
Foley or NG/OG tube placement, transesophageal echo, or bronchoscopy, discuss the procedure with
the interventional cardiologist and allow only highly skilled clinicians to perform the procedure.

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Delayed closure using Perclose

The definitive closure procedure of pre-close sutures should be performed in cardiac catheterization lab
once hemodynamic support is successfully weaned. This is a crucial step to achieve successful and patent
hemostasis. Variation in practice patterns in device closure of MCS does exist.

Preparation
Anticoagulation should not be tuned off in advance of pre-closure as large bore devices are prone to
thrombosis. The sterile techniques and preparation take time. Once preparation for removal of the large
bore device is complete, the interventional cardiologist determines when to stop anticoagulation in the
cardiac cath lab.

When the patient arrives in cardiac cath lab, standard sterile techniques should be in place. Remove
the Tegaderm and sterile towel and clean with standard sterile solution. No additional local or systemic
antibiotic prophylaxis is needed. Inspect the pre-close sutures for integrity. The interventional
cardiologist removes the large bore device in customary manner. If the large bore device does not have
a sheath then obtain contralateral access as described below and prepare to place the crossover sheath
from other side. The hemodynamic device without sheath can be pulled up to the common iliac/external
iliac and the crossover sheath can be placed with balloon just above the large bore device. The device is
then removed and pre-close sutures deployed in the usual fashion.

Technique
1. Check ACT at the initiation of the pre-close deployment.
2. Perform ipsilateral imaging through large bore sheath to ensure the patency of the vessels.
3. To achieve dry hemostasis, contralateral femoral access or a radial access is necessary. Advance a
6 Fr diagnostic inframammary artery catheter (IMA) through the additional contralateral femoral or
radial access and perform infrarenal abdominal angiogram to delineate the route.
4. Use the same catheter to engage the iliac artery and advance a 0.35 crossover wire through the
IMA and through the side of the large bore sheath and at least up to the distal superficial femoral
artery or popliteal artery.
5. Exchange the IMA catheter for a 6 Fr crossover long sheath from the contralateral site placed at the
ipsilateral (to side of large bore sheath) external iliac artery.
6. Attach manifold to the large bore sheath.
7. Place an appropriate size peripheral balloon, ideally 1:1 to the artery, over the 0.35 wire and inflate
proximally to the large bore sheath until the pressure waveform at large bore sheath is flattened.
Low pressure is usually enough to achieve this flattened waveform if an appropriate size balloon is
used. Low inflation pressure prevents traumatic injury to the vessel wall.
8. Remove the large bore sheath and push the existing pre-close sutures knot further and tie to
complete closure of first Perclose. Then close the second Perclose.
9. Balloon tamponade helps in deployment of Perclose sutures in a bloodless field. If the Perclose
suture fails to achieve hemostasis, the balloon can be inflated to achieve complete hemostasis.
10. Perform final angiogram through the balloon to long sheath and remove all catheters and
guidewires to conclude the procedure.
11. Exchange long sheath for short sheath and obtain hemostasis with either manual compression or
closure device.

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Complications
Complications of large bore access may include perforation, thrombosis, or distal embolization. Each
of these complications should be managed in the standard way. Meticulously following the technique
described above provides a controlled environment in which to deal with complications in the event they
arise. Delayed closure using Perclose sutures is not a risk for additional vascular complications.

Tips and tricks

• Once the patient reaches the cath lab for device removal, remove the sterile towels and Tegaderm
under strict sterile precautions. Clean the entire area around the sheath with sterile solutions and
examine the intactness of the pre-close sutures.
• After removal of the large bore device, perform dry closure with deployment of pre-close sutures.
• Pre-close sutures can be left in place as many days as the device is left in place.4
• Hemostasis after device removal is recommended in the cardiac cath lab.

QUICK READ SUMMARY

✓ Delayed closure for large bore sheath procedures is feasible and can be safely performed.

✓ Pre-close techniques are much safer than postprocedural closure because we place the
sutures during initial access before any anticoagulation.

✓ Delayed closure of large bore sheath device with pre-close sutures can be performed safely
as the pre-close sutures may be left in place for as many days as the device is left in place.

References
1. O’Neill WW, Kleiman NS, Moses J, et al. A prospective randomized clinical trial of hemodynamic support with Impella
2.5 versus intra-aortic balloon pump in patients undergoing high-risk percutaneous coronary intervention: the
PROTECT II study. Circulation. 2012;126(14):1717-27.

2. Werdan K, Gielen S, Ebelt H, Hochman JS. Mechanical circulatory support in cardiogenic shock. Eur Heart J.
2014;35(3):156-67.

3. Kaki A, Blank N, Alraies MC, et al. Access and closure management of large bore femoral arterial access. J Interv
Cardiol. 2018;31(6):969-77. doi: 10.1111/joic.12571. Epub 2018 Nov 19. PMID: 30456854.

4. Lata K, Kaki A, Grines C, et al. Pre-close technique of percutaneous closure for delayed hemostasis of large-bore
femoral sheaths. J Interv Cardiol. 2018;31(4):504-10. doi: 10.1111/joic.12490. Epub 2018 Feb 5. PMID: 29405431.

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10.10
Percutaneous
Axillary Artery
Access Best
Practices
James M. McCabe, MD, FSCAI
Department of Medicine, Division of Cardiology
University of Washington
Seattle, WA
jmmcabe@[Link]

Kathleen Kearney, MD, FSCAI

Department of Medicine, Division of Cardiology
University of Washington
Seattle, WA

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Introduction
Growth in percutaneous transcatheter technology is driving a demand for expanded large bore access
options beyond the femoral arteries. Axillary arterial access is typically considered for structural heart
interventions or delivery of temporary mechanical circulatory support in situations involving:
• Femoral-iliac arterial vascular disease
• Morbid obesity or other anatomical considerations favoring axillary over femoral access
• Desire for early ambulation, especially for patients with prolonged indwelling axillary devices
Surgical graft implantation is the historical standard for axillary access, but a percutaneous axillary
approach offers advantages in urgent scenarios and may carry less morbidity than general anesthesia
and surgery. In contrast to long-standing beliefs that the axillary artery is not compressible, the mid-
axillary portion is compressible against the second rib. This was shown using cadaveric models1 and
has been borne out in clinical experience. While there was early speculation that the less muscular
media layer of the axillary artery would result in more complications than femoral access, rates of
arterial laceration or disarticulation have not increased with growing experience, demonstrating safe
utility of large bore access.2

Strategic planning
When assessing the suitability of the axillary artery for access, it is important to assess axillary artery
caliber (ideally ≥ 6.0 mm in diameter), tortuosity, and calcification or atheroma at the implantation site.3,4
For transcatheter aortic valve replacement, these anatomic features are evaluated using pre-procedure
CT angiography. In urgent cases, such as temporary mechanical circulatory support device implantation,
ultrasound and peripheral angiography are used, occasionally substituting intravascular ultrasound
when contrast must be limited. Collateralization around the axillary artery may be sufficient for short-
term use in cases with borderline vessel size, and vessel size should be interpreted remembering that
the vasoconstricted peripheral arterial tree underestimates the ability of vessels to accommodate large
bore access in the setting of cardiogenic shock. The decision of which axillary artery to choose for
access is based on patient handedness, aortic arch type with attention to retroflexion of the innominate
or left subclavian artery, and avoiding puncture through pacemaker or ICD pockets.

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Equipment and procedural considerations

1. Perform peripheral angiography via femoral access. Advance a 0.018 inch wire across the
respective axillary artery. This wire serves as a marker for fluoroscopic correlation with the course
of the artery (see Figure 1). Map the course on the skin surface to orient the operator to the cranial-
medial trajectory of the vessel, typically toward the earlobe.

A B

C D

Figure 1. Axillary Access

(A) The axillary artery originates as the subclavian artery crosses lateral to the first rib and terminates as the brachial artery as it crosses the
inferior border of teres minor muscle attachment to the humerus. Access is obtained in the proximal segment to ensure compressibility against
the 2nd rib and to avoid many of the branches. (B & C) Micropuncture access is obtained at a shallow angle. The fluoroscopic landmarks from the
indwelling wire down the axillary artery are used to mark the skin, aiming puncture just lateral to the 2nd rib. (D) Note shallow angle of sheath
entry of the large bore sheath, which remains protruding during the procedure.

2. Identify the proximal segment of the axillary artery on ultrasound with respect to the subclavian vein
and, often, the brachial plexus. While you can enter the axillary artery in its lateral segment via the
armpit, we do not recommend this location due to difficulty with manual compression hemostasis
and patient comfort. Liberal use of a local anesthetic is needed as this area is well-innervated.

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3. Identify the thoracoacromial branch near the access point to avoid transection. As shown in Figure
1, use ultrasound-guided micropuncture technique at a shallow angle (approximately 30 degrees)
with entry near the lateral border of the 2nd rib. A shallow angle of entry is critical to allow for
sheath delivery into the artery as it courses between the clavicle and the second rib. A steep angle
results in kinking of the sheath and is a common reason for failure with axillary access. The artery is
usually ‘pre-closed’ with Perclose suture devices deployed at minimal angulation. Contraindications
to closure devices do not differ from femoral access. This step may be deferred in preference for
late closure at the time of device removal, or a single suture deployed pre-procedure with a second
deployed at the time of device explant.
4. Place a 10 cm 8 Fr sheath for ease of delivering equipment intravascularly before upsizing to the
large delivery sheath. Advance the large bore sheath no further than the mid subclavian to avoid
trauma crossing the subclavian flexure. Note that even when the sheath is advanced into the aorta
for procedures such as percutaneous valve delivery in TAVR, the sheath remains protruding.
5. The existing 0.018 inch wire may be used to deliver a compliant balloon sized to assist with
hemostasis as needed, although this is usually unnecessary for sheath exchanges.
6. At the time of explantation, tighten the Perclose sutures in the usual fashion and repeat peripheral
angiography to ensure normal flow and the absence of significant stenosis from the closure device,
significant thrombus, or bleeding.
Prolonged angioplasty is usually adequate treatment, but in cases of long-dwelling ventricular assist
devices, thrombus burden may require thrombectomy. Covered stents are prone to deformation against
the bony structures in this region and are thus reserved for severe or refractory cases of bleeding.

PRO TIPS
• Maintain a shallow angle of entry into the axillary
artery with micropuncture access. The wire may
navigate a steep angle crossing between the
clavicle and the 2nd rib but a sheath will kink; this
is a common reason for failure.
• Set up a table as an extension from the left
arm and have a second operator or technician
assist in advancing catheters or stabilizing the
partially advanced sheath. Ensure monitors are
easily visible so that you can comfortably view
fluoroscopic images. Monitors are typically placed
on the patient’s contralateral side (as normal) or
at the ipsilateral ear facing the feet (Figure 2).
• Use a second access point to advance a 0.018
inch wire across the axillary artery to use Figure 2. Room Setup
as a marker during access and for balloon- Proper room setup is imperative for facile left axillary
assisted hemostasis in the event of bleeding arterial device implantation.
complications.
• Apply manual pressure hemostasis against
the second rib. This is effective and sufficient
for sheath exchanges, and while not ideal,
is adequate for sheath removal in certain
circumstances.

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Case examples

Case 1: Bleeding after failed closure—balloon-assisted tamponade compression after

failed Perclose
Following TAVR, extravasation is noted on post-procedure angiogram after Perclose deployment and
wire removal (Figure 3A, video). Bleeding is controlled following balloon occlusion for 5 minutes and
half-reversal of heparin (Figure 3B). A covered stent is not required.

A B

Figure 3 (video). Bleeding and Balloon-assisted Tamponade Compression After Failed Perclose

Case 2: Obstructive thrombus—collateralization and atherectomy

Large bore sheath has remained in place for over 14 days, with laminar thrombus noted on pre-explant
angiography. Occlusive thrombus post-explantation, though flow is maintained via collaterals (Figure
4A, video). Following thrombectomy, flow is improved (Figure 4B) and managed with intravenous
heparin drip for 48 hours.

A B

Figure 4 (video). Obstructive Thrombus, Collateralization, and Atherectomy

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References
1. M
 athur M, Krishnan SK, Levin D, Aldea G, et al. A step-by-step guide to fully percutaneous transaxillary transcatheter
aortic valve replacement. Structural Heart. 2017;1(5-6):209-215. doi:10.1080/24748706.2017.1370156.

2. McCabe JM, Kaki AA, Pinto DS, et al. Percutaneous axillary access for placement of microaxial ventricular support
devices: the Axillary Access Registry to Monitor Safety (ARMS). Circ Cardiovasc Interv. 2021;14(1):e009657. doi:
10.1161/CIRCINTERVENTIONS.120.009657. Epub 2020 Dec 16. PMID: 33322918; PMCID: PMC7813449.

3. A
 rnett DM, Lee JC, Harms MA, et al. Caliber and fitness of the axillary artery as a conduit for large-bore cardiovascular
procedures. Catheterization and Cardiovascular Interventions. 2017;91(1):150-156. doi:10.1002/ccd.27416.

4. T
 ayal R, Iftikhar H, LeSar B, et al. CT angiography analysis of axillary artery diameter versus common femoral
artery diameter: implications for axillary approach for transcatheter aortic valve replacement in patients with hostile
aortoiliac segment and advanced lung disease. International Journal of Vascular Medicine. 2016;2016(3):3610705-
3610705. doi:10.1155/2016/3610705.

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PREVIOUS CHAPTER Chapter 10.11: Distal Limb Perfusion Strategies NEXT CHAPTER

10.11
Distal Limb
Perfusion
Strategies
Chirdeep Patel, MD, FSCAI
Interventional Cardiologist
Lehigh Valley Health Network
Allentown, PA
chirdeeppatel@[Link]

Pooja Swamy, MD
Assistant Professor of Medicine
Division of Interventional Cardiology
Loma Linda University Health
Loma Linda, CA
Docpoojamahadev@[Link]

Amir Kaki, MD, FACC, FSCAI

Clinical Associate Professor of Medicine
Director, Mechanical Circulatory Support and Complex Coronary Intervention
Associate Director, Interventional Cardiology
Ascension St. John Hospital
Detroit, MI
amirkaki@[Link]

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Introduction
Modern percutaneous left ventricular assist devices (pLVADs) and extracorporeal life support (ECLS) require
large-bore arterial access (13-24 Fr). The combination of hypoperfusion, vasoconstriction, and obstruction of
arterial flow by large indwelling catheters may lead to limb ischemia in up to 70% of patients.1-3 The survival
rate of patients in cardiogenic shock (CS) is around 50% in the modern era.4 Limb ischemia significantly
decreases these survival rates and negatively impacts the quality of life.5, 6 Therefore, it is paramount to
establish and maintain adequate distal limb perfusion when large-bore arterial access is in place.7 Strategies
to reduce the risk of limb ischemia include the placement of antegrade distal perfusion catheters (DPCs).8, 9
In this chapter, we aim to provide a comprehensive review of strategies to assess and re-establish distal limb
perfusion in patients with temporary mechanical circulatory support (MCS) systems.

Assessment of distal perfusion

Assessment of distal limb perfusion prior to departing the procedural suite is preferred, as prevention of
ischemia is likely to provide the best outcomes.

Femoral approach
Lower extremity perfusion can be assessed via angiography or Doppler assessment. For Impella®
devices, selective angiography may also be performed via the side port of the introducer sheath. With
TandemHeart® or ECLS cannulas, angiography can alternatively be performed in an antegrade fashion
via radial, brachial, or contralateral femoral access. Visualization of contrast passage below the access
site can often (but not always) provide reassurance of perfusion (Figure 1).

Figure 1. Assessing Distal Limb Perfusion

Using the large-bore access side port (orange), right iliofemoral angiography was
performed demonstrating adequate flow into the superficial (green) and deep
femoral arteries (black).10

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Axillary approach
The coexistence of coronary disease and lower extremity arterial disease is well established.11 As a
result, a small percentage of patients may not be appropriate candidates for femoral MCS. The axillary
artery has been shown to be of adequate size and free of significant atherosclerotic disease in a
majority of these patients and an axillary approach can be a safe and lifesaving option in these patients
(Figure 2).12 Additionally, femoral access requires persistent bedrest in patients who may otherwise
greatly benefit from in-hospital conditioning programs and physical therapy.13

Figure 2. Angiography Guided Axillary Access

(A) Assessment and identification of the axillary artery branches is important to precisely define an access point that is lateral to the
thoracoacromial artery and medial to the circumflex humeral and subscapular arteries (ie, the “sweet spot,” highlighted in image A). (B) A JR4 or
multipurpose (MP) catheter is used to engage the innominate artery to perform contrast angiography to identify the axillary artery anatomy. (C)
Introduction of the large sheath in the right axillary artery over the stiff wire.10

Upper extremity perfusion is easier to assess, typically via palpation of brachial, radial, or ulnar pulses.
Placement of a brachial or radial arterial line can provide continuous hemodynamic monitoring. Doppler
A B
assessment may also be used. Angiography may be performed via the introducer sheath side port or in
an antegrade fashion by placing a catheter (ie, Vitek, Simmons, Cobra, or JR4) in the subclavian artery via
femoral or contralateral radial approach. Our recommendation is to place an ipsilateral radial arterial line
(typically using a 4-5 Fr Terumo Slender® or Cordis Rain® sheath) for monitoring in all these patients.

Monitoring of distal perfusion

Frequent monitoring of distal limb perfusion in the ICU is critical for early detection of ischemia as “time
is tissue.” Our routine is for bedside nurses to perform hourly visual inspection and physical examination
(appearance, temperature, capillary refill time, neurological assessment) of the at-risk extremity. The
nurses also perform distal Doppler assessment at least every shift or when a change in perfusion is
suspected. Continuous radial arterial line pressure monitoring is also the routine for axillary access in
our institution. Although it is possible to employ invasive pressure monitoring of lower extremity (via
antegrade superficial femoral, popliteal, dorsalis pedis, or posterior tibial lines), we do not routinely
employ this strategy purely for perfusion monitoring purposes.

These patients are typically maintained on anticoagulation with heparin for the patency of their MCS
devices. While each institution has its own target ranges, our usual target ACT and aPTT ranges are
180-220 and 70-100 seconds, respectively. We do not specifically alter our anticoagulation goals due
to the mere presence of a perfusion circuit. The patency of these circuits depends on many factors
including patient specific systemic milieu and the amount of flow through these circuits. We generally
leave these perfusion circuits in place for as long as they are functional and necessary. We find
replacing these circuits routinely for infection control purposes to be a difficult proposition as this carries
a significant risk of vascular complications.

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Reperfusion—or continued perfusion—strategies

The term reperfusion in this case is a bit of a misnomer as it implies absence of perfusion at some
point. Our preference is to use the term “continued perfusion” as we strongly believe in preventing
limb ischemia even for the shortest period. This starts initially with choosing the optimal access site to
reduce ischemia risk. We recognize that there may be patient or device constraints where limb ischemia
will occur if interventions are not implemented from the very beginning.

There are many options for continued perfusion. Here we discuss the following techniques at our disposal:
• Removal of peel-away sheath on Impella®
• External femoral ipsilateral bypass circuit
• External femoral contralateral bypass circuit
• External upper to lower extremity bypass circuit
• Internal femoral contralateral bypass circuit
• External axillary bypass circuit
• Internal axillary bypass circuit

Removal of peel-away sheath on Impella®

The percutaneous Impella® catheters come with two sheaths (13-14 Fr introducer sheath and a tapered
repositioning sheath). Impella CP® is implanted more frequently for shock patients as it provides more flow
than the Impella 2.5® device. The Impella CP comes with a 14 Fr peel-away introducer sheath for insertion
of the device. Although maintaining this sheath increases options for closure, this does increase the risk
of limb ischemia as it is 14 Fr in size throughout its entire length. For patients at high risk or with signs of
such complications, removal of the peel-away sheath can be tried first.

The introducer sheath should be pulled back from the arteriotomy while manual pressure is held
over the access site. Once it is fully removed from the body, the sheath can then be peeled away and
removed. Note that injury to the arteriotomy and bleeding may occur if the peel-away sheath is broken
while still fully or partially within the artery. The smaller repositioning sheath (14 Fr base tapering down
to a 9 Fr tip) can then be advanced from its position at the back of the catheter to the arteriotomy site
over the catheter. One potential complication of this exchange is catheter migration and therefore this
maneuver should be performed by two people under direct fluoroscopic visualization (Figure 3). Another
potential complication may be an increased risk of bleeding as the sheath size is tapered down. If the
site has been preclosed with Perclose ProGlide™ sutures, tightening the sutures (pulling the longer blue
rail suture limb) may help reduce the bleeding. Hubbing the sheath also ensures that the 14 Fr portion
of the sheath fully “plugs” the 14 Fr arteriotomy. In some cases, this simple exchange is enough to allow
for adequate distal blood flow and no further intervention is required.

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Figure 3. Impella® Peel-away Sheath Removal

(A) One operator holds pressure and stabilizes the catheter while a
second operator pulls the introducer sheath back, (B) peels it away,
and (C) places the repositioning sheath in place. (photographs
courtesy of Abiomed®)

External femoral ipsilateral bypass circuit

TandemHeart (15-17 Fr) and ECLS (17-24 Fr) cannulas are large in size and likely to cause limb
ischemia. Although not recommended, there may be clinical scenarios where the operator may elect
to leave the peel-away Impella® sheath in place even if it is occlusive. In these at-risk patients, it is
necessary establish a limb perfusion circuit7 and infusion through a DPC is recommended in these
cases. The DPC can be inserted in the superficial femoral artery (SFA) in an antegrade approach or in
the popliteal to tibial vessels in a retrograde fashion for femoral cannulations.

Note that all perfusion bypasses in this chapter are labeled in a donor to recipient format. The donor
sheath should be equal to or one French size larger than the recipient sheath.

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External fem-fem bypass: ipsilateral CFA to antegrade SFA

Antegrade SFA access is the most common mode of continued perfusion. Note that antegrade SFA
access after the insertion of a large-bore sheath is difficult. Thus, we recommend obtaining antegrade
access prior to the placement of the large sheath if risk of hypoperfusion is anticipated to be at least
moderate.

1. Obtain antegrade access in the ipsilateral SFA using micropuncture access. Fluoroscopy
(intermittent contrast injections or the use of roadmap angiography) or ultrasound guidance is
necessary. Fluoroscopic guidance may be preferred for beginners who are not accustomed to the
use of ultrasound.
2. Insert a 5-6 Fr sheath in an antegrade fashion. We prefer longer (20-25 mm) and flexible braided
(ie, Teleflex Arrow-Flex®) sheaths to prevent accidental slippage or kinking if possible.
3. Connect the side port of the Impella® introducer sheath or the wire access port of the repositioning
sheath to the side port of the antegrade sheath via a male-to-male (M-M) connector (Figure 4). The
latter provides minimal passive flow and should only be considered for short-term use.

A B C
Figure 4. External Femoral Ipsilateral Bypass Circuit: Ipsilateral CFA to Antegrade SFA Bypass
(A) Right CFA with an occlusive Impella repositioning sheath. To maintain flow to the leg, an external bypass circuit was created by connecting
the repositioning sheath and an antegrade SFA sheath (photo courtesy of Alex Truesdell, MD). (B) Left CFA with occlusive MCS sheath in situ. To
maintain flow to the left leg, an external bypass circuit was created. Left CFA was accessed in an antegrade position with a puncture distal to the
large sheath. The sidearm of the antegrade sheath was then connected to the large sheath using a M-M connector, creating flow (dotted arrow).14
(C) Male-to-male connector (photo courtesy of Alex Truesdell, MD).

Keep in mind that the flow through the repositioning sheath may not be adequate for perfusion and
other modes may need to be considered. ECLS cannulas typically include side vents for connection to
perfusion sheaths. The TandemHeart® cannulas do not come with a side vent. The cannulas without a
vent can be attached to a barbed connector with a side vent. These side vents can then be connected to
the antegrade sheath via a M-M connector (Figure 5).

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A B C
Antegrade
SFA
perfusion
sheath

Side vent

Barbed
.
connector with
side vent
ECLS
cannula
side vent

Figure 5. ECLS Arterial Cannula Connections

(A) ECLS arterial cannulas come with or without a side vent for perfusion. (B) The cannulas without a vent can be attached to a separate
connector with a vent. (C) The antegrade perfusion sheath can then be connected to the cannula for perfusion using a M-M connector to create
an external femoral ipsilateral bypass circuit. (image A courtesy of Medtronic®)

External fem-distal bypass: ipsilateral CFA to retrograde distal lower extremity

1. Obtain retrograde access in the ipsilateral popliteal, posterior tibial (PT), or dorsalis pedis (DP)
arteries using fluoroscopic or ultrasound guidance as described above. We favor ultrasound in these
cases. Popliteal access in a supine patient is more technically complex although “frog-leg” position
can often be utilized.
2. Place 4-5 Fr hydrophilic (ie, Terumo Glide® or Cordis Rain®) sheath at the site and connect to the
large-bore via a M-M connector tubing (Figure 6).

DP access

Figure 6. External Femoral Ipsilateral Bypass Circuit: Ipsilateral Antegrade

SFA to DP Bypass
Left CFA with an occlusive Impella repositioning sheath. Ultrasound guided left DP access was
obtained. To maintain flow to the leg, an external bypass circuit was then created by connecting
the repositioning sheath to the DP sheath.

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External femoral contralateral bypass circuit

For some femoral approach patients, such as the ones with the Impella® repositioning sheath in place,
contralateral access for perfusion may be necessary. This technique employs a similar principle for limb
perfusion as above but from contralateral access.
1. Obtain routine 5-6 Fr access in the contralateral common femoral artery (CFA).
2. Obtain ipsilateral access as described above.
3. Connect the side ports via M-M connector tubing (Figure 7).

It is imperative to monitor both lower extremities in these cases for signs of complications.

Figure 7. External femoral contralateral bypass circuit

Right CFA large-bore sheath placed for MCS. It was occlusive to distal flow. An external contralateral conduit was created from the contralateral
CFA. A sheath was placed in the left CFA. A perfusion sheath was placed in an antegrade fashion in the right SFA. Both sides were then
connected with M-M tubing. The arrows in these images depict the direction of blood flow.13,14

External upper to lower extremity bypass circuit

Peripheral arterial disease (PAD) may prevent contralateral femoral access in some patients. Limiting
femoral access points can also be desirable to decrease bleeding risk. Upper to lower extremity external
bypasses can be utilized in these patients.
1. Obtain 5-6 Fr access using a hydrophilic sheath in a brachial or radial artery.
2. Obtain ipsilateral lower extremity access in the SFA antegrade or in the popliteal/DP/PT arteries
retrograde as described above.
3. Connect these sheaths with M-M connector tubing (Figure 8).

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Figure 8. External Upper to Lower Extremity Bypass Circuit (“Lend a

Hand Technique”): Radial to Ipsilateral Antegrade SFA Bypass
Right CFA with an occlusive Impella® repositioning sheath. Right radial and antegrade
SFA accesses were obtained. To maintain flow to the leg, an external bypass circuit was
created by connecting the radial and SFA sheaths.13

Internal femoral contralateral bypass circuit

Antegrade SFA access can be challenging in some patients. In others significant PAD may limit
ipsilateral options. Limiting arterial access points can help decrease the risk of complications. Internal
contralateral bypass can instead be employed in these patients. Again, both lower extremities should be
monitored closely for signs of complications in these cases.

Internal fem-fem bypass: ipsilateral CFA to ipsilateral SFA

1. Obtain routine access in the contralateral CFA.
2. Engage ipsilateral iliac artery using a crossover (ie, IM, SOS, flush, RIM) catheter.
3. Advance a 0.035 wire (ie, Terumo Glide Advantage®) to the contralateral SFA.
4. Advance a 5-6 Fr long (45-65 cm) sheath over the wire and position it with the tip in the ipsilateral SFA.
5. Connect this long sheath to the side port/vent of the large bore access as described above (Figure 9).

Contralateral CFA
long sheath with tip
in ipsilateral SFA

Figure 9. Internal Fem-Fem Bypass Circuit: Ipsilateral CFA to

Ipsilateral SFA Bypass
Left CFA with an occlusive ECLS cannula. Access is obtained in the
contralateral CFA. A long sheath (orange arrow) is advanced to the ipsilateral
SFA from this access. An internal bypass (red arrows) is created by connecting
the sheath to the ECLS side vent with a M-M adapter.

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Internal fem-fem bypass: ipsilateral CFA to ipsilateral SFA, contralateral CFA to ipsilateral SFA,
or profunda femoris artery (PFA) also known as the “parent-child sheath technique”

This technique is useful in the event of a pre-existing occlusion of the ostial-proximal SFA, difficult
antegrade SFA access, or if the anatomy does not allow for the passage of a long 5-6 Fr sheath to the
ipsilateral femoral.

Note: To achieve adequate flow, the “parent” sheath has to be at least 3 sizes bigger than the “child”
sheath.
1. Obtain routine access in the contralateral CFA (7-8 Fr “parent” sheath).
2. Engage the ipsilateral iliac artery using a crossover (ie, IM, SOS, flush, RIM) catheter.
3. Advance a 0.035 wire (ie, Terumo Glide Advantage) to the contralateral SFA or PFA.
4. Advance a hydrophilic 4 Fr long (45-55 cm) “child” sheath over the wire and position it with the tip
in the ipsilateral SFA or PFA.
5. Connect this 4 Fr long sheath to the side port of the short contralateral sheath (Figure 10).

A B

Figure 10. Internal Fem-Fem Bypass “Parent-Child Sheath Technique” Circuit

(A) Blood flows through the left 7 Fr sheath (blue arrow) to the 4 Fr child sheath (green arrow) and through the 45 cm catheter to the contralateral
right side. The catheter then passes along the large-bore sheath (yellow arrow) and to the right SFA to bypass the occlusion and provide
perfusion to the right leg. (B) 7 Fr short “parent” and 4 Fr long “child” sheaths in the right CFA are connected (red arrow) to perfuse the left leg.14

External axillary bypass circuit

For axillary access, ipsilateral brachial or radial arteries can be utilized to maintain perfusion.13 The need
for such a bypass is generally lower than in femoral access.
1. Place a 4-5 Fr hydrophilic sheath at the desired location. Strong preference should be given
to the use of the radial artery to decrease brachial complications and ultrasound guidance is
recommended.
2. Connect to the large bore as above (Figure 11).
3. If Impella peel-away sheath has been removed, obtain access at an additional arterial site (femoral
or contralateral radial).
4. Connect the ipsilateral sheath with M-M tubing as above.

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A B

Figure 11. External Axillary Bypass Circuit

Upper extremity with an occlusive axillary large bore sheath. (A) 6 Fr sheath is placed in the ipsilateral radial artery. This sheath is then connected
to the sidearm of the Impella introducer sheath to maintain flow to the upper extremity (red arrows). (B) 6 Fr sheath is placed in an antegrade
fashion in the ipsilateral brachial artery. This sheath is then connected to the large bore sheath to maintain flow (red arrows).15

Internal axillary bypass circuit

In patients where brachial or radial perfusion sheath placement is difficult, an internal bypass circuit can
be utilized.
1. Obtain routine access in the CFA (7-8 Fr “parent” sheath).
2. Engage subclavian artery using a JR4 or a multipurpose (MP) catheter.
3. Advance a 0.035 wire (ie, Terumo Glide Advantage) to the ipsilateral brachial artery.
4. Advance a hydrophilic 4 Fr long (100 cm) “child” Glidecath® over the wire and position it with the tip
in the axillary or brachial artery.
5. Connect this 4 Fr long catheter to the side port of the femoral sheath (Figure 12).

Figure 12. Internal Axillary Bypass Circuit: Fem-Brachial Bypass

Upper extremity with an occlusive axillary large-bore sheath. Small radial artery precluded
placement of a perfusion sheath. 6 Fr “parent” sheath is placed in the CFA. 4 Fr “child”
Glidecath is advanced to the ipsilateral brachial artery and connected to the CFA sheath to
maintain flow (red arrows).15

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QUICK READ SUMMARY

✓ Large-bore access necessary for modern MCS systems poses a risk of limb ischemia and
other adverse vascular and bleeding events.

✓ Proactive planning and assurance of continued distal perfusion in every patient before
departing the procedural suite can help avoid complications.

✓ Continued perfusion strategies for patients with temporary MCS include:

• Removal of 14 Fr Impella® peel-away sheath

• External femoral ipsilateral bypass circuit
• External femoral contralateral bypass circuit
• External upper to lower extremity bypass circuit
• Internal femoral contralateral bypass circuit
• External axillary bypass circuit
• Internal axillary bypass circuit

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References
1. Bisdas T, Beutel G, Warnecke G, et al. Vascular complications in patients undergoing femoral cannulation for
extracorporeal membrane oxygenation support. Ann Thorac Surg. 2011;92(2):626-31.

2. Foley PJ, Morris RJ, Woo EY, et al. Limb ischemia during femoral cannulation for cardiopulmonary support. J Vasc Surg.
2010;52(4):850-3.

3. Zimpfer D, Heinisch B, Czerny M, et al. Late vascular complications after extracorporeal membrane oxygenation
support. Ann Thorac Surg. 2006;81(3):892-5.

4. Hajjar LA, Teboul JL. Mechanical circulatory support devices for cardiogenic shock: state of the art. Crit Care.
2019;23(1):76.

5. Tanaka D, Hirose H, Cavarocchi N, Entwistle JW. The impact of vascular complications on survival of patients on
venoarterial extracorporeal membrane oxygenation. Ann Thorac Surg. 2016;101(5):1729-34.

6. Kaushal M, Schwartz J, Gupta N, et al. Patient demographics and extracorporeal membranous oxygenation (ECMO)-
related complications associated with survival to discharge or 30-day survival in adult patients receiving venoarterial
(VA) and venovenous (VV) ECMO in a quaternary care urban center. J Cardiothorac Vasc Anesth. 2019;33(4):910-7.

7. Kaki A, Alraies MC, Kajy M, et al. Large bore occlusive sheath management. Catheter Cardiovasc Interv.
2019;93(4):678-84.

8. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus
conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and
propensity analysis. Lancet. 2008;372(9638):554-61.

9. Lamb KM, DiMuzio P, Moudgill N, et al. Fate of the lower extremity in patients after VA-ECMO via femoral
cannulations: limb salvage protocol can decrease ischemic complications. Journal of Vascular Surgery. 2015;61(6).

10. Kaki A, Alraies MC. Large-bore access site management. Cardiac Interventions Today. 2019;13(4):59-66.

11. Leng GC, Fowkes FG, Lee AJ, et al. Use of ankle brachial pressure index to predict cardiovascular events and death: a
cohort study. BMJ. 1996;313(7070):1440-4.

12. McCabe JM, Kaki AA, Pinto DS, et al. Percutaneous axillary access for placement of microaxial ventricular support
devices: the Axillary Access Registry to Monitor Safety (ARMS). Circ Cardiovasc Interv. 2021;14(1):e009657.

13. Zhang L, Hu W, Cai Z, et al. Early mobilization of critically ill patients in the intensive care unit: a systematic review and
meta-analysis. PLoS One. 2019;14(10):e0223185.

14. Kaki A, Schreiber T, Alraies M. The challenge of large bore occlusive sheath management: strategies for success.
Cardiology Today Intervention. 2018;7(5):26-30.

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PREVIOUS CHAPTER Chapter 11: Anticoagulation Strategies and Patient Considerations When Using MCS NEXT CHAPTER

Anticoagulation
Strategies and
Patient Considerations
When Using MCS
Manoj Ambalavanan, MD Stephanie Dwyer Kaluzna, PharmD, BCCP
Resident Physician, Cardiovascular Clinical Pharmacist
Department of Internal Medicine Clinical Assistant Professor, Department of
University of Illinois-Chicago Pharmacy Practice
[Link]@[Link] University of Illinois-Chicago
smdwyer2@[Link]
Anish Shah, MD, MS
Fellow Physician, Department of Cardiology Adhir R. Shroff, MD, MPH, FSCAI
University of Illinois-Chicago Professor of Medicine
Ashah282@[Link] University of Illinois-Chicago
arshroff@[Link]
Helena Dickens, BS
University of Illinois-Urbana/Champaign
Hdicke2@[Link]

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Introduction
Temporary mechanical circulatory support (MCS)—ranging from intra-aortic balloon pumps (IABP)
and percutaneous ventricular assist devices (eg, TandemHeart®, Impella®) to extracorporeal membrane
oxygenation (ECMO) systems, including venovenous (VV) and venoarterial (VA) bypass—is often used
in the setting of cardiogenic shock to help support and prevent end organ failure. The introduction of
these devices comes with additional thrombosis and coagulopathy risks from both the anticoagulation
strategies and the devices themselves. The appropriate use of MCS requires a nuanced balance in the
management of anticoagulation to minimize bleeding and thrombotic risk. The objective of this chapter
is to describe expert consensus and evidence-based best practices when considering anticoagulation
management with MCS.

Literature review
The major hematologic complications in MCS are thrombosis and bleeding. Bleeding complications
include major bleeding events, minor bleeding events, and access site related events, as described in
Table 1.

Table 1. Types of Bleeding Complications

Major bleeding events Broadly defined as requiring transfusions unrelated to access site complications

Minor bleeding events Do not meet criteria for major bleeding events

Access site complications Localized bleeding events related to:

• Anatomic issues

• Sheath size

• Access/closure technique

• Anticoagulation status

The incidence of major bleeding varies widely based on the breadth of the definition in studies and the
specific device being used. Additional complications include hemolysis and thrombocytopenia. Incidence
of these complications varies based on patient risk factors, operator factors, device types, and study
measures. The reported rates vary from as low as <1% major bleeding events with IABP to up to 81%
with ECMO.1

The three most common thrombotic events are limb ischemia, stroke, and thromboembolism. In severe
cases, limb ischemia can lead to amputation. Thrombotic complications can often be life threatening.
Table 2 lists the incidence of these complications from published datasets.

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Table 2. Incidence of Major Complications Associated with MCS1,5,29-31

COMPLICATION IABP (%) IMPELLA (%) TANDEMHEART (%) ECMO (%)

Hematologic

Major bleeding 0.8–47 0.05–54 3.6–59 5–81

Access site bleeding 2–27 2–40 8–53 6

Hemolysis 0.7–7.2 10–46 5.3 9.2–18

Thrombocytopenia 43 – – 8.3 (HIT)

Neurologic

Cerebrovascular accident 1–7 2.4–6.3 1.6–17.6

Neuropathy 0.4–24 – – –

Vascular

Limb ischemia 0.3–42 0.07–10 3.4–11 4.3–50

Amputation 0.1–1 – – 0–1.1

Thromboembolism 1.1–8.6 – – 18

Aortic rupture/dissection 0.09–9 – – <1

A
Vascular injury requiring surgery 0.01–13.3 B 1.3–2 0.85–13 4.7

Infectious

Access site infection 0.5–35 1.1 16 1.1–17.7

Sepsis 1–15.7 0.16–19 29.9 12.9–31

Mechanical

Device migration 1–8 0.05–23 8 –

Device malfunction 0.9–8.3 0.16–17 – 16.8–29

Preoperative considerations
The choice and placement of specific types of MCS is dependent on many clinical factors. Generally
speaking, a history of coagulopathies and intolerance to anticoagulation should be considered relative
contraindications to anticoagulation in the setting of MCS. The contraindications for devices evolve
throughout the course of treatment. For example, platelet consumption in patients with IABP or the
amount of hemolysis with Impella may require withdrawal of these MCS therapies.2

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Pharmacology
Unfractionated heparin is the primary pharmacologic agent used for anticoagulation. To date, there is no
universal algorithm for anticoagulation titration. Many proposed protocols are based on manufacturer’s
recommendations along with institutional guidelines, which include monitoring frequency and method.3,4
• A minimum of daily monitoring of complete blood counts is recommended to monitor for occult
bleeding or destruction of red blood cells.
• Hemolysis labs (eg, total bilirubin and LDH) should be considered when unexplained anemia is
found.
• ACT, PTT, and anti-Xa levels are commonly used to monitor anticoagulation:

· ACT is a point of care test that is best used with heparin but not practical outside of procedural
settings
· PTT is more accessible, but ranges are institution dependent, and value may be influenced by
other factors
· Anti-Xa has been found to improve time to therapeutic anticoagulation with heparin compared
to PTT, but established reference ranges have not been validated through larger studies,
particularly in the setting of MCS
Table 3 lists device specific ranges and considerations for anticoagulation with MCS.5-7

Table 3. Suggested Anticoagulation Ranges for MCS

INSERTION FREQUENCY OF
DEVICE MAINTENANCE CONSIDERATIONS
OF DEVICE MONITORING

Inflation-deflation ratios >1:1

* * * (such as 2:1 or 3:1) increase the
risk of thrombosis due to stasis
of the balloon. When using this
modality for a prolonged period
IABP
as is seen during the weaning
process, consider providing
systemic anticoagulation and
should warrant consideration of
anticoagulation

Q2-4 hours for first

ECMO ACT: 180-220 sec. ACT: 180-220 sec.
24 hours until stable

ACT: 160-180 sec. Q3 hours for first 24

Impella ACT: >250 sec. see Figure 1
PTT: 60-80 hours until stable

ACT: 180-200 sec. Q4-6 hours until

TandemHeart ACT: 400 sec. see Figure 2
PTT: 60-80 sec. stable
*Generally speaking, anticoagulation is recommended when using IABP unless there is a clear contraindication, although preference may vary by
operator. Guidelines for monitoring anticoagulation are institution dependent with no universal or evidence-based recommendations.

The Impella and TandemHeart devices use a purge solution that may contain unfractionated heparin.

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Figure 1. Management of Impella Device5,6,19

Figure 2. Management of TandemHeart Device5,34

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Other forms of anticoagulation are not standard of care with MCS. Low molecular weight heparin (LMWH),
direct oral anticoagulants (DOAC), and antiplatelet agents do not currently have enough data to support their
use in MCS. Figure 3 illustrates sites of activity and measurement within the coagulation cascade.

GPIIB/IIIA
Platelet

Endothelial damage will expose vWF,

which will allow for platelet binding –
Fibrinogen damage to this molecule will weaken
the ability for clot formation
Platelet

TISSUE
FACTORS Endothelial damage will release
GPIB tissue factor, a key molecule that
RELEASED
vWF will convert VII to VIIa and start the
extrinsic pathway

Subendothelial collagen

TISSUE FACTOR
VII VIIa

CLOTTING CASCADE

INTRINSIC PATHWAY

EXTRINSIC PATHWAY
FXIIa
VIIa UFH
aPTT
Activated FXa
Anti-FXa FXIa

Antithrombin
FIXa

Site of action of
unfractionated heparin Inactivated FXa
FXa
and low molecular
weight heparin
THROMBIN (FIIa) Anti-Xa directly
measures the ability
Site of action of
of this complex (UFH
argatroban and
THROMBIN-FIBRIN CLOT + antithrombin) to
bivalirudin
inhibit activated FXa

Figure 3. Coagulation Cascade Activity12,35

In the setting of heparin induced thrombocytopenia (HIT) or heparin intolerance, agents such as
bivalirudin or argatroban may be considered. Alternative forms of anticoagulation and management of
HIT are discussed later in this chapter.

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Management of complications
Therapeutic anticoagulation and active monitoring of access sites for bleeding and thrombosis helps
minimize or prevent complications. The specific management of bleeding and thrombotic complications
is described below.

Treatment of acute bleeding

Bleeding concerns may be secondary to hemolysis or supratherapeutic anticoagulation or may be
device related. Additional access site imaging, such as CT or angiography, may be required for further
evaluation of bleeds.8

Prompt discontinuation of anticoagulation should be considered, while balancing the risk of thrombosis
with the duration of anticoagulation. Administration of protamine sulfate may be used. While protamine
sulfate administration may be institution dependent, the general approach is that 1 mg of protamine
sulfate will reverse approximately 100 units of heparin. Since heparin is administered as a continuous
infusion in the setting of MCS, it is recommended to calculate the protamine dose based on the amount
of heparin administered in the preceding 2 to 3 hours. The maximum single dose of protamine sulfate
is 50 mg. The dose should be administered slowly over 10 minutes. If PTT remains elevated, additional
administration of 0.5 mg of protamine sulfate for every 100 units of heparin can be attempted.9

When argatroban is used, the half-life is approximately 45 minutes upon discontinuation. If prompt
reversal is needed, idarucizumab may be used, although availability is a significant limiting factor in
emergency settings. Typical administration of idarucizumab is two doses of 2.5 mg administered no
more than 15 minutes apart.10

There are no known, well-studied reversal agents for bivalirudin. The suggested measures to mitigate
bleeding with bivalirudin are discontinuation of the drug and attempts at hemostasis.

von Willebrand syndrome

Increased rates of transfusion have been seen in patients with continuous flow devices compared to
pulsatile devices.11 Some of these differences are thought to be secondary to acquired von Willebrand
syndrome.

Generally speaking, acquired von Willebrand syndrome is more frequently reported in patients with
durable or long-term MCS, although it should be considered in patients with nondurable MCS as well.
The mechanism through which patients with continuous flow MCS acquire von Willebrand syndrome
is centered around the amount of shear stress.12 The amount of shear stress is higher in patients with
continuous flow circuits leading to a greater proteolysis of the von Willebrand multimer. As a result, lysis
of this protein leads to an acquired impediment to coagulation causing an increased risk of bleeding.
Moreover, the activity of ADAMS-13, the enzyme naturally involved in breakdown of von Willebrand
factor, is thought to be enhanced,13 further exacerbating any bleeding complications.

In cases where rapid reversal is necessary, the use of von Willebrand-containing factor VIII
concentrates, desmopressin, and tranexamic acid have all been used, although their efficacy specifically
in MCS has not been evaluated.14

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Treatment of acute thrombosis

Heparin-induced thrombocytopenia (HIT) is the most common thrombotic complication of patients
with MCS. Table 4 lists criteria for suspicion for HIT.15 The first two criteria are thought to be the most
predictive.16

Table 4. Criteria for Suspicion of HIT32,33 (Based on Lo 2006 and Vatanparast 2012)

>50% drop in platelets and platelet nadir >20,000 2 points

Persistent
thrombocytopenia at or
30-50% drop in platelets and platelet nadir 10,000-19,000 1 point
after 5 days following
device implantation
<30% drop in platelets and platelet nadir <10,000 0 points

5-10 days after heparin exposure or <1 day after if exposed in last 30 days 2 points
A second fall in platelet
Suspected 5-10 days, >10 days after exposure or <1 day after if exposed
count 5 to 14 days after 1 point
in last 30 -100 days
initial heparin exposure
Platelet drop < 4 days without recent exposure 0 points

New thrombus or skin necrosis or systemic reaction following IV heparin 2 points

Presence of a thrombus Progressive or recurrent thrombus or suspected (not proven) 1 point

No thrombus present 0 points

No other causes 2 points

No other reasonable
explanation for Possible other cause 1 point
thrombocytopenia
Definite other cause 0 points

Total score

TOTAL SCORE LIKELIHOOD OF HIT NEXT STEPS

0-3 Low Evaluate for other causes of thrombocytopenia

4-5 Intermediate Order Anti-PF4

Order Anti-PF4
6-8 High
Order Serotonin Release Assay

Clinical presentation of thrombosis may occur with changes in pulsatility indices, device alarms, or
LV failure.17 If HIT is suspected, heparin products should be promptly discontinued, and laboratory
evaluation should be sent off. Figure 4 depicts the complete algorithm for management of HIT.18

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Suspected HIT?
(see Table 4)

1. Discontinue all forms of heparin and heparin purge solutions

2. Avoid platelet transfusions
3. Avoid vitamin K antagonists
4. Send off diagnostic testing

HIT confirmed HIT ruled out

Are there absolute Look for other causes of

contraindications to thrombocytopenia
anticoagulation?

YES NO

Monitor for resolution Normal renal

function?
Consider IVIG or
plasmapheresis
YES NO
Consider regional
citrate for ECMO
Bivalirudin Argatroban

Figure 4. Management of HIT in MCS

The first step in treatment in suspected HIT is to stop the heparin related products. For devices that require a
purge solution (ie, TandemHeart and Impella), manufacturers often recommend using purge solution without
anticoagulation.3 For patients with Impella devices, a sodium bicarbonate-based purge solution (25 mEq of
sodium bicarbonate in 1 liter of D5W) is the recommended alternative.36,37 It should be noted that heparin
coating and line flush solutions can also contribute to HIT and should be promptly discontinued.

Diagnostic testing should be sent off in patients with suspected HIT. Anti-PF4 is a more sensitive test
and useful screening tool, while the serotonin release assay (SRA) is more specific and diagnostic. Both
anti-PF4 antibodies and SRA should be sent off if suspicion for HIT is high.

In scenarios where anticoagulation is absolutely contraindicated, intravenous immunoglobulins or

plasmapheresis can be considered. In ECMO circuits, the use of citrate anticoagulation can also be
considered.

When anticoagulation is not contraindicated, HIT necessitates the use of an alternative anticoagulant.
The most commonly used agents are direct thrombin inhibitors. As outlined in Figure 3, these agents
bind directly to thrombin versus factor Xa. In clinical situations such as HIT, the most common agents
used are argatroban and bivalirudin.

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There is limited data about specific dosing recommendations in patients with Impella, TandemHeart, or
IABP. Small studies have demonstrated success using either argatroban or bivalirudin as replacements
in the purge solution and as systemic anticoagulation.19-21 In patients with hepatic dysfunction,
bivalirudin may be preferred over argatroban, although argatroban can be dose adjusted initially for
hepatic impairment.22 Bivalirudin requires renal dose adjustments, and its clearance is altered in patients
receiving continuous renal replacement therapy, rendering argatroban preferred in the setting of severe
renal impairment.23,24 For patients receiving ECMO, argatroban or bivalirudin may be used in the setting
of HIT.25 Specific dosing requirements of these agents are outlined in Table 5.

Table 5. Anticoagulant Dosing for Mechanical Circulatory Support26-28

ANTICOAGULANT MECHANISM OF ACTION INITIAL DOSING ELIMINATION

Non-renal
Unfractionated Potentiates action of mechanisms via
12-18 units/kg/hr
heparin antithrombin III reticuloendothelial
system

1-2 mcg/kg/min

Argatroban Direct thrombin inhibitor 0.25-0.5 mcg/kg/min in critically Hepatic

ill, moderate to severe hepatic
impairment, and heart failure patients

0.15-0.2 mg/kg/hr

Renal dose adjustments:

Bivalirudin Direct thrombin inhibitor CrCl 30-60: 0.08-0.12 mg/kg/hr Renal
CrCl < 30 or hemodialysis or CRRT:
0.04-0.07 mg/kg/hr

QUICK READ SUMMARY

✓ The use of MCS in patients with cardiogenic shock has significant clinical benefit but is
associated with anticoagulation risks that require careful and meticulous observation by all
members of the care team.

✓ While robust guidelines and clinical trials are lacking, the use of expert consensus, available
evidence-based practices, and interdisciplinary care coordination can help ensure safe and
appropriate anticoagulation practices.

✓ Clinical concern for thrombosis in MCS should raise suspicion for HIT, which should be
evaluated and managed in a timely fashion.

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References
1. Subramaniam AV, Barsness GW, Vallabhajosyula S, Vallabhajosyula S. Complications of temporary percutaneous
mechanical circulatory support for cardiogenic shock: an appraisal of contemporary literature. Cardiol Ther.
2019;8(2):211-28.

2. Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/STS Clinical expert consensus statement on the
use of percutaneous mechanical circulatory support devices in cardiovascular care: endorsed by the American
Heart Association, the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencion;
affirmation of value by the Canadian Association of Interventional Cardiology-Association Canadienne de Cardiologie
d’intervention. J Am Coll Cardiol. 2015;65(19):e7-e26.

3. ABIOMED. Impella ventricular support systems for use during cardiogenic shock and high-risk PCI: instructions
for use and clinical reference manual. 2017. Available at: [Link]
[Link]. Accessed 24 September 2021.

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long-term cardiac assist devices. Radiographics. 2015;35(2):327-56.

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10. Pollack CV, Jr, Reilly PA, van Ryn J, et al. Idarucizumab for dabigatran reversal - full cohort analysis. N Engl J Med.
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11. Uriel N, Pak SW, Jorde UP, et al. Acquired von Willebrand syndrome after continuous-flow mechanical device support
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13. Bartoli CR, Restle DJ, Zhang DM, et al. Pathologic von Willebrand factor degradation with a left ventricular assist
device occurs via two distinct mechanisms: mechanical demolition and enzymatic cleavage. J Thorac Cardiovasc Surg.
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14. Tiede A. Diagnosis and treatment of acquired von Willebrand syndrome. Thromb Res. 2012;130 Suppl 2:S2-6.

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18. Pollak U. Heparin-induced thrombocytopenia complicating extracorporeal membrane oxygenation support: review of
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22. Williamson DR, Boulanger I, Tardif M, et al. Argatroban dosing in intensive care patients with acute renal failure and
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23. Selleng K, Warkentin TE, Greinacher A. Heparin-induced thrombocytopenia in intensive care patients. Crit Care Med.
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24. Chanas T, Surabhi P, Maitland, HS, Liszewski, A. Evaluation of the use of argatroban or bivalirudin for the
management of suspected heparin-induced thrombocytopenia in the setting of continuous renal replacement therapy.
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25. Taylor T, Campbell CT, Kelly B. A review of bivalirudin for pediatric and adult mechanical circulatory support. Am J
Cardiovasc Drugs. 2021;21(4):395-409.

26. Junqueira DR, Zorzela LM, Perini E. Unfractionated heparin versus low molecular weight heparins for avoiding
heparin-induced thrombocytopenia in postoperative patients. Cochrane Database Syst Rev. 2017;4:Cd007557.

27. Argatroban. Package Insert. GlaxoSmithKline; 2011.

28. Bivalirudin(Angiomax). Package Insert. Pfizer; 2019.

29. Perera D, Stables R, Thomas M, et al. Elective intra-aortic balloon counterpulsation during high-risk percutaneous
coronary intervention: a randomized controlled trial. JAMA. 2010;304(8):867-74.

30. Schrage B, Ibrahim K, Loehn T, et al. Impella support for acute myocardial infarction complicated by cardiogenic shock.
Circulation. 2019;139(10):1249-58.

31. Dhruva SS, Ross JS, Mortazavi BJ, et al. Association of use of an intravascular microaxial left ventricular assist device
vs intra-aortic balloon pump with in-hospital mortality and major bleeding among patients with acute myocardial
infarction complicated by cardiogenic shock. JAMA. 2020;323(8):734-45.

32. Lo GK, Juhl D, Warkentin TE, et al. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced
thrombocytopenia in two clinical settings. J Thromb Haemost. 2006;4(4):759-65.

33. Vatanparast R, Lantz S, Ward K, et al. Evaluation of a pretest scoring system (4Ts) for the diagnosis of heparin-
induced thrombocytopenia in a university hospital setting. Postgrad Med. 2012;124(6):36-42.

34. Abnousi F, Yong CM, Fearon W, Banerjee D. The evolution of temporary percutaneous mechanical circulatory support
devices: a review of the options and evidence in cardiogenic shock. Curr Cardiol Rep. 2015;17:40.

35. Halpin N, Snadden D. Exercise on both sides of the curriculum. Br J Sports Med. 2000;34(2):124.

36. Moretz JDS, Das S, Beavers C, et al. Bicarbonate purge solution to support Impella devices for patients with clinically
suspected or confirmed heparin-induced thrombocytopenia. ASAIO J. 2021;67.

37. Bergen K, Sridhara S, Cavarocchi N, et al. Analysis of bicarbonate-based purge solution in patients with cardiogenic
shock supported via Impella ventricular assist device. Ann Pharmacother. 2023;57(6):646-52.

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Vasoinotropic
Considerations
with Short-Term
MCS
Michael J. Lim, MD, FSCAI, FACC, FAHA
Poplar Bluff Regional Medical Center

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Introduction
Vasopressors and inotropic agents remain commonly used tools for treatment of patients with
hypotension or impaired cardiac output. As they are primarily used for patients with life-threatening
hemodynamic perturbations, much of what we know from an efficacy standpoint comes from an
examination of their hemodynamic effects. In this chapter, we discuss vasopressors and inotropic agents
commonly used in current practice. We emphasize the essential role of hemodynamic assessment in
patient management and decision making and the role of cardiac power output (CPO) in driving decision
making for vasoinotropic agents while a patient is on mechanical circulatory support (MCS). We also
briefly review the clinical data that is currently available to guide practice.

Vasoinotropic agents
Catecholamines
Otherwise known as “sympathomimetics,” catecholamines act through beta-1, beta-2, alpha-1, and
dopaminergic receptors. Beta-1 activation results in enhanced calcium cycling and enhanced myocardial
contractility. Beta-2 receptors are predominately found on smooth muscle and stimulation results in
overall vasodilation. Alpha-1 adrenergic receptor activation results in smooth muscle contraction and
increased systemic vascular resistance. Table 1 lists commonly used catecholamines, dosing, and
receptor binding activity.

Table 1. Commonly Used Vasoinotropic Agents

DRUG α1 ß1 ß2 DOPAMINE (D) VASOPRESSIN

PRIMARY EFFECTS
(DOSE RANGE) ACTIVITY ACTIVITY ACTIVITY ACTIVITY (V1) ACTIVITY

Dopamine +++ ++++ ++ +++ Low dose effect may

2 – 20 mcg/kg/min cause vasodilation, high
doses increase SVR
Dobutamine + +++++ +++ Increase inotropy and
2 – 20 mcg/kg/min chronotropy (increase CO)
Norepinephrine +++++ +++ ++ 0 0 Increases SVR, small
0.01 – 3 mcg/kg/min inotropic/chronotropic
effect
Epinephrine +++++ ++++ +++ 0 0 Chronotropic and
0.01 – 0.10 mcg/kg/min inotropic effect increases
CO, increases SVR
Phenylephrine +++++ 0 0 0 0 Increases SVR,
0.4 – 9.1 mcg/kg/min venoconstriction results in
increased preload
Milrinone 0 0 0 0 0 Increases intracellular
0.375 – 0.75 mcg/kg/min cAMP resulting in
increased cardiac output
and decreased SVR
Vasopressin 0 0 0 0 ++++ Increases SVR
0.01 – 0.1 U/min

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Milrinone
Milrinone is a phosphodiesterase inhibitor that results in an increase in cellular cAMP which leads to
enhanced myocardial contractility. It also has a corresponding vasodilatory effect on smooth muscle
cells. Recommended dosing is a bolus of 50 mcg/kg over 10 to 30 minutes, followed by an infusion of
0.0375-0.75 mcg/kg/min.

Vasopressin
Vasopressin is a naturally produced nonapeptide secreted from the posterior pituitary gland and
released naturally in response to pain or hypoxia. It predominately works by stimulating V1 and V2
receptors on smooth muscle, resulting in smooth muscle constriction. This agent is thought to have a
lesser direct effect on coronary constriction than catecholamines. Vasopressin is dosed as an infusion of
0.01-0.1 U/min.

Hemodynamic considerations
There are several hemodynamic factors to consider when assessing the status of a patient being
supported by MCS, or even before support is initiated. These encompass basic vital signs as well as
those derived from invasively measured hemodynamics.

HEMODYNAMIC CONSIDERATIONS
• Blood pressure (BP)
• Oxygenation
A B
• Heart rate (HR)
• Right atrial pressure (RAP)
• Pulmonary capillary wedge pressure (PCWP)
• Cardiac power output (CPO)
• Pulmonary artery pulsatility index (PAPi)

Blood pressure
We’ve all been trained to assess blood pressure, heart rate, and oxygenation status of all patients as
these measures provide an instant assessment of their “well-being.” When utilizing MCS support, this
does not change.

Blood pressure assessment is highly subjective and many continue to categorize it as “stable” vs.
“unstable.” While these categorizations are somewhat beneficial, consider the following when assessing
blood pressure:
• How is BP being measured? (eg, non-invasive BP cuff, invasive arterial line)
• Is the measurement accurate?
• Is the pressure adequate to support end organ perfusion?
• Is the pressure supported by mechanical circulatory support (MCS) or other agents or is BP
unsupported?

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If blood pressure is accurately assessed and subjectively viewed as able to support end organ perfusion,
the patient is likely “stable.” Clinical trials have frequently used a systolic blood pressure of 90 mmHg
to define adequate perfusion. However, corrective measures must be taken quickly if blood pressure is
inaccurately assessed and unable to support end organ perfusion.

Oxygenation
Oxygenation status is relatively more objective than blood pressure, and lower oxygen saturation
(typically below 90%) is associated with a potentially unstable patient state. While much of the
oxygen saturation level is an assessment of gas exchange in the lungs, it is also dependent upon the
hemodynamic status and cardiac output.

Heart rate
Heart rate reflects both relative tachycardia or bradycardia and overall rhythm. Keep in mind the
contribution of heart rate to cardiac output (CO = heart rate x stroke volume). Many patients found to be
tachycardic are attempting to generate higher cardiac output. Most frequently, unstable patients present
with atrial fibrillation with rapid rates that do not have a true ventricular electrical synchronization and
overall decreased cardiac output.

RV function
While pulmonary arterial (PA) catheter use was shunned in the past as being potentially harmful to the
patient, more recent data have clarified the role of invasively measured pressures to guide management,
especially in patients in shock and decompensated heart failure supported with MCS devices. Right
atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP) can be measured directly with
the balloon-tipped PA catheter, providing a more sensitive snapshot of the patient’s overall volume
status and left ventricular function. Ultimately, these 2 measures may guide decisions regarding adding
or weaning vasoinotropic agents during MCS when attempting to optimize a patient’s hemodynamic
support. As Figure 1 shows, in a patient needing better overall blood pressure and cardiac output, the
right atrial pressure can suggest inadequate preload to guide volume resuscitation or, if it is elevated,
prompt further assessment of right ventricular function. The pulmonary artery pulsatility index
(PAPi=(PA systolic - PA diastolic)/mean RA) should be calculated and when less than 0.9, consideration
for supporting the RV is necessary to improve the patient’s hemodynamic status.

RA PRESSURE > 15 mmHg? PCWP > 25 mmHg?

NO YES NO YES

Volume resucitation Increased PVR? Septic shock Likely LV dysfunction

(calculate SVR)? and decreased
LV stroke volume
Decreased RV function
(calclate PAPi)?
Primary RV failure
(calculate PAPi)?

PVR (dynes-sec/cm-5) = 80 x [mean PAP (mmHg) – LAP (mmHg)] / CO (L/min)

SVR (dynes-sec/cm-5) = 80 x [MAP (mmHg) – CVP (mmHg)] / CO (L/min)

Figure 1. Using RAP and PCWP to Guide Decision Making

Mechanical circulatory support devices, such as the Impella heart pump, rely on these hemodynamic
variables (Figure 2).

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Flow MAP LVEDP and LVEDV

Wall LAP Mechanical work

tension

Microvascular Cardioprotective
resistance signaling*

Myocardial Pulmonary
perfusion congestion

Cardiac power O2 supply O2 demand Reperfusion

output injury*
End-organ perfusion Unloading to myocardial recovery
CPO: cardiac power output; LAP: left atrial pressure; LVEDP: left ventricular end diastolic pressure;
LVEDV: left ventricular end diastolic volume; MAP: mean arterial pressure;
*Cardioprotective signaling and reperfusion injury are areas under active investigation (STEMI DTU trial)

Figure 2. Hemodynamic Effects of Impella Support

When an Impella catheter is placed in a patient with low PCWP (eg, 10 mmHg), there is insufficient
volume to allow the device to provide full support (ie, operate at maximum RPMs). An alarm will occur
and the level of support (P-level) should be reduced and the RA pressure assessed. When supporting
a patient with Impella, it is important to balance the patient’s loading conditions, vasoinotropic agents,
and the level of support from the Impella device.

Cardiac power output (CPO)

Perhaps the most important hemodynamic factor to consider when assessing patient status is cardiac
power output (CPO), which assesses overall blood flow to body tissues and is calculated as follows:

CPO (watts) = CO (liters/min) x MAP (mmHg) / 451

Multiple studies have shown:

• CPO < 0.6 watts is strongly associated with increased mortality
• Achieving a CPO of 0.8 – 1 watt likely provides adequate tissue perfusion to support normal
aerobic metabolism and improved survival
Data from the SHOCK registry identified CPO as a significant marker for in-hospital mortality1 (Figure 3).

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100%

90%

80%
Est. In-hospital Mortality

70%

60%

50%

40%

30%

20%

10%

0%
0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 Figure 3. SHOCK Registry Identified
CPO as Significant Marker for In-
Cardiac Power Output (watts)
Hospital Mortality1

Pulmonary artery pulsatility index (PAPi)

Adequate left ventricular preload is essential for the left-sided Impella to provide maximal support.
Right ventricular dysfunction impairs filling of the left ventricle and must be considered as a cause of
inadequate support despite the use of a left-sided MCS device. Most clinicians calculate PAPi to assess
the function of the right ventricle:

PAPi = (PAsystolic – PAdiastolic) / RA

Inotropic or vasopressor agents have little to no ability to change right ventricular function, so when
PAPi < 0.9, the initiation of an MCS strategy (eg, Impella RP®, TandemHeart, or extracorporeal
membrane oxygenation (ECMO)) that directly supports the right ventricle should be performed.

Competing interests?
With multiple and interrelated variables to appreciate at any given time, the ability to add or remove a
vasopressor or inotrope and have a single desired effect remains highly challenging. This is especially
true in patients who are the least stable. However, vasopressor agents universally will directly increase
afterload while inotropic agents will increase left ventricular wall tension and mechanical work. In turn,
this increases myocardial oxygen demand (Figure 4).

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VASOPRESSOR / INOTROPE

Flow AOP EDV, EDP

Wall Mechanical work

tension

Microvascular
resistance

Coronary flow

Cardiac power O2 supply O2 demand

output
Hemodynamic protection Loads the heart

APO: aortic pressure; CPO: cardiac power output; EDP: end diastolic pressure; EDV: end diastolic volume

Figure 4. Hemodynamic Effects of Vasopressors and Inotropes

Investigators have attributed these hemodynamic effects of vasopressors and inotropes to the higher
mortality rates seen in patients with increasing doses of these agents or multiple agents (Figure 5). In
patients with compromised left ventricular function, these effects represent the unwanted or negative
aspects that must be balanced against the desired increase in MAP or CO and systemic organ perfusion.

80%
Mortality Risk (N=3462)

42%

21%

7.5%
2% 3%
NO LOW MODERATE ONE HIGH TWO HIGH THREE HIGH
INOTROPE DOSE DOSE DOSE DOSE DOSE

Figure 5. Mortality Risk with Inotropes/Vasopressors2

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To better understand the balance between positive and negative effects of vasopressors, inotropes, or
MCS we can turn to the pressure-volume (PV) loop (Figure 6). Although not commonly utilized in everyday
clinical practice, the PV loop can give a wealth of information about the mechanics of the left ventricle.

End-systolic
pressure-volume PVA=SW+PE
relationship (ESPVR)
Stroke work (SW):
A measure of mechanical energy
Potential energy (PE):
Left Ventricular Pressure

A measure of stored energy

SW End-diastolic
pressure-volume
relationship
(EDPVR)
PE

Left Ventricular Volume

Figure 6. Pressure-Volume Loop

The entire shaded region in Figure 6 represents the pressure-volume area (PVA) and the total
mechanical energy of the left ventricle, approximating myocardial oxygen consumption. Left ventricular
“unloading” decreases the area representing stroke work (SW) and therefore results in decreased
oxygen consumption. Anything that increases heart rate, left ventricular pressure, and/or left
ventricular volume will “load” the heart and result in a net increase in myocardial oxygen consumption.
Vasopressors and inotropes, in general, increase load on the left ventricle, thereby informing decisions to
minimize pharmacologic agents and rely on MCS.

Potential decision-making algorithm

If RAP has been optimized (>12 mmHg) and PCWP remains elevated (~>20 mmHg), consider using
CPO to guide decision making regarding the use of MCS support, vasopressors, and/or inotropes. The
proposed algorithm in Figure 7 relies on the following assumptions:
1. If an MCS device is needed, MCS support is favored over pharmacologic support.
2. Norepinephrine represents a reasonable first choice vasopressor.
3. A vasopressor likely has a greater chance of increasing CPO than an inotrope.
4. Epinephrine is probably the most effective inotrope in this scenario as milrinone and dobutamine
have untoward effects that hamper their ability to effectively increase CPO.

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PATIENT ON MCS

CPO ≥ 0,8 watts?

YES NO

Are any vasoinotropic agents Is MCS at maximal

being given? support/flow?

NO YES NO YES
NO
PAPi > 0.9? Add RV support
Wean MCS
( support level) Wean agent Increase support level YES

Add norepinephrine
(and titrate)
< 0.8 watts

≥ 0.8 watts < 0.8 watts

Re-assess CPO
Re-assess CPO Re-assess CPO

CPO ≥ 0.8 watts < 0.8 watts

Continue present Add/change to

management/reassess epinephrine

CPO < 0.8 watts Consider upgrading

MCS

Figure 7. Patient Support Decision Making Algorithm

The goal for patient support is to achieve CPO ≥ 0.8 watts, and if this is achieved, to then reduce the
support (MCS and vasoinotropic agents) to the lowest level necessary. If this goal is not achievable, then
(assuming the patient is adequately volume supported) MCS support should be maximized. If maximal
MCS support is not able to sufficiently increase CPO, check for right ventricular failure and consider
adding norepinephrine as a vasopressor, and potentially switching/adding epinephrine as an inotrope.

As patients with a low CPO accumulate lactate quickly due to tissue malperfusion, consideration for
upgrading the MCS support should be done without delay.

Where’s the data?

Unfortunately, the medical literature is not replete with randomized controlled trials to inform use of
vasoinotropic agents – with or without MCS. Much of what can be gained from the published data to
date comes from the cardiogenic shock population and is in the form of registry or case-series data.
Two randomized controlled trials evaluating cardiogenic shock being treated with MCS have now
been completed in Europe. The ECLS-SHOCK8 trial looked at the ability of ECMO in conjunction with
percutaneous coronary revascularization to reduce 30-day mortality. The trial found no benefit of
routine ECMO utilization compared to standard, usual therapy. The second, DanGer Shock,9 evaluated
the use of the Impella micoraxial flow pump in patients with cardiogenic shock and found a significantly
lower risk of death from any cause at 180 days in patients receiving the device compared to usual care.
It is always difficult to compare trials given the different patient populations studied, but one of the
likely explanations for the different results is that the successful treatment of patients with cardiogenic
shock is not all about the device; rather, early recognition of shock and understanding of the specific
hemodynamic manifestations likely provides better insight into the differences.

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The cVAD registry3 collected data and analyzed patient outcomes stratified by the placement of an
Impella MCS device before PCI compared to those patients treated with intra-aortic balloon pumps and/
or vasoinotropic drugs. In 154 patients, 30-day survival was markedly higher in those receiving Impella
pre-PCI (Figure 8) and supportive of the assumption that an Impella MCS device should be prioritized
over vasoinotropic agents to stabilize hemodynamics.

30 DAY SURVIVAL
1.0 cVAD Study
N=154

0.8

Impella Pre-PCI
Survival rate

0.6

0.4
IABP and/or inotropes
Pre-PCI
0.2

Log-rank, p=0.004

0 5 10 15 20 25 30

Days from initiation of Impella

Figure 8. Comparison of 30-Day Survival Rate3

Comparing inotrope/vasopressor usage across available published trials, one can see a consistent usage
of these agents that exceeds 85% along with very high overall in-hospital mortality rates (Table 2).

Table 2. Inotrope/Vasopressor Usage and In-hospital Mortality

TRIAL INOTROPE OR
SURVIVAL
(N) VASODILATOR USAGE

SHOCK
99% 49%
(N=302)

IABP-SHOCK
90% 60%
(N=600)

IMPRESS
96% 52%
(N=45)

CULPRIT-SHOCK
90% 52%
(N=686)

NSCI
85% 71%
(N=406)

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The National Cardiogenic Shock Initiative (NCSI) closely tracked patients in cardiogenic shock secondary
to acute myocardial infarction. This was a voluntary registry involving multiple institutions throughout
the United States and relied on the following guiding principles:
• Early recognition of cardiogenic shock and transport to the catheterization lab
• Impella placement encouraged prior to coronary revascularization
• Investigators strongly encouraged to invasively assess hemodynamics with a PA catheter and
titrate care accordingly
The NCSI investigators collected data on vasopressors and inotropes and analyzed the impact of these
agents on the outcome in these shock patients. They found that of 300 patients analyzed, 43% were
on 1 vasopressor and 20% were on 2 or more agents. Norepinephrine was used in 48% of these,
while dopamine (19%) and epinephrine (13%) were also frequently used. When an analysis was done
comparing CPO to predicted mortality, they showed that the higher number of vasopressors used was
independently associated with an increase in mortality (Figure 9). While the use of increasing numbers
and doses of vasopressors in patients with shock likely do not "directly" result in higher mortalities,
clinicians should clearly be cautioned that patients whose hemodynamics are not improving with these
medications should be considered for potential mechanical support.

100%

90%
Estimated Probability of Mortality

80%

70%

60% 0 Vasopressor
1 Vasopressor
50% ≥ 2 Vasopressors

40%

30%

20%

10%

0%
0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 2.0 2.2 2.4 2.6 2.8

Cardiac Power Output (watts)

Figure 9. Unadjusted Estimated In-Hospital Mortality by CPO & Vasopressor Use4

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QUICK READ SUMMARY

✓ Best treatment for patients with cardiogenic shock remains elusive, as clinical trials done
to date have only evaluated the effect of a single device compared to no device in differing
patient populations.

✓ Better understanding of basic hemodynamic data and the potential impact of therapies on the
PV loop can inform clinical decision making.

✓ Overall goals for supporting the patient are:

• Maintain CPO ≥0.8 watts on MCS support only (lowest possible level of support)
• If CPO ≥0.8 watts is not achievable and MCS support is at maximal level, adding
pharmacologic support is a reasonable next step
• If reasonable doses of pharmacologic support are not sufficient, upgrade MCS support to a
higher-powered device

RECOMMENDED READING

Basir MB, Lemor A, Gorgis S, et al. Vasopressors independently associated with mortality
in acute myocardial infarction and cardiogenic shock. Catheter Cardiovasc Interv. 2021; doi:
10.1002/ccd.29895.
Overgaard CB, Dzavík V. Inotropes and vasopressors: review of physiology and clinical use in
cardiovascular disease. Circulation. 2008;118(10):1047-56.
Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support. J Am
Coll Cardiol. 2015; 66(23):2663-74.
Burkhoff D, Naidu SS. The science behind percutaneous hemodynamic support: a review and
comparison of support strategies. Catheter Cardiovasc Interv. 2012;80(5):815-29.
Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction
complicated by cardiogenic shock. N Eng J Med. 1999;341(9):625-34.
Thiele H, Zeymer U, Thelemann N, et al. Intraaortic balloon pump in cardiogenic shock
complicating acute myocardial infarction. Long-term 6-year outcome of the randomized IABP-
SHOCK II Trial. Circulation. 2019;139(3);395-403.

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shock: challenges and importance of randomized control trials. Catheter Cardiovasc Interv. 2021; doi: 10.1002/
ccd.29593.

5. Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous mechanical circulatory support versus intra-aortic balloon
pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69:278-87.

6. Thiele H, Akin I, Sandri M, et al. PCI strategies in patients with acute myocardial infarction and cardiogenic shock.
N Engl J Med. 2017;377:2419-32.

7. Basir MG, Kapur NK, Patel K, et al. Improved outcomes associated with the use of shock protocols: Updates from the
National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):1173-83.

8. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock. N Engl J Med.
2023;389(14):1286-97.

9. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl J Med. 2024;390(15):1382-93.

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SECTION 3

In-Depth Review
of Devices

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

13
PREVIOUS CHAPTER Chapter 13: Pulsatile Devices NEXT CHAPTER

Pulsatile Devices

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PREVIOUS CHAPTER Chapter 13.1: IABP and iVAC2L Mechanism of Action & Clinical Data NEXT CHAPTER

13.1
IABP and iVAC2L
Mechanism of
Action & Clinical
Data
Paul Brocklebank, BS
Medical Student
Medical University of South Carolina
Charleston, SC

Maxwell Kilcoyne, DO
Integrated Cardiac Surgery Resident, PGY-2
Medical University of South Carolina
Charleston, SC

Arman Kilic, MD, FACS, FACC

Associate Professor of Surgery
Surgical Director, Heart Failure and Heart Transplant Program
Medical University of South Carolina
Charleston, SC
kilica@[Link]

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Introduction
Temporary mechanical circulatory support (MCS) plays an important role in the management of
refractory cardiogenic shock. At the cost of increased invasiveness, MCS addresses some of the
principal goals of cardiogenic shock management:1
• Support systemic circulation and end-organ perfusion
• Unload the left ventricle
• Perfuse the coronary arteries
In patients with shock secondary to acute myocardial infarction, coronary artery perfusion is an
especially important consideration for avoiding the vicious cycle of myocardial infarction, decreased
coronary artery perfusion, and expansion of myocardial infarction. Pulsatile MCS devices, such as
an intra-aortic balloon pump (IABP), have become a staple of intervention in cardiogenic shock due
to low cost and ease of insertion.1 However, the IABP-SHOCK-II trial cast doubt over the mortality
benefit of the IABP and in its wake additional pulsatile devices have been developed, one of which is
the PulseCath iVAC2L®.1 The IABP and iVAC2L achieve hemodynamic support through fundamentally
different mechanisms of action. This chapter elaborates these mechanisms and compares clinically
important parameters and outcomes between the IABP and iVAC2L.

Mechanisms of action: IABP and iVAC2L

The IABP and iVAC2L are considered pulsatile MCS devices because they perform different actions
depending on whether the heart is in ventricular systole or diastole. Both devices create retrograde
diastolic flow that increases coronary artery perfusion via accumulation of blood against a closed aortic
valve. However, the IABP and iVAC2L increase cardiac output and unload the left ventricle via different
mechanisms. Deflation of the IABP during systole creates a vacuum effect that siphons blood out of the
left ventricle thereby augmenting stroke volume while simultaneously decreasing stroke work. The iVAC2L
also uses suction to decrease stroke work during systole. However, during systole the suctioned blood is
stored within the pump and returned to the ascending aorta during diastole, adding to the stroke volume
produced by the left ventricle during the next systolic cycle. In both cases, unloading the left ventricle
decreases myocardial oxygen demand helping to break the vicious cycle associated with cardiogenic
shock. Figure 1 provides more detailed explanations of the mechanics of the IABP and iVAC2L.2,3

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VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE

IABP

1. The driver 1. The driver inflates

deflates the the balloon
balloon
2. Inflation forces
2. Because the blood both
cardiac system is anterograde and
a closed system, retrograde
deflation of the
balloon creates 3. Anterograde flow
a vacuum effect increases cardiac
that pulls blood output
out of the left 4. Because the
ventricle aortic valve is
3. Cardiac output closed, retrograde
and coronary flow increases
artery perfusion coronary artery
are increased perfusion

iVAC2L

1. The driver creates negative pressure that pulls on 1. The driver creates positive pressure that pushes
the membrane within the pump chamber on the membrane within the pump chamber
2. Negative distention of the membrane creates a 2. Positive distention of the membrane forces blood
vacuum effect that draws blood out of the left out of the pump chamber
ventricle and into the pump chamber 3. Retrograde flow through the catheter opens the
3. Anterograde flow of blood keeps the two-way two-way valve allowing blood to escape
valve closed 4. Escaped blood accumulates against the closed
aortic valve and increases coronary artery perfusion
5. During the next ventricular systole, the
accumulated blood adds to ventricular stroke
volume thereby increasing cardiac output and
coronary artery perfusion

Figure 1. IABP and iVAC2L Mechanisms of Action

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Pump synchronization
The IABP console used to drive both the IABP balloon and the iVAC2L chamber membrane can be
synchronized to either EKG or arterial pressure waveforms.2 Synchronization with systole and diastole
of the heart is critical to maximize cardiac support and avoid active pump interference with cardiac
function. The specific components of the EKG and arterial pressure waveform that trigger pump
functions are elaborated in Figure 2.

Dicrotic
120 Notch
pressure (mmHg)
Arterial blood

100

80

60
0.5 1.0 1.5 t (s)
Deflation

Inflation
Balloon

Balloon

IABP
Aspirative
Deflation

Inflation
Ejective

iVAC2L

R
1.0
Lead II voltage
(mV)

0.5 T
P

0
Q 0.5 1.0 1.5 t (s)
S
–.05

SYSTOLE DIASTOLE
EKG Arterial Pressure EKG Arterial Pressure

Balloon
Balloon deflation Balloon inflation
state
IABP
Trigger R wave Upstroke Middle of T wave Dicrotic notch

Chamber
Aspirative deflation Ejective inflation
state
iVAC2L
Start of QRS
Trigger Upstroke T wave Dicrotic notch
complex

Figure 2. Synchronization of IABP and iVAC2L to Cardiac Cycle

Electrocardiographic and arterial pressure waveform features utilized in the synchronization of the IABP and iVAC2L to the cardiac cycle.2,3

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Surgical considerations
The IABP and iVAC2L are both considered temporary MCS devices and therefore are not intended for
cardiac support beyond 30 days.1 Both devices are typically inserted through the femoral artery and
while ultrasound guidance is recommended, it is not required in the emergent setting. Transaxillary
IABP insertion can also be performed with either direct percutaneous or open surgical insertion of
the device in the axillary artery on either the right or left side and is increasingly utilized in acute
decompensated heart failure cardiogenic shock. Furthermore, the iVAC2L was designed to be driven
by an IABP console and therefore the two devices use the same hardware.2 With respect to additional
cardiac output generated the IABP produces an additional 0.5-1.0 L/min which is slightly less than the
1.5-1.8 additional L/min generated by the iVAC2L.2,3

Clinical data: IABP and iVAC2L

Direct comparisons between IABP and iVAC2L with respect to clinical outcomes are limited by the
novelty of the iVAC2L and consequent paucity of data. The IABP has failed to show a mortality benefit
in multiple randomized clinical trials in cardiogenic shock in the setting of acute myocardial infarction,
but has been shown to significantly increase a number of vital parameters in cardiogenic shock
including mean arterial pressure (MAP), cardiac output (CO), cardiac power output (CPO), and mixed
venous oxygen saturation (SvO2).4 The iVAC2L has been demonstrated to be a safe and feasible way
to support low EF patients during high-risk percutaneous coronary intervention (PCI) and off-pump
coronary artery bypass grafting (CABG) but prospective randomized clinical trials are still ongoing.3

Short-term pulsatile devices currently under development

Venoarterial extracoporporeal membrane oxygenation (VA ECMO) is another form of temporary MCS
used in the management of refractory cardiogenic shock. IABP can be added to ECMO for the purposes
of pressure unloading the left ventricle and, secondarily, producing pulsatile flow.

A device currently under development, called K-beat, consists of a pulse generator and tamper that
when affixed to VA ECMO produces pulsatile ECMO flow. Although K-beat readily produces pulsatility,
it has not yet been shown to be effective at pressure unloading the left ventricle.5

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Case Study
61-year-old male with no significant past medical history presented with shortness of breath and
substernal chest pain.

Emergency room
• Afebrile, heart rate 105 bpm, BP 89/60, SpO2 86% on room air, 96% on 6L NC
• Exam: Bilateral rales appreciated on lung auscultation, moderate lower extremity edema
• Chest x-ray consistent with pulmonary edema
• EKG revealed sinus tachycardia with ST depressions in leads II and III
• Developed significant troponin increase (88 à 1101 à 40,000) and diagnosed with an NSTEMI
• BP was refractory to low-dose Levophed (norepinephrine)
• ACS protocol activated and patient taken for emergent left heart catheterization

Catherization laboratory
• Left heart catheterization – LM: severe distal LM disease, LAD: diffuse mild disease, LCx: non-
dominant, diffuse mild disease, RCA: dominant, significant lesion in mid-RCA, LVEDP: 25 mmHg
• Right heart catheterization – RAP 18, PA 38/26, PCWP 24, CI 1.7
• Intra-aortic balloon bump was placed via the right common femoral artery
• Transferred to cardiac ICU

Cardiac ICU
• Optimized with inotropes and diuresis
• Remained hemodynamically stable prior to undergoing an uneventful 3-vessel CABG (LIMA-LAD,
SVG-OM, SVG-RCA)
• IABP removed on POD2 and vasoactive medications weaned off by POD3
• Transferred to the floor on POD4
• Discharged to home on POD6

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QUICK READ SUMMARY

✓ In cardiogenic shock, temporary MCS devices that support systemic circulation and end-
organ perfusion, unload and augment the left ventricle, and perfuse the coronary arteries
can be highly effective.

✓ The IABP and iVAC2L reduce left ventricular afterload, increasing cardiac output and
reducing ventricular oxygen demand, and create retrograde diastolic flow which increases
coronary artery perfusion.

✓ Both the IABP and iVAC2L can be placed through percutaneous femoral approaches.

✓ Clinical data regarding the IABP is extensive and while it has not shown a substantial
mortality benefit, it does demonstrate significant improvement in a number of
hemodynamic and metabolic parameters.

✓ The iVAC2L has been shown to be a safe and feasible choice for temporary MCS with
randomized clinical trials currently underway.

References
1. Jiritano F, Lo Coco V, Matteucci M, et al. Temporary mechanical circulatory support in acute heart failure. Card Fail
Rev. 2020;6:e01. Published 2020 Mar 16. doi:10.15420/cfr.2019.02

2. Bastos MB, van Wiechen MP, Van Mieghem NM. PulseCath iVAC2L: next-generation pulsatile mechanical circulatory
support. Future Cardiol. 2020;16(2):103-12. doi:10.2217/fca-2019-0060

3. Parissis H, Graham V, Lampridis S, et al. IABP: history-evolution-pathophysiology-indications: what we need to

know. J Cardiothorac Surg. 2016;11(1):122. doi:10.1186/s13019-016-0513-0

4. Brown MA, Sheikh FH, Ahmed S, et al. Intra-aortic balloon pump as a bridge to durable left ventricular assist device.
J Am Heart Assoc. 2021;10(15):e019376. doi:10.1161/JAHA.120.019376

5. Fujii Y, Akamatsu N, Yamasaki Y, et al. Development of a pulsatile flow-generating circulatory assist device
(K-Beat) for use with veno-arterial extracorporeal membrane oxygenation in a pig model study. Biology (Basel).
2020;9(6):121. Published 2020 Jun 12. doi:10.3390/biology9060121

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13.2
Pulsatile Devices:
Troubleshooting
Complications
Matthew C. Evans, MD
Fellow, Cardiovascular Disease
Division of Cardiology
Medical University of South Carolina, Charleston, SC

Anbukarasi Maran, MD
Associate Professor
Division of Cardiology
Medical University of South Carolina, Charleston, SC
maranarasi@[Link]
@ArasiMaran

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Overview
Percutaneous mechanical circulatory support (MCS) devices offer the ability to support hemodynamics
and prevent acute organ failure in cardiogenic shock. The most commonly used device is the intra-aortic
balloon pump (IABP). The IABP increases coronary artery perfusion by inflating during diastole and
reduces ventricular afterload by deflating during systole. Identification and management of IABP-related
complications remains an important issue.

Vascular complications
IABP insertion can lead to access site complications due to the large-bore peripheral arterial and/or
venous access required to deliver these devices. Commonly reported vascular complications include
pseudoaneurysm and hematoma formation and development of retroperitoneal hemorrhage.1 Although
patients in cardiogenic shock frequently require emergent access under suboptimal clinical conditions,
implementation of contemporary femoral access techniques such as combined use of fluoroscopy and
ultrasound, micropuncture access, femoral angiography, and vascular closure devices can decrease the
incidence of these access complications.

Limb ischemia—defined as loss of pulses, Doppler signal, or arterial thrombus requiring thrombectomy
or surgical intervention—is one of the most feared and common complications across all forms of MCS,
and prolonged limb ischemia can necessitate the rare need for limb amputation. In the IABP-SHOCK II
trial, which prospectively compared IABP placement to medical therapy in 600 patients with cardiogenic
shock complicating acute myocardial infarction, the incidence of peripheral ischemic complications in
patients who received an IABP was 4.3%.2 Risk factors for limb ischemia include larger sheath size
and longer duration of support. Distal pulses and surveillance for the development of compartment
syndrome should be regularly assessed.

An incorrectly positioned or migrated IABP can lead to compromised abdominal visceral perfusion; the
incidence of mesenteric ischemia varies widely in the literature but is typically reported at around 1-4%.3

Bleeding
Anticoagulation is an essential component of MCS management to prevent device-related
thrombosis. While a suggested activated partial thromboplastin time (aPTT) of 60-80 seconds is
customary, an aPTT goal of 40-60 seconds can be used in patients at particularly high bleeding risk.
Thrombocytopenia is common (43%) but generally mild, and does not appear to be associated with
administration of heparin or with an increased risk of major bleeding or in-hospital death.4,5 IABP may
also be used when necessary without systemic heparinization.6

Hemolysis, produced by shear stress associated with mechanical pumping, can be directly measured by
plasma-free hemoglobin, which is more accurate than traditional methods of laboratory evaluation such
as lactate dehydrogenase (LDH) and haptoglobin. In combination with hemolysis, systemic inflammation
and thromboembolism can lead to pigment-induced nephropathy and renal failure.7

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Device migration
Proximal migration of the IABP to the ascending aorta is much more frequently associated with axillary
(rather than femoral) artery placement and can lead to several potential consequences, including
ventricular migration and arrhythmias or obstruction of cerebral blood flow resulting in cerebrovascular
accident (CVA) (Figure 1)8. In instances where femoral IABP placement is undesirable (such as those
awaiting cardiac transplantation) a longer 25 cm arterial sheath or a metallic braided sheath can be
placed to minimize device migration or the IABP placed via surgical cutdown. Routine chest x-rays
should be obtained daily to monitor for migration. Assessment of the left radial pulse can also provide
early indication of proximal device migration due to obstruction of the left subclavian artery.

A B

Figure 1. Transaxillary Intra-aortic Balloon Pump Migration

(A) Lateral chest x-ray with proximal and distal markers (arrows). (B) Fluoroscopy with outlined inflated balloon.

Infection
Sterile techniques and controlled implantation (in the operating room or cardiac catheterization
laboratory) are associated with better outcomes in comparison to emergent bedside initiation.
Prolonged use of MCS is associated with a higher risk of infection, presumably due to a greater duration
of indwelling catheters. A broad infectious work-up should be performed in patients with prolonged
MCS, with low threshold to start empiric broad-spectrum intravenous antibiotics.

Conclusion
IABP remains a valuable tool for the treatment of cardiogenic shock as a means for increasing coronary
perfusion and decreasing left ventricular afterload. While the incidence of complications reported in the
literature is relatively low, major complications including limb ischemia, CVA and vascular access issues
such as pseudoaneurysm and hematoma formation have the potential to limit the overall net clinical
benefit to patients. Fortunately, knowledge and awareness of major potential problems can allow for
prompt recognition and management of these complications.

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QUICK READ SUMMARY

✓ IABP remains a valuable tool for the treatment of cardiogenic shock as a means for
increasing coronary perfusion and decreasing left ventricular afterload.

✓ While the incidence of complications reported in the literature is relatively low, major
complications, including limb ischemia, CVA, and vascular access issues such as
pseudoaneurysm and hematoma formation, have the potential to limit the overall net clinical
benefit to patients.

✓ Fortunately, knowledge and awareness of major potential problems can allow for prompt
recognition and management of these complications.

References
1. de Jong MM, Lorusso R, Al Awami F, et al. Vascular complications following intra-aortic balloon pump implantation: an
updated review. Perfusion. 2018;33(2):96-104. doi:10.1177/0267659117727825

2. Thiele H, Zeymer U, Neumann F-J, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock.
N Engl J Med. 2012;367(14):1287-96. doi:10.1056/NEJMoa1208410

3. Yildirim Y, Pecha S, Kubik M, et al. Efficacy of prophylactic intra-aortic balloon pump therapy in chronic heart failure
patients undergoing cardiac surgery. Artif Organs. 2014;38(11):967-72. doi:10.1111/aor.12276

4. Roy SK, Howard EW, Panza JA, Cooper HA. Clinical implications of thrombocytopenia among patients undergoing
intra‐aortic balloon pump counterpulsation in the coronary care unit. Clin Cardiol. 2010;33(1):30-5. doi:10.1002/
clc.20694

5. Parissis H, Leotsinidis M, Akbar MT, et al. The need for intra aortic balloon pump support following open heart
surgery: risk analysis and outcome. J Cardiothorac Surg. 2010;5:20. doi:10.1186/1749-8090-5-20

6. Pucher PH, Cummings IG, Shipolini AR, McCormack DJ. Is heparin needed for patients with an intra-aortic balloon
pump? Interact Cardiovasc Thorac Surg. 2012;15(1):136-9.

7. Kapur NK, Whitehead EH, Thayer KL, Pahuja M. The science of safety: complications associated with the use of
mechanical circulatory support in cardiogenic shock and best practices to maximize safety. F1000Res. 2020;9.
doi:10.12688/f1000research.25518.1

8. Karimianpour A, Fernandes V. Transaxillary intra-aortic balloon pump migration minimized with a long introducer
sheath. J Am Coll Cardiol. 2020 March, 75 (11_Supplement_1). 1286.

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13.3
Axillary-Subclavian
Intra-aortic
Balloon Pump
Insertion
Neha Yadav, MD
Director, Cardiac Catheterization Laboratory
Director of Quality and Patient Safety, Division of Cardiology
Cook County Health
Associate Professor of Medicine
Chicago, IL
nyadav@[Link]

Kameel Kassab, MD, FSCAI

Cardiovascular Medicine Fellow
Cook County Health
Chicago, IL

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Overview
Intra-aortic balloon pumps (IABP) are the most commonly used temporary mechanical support devices
in cardiogenic shock and in patients with advanced heart failure. While the transfemoral approach
remains the most widely used for IABP placement, axillary or subclavian access sites may be better
suited for patients with prohibitive aorto-iliac disease, or patients with advanced heart failure in whom
ambulation is important due to the need for longer duration of support.

Axillary anatomy
Safe axillary access requires familiarity with axillary artery anatomy and fluoroscopic techniques for
identifying key landmarks. While axillary arteries are smaller than the arteries in the iliofemoral system
(6.0 ± 1.1 mm), they are less frequently diseased. The axillary artery is an extra-thoracic continuation
of the subclavian artery and is divided into 3 main segments (Table 1). The ideal site of access is in the
second segment above the brachial plexus and distal to the outer margin of the chest wall. Figure 1
depicts axillary artery course and anatomy.

ACCESS
POINT

1
Circumflex
humoral
2

Superior
thoracic
3
Thoracoacromial
Subscapular
Figure 1. Axillary Artery Angiography Depicting
Optimal Access Site In Segment 2

Table 1. Axillary Artery Anatomy

SEGMENT LOCATION BRANCHES ACCESS NOTES

Lateral border of first rib, medial Superior thoracic artery Avoid access, so as not to enter the
1
to pectoralis minor chest/pneumothorax

Underneath pectoralis minor Thoracoacromial and lateral thoracic Ideal site of vascular access
2
artery

Lower border of pectoralis minor Subscapular, anterior and posterior Avoid vascular access in brachial
3
circumflex plexus

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Technique
1. Preparation. Prepare the site with the patient in supine position with arm abducted 90 degrees.
The site of insertion varies based on institutional experience and patient characteristics. The right
axillary site is usually easier to prepare; however, it may have a more tortuous course than the left.
Avoid left sided access if a LIMA graft is present. Avoid access on the side of an AV fistula. The
presence of pacemakers/defibrillators is not a contraindication as long as the site of access is lateral
to the device.
2. Roadmapping. In early experience, obtaining ipsilateral transfemoral access with a 5 to 6 Fr
catheter may be best. Alternately, ipsilateral brachial or radial access can be obtained. There are two
common ways of delineating the course of the axillary artery:

• Angiography: Inject 3-5 mL of contrast and utilize the roadmap feature of the lab system. If
access is femoral, engage the subclavian artery with a JR4 catheter. If access is radial, use a
standard radial diagnostic catheter or a 4 to 5 Fr JR4.
• Fluoroscopy: Advance a regular J-tip guidewire through the ipsilateral femoral or radial/brachial
access into the axillary artery to roadmap the course and help facilitate direct arterial puncture.
In addition, or alternately, ultrasound guidance can be used to access or facilitate access to the
axillary artery. We recommend operators refer to the SCAI position statement on best practices for
percutaneous axillary arterial access and training.5

3. Needle puncture. Advance the standard 21G micropuncture needle at a 45° angle targeting the
second segment of the axillary artery guided fluoroscopically by the guidewire or the angiography
roadmap. Alternatively, ultrasound-guided access can be obtained after fluoroscopically identifying
the optimal entry location.
4. Wire and sheath insertion. Once pulsatile flow is observed, advance the micropuncture wire
through the needle under fluoroscopy to avoid side branches. Once wire location is confirmed and
satisfactory, insert the 4 Fr micropuncture arterial sheath with the 3 Fr dilator over the 0.018 inch
wire and remove the dilator with wire.
5. Balloon pump insertion. Introduce the IABP J-tip guidewire through the micropuncture sheath and
advance into the descending aorta. Exchange the micropuncture sheath for an 8 Fr balloon pump
sheath. Advance IABP through the IABP sheath with the distal edge positioned just below the level
of the aortic arch beneath the left subclavian artery origin. (Figure 2)

Figure 2. Left Sided Axillary Artery IABP in Upright Seated Patient

(image courtesy of Arvind Bhimaraj, MD, Houston Methodist)
Note the location of IABP lateral to a left sided ICD device

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IABP management
Management of axillary IABP is similar to that of femoral insertion.
• Therapeutic anticoagulation with heparin targeting APTT of 1.5-2 times the institutional upper
limit of normal or anti-factor Xa of 0.25-0.5 U/mL
• Daily chest x-rays and physical exams to assess appropriate positioning and extremity perfusion

IABP exchange/removal technique

Exchange
1. Place a guidewire through the arterial lumen of the IABP and position infrarenally.
2. Remove the IABP together with the sheath.
3. Place a new 8 Fr sheath over the guidewire.

Removal
1. Perform angiography through the 8 Fr sheath to screen for vascular injury or thrombus formation.
2. If there is no injury, closure can be performed with percutaneous closure device (eg, Angio-Seal™ or
Perclose ProGlide™).
3. Alternatively, in case of vascular injury or thrombus formation, manual pressure can be performed
to achieve hemostasis. This strategy also applies in case of unsatisfactory hemostasis with
percutaneous closure.

Complications
Complications are predominantly related to access site. The axillary artery has higher elastic properties
and thinner walls than the femoral artery, hence it is more prone to injury. It is vital to angiographically
verify distal flow, as acute limb ischemia occurs when the sheath is occlusive. In case of acute limb
ischemia where IABP placement is utilized for acute shock without alternative access, connecting the
IABP sheath to a brachial or preferably radial sheath through a male-to-male connector may reestablish
flow to the arm.

Table 2. Potential Access- and Insertion-related Complications

ACCESS-RELATED COMPLICATIONS INSERTION-RELATED COMPLICATIONS

• Pneumothorax may result from a site access proximal • Acute limb ischemia may result from sheath occlusion
to the first segment of the axillary artery

• Arm paresthesia may result from injury to the brachial • Perforations/bleeding may result predominantly from
plexus due to access distal to the second segment advancing the sheath against vascular tortuosity;
manage with deployment of covered stents or balloon
• Avascular necrosis of the humeral head may result from tamponade
access distal to the second segment and deployment of
covered stents in case of perforation and occlusion of • Risk of stroke/TIA is theoretically minimized using the
the circumflex humeral artery left axillary artery by avoiding cerebral artery vessels
(with the exception of the left vertebral)

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Subclavian intra-aortic balloon pump placement

SC-IABP insertion is another alternative access circulatory support technique that provides the
advantage of early ambulation. It is predominantly used as a bridge to advanced therapies in patients
with heart failure. Although minimally invasive, the primary mode of insertion remains through a
surgically attached graft to the subclavian artery. It provides a safe approach with minimal morbidity
and mortality in end-stage heart failure patients. At the present time, this insertion is performed by
cardiothoracic or vascular surgeons in the operating room.

QUICK READ SUMMARY

✓ Axillary IABP insertion is feasible and safe, and provides the advantage of early
ambulation in advanced heart failure patients and an alternate access site option in
acute shock patients with challenging iliofemoral anatomy.

✓ Familiarity with axillary anatomy and accurate roadmapping of the arterial course is
vital to achieving safe access.

✓ Using angiographic or fluoroscopic wire guidance together with micropuncture

technique and/or ultrasound guidance at the second segment of the axillary artery
helps minimize complications.

✓ Gentle sheath advancement technique and verification of adequate flow to the distal
extremity help minimize vascular and limb complications.

✓ Subclavian IABP insertion may offer safe alternative access in patients with heart
failure requiring bridge to advanced therapies.

References
1. Estep JD, Cordero-Reyes AM, Bhimaraj A, et al. Percutaneous placement of an intra-aortic balloon pump in the left
axillary/subclavian position provides safe, ambulatory long-term support as bridge to heart transplantation. JACC
Heart Fail. 2013;1(5):382-8.

2. Moussa Pacha H, Al-Khadra Y, Alraies MC. Transaxillary intra-aortic balloon pump placement: a new approach with
great potential. Mayo Clin Proc. 2018;93(4):539-40.

3. Umakanthan R, Hoff SJ, Solenkova N, et al. Benefits of ambulatory axillary intra-aortic balloon pump for circulatory
support as bridge to heart transplant. J Thorac Cardiovasc Surg. 2012;143(5):1193-7.

4. Tanaka A, Tuladhar SM, Onsager D, et al. The subclavian intraaortic balloon pump: a compelling bridge device for
advanced heart failure. Ann Thorac Surg. 2015;100(6):2151-7; discussion 2157-8.

5. Seto AH, Estep JD, Tayal R, et al. SCAI position statement on best practices for percutaneous axillary arterial access
and training. Open Access. 2022;1(3):100041

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 191

14
PREVIOUS CHAPTER Chapter 14: Impella® Family of MCS Axial Flow Pumps NEXT CHAPTER

Impella Family ®

of MCS Axial
Flow Pumps

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PREVIOUS CHAPTER Chapter 14.1: Impella® Mechanism of Action NEXT CHAPTER

14.1
Impella ®

Mechanism of
Action
Francesco Burzotta, MD, PhD Cristina Aurigemma, MD, PhD
Dipartimento di Scienze Cardiovascolari Dipartimento di Scienze Cardiovascolari
Fondazione Policlinico Universitario A. Fondazione Policlinico Universitario A.
Gemelli IRCCS Gemelli IRCCS
Università Cattolica del Sacro Cuore Rome, Italy
Rome, Italy [Link]@[Link]
[Link]@[Link]
@BURZOTTA_F Carlo Trani, MD
Dipartimento di Scienze Cardiovascolari
Fondazione Policlinico Universitario A.
Gemelli IRCCS
Università Cattolica del Sacro Cuore
Rome, Italy
[Link]@[Link]

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Introduction
The Impella (Abiomed Inc, Danvers, MA) family of mechanical circulatory support devices are microaxial
pumps delivering blood from the left ventricle (LV) to the ascending aorta, or in the case of the right
side Impella device (Impella RP®), delivering blood from the inferior vena cava to the pulmonary artery.
The most common percutaneous insertion site is the femoral artery (or femoral/internal jugular vein for
Impella RP platform). Alternative insertion sites for the left side devices include the axillary artery (either
percutaneous or surgical) or the aorta (surgical). Once arterial access for left side support has been
achieved, the Impella catheter is advanced from the aorta, across the aortic valve, into the LV. Therefore,
significant aortic valve disease represents a relative contraindication for use of left side devices.

Figure 1 illustrates the Impella devices and Table 1 lists the key properties of both the left and right side
Impella catheters.

LV IMPELLA PUMPS RV IMPELLA PUMPS

Impella CP with Impella 5.0 Impella LD Impella 5.5 with Impella RP Impella RP Flex
SmartAssist (21 Fr) (21 Fr) SmartAssist (22 Fr) (22 Fr)
(14 Fr) (21 Fr)

6 Fr 6 Fr

6 Fr

6 Fr

9 Fr 9 Fr 9 Fr 9 Fr 11 Fr 11 Fr

Figure 1. Left and Right Ventricle Impella Microaxial Flow Pumps

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Impella pumps
Each Impella catheter consists of a microaxial rotary blood pump, which includes an impeller, integrated
motor, and inflow/outflow cannula, mounted on a 9 Fr drive catheter. Impella CP is designed for
percutaneous peripheral insertion with a 14 Fr maximal diameter at the pump level. The Impella CP can
provide up to 4.1 L/min of support . Impella 5.0 and Impella LD have a 21 Fr maximal diameter at the
pump level and are designed for surgical insertion through, respectively, a peripheral artery (femoral or
axillary) or the aorta (although several centers also utilize percutaneous venous access for a transcaval
approach to the aorta). Impella 5.5 has a 21 Fr maximal cannula diameter and is inserted surgically
through the axillary artery or aorta. Impella CP and Impella 5.0 have a pigtail catheter at their tip to
facilitate placement and stabilization. The Impella 5.5 and Impella LD, which are placed surgically, do not
require a pigtail for stability and placement. Impella RP is designed for femoral vein insertion with 21 Fr
maximal diameter at the pump level and delivers blood from inferior vena cava (inlet area), through the
cannula to the pulmonary artery (outlet area). Impella RP Flex is designed for internal jugular or femoral
vein insertion and has a 21 Fr maximal diameter at the pump level. Both Impella RP and Impella RP Flex
provide right ventricular unloading with 4.0+ L/min of continuous flow.

All Impella catheters for left ventricular support are placed with the cannula inflow located in the LV and
the outflow located in the ascending aorta, as shown in Figure 2. Blood is continuously drawn through
the cannula and expelled into the aorta. The Impella catheters also have pressure sensing capability
for monitoring the position of the device during ventricular support. The Impella CP has a fluid-filled
pressure sensing system that measures the aortic pressure just proximal to the outflow window. The
Impella 5.0 and LD each have a differential pressure sensor mounted directly on the axial flow pump
assembly that measures the pressure drop across the pump’s impeller.1 The Impella 5.5 has a fiber-optic
sensor
A for monitoring positioning during placementBand catheter operation.

Figure 2. Placement of Impella Pumps

(A) Left ventricle Impella catheter implant through peripheral femoral access (Impella CP or 5.0), or (B) direct surgical (Impella LD shown here), or
(C) axillary access (Impella 5.5 shown here) and (D) right ventricle Impella catheter implant through femoral vein (Impella RP)

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Table 1: Key Technical Characteristics of the Impella Left and Right Ventricular Support Catheters

IMPELLA
PUMP TYPE IMPELLA CP IMPELLA 5.0 IMPELLA LD IMPELLA 5.5 IMPELLA RP
RP FLEX

Maximal flow
3.3 L/min 5.0 L/min 6 L/min 4.0 L/min
rate

Maximal pump 33,000

46,000 rpm 33,000 rpm 33,000 rpm
speed rpm

Pump length 152 mm 155 mm 96 mm 114 mm 170 mm

Not Not
Pigtail length 40 mm 30 mm 40 mm
available available

Cannula/inflow
90 mm 86 mm 57 mm 70 mm 73 mm
cage length

Cannula shape Angled Straight Angled

Pump motor
14 Fr 21 Fr 19 Fr 22 Fr
diameter

Drive catheter 9 Fr 11 Fr

Pump bearing
Hydrodynamic purged (dextrose) through the Impella purge cassette
type

Fluid-filled Fiber-optic
Pressure sensing Differential sensor Differential sensor
sensor sensor

Ideal insertion
Percutaneous Surgical Percutaneous
technique

Axillary Internal
Femoral or
Ideal access Axillary artery Aorta artery or Femoral vein jugular vein or
axillary artery
aorta femoral vein

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Automated Impella Controller™ (AIC)

Each Impella catheter is connected to an AIC (see Figure 3), which controls the Impella catheter
performance, monitors position, and provides step-by-step guidance for troubleshooting. Impella
catheters with the SmartAssist platform are able to provide advanced hemodynamic information (eg,
LV end-diastolic pressure, mean arterial pressure, and cardiac power output) to facilitate proper Impella
positioning in the intensive care unit, real-time hemodynamic monitoring, and serial assessment of
hemodynamic trends to guide escalation and weaning.

B. Incorrect position (pump in ventricle)

C. Reposition

A. AIC interface
D. Continuous suction (check Impella position)

E. Diastolic suction (check filling)

Figure 3. Automated Impella Controller (AIC) Connected to Impella CP® with SmartAssist®
(A) The AIC is the control interface and displays Impella catheter performance and position information. (B) If the pump is incorrectly positioned in
ventricle, the optical sensor reveals a ventricle waveform curve. (C) Pump is correctly repositioned when an aortic waveform is displayed. (D) The
left ventricular placement signal can provide information to assist in suction resolution. In the case of continuous suction, it is likely that the patient is
experiencing suction related to positioning. (E) In case of diastolic suction, it is likely that the patient is experiencing suction related to volume.

The AIC is a standalone console capable of powering and purging the Impella catheter by connecting
to both the Impella catheter and the Impella purge cassette, as shown in Figure 4. The purge solution,
which flows through the purge cassette, flows to the microaxial rotary blood pump bearings to prevent
blood from entering the motor.

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Figure 4. Impella Left Ventricular Support System

(A) Impella CP and (B) zoomed image of microaxial pump showing inflow where blood is pulled from the left ventricle and outflow where blood
exits into the ascending aorta. Both the Impella catheter and (C) purge cassette connect to the (D) Automated Impella Controller.

Left ventricular placement of Impella catheters

The devices designed for peripheral insertion (Impella CP and Impella 5.0) have a pigtail catheter
mounted on their distal tip. This pigtail catheter has a lumen allowing for 0.018" guidewire insertion.
Retrograde aortic valve crossing with the peripheral Impella pumps can be performed through direct
advancement by pushing the catheter against the aortic valve or, more commonly, by advancing the
Impella catheter over a 0.018" guidewire previously placed across the aortic valve in the LV. Although
direct advancement is feasible, it may be associated with higher risk of failure and catheter tip damage,
so whenever fluoroscopic guidance is available, the guidewire tracking method is advised.

Guidewire-assisted placement requires fluoroscopy and may be performed in a number of ways.

Usually, a 6 Fr diagnostic catheter (Judkins right is advised to avoid incorrect position through mitral
valve structure and to facilitate 0.018" extra support wire delivery) is advanced into the LV. Then, the
Impella kit 300 cm 0.018” extra-support wire is shaped to create a wide loop (which may limit the risk
of LV damage) and is advanced through the diagnostic catheter in the LV. After diagnostic catheter
removal, the Impella is advanced over the wire into the LV. At this stage, the wire is removed and the
Impella pump may be activated.

Hemodynamic principles for left ventricle Impella mechanical

circulatory support
The aim of hemodynamic support in cardiogenic shock (CS) is to normalize mean aortic pressure (MAP),
cardiac output (CO), and cardiac power output (CPO = MAP x CO/451), decrease pulmonary wedge
pressure (PWP), and thereby provide myocardial protection by both reducing oxygen consumption (reducing
myocardial work) and improving oxygen delivery to the myocardium (increasing coronary blood flow).

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Impella increases MAP, CO, and systemic and coronary perfusion. It has no direct effect on contractility,
but it provides significant LV unloading, resulting in reduction of filling pressures (LV end-diastolic
pressure and PCWP) and afterload. The direct LV unloading leads to significant improvement of oxygen
supply, increasing coronary blood flow and reducing myocardial oxygen consumption (MVO2), with
cardioprotective effects. The final native stroke volume may be reduced, although the pump function
and cardiac output is replaced by the device.

During Impella support the pressure-volume loop is transformed from the normal trapezoidal shape to a
triangular shape (due to the continuous pumping of blood from LV to aorta and the loss of the isovolumic
periods) and shifts progressively leftward and downward, as shown in Figure 5. The consequent reduction
in pressure volume area (in terms of both stroke work and potential energy) depicts the clinically important
reduction in oxygen consumption. In addition, pharmacological or spontaneous increases in contractility
and decreases in peripheral resistance can enhance device-related unloading effects.2 Of note, the action
of the devices is strongly dependent on LV preload and right ventricle contractility, and so appropriate
administration of IV fluids to achieve adequate filling pressures is pivotal.

According to manufacturers’ instructions, Impella is intended for short-term use (up to 4 days in cases
of cardiogenic shock) although multiple centers worldwide have successfully utilized Impella support
for far longer periods in a variety of clinical scenarios. In addition, a recent study demonstrates beneficial
effects of Impella LV unloading on top of extracorporeal membrane oxygenation (ECMO) in the setting
of cardiogenic shock. This combination of Impella and ECMO support, called ECpella™, is associated with
favorable outcome in patients with cardiogenic shock compared to isolated ECMO.3 The counterbalancing
hemodynamic effect of Impella on top of ECMO, specifically reductions in afterload and myocardial oxygen
demand via active left ventricular unloading in addition to complete circulatory support, may both shorten
duration of ECMO support and enhance myocardial recovery compared to ECMO alone.

150

NORMAL HEART
125
CARDIOGENIC SHOCK
LV PRESSURE (mHg)

HEMODYNAMIC EFFECTS OF IMPELLA:

100
Mean aortic pressure
75 IMPELLA 2.5 Cardiac output
Coronary blood flow
50
IMPELLA CP Left ventricle end-diastolic pressure
Pulmonary wedge pressure
25
Myocardial oxygen consumption

0
25 50 75 100 125 150
LV VOLUME (mL)

Figure 5. Effect of Left Ventricle-to-aorta Circulatory Support on Pressure-volume Loop

Available data do not support the routine use of Impella in patients with CS, and its use should be
carefully evaluated on a case-by-case basis. However, recent data from the DanGer Shock randomized
controlled trial demonstrates that the routine use of Impella with standard care reduces the risk of death
for any cause in patients with STEMI-related cardiogenic shock.4

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Patients with severe LV dysfunction and persistent systemic hypoperfusion may theoretically benefit
from Impella LV support provided that medical futility does not exist (Figure 6).5 While patients with
refractory CS or biventricular dysfunction may not benefit from Impella LV support alone, they may
benefit from a “BiPella” approach that combines Impella LV and RV support.

Absence and very

B low pulsatility
(approximately 10
minutes) at the
beginning of
support. Quickly
improving and
stabilizing.

B D

Figure 6. Hemodynamic Effects of Impella Pumps in Cardiogenic Shock

(A) Hemodynamics degenerate to cardiac arrest and (B) patient completely depends on Impella CP support. (C) After 10 minutes of Impella CP
support, as demonstrated in Impella function curves, (D) significant LV unloading and reduction of filling pressures and afterload from Impella CP
support have an indirect effect on contractility.

Right ventricle Impella pump

Over the last few years, the Impella family has been enriched with the addition of the Impella RP® and
Impella RP Flex® with SmartAssist®. They are indicated for temporary right ventricular support for up
to 14 days in patients developing acute right heart failure or decompensation following left ventricular
assist device implantation, myocardial infarction, heart transplant, or open-heart surgery. The primary
contraindications are right side valvular heart disease, mural thrombus of the right atrium or vena
cava, and anatomic conditions precluding insertion of the pump. Currently, data regarding the use of
BiPella support with the Impella RP are scarce. A retrospective study of 20 patients on BiPella support
demonstrated its feasibility and efficacy although cardiogenic shock causes were heterogeneous and in-
hospital mortality was high at 50%.6

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QUICK READ SUMMARY

✓ Impella microaxial pumps provide left ventricular assistance by delivering 4.0 to

5.5 L/min of blood from the left ventricle to the ascending aorta.

✓ Impella pumps that deliver higher flow (eg, Impella CP, 5.0, and 5.5) are commonly
selected for cardiogenic shock patients.

✓ Impella increases MAP and CO as well as systemic and coronary perfusion and unloads
the LV, thereby reducing filling pressures and afterload.

✓ LV unloading and increased coronary blood flow can significantly increase myocardial
oxygen supply and reduce myocardial oxygen consumption, offering cardioprotective
effects.

✓ Impella can help unload the LV when used with ECMO in the setting of cardiogenic
shock.

✓ Impella RP provides up to 4 L/min of flow from the inferior vena cava to the pulmonary
artery for right ventricular support and is indicated in patients developing acute right
heart failure.

References
1. Burzotta F, Russo G, Previ L, et al. Impella: pumps overview and access site management. Minerva Cardioangiol.
2018;66(5):606-11. doi: 10.23736/S0026-4725.18.04703-5. Epub 2018 Apr 20. PMID: 29687700

2. Basile E, Russo G, Leone AM. Principles of hemodynamics for mechanical circulatory support: patho-physiological
key aspects of assisted PCI. Minerva Cardioangiol. 2018;66(5):600-5. doi: 10.23736/S0026-4725.18.04658-3. Epub
2018 Mar 15. PMID: 29546747

3. Pappalardo F, Schulte C, Pieri M, et al. Concomitant implantation of Impella® on top of veno-arterial extracorporeal
membrane oxygenation may improve survival of patients with cardiogenic shock. Eur J Heart Fail. 2017;19(3):404-12.

4. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl J Med. 2024;390(15):1382-93.

5. Russo G, Burzotta F, Auirgemma C, et al. Rationalized selection of intra-aortic balloon pump, Impella and
extracorporeal membrane oxygenation in the catheterization laboratory. In press.

6. Kapur NK, Bretón C, O’Kelly R, et al. TCT-126 Simultaneous, not staged, deployment of biventricular micro-axial flow
Impella catheters (BiPella) is associated with improved survival for cardiogenic shock involving biventricular failure. J
Am Coll Cardiol. 2016;68(18)B51.

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PREVIOUS CHAPTER Chapter 14.2: Troubleshooting Complications for Impella Left-sided Devices NEXT CHAPTER

14.2
Troubleshooting
Complications for
Impella Left-sided
Devices
Miguel Martillo, MD Mauricio G. Cohen, MD, FACC, FSCAI
Cardiology Fellow Director, Structural Heart Interventions
University of Miami Miller School of Medicine Staff, Interventional Cardiology
Miami, FL Cleveland Clinic Florida
@MguelMartilloMD Weston, FL
cohenm10@[Link]
Tawseef Dar, MD @DrMauricioCohen
Cardiology Fellow
University of Miami Miller School of Medicine
Miami, FL
@DarTauseef022

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Overview
The Impella® heart pump is a microaxial flow device widely utilized for hemodynamic support in patients
undergoing high-risk percutaneous coronary interventions (PCI), or who are suffering cardiogenic shock.
Clinicians caring for such patients must be familiar with the alarms related to incorrect Impella position,
suction events, and inadequate purge pressures, among others. In this chapter we discuss how to
recognize and address these technical issues.

Impella position alarms

Correct Impella positioning
A correct position is crucial for the normal functioning of Impella and provision of optimal hemodynamic
support. The Impella catheter is correctly positioned when the inlet area is in the mid-ventricular space,
approximately 3.5 cm below the aortic valve annulus, and the outlet area is in the ascending aorta, well
above the aortic valve. Additionally, the catheter should be angled toward the apex away from the left
ventricular wall and not entangled within or blocking the mitral valve.

The Automated Impella Controller (AIC) displays placement signal and motor current waveforms
indicating the Impella catheter position across the aortic valve. When the Impella catheter is in correct
position, the placement signal displays both an aortic and left ventricular tracing, and the motor current
displays a pulsatile waveform (Figure 1). The console home screen also provides visual information
about the location of the Impella catheter (Figure 2).

Figure 1. Placement Signal and Motor Current Figure 2. Home Screen

Waveforms Indicative of Correct Impella CP® with
SmartAssist® Positioning (image used with permission
from Abiomed)

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Troubleshooting Impella position alarms

The AIC displays an alarm if the Impella is in an inappropriate position in the ventricle or aorta (Figure
3). Table 1 describes various incorrect Impella positions and provides troubleshooting tips for restoring
optimal positioning.

Table 1. Troubleshooting Incorrect Impella Position

IMPELLA DESCRIPTION TROUBLESHOOTING

Impella Position • Occurs when the inlet and the outlet of the Impella catheter • Drop P-level to P2.
in the Aorta are both in the aorta.
• Reposition Impella under
• Placement signal waveform overlaps the LV pressure echocardiographic guidance.
waveform.
• Return to preferred P-level
• Motor current displays a flat signal. once correct position has been
confirmed.

Impella Position • Occurs when the Impella device is too far into the left • Drop P-level to P2.
in Ventricle ventricle and the optical sensor is below the aortic valve.
• Reposition Impella under
• Also occurs when the outlet of Impella is impinging on the echocardiographic guidance.
aortic valve (Impella too low)

• Placement signal waveform overlaps the LV pressure

waveform and shows a ventricular tracing signal.

• Motor current waveform displays a flat signal.

Impella Position • The controller might not be able to display waveforms in • Monitor Impella position
Unknown patients with low native heart pulsatility. using patient hemodynamics
and periodic bedside
• Placement algorithms require a minimum cardiac function echocardiographic
to generate a pressure difference across the aortic valve. assessments.
• When native cardiac function is depressed, Impella will • If flows are higher than
provide an appropriate amount of forward flow. However, predicted for the current
the placement signal might be pulsatile with a dampened P-level, incorrect catheter
amplitude because of low aortic pressure and depressed position caused by catheter
cardiac function. migration may be suspected.
• Similarly, the motor current signal might be dampened
because of the small pressure gradient between the inlet
and outlet areas.

• The home screen might display a yellow question mark with

the message: Impella position is unknown.

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INCORRECT IMPELLA POSITION

Impella position in the Impella position in the Impella position unknown

aorta ventricle

Inlet and outlet are Too far in the ventricle Might occur in low native
in the aorta and sensor cardiac pulsatility
below the aortic valve

1. Drop P-level to P2.

2. Reposition Impella under echo guidance.
3. Confirm Impella position and resume preferred P-level.
4. Lock Tuohy valve.

Figure 3. Troubleshooting Incorrect Impella Position

Evaluating Impella position with TTE

Parasternal long axis is the preferred view for transthoracic echocardiography (TTE) of Impella position.
When the Impella is correctly positioned you should see the following:
• The inlet area of the Impella catheter in the mid-ventricular space, approximately 3.5 cm below
the aortic valve annulus
• A dense mosaic pattern of turbulence on color doppler above the aortic valve near the outlet of
the aorta
When the Impella is incorrectly positioned you may see the following:
• A dense mosaic pattern of turbulence on color doppler underneath the aortic valve indicating the
catheter is too far into the ventricle or entangled in a papillary muscle.
• Impella rocking back and forth or inlet impinging on the anterior mitral valve leaflet.

Suction events/alarms
What causes suction?
Suction results in lower than expected flows with inadequate hemodynamic support leading to
hypotension and increased risk of hemolysis. Suction events may be caused by:
• Inadequate volume status
• Incorrect Impella position
• Obstruction
• Inadequate LV filling due to RV failure

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Troubleshooting suction
To recognize suction events, monitor for suction alarms like low flow alarms, lower than expected
flow rates, reduced mean motor current, and hypotension. Diastolic suction presents with normal
systolic pressure, negative diastolic pressure that recovers by the end of diastole, and low diastolic
flow. Continuous suction presents with low systolic pressure, negative diastolic pressure that does not
recover, and presence of low systolic and diastolic flows.

When suction alarms are present, decrease P-level 1 or 2 levels below the set level until the alarms
resolve. Assess volume status and consider volume resuscitation if right (central venous pressure) and
left sided (pulmonary capillary wedge pressure) filling pressures are less than 10 mmHg. Also evaluate
catheter position using echocardiography and evaluate right ventricular (RV) function (Figure 4).

SUCTION EVENTS

Diastolic suction Continuous suction

Caused by:
• Inadequate volume status
• Incorrect Impella position
• Obstruction
• Inadequate LV filling due to RV failure

Look for:
• Impella flow reduced alarm
• Suction alarm
• Lower than expected flow rates
• Reduced mean motor current
• Worsening hypotension

Response:
1. Decrease 1 or 2 P-levels or until suction resolves
2. Assess volume status
3. Evaluate catheter position with imaging and reposition if needed
4. Evaluate RV function; the following may indicate RV failure:
• PAPi < 1.0 (PAPi = PAS – PAD/ RA)
• RV hypokinesis
• TAPSE score <14mm
• RV diameter at base >42 mm or mid-cavity >35 mm

Figure 4. Troubleshooting Suction Events

Persistent suction events despite correcting position and volume status suggest RV failure. The
presence of suction alarms in the context of an elevated CVP requires an assessment of the RV function
using combined hemodynamics and echocardiography. A pulmonary artery pulsatility index (PAPi) <1.0
and the presence of moderate to severe global RV dysfunction on echocardiography with evidence of
global RV hypokinesis, TAPSE score <14 mm, or RV diameter at base >42 mm support the diagnosis
of RV failure. If RV failure is confirmed, consider timely escalation of inotropic therapy for RV support or
mechanical support, including Impella RP® or Protek Duo.

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Hemolysis in patients while on Impella support

What is hemolysis?
Hemolysis is defined as plasma free hemoglobin levels (PfHgb) >40 mg/dL on more than 2
measurements, taken 8 hours apart within 24 hours of device placement.1,2 Impella rarely causes
significant hemolysis by itself. Suboptimal device position and suction are the two major drivers of
hemolysis in patients supported with Impella.

Pathophysiology underlying hemolysis

The pathophysiology underlying hemolysis is related to shear stresses to red blood cells (RBCs). These
stresses are directly related to:
• Differences in velocity across the RBC surfaces, which in turn is inversely related to the diameter
of flow channels in mechanical devices (ie, smaller flow channels cause high velocities and
therefore higher shear stress)
• Time and area of contact
RBC membrane damage caused by shear stress accumulates over time until cell lysis. Therefore, the
longer the time and area of contact, the higher the risk of hemolysis.

The velocity of the impeller blade tip, rather than rotations per minute (RPM), damages RBCs. Velocity
(v) is the product of radius (r) and rotational speed (ω): v = r × ω. Thus, the small diameter of the impeller
in the Impella device allows higher RPMs while maintaining blade tip velocity below 10 m/sec, with
lower risk of hemolysis.3

Confirming hemolysis
Hemolysis may be suspected if lactate dehydrogenase (LDH) levels increase or the patient’s urine is
red. Keep in mind, however, that LDH levels can increase in response to any type of tissue necrosis
(red blood cells, platelets, myocardial tissue, and liver) or infection (ie, pneumonia). In addition, blood
(RBCs) in the urine can cause red urine, so it is important to perform a simple urinalysis to determine
whether urine discoloration is due to RBCs or hemoglobin. To confirm hemolysis, measure plasma free
hemoglobin (PfHgb) levels by a simple colorimetric test (40 mg /dL is the clinical limit) or spun plasma
color if PfHgb is not available.

Troubleshooting hemolysis
As previously mentioned, Impella, with its unique design and impeller that achieves <10 m/sec
peripheral blade velocity even at maximum RPMs, infrequently causes significant hemolysis by itself.
Suboptimal position and suction are the two major drivers of hemolysis (Figure 5).

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HEMOLYSIS SUSPECTED IF:

• Hb levels
• LDH levels
• Red urine

HEMOLYSIS CONFIRMED IF:

• Urine negative for RBCs
• PfHgb >40 mg/dL

Assess position (TTE) Hemodynamics

TOO LOW TOO HIGH UNSTABLE • Use lowest RPM required to

maintain hemodynamics
Address suction alarms
• Assess volume status
• Evaluate RV function

Steps to take:
• Reposition Impella under TTE guidance
• Volume resuscitation (if CVP and PCWP <10 mmHg)
• RV support
If hemolysis is not resolved, may need to remove Impella

Figure 5. Troubleshooting Hemolysis in a Patient on Impella Support

In addition to addressing suction alarms and volume resuscitation as described above, it is important to
assess Impella position if hemolysis is present. Ensure proper positioning of Impella using fluoroscopy
and echocardiographic guidance. Improper positioning causing obstruction of either inflow or outflow
increases velocity through the unobstructed windows and therefore increases shear stress.

Bedside echocardiography, which is quick and easy, is the best method to confirm proper positioning of
the Impella device. The parasternal long axis TTE (Figure 6) and mid-esophageal long axis TEE views
are preferred for confirming proper Impella placement. Look for the following on echo:
• Position of the Impella device in relation to other cardiac structures, such as the aortic valve, mitral
valve, and septum. Live images help confirm whether the position changes with the cardiac cycle
and while repositioning Impella.
• The inlet should be 3.5 cm below the aortic valve and away from anterior mitral valve leaflet.
Usually, a suction alarm will go off if there is an obstruction.
• The outlet should be well above the aortic valve within the ascending aorta. Outflow near the
aortic valve causes obstruction as well as instability of the device and usually a position alarm
goes off if there is an outlet obstruction.
• Ensure device stability, that is, no rocking movements of the Impella.

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CORRECT IMPELLA POSITION IMPELLA TOO HIGH IMPELLA TOO LOW INLET IMPINGING ON
MITRAL VALVE LEAFLETS

Figure 6. Assessing Impella Position During Hemolysis with TTE Parasternal Long Axis View

Purge flow and pressures

Importance of purge flow and pressure
A purge solution runs through the Impella catheter in the opposite direction of the flow of blood to
create a pressure barrier, preventing blood from entering the Impella motor. A pressure range of 300-
1100 mmHg is required for optimal pump flow and an activated clotting time (ACT) range of 160-180
seconds for sustained pump function. The built-in pressure sensors within the Impella automatically
adjust the purge solution flow rate to between 2-30 mL/hr to maintain adequate purge pressure. The
recommended purge solution for Impella heart pumps is a mixture of 25 U/mL of unfractionated heparin
with 5% dextrose in water (D5W).

Troubleshooting purge pressure alarms

Alarms will occur if Impella purge pressure is too high or too low (Figure 7).

High purge pressure. The high purge pressure alarm will occur if purge pressure exceeds 1100 mmHg
with a flow ≤2 mL/hr. Potential causes include:
• Device related factors—look for kinks in the purge tubing, the catheter, or the clear sidearm, and
straighten them
• Purge solution concentration too high—decrease the dextrose concentration to 5% if current
concentration is higher
If these steps do not resolve high purge pressure, monitor motor current. High motor current indicates
impending pump failure and Impella may need to be replaced.

Low purge pressure. The low purge pressure alarm will occur if purge pressure is less than 300 mmHg
with a flow of 30 mL/hr. Potential causes include:
• Device-related factors—look for leaks in the purge cassette, Y connector, or luer connections to
the catheter, and replace the purge cassette or tighten the connections
• Purge solution concentration too low—increase the dextrose concentration from 5% to 20%
If these steps do not resolve high purge pressure, monitor motor current. High motor current indicates
impending pump failure and Impella may need to be replaced.

Note: If you change the dextrose concentration, the LV placement signal will need to be adjusted.

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Summary
DESCRIPTION EFFECT TROUBLESHOOTING
DEVICE-RELATED ALARMS DISPLAYED ON AIC

Suction • Secondary to low filling • Low flow leading to • Assess hemodynamics and
pressures (low CVP and inadequate support and resuscitate if low CVP or
PCWP) if diastolic in hypotension PCWP
nature
• Hemolysis • TTE to assess position and
• Device malposition if reposition if needed
systolic in nature
• Escalate RV support if
• RV failure if continuous in signs of RV failure on TTE
nature or high CVP

• Device inlet impinging on

nearby structures (likely
papillary muscle or mitral
valve leaflets) can also lead
to suction alarms

Position • Device migration to • Inadequate support • Reduce the support to P1

either aorta or ventricle leading to hypotension or P2
(placement signal overlaps
LV tracing and motor • Hemolysis • Bedside TTE to confirm
current dampens) Impella position; if
needed, reposition under
• Outlet impinging on aortic echo guidance or in the
valve can display as device catheterization laboratory
in ventricle

Purge pressure • Too high due to kinks • Can damage the motor • Straighten the tubes
or high purge solution
concentration • Tighten the connections

• Too low due to leaks, loose • Change the concentration

connections, or low purge of the purge solution
solution concentration

PATIENT-RELATED CONDITIONS (eg, red urine, âHb, áLDH)

Hemolysis confirmed • Device too high in the • Decreasing hemoglobin • Bedside TTE to reposition
by PfHgb >40 mg/dL aorta with inlet impinging the Impella even if position
on nearby structures; can seems correct
cause suction alarm
• Address all the other
• Device too low in the alarms as needed
ventricle with device outlet
impinging on AV; can • Minimum RPMs to
cause position in ventricle maintain hemodynamic
alarm support

• Instability of the Impella

device

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PURGE PRESSURE ALARMS

High pressure in the Low pressure in

purge system the purge system

Purge flow <2mL/hr and Purge flow 30mL/hr and

Purge pressure >1100 mmHg Purge pressure <300 mmHg

Look for kinks in the purge Purge fluid concentration Look for leaks in the purge Purge fluid concentration
tubing, the clear sidearm, or may be too high cassette, Y-connector, or Iuer may be too low
anywhere along the catheter connections to the catheter

Straighten the tubing, the clear Reduce the purge fluid Tighten any loose connections Increase the purge fluid
sidearm, or catheter (dextrose) concentration or replace purge cassette (dextrose) concentration

If alarm does not resolve, monitor for increase in motor current

which can indicate impending pump failure

Figure 7. Troubleshooting Purge Pressure Alarms

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References
1. Anderson MB, Goldstein J, Milano C, et al. Benefits of a novel percutaneous ventricular assist device for right heart failure:
the prospective RECOVER RIGHT study of the Impella RP device. J Heart Lung Transplant. 2015;34(12):1549-60.

2. O’Neill WW, Schreiber T, Wohns DHW, et al. The current use of Impella 2.5 in acute myocardial infarction
complicated by cardiogenic shock: results from the USpella Registry. J Interv Cardiol. 2014;27(1):1-11.

3. Roberts N, Chandrasekaran U, Das S, et al. Hemolysis associated with Impella heart pump positioning:
in vitro hemolysis testing and computational fluid dynamics modeling. Int J Artif Organs. 2020. doi:
10.1177/0391398820909843.

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PREVIOUS CHAPTER Chapter 14.3: Impella RP® Insertion, Tips & Tricks, and Challenges NEXT CHAPTER

14.3
Impella RP
®

Insertion, Tips
& Tricks, and
Challenges
Joaquim Spadoni Barboza, MD, FSCAI, FACC
Interventional Cardiology
University of Illinois Chicago Hospital
Chicago, IL
Jbarboza@[Link]

Khalil Ibrahim, MD, FSCAI, FACC

Interventional Cardiology
University of Illinois Chicago Hospital
Chicago, IL
khalil8@[Link]

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Overview
Impella RP® (Abiomed) is a percutaneously placed temporary intracardiac microaxial blood pump
designed to provide right ventricular (RV) support. It delivers up to 4 L/min from the vena cava/
right atrium to the pulmonary circulation, bypassing the right ventricle. The primary indication for
its use is RV failure, which may be related to acute RV insult (eg, RV acute myocardial infarction) or
RV decompensation in the setting of volume/pressure overload (eg, RV failure after left ventricular
(LV) support, left ventricular assist device (LVAD) implantation, or heart transplant).1 The main
contraindications include any anatomic considerations that impede safely implanting the device, such
as right-sided mechanical valves and thrombus (Table 1). Full anticoagulation while Impella RP is
in place is recommended, as pump failure secondary to thrombosis has been reported. Appropriate
anticoagulation is even more critical when there are central venous lines, as clots from these lines can
embolize to the device and cause it to malfunction. Impella RP requires a purge solution of dextrose 5%
with either heparin 25 u/mL or bicarbonate 25 mEq/L.

Table 1. Indications and Contraindications for Impella RP

INDICATIONS

• Acute right ventricular failure, such as in right ventricular myocardial infarction (RVMI)

• RV failure following left ventricular assist device (LVAD) implantation

• RV decompensation after heart transplantation

• RV failure post cardiac surgery

• RV support in the setting of left ventricular support (eg, in a BiPella configuration)

• Refractory RV shock after pulmonary embolism

CONTRAINDICATIONS

• Presence of right-sided mechanical heart valves

• Significant right ventricular thrombus

• Anatomic abnormalities that prevent safe device placement (eg, congenital heart defects, tumors, severe tricuspid/
pulmonary stenosis)

• Inability to tolerate anticoagulation (eg, severe coagulopathy that cannot be managed, uncontrolled bleeding)

• Known or suspected pulmonary artery injury

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Strategic planning
When placing Impella RP, careful planning of vascular access is essential. While the standard Impella
RP can only be placed via femoral access, the newer Impella RP Flex® (Abiomed) can be introduced
via either the common femoral or internal jugular veins. The anticipated duration of support should
be considered when selecting an access site, as jugular access allows patients to ambulate while
on support. This is particularly important in cases where extended support is necessary to prevent
deconditioning, which can significantly worsen outcomes.

The Impella RP should always be placed under fluoroscopic guidance. Ideally, a pulmonary artery
(PA) catheter should be placed prior to Impella implantation to assist with patient selection, device
management, and weaning. It is important to turn off Impella RP when repositioning/introducing
a pulmonary artery catheter after Impella is in place, as the catheter can enter the inlet, potentially
damaging the device.

Equipment and procedural considerations

While the Impella RP is still available on the market, the new Impella RP Flex is currently the most
commonly implanted model. The Impella RP Flex is more flexible, easier to implant, and can be
implanted via a jugular approach (Figure 1). This extra flexibility is more important when the right
ventricle is very dilated. In this scenario, the standard Impella RP is easier to implant via the right
femoral vein instead of the left. The authors recommend the jugular access site as the preferred option
for Impella RP Flex because it facilitates patient mobility, reduces the risk of infection, and allows for
easier hemostasis management. Other anatomic considerations include the presence of other right-
sided devices (eg, pacemakers, long term-dialysis catheters) that could predispose to venous chronic
occlusions. In this situation, alternative access should be considered. Special care should be taken to
avoid pacemaker lead dislodgment during Impella RP introduction.

Figure 1. Impella RP vs Impella RP Flex

Impella RP (left) is pre-shaped and stiffer; Impella RP Flex (right) is straight and flexible.

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Insertion steps
Figure 2 illustrates Impella RP placement and removal under fluoroscopy. Specific steps are described below.

Figure 2 (video). Impella RP Placement and Removal Under Fluoroscopy

1. We recommend placing a long-term PA catheter via a secondary venous access prior to Impella RP
placement for reasons previously mentioned above.
2. Obtain internal jugular or femoral access and place a 6-8 Fr sheath under ultrasound guidance. As
previously mentioned, only Impella RP Flex can be introduced via jugular access while Impella RP
can only be placed via femoral vein.
3. Place a modified purse string suture to facilitate hemostasis (Figure 3), but do not tie it down.

Figure 3 (video). Modified Purse String Suture

4. Introduce the stiff 0.035″ wire provided, perform skin nick with a scalpel, dilate the track with the
provided dilators (8 Fr, 12 Fr, 16 Fr, and 20 Fr), and place the 23 Fr introduction sheath. Remove the
dilator and flush the sheath.

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5. After the 23 Fr sheath is introduced, administer heparin to achieve an ACT of 250 seconds before
advancing the device.
6. Place a flow-directed catheter that can accommodate a 0.027″ guidewire in the pulmonary artery.
For the Impella RP, the left pulmonary artery is preferred. Impella RP Flex can be placed in either
pulmonary artery.
7. Shape a bend on the soft radiopaque end of the 0.027″ x 260 cm placement guidewire provided
and position it in the pulmonary artery using the flow-directed catheter. Remove the catheter,
maintaining stable guidewire position.
8. Backload the Impella to the 0.027″ placement guidewire and introduce the Impella RP while
maintaining tension on the wire. The cannula outlet should be 2-4 cm above the pulmonary valve.
Having a PA catheter in the contralateral pulmonary artery facilitates identification of the pulmonary
valve location.
9. Impella RP should be zeroed once the pressure sensor exits the sheath in the inferior vena cava,
while this is not necessary for the Impella RP Flex.
10. The stiffer Impella RP is preferably placed in the left pulmonary artery. Rotating the catheter while
traversing the right ventricle to make the tip face upward facilitates placement. The Impella RP Flex
can usually be advanced to either pulmonary artery without any special maneuver.
11. Remove the 0.027″ guidewire.
12. Initiate support at the P-2 level and gradually increase until the required support is achieved.
13. Under fluoroscopic guidance, completely remove the 23 Fr peel-away sheath while monitoring the
Impella position. While an assistant applies pressure on the puncture site to maintain hemostasis,
peel away the sheath by bending the two wings of the introducer.
14. Slide the reposition sheath in the jugular/femoral vein and tighten down the previously placed
modified purse string.

Removing Impella RP
1. Remove the hemostatic suture placed during implantation.
2. Place new purse string suture but do not tie it down.
3. Turn off the Impella and remove it from the body. Allow bleedback of 15-20 mL and apply manual
compression.
4. Tighten the suture and perform manual compression until hemostasis is achieved. A secondary
purse suture can be placed if needed.

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CASE EXAMPLE
An elderly woman presented at an outside hospital with inferior ST-elevation myocardial infarction. She
underwent primary percutaneous intervention of the proximal right coronary artery complicated by no-
reflow phenomenon. The patient deteriorated despite intra-aortic balloon pump placement and required
high dose of vasopressors (norepinephrine 40 mcg/min and epinephrine 20 mcg/min). She was transferred
for escalation of care. Upon arrival, a pulmonary catheter was placed, showing profound shock with a
cardiac index of 1.4 and RV failure with a pulmonary artery pulsatility index (PAPi) of 0.6. Lactate was
8.9 mmol/L. Impella RP was placed via right femoral vein access with rapid improvement of the cardiac
index to 2.2. Pressors were weaned, and lactate cleared in less than 24 hours. The patient improved, and
Impella RP was removed after 5 days of support. Teaching points: Early diagnosis (less than 48 hours) and
support of right ventricular shock with Impella RP is associated with better outcomes.

Summary
• The Impella RP system is indicated for circulatory support of the right ventricle in the setting of
acute right ventricular failure (eg, RV acute myocardial infarction) or decompensation after left
ventricular mechanical devices implantation, heart transplant, or open-heart surgery.
• Impella RP pumps blood from the vena cava/right atrium to the pulmonary artery, bypassing the
right ventricle.
• The Impella RP Flex can be introduced via jugular or femoral vein approach.
• All patients with Impella RP should be anticoagulated unless contraindicated.

Reference
1. Anderson MB, Goldstein J, Milano C, et al. Benefits of a novel percutaneous ventricular assist device for right heart
failure: the prospective RECOVER RIGHT study of the Impella RP device. J Heart Lung Transplant. 2015;34:1549–60.
doi: 10.1016/[Link].2015.08.018.

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PREVIOUS CHAPTER Chapter 14.4: Transcaval Access for Large Caliber Transcatheter Aortic Implants NEXT CHAPTER

14.4
Transcaval Access
for Mechanical
Circulatory
Support
Toby Rogers, MD, PhD Robert J. Lederman, MD, FSCAI
Scientific Lead for Structural Heart Disease Senior Investigator
Section of Interventional Cardiology Cardiovascular Branch, Division of Intramural
MedStar Washington Hospital Center Research
Washington, DC National Heart, Lung, and Blood Institute,
Associate Professor of Medicine (Cardiology) National Institutes of Health
Georgetown University Bethesda, MD
Washington, DC ledermar@[Link]
Interventional Cardiologist
Adam B. Greenbaum, MD
Cardiovascular Branch, Division of
Co-director
Intramural Research
Emory Structural Heart and Valve Center
National Heart, Lung, and Blood Institute,
Emory Midtown Hospital
National Institutes of Health
Atlanta, GA
Bethesda, MD
[Link]@[Link]
[Link]@[Link]
@AdamGreenbaumMD

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Overview
Transcaval access enables delivery of large caliber transcatheter devices and implants to the aorta
in patients with small or diseased iliofemoral arteries. The technique involves crossing over from
the inferior vena cava into the abdominal aorta and then, after removal of the large caliber device or
following the aortic intervention, closing the aorto-caval tract with a nitinol cardiac occluder. This
chapter discusses patient selection based on contrast-enhanced CT, describes technical and procedural
considerations and reviews current clinical data.

Introduction
Latest generation mechanical circulatory support (MCS), transcatheter aortic valve replacement
(TAVR), and thoracic endovascular aneurysm repair (TEVAR) devices have benefitted from engineering
advances resulting in smaller delivery catheters, but despite this miniaturization process, some
patients with small iliofemoral arteries and/or severe peripheral vascular disease remain ineligible for
transfemoral artery access. Transcaval access takes advantage of the high compliance of the iliofemoral
veins and the proximity of the inferior vena cava (IVC) and abdominal aorta to deliver large introducer
sheaths by crossing from the IVC into the aorta (Figure 1). The aorto-caval tract is closed using nitinol
cardiac occluder devices. Most of the clinical experience and data for transcaval access hail from the
structural heart world, where transcaval has been shown to be an effective and safe alternative for
TAVR patients who are ineligible for transfemoral access.1-3

A
Abdominal aorta

Inferior vena cava

Crossing guidewire
exchanged for stiff
interventional 0.035"
guidewire

Gooseneck
snare in aorta

Interventional sheath
through which aorta
implant is delivered is
advanced from IVC
to aorta

Aorto-caval tract
closed with
nitinol-cardiac
occluder device

Figure 1. Transcaval Aortic Access and Closure

(A) A catheter is used to direct the 0.014″ crossing wire toward the aorta. A gooseneck snare serves as the target in the aorta. The wire tip is
energized with an electrosurgery pencil attached to the distal end to puncture into the aorta. (B) The crossing 0.014″ guidewire is exchanged for
a stiff interventional 0.035″ guidewire using sequentially larger catheters. (C) The large interventional sheath is advanced from the IVC into the
aorta, through which the aortic implant is delivered. (D) The aorto-caval tract is closed with a nitinol cardiac occluder device.

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Patient selection
Pre-procedural CT analysis
Transcaval access is preferably planned using contrast-enhanced computed tomography (CT) images of the
abdominal aorta and iliofemoral arteries. Non-contrast enhanced CT imaging is possible but risks missing
aortic dissection or other intraluminal pathology. Thin-slice reconstructions are preferable. Systematic
analysis includes:
• Segmentation of the aorta and IVC
• Assessment of aortic calcification
• Selection of suitable calcium-free windows in the aorta
• Identification of anatomic contraindications that would preclude transcaval access
• If eligibility is confirmed, formulation of a transcaval plan for use during the procedure4,5

A number of key CT measurements and observations are made and can be divided into three broad
categories: anatomic descriptors, location of the proposed target site (including anatomic landmarks
for target identification under fluoroscopy), and criteria for bailout. Ad hoc transcaval access can
be obtained without pre-procedural CT for patients with cardiogenic shock. Special procedural
considerations are summarized later in this chapter.

How to perform transcaval access and closure

Technical overview
The transcaval technique is founded on four key assumptions:
• The iliofemoral veins are larger, more compliant, and rarely diseased compared with the
iliofemoral arteries.
• The infrarenal IVC is close to the aorta typically without interposed anatomic structures.
• Arteriovenous tracts with substantial flow are usually not immediately life threatening.
• Catastrophic bleeding into the extravascular space (ie, retroperitoneum in the case of transcaval)
does not occur so long as bleeding from the artery can decompress directly into the adjacent low-
pressure vein. Because IVC pressure is lower than retroperitoneal pressure, any bleeding from the
aorta will preferentially shunt into the vein rather than collecting in the extravascular space.

Vascular access
We prefer to pre-close the right femoral venous access site to facilitate rapid hemostasis at the end
of the procedure (Perclose ProGlide®, Abbott Vascular), although manual hemostasis or figure-of-
eight suture is also adequate. We use the right femoral vein exclusively and do not recommend that
transcaval access is performed from the left femoral vein. A single femoral arterial access (can be from
either side) is required for aortic angiography and to deliver a gooseneck snare into the abdominal
aorta. The gooseneck snare serves as the crossing target and also snares and tensions the transcaval
guidewire, as shown in Figure 1. Select the largest and least diseased iliofemoral artery, as this same
access will be used for adjunctive balloon aortic tamponade or bailout endograft deployment.

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Transcaval access site selection

The transcaval access site is selected from pre-procedural contrast enhanced CT,4,5 based on location
of a calcium free window in the aorta and proximity to other critical structures. It is important to ensure
that the distance from skin to transcaval crossing site is appropriately less than the working length of
the introducer sheath. We describe the location relative to the lumbar vertebrae for easy identification
on fluoroscopy. Perform contrast-enhanced cineangiography in the projection angle prescribed from CT
analysis. Cineangiography without contrast injection can be useful to visualize aortic calcification.

Transcaval access
1. Immediately after obtaining vascular access, administer heparin to achieve ACT>250 seconds.
2. Position a single loop snare (Gooseneck Amplatz, Medtronic) loaded into a 6 Fr JR4 guiding catheter
in the aorta to serve as a target and to snare the transcaval wire after crossing. The snare should be
sized to be 5 mm larger than the aortic lumen diameter.
3. The coaxial crossing system is a fundamental component (Figure 2).

• Load a stiff 0.014″ coronary CTO guidewire (Astato XS 20, Asahi) into a 0.014″ to 0.035″ wire
converter (PiggyBack®, Teleflex) or 0.014″ microcatheter (eg, Finecross®, Terumo), which is in turn
loaded into a 0.035″ microcatheter (eg, Navicross®, Terumo).
• Connect the back end of the 0.014″ guidewire to a unipolar electrosurgery pencil. The PTFE
coating of the guidewire may need to be scraped off with a scalpel to optimize conductivity.
• Attach the ground pad to the patient, taking care to avoid electrical coupling with other
conductive structures.
• Set the pencil to ‘cutting’ and ‘pure’ modes with typical energy of 50W.

A B

Figure 2. Transcaval Crossing Assembly

(A) The crossing assembly consists of a 0.014″ guidewire, inside a
0.014″ to 0.035″ wire converter, inside a 0.035″ microcatheter. (B)
A unipolar electrosurgery pencil is attached to the distal end of the
0.014″ guidewire to energize the tip during crossing. The ground
pad is attached to the patient.

4. Use a short (renal length 55 cm) 6-8 Fr internal mammary or renal-curve guiding catheter to
position the coaxial crossing system in the IVC, pointing horizontally toward the aorta, aiming for the
center of the gooseneck snare (Figure 3). Confirm the trajectory in orthogonal projections.

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Figure 3. Transcaval Access and

Closure
(A) Procedure plan obtained from contrast-
enhanced CT showing two potential target
crossing sites. (B) Simultaneous aortic and caval
angiography. (C-D) The caval guiding catheter
directs the 0.014″ crossing wire toward the
aorta. The aortic snare acts as a target. (E) The
large aortic valve introducer sheath is advanced
from IVC to aorta. (F) A nitinol cardiac occluder
is deployed across the aorto-caval tract. (G)
Completion angiogram showing complete
occlusion of the aorto-caval tract.

5. Advance the 0.014″ guidewire independent of the wire converter during 1–2 seconds activation
of the electrosurgery pencil. If the trajectory is correct and the correct calcium-free window is
targeted, the wire should traverse easily into the aorta and through the open loop of the snare. If
using moderate sedation (and not general anesthesia), we recommend giving additional bolus of
analgesia before energizing the wire.
6. Snare the wire, then advance both snare and guiding catheter in tandem up the aorta.
7. Sequentially advance the wire converter and the microcatheter into the aorta over the 0.014″
guidewire. If difficulty is encountered while crossing, the tract may require dilatation with a
noncompliant coronary angioplasty balloon.
8. Once the 0.035″ microcatheter is in the aorta, exchange the 0.014″ guidewire and wire converter
for a stiff 0.035″ interventional guidewire (eg, Lunderquist® Extra-Stiff Wire, Cook Medical).
9. Advance the large caliber sheath over the stiff guidewire until the sheath tip is well into the aorta.
We prefer to use Dryseal (Gore) sheaths for MCS devices, because the inflatable hub/valve allows
coronary guide catheters to be introduced alongside the MCS shaft while maintaining hemostasis.

Aorto-caval tract closure

To close the aorto-caval tract, we recommend nitinol cardiac occluder devices marketed to close patent
ductus arteriosus (Amplatzer™ Duct Occluder, Abbott). Typically, we recommend using the ADO
10/8mm device for all but the largest sheaths.
1. Administer protamine first to reverse anticoagulation fully and encourage tract closure.
2. Advance a 0.014″ medium-support buddy guidewire through the large caliber sheath into the aorta
to serve as a rail over which aortic access can be re-established in case of inadvertent occluder pull
through.
3. We recommend delivering the occluder through a deflectable sheath (eg, 8.5 Fr, 16.8 mm small curl
dimension Agilis™ Steerable Introducer, Abbott) to allow the device to be oriented horizontally. The
distal disc of the occluder should first be deployed within the aorta.
4. Pull the large caliber sheath back into the IVC. Incomplete or partial withdrawal of the sheath
(ie, out of the aorta but not fully back into the IVC) causes torrential retroperitoneal bleeding by
obstructing blood return to the vein.

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5. Deploy the proximal portion—or ‘neck’—of the device across the aortic wall. At this stage, the
device can still be captured, repositioned, or replaced as necessary.
6. Figure 4 summarizes typical transcaval tract angiographic patterns in the cath lab. Incomplete
closure of the aorto-caval tract is usually well tolerated and, in our experience, complete closure
usually occurs in hours to weeks. It is imperative to pay close attention to the final angiogram before
removing all remaining catheters.
7. In patients with small aorta (eg, <12 mm diameter), primary closure with a covered stent may be
preferred because opening the 16 mm disc on the ADO in a small aorta can be challenging. A
balloon-expandable covered stent with low delivery profile (eg, 11x39 mm Viabahn VBX Gore,
which can be post-dilatated to a diameter of 16 mm) is recommended in this scenario.

Figure 4. Angiographic Patterns of Aorto-caval Tract Closure

Type 0: Complete occlusion of aorto-caval tract. Type 1: Patent fistula with a long tunnel. Type 2: Patent fistula with a ‘cruciform’ pattern of
contrast around the neck of the occluder. Type 3: Extravasation into the retroperitoneum. Arrows indicate nitinol occluder.

Special considerations for transcaval tract closure after MCS

If the MCS device is removed at the completion of the index procedure, the procedural steps for closure
should be followed as above. However, if the transcaval MCS device is left in for any length of time (ie,
hours or days), additional precautions should be taken when the patient returns to the cath lab for MCS
removal and aorto-caval tract closure.6
1. Always maintain continuous heparinized-saline flush on the sidearm of the large caliber transcaval
sheath while the MCS device is in place to prevent thrombus formation in the dead space around the
(much smaller) shaft of the MCS device.
2. After removal of the MCS device, aspirate the large caliber sheath. If unable to aspirate, or if there
is heavy thrombus burden, we recommend exchanging the sheath for a new identical sheath over a
stiff wire to ensure thrombus is not pushed into the aorta when introducing the nitinol occluder.
3. Consider upsizing the nitinol occluder device (eg, ADO 12/10mm) instead of typical 10/8mm device)
as less aortic wall recoil is expected after a sheath has been in place for a prolonged duration.

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Managing complications
Failure to cross
Aortic calcification at the attempted crossing site is the most common reason for failure to cross. This
typically results in buckling of the 0.014″ crossing wire and the need to select a different crossing site.
Other reasons for failure to cross include char accumulated at the tip of the wire from repeated crossing
attempts, incorrect energy selection, or a short circuit in the electrosurgery pencil-wire assembly. Char
can be cleaned off with a wet gauze, but a fresh wire should be used if the tip is damaged.

Recapture of the nitinol occluder

If the device needs to be recaptured, the exchange-length 0.014″ buddy guidewire in the aorta serves
as the rail over which a 0.035″ catheter can be re-advanced across the aorto-caval tract. Exchange the
0.014″ guidewire for a 0.035″ stiff interventional guidewire to facilitate re-advancement of another
large sheath into the aorta with its introducer. Expandable sheaths do not recoil completely and should
be replaced with a new sheath for re-crossing.

Incomplete closure of the aorto-caval tract

Small residual shunting around the occluder device is usually well tolerated and will cease in hours to days
as the ADO thromboses,7 as shown in Figure 4. Hypotension may be caused by extravasation or by inability
to tolerate acute arteriovenous shunting in patients with pre-existing severe right ventricular dysfunction.
Persistent mild extravasation can be managed with volume infusion, blood products, or vasopressors. More
severe extravasation can be managed with 3 minutes aortic balloon tamponade (eg, Tyshak II®, B. Braun).
Balloon tamponade can be repeated, but a covered stent should be deployed if extravasation persists.

Clinical experience
The National Heart, Lung, and Blood Institute (NHLBI) sponsored a 100-subject prospective
investigational device exemption (IDE) study in the US.2 Transcaval access and closure was successful
in 99 of the 100 high-risk subjects undergoing TAVR with mean STS-PROM score 9.6%. Thirty-day
mortality was 8%. Long-term follow up with serial CT scans demonstrated no late sequelae of the
transcaval access or closure.7 Ongoing clinical experience has confirmed excellent transcaval access and
closure success rates, alongside marked improvement in procedural outcomes with lower completion
angiogram scores, fewer blood transfusions or endografts, shorter hospital lengths of stay, and low
mortality compared to early experience.8 In a contemporary US multicenter study, patients undergoing
transcaval TAVR had lower rates of stroke and similar bleeding compared with transaxillary access.3
Furthermore, more patients were discharged directly home and without stroke or transient ischemic
attack after transcaval than transaxillary access.

Unusual case considerations and ad hoc transcaval access for

mechanical circulatory support
We have performed transcaval access successfully in patients with abdominal aortic aneurysms, crossing
from the IVC directly into the aneurysmal segment. We have used excimer laser to cross calcified aortic
walls.9 We have also successfully entered the aorta by puncturing through a polyester aortic graft.10,11
Additionally, transcaval access has been used to deliver large caliber thoracic endovascular aneurysm
repair devices.12 These examples demonstrate the versatility of the transcaval technique, but a thorough
analysis of the pre-procedural CT is important to determine individual patient eligibility.

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Transcaval access has been performed ad hoc for insertion of mechanical circulatory support devices in
patients with fulminant myocarditis and cardiogenic shock.6,13-15 Typically, a pre-procedural abdominal and
iliofemoral CT is not available, in which case two pigtail catheters can be used to obtain the transcaval
crossing angles in the cath lab.

AP=anteroposterior projection angle;

LAO=left anterior oblique

Figure 5. How to Obtain Transcaval Angles in

the Cath Lab (reprinted with permission)5
Abdominal cross-section at the level of intended transcaval
crossing, with a typical relationship of inferior vena cava (IVC),
aorta, and spine. Two pigtail catheters are placed in the IVC
and the aorta and rotated in the anteroposterior projection
until the pigtail curve is no longer visible. Fluoroscopy gantry
rotated left-right until the 2 pigtail catheters overlap. Over-
rotation removes pigtail catheter overlap.

Dedicated devices for aorto-caval tract closure

Worldwide transcaval experience has shown that closure is feasible and safe using off-the-shelf nitinol
cardiac occluder devices. However, dedicated devices are designed to achieve immediate hemostasis and
resist inadvertent pull through. The first of these dedicated devices underwent early feasibility testing
in the United States, revealing faster and more reliable hemostasis compared to off-label Amplatzer
devices.16 As of the time of writing, however, no dedicated closure devices are commercially available.

QUICK READ SUMMARY

✓ Transcaval access is transfemoral, does not require general anesthesia, and enables non-
surgical access for MCS in patients with small or diseased iliofemoral arteries.

✓ We strongly advocate for thorough pre-procedural CT analysis to determine eligibility,

if possible, as well as for procedure planning, alongside expert proctoring to teach new
operators.

✓ Ad hoc transcaval access for MCS device insertion during cardiogenic shock has been
shown to be feasible without pre-procedural CT imaging guidance.

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References
1. Greenbaum AB, O’Neill WW, Paone G, et al. Caval-aortic access to allow transcatheter aortic valve replacement in
otherwise ineligible patients: initial human experience. J Am Coll Cardiol. 2014;63:2795-804.

2. Greenbaum AB, Babaliaros VC, Chen MY, et al. Transcaval access and closure for transcatheter aortic valve
replacement: a prospective investigation. J Am Coll Cardiol. 2017;69(5):511-21.

3. Lederman RJ, Babaliaros VC, Lisko JC, et al. Transcaval versus transaxillary TAVR in contemporary practice: a
propensity-weighted analysis. JACC Cardiovasc Interv. 2022;15(9):965-75.

4. Lederman RJ, Chen MY, Rogers T, et al. Planning transcaval access using CT for large transcatheter implants. JACC
Cardiovasc Imaging. 2014;7(11):1167-71.

5. Lederman RJ, Greenbaum AB, Rogers T, et al. Anatomic suitability for transcaval access based on computed
tomography. JACC Cardiovasc Interv. 2017;10(1):1-10.

6. Afana M, Altawil M, Basir M, et al. Transcaval access for the emergency delivery of 5.0 liters per minute mechanical
circulatory support in cardiogenic shock. Catheter Cardiovasc Interv. 2021;97(3):555-64.

7. Lederman RJ, Babaliaros VC, Rogers T, et al. The fate of transcaval access tracts: 12-month results of the prospective
NHLBI Transcaval Transcatheter Aortic Valve Replacement Study. JACC Cardiovasc Interv. 2019;12(5):448-56.

8. Costa G, De Backer O, Pilgrim T, et al. Feasibility and safety of transcaval transcatheter aortic valve implantation: a
multicentre European registry. EuroIntervention. 2020;15:e1319-e1324.

9. Rogers T, Waksman R, Slack M, Satler L. Laser-assisted transcaval access for transcatheter aortic valve replacement.
JACC Cardiovasc Interv. 2018;11(1):e3-e4.

10. Lederman RJ, O’Neill WW, Greenbaum AB. Transcaval access for TAVR across a polyester aortic graft. Catheter
Cardiovasc Interv. 2015;85(7):1270-3.

11. Lanz J, Pilgrim T, Greenbaum AB, et al. Sheathless transcaval transcatheter aortic valve implantation through an
abdominal aortic graft. Can J Cardiol. 2018;34(12):1688 e17-1688 e19.

12. Uflacker A, Lim S, Ragosta M, et al. Transcaval aortic access for percutaneous thoracic aortic aneurysm repair: initial
human experience. J Vasc Interv Radiol. 2015;26(10):1437-41.

13. Cui CQ, Cook BS, Cauchi MP, Foerst JR. A case series: alternative access for refractory shock during cardiac arrest. Eur
Heart J Case Rep. 2019;3(3):ytz101.

14. Arnautovic JZ, Connor-Schuler R, Ip R. Mechanical circulatory support in management of cardiogenic shock and
myxedema coma. Case Rep Cardiol. 2019; 2019:2595736.

15. Maidman SD, Eberly LM, Greenbaum AB, et al. Postinfarction Ventricular septal rupture and hemopericardium with
tamponade physiology. CASE (Phila) 2021;5(1):48-50.

16. Rogers T, Greenbaum AB, Babaliaros VC, et al. Dedicated closure device for transcaval access closure: from concept
to first-in-human testing. JACC Cardiovasc Interv 2019;12(21):2198-206.

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14.5
Single Access
Technique for
Impella Assisted
High-risk PCI
Jason Wollmuth, MD, FACC, FSCAI
Director, Complex Coronary Interventions
Interventional Cardiologist
Providence Heart and Vascular Institute
Portland, OR
[Link]@[Link]
@jason_wollmuth

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Overview
Percutaneous techniques for complex coronary revascularization have grown dramatically with the use of
hemodynamic support to facilitate safe and durable outcomes. Historically, 2, or even 3, separate access
sites have been necessary; one for the hemodynamic support device and a second (and occasionally third)
for guide catheter delivery. Separate access sites can be challenging in patients with peripheral vascular
disease and limited access options, and can also increase the risk of vascular complications.

Recently, a single access technique has been described1,2 wherein the second access for the coronary
guide catheter is gained through the 14 Fr sheath provided in the Impella CP® kit alongside the 9 Fr
catheter of the Impella CP®. Although the motor unit of the Impella requires a 14 Fr sheath, the remaining
catheter of the Impella is 9 Fr, leaving room for a second sheath/catheter. This chapter provides an
overview of this single access technique.

Equipment
Equipment for the single access technique:
• 14 Fr Impella sheath that comes with the Impella CP (technique is not compatible with the Impella
13 Fr sheath)
• 21G micropuncture needle, stiff 4 Fr micropuncture kit, or standard 18G needle (to gain access
through the diaphragm of the Impella sheath)
• 0.035″ wire
• 6 or 7 Fr sheath

Technique
1. Obtain arterial access (common femoral or axillary) using standard techniques. Typically, safe
femoral or axillary access is performed with the aid of a micropuncture kit. This same micropuncture
kit can be used to gain additional access through the diaphragm of the 14 Fr Impella sheath.
2. Obtain secondary access through a separate hole in the diaphragm of the Impella sheath
with an access needle away from the slits as shown in Figure 1. Note that the Impella sheath has
slits in the center of the diaphragm through which the Impella is inserted and longitudinal slits that
facilitate separation of the valve during peel away. If access with the second sheath disrupts this
entry point for the Impella, or the breakline slits, excessive bleeding can occur.

Figure 1. Potential Secondary Entry Sites Through Impella

Diaphragm (Red Dots)

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3. Once the needle is introduced, pass the 0.018″ guidewire into the sheath and remove the needle.
4. Advance the 4 Fr or 5 Fr micropuncture sheath (preferably with a stiff introducer) through the
diaphragm over the wire.
5. Remove the dilator and wire.
6. Pass a 0.035″ wire through the micropuncture sheath. The stiff 0.035″ wire that comes with
the Impella CP works well for this. Alternatively, you can use an 18-gauge standard access needle,
however, be sure to avoid sticking the shaft of the Impella.
7. Confirm proper Impella position prior to insertion of the second sheath.
8. Place a sheath over the 0.035″ wire. A variety of sheaths have been used with this technique.
Sheath size is limited to 7 Fr as larger sheath sizes are not compatible within the Impella sheath. The
position of the Impella cannot be adjusted with a 6 Fr or 7 Fr sheath next to the 9 Fr catheter.

Braided sheaths work best as they have enough radial strength to consistently allow for guide
catheter manipulation. Abiomed recently released the 7Fr low profile Companion Sheath which is
specifically designed for the single access technique. This 30 cm braided sheath has a hydrophilic
coating that allows full body insertion of the sheath with minimal interaction with the Impella
driveshaft. It is coil-reinforced which resists compression and allows for easy and durable guide
catheter manipulation.
A variety of other sheaths have been used. Originally, a 45 cm 6 Fr or 7 Fr Pinnacle® Destination®
sheath (Terumo) with extended hydrophilic coating (35 cm) was described. It is important to note
that the last 10 cm of this sheath is not hydrophilically coated and is difficult to advance through the
diaphragm.

• The 6 Fr version of this sheath can be pushed all the way to the hub of the Impella sheath.
• The 7 Fr version is difficult to advance further and a portion of this sheath extends from the
Impella sheath (Figure 4). If the sheath needs to be advanced further so that the guide can
reach the coronary artery, pass a dilator from the Impella sheath kit over the wire to "dilate"
the Impella sheath diaphragm. This leaves some hydrophilic coating and can allow for deeper
insertion of the non-coated portion of the Destination sheath.

Standard 10 cm or 25 cm Pinnacle sheaths have been used successfully, although manipulation

of the guide catheter may be difficult due to compression of the sheath by the diaphragm and
interaction with the Impella catheter. One benefit of these sheaths is that they can be manipulated
all the way to the hub of the Impella sheath (even with the 7 Fr sheath). This may be helpful so that
guide catheters can reach the coronary arteries in tall patients or those with tortuous anatomy.
Slender radial sheaths have also been used. The Merit 6/7 Fr radial slender sheath works best as it
is braided, giving it excellent radial strength. It can be advanced to the hub of the sheath, so it is a
good alternative in tall patients or those with tortuous vasculature. When used with the short 14 Fr
Impella sheath, there is minimal interaction with the Impella shaft.
Two sheaths—a 7 Fr Brite-Tip® (Cordis) and 7 Fr Flexor® Raabe (Cook Medical)—have been
attempted without success. The 7 Fr Brite-Tip sheath was unable to advance through the
diaphragm. The hydrophilic coating on the 7 Fr Raabe sheath was not long enough, leading to an
excessive amount of the sheath out of the body.
Glidesheath Slender sheaths have been used with mixed success. Due to their minimal wall
thickness, they may not have enough radial strength to pass through the Impella sheath diaphragm
making guide catheter manipulation difficult. Once a sheath has been placed, standard guide
catheters are used.

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Sheathless guides have also been attempted with varying degrees of success. Guides with
hydrophilic coating (Asahi Eaucath 7.5 Fr) have been used successfully. Standard guide catheters
can be delivered over long sheath dilators or using a Cordis Railway access system. Guide catheter
manipulation can be difficult and can get more difficult throughout the course of the procedure.
There is often an unacceptable amount of interaction with the Impella catheter as well with frequent
guide catheter manipulation.
A new technique for delivering an 8 Fr guide (Figure 2) has recently been published.3 The 8 Fr
guide catheter is delivered through the Impella sheath diaphragm over the dilator from a Cook 6 Fr
110 cm Flexor sheath (which is then removed after successful guide catheter delivery). Rotaflush
or Viperslide solution is injected into the 14 Fr Impella sheath prior to passing the guide catheter/
dilator combination to lubricate the system and allow for better torque control of the guide catheter.
During the procedure, guide catheter manipulation can become more difficult but can be overcome
by injecting more Rotaflush or Viperslide.

9. Fix the shaft of the Impella while advancing the 6 Fr or 7 Fr sheath through the diaphragm to
maintain proper pump position and not advance the pump outlet into the ventricle. One advantage
of choosing a longer sheath is the lack of interaction between the guide catheter and Impella
catheter even when using the long Impella sheath.
10. After the intervention is completed, remove the guide and sheath from the Impella sheath simply
by pulling them out. The Impella must be fixed during removal of the 6 Fr or 7 Fr sheath to
prevent pump removal from the ventricle. The diaphragm seals immediately without any further
bleeding. The Impella can then be removed or left in place, depending on the patient’s clinical status.

Figure 2. Technique for Delivering 8 Fr Guide Through Impella Sheath

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Figure 3 (video). Obtaining Access

Through the Impella Sheath
Diaphragm with a Micropuncture Kit

Potential limitations/complications
There are potential limitations and complications associated with the use of single access for Impella
assisted intervention. One is the limitation on sheath size to 7 Fr and sheathless guide to 8 Fr. Larger
bore guide catheters necessitate a second access site. A second access site for a contralateral
guide catheter for dual angiography and retrograde access is also needed for chronic total occlusion
intervention.

Another potential limitation is in reaching the coronaries with the guide catheter due to inability to
advance the second access sheath to the hub of the Impella sheath, leaving some of the sheath outside
of the body, as shown in Figure 4. If the patient is tall or has a tortuous aorta and/or iliac arteries, a
standard 100 cm guide may not reach the coronaries if a significant amount of the sheath is out of the
body. Additionally, guide catheter choice may need to be altered or a separate access for intervention
may be necessary in these circumstances. Use of the Abiomed Companion Sheath or the Merit radial
slender sheath may be beneficial in this scenario as it is able to be inserted to the hub.

Figure 4. 7 Fr Pinnacle® Destination® Sheath Introduced into the

Impella® Sheath up to the Non-hydrophilic Portion of the Sheath

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When using the single access technique, care must be taken to not inadvertently stick the drive shaft
of the Impella with the access needle. In addition, once the sheath and guide catheter are in place, the
ability to manipulate the Impella is limited. It is important to assure proper Impella positioning prior to
placing the PCI sheath. When placing the second sheath or during any subsequent sheath manipulation,
it is important to fix the driveshaft of the Impella to prevent any movement of the Impella which could
lead to device malposition, ventricular arrhythmia, or even ventricular injury.

Bleeding from the diaphragm can be an issue if the second access disrupts the diaphragm of the Impella
insertion site. It is important to observe the Impella diaphragm after sheath insertion to assess for any bleeding
or oozing. Bleeding from around the sheath has been described. If this occurs, tightening a preplaced Perclose
suture or adjusting the depth or angle of the peel-away sheath can help minimize bleeding.

Another possible complication is disrupting the peel-away Impella sheath, although this has yet to be
described. This would necessitate removing the peel-away sheath and advancing the repositioning
sheath while also gaining a second access for the coronary intervention.

Another potential limitation of the single access technique is the lack of a second access to assist
Finally, the lack of a second access site for post closure angiography and management of access site
complications is a limitation of the single access technique. Typically, the arteriotomy is pre-closed with
1 or 2 Perclose ProGlide® Suture-Mediated Closure devices. At the end of the procedure, the sheath
is removed and the sutures are tightened on the arteriotomy. A contralateral dry closure technique is
usually accomplished by passing a balloon proximal to the arteriotomy from a second access site. A
modified version of this approach can still be accomplished with the single access technique.4 Prior to
removing the 14 Fr sheath, you may place a peripheral angioplasty balloon sized 1:1 to the proximal
vessel over a 0.035″ guidewire proximal to the arteriotomy and inflate at low pressure (2 to 4 atm).
The inflated balloon limits bleeding as the sheath is removed. Pull the Perclose sutures down onto
the arteriotomy but do not tighten. Deflate the balloon to check for bleeding and hemostasis. If there
is reasonable hemostasis, remove the balloon and wire and tighten and cut the sutures. If adequate
hemostasis is not achieved, the balloon can be reinflated before deploying an additional closure device
over the wire or hold manual pressure.

QUICK READ SUMMARY

✓ Hemodynamic support for high-risk percutaneous coronary intervention traditionally

has required an access site for Impella placement and a secondary access site for the
interventional equipment.

✓ The single access technique eliminates the need for second access for the coronary
intervention for 6 Fr and 7 Fr sheaths.

✓ This technique decreases the risk associated with multiple access sites and represents a
significant advance, especially in patients with limited access options.

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References
1. Kumar K, Reddy S, Acharya D, Lotun K. Novel technique of performing multivessel PCI through an Impella sheath.
Catheter Cardiovasc Interv. 2019;1-4.

2. Wollmuth J, Korngold E, Croce K, Pinto DS. The single-access for hi-risk PCI (SHiP) technique. Catheter Cardiovasc
Interv. 2019;1-3.

3. Verreault-Julien L, Shekiladze N, Wollmuth J, Rinfret S. Single-access for Impella-supported percutaneous coronary

intervention using a sheathless technique with an 8 Fr guide. Catheter Cardiovasc Interv. 2022;100(6):1039-42.

4. Lichaa H, Wollmuth J, Tayal R. Dry field closure of large-bore access with iliac artery angioplasty through the
ipsilateral sheath: the single-access dry closure technique. J Invasive Cardiol, 2021;33(7):E516-21.

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14.6
Initial
Management of
the Impella in ®

the ICU
Kari Gorder, MD
Cardiovascular Critical Care and Emergency Medicine
OhioHealth Riverside Methodist Hospital
Columbus, OH
[Link]@[Link]

Timothy D. Smith, MD, FSCAI

Interventional Cardiovascular and Critical Care Medicine
OhioHealth Riverside Methodist Hospital
Columbus, OH
Timothy.Smith3@[Link]

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Introduction
Despite advances in care, cardiogenic shock (CS) remains a highly morbid condition fraught with
complications and high rates of mortality.1 The Impella family of mechanical circulatory support (MCS)
devices offers advanced treatment strategies for patients with CS and other complex cardiac conditions.
As with any invasive, large-bore MCS device, complications can and do occur. While appropriate patient
selection and skilled technical placement are of the utmost importance for the patient with the Impella,
diligent care and management in the intensive care unit (ICU) also significantly improves outcomes
and mitigates complications. This chapter discusses considerations for the initial care of patients with
the Impella in the ICU setting. While this chapter focuses on the femorally-placed Impella CP®, most
principles can be extended to the entire complement of Impella devices.

Initial ICU management of the patient with an Impella

Patients requiring an Impella for MCS are, by definition, critically ill, and should be cared for in an ICU
setting—ideally a cardiovascular intensive care unit (CICU) with a multidisciplinary shock team, which
has been proven to improve clinical outcomes for patients with CS2—with nursing and physician staff
who have additional training and demonstrated competency in the management of these MCS devices
and complex patients.

Transfer to the ICU and access site management

Most patients with Impella devices in place will be transferred to the ICU from the coronary
catheterization lab or the operating room. It cannot be overstated that appropriate ultrasound-guided
vascular access, positioning, and securement of the Impella device and sheath are integral to mitigating
any future complications that may arise during patient movement.3,4 Hemostasis should be assured prior
to transport, and the use of a femoral compression system to mitigate bleeding is strongly discouraged.
The access site must be monitored diligently during patient transfer, as any migration of the tapered
conical sheath can lead to extensive bleeding.

Figure 1. Stabilizing the Access Site

(A) Angle of entry should be 30-45°. (B) Stabilize access site by propping
up catheter with 4x4 gauze, if necessary. (C) Let catheter settle at natural
angle of insertion. (D) Forcing conical sheath to lay flat on skin can cause
tenting, pulling, and ultimately bleeding.

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In the ICU, meticulous site management by nursing staff is key. Knee immobilizers and slings are
recommended for patients with femoral and axillary Impellas, respectively. Simplicity in site care is
best, as bulky dressings may place unnecessary tension on the Impella at its insertion site, creating
drag on the arteriotomy and increasing bleeding around the sheath. Large dressings may also obscure
visualization of the access site, leading to a delay in diagnosis of a site hematoma or other vascular
complication during transfer or in the ICU.

Initial device management & hemodynamic goals

Upon arrival to the ICU, the initial priority is to ensure hemodynamic stability, as patients can and often
do deteriorate during transfer. Change in position of the Impella is possible during transport, and a chest
x-ray and bedside cardiac echocardiogram are recommended to ensure proper placement after any
significant patient movement.

Access for invasive monitoring devices is often needed, if not already present. The mean arterial pressure
displayed from the placement signal on the Impella console may not accurately correlate with peripheral
invasive arterial pressure measurements but may be used as a surrogate value to guide initial hemodynamic
management. Many patients with CS will see improved outcomes with the use of pulmonary arterial catheter
(PAC) monitoring to guide the titration of vasoactive agents and the weaning of mechanical circulatory
support.5 Like many ventricular support devices, the Impella is preload-dependent and afterload-sensitive.6
Care must be taken to ensure adequate device preload—for instance, managing right ventricular failure or
elevated pulmonary vascular resistance—and to reduce unnecessary afterload due to systemic hypertension.
Maintaining an LVEDP of 15-20 mmHg, measured either via Impella SmartAssist or via pulmonary arterial
wedge pressure, may mitigate suction events and decrease hemolysis rates. Titration of the device via its
P-level setting should be dynamic and based on the patient’s clinical trajectory.

Patient management & complication mitigation in the ICU

In general, standard ICU principles apply to patients with these devices. Additionally, it is recommended
to utilize Impella-specific multidisciplinary protocols drafted collaboratively by nursing, physician, and
pharmacy leadership.

Patient management protocols may include:7

• Standardizing neurovascular exams and device-specific documentation
• Following best-practice guidelines for the reduction of hospital acquired infections
• Encouraging mobility and physical therapy as possible
• Standardizing approaches to glycemic control, delirium prevention, and pain management

Device-specific protocols for the Impella should address:8,9

• Systemic anticoagulation
• Management of the purge solution, which must always contain dextrose for proper device function
• Standardized laboratory monitoring schedule, including markers of hemolysis (eg, plasma free
hemoglobin)

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Utilizing a care checklist or electronic nursing protocol is integral to ensuring no step is missed in the
care of these complex devices and is best implemented as part of the admission order set for patients
with mechanical circulatory support devices.

As with any patient who is critically ill and on mechanical circulatory support, patients with Impellas in
place are at risk for developing complications that may have the potential to derail their recovery. Based on
clinical trial data and clinician experience, some of the most common complications with the Impella device
are bleeding, limb ischemia, and hemolysis.10,11 While many complications can be avoided by meticulous
vascular access, angiographic evaluation at the time of placement, and for some patients, the placement of
distal perfusion sheaths, the guiding principle with any device-related complications is that early detection
and mitigation is key to preventing long-term or clinically significant problems. Finally, the importance
of multidisciplinary care for these patients—care that involves a cardiac intensivist, interventional
cardiologist, heart failure cardiologist, and cardiac surgeon—cannot be understated.

Summary
The Impella family of devices offers a great range of mechanical circulatory support options for critically
ill patients with cardiogenic shock or other acute cardiac emergencies. Successful ICU management
of the patient with an Impella in place is contingent upon timely and frequent reassessment, dynamic
monitoring, early intervention, and careful titration of vasoactive medications in the context of a
multidisciplinary team that has a working familiarity with the Impella devices.

QUICK READ SUMMARY

✓ Upon arrival to the ICU, the initial priority is ensuring hemodynamic stability.

✓ Meticulous site management by nursing staff is key.

✓ Access for invasive monitoring devices is often needed.

✓ Utilize patient management protocols and Impella-specific multidisciplinary protocols.

✓ Early detection and mitigation are key to preventing device-related complications.

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References
1. Vahdatpour C, Collins D, Goldberg S. Cardiogenic Shock. J Am Heart Assoc. 2019;8(8):e011991.

2. Papolos AI, Kenigsberg BB, Berg DD, et al. Management and outcomes of cardiogenic shock in cardiac ICUs with
versus without shock teams. J Am Coll Cardiol. 2021;78(13):1309-17.

3. Seto AH, Abu-Fadel MS, Sparling JM, et al. Real-time ultrasound guidance facilitates femoral arterial access and
reduces vascular complications: FAUST (Femoral Arterial Access With Ultrasound Trial). JACC Cardiovasc Interv.
2010;3(7):751-8.

4. Hind D, Calvert N, McWilliams R, et al. Ultrasonic locating devices for central venous cannulation: meta-analysis. BMJ.
2003;327(7411):361.

5. Ranka S, Mastoris I, Kapur NK, et al. Right heart catheterization in cardiogenic shock is associated with improved
outcomes: insights from the Nationwide Readmissions Database. J Am Heart Assoc. 2021;10(17):e019843.

6. Castelein T, Balthazar T, Adriaenssens T, et al. Impella to resist the storm. Circ Heart Fail. 2020;13(5):e006698.

7. Klompas M, Branson R, Eichenwald EC, et al. Strategies to prevent ventilator-associated pneumonia in acute care
hospitals: 2014 update. Infect Control Hosp Epidemiol. 2014;35(8):915-36.

8. Abiomed. FAQ: Anticoagulation. Aug 19, 2021. Available from: [Link]

library/faq-anticoagulation. Accessed on 22 February 2022.

9. Abiomed. Impella 2.5 with the Automated Impella Controller Circulatory Support System: Instructions for Use &
Clinical Reference Manual (US). 2016.

10. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous
left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by
myocardial infarction. J Am Coll Cardiol. 2008;52(19):1584-8.

11. O’Neill WW, Grines C, Schreiber T, et al. Analysis of outcomes for 15,259 US patients with acute myocardial
infarction cardiogenic shock (AMICS) supported with the Impella device. Am Heart J. 2018;202:33-8.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 239

15
PREVIOUS CHAPTER Chapter 15: TandemHeart Device NEXT CHAPTER

TandemHeart ®

Device

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15.1
TandemHeart:
Clinical Data and
Mechanism of
Action
Katherine J. Kunkel, MD, MSEd, FSCAI Brian O’Neill, MD
Fellow in Complex, High-Risk Indicated Interventional Cardiologist
Percutaneous Coronary Intervention and Center for Structural Heart Disease
Advanced Hemodynamic Care Henry Ford Hospital
Henry Ford Hospital Detroit, MI
Detroit, MI BOneil3@[Link]
[Link]@[Link]
@kjkunkelmd Khaldoon Alaswad, MD, FSCAI
Director, Cardiac Catheterization Laboratory
Hussayn J. Alrayes, DO Henry Ford Hospital
Fellow in Cardiovascular Diseases Detroit, MI
Henry Ford Hospital KAlaswa1@[Link]
Detroit, MI @KAlaswadMD
HAlraye1@[Link]

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Introduction
The TandemHeart is a left-sided hemodynamic support device that provides 3.5 to 5 L/min of flow via
a centrifugal cardiac bypass pump. The TandemHeart drains oxygenated blood from the left atrium via
a transseptal cannula and returns blood via an outflow cannula that is typically inserted in the common
femoral artery. The TandemHeart provides left ventricular preload reduction and systemic perfusion. The
hemodynamic characteristics of the TandemHeart offer important benefits, particularly in patients with
cardiogenic shock, decompensated heart failure, certain aortic and mitral valvular abnormalities, and
during high-risk percutaneous coronary interventions (HRPCI). While expertise in transseptal puncture
has limited widespread use, the use of TandemHeart in selected patients with cardiogenic shock can
play a critical role in hemodynamic stabilization and recovery.

Clinical data
Limited data is available to inform the use of TandemHeart in cardiogenic shock and HRPCI. Available
data from 2 small, randomized controlled trials (RCTs) and the largest of several registries show that
TandemHeart effectively improves hemodynamic parameters in patients with cardiogenic shock (Table 1).
Although treatment with Impella CP has been shown to improve outcomes of patients with cardiogenic
shock associated with myocardial infarction, it is not known if the TandemHeart provides the same benefits
in this cohort of patients.7

Table 1. Prospective TandemHeart Studies in Cardiogenic Shock

HEMODYNAMIC
TRIAL INTERVENTIONS COMPLICATIONS MORTALITY
OUTCOMES

Thiele et al. TandemHeart vs. á CPO â PCWP In TandemHeart patients: No difference at 30

(2005) IABP in AMICS á UOP á Limb ischemia days
á CO/CI á Blood transfusions
Randomized trial á DIC
(n=41)

Burkhoff et al. TandemHeart vs. á CO/CI â PCWP No difference between No statistically

(2006) IABP in CS á UOP groups significant
difference at
á MAP
30 days
Randomized trial
(n=42)

Kar et al. Escalation to á CI â PCWP N/A 40.2% at 30 days

(2011) TandemHeart in á MAP â LA 45.3% at 6 months
CS
á SvO2 â Cr
Prospective
registry (n=117)

AMICS=acute myocardial infarction cardiogenic shock; CS=cardiogenic shock; CI=cardiac index; CO=cardiac output;
CPO=cardiac power output; Cr=creatinine; DIC=disseminated intravascular coagulation; IABP=intra-aortic balloon pump;
LA=lactic acid; MAP=mean arterial pressure; PCWP=pulmonary capillary wedge pressure; SvO2=mixed venous oxygen
saturation; UOP=urine output

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The first randomized study of TandemHeart was conducted by Thiele et al. in 2005.1 Forty-one patients
who presented with acute myocardial infarction cardiogenic shock (AMICS) were randomized to IABP
or TandemHeart at the time of PCI. Despite favorable hemodynamic and metabolic outcomes in the
TandemHeart group as demonstrated by cardiac power output (CPO), pulmonary capillary wedge
pressure (PCWP), urine output (UOP), and serum lactate, the investigators were unable to demonstrate
a difference in mortality at 30 days. The authors did note an increased risk of limb ischemia and severe
bleeding in the TandemHeart group.

In 2006, Burkhoff et al. presented similar findings.2 These investigators randomized 42 patients in
cardiogenic shock to IABP or TandemHeart. Compared to patients in the IABP group, the TandemHeart
group had superior hemodynamic parameters, with greater increases in cardiac index and MAP and
greater decreases in PCWP. Although the 30-day survival in the TandemHeart group was numerically
higher than the IABP group (64% vs. 53%), the difference was not statistically significant.

The largest prospective study of TandemHeart was published by Kar et al. in 2011. This registry
included 117 patients in cardiogenic shock refractory to IABP and pressors. After TandemHeart
insertion, the authors found improvement in multiple hemodynamic and metabolic parameters, including
urine output, lactic acid levels, MAP, and cardiac index. The 30-day in-hospital mortality rate with
TandemHeart was 40.2%. While there was no comparator group in this study, these findings were
encouraging in the context of the 47% mortality rate found in the SHOCK trial.3,4

In addition, some retrospective studies reported the use of TandemHeart for mechanical circulatory
support during high-risk PCI. The largest study, Alli et al., retrospectively analyzed data from 54 patients
undergoing HRPCI using the TandemHeart device for hemodynamic support, observing a 90% 30-
day survival which compared favorably to EuroSCORE predicted survival of 67% and STS predicted
survival of 87% in this cohort.5 Neupane et al. reported 13 patients who underwent high-risk chronic
total occlusion PCI with TandemHeart for circulatory support with good outcomes and no device related
complications.6

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Mechanism of action
The TandemHeart is a left-sided hemodynamic support device with unique insertion and hemodynamic
characteristics. The pump inflow is a 21 Fr cannula placed via the femoral vein and inserted into the left
atrium via a transseptal puncture. Oxygenated blood from the left atrium passes through the centrifugal
TandemHeart pump into a 15 or 17 Fr outflow cannula in the common femoral artery (Figure 1).

Figure 1. TandemHeart Configuration

TandemHeart provides up to 4 - 5.0 L/min of flow and directly unloads the LA, resulting in a reduced LV
preload and LVEDP. Other hemodynamic effects of the TandemHeart device include increased cardiac
output and mean arterial pressure as well as decreased myocardial oxygen demand and improved
tissue perfusion. Given the retrograde flow of arterial blood in the aorta, afterload is increased. This
combination of increased afterload and decreased LVEDP typically results in a neutral effect on coronary
perfusion. Although considered a left-sided device, studies have also reported a significant reduction in
right‐sided pressures.

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TandemHeart offers several distinct advantages among hemodynamic support devices. With indirect LV
and direct LA unloading, the TandemHeart is generally the MCS device of choice in patients with mitral
valve stenosis. The TandemHeart is safe to use in the presence of an LV thrombus or a pre-existing
mechanical aortic valve given the cannulation configuration. TandemHeart provides almost equivalent
support to venoarterial (VA) ECMO. The TandemHeart can also be converted to a VA ECMO circuit
by adding an oxygenator to the circuit with the LA cannula in place or after being pulled back into the
right atrium to provide venous drainage. The TandemHeart with added right atrial drainage constitutes
left atrium veno-arterial ECMO (LAVA ECMO) that offloads both ventricles and provides superior
hemodynamic support in certain patients.

The major disadvantage of TandemHeart is that it must be placed using a transseptal puncture that
requires specific expertise, which may not be available in emergency situations in all centers. In addition,
it is associated with the typical complications associated with large-bore arterial access, namely
bleeding and vascular injury. Finally, retrograde flow from the outflow cannula might increase the LV
afterload resulting in increased myocardial oxygen consumption; however, this is much less of a concern
than with VA ECMO given direct LA unloading.

Table 2. Major Advantages and Disadvantages of TandemHeart

ADVANTAGES DISADVANTAGES

• Direct LA unloading • Requires transseptal puncture for insertion

• Ideal support device for patients with severe aortic or • Large bore arterial access with associated risk of
mitral valvular abnormalities vascular injury and bleeding

• Safe in the presence of LV thrombus and mechanical • Retrograde arterial blood flow
aortic valve

• Can be easily converted to VA or LAVA ECMO

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Case study
A 63-year-old man with a history of hypertension, hyperlipidemia, and tobacco use presented with
ventricular fibrillation cardiac arrest. After multiple defibrillation attempts, spontaneous circulation
was restored. In the setting of ischemic EKG changes, the patient underwent coronary angiography,
which showed diffuse coronary artery disease with no focal lesion, and a right heart catheterization,
which was notable for elevated PCWP with severely reduced cardiac index (Figure 2). An Impella CP®
(Abiomed, Danvers, MA) was placed, and the patient was transferred to the ICU. On arrival to the ICU,
transthoracic echocardiography (TTE) showed a severely reduced LVEF (25%) with severe apical and
lateral hypokinesis and an apical LV thrombus. Initially, the Impella CP was removed, and an IABP
was placed. The IABP provided inadequate hemodynamic support over the next 24 hours. The serum
lactate continued to rise with worsening hemodynamic parameters. The patient ultimately underwent
escalation of hemodynamic support to a TandemHeart via the right femoral artery and vein with
stabilization of hemodynamic parameters. Four days later, the patient’s hemodynamics were adequately
stabilized to remove the TandemHeart. The patient had a prolonged hospital course but was ultimately
discharged to skilled nursing rehabilitation one month later.

Figure 2. Case Study Images

(A-C) Coronary angiography with no culprit lesion or critical stenosis; (D) TTE demonstrating a 1.0 x 0.5 cm LV apical thrombus (arrow);
(E)TandemHeart insertion in the right femoral artery and vein; (F) TandemHeart venous inflow cannula placed transseptally into the left atrium.

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QUICK READ SUMMARY

✓ Limited clinical data to date show that TandemHeart effectively improves hemodynamic
and metabolic parameters (eg, increases CPO, UOP, and reduces PCWP) in patients with
cardiogenic shock.

✓ TandemHeart provides left-sided hemodynamic support via a centrifugal cardiac bypass

pump, draining oxygenated blood from the left atrium via transseptal cannula and returning
oxygenated blood to the common femoral artery.

✓ TandemHeart reduces LV preload and LVEDP and provides systemic perfusion. Retrograde
flow of arterial blood increases afterload, however, the overall effect on coronary perfusion is
neutral.

✓ Advantages of TandemHeart include direct LA unloading, appropriateness in patients

with severe aortic or mitral valve abnormalities, safety in the presence of LV thrombus and
mechanical aortic valve, and easy conversion to VA or LAVA ECMO.

✓ Disadvantages include expertise required for transseptal puncture, large bore arterial access and
associated risks of vascular injury and bleeding, and retrograde arterial blood flow.

References
1. Thiele H, Sick P, Boudriot E, et al. Randomized comparison of intra-aortic balloon support with a percutaneous left
ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock.
Eur Heart J. 2005;26(13):1276-83.

2. Burkhoff D, Cohen H, Brunckhorst C, O’Neill WW. A randomized multicenter clinical study to evaluate the safety
and efficacy of the TandemHeart percutaneous ventricular assist device versus conventional therapy with intraaortic
balloon pumping for treatment of cardiogenic shock. Am Heart J. 2006;152(3):469.e1-8.

3. Kar B, Gregoric ID, Basra SS, et al. The percutaneous ventricular assist device in severe refractory cardiogenic shock.
J Am Coll Cardiol. 2011;57(6):688-96.

4. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by
cardiogenic shock. N Engl J Med. 1999;341(9):625-34.

5. Alli OO, Singh IM, Holmes Jr DR, et al. Percutaneous left ventricular assist device with TandemHeart for high-risk
percutaneous coronary intervention: the Mayo Clinic experience. Catheter Cardiovasc Interv. 2012;80(5):728-34.

6. Neupane S, Basir MB, Alqarqaz M, et al. High-risk chronic total occlusion percutaneous coronary interventions
assisted with TandemHeart. J Invasive Cardiol. 2020;32(3):94-7.

7. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl. J Med. 2024;390:1382-93.

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PREVIOUS CHAPTER Chapter 15.2: Transseptal Access NEXT CHAPTER

15.2
Transseptal
Access
Elliott M. Groves, MD, MEng, FACC, FSCAI
Interventional and Structural Cardiology
Palo Alto Medical Foundation
San Francisco, CA
emgroves@[Link]
grovesem@[Link]
@ElliottMGroves

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Introduction
TandemHeart® (LivaNova, London, UK) is an extracorporeal, centrifugal, continuous flow mechanical
circulatory support (MCS) device that withdraws blood from the left atrium (inflow cannula) and pumps
it back into the arterial circulation (outflow cannula).1 The unique nature of TandemHeart is that it has
an oxygenator like extracorporeal membrane oxygenation (ECMO), but unlike ECMO, it also unloads
(vents) the left ventricle via its inflow cannula being placed in the left atrium. Whereas ECMO increases
left ventricular stress, TandemHeart reduces left ventricular preload and stroke volume, which in turn
reduces LV workload and myocardial oxygen demand.2 However, the LA cannula does introduce an
added level of complexity to the procedure through the need for a transseptal puncture and delivery of a
large bore device across the interatrial septum.

Due to the advent of transseptal structural heart procedures with large bore devices, many techniques
have been developed for safe and effective delivery of devices across the interatrial septum in the
fossa ovalis. The most critical step to achieve a safe and successful procedure is preparation. Before
transseptal delivery of the LA TandemHeart cannula is attempted, the proper equipment and support
must be in place. Imaging is critical to a safe and properly located transseptal puncture. Under ideal
circumstances this would include echocardiographic and fluoroscopic imaging. Thus, the ideal location
for TandemHeart cannulation is in a cardiac catheterization laboratory or a hybrid operating room. Either
transesophageal echocardiography (TEE) or intracardiac echocardiography (ICE) may be used to guide
cannula delivery into the LA.

Procedure setup
Proper preparation is an important aspect of the insertion of a transseptal cannula during the initiation
of TandemHeart.
• Patient. The patient should be supine, under adequate anesthesia and typically have the right
inguinal region prepped.
• Access. Any procedure starts with proper vascular access and while not the purpose of this
section, it is important to note that ultrasound and fluoroscopic guidance reduces complications,
particularly in large bore access.3
• Anticoagulation. Half to full dose heparin can be administered once arterial and venous access
has safely been obtained. This is to reduce the risk of catheter thrombosis during the procedure.
• Imaging. Use TEE biplane imaging to visualize landmarks; some variations of the 90-degree
bicaval view and 30-degree aortic short axis views should be established. If ICE is being used, a
posterior tilt with clockwise rotation will demonstrate the fossa ovalis and can be used to judge
height (superior versus inferior). Further manipulation of the catheter with counterclockwise
followed by clockwise rotation can be used to judge the anterior and posterior fossa.4 Identifying
optimal imaging windows is critical prior to catheter insertion.

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Catheter and needle positioning

1. After obtaining femoral venous access, pass a 0.032" or 0.035" wire (depending on transseptal
system) into the superior vena cava (SVC).
2. Introduce a transseptal sheath over the wire in the SVC through the femoral venous puncture site.
Typically, transseptal sheaths—such as the Mullins (Medtronic, Minneapolis, MN, USA), Swartz™ SL
series (Abbott, Abbott Park, IL, USA), VersaCross (Boston Scientific, Marlborough, MA, USA) and
TorFlex™ (Boston Scientific, Marlborough, MA, USA)—are 8-8.5 Fr, and while they can be safely
inserted directly over a wire, they can also be passed through a larger sheath which can serve to
predilate the tract for the 21 Fr venous cannula to pass through once the wire is secured in the
LA. (Of note there are several steerable sheaths that can be used; however, due to the desire for a
mid, mid fossa puncture in this procedure, those are rarely necessary and come with a significant
increase in cost and add unnecessary complexity.)
3. Advance the transseptal sheath into the SVC with the tip pointed to the patient’s left in the AP or
LAO view. The tip should be 3-4 cm cranial to the cavoatrial junction.
4. Remove the wire, or if using the VersaCross system, withdraw it into the transseptal sheath.
5. Once the transseptal sheath is appropriately placed in the SVC, introduce the needle or radiofrequency-
based system. Currently several needle and radiofrequency-based options are available.
• BRK™ Transseptal Needles. The original transseptal needle designed by Ross in the 1950s was
modified by Brockenbrough, a version of which, the BRK, is the most commonly used transseptal
needle.5 BRK comes in different shapes and can be used in a variety of different atrial sizes. The
BRK is a hollow needle and comes with a stylet. The stylet should be left in the needle until the
needle is 4-5 cm from the tip of the sheath. Alternatively, the stylet can be removed, and the
needle can be hooked up to continuous saline flush as it is advanced. The reason for this is to avoid
scraping the inner lumen of the plastic dilator into the needle which could potentially embolize into
the LA or RA.
• Radiofrequency (RF) NRG® Transseptal Needle and VersaCross (Boston Scientific, Marlborough,
MA, USA)
• Nykanen RF Wire (Baylis Medical, Austin, TX, USA)
• SafeSept® transseptal access system (Pressure Products Medical Supplies Inc, San Pedro, CA, USA)

6. When the needle is in place, in an LAO or AP view, pull the needle and sheath down toward the
fossa ovalis. Under live imaging, observe the sheath and the needle, first in the lowest section of the
SVC, then in the fossa.
7. The goal for TandemHeart is to puncture the fossa in a mid, mid location6 (Figure 1). A mid, mid
puncture of the fossa is preferred for several reasons.7
• The aorta is an anterior structure and puncture into the aorta is a potentially devastating
complication. A puncture that is too low can traverse the reflection between the right and left
atria. This would result in tamponade when the cannula was removed.
• Cannula and LA wall interaction will impair inflow and a mid, mid puncture provides the optimal
spacing away from walls of the LA.
• If the patient is successfully decannulated and has significant residual left to right or bidirectional
shunting, the iatrogenic atrial septal defect may need to be closed with a septal occluder. A mid,
mid puncture will leave the defect with adequate rims and a favorable angle for closure.

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8. Once the tip of the dilator is in the fossa, specific movements can be made to achieve the optimal
position.
• Pull further down to be more inferior in the septum. If the initial position is too low, withdraw into
the inferior vena cava (IVC) and use a wire to readvance into the SVC.
• Anterior-posterior position is accomplished by clockwise or counterclockwise rotation of the
catheter and can be checked in an RAO view on fluoroscopy where the tip of the dilator should
be pointed to the left of the screen away from the aorta which can be marked with a catheter as
arterial access is needed as well. Clockwise rotation will bring the tip of the dilator more posterior
and conversely counterclockwise rotation will bring the system more anterior.

LA
LA
IVC
Aorta

RA SVC
RA

Figure 1. Mid, Mid Fossa Puncture Location

(A) Bicaval view on TEE demonstrating the cavoatrial junction, with the SVC representing the most superior portion of the fossa and the RA
junction with the IVC representing the most inferior portion of the fossa; (B) Aortic short-axis view on TEE in which the border with the aorta
represents the most anterior portion of the fossa (which moves more posterior as the puncture site and catheter travel away from the aorta).

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Septal traversal
After the dilator has been positioned in a mid, mid location in the fossa, complete the puncture under
live imaging guidance.7
1. With a traditional needle, apply gentle forward pressure until the needle crosses the septum.
• If an RF needle/wire is used, then the crossing requires little to no pressure.8
• Using the SafeSept system also requires very little force and can allow for confirmation of
puncture position before proceeding.

2. Watch for signs of successful transseptal puncture.

• If the transseptal needle is attached to a manifold or other pressure transducer, look for a left
atrial waveform immediately upon crossing. Do not advance the needle and catheter if any other
waveform is seen and conduct further imaging.
• If using imaging, signs of successful transseptal puncture include release of the “tenting” seen
with pressure on the fossa and the presence of the needle tip in the left atrium.

Figure 2. Transseptal Puncture for TandemHeart

(A) Successful transseptal puncture in the fossa; (B) dilator inserted over wire into LA; (C) Cannula inserted until all side holes of the 21 Fr
TandemHeart cannula are in LA

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Wire and cannula insertion

1. After successful transseptal puncture, gently advance the system until 1-2 cm of the sheath/dilator
are in the left atrium. You can then proceed with a traditional, alternative, or hybrid strategy.
Traditional strategy
A. Fix the needle and advance it until the sheath tip is across the septum.
B. Fix the dilator and advance the sheath over the dilator into the mid left atrium under imaging
guidance to avoid the back wall of the atria.
C. Following dilator and needle removal, insert a guidewire, directing it into a left sided pulmonary
vein. This can be aided by inserting a multipurpose catheter through the transseptal sheath.
D. Confirm that the wire is in the pulmonary vein using imaging and fluoroscopy.
E. Pass either a stiff buddy wire into the vein through the same sheath or pass a soft tip catheter
over the wire in the pulmonary vein and then exchange it for a stiff wire. Typically, the stiff wire
of choice is a 0.035" Amplatz extra or super stiff wire to provide maximal support for devices.
Alternative strategy
A. Once the tip of the needle and dilator complex is just into the left atrium, remove the needle and
pass a 0.025" pigtail wire—such as an TorayGuide™ (Toray International Inc, Tokyo, Japan) or
ProTrack™ (Boston Scientific, Marlborough, MA, USA)—into the LA to pass the sheath and the
dilator into the LA to dilate the septum. If using the VersaCross system, then conveniently, you are
able to pass the relatively stiff RF 0.035" pigtail wire into the LA or preferably, the pulmonary vein.
Use of the VersaCross system can save a significant amount of time and exchanges.
B. The operator can then further dilate the septum with a balloon over this wire, or simply pass the
cannula over the wire into the LA, as most large bore devices will pass over this wire without
difficulty. This technique is very safe as the needle and sheath/dilator complex is not advanced
into the LA. It is also more expeditious, as the operator does not need to engage or wire the
pulmonary vein.
Hybrid strategy
A. Advance the sheath tip into the LA as described above.
B. Remove the dilator and insert a 0.035" pigtail wire—such as a Safari2™ (Boston Scientific,
Marlborough, MA, USA)—into the LA, over which the cannula can be delivered. This strategy,
however, may result in more risk given the fact that the 0.035" pigtail wires were designed for
use in the thick-walled LV and not the thin-walled LA.

2. Regardless of the technique, once access to the LA is secured, the patient should be fully anticoagulated.
3. Once the wire of choice is secured in the LA, carefully remove the transseptal sheath and introducer
sheath (if used) in the venotomy, using care not to disrupt wire position.
4. Under fluoroscopy, pass the 21 Fr transseptal cannula and dilator complex over the wire into the LA.
All side holes should be in the LA and not in the RA. If difficulty is encountered, a 6 mm diameter
peripheral angioplasty balloon can be used to dilate the septum.9
5. Remove the dilator and if the arterial cannula is in place, initiate support.10
6. Secure the cannula in place with great care, as cannula migration is one of the limitations to use
of this device. Multiple suture locations are helpful along with other dedicated devices to affix
the cannula to the leg. Complications can occur and should be managed expeditiously. Specific
management of each challenge is beyond the scope of this chapter, but careful technique can help
avoid nearly every common issue.11

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QUICK READ SUMMARY

✓ TandemHeart is a valuable tool in the mechanical support armamentarium.

✓ The need for a transseptal puncture to introduce a cannula into the LA adds a layer of
complexity that can be overcome with proper technique and an understanding of the
steps for successful LA access.

✓ Consistently following a protocol that involves high quality continuous imaging will lead
to consistent success in placement of the LA inflow cannula.

References
1. Saffarzadeh A, Bonde P. Options for temporary mechanical circulatory support. J Thorac Dis. 2015;7(12):2102-11.

2. Kapur NK, Paruchuri V, Urbano-Morales JA, et al. Mechanically unloading the left ventricle before coronary reperfusion
reduces left ventricular wall stress and myocardial infarct size. Circulation. 2013;128:328-36.

3. Vincent F, Spillemaeker H, Kyheng M, et al. Ultrasound guidance to reduce vascular and bleeding complications of
percutaneous transfemoral transcatheter aortic valve replacement: a propensity score–matched comparison. JAHA.
2020:9(6).

4. Merchant FM, DeLurgio, DB. Site-specific transseptal cardiac catheterization guided by intracardiac echocardiography
for emerging electrophysiology applications. J Innov Card Rhythm Manage. 2013;4:1415–27.

5. Ross J Jr, Braunwald E, Morrow AG. Transseptal left atrial puncture; new technique for the measurement of left atrial
pressure in man. Am J Cardiol. 1959;3(5):653-5.

6. Bazaz R, Schwartzman D. Site-selective atrial septal puncture. J Cardiovasc Electrophysiol. 2003;14(2):196-9.

7. Bayrak F, Chierchia GB, Namdar M, et al. Added value of transoesophageal echocardiography during transseptal
puncture performed by inexperienced operators. Europace. 2012;14(5):661-5.

8. Hsu JC, Badhwar N, Gerstenfeld EP, et al. Randomized trial of conventional transseptal needle versus radiofrequency
energy needle puncture for left atrial access (the TRAVERSE-LA study). J Am Heart Assoc. 2013;2(5):e000428.

9. Sy RW, Klein GJ, Leong-Sit P, et al. Troubleshooting difficult transseptal catheterization. J Cardiovasc Electrophysiol.
2011;22(6):723–7.

10. Chiam PT, Ruiz CE, Cohen HA. Placement of a large transseptal cannula through an inferior vena cava filter for
TandemHeart percutaneous left ventricular assist. J Invasive Cardiol. 2008;20:E197–9.

11. Alkhouli M, Rihal CS, Holmes DR Jr. Transseptal techniques for emerging structural heart interventions. JACC
Cardiovasc Interv. 2016;9(24):2465–80.

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15.3
Troubleshooting
TandemHeart ®

Complications
Katrine A. Zhiroff, MD, FSCAI
Interventional Cardiology
Department Chair of Cardiovascular Services
PIH Health Physicians
Downey, CA
kzhiroff@[Link]

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Introduction
While some complications are common to all mechanical circulatory support (MCS) devices, reported
complication rates vary for each type of device. TandemHeart® is associated with some unique
complications that operators must consider. Careful procedural planning as well as close clinical and
laboratory monitoring of the patient can prevent the occurrence or allow rapid identification and
treatment of these complications.

Complications associated with TandemHeart

Most MCS devices are associated with some hematologic, vascular, infectious, neurologic, and
mechanical or device-specific complications. Table 1 lists the complications associated with
TandemHeart in each of these categories. These complications are discussed in more detail below.

Table 1. TandemHeart Complications

• Major bleeding

• Access site bleeding

Hematologic complications
• Hemolysis

• Thrombosis

Vascular complications • Limb ischemia

• Access site infection

Infectious complications
• Sepsis

• Stroke
Neurologic complications
• TIA

• Device migration

• Atrial perforation
Mechanical/device-specific • Cardiac tamponade
complications
• Air embolism during insertion

• Right to left shunting in patients with iatrogenic residual atrial septal

defect (ASD)

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Handling hematologic complications

Hematologic complications observed with the use of TandemHeart include major bleeding, access site
bleeding, hemolysis, and thrombosis.

Major bleeding
Reported rates of major bleeding associated with TandemHeart, defined as need for a blood
transfusion, are variable and typically range from 53-59%.1 Thomas et al.4 reported the highest rate of
procedure-related bleeding—82%—resulting in the need for blood transfusion. Gastrointestinal sources
of major bleeding were reported in 19% of cases, and access-related bleeding in 8-53% of patients.2

Given that optimal operation of the TandemHeart circuit depends on adequate preload and filling
pressures, it is imperative to identify the etiology of bleeding and reverse blood loss as soon as possible.
The operator must consider sources of bleeding that are both patient-related and device-related. In
a subset of critically ill patients receiving therapeutic anticoagulation, for example, it is important to
consider gastrointestinal bleeding. Device-related bleeding in the device circuit can account for more
than 250 mL of blood loss.

Device placement increases the risk of atrial perforation and pericardial tamponade. Recognition of
tamponade may be difficult in these patients given a non-pulsatile arterial waveform. This complication
occurs early after device placement and is often recognized shortly after transseptal puncture,
underscoring the importance of echocardiographic and fluoroscopic evaluation of cannula placement
shortly after device insertion.

Access site bleeding

Access site bleeding is another common source of device-related blood loss and has been reported to
be as high a 53%.1 Use of 2 percutaneous access sites with large bore cannula incrementally increases
the risk of this complication compared to other MCS devices. Access sites should be closely monitored.
Use of transparent dressings and frequent assessment for hematoma formation is imperative. Special
care should be taken when moving or turning the patient to avoid moving or dislodging the cannulae,
which may result in bleeding.

Hemolysis
Hemolysis is another source of observed decline in hematocrit, which is related to shear stress with all
axial pump MCS devices. Hemolysis with TandemHeart is reported at a lesser rate compared to other
devices, occurring in 5.3% of patients according to Burkhoff et al.5 Similar to other MCS devices, there is
probably a temporal relationship between development of clinically significant hemolysis and duration
of temporary MCS support. Laboratory assessment of the degree of hemolysis is further complicated
in a setting of cardiogenic shock when baseline elevations in LDH make it an unreliable marker. Serial
monitoring of serum hemoglobin and free plasma hemoglobin allows early identification of presence
and severity of hemolysis.6 Use of lower motor speed (rpm) to achieve maximal flow rates may reduce
observed rates of hemolysis. Notably, thrombocytopenia has not been reported with the use of
TandemHeart.1

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Thrombosis
Thrombotic complications with TandemHeart are uncommon and can usually be prevented with adequate
anticoagulation. Consider evaluation for thrombus formation in the setting of prolonged periods of
subtherapeutic anticoagulation or prolonged periods of low flow states. Per manufacturer instructions,
in order to avoid thrombosis one must avoid stopping TandemHeart for more than 5 minutes and avoid
low flow rates (<1.5 L/min) for more than 30 minutes. Increasing wattage requirements may indicate clot
formation either at the tip of a cannula or within the circuit. Promptly consult with a cardiothoracic surgeon
if thrombus is seen at the tip of the left atrial cannula. The surgeon can surgically remove the cannula and
thrombus with preemptive cross-clamping of the aorta and cardiopulmonary bypass to avoid systemic
embolization.3

Handling vascular complications

Vascular complications are another clinically significant consequence of MCS use. Reported rates of limb
ischemia in patients supported with TandemHeart appear to be comparable to IABP and Impella® and
lower than VA ECMO.1 No amputations have been reported with this device. The true rate of vascular
complications is difficult to ascertain given variability in reporting.

Rates of limb ischemia are related to the caliber of arterial cannula relative to the diameter of femoral
and iliac arteries. TandemHeart requires evaluation of iliofemoral circulation to assess the feasibility of
placing the 17 Fr femoral cannula. Alternatively, two 12 Fr cannulae may be placed in bilateral femoral
arteries at the expense of reducing maximal flow rate to approximately 2.5 L/min.7

Limb ischemia is difficult to identify in a patient supported with TandemHeart due to the absence of
pulsatile flow. Therefore, identification of limb ischemia is based on clinical assessment of temperature
and color of the limb. If there is concern for adequate perfusion to the ipsilateral limb at the time of
cannula insertion, placement of an antegrade femoral sheath may reduce the rate of limb ischemia as
has been described with use of other large bore devices.9 Recent adoption of near-infrared spectroscopy
(NIRS) offers a more accurate and objective method of monitoring regional tissue perfusion as well as
an opportunity for early identification of critical limb ischemia.10

Handling infectious complications

Infectious complications represent another major source of morbidity for patients with temporary MCS
devices. Reported rates of sepsis and access site infection with TandemHeart are 29.9% and 16%,
respectively.1 These rates are higher than those reported for Impella and IABP and similar to those
observed with VA ECMO. The use of 2 percutaneous insertion sites with large bore cannula likely accounts
for this observation. This underscores the importance of using meticulous sterile technique during
insertion as well as limiting the duration of MCS support. There is no data to support the use of antibiotics
other than the standard institutional prophylaxis protocols for preventing device-related infections.

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Handling neurologic complications

Neurologic complications, specifically stroke and TIA, have been reported with all MCS devices.1 These
complications may be due to patient-factors, such as underlying cerebrovascular disease and global
hypoperfusion, or device-related risk. The need for transseptal puncture in the placement protocol
for TandemHeart increases the risk of such neurologic events. To help reduce complications, achieve
a therapeutic ACT greater than 250 seconds prior to instrumentation of the left atrium. Meticulously
de-air the atrial cannula according to manufacturer instructions to avoid air embolism. During the
maintenance phase of MCS support, regularly check the cannula for air to avoid embolization.

Handling mechanical/device-specific complications

As mentioned above, atrial perforation and cardiac tamponade are two mechanical complications
unique to TandemHeart. While the reported rate is below 1%,1 it is important that institutions and
operators using TandemHeart have extensive experience in transseptal2 technique.

Device malfunction has not been reported. Dislodgement of cannula was only reported in an early
feasibility study with no significant prevalence in more contemporary case series.1 In cases of
inadequate preload, suction of the atrial cannula in the left atrium can limit the maximal achievable rpms
and resultant flow rates. It can also result in atrial arrhythmias as well as cannula migration from the left
atrium across the interatrial septum.

A unique complication of TandemHeart that deserves special mention is the development of a persistent
right to left shunt following device removal. True incidence of this complication is unknown because of
limited published long-term follow-up data. From recent data in patients who underwent percutaneous
mitral valve repair, the reported incidence of iatrogenic atrial septal defect (ASD) with resultant right
to left shunting following transseptal instrumentation with a large bore sheath was 5%, with a third of
patients experiencing associated hypoxemia.8 The majority of patients experienced complete resolution
of iatrogenic ASD within 4 to 6 weeks after device removal.11 Thus, identification and evaluation for
closure of a persistent ASD should be considered during long-term follow up of these patients.

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QUICK READ SUMMARY

✓ Several complications may occur during the hospital course of a patient requiring
TandemHeart support.

✓ Complications can be rapidly identified or prevented through careful procedural planning

and close clinical and laboratory monitoring.

✓ When handling bleeding complications, be sure to consider both device-and patient-related

sources of bleeding.

✓ Serial monitoring of serum hemoglobin and free plasma hemoglobin enable early
identification and severity assessment of hemolysis.

✓ To identify limb ischemia, color and temperature are used in the absence of pulsatile flow
with TandemHeart.

✓ Use of 2 percutaneous insertion sites with large bore cannula increase the risk of infectious
complications and necessitate use of meticulous sterile technique during insertion of
TandemHeart as well as limited duration of MCS support.

✓ To help avoid air embolism and the risk of TIA or stroke, meticulously de-air atrial cannula
and regularly check cannula during the maintenance phase of TandemHeart support.

✓ To avoid complications such as atrial perforation and cardiac tamponade,

institutions and operators of TandemHeart should have extensive experience in transseptal2
technique.

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References
1. Subramaniam AV, Barsness GW, Vallabhajosyula S, Vallabhajosyula S. Complications of temporary percutaneous
mechanical circulatory support for cardiogenic shock: an appraisal of contemporary literature. Cardiol Ther.
2019;8(2):211-28.

2. Ali JM, Abu-Omar Y. Complications associated with mechanical circulatory support. Ann Transl Med. 2020;8(13):835.

3. Gregoric ID, Bruckner BA, Jacob L, et al. Techniques and complications of TandemHeart ventricular assist device
insertion during cardiac procedures. ASAIO J. 2009;55(3):251-4.

4. Thomas JL, Al-Ameri H, Economides C, et al. Use of a percutaneous left ventricular assist device for high-risk cardiac
interventions and cardiogenic shock. J Invasive Cardiol. 2010;22(8):360-4.

5. Burkhoff D, Cohen H, Brunckhorst C, O’Neill WW, TandemHeart Investigators Group. A randomized multicenter
clinical study to evaluate the safety and efficacy of the TandemHeart percutaneous ventricular assist device
versus conventional therapy with intraaortic balloon pumping for treatment of cardiogenic shock. Am Heart J.
2006;152(3):469.e1-8.

6. Dufour N, Radjou A, Thuong M. Hemolysis and plasma free hemoglobin during extracorporeal membrane oxygenation
support: from clinical implications to laboratory details. ASAIO J. 2020;66(3):239-46.

7. Naidu SS. Novel percutaneous cardiac assist devices: the science of and indications for hemodynamic support.
Circulation. 2011;123(5):533-43.

8. Morikawa T, Miyasaka M, Flint N, et al. Right-to-left shunt through iatrogenic atrial septal defect after MitraClip
procedure. JACC Cardiovasc Interv. 2020;13(13):1544-53.

9. Kizner L, Flottmann C, Horstkotte D, Gummert J. Bilateral antegrade perfusion of the superficial femoral artery
to prevent limb ischaemia during combined use of Impella CP left ventricular assist device and extracorporeal life
support, Interactive Cardiovascular and Thoracic Surgery. 2016;23(2):335-7.

10. Bonicolini E, Martucci G, Simons J, et al. Limb ischemia in peripheral veno-arterial extracorporeal membrane
oxygenation: a narrative review of incidence, prevention, monitoring, and treatment. Crit Care. 2019;23(1):266.

11. Thiele H, Lauer B, Hambrecht R, et al. Reversal of cardiogenic shock by percutaneous left atrial-to-femoral arterial
bypass assistance. Circulation. 2001;104(24):2917-22.

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ECMO Overview

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16.1
ECMO Program
Development
Eric M. Gnall, DO, FACC
Director, ECMO/Acute Mechanical Circulatory Support
Lankenau Medical Center, Main Line Health
Wynnewood, PA
ericgnall@[Link]
@ericgnall

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Introduction
Developing a program for extracorporeal membrane oxygenation (ECMO), or extracorporeal life
support (ECLS), is a complex undertaking. An ECMO/ECLS program (referred to as an ECMO program
throughout this chapter) is established at an institutional level and requires commitment from multiple
clinical and administrative parties. This chapter highlights some key elements of establishing an ECMO
program, as depicted by the ECMO program pathway in Figure 1.

CARE TEAM
PRIVILEGING MODEL AND CAPACITY PLATFORMS OUTCOMES

Figure 1. Key Elements of Establishing an ECMO Program

Privileging

Privileging is one of the first steps along the road to building an ECMO program. While the privileging
process varies among institutions, federal guidelines provide credentialing and privileging oversight.
The Joint Commission, which accredits and certifies healthcare organization in the Unites States, defines
credentialing as “the process of obtaining, verifying, and assessing the qualifications of a practitioner
to provide care or services in or for a healthcare organization.” It defines privileging as “the process
whereby a specific scope and content of a patient care services (that is clinical privileges) are authorized
for a healthcare practitioner by a healthcare organization, based on an evaluation of the individual’s
credentials and performance.”1

For most institutions, privileging for a new ECMO program will need to be drafted and submitted to
either the department of medicine, the department of surgery, or both. Once the new privileges are
established, physicians must apply for them.

Many institutions have 2 different types of ECMO privileges:

• Privileges for cannulation
• Privileges for management
Cannulating physicians would require both types of privileges.

Privileging requires training and proctoring that is approved by the credentialing committee. Performing
ECMO procedures without proper privileges will result in various levels of penalties in addition
to malpractice liability. Although the minimum number of supervised cannulations varies among
institutions, 5 is the lowest surveyed. In terms of supervised management, this may be quantified by
either numbers of managed patients or hours of management. Management privileges should reflect a
greater minimum bar compared with cannulation.

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Model

An ECMO program may follow a hub model or a spoke model. Although there may be some fluidity
between the two models, the initial decision of which model to follow impacts the program development
pathway.

SPOKE

SPOKE SPOKE

SPOKE HUB SPOKE

SPOKE SPOKE

SPOKE

Spoke models
An ECMO program following a spoke model likely will not have an organized ECMO intensive care
unit for the post cannulation care of patients. A spoke model typically relies on formal or informal
agreements with a hub facility for the transfer and continued care of patients. Patient selection is usually
heavily impacted by the spoke-hub relationship and transfer is dependent on the hub’s capacity.

A spoke model allows dissemination of life saving technology to more hospitals, especially with ECMO
platforms that do not require a perfusionist to prepare the circuit. The spoke model also reduces the
overall care team and capacity requirements of the program, and financials are favorable in most cases.

Hub models
A hub model is a referral center with a fully trained ECMO care team. A hub center offers specialized
care to multiple ECMO patients for longer durations. One hub per health network enables all care team
members to maintain proficiency. In addition, the concentrated experience at a single hub center allows
for better patient selection and outcomes. Hub centers that only service their own health network can
more easily utilize predictable ground transportation, although ambulances used for ECMO transport
are often required to be larger than traditional ambulances.

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Care team and capacity

In a spoke facility, the care team may be limited to a physician trained in both cannulation and
management of ECMO and a small group of ECMO specialists. In addition, a physician program director
should be established for oversight and accountability. In the spoke model, it is common for the hub’s
multidisciplinary team to provide joint evaluation and decision-making regarding implementation of
circulatory support.

The Extracorporeal Life Support Organization (ELSO) recognizes care team members as ECMO
specialists and recommends basic training requirements to obtain this designation.2 An ECMO specialist
may be a registered nurse (RN), respiratory therapist (RT), or perfusionist with specialized training
in running ECMO devices. A cannulating physician should also be an ECMO specialist. Institutional
oversight of initial specialist training and ongoing training is imperative. Most organizations evaluate and
document competency annually. Physician privileges are typically reviewed each recredentialing cycle.

Establishing a hub program requires system investment. Most hubs will start with a low capital/low
operating budget. In this model, a single capital investment is made for hardware/disposables for ECMO
circuits, cost of training a dedicated small group of ECMO specialists, and initial in-house supervision by
a perfusionist or established specialist. Required flight time (ECMO patient care experience) varies by
institution and can range from 20 to 100 hours per specialist before allowing independent care. Apart
from cardiac ECMO, a robust pulmonary ECMO program provides additional flight time hours for most
medium to large centers.

In addition to initial certification, yearly recertification and documented proficiency testing should be
recorded for each specialist. ELSO recommends recertification for those who have not participated in
ECMO care for more than 3 months. Most established ECMO nurse specialist models are hybrid, utilizing
a perfusionist for most initiations. The perfusionist often remains bedside until the patient is clinically
stable, although he or she will not stay in house 24 hours a day. Perfusionists will perform circuit checks
every 12 or 24 hours, in addition to the surveillance checks completed by the ECMO nurses.

Non-cath lab cannulation allows for greater programmatic growth. This requires the ability to move the
cannulators, the circuit, the cannulating equipment and cannulas, the ECMO drug box, and vascular
ultrasound as well as a perfusionist/ECMO specialist who can initiate the circuit, to the desired location.
The use of a mobile ECMO cart is vital. Larger programs will place ECMO carts in several locations
around the hospital including the cath lab, intensive care unit, and emergency departments. Housing
pre-primed circuits at all locations is usually not feasible, but 1 pre-primed circuit is always kept
available within the hub. In the absence of a perfusionist, an ECMO specialist is trained to initiate the
pre-primed circuit for the team.

At our institution we use a model of “ECMO ACTIVATION.” The decision to place someone on ECMO
is shared by the physician cannulator and requesting physicians. Once the patient is determined to
be an ECMO candidate, an ECMO ACTIVATION is sent by telecommunications to the team members.
The notification is sent to cannulators, ECMO unit nurse managers, perfusion, pharmacy, blood bank,
and anesthesia. The blood bank prepares for the possible need for emergent blood products, and the
pharmacy prepares the ECMO drug box. An ECMO ACTIVATION should be initiated only by the ECMO
team to prevent erroneous activations. Following cannulation, post-ECMO order sets and protocols are
initiated. These may involve CT scans and cath lab imaging prior to transfer to the ECMO unit.

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Post-initiation, multidisciplinary team members may include intensivist/pulmonary critical care, palliative
medicine, heart failure cardiology, clinical pharmacy, spiritual care, and other clinical subspecialists. The
operating budget should factor the continuous care by an ECMO specialist nurse, which affects nurse
to patient ratios. In the absence of in-house ECMO physician specialists, a physician assistant or nurse
practitioner ECMO specialist is often required for unit supervision during after hour care.

As evident in any other procedure, limiting the number of cannulators reduces complications and will
improve outcomes. Establishing a call schedule for cannulators is important as it allows the program
to offer a 24-hour service line. ECMO consults often occur after hours when a large multidisciplinary
team evaluation may not be possible, sometimes leaving the cannulating physician specialist to make
the decision rapidly with limited patient information. To limit inappropriate use of ECMO, ELSO provides
a list of relative contraindications.3 Physician experience and the accumulated knowledge of ECMO
outcomes often becomes the deciding factor in cases. In addition, hub capacity—defined by available
equipment, beds, and all personnel—may impact this decision. The program director should interface
daily with perfusion and the ECMO unit manager to determine the capacity of the unit to provide care to
an additional ECMO patient. During a surge, neighboring hubs are often contacted (ideally proactively)
for overflow. To ensure efficient and responsible use of this technology, it is important for hubs and their
respective spoke centers to develop standards for patient selection and standard protocols.

Platforms

There are currently multiple platforms of ECMO/ECLS pump/oxygenators, and the number continues
to grow. Spoke models usually are limited to a single platform that meets their institution’s needs. Hub
models typically utilize multiple platforms.

ECMO/ECLS pump/oxygenator systems require varying degrees of technical knowledge and expertise
to prepare and manage. Most notably, most platforms are perfusionist dependent, thus often limiting
those platforms to hub models. In addition, “mobile ECMO”—offering ECMO services to hospitals
outside the hub’s network—requires platforms that are portable and transport friendly. Mobile ECMO is
the final stage in program growth as a hub. The ability to cannulate a patient out-of-network requires
involvement of hospital administration, as mobile cannulators would require emergency privileges at
an out-of-network hospital. Platform decisions are heavily impacted by this advanced service line. It
must be noted that an out-of-network ECMO initiation hospital is not considered a spoke as it is not
intrinsically ECMO capable.

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Outcomes

In addition to developing protocols and algorithms involving ECMO/ECLS patient care, it is important
to have periodic evaluations of program outcomes and programmatic financials. Outcomes are usually
discussed in a peer-reviewed setting. The venue for such reviews varies by institution.

Hub models should participate in an ELSO database. This database provides annual reports comparing
participating programs with both national and international outcomes. The database is voluntary,
however, and the self-reporting nature is one of its main limitations.

Periodic financial evaluations provide important data for an ECMO program. An understanding of
financial data can enable changes in patient care pathways to adjust cost. Such data, in many cases,
also provides an incentive to expand the program.

Successful programs expand mostly by spreading a culture of ECMO throughout all service lines. This
is accomplished through education, spotlighting success stories and successful program outcomes with
favorable financials. Growth into a mobile ECMO hub requires significant administrative oversight as
outcomes and financials are usually evaluated before this step.

QUICK READ SUMMARY

✓ Many institutions have separate ECMO privileges for cannulation and management.

✓ ECMO programs may follow a hub or spoke model and the model they follow impacts care
team and capacity requirements.

✓ Care team and capacity requirements are greater at hub facilities.

✓ Most spoke models are limited to a single ECMO/ECLS platform while hub models utilize
multiple platforms.

✓ Periodic evaluations of program outcomes and financials provide valuable feedback for
strengthening an ECMO program.

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References
1. The Joint Commission. Ambulatory Care Program: The Who, What, When and Where’s of Credentialing
and Privileging. Available at [Link]
imported-assets/tjc/system-folders/blogs/ahc_who_what_when_and_where_credentialing_bookletpdf.
pdf?db=web&hash=CD838EB80D69FE2FA517285B4F3A0537. Accessed June 3, 2021.

2. ELSO Guidelines for ECMO Centers. Available at [Link]

[Link]. Accessed June 15, 2021.

3. ELSO Guidelines. Available at [Link] Accessed June 15, 2021.

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16.2
ECMO Approved
Devices
Donald Quimby Jr., MD
Assistant Professor
University of South Florida Morsani College of Medicine,
Department of Cardiology
Tampa, FL
dlquimby@[Link]

Nick Martini, CCP

Manager Cardiac Perfusion Services
Tampa General Hospital
Tampa, FL
nmartini@[Link]

Hiram Grando Bezerra, MD, PhD

Professor
University of South Florida Morsani College of Medicine,
Department of Cardiology
Director, Interventional Cardiology Center
Tampa General Hospital
Tampa, FL
hbezerra@[Link]

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Introduction
Extracorporeal membrane oxygenation (ECMO) serves as a potentially lifesaving therapy for critically
ill patients who require complete cardiopulmonary bypass and is used as a bridge to recovery or
more durable therapies (LVAD or transplant). Small trials have shown promising results with quick
implementation of VA ECMO in the setting of cardiac arrest.1 Increase in demand has led to advances in
the technology and new devices which include more complex configurations. In this section, we review
the essential components of the ECMO circuit and various commercially available devices.

Components
Pumps
Familiarity with the available ECMO products is crucial for implementation in the clinical arena. Clinicians
should be familiar with the specifications of the major components – mechanical pump, heat exchange
device, and large bore cannulae – as well as the battery life for portable units. The original roller pumps
have since been replaced with centrifugal pumps, which have a lower adverse event profile. Each device
consists of an inlet and outlet port and a polymer coated rotor. Table 1 presents technical specifics for
devices of the major manufacturers.

Table 1. Centrifugal Pump Characteristics

EUROSETS
ABBOTT MEDTRONIC CARDIOHELP- SORIN-
(not available NOVALUNG
CENTRIMAG™ AFFINITY MAQUET REVOLUTION
in US)

Blood flow
0-10 L/min 0-10 L/min 0.5-10 L/min 0.5-7 L/min 0.5-8 L/min 1-7 L/min
range

Pump
0-5000 rpm 0-5500 rpm 0-4000 rpm 0-5000 rpm 0-3500 rpm 0-10000 rpm
Speed

Max blood
pathway 800 mmHg 600 mmHg 760 mmHg 900 mmHg 800 mmHg 600 mmHg
pressure

5 hours
Battery life 90 min
120 min NA 90 min NA (2 batteries;
(transport) (max 6 hrs)
2.5 hour each)

Total
priming 39 mL 31 mL 40 mL 600 mL 57 mL 17 mL
volume

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Oxygenators/heat exchange systems

The second aspect of the ECMO circuit, after the pump, is the gas exchange system or oxygenator,
which allows oxygen to enter the blood and carbon dioxide to be removed. Formerly these were
silicone rubber membrane lungs but over the years these older systems have been replaced with newer
technology.

Most devices today are composed of a hollow fiber polymethylpentene. This substance offers multiple
benefits:
• Optimized flow pattern that allows for smaller devices
• Combined heat exchange
• Small volume priming requirement that leads to faster execution
• Smaller surface area limits inflammatory response and reduces hemolysis

The exchange of gas is usually dictated by the flow of blood through the circuit. Most oxygenators now
contain their own temperature control mechanism that negates the need for a separate device to control
temperature. As such, we will not discuss separate temperature control units in detail. Table 2 presents
technical specifics of devices from major manufacturers.

Table 2. ECMO Oxygenators/Heat Exchange Systems

MEDTRONIC- MAQUET-QUADROX-
EUROSETS-AMG SORIN-LIVANOVA NOVALUNG
NAUTILUS™ ID ADULT

Recommended
0.5-7 L/min 0.5-7 L/min 0.5-7 L/min 0-5 L/min 1-7 L/min
flow rating

Maximum gas 0.5:1 – 3:1

14 L/min 14 L/min 0-14 L/min
flow (gas:blood)

Priming
220 mL 226 mL 215 mL 150 mL 320 mL
volume

Effective gas
exchange 1.81 m2 1.8 m2 1.8 m2 1.2 m2 1.9 m2
surface area

Effective heat
exchange 0.08 m2 0.3 m2 0.4 m2 0.14 m2 0.45 m2
surface area

Gas exchange Polypropylene and

Polymethylpentene Polymethylpentene Polymethylpentene Polymethylpentene
material Polymethylpentene

Heat exchange Polyethylene

Stainless steel Polyurethane Stainless steel Polyethylene
material terephthalate

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Cannulae
Most cannulas utilized to access venous and arterial systems are composed of polyurethane or other
inert polymers and lined with biological coating to minimize interaction with blood. These cannulas
are placed using percutaneous technique or surgical cutdown and are usually paired with a series of
dilators to allow for an easy transition to the larger bore access. Cannulas are then connected to the
ECMO circuit using large 3/8" tubing. Table 3 presents specific cannula sizes available through various
manufacturers.

Table 3. ECMO Vascular Access Cannulae

EUROSETS ABBOTT CENTRIMAG™ MEDTRONIC CARDIOHELP-MAQUET

Arterial size (Fr) 20, 22, 24 24 15, 17, 19, 21, 23, 25 13, 15, 17, 19, 21, 23

15, 17, 19, 21, 23, 25,

Venous size (Fr) 22, 24, 26 34 19, 21, 23, 25, 29
27, 29

QUICK READ SUMMARY

✓ The major components of the ECMO circuit are the pump, oxygenator/heat exchange
device, and vascular access cannulas.

✓ The original roller pumps have since been replaced by centrifugal pumps, which have a
slightly lower adverse event profile. Each device consists of inlet and outlet ports and a
polymer coated rotor, which operates within a certain speed and is capped at a certain
flow threshold (L/min).

✓ Most oxygenators include a temperature control unit, and the rate of gas exchange
depends heavily on blood flow through the circuit.

✓ We recommend working with the various manufacturers to familiarize all medical

staff with the main components of the ECMO circuit. This aids tremendously when
troubleshooting is needed.

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References
1. Shin TG, Choi J-H, Jo IJ, et al. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: a
comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011;39(1):1-7.

2. ECMOLIFE Brochure. Eurosets S.r.l.; 2021;2021. Available from: [Link]

Accessed 21 October 2021.

3. HLS Cannulae Solutions from tip-to-tip brochure. Gentinge group; 2021. Available from: [Link]
dam/hospital/documents/english/hls_cannulae_brochure-en-non_us_japan.pdf. Accessed 21 October 2021.

4. Gentinge: Cardiohelp System - The world’s most versatile heart-lung support system. Available at: [Link]
[Link]/us/product-catalog/cardiohelp-system/. Accessed 21 October 2021.

5. Crescent™* Jugular Dual Lumen Catheter Brochure, NAUTILUS™* ECMO Oxygenator Quick Reference Guide.
Medtronic; 2020. Available from: [Link]

6. Novalung Heart and Lung Therapy System brochure. Fresenius Medical Care North America; 2020.

7. CentriMag™ Blood Pump Instructions for Use (IFU) manual, CentriMag™ 24Fr Return (Arterial) Cannula Kit
Instructions for Use (IFU), CentriMag™ 34Fr Drainage (Venous) Cannula Kit Instructions for Use (IFU). Abbott; 2019.
Available from: [Link]

8. EOS ECMO Intended for Long-Duration Procedures Hollow Fiber Oxygenator. LivaNova; 2016. Available from: https://
[Link]/livanova-media/livanova-public/media/resources01/ous_only_livanova_livanova_
eos_ecmo_09295-[Link]?ext=.pdf.

9. QUADROX-i Small Adult and Adult Choose maximum safety brochure. Maquet Gentinge Group; 2015. Available
from: [Link]

10. AFFINTYTM CP Centrifugal Blood Pump Brochure. Medtronic; Available from: Affinity CP Centrifugal Blood Pump
Brochure - Medtronic - PDF Catalogs; Technical Documentation ([Link]).

11. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus
conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and
propensity analysis. Lancet. 2008;372(9638):554-61.

12. Extracorporeal Life Support Organization. ECLS Registry Report: International Summary. Available at: [Link]
[Link]/Registry/InternationalSummaryandReports/[Link] Accessed 17 February 2022.

13. Lequier L, Horton SB, McMullan DM, Bartlett RH. Extracorporeal membrane oxygenation circuitry. Pediatr Crit Care
Med. 2013;14(5 Suppl 1):S7-S12.

14. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support
versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised
controlled trial. Lancet. 2009;374(9698):1351-63.

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16.3
VA vs VV ECMO:
Why, When and
How?
Christopher M. Fernandez, MD, MHS
Cardiovascular Disease Fellow
University of Chicago Medicine
Department of Medicine, Section of Cardiology
Chicago, IL
[Link]@[Link]

Sandeep Nathan, MD, MSc

Professor of Medicine
University of Chicago Medicine
Department of Medicine, Section of Cardiology
Chicago, IL
snathan@[Link]

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Introduction
Extracorporeal membrane oxygenation (ECMO) offers the highest level of mechanical circulatory
support achievable percutaneously, with the ability to circulate oxygenated blood at flow rates
comparable to or even greater than normal physiologic values. The decision to initiate a patient on veno-
arterial ECMO (VA ECMO) versus veno-venous ECMO (VV ECMO) depends on the degree of cardiac
vs. pulmonary dysfunction and the magnitude of hemodynamic compromise as well as the therapeutic
needs of the patient balanced against the projected clinical trajectory of the individual. This chapter
provides an overview of the essential differences between VA and VV ECMO, rationale and indications
for ECMO, timing of ECMO initiation, and focus on the essentials of percutaneous cannulation.

Rationale and indications for VA and VV ECMO

ECMO may be used to provide full cardiopulmonary support in the setting of severe cardiac and/or
respiratory failure using a VA configuration and total pulmonary support for isolated severe respiratory
failure using a VV configuration. Other configurations may be considered to address specific clinical
needs, such as north-south syndrome. Multiple societies have published specific indications and
guidelines for the use of VA and VV ECMO; however, the strength of recommendations overall are
somewhat low due to uncertain benefit across the range of clinical scenarios.1-3

Several landmark trials published recently have reinforced the lack of mortality benefit with routine, early
initiation of VA ECMO in cardiogenic shock not complicated by persistent cardiac arrest. An individual
patient data meta-analysis inclusive of 567 (mostly ischemic) cardiogenic shock patients from the ECLS-
Shock (Extracorporeal Life Support in Infarct-Related Cardiogenic Shock), Euro Shock, and ECMO-CS
(Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock) trials found that VA ECMO
did not reduce 30-day mortality compared with medical therapy and was associated with increased major
bleeding events and vascular complications.4 Furthermore, the individual component studies, ECLS-Shock
and Euro Shock, neither demonstrated improved survival at 30 days in the overall population, nor identified
any specific subgroup who may benefit differentially from early use of VA ECMO.5,6 In ECMO-CS, 122 all-
comer cardiogenic shock patients were randomized to immediate VA ECMO or early conservative therapy.
Once again, there was no significant difference in the primary composite outcome of death, resuscitated
circulatory arrest, and implementation of another mechanical circulatory support device at 30 days.7

The use of VA ECMO to support ongoing resuscitative efforts in the context of in-hospital and out-of-
hospital cardiac arrest (OHCA), known as ECPR (extracorporeal cardiopulmonary resuscitation), has also
been under close scrutiny recently. In 2023, the American Heart Association’s (AHA) Focused Update on
Adult Advanced Cardiovascular Life Support upgraded the recommendation for ECPR in patients with
cardiac arrest refractory to standard ACLS to Class 2a (Level of evidence B) following the publication of 2
randomized controlled trials.8 The ARREST trial (Advanced Reperfusion Strategies for Refractory Cardiac
Arrest) randomized 30 OHCA patients with refractory ventricular fibrillation to VA ECMO versus standard
ACLS.9 The primary outcome of survival to hospital discharge was significantly higher in the ECMO
group compared to the standard ACLS arm and the study was terminated early due to the probability
of superiority of the ECMO arm. The Hyperinvasive trial randomized 256 OHCA patients to early ECPR
versus standard ACLS with a primary outcome of neurologically favorable recovery at 180 days.10 The
trial was stopped early due to futility, however, the authors note that wide confidence intervals observed
in the occurrence of the primary outcome may suggest that the study was underpowered. The upgraded
practice recommendation, notwithstanding the 2 aforementioned trials, highlights the challenges of
treating and studying this patient population. These data should be interpreted with caution given the very
small sample size in the former trial, and the outcome heterogeneity noted in the latter.

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Despite the lack of demonstrable benefit with routine, early VA ECMO use in cardiogenic shock and
inconsistent benefit in OHCA, ECMO should be considered a life-saving or life-sustaining therapy in
selected patients with isolated severe cardiopulmonary dysfunction as a bridge to native organ recovery,
durable surgical ventricular assist device implantation, or cardiac transplantation.

VV ECMO for severe respiratory failure

The basic VV ECMO cannula configuration drains venous blood from a large central vein (often the
inferior vena cava (IVC)), circulates blood through a membrane lung (oxygenator), and then returns
blood to the right heart via a second central venous access site (either superior vena cava (SVC) or a
second cannula in the IVC, placed in close proximity to the right atrium/tricuspid valve annulus) where it
can pass through the pulmonary bed to the systemic circulation (Figure 1).

Figure 1. VV ECMO Configuration

The ECMO oxygenator uses a countercurrent gas exchange mechanism to add oxygen and remove CO2
from the circulating blood and is efficient enough to meet the physiologic demands of patients even in
the absence of any meaningful lung function. As such, VV ECMO is indicated for patients with severe
respiratory failure such as those with severe acute respiratory distress syndrome (ARDS). Several
meta-analyses have shown reductions in mortality in ARDS patients treated with ECMO as compared
to those who had more conservative management, and ARDS is among the most common indications
for VV ECMO use.11,12 The use of VV ECMO increased substantially during the initial surges of the
SARS-CoV-2 (COVID-19) pandemic to support critically ill, but otherwise recoverable or transplantable,
patients with severe COVID-19 pneumonia/ARDS.

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A number of objective measures may be used to help guide clinicians to consider VV ECMO, regardless
of the cause of respiratory failure. The Extracorporeal Life Support Organization (ELSO) is an
international group that collects data and publishes guidelines on the use of ECMO. According to the
June 2021 ELSO guidelines, VV ECMO is indicated in patients with refractory hypoxemia (PaO2 /FiO2
<80 mmHg), severe hypercapnic respiratory failure (pH <7.25 with PaCO2 ≥60 mmHg) despite optimal
ventilator settings, patients who require ventilatory support as bridge to transplant, or patients with
graft dysfunction following lung transplant (Table 1).2

Table 1. Indications, Contraindications, and Technical Considerations for VV/VA ECMO

VENO-ARTERIAL VENO-VENOUS
General Severe cardiac failure +/- respiratory failure Severe respiratory failure
indications
Specific • Cardiogenic shock (SCAI stage C-E) with • ARDS from any cause refractory to medical
indications severe LV, RV, or BiV failure and ventilatory support
• Post myocardial infarction • Hypoxemic respiratory failure with PaO2 /FiO2
• Failure to wean from cardiopulmonary bypass <80 mmHg despite optimal vent settings
• Post-cardiotomy • Hypercapnic respiratory failure with arterial
pH<7.25 and PaCO2 ≥60 mmHg
• Cardiac arrest
• Bridge to decision or lung transplant
• Massive pulmonary embolism
• Post lung transplant rejection
• Myocarditis
• Concomitant cardiac and respiratory failure
• Bridge to decision, transplant, or ventricular
assist device
Absolute • Pre-existing terminal illness or catastrophic • Pre-existing terminal illness or catastrophic
& relative neurologic injury neurologic injury
contraindications • Aortic dissection / significant aortic • Severe irreversible noncardiopulmonary organ
insufficiency failure
• Severe irreversible noncardiopulmonary organ • Severe coagulopathy and/or active
failure hemorrhage (relative)
• Severe coagulopathy and/or active • Poor vascular access (relative)
hemorrhage (relative) • Advanced age (relative)
• Inability to tolerate anticoagulation (relative)

Timing • Early initiation in cardiogenic shock • Early initiation (within a few days; less
• ECPR 10-15 minutes after failure of favorable after 7 days of intubation) or early
conventional CPR to regain ROSC referral to an ECMO center

Access sites Peripheral: • Femoral-femoral

• Femoral V; femoral A • Femoral-IJ
• IJ or femoral V; axillary/ innominate A • RIJ w/ dual lumen cannula
Central:
• RA V; aorta A
• LV to aorta
Special • May require LV venting in setting of severe LV • Requires adequate right ventricular function
considerations dysfunction and relatively stable hemodynamics
• North/South syndrome
• Vascular complications
• Need for distal limb perfusion

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VA ECMO for severe cardiac or combined cardiopulmonary failure/collapse

The basic VA ECMO configuration withdraws blood from a large central vein, circulates blood through
an oxygenator, and then returns the blood into a large systemic artery (Figure 2). Unloading of the
RV and pulmonic circulation results in a passive decrease in flow into the left ventricle (LV) but also
dramatically increases LV afterload when percutaneous VA ECMO is performed, as oxygenated blood
is typically returned against the physiologic direction of blood flow.13 In cases of severely decreased LV
systolic function, pulmonary edema and resultant lung injury may ensue as a consequence of increased
LV afterload. In extreme cases, failure of the aortic valve to open can set the stage for stasis and clot
formation within the LV.14

Figure 2. VA ECMO Configuration

If LV dysfunction is known or suspected, consider LV venting—either passive venting using an

intra-aortic balloon pump (IABP) or atrial septostomy or active venting using an Impella® microaxial
transvalvular pump—at the time the patient is placed on peripheral VA ECMO.13,15 Given that
pressurized blood flow enters the aorta in a retrograde fashion, usually from a femoral arterial return,
moderate to severe aortic insufficiency, aortic dissection, severe obstructive iliofemoral peripheral
arterial disease or dissection, and Leriche Syndrome (aortoiliac occlusive disease) are all regarded as
contraindications for peripheral VA ECMO.

VA ECMO, which can provide complete to super-physiologic circulatory support as well as oxygenation,
is well-suited for patients with severe cardiac failure with or without concomitant respiratory failure
inclusive of impending or resuscitated cardiopulmonary collapse. Common applications for VA ECMO
include severe cardiogenic shock with isolated LV or biventricular failure from a variety of etiologies,
failure to wean from cardiopulmonary bypass following open heart surgery, post-cardiac arrest, and
bridge to decision, transplant, or ventricular assist device (VAD).

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Mortality data varies greatly dependent on the etiology of cardiopulmonary failure and patient selection,
but the lowest short-term mortality appears to occur for patients who are post-heart transplant and
those with myocarditis, followed by patients with pulmonary embolism, heart failure, post-cardiotomy,
and post-myocardial infarction.16 The highest short-term mortality occurs in post-arrest patients,
although some studies suggest that short-term mortality in these patients is still reduced with ECMO
use compared to conventional cardiopulmonary resuscitation (CPR).17

While clinicians have several percutaneous mechanical circulatory support devices to choose from,
ECMO is typically preferred over other devices for patients with the most severe stages of cardiogenic
shock (SCAI shock stages D and E), those who require biventricular and respiratory support, or those
with evidence of worsening shock despite more conservative measures.18

When to initiate VV and VA ECMO

While the optimal timing for the initiation of ECMO is not well-defined, available evidence supports
relatively early evaluation and initiation of VV or VA ECMO in patients with a reasonable chance of
survival and meaningful recovery.

VV ECMO support should be initiated once the patient has failed an adequate trial of medical
treatment, proning, and invasive mechanical ventilation. It should not be reserved solely for use as a
salvage therapy. This typically corresponds to initiation of ECMO within a couple days after intubation
as there is diminishing benefit with further delay. Some guidelines even state that there is a relative
contraindication to starting ECMO in patients who are ventilated for more than 7 days (with plateau
pressures >30 cm H20 and FiO2 > 90%).2 This early intervention strategy has been shown to be
beneficial in the EOLIA trial and is part of the most recent ELSO guidelines.2,19 If a patient is not at an
ECMO capable facility, the care team should refer the patient to an ECMO capable facility if transfer is
reasonably safe. Early referral to an ECMO center is supported by reductions in mortality as shown by
the CESAR trial and is also part of the most recent ELSO guidelines.2,20

Timing of initiation of VA ECMO support depends on the indication for support. In the setting of
extracorporeal cardiopulmonary resuscitation (ECPR) for cardiac arrest, cannulation, by necessity, takes
place when regular CPR fails to achieve return of spontaneous circulation (ROSC) or when ROSC is
achieved but another arrest is imminent. In experienced centers offering 24-hour coverage, cannulation
may be performed at the bedside using ultrasound guidance for vascular access and echocardiographic
imaging for venous cannula advancement. Figure 3 shows bedside cannulation for VA ECMO in a
patient with SCAI stage E cardiogenic shock.

Figure 3. Bedside Cannulation

for VA ECMO
25 Fr Biomedicus vented, multistage
venous cannula in RCFV; 19 Fr Biomedicus
arterial cannula in RCFA; 8 Fr antegrade
perfusion cannula in RSFA; circuit at 3,600
rpm with 2.67 L/min flow; Impella CP® at
P-6 with 2.4 L/min flow

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Recent ELSO guidelines for ECPR recommend consideration of ECMO after 10-15 minutes of
unsuccessful conventional resuscitation efforts.21 Our institutional practice has evolved to cannulation
of patients who are believed to have had a short “down time” with bystander CPR and a presumed
reversible cause of arrest or if they are candidates for advanced heart failure options (VAD or
transplant), and are without known contraindications to ECMO (see Table 1). While early restoration of
circulation with ECMO has been shown to improve recovery, when the cause of arrest is immediately
reversible (eg, tension pneumothorax, tamponade, ventricular fibrillation responsive to cardioversion), it
may be desirable to avoid ECMO and its high-rate of complications.

For cardiogenic shock due to a variety of causes, it is generally accepted that early cannulation should
be considered. Early initiation of ECMO has the benefit of avoiding further circulatory collapse and
has been suggested to improve outcomes in selected patient populations.22 The optimal timing of
cannulation is still poorly defined in cardiogenic shock as there are few studies that specifically evaluate
timing; however, many experienced centers, including ours, choose to cannulate patients in SCAI shock
stage D or E as quickly as possible and in the context of a real-time guidance from a multidisciplinary
shock team. Further deliberation is often required for patients who are in SCAI shock stage C,
particularly if they are clinically stable.

How to initiate percutaneous ECMO: cannulation and pump

configuration strategies
When the decision has been made to cannulate a patient for ECMO, there are several logistic and
procedural considerations. First, the patient must be physically located in a care area that has the staff
(including physicians, nurses, perfusionists, and in some institutions, ECMO specialists) and supplies
to perform the cannulation as well as trained support staff to help initiate and maintain an ECMO
circuit. Second, the physician(s) performing the cannulation must consider the anatomic locations of
cannulation and the size of cannulae required to achieve adequate flow through the circuit.

Flow through an ECMO circuit is determined, in part, by cannula radius as shown by Poiseuille’s law:
Q=πPr4/8ηl where Q=flow, r=cannula radius, and l=cannula length.23 Flow rates for VV ECMO are
typically higher than VA. Possible cannulae to use for VV ECMO include two large single-lumen (21 Fr
or higher) cannulae or a single large double-lumen cannula (typically 29-31 Fr). For percutaneous VA
ECMO initiation, venous cannulae typically range from 19 to 25 Fr while arterial cannulae are usually
15 to 19 Fr. Vessel access may be obtained by cutdown or by percutaneous insertion via modified
Seldinger technique. The percutaneous approach, which is associated with lower risk of bleeding and
infection, is our preferred approach.

ECMO CANNULA TERMINOLOGY

For the purpose of consistent cannula direction nomenclature:
• The inflow cannula carries blood toward the ECMO apparatus away from the patient
• The outflow cannula carries blood away from the ECMO apparatus toward the patient

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Percutaneous VV ECMO cannulation strategies

Three major cannulation strategies exist for percutaneous VV ECMO; the first two are dual-cannulation
strategies and the third, a single-site cannulation option.
• Strategy 1: Insert an inflow cannula into the inferior vena cava (IVC) via the femoral vein and an
outflow cannula in the right atrium (RA) via the left or right internal jugular (IJ) vein (Figure 4).
• Strategy 2: Insert bilateral femoral venous cannulae with the vented, multistage inflow cannula
terminating in IVC and the endhole outflow cannula terminating in the RA.
• Strategy 3: Insert a single dual-lumen cannula via the right IJ, allowing one lumen to drain
blood from the superior vena cava (SVC) and IVC and oxygenated blood to return through
the second lumen to the RA, directed toward the tricuspid annulus under fluoroscopic and/or
echocardiographic guidance (Figure 5).

Figure 4 (video). VV ECMO via RIJ and RCFV - Dual Cannulation Approach

Figure 5 (video). VV ECMO via RIJ - Single Cannulation Approach

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Dual cannulation strategies, while capable of providing high flow rates, limit patient mobility and
effectiveness may be limited by recirculation of oxygenated blood. Thus, single-site cannulation
strategies, using specialty dual-lumen cannula and internal jugular (IJ) vein access, are preferred in
patients with suitable anatomy. It should be noted however that a single, dual-lumen cannula can carry
a higher risk of malposition given the lower margin for error in cannula placement.

The use of percutaneous right ventricular (RV) bypass with oxygenation may also be considered in
patients requiring both oxygenation as well as support for a failing RV. Typically a different type of IJ dual
lumen sidehole/endhole specialty cannula is used, draining blood from the SVC/right atrium, oxygenating
the blood, and returning it via the endhole positioned in the main pulmonary artery (Figure 6). This
configuration is often referred to as a percutaneous oxygenated right ventricular assist device (oxy-RVAD)
and can also be achieved using 2 separate venous cannulae.

Figure 6 (video). Percutaneous Oxygenated Right Ventricular Assist Device (oxy-RVAD) from RIJ Approach

VA ECMO cannulation strategies

Like VV ECMO, cannulae for VA ECMO may be placed using a variety of configurations. The most
common VA ECMO configuration is peripheral cannulation using femoral access due to its ease of
implantation. This is achieved by cannulating the femoral artery and femoral vein using contralateral
or ipsilateral vessels. The end of the arterial cannula terminates in the common iliac artery, or distal
abdominal aorta, while the venous cannula terminates at the IVC/RA junction. Placement of large-bore
femoral cannulae must be done with extreme caution as vascular complications or major bleeding can
be catastrophic in critically ill patients. Moreover, the chances of limb ischemia must be minimized by
maintaining antegrade limb perfusion, especially if a 17 Fr or larger arterial cannula is being placed.
This is achieved by obtaining antegrade arterial access into the superficial femoral artery (SFA) on the
ipsilateral side with a 6-8 Fr metal braided (kink-resistant) introducer sheath connected to the sideport
of the arterial cannula (Figure 7).

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Figure 7 (video). Femoral VA ECMO with Limb Perfusion

17 Fr arterial, 25 Fr vented multistage venous cannulae, and 6 Fr antegrade limb perfusion; video is representative of VA ECMO with Impella
placement

Alternative sites may be used for the inflow cannula including placement into the SVC, IVC, or RA
via the IJ or subclavian veins. Other sites may also be used for arterial outflow cannulae including the
axillary, subclavian, or innominate arteries, although placement for this type of access may require
artery-to-graft anastomosis and placement in an operating suite.

Central VA ECMO cannulation is possible using an open approach to directly cannulate the right atrium
for a venous inflow cannula and aorta for an arterial outflow cannula. This strategy is the most invasive
and time consuming and requires greater patient stability as well as cannulation in an operating suite.

QUICK READ SUMMARY

✓ Extracorporeal membrane oxygenation may be used to provide full cardiopulmonary support

in the VA configuration or full respiratory support in the VV configuration.

✓ There are numerous specific indications for VV and VA ECMO, but cannulation is typically
reserved for patients with severe cardiac or respiratory failure.

✓ While each cannulation strategy has benefits and drawbacks, peripheral access with two
cannulae (and antegrade limb perfusion) is often the preferred approach due to its relative
ease and the speed at which it can be performed.

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versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised
controlled trial. Lancet. 2009;374(9698):1351-63. doi:10.1016/S0140-6736(09)61069-2

21. Richardson ASC, Tonna JE, Nanjayya V, et al. Extracorporeal cardiopulmonary resuscitation in adults. Interim guideline
consensus statement from the Extracorporeal Life Support Organization. ASAIO J. 2021;67(3):221-8. doi:10.1097/
MAT.0000000000001344

22. Choi KH, Yang JH, Hong D, et al. Optimal timing of venoarterial-extracorporeal membrane oxygenation in acute myocardial
infarction patients suffering from refractory cardiogenic shock. Circ J. 2020;84(9):1502-10. doi:10.1253/[Link]-20-0259

23. Rao P, Khalpey Z, Smith R, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and
cardiac arrest: cardinal considerations for initiation and management. Circ Heart Fail. 2018;11(9). doi:10.1161/
CIRCHEARTFAILURE.118.004905

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VA ECMO

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17.1
Introduction to
VA ECMO
Siddharth Sarangi, MD
Surgical Director, ECMO
Cardiac Surgeon
St Francis Medical Center
Clinical Assistant Professor
Dept of Surgery
University of Illinois College of Medicine
Peoria, IL
[Link]@[Link]

John M. Lasala, MD, PhD, FACC, FSCAI

Professor of Medicine
Director, Structural Heart Disease
Washington University School of Medicine
St Louis, MO
jlasala@[Link]

Akinobu Itoh, MD, PhD

Surgical Director
Heart Transplantation and Mechanical and Circulatory Support
Associate Surgeon
Division of Thoracic and Cardiac Surgery
Brigham and Women’s Hospital
Boston, MA
aitoh@[Link]

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Introduction to VA ECMO
Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is a form of temporary mechanical
circulatory support (MCS) and simultaneous extracorporeal gas exchange for acute cardiorespiratory
failure. The initiation of VA ECMO has emerged as a salvage intervention in patients with cardiogenic
shock, even with cardiac arrest refractory to standard medical therapies. Analogous to veno-venous
ECMO (VV ECMO) for acute respiratory failure, VA ECMO provides circulatory support to reverse end-
organ dysfunction, allow time for other treatments to promote recovery, or may serve as a bridge to a
more durable mechanical solution in the setting of acute or acute on chronic cardiopulmonary failure.1

Accepted indications for VA ECMO include patients presenting in cardiogenic shock due to acute
myocardial infarction (AMI), myocarditis, intoxication with cardiotoxic drugs, end-stage dilated
cardiomyopathy, postpartum cardiomyopathy, post-cardiotomy, or post-transplantation, refractory
to conventional treatments. Emerging indications include massive pulmonary embolism (PE) either
as single therapy or coupled with thrombectomy, sepsis associated cardiomyopathy, and stress
cardiomyopathy. Most of these patients receive the treatment as salvage therapy after having developed
signs of refractory cardiogenic shock with multiple organ failure. In these situations, VA ECMO is used
as a bridge to decision making if the patient survives the initial cardiogenic shock phase. For patients
with potentially reversible heart failure (eg, myocarditis, myocardial stunning post-infarction), VA ECMO
may also be used as a bridge to cardiac recovery.

With the improvement of biomaterials and technologies, VA ECMO may now be utilized for several days
or even weeks, as a bridge to “decision” that includes recovery, durable long-term MCS, or withdrawal
in case of futility. Compared to percutaneous microaxial circulatory support devices, VA ECMO allows
rapid improvement in oxygenation and is the only short-term therapy suitable for patients with severe
biventricular failure.2

Setup and configuration

Figure 1. VA ECMO Cannulation Techniques

(A) Femoral-femoral; (B) central aortic and right atrial; (C) axillary artery and internal jugular vein.

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All VA ECMO circuits consist of a venous cannula, a pump, an oxygenator, and an arterial cannula. For
VA ECMO one cannula is inserted for draining blood from the venous system (inflow, drainage cannula)
to the ECMO circuit, and the other cannula for returning oxygenated blood to the arterial system
(outflow, return cannula). During VA ECMO oxygenated blood is returned into systemic circulation thus
fulfilling two functions: gas exchange and circulatory support. The distinct feature of peripheral VA
ECMO is that oxygenated blood is delivered to the aorta via the femoral artery in retrograde fashion and
competes with native antegrade circulation generated by the heart.

A B

Figure 2. ECMO Circuit Parts

(A) Controller with monitor; (B) Centrifugal pump with oxygenator; (C) Blender with controller; (D) Post oxygenator gas sample collection 3-way
with flow probe; (E) VA tubing set; (F) Dialysis pigtail setup.

Central cannulation
Central ECMO usually involves sternotomy and direct surgical cannulation of the right atrium and aorta.
The main advantages of central ECMO cannulation are:
• Large cannulae can provide optimal venous drainage and reliable arterial return to the proximal
aorta in antegrade fashion
• Access to the right superior pulmonary vein or the LV apex for left ventricular decompression if
necessary

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The adequate size of the cannula is defined by body surface area and the calculated ECMO flow
necessary to achieve metabolic requirements of the patient. Aortic cannulation and standard venous
cannulation for full cardiopulmonary bypass typically use 18-24 Fr cannulae. The cannulae are
secured in position to prevent any bleeding from the cannulation site or displacement during ICU care.
The venous cannulation site should be well reinforced to prevent air suction to the circuit. Multilevel
measures (eg, purse string, snuggers, Ioban™) are employed to secure the cannulae to the right atrium
and chest wall.

Central ECMO cannulation can be used as a first-choice modality for cardiorespiratory support (post-
cardiotomy shock being the most typical indication) or as an upgrade from peripheral configuration
when it does not achieve adequate flows to provide good end-organ function or overcome problems
inherent to peripheral ECMO like LV distention and differential hypoxia (Harlequin syndrome), or for
patients with severe peripheral arterial disease.

A primary disadvantage of central cannulation is its invasive nature including sternotomy related issues, such
as bleeding and infection, aortic dissection, and inability to mobilize the patient if the chest was left open.3

Peripheral cannulation
The Society for Cardiovascular Angiography and Interventions (SCAI) classified cardiogenic shock into 5
stages (Figure 3). VA ECMO can be indicated in patients with stages C, D, or E cardiogenic shock.4

STAGE E: A patient with refractory shock or actual/impending

E
circulatory collapse.
EXTREMIS
STAGE D: A patient who has clinical evidence of shock that

D
worsens or fails to improve despite escalation of therapy.
DETERIORATING
STAGE C: A patient who has clinical evidence of

C
hypoperfusion that initially requires pharmacologic or
CLASSIC mechanical support. Hypotension is usually present.

STAGE B: A patient who has clinical evidence of

B
hemodynamic instability (including hypotension,
BEGINNING tachycardia, or abnormal systemic
hemodynamics) without hypoperfusion.

STAGE A: A patient who is hemodynamically

A
stable and is NOT experiencing signs or
AT RISK symptoms of cardiogenic shock, but is at
risk for its development (ie, large AMI or
decompensated heart failure).

STAGE
Figure 3. SCAI Classification of Stages of Cardiogenic Shock4

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Major advantages of percutaneous peripheral cannulation are:

• Rapid initiation at the bedside under ultrasound guidance
• Avoidance of sternotomy for central approach

Potential pitfalls of this method are critical limb ischemia and differential hypoxia. Limb ischemia can be
averted by the use of distal limb perfusion catheters placed in the superficial femoral artery (Figure 4).
Limb perfusion should be monitored frequently by gross observation and Doppler ultrasound.

Figure 4. Peripheral VA ECMO

Femoral-femoral cannulation with distal perfusion catheter in superficial femoral artery.

Cannulation techniques
Peripheral configuration uses the standard venous access either via the femoral or internal jugular (IJ)
vein. The arterial return can be achieved on the axillary or femoral arteries by percutaneous technique
or surgical cutdown employing an end-to-side Dacron graft or direct insertion of cannula. The venous
drainage is provided by the cannula (19–25 Fr) in the femoral or IJ vein with the tip positioned in the
right atrium. Flow rates can be limited by the size of both the venous drainage cannula and the arterial
cannula. The common femoral and axillary arteries are the most common arteries used for arterial return
in adults. Axillary cannulation provides easier ambulation, antegrade flow, potentially higher upper body
saturation (including the brain) but requires a surgical approach to establish vascular access and has a
higher risk of cannulation site bleeding.5

The size of the cannula depends on the caliber of the target vessels. The following formula can be used
to select the diameter (D) of the cannula in French (Fr) gauge system: Fr = D (mm) × 3.14

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Table 1. Cannula Sizes for Desired Flow

EXTERNAL
FLOW (mL/min) SIZE (Fr)
DIAMETER (mm)

0-350 8 2.66

350-600 10 3.33

600-1000 12 4

1000-1400 14 4.66

750-1000 15 5

1000-1500 17 5.66

1500-2300 19 6.33

2000-2500 21 7

2500-5000 23 7.66

3000-3600 25 8.33

3600-4500 27 9

>4500 29 9.66

Initiation of peripheral VA ECMO

The following steps are used to initiate VA ECMO with peripheral cannulation.
1. Use long venous multistage drainage cannula – 60 cm long and 25 Fr.
2. Use return arterial cannula 20-25 cm long and 15-21 Fr.
3. Use 6-8 Fr wire reinforced sheath for distal limb perfusion.
4. Perfusionist primes circuit.
5. Once placed under ultrasound guidance, give bolus of IV heparin (dosed to maintain ACT>200).
6. Ensure O2 line is connected to oxygenator and initiate 100% O2 flows >2 liters per minute.
7. Ensure circuit is connected to the cannula with tubing connectors without any air in the circuit.
8. Gradually increase flow.
9. Check arterial oxygen saturation (blood gas) and circuit post oxygenator gas.
10. Secure cannulae after insertion.

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Conversion to VAV ECMO

Figure 5. Harlequin Syndrome or North-South Syndrome

Blood travels in a retrograde direction with peripheral VA ECMO support and there is therefore a
watershed area within the aorta where oxygenated blood from the ECMO circuit meets blood from the
LV which may be deoxygenated from impaired pulmonary gas exchange in the setting of cardiogenic
shock or pulmonary edema (Figure 5). If this watershed region is distal to the left subclavian artery, the
patient may be at risk for significant hypoxemia in the upper extremities, heart, and brain. Monitoring of
cerebral oxygenation can be done with serial blood gas from the upper extremities. This phenomenon
is known as Harlequin syndrome or North-South syndrome.6 Central cannulation to the proximal aorta
or axillary artery can solve this problem. Adding another cannula to the arterial return of the peripheral
VA circuit, preferably in the internal jugular vein, the so called veno-arterio-venous (VAV) or veno-
veno-arterial (VVA) ECMO configuration, may also be beneficial. VAV ECMO increases the amount of
oxygenated blood in the LV.7

LV unloading in VA ECMO
After initiation of VA ECMO, LV end-diastolic pressure can be increased if the LV ejection is limited due
to myocardial damage and the aortic valve is hardly opening. On echocardiography, a “smoke sign” in
the left atrium, ventricle, or aortic root indicates blood stasis, which may result in pulmonary edema
and thrombus formation. In these circumstances, a few strategies should be considered within the first
several hours of VA ECMO initiation to reduce the LV diastolic pressure and myocardial oxygen demand.
This also helps to mitigate pulmonary edema and facilitate myocardial recovery.

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For patients with residual LV function, one can attempt reducing VA ECMO flow and pharmacologic
afterload reduction to enhance LV ejection. This partial ECMO technique is useful in cases of prosthetic
valve replacement of the left side valves or post heart transplant primary graft failure.8 Intra-aortic
balloon pumps are often used to enhance LV ejection; however, their efficacy can be limited due
to their indirect characteristics. Direct LV venting methods include transcatheter atrial septostomy,
surgical direct LA or LV venting through the right superior pulmonary vein or LV apex, and Impella
devices (percutaneous Impella CP® or surgically implanted Impella 5.5®).9 Prompt deployment of the
LV unloading strategy is desired to enhance myocardial recovery or increase the possibility of being
bridged to the next steps, such as durable LVAD or heart transplant if indicated.

CRRT circuit in ECMO

Continuous renal replacement therapy (CRRT) can be initiated with the ECMO circuit by connecting
the circuit to the venous and arterial limbs. The inherent advantages over separate insertion of a
hemodialysis (HD) line include the need to access fewer blood vessels and a lower risk of infectious
complications. Disadvantages include potential air embolism in the ECMO circuit and the potential
need to change alarm parameters as changing ECMO flows may initiate high or low flow alarms in the
CRRT machine. The duration of CRRT on ECMO patients has been similar to conventional HD access,
nevertheless, it seems to be an extremely feasible option in this subgroup of patients.10

QUICK READ SUMMARY

✓ VA ECMO is a form of temporary mechanical circulatory support and simultaneous

extracorporeal gas exchange for acute cardiorespiratory failure to help reverse end-organ
dysfunction and allow time for other treatments to promote recovery or bridge to decision
making or more durable solutions.

✓ Central ECMO cannulation usually involves sternotomy and direct surgical cannulation of the
aorta and right atrium. It can be a first-choice modality or an upgrade if peripheral cannulation
does not achieve adequate flows.

✓ Peripheral ECMO cannulation can be rapidly initiated at bedside without need for sternotomy
but can be associated with critical limb ischemia and differential hypoxia.

✓ Peripheral VA ECMO may lead to Harlequin or North-South syndrome, necessitating VAV

ECMO to increase oxygenated blood in the LV.

✓ CRRT with the ECMO circuit seems to be an extremely feasible option in patients requiring
hemodialysis.

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References
1. Rao P, Khalpey Z, Smith R, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac
arrest. Circ Heart Fail. 2018;11(9):e004905.

2. Pineton de Chambrun M, Bréchot N, Combes A. Venoarterial extracorporeal membrane oxygenation in cardiogenic

shock: indications, mode of operation, and current evidence. Curr Opin Crit Care. 2019;25(4):397-402.

3. Pavlushko E, Berman M, & Valchanov K. Cannulation techniques for extracorporeal life support. Ann Transl Med.
2017;5(4):70.

4. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic
shock. Catheter Cardiovasc Interv. 2019;94(1):29-37.

5. Yang C, Peng G, Xu X, et. al. The technique of intraoperative axillary artery cannulation for extracorporeal membrane
oxygenation in lung transplantation. J Thorac Dis. 2019;11(7):2939-44.

6. Hoeper MM, Tudorache I, Kühn C, et al. Extracorporeal membrane oxygenation watershed. Circulation.
2014;130(10):864-5.

7. Cakici M, Gumus F, Ozcinar E, et al. Controlled flow diversion in hybrid venoarterial-venous extracorporeal membrane
oxygenation. Interact Cardiovasc Thorac Surg. 2018;26(1):112-8.

8. Guo A, Kotkar K, Schilling J, et al. Improvements in extracorporeal membrane oxygenation for primary graft failure
after heart transplant. Annals Thorac Surg. 2023;115(3):751-7.

9. Lorusso R, Meani P, Raffa GM, Kowalewski M. Extracorporeal membrane oxygenation and left ventricular unloading:
What is the evidence? JTCVS Tech. 2022;101-14.

10. Schetz M, Legrand M. CRRT and ECMO: Dialysis catheter or connection to the ECMO circuit? Anaesth Crit Care Pain
Med. 2018;37(6):519-20.

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17.2
Common Access
Strategies for
VA ECMO
Rami Zein, DO Theodore L. Schreiber, MD, FSCAI
Interventional Cardiologist Chief of Cardiology
Ascension St. John Hospital Ascension Macomb Hospital
Detroit, Michigan Detroit, Michigan
Rzein10@[Link]
@RamiZeinDO Amir Kaki, MD, FACC, FSCAI
Director of Mechanical Circulatory Support
Chirdeep Patel, MD, FSCAI Ascension St. John Hospital
Interventional Cardiologist Detroit, Michigan
Ascension St. John Hospital
Detroit, Michigan

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Introduction

“Cardiogenic shock and large bore access is a nasty business.”

– Theodore Schreiber, MD

Venoarterial extracorporeal membrane oxygenation (VA ECMO) cannulation is a complex procedure that
requires vascular expertise. Multiple sites may be necessary for cannulation, as shown in Figure 1. To
maximize outcomes, operators must be familiar with multiple modalities for optimal large-bore access at
different locations. In this chapter, we review common access strategies for VA ECMO cannulation.

Figure 1. VA ECMO Circuit in COVID-positive Patient with Myocarditis

Patient upgraded to VA ECMO following worsening pulmonary function and worsening hemodynamics. 29 Fr Protek Duo™ in right IJ used as
drainage cannula where both lines “Y” together (red arrow) to form single drainage line (yellow arrow) into oxygenator. 17 Fr arterial return
cannula (blue arrow). 26 Fr Gore Dryseal™ sheath in right common femoral vein used as transcaval access for a microaxial flow pump.

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Cannula selection
Venoarterial extracorporeal membrane oxygenation (VA ECMO) requires large-bore access in both
the venous and arterial systems to maintain tissue perfusion.1 Percutaneous cannulation strategies
should be able to provide flow rates above 2.0 L/min/m2 and optimally close to 2.5 L/min/m2.1 Adequate
flows sustained by extracorporeal support are necessary for reduction in anaerobic metabolism. Rapid
clearance of lactate during the initial hours of extracorporeal life support (ECLS) has been associated
with decreased mortality.2,3 ECMO cannulation can carry a high risk of vascular complications,
therefore thoughtful preprocedural planning is required. The size and site of cannulation are important
considerations to provide the necessary balance between perfusion and safety.4

For VA ECMO, one should choose cannulas based on body surface area (BSA),5 as shown in Table 1, or
cannulas that can provide a cardiac index of >2.4 L/min/m2.1,6 Flow rates are more often limited by the
size of the inflow (venous) drainage cannulas than the outflow (arterial) cannulas.1 The venous drainage
is provided by a cannula (15-29 Fr) in the femoral or internal jugular vein with the tip positioned distal to
the right atrium. The arterial return is provided by a cannula (15-19 Fr) in the femoral or axillary arteries.

Table 1. Cannula Size Per BSA (Adapted from Lamelas et al.)5

CANNULATION SITE BSA CANNULA SIZE

<1.6 15 Fr
Femoral artery 1.7 -2.1 17 Fr
>2.1 19 Fr

A <1.6 B 15 Fr
Axillary artery 1.7-2.1 15 Fr
>2.1 17 Fr

Femoral or internal jugular vein Regardless of BSA 25 Fr

Table 2 highlights the most commonly used peripheral cannulas. The size of the cannula depends on
the caliber of the vessels and flows required to achieve adequate circulatory support.7 A 25 Fr venous
cannula and a 17 Fr arterial cannula are adequate for most adults.

Table 2. Cannula Sizes and Lengths Per Manufacturer11,12

MANUFACTURER SIZE [FR] LENGTH, CM

Arterial [15-23] 15 & 23

Maquet
Venous [19-29] 38 & 55

Arterial [15-25] 18
Medtronic
Venous [15-29] 50 & 60

Arterial [15 & 17] 17

LivaNova
Venous [24] 62

Table 3 exhibits the minimal recommended vessel size for peripheral cannulation. Some patients,
particularly smaller women, may not accommodate these sizes.5 In these cases cannulas should be
chosen based on ultrasound measurements of the artery and the desired flow rate.8

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Table 3. Minimum Vessel Size Per Cannula

CANNULA SIZE MINIMUM ARTERIAL DIAMETER

15 Fr 5 mm

17 Fr 5.5 mm

19 Fr 6 mm

Arterial size assessment

The assessment of arterial caliber is necessary prior to cannulation. If the patient has arterial access, an
angiogram can be used to quantify the vessel size and anatomy. For enhanced safety and efficiency, use
vascular ultrasound in tandem with angiography for evaluation.7

Venous cannulation
In patients who are undergoing VA ECMO, the venous cannula drains blood to the oxygenator/pump
where gas exchange occurs. This blood is then returned via the arterial cannula. The 2 most common
locations for venous cannulation are the femoral vein and internal jugular (IJ) vein.

Femoral vein access

Box 1 presents step-by-step instructions for femoral vein canulation.

BOX 1. FEMORAL VEIN ACCESS

1. Prep patient by sterilizing the groin site and exposing the site for common femoral vein puncture.
2. Administer local anesthesia and advance a micropuncture needle toward the access point
using ultrasound imaging guidance. Visualization of the needle tip into the vessel is important.
3. Place a 6 Fr sheath via Seldinger technique.
4. Advance a 0.035 inch stiff wire (eg, Lunderquist™, Amplatz Super Stiff™ or Supra Core™)
into the SVC and make an incision over the wire to help with further dilations.
5. Sequentially dilate the venous site in a corkscrew fashion (eg, 12, 16, 20, & 24 Fr dilators)
over the stiff wire of choice before introducing of the cannula.
6. Maintain the freedom of the wire and avoid kinking or bending the wire as this may damage
the vessel.
7. Advance the venous cannula over the stiff wire until the distal ports are in the SVC, the middle
ports are in the right atrium, and the proximal ports in the IVC.
8. Remove the dilator and the wire and clamp the open end of the cannula.
9. Use a bulb syringe to flush the tubing and cannula to ensure that no air is introduced.
10. Connect the cannula to the tubing.

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Internal jugular vein access

Figure 2 illustrates IJ vein cannulation and Box 2 describes the steps for IJ venous cannulation.

Figure 2. Internal Jugular Vein Cannulation

Patient has Maquet 25 Fr-38 cm IJ venous cannula sutured in place.

BOX 2. IJ VEIN ACCESS

1. Prep patient by sterilizing the right neck and exposing the site for IJ puncture.
2. Administer local anesthesia and advance a micropuncture needle toward the access point
using ultrasound imaging guidance. It is important to visualize the carotid artery in relation
to the IJ vein. Visualization of the needle tip into the IJ vein is important to ensure venous, not
arterial, access.
3. Place a 6 Fr sheath via Seldinger technique.
4. Advance a 0.035 inch stiff wire (eg, Lunderquist™, Amplatz Super Stiff™ or Supra Core™)
into the inferior vena cava (IVC) and make an incision over the wire to help with further
dilations.
5. Sequentially dilate the venous site in a corkscrew fashion (eg, 12, 16, 20, & 24 Fr dilators)
over the stiff wire of choice before introducing the cannula.
6. Maintain the freedom of the wire and avoid kinking or bending the wire as this may damage
the vessel.
7. Advance the venous cannula over the stiff wire until the distal ports are in the proximal IVC,
the middle ports in the right atrium, and the proximal ports in the superior vena cava (SVC).
8. Remove the dilator and the wire, and clamp the open end of the cannula.
9. Use a bulb syringe to flush the tubing and cannula to ensure that no air is introduced.
10. Connect the cannula to the tubing.

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Arterial cannulation
The 2 most common locations for arterial cannulation with VA ECMO are the femoral artery and the
axillary artery.

Femoral artery access

The femoral artery is the most commonly used site for large-bore access (see Figures 3 and 4). With the
rise of percutaneous left ventricular assist device insertion and removal, large-bore access has become
commonplace in most large cath labs. Box 3 outlines the steps for femoral arterial cannulation.

Figure 3. Femoral Artery Cannulation

Figure 4. Femoral Artery Access for VA ECMO and

Microxial Flow Pump
This configuration for VA ECMO shows the importance of an IJ-Fem cannulation.
Transcaval access obtained using 26 Fr Gore DrySeal™ sheath (green arrow). Microaxial
flow pump inserted into sheath and maintained as LV vent. 6 Fr sheath (red arrow) with
side port connected to antegrade sheath via external bypass (blue arrow). 17 Fr return
cannula (yellow arrow).

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BOX 3. FEMORAL ARTERY ACCESS

1. Prep the patient by sterilizing the groin site and exposing the site for common femoral artery
puncture.
2. Placement of the arterial and venous cannulas on opposite sides may be preferred due to their
close proximity.8 While both arterial and venous cannulas can be inserted in the same side,
decannulation may be difficult.
3. If the femoral artery caliber is small and there is a concern for leg ischemia, placement of an
antegrade catheter, as described in chapter 17.4, may be helpful.
4. After administration of local anesthesia, advance a micropuncture needle toward the access
point using ultrasound imaging guidance. Visualization of the needle tip into the vessel is
important.
5. Place a 6 Fr sheath via Seldinger technique.
6. Using a pre-close technique, deploy 2 suture-mediated closure devices (Perclose ProGlide,
Abbott) at the 10 o’clock and 2 o’clock positions and leave uncinched.
7. Advance a long sheath to the aorta to traverse the iliac vessels.
8. Advance a 0.035 inch stiff wire (eg, Lunderquist™, Amplatz Super Stiff™ or Supra Core™)
into the aorta. It is important to make an incision over the wire to help with further dilations.
9. Sequentially dilate the arterial site in a corkscrew fashion (eg, 8, 12 and 16 Fr dilators) over
the stiff wire of choice before introducing the cannula.
10. Maintain the freedom of the wire and avoid kinking or bending the wire as this may damage
the vessel.
11. Advance the arterial cannula to position. The outflow should be in the common iliac artery or
the distal aorta.
12. Remove the dilator and the wire, and clamp the open end of the cannula.
13. Use a bulb syringe to flush the tubing and cannula to ensure no air is introduced.
14. Connect the cannula to the tubing.

Axillary artery access

For patients with severe PAD or those with small caliber iliac and/or femoral arteries (<5 mm), the
axillary artery is a viable alternative for arterial cannulation. Similarly, patients with heavy calcification
or severe tortuosity should be considered for axillary cannulation. Axillary access also allows for greater
patient mobility, which is an important advantage.9 As shown in Figures 5 and 6, the right axillary is
preferred due to the anterograde flow into the aorta. Box 4 outlines axillary cannulation.

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Figure 5. Axillary Artery Cannulation

Figure 6. Axillary Cannulation in Patient with Severe

PAD
Patient had severe PAD prohibiting femoral cannulation. Insertion site
of the cannula (blue arrow). Bypass circuit (yellow arrow) attached to
right radial artery (not shown).

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BOX 4. AXILLARY ARTERY ACCESS

1. Place the patient in supine position with the arm abducted at 90 degrees away from the body
as you prep the patient.
2. Place a 5 Fr sheath in the ipsilateral radial artery. To evaluate for suitable vessel anatomy,
advance an angiographic catheter (eg, Multipurpose) from the ipsilateral radial or the femoral
artery to selectively engage the left subclavian artery or innominate artery.
3. Obtain an angiogram or fluoroscopic subtraction image of the subclavian and axillary arteries
for “roadmapping.”
4. Angiographic assessment of the axillary artery and all branches is an important step to define
the access point that is lateral to the thoracoacromial artery and medial to the circumflex
humeral artery, as shown in Figure 7.
A Thoracoacromial B C
Circumflex humeral

Subscapular

Figure 7. Angiography Guided Axillary Access (used with permission)10

(A) Assessment and identification of the axillary artery branches is important to precisely define the access point that is lateral to the
thoracoacromial artery and medial to the circumflex humeral and subscapular arteries (ie, the “sweet spot” indicated by the dotted green
box); (B) A JR4 or Multipurpose catheter is used to engage the innominate artery to perform contrast angiography to identify the axillary
artery anatomy; (C) Introduction of the large sheath in the right axillary artery over the stiff wire.10

5. After administration of local anesthesia, advance a micropuncture needle at a shallow angle

(30-45 degrees from skin) toward the access point using angiographic or ultrasound guidance.
6. Place a 4 Fr microcatheter sheath and perform an access site angiogram to confirm the
appropriate access point.
7. Using a pre-close technique, deploy 2 suture-mediated closure devices (Perclose ProGlide,
Abbott) at the 10 o’clock and 2 o’clock positions and leave uncinched.
8. Advance a long sheath to the aorta to traverse the subclavian artery.
9. Advance a 0.035 inch stiff wire (eg, Lunderquist™, Amplatz Super Stiff™ or Supra Core™) into
the aorta. It is important to make an incision over the wire to help with further dilations.
10. Sequentially dilate the arteriotomy prior to introducing the large bore sheath over the stiff
0.035 inch wire of choice.
11. Advance the arterial cannula to the tapered portion. It is important not to advance past the
tapered portion as this can overdilate the site and cause bleeding.
12. Remove the dilator and the wire, and clamp the open end of the cannula.
13. Use a bulb syringe to flush the tubing and cannula to ensure no air is introduced.
14. Connect the cannula to the tubing.

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QUICK READ SUMMARY

✓ VA ECMO may require multiple cannulation sites and operators must be familiar with
multiple large bore access techniques to maximize outcomes.

✓ The femoral and internal jugular veins are the most common locations for inflow drainage
cannulas for VA ECMO.

✓ The femoral and axillary arteries are the most common locations for outflow cannulas for VA
ECMO.

✓ Taking careful measures at the time of access ensures a safe and successful decannulation
when the patient recovers.

References
1. Extracorporeal Life Support Organization. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support.
Extracorpor Life Support Organ. 2017;1-26. [Link]

2. Ganushchak YM, Kurniawati ER, Maessen JG, Weerwind PW. Peripheral cannulae selection for
veno-arterial extracorporeal life support: a paradox. Perfus (United Kingdom). 2020;35(4):331-7.
doi:10.1177/0267659119885586

3. Pavlushkov E, Berman M, Valchanov K. Cannulation techniques for extracorporeal life support. Ann Transl Med.
2017;5(4):70. doi:10.21037/atm.2016.11.47

4. Murphy DA, Hockings LE, Andrews RK, et al. Extracorporeal membrane oxygenation-hemostatic complications.
Transfus Med Rev. 2015;29(2):90-101. doi:10.1016/[Link].2014.12.001

5. Lamelas J, Aberle C, Macias AE, Alnajar A. Cannulation strategies for minimally invasive cardiac surgery. Innov
Technol Tech Cardiothorac Vasc Surg. 2020;15(3):261-9. doi:10.1177/1556984520911917

6. Jayaraman A, Cormican D, Shah P, Ramakrishna H. Cannulation strategies in adult veno-arterial and veno-venous
extracorporeal membrane oxygenation: Techniques, limitations, and special considerations. Ann Card Anaesth.
2017;20(5):S11-S18. doi:10.4103/0971-9784.197791

7. Grasselli G, Pesenti A, Marcolin R, et al. Percutaneous vascular cannulation for extracorporeal life support (ECLS): a
modified technique. Int J Artif Organs. 2010;33(8):553-7. doi:10.1177/039139881003300806

8. Ramaiah C, Babu A. ECMO Cannulation Techniques. In: Extracorporeal Membrane Oxygenation: Advances in Therapy.
InTech; 2016. doi:10.5772/64338

9. Peripheral Matters | Axillary Artery: Alternate Access for Large Bore Interventional Procedures - American College of
Cardiology. Accessed May 4, 2021. [Link]
matters-axillary-artery-alternate-access-for-large-bore-interventional-procedures

10. Kaki A, Alraies C. Large-bore access site management: state-of-the art closure techniques for large bore access.
Cardiac Interv Today. 13(4):59-66.

11. HLS Cannulae Solutions from tip-to-toe. Getinge brochure. Accessed May 5, 2021. [Link]
hospital/documents/english/hls_cannulae_brochure-en-non_us_japan.pdf

12. Find Your Ideal Bio-Medicus™ Nextgen Cannulae. Medtronic brochure. Accessed May 5, 2021. [Link]
com/content/dam/medtronic-com/products/cardiovascular/cannulae/soft-flow-arterial-cannulae/documents/Bio-
Medicus_NextGen_Brochure_1.pdf

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17.3
LAVA ECMO
Marvin Eng, MD, FACC, FSCAI
Medical Director, Structural Heart Program
Banner University Medical Center- Phoenix
Phoenix, AZ
[Link]@[Link]
@EngmdMarvin

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Introduction
Cardiogenic shock (CS) complicates 5-10% of cases of myocardial infarction (MI) and is associated with a
30-day mortality as high as 60%.1,2 Several mechanical circulatory support (MCS) devices are used for CS
and more recently venoarterial extracorporeal membrane oxygenation (VA ECMO) has been utilized more
frequently. A disadvantage of peripheral VA ECMO is the lack of left ventricular (LV) unloading. VA ECMO
pressurizes the arterial system thereby increasing LV afterload, end-diastolic filling pressure, wall stress, and
myocardial oxygen demand.3 One method of indirectly unloading the left ventricle is with a left atrial cannula.
Left atrial venous arterial (LAVA) ECMO utilizes a single cannula (RAP Femoral Venous 22 Fr Cannula,
LivaNova) with a long fenestrated segment (15 cm), decompressing the left and right atria simultaneously.
Inserted via femoral venous access, LAVA ECMO requires transseptal puncture and provides biventricular
support with a single large bore arterial access.

AORTA

PULMONARY TRUNK

LEFT
RIGHT ATRIUM
ATRIUM
LEFT
VENTRICLE

RIGHT
VENTRICLE

Figure 1. Transseptal Configuration for LAVA ECMO (Permissions granted from ASAIO)
A long cannula that is fenestrated for a length of 15 cm is inserted across the atrial septum from the right femoral vein. This cannula draws blood
from the left and right atrium simultaneously, takes it through the ECMO circuit to be oxygenated, and then returns the blood to the femoral artery.

Technique
LAVA ECMO requires the equipment recommended in Table 1, although alternative pieces of equipment
can be substituted for several of the recommended items.

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Table 1. Recommended Equipment for LAVA ECMO

VASCULAR ACCESS TRANSSEPTAL ACCESS ECMO CANNULATION

• Micropuncture kit • SL-1 sheath (Abbott Vascular, • 10x40 mm peripheral balloon

• Serial large bore dilators Santa Clara, CA) • Amplatz super stiff wires (Cook,
• 6 Fr 11 cm Arrow sheath • BRK-1 XS (Abbott Vascular, Santa Bloomington, IN)
(antegrade perfusion sheath) Clara, CA) • 15-21 Fr arterial cannula
• Fluoroscopy, transesophageal or • Vascular clamps
intracardiac echo • Male-male connector/tubing
• RAP Femoral Venous Cannula
(LivaNova)

The following steps provide an overview of the LAVA ECMO technique.

1. Establish femoral venous and arterial access in the routine fashion.
2. Direct a transseptal catheter and needle against the interatrial septum and complete transseptal
access (Figure 2). Use your discretion regarding performing transseptal puncture with or without
echocardiographic imaging (transesophageal or intracardiac echocardiography).

A B

*
A B

C D
LA

RA AoV

RV

AoV= aortic valve, LA= left atrium, RA= right atrium, RV=right ventricle

Figure 2. Transseptal Access and Insertion of RAP Femoral Venous Cannula Across Atrial Septum for Left and
Right Sided Unloading for ECMO (Permissions granted from ASAIO)
A) Intracardiac echocardiographic (circle) guided transseptal puncture using a transseptal crossing system (arrow). 0.014" Grandslam guidewire
(*) provides support for catheter traversal of the interatrial septum in patient supported by an Impella CP®. B) Balloon dilation of the interatrial
septum using an 8 x 40 mm Armada peripheral balloon (dagger) (Abbott Vascular, Santa Clara, CA) to facilitate cannula traversal. C) Insertion of
a 24 Fr RAP Femoral Venous Cannula (double dagger) across the atrial septum. D) Transesophageal echocardiography visualizing the transseptal
cannula (double arrow) withdrawing blood from both the left and right atrium simultaneously.

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3. Once across the atrial septum, exchange the transseptal catheter and needle for the RAP Femoral
Venous Cannula using a stiff wire, being careful to stop in the middle of the atrium. We caution
operators that the dilator accompanying the cannula is not radiopaque, therefore exchanging the
RAP Femoral Venous Cannula should be done carefully (Figure 2).
4. Exchange the arterial sheath for an arterial cannula. Choose an arterial cannula size (15-19 Fr)
commensurate with the flow needed to perfuse the patient. Routine clinical practice in our center
consists of placing an antegrade sheath ipsilateral to the large bore arterial cannula to maintain limb
perfusion (Figure 3).
5. Place a right radial arterial line for invasive pressure monitoring and to check for “North-South” syndrome.
Consider arterial pre-close with 2 ProGlide devices. Following vascular access, administer
anticoagulation to achieve an activated clotting time (ACT) >300 seconds.

6 Fr antegrade
reperfusion sheath
(LSFA)

19 Fr arterial
cannula (LCFA)

14 Fr sheath for
ICE (LCFV)

22 Fr venous
cannula (RCFV)
Fr=French, ICE= intracardiac echocardiography, LSFA= left superficial femoral artery,
LCFA=left common femoral artery, LCFV= left common femoral vein, RCFV= right common femoral vein

Figure 3. Cannula Configuration in Patient

The yellow arrows denote flow from the arterial cannula traveling to the antegrade 6 Fr sheath to perfuse the left lower limb.

Discussion
The merit of using LAVA ECMO in patients with biventricular dysfunction is rapid decompression of
the central venous and pulmonary pressures. In one representative case, LAVA ECMO caused rapid
lowering of the right atrial and pulmonary pressures (Figure 4) while improving perfusion in a 78-year-old
cardiogenic shock patient with concomitant mitral and aortic regurgitation. This is one of several examples
where rapid right atrial and pulmonary artery diastolic pressure reduction reflect the unloading of the right
and left ventricular preload. Although unloading is an established concept, the merits of the LAVA ECMO
configuration includes simplification of arterial access to avoid using several arterial large bore catheters.

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25
LAVA LAVA
70

60
20 PA-S
(mmHg)

50

15
40

PA-M
CVP (mmHg)
(mmHg)
30
10
PA-D
(mmHg)
20
CO
(L/min)
5

10
Lactate
(mmol/L)

0 0
Baseline Pre-LAVA Post-LAVA Pre-TAVR Baseline Pre-LAVA Post-LAVA
(3 days prior) (2 days after)

CVP= central venous pressure, CO= cardiac output, LAVA= left atrial venous arterial ECMO,
TAVR=transcatheter aortic valve replacement, PA-S= pulmonary artery systolic pressure,
PA-D= pulmonary artery diastolic pressure, PA-M= pulmonary artery mean pressure

Figure 4. Hemodynamic Impact of LAVA ECMO

A 78-year-old man with a regurgitation aortic bioprosthesis, severe mitral regurgitation, and left ventricular systolic dysfunction was in
cardiogenic shock with a rising lactate. The patient was assessed by right heart catheterization 3 days prior and found to have a CVP near
10 mmHg and severe pulmonary hypertension (A and B, baseline). However, the patient presented with respiratory and hemodynamic
embarrassment prompting emergent intubation and repeat hemodynamic assessment. His CVP had spiked to 23 mmHg and concerns for right
ventricular failure arose (pre-LAVA). With insertion of LAVA ECMO, the CVP dropped precipitously as did the pulmonary artery pressures along
with improvement of perfusion. Fick derived CO improved and the lactate cleared.

Increased left ventricular wall stress, indicated by elevated left ventricular end diastolic pressure (LVEDP),
results in increased LV myocardial work and has been associated with myocardial ischemia, reduced
myocardial salvage, and increased mortality. Reduction in left ventricular work has correlated with
improved outcomes. A meta-analysis by Russo et al. demonstrated that LV venting was associated with
lower mortality (OR 0.79 [95%CI 0.72-0.87] p<0.00001), but higher rates of hemolysis.4 Al-Fares et
al. observed that LV unloading improved the ability to wean from MCS (OR 0.62 [0.47-0.83] p=0.001),
however it did not significantly impact survival.5 Schrage et al. investigated the impact of Impella® to
unload the left ventricle when using VA ECMO. A mortality reduction with LV unloading was seen with
the combination of Impella and ECMO (ECpella™) when compared to VA ECMO alone (47% vs. 80%,
p<0.0001). This series observed higher rates of successful weaning with ECpella as opposed to VA ECMO
(successful wean 68% vs. 28%, p<0.0001). However, bleeding and access site-related ischemia rates
were higher in those treated with Impella.8 LAVA ECMO addresses the need to minimize adverse vascular
outcomes as it uses a single large bore arterial access while providing biventricular support.

Techniques to unload the LV include left atrial septostomy6 and direct left atrial cannulation.7 Kotani et al.
reported a single center experience where 12.9% of pediatric patients with VA ECMO had additional
left sided decompression.7 In this cohort, 70% of the patients with left and right atrial cannulation were
eventually decannulated and there was 52% survival.7

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Limitations of the technique

LAVA ECMO may not be generalizable to every operator as it requires the technical expertise of
transseptal puncture and possible need for septal closure post-decannulation. Post-decannulation left-
to-right shunting would render pulmonary artery mixed venous values inaccurate and complicate critical
care management. High degree of left-to-right shunting could exacerbate right ventricular failure and
tricuspid regurgitation due to the increased volume load. Right-to-left shunting may cause hypoxia.
Also weaning from a biventricular device is challenging as the hemodynamic compromise of losing
biventricular unloading is difficult to manage. This likely reflects the extremely dire condition of the
patient requiring the support of LAVA ECMO.

QUICK READ SUMMARY

✓ LAVA ECMO provides biventricular hemodynamic support with single arterial large
bore access and without additional MCS devices.

✓ LAVA ECMO can rapidly decompress central venous and pulmonary pressures in
patients with biventricular dysfunction.

✓ Reducing ventricular load is correlated with improved outcomes.

✓ Use of LAVA ECMO may be limited by required expertise in transseptal puncture and
possible need for septal closure post-decannulation.

✓ Further research is needed to understand the safety and efficacy of this strategy across
cardiogenic shock patients.

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References
1. Aissaoui N, Puymirat E, Tabone X, et al. Improved outcome of cardiogenic shock at the acute stage of myocardial
infarction: a report from the USIK 1995, USIC 2000, and FAST-MI French Nationwide Registries. Eur Heart J.
2012;33(20):2535-43.

2. Goldberg RJ, Makam RCP, Yarzebski J, et al. Decade-long trends (2001-2011) in the incidence and hospital death
rates associated with the in-hospital development of cardiogenic shock after acute myocardial infarction. Circ
Cardiovasc Qual Outcomes. 2016;9(2):117-25.

3. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support. J Am Coll Cardiol.
2015;66(23):2663-74.

4. Russo JJ, Aleksova N, Pitcher I, et al. Left ventricular unloading during extracorporeal membrane oxygenation in
patients with cardiogenic shock. J Am Coll Cardiol. 2019;73(6):654-62.

5. Al-Fares AA, Randhawa VK, Englesakis M, et al. Optimal strategy and timing of left ventricular venting during veno-
arterial extracorporeal life support for adults in cardiogenic shock: a systematic review and meta-analysis. Circ Heart
Fail. 2019;12(11):e006486.

6. Koenig PR, Ralston MA, Kimball TR, et al. Balloon atrial septostomy for left ventricular decompression in patients
receiving extracorporeal membrane oxygenation for myocardial failure. J Pediatr. 1993;122(6):S95-9.

7. Kotani Y, Chetan D, Rodrigues W, et al. Left atrial decompression during venoarterial extracorporeal membrane
oxygenation for left ventricular failure in children: current strategy and clinical outcomes. Artif Organs. 2012;37(1):29-36.

8. Ouweneel DM, de Brabander J, Karami M, et al. Real-life use of left ventricular circulatory support with Impella in
cardiogenic shock after acute myocardial infarction: 12 years AMC experience. Eur Heart J Acute Cardiovasc Care.
2019;8(4):338-49.

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17.4
Common
VA ECMO
Management
Issues
Ranya Sweis, MD, MS, FACC, FSCAI Duc Thinh Pham, MD, FACS
Associate Professor of Associate Professor of Surgery
Medicine, Interventional Cardiology Division of Cardiac Surgery
Division of Cardiology, Northwestern University,
Department of Medicine Feinberg School of Medicine
Northwestern University Feinberg Surgical Director,
School of Medicine Center for Advanced Heart Failure
Clinical Practice Director, Northwestern Medicine,
Bluhm Cardiovascular Institute Bluhm Cardiovascular Institute
Chicago, IL Chicago, IL
rsweis@[Link] dpham1@[Link]
@DrRanyaSweis @DTPham_CVSurg

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Introduction
Extracorporeal life support (ECLS) using VA ECMO is indicated to temporarily support heart and lung
function during cardiopulmonary failure with a goal of ultimate organ recovery or replacement.1 To
achieve this, VA ECMO is necessary to maintain adequate oxygen delivery to the tissues. Oxygen
delivery is determined by cardiac output and oxygen content which in turn is dependent on hemoglobin
level and oxygen saturation.

Cardiac output for a patient on ECMO is the sum of native cardiac output as well as ECMO flow. Initial
target flow is generally 50–70 mL/kg/min. Achieving this flow is dependent on preload, afterload,
and impeller revolutions per minute (RPM) of the pump. Optimal ECMO function usually depends
on receiving approximately 80% of total venous return. This contributes the preload, which can be
impacted by factors such as bleeding or hypovolemia. Initiation of ECMO often results in an increase in
the patient's mean artery pressure (MAP) that contributes to significant LV afterload, which can in turn
reduce LV stroke volume and pulse pressure. This may still contribute to an increase in the LV workload.

Furthermore, since VA ECMO is used to support cardiopulmonary failure, it is critical that while maintaining
tissue oxygen delivery as mentioned above, the heart is given the optimal conditions for recovery. Optimizing
myocardial oxygen demand and LV unloading are important to support myocardial recovery.

This chapter covers patient- and circuit-related factors that are important for daily management of the
VA ECMO patient. We also include a discussion of common special circumstances that necessitate
careful attention as well as a brief overview of ECMO weaning.

Patient management
Hemodynamic monitoring
Hemodynamic monitoring during ECMO support is essential to assess cardiac function, oxygen delivery,
and tissue perfusion.2 Pulmonary artery catheter placement enables monitoring of pulmonary artery
pressures, and by extrapolation, LV filling pressures. These values allow for better assessment of LV
unloading. It is also critical to follow mean arterial pressure, heart rhythm, and pulsatility.

Rhythm evaluation
Arrhythmias in patients on ECMO can contribute to hemodynamic instability and worsening clinical
status. In cases where myocardial recovery is the goal, prevention and control of arrhythmias is critical.
Tachyarrhythmias, such as atrial fibrillation or ventricular fibrillation, may be due to ischemia, LV
distension, electrolyte derangements, or medication effects. Electrical or pharmacological cardioversion
and antiarrhythmic medications may be needed to abort these rhythms and prevent recurrences.
Bradyarrhythmias may require temporary or permanent pacemaker implantation.

In the rare scenario in which myocardial recovery is unlikely and transplantation is likely, the treatment
of arrhythmias is less critical and unlikely to affect ECMO circuit function.

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Blood pressure
ECMO flow is continuous and therefore close monitoring of the mean arterial pressure is critical to
ensure adequate end-organ perfusion. It is generally agreed that a MAP > 65 mmHg will achieve this
end. Since MAP is a product of the cardiac output (in this case the ECMO flow plus native cardiac
output) and the systemic vascular resistance (SVR), the MAP can be manipulated by increasing the
ECMO flow or increasing the SVR with vasoactive agents.

The pulsatility of the arterial waveform is the result of the LV contractility. It is important to allow the
heart to maintain a pulse pressure of at least 10-20 mmHg to prevent LV distension, stasis of the
blood, or pulmonary edema. If this is not possible, LV decompression may be achieved by a number of
methods, such as a catheter in the left ventricle or pulmonary artery connected to the circuit, placement
of an intra-aortic balloon pump, or use of microaxial flow ventricular assist devices. Surgical methods,
such as placement of LV catheters, are also routinely used to decompress the ventricle.

Daily monitoring of pulsatility and MAP, especially as ECMO flow is decreased, allows for assessment of
LV status and signs of contractile recovery.

Neurologic status
Up to 4% of VA ECMO patients may develop strokes—more often ischemic than hemorrhagic3—and
thus regular neurologic assessment is important. Stroke risk factors include emboli from the circuit,
anticoagulation, hemodynamic instability, and other patient-specific comorbidities. Adequate cerebral
blood flow can be continuously monitored using near-infrared spectroscopy (NIRS). Routine, regular,
clinical neurologic examination should also be performed.

A perfusion
Limb B
Limb ischemia is a frequent complication in ECMO patients who are cannulated peripherally (eg, femoral
arterial cannulation). Limb ischemia rates up to 20% have been reported and overall patient outcomes
are worse when this occurs. Routine clinical examination and NIRS are used to monitor limb perfusion.
Distal limb catheter perfusion is recommended to prevent limb ischemia. This is performed by antegrade
cannulation of the superficial femoral artery prior to full ECMO cannulation, as shown in Figure 1.

Figure 1. Antegrade Cannulation of Superficial Femoral Artery Prior to Full ECMO Cannulation

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Recommended laboratory tests

Daily bloodwork for patients on VA ECMO helps to monitor the degree of oxygen delivery, organ
perfusion, and function and circuit condition, as well as monitor for early signs of complications.
Essential blood work includes complete blood count (CBC), complete metabolic panel (CMP), lactate,
lactate dehydrogenase (LDH), coagulation panel, arterial blood gas (ABG), as well as pre- and post-
oxygenator blood gas values.1 Stable and adequate hemoglobin levels are necessary to ensure adequate
oxygen delivery. Lactic acidosis may be a sign of anaerobic glycolysis and inadequate oxygen delivery
but may also be a sign of end-organ ischemia, especially the small bowel. Monitoring renal function is
important to determine if renal replacement therapy is needed. Liver function derangements may point
to liver congestion from RV failure or inadequate drainage. Coagulation panels are used to monitor the
degree of anticoagulation as described elsewhere. Pre- and post-oxygenator gas values may indicate
failing oxygenator function due to fibrin deposition.

Figure 2. VA ECMO Patient Management and Circuit Management

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Circuit considerations
Pump types
When managing VA ECMO patients, it is important to understand the features of the ECMO pump
supporting the patient and its specific safety features. Unlike earlier roller pumps that largely depended
on suction, today most ECMO pumps are centrifugal pumps, designed to decrease the risk of hemolysis
and blood stasis.4 Commonly used ECMO pumps include:
• CentriMag (Levitronix LLC, Waltham, MA, USA), which uses a magnetically levitated rotary pump
• ROTAFLOW (MAQUET Cardiopulmonary AG, Hirrlingen, Germany), which consists of a
magnetically stabilized rotor on a one-point sapphire bearing
• MECC-i for Cardiohelp (MAQUET Cardiopulmonary AG, Hirrlingen, Germany), which relies on
pump technology similar to ROTAFLOW but is smaller and more portable
Table 1 highlights the safety features of each of these ECMO pumps.

Table 1. ECMO Pump Safety Features (adapted from Palanzo, et al.4)

PUMP CENTRIMAG ROTAFLOW CARDIOHELP

Flow alarms

Power alarms

Power supply status

Hand crank

Alarms reactivate

Can set interventions

Portability

Cannulation
ECMO management issues largely depend on the type of ECMO cannulation. The majority of ECMO is
delivered via peripheral cannulation. Management issues associated with peripheral cannulation include
limb ischemia (which can be avoided by using a distal perfusion catheter), differential cyanosis, and
peripheral vascular complications at the entry site in the setting of previous peripheral vascular disease.

Patients with postcardiotomy shock may have central ECMO cannulation (via the RA and ascending
aorta similar to the cannulation for cardiopulmonary bypass). Central cannulation avoids limb ischemia
and differential cyanosis but requires surgical exploration for decannulation and carries an increased risk
of bleeding and mediastinitis.

Blood flow in the cannulas is impacted by the resistance to flow (Poiseuille’s Law): directly with the
length of the cannula and inversely with the fourth power of the radius of the cannula. Arterial catheter
sizes range from 15-20 Fr while venous catheter sizes range from 10-25 Fr. It is important that the
cannulas can support a flow equivalent to a cardiac index of 2.2-2.5 L/min/m2.

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Circuit configuration
The configuration of the ECMO circuit also impacts management issues. Peripheral VA ECMO most
commonly utilizes femoral vein and femoral artery access obtained percutaneously via Seldinger
technique. If axillary artery cannulation is required, this is generally achieved via cut-down with end to
side graft anastomosis. In certain situations, VA ECMO may need to be converted to VVA or VAV ECMO.

If a patient develops LV distension secondary to inadequate venous drainage from the single IVC cannula,
a right internal jugular venous cannula may be placed. It is then Y-connected with the femoral venous
line to allow for dual venous drainage and thus creates a VVA configuration. This may also be achieved
by inserting a ProtekDuo cannula. The ProtekDuo (LivaNova, Boston, MA) is a dual lumen cannula that is
placed from the right internal jugular artery into the pulmonary artery. It drains de-oxygenated blood from
the right atrium while oxygenated blood is ejected into the main pulmonary artery.

Patients may experience differential cyanosis resulting from LV recovery despite persistent pulmonary
dysfunction. In this situation, it may be necessary to convert the VA ECMO configuration to a VAV
ECMO configuration. To achieve this, the right internal jugular catheter (either single or double lumen) is
Y-connected to the arterial line. This allows oxygenated blood to enter the LV.

If the pulmonary dysfunction persists beyond the point of LV recovery, the patient may be converted to
VV ECMO. Prior to doing this, it is critical to determine if RV support is needed. If the patient has had
RV recovery, then converting to VV ECMO requires converting the arterial outflow to a jugular outflow.
However, if the patient requires RV support, then the ProtekDuo cannula can be placed and the VV
ECMO will essentially bypass the RV.

Figure 3. VA ECMO Circuit Configurations

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Circuit management
Management of the ECMO circuit includes careful and regular assessment of 4 settings:
• Flow
• RPM
• Gas sweep
• Fraction of delivered oxygen (FDO2)
The membrane lung in the oxygenator consists of a network of thousands of small tubes carrying venous
blood that passes through gas containing 100% oxygen. The sweep refers to the amount of carbon
dioxide the circuit removes from the blood. A sweep of 0 means there is no O2 or CO2 exchange. To avoid
right to left shunting, the FdO2 must never be < 100% and the sweep should always be >1. Regular
evaluation of the gas tubing connections as well as the O2 tank is appropriate. In addition, it is important to
monitor the cannulas, ECMO tubing, and oxygenator for evidence of fibrin and thrombus buildup.

Management of special circumstances and complications

Limb ischemia
Lower limb ischemia in patients with peripheral ECMO cannulation is common and occurs in 10-20% of
patients.3 The risk is increased with pre-existing peripheral vascular disease, shock, as well as the use of
high dose vasopressors. Lower extremity ischemia is associated with twice the risk of in-hospital mortality.

To anticipate, detect, and manage clinically significant limb ischemia:

1. Regularly monitor and assess arterial pulse, ankle brachial index, tissue oximetry, and lab work
(including creatinine, lactate, and phosphokinase).
2. Use smaller cannulas (16 or 18 Fr is usually sufficient) to reduce the risk of limb ischemia while
maintaining adequate ECMO flows.
3. Use distal perfusion cannulas (DPC) to maintain circulation to the lower limb. Place a sheath in the
superficial femoral artery using ultrasound guidance and connect it to the arterial cannula, allowing
antegrade perfusion of the lower extremity. Routine use of DPCs has drastically diminished the risk
of limb loss in ECMO patients.

Differential cyanosis
Differential cyanosis, also known as Harlequin syndrome, is a result of mixing of oxygenated retrograde
ECMO flow from a peripheral cannula with deoxygenated antegrade flow from the LV. This may occur in
patients with a recovering LV but residual poor lung function. When this occurs, venous blood bypasses the
ECMO circuit going through the pulmonary system without gas exchange and is then ejected though the LV
thereby delivering deoxygenated blood to the very proximal vessels off the ascending aorta and aortic arch.
This may result in inadequate oxygen supply to the coronary arteries and recovering myocardium.

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Figure 4. Differential Cyanosis

To monitor for differential cyanosis:

1. Place a right radial artery line in all patients with VA ECMO. A drop in oxygen saturation in the right
radial artery suggests coronary and cerebral hypoxemia.
2. If hypoxia is detected, provide complete drainage with the use of an additional venous cannula in
the right internal jugular vein, optimize lung function, or convert to VV, VAV, or central cannulation.
3. Note that increasing ECMO flow serves to move the mixing point of the oxygenated and
deoxygenated blood further proximal. If the mixing point moves proximal to the innominate artery,
it will appear that the arterial saturations have improved yet the coronary arteries and myocardium
remain ischemic.

Low flow states

ECMO flow is preload dependent and as a result optimal intravascular volume must be maintained.
When the patient does not have adequate preload, the circuit will generally signal “low flow” alarms and
the venous line may be noted to be “chugging.” Chugging refers to the motion of the venous cannula
due to suction on the vein walls given inadequate volume in the setting of high suction or high RPMs.
• If low flow and chugging occur, decrease the RPMs, provide volume, or both.
• If the situation cannot be immediately resolved, clamp the cannulas to prevent this flow reversal.
In an extreme low volume state, the circuit may completely stop, resulting in reversal of the flow
from the patient to the circuit.

Management during recovery and weaning

Weaning VA ECMO is considered when the cause of cardiogenic shock has been addressed and treated,
the RV and LV have recovered while being decompressed, and the patient’s volume, vasopressors,
inotropes, and oxygenation have been optimized. Echocardiography and hemodynamic evaluation are
critical to the weaning process.

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Weaning is achieved by decreasing the ECMO flow and allowing the heart to provide more cardiac
output. As the ECMO flow decreases, the recovered RV and LV receive more preload and this stimulates
the heart to increase its native output to maintain the mean arterial pressure and increase the pulse
pressure. Ventricular function, distension, and valvular function can be assessed with echocardiography
during ECMO turndown. A few things to keep in mind during ECMO weaning:
• Optimize the patient’s volume with diuretics as appropriate. It may also be necessary to start
inotropes or pulmonary vasodilators.
• Prior to decannulation, turn down ECMO flow to 1 L/min and evaluate the hemodynamics and gas
exchange. If these parameters remain acceptable, disconnect the patient from the ECMO pump.
• The circuit is connected to itself to allow for recirculation. Prior to removing the cannulas, reassess
hemodynamic parameters and gas exchange.
• We typically do not wean the FdO2 and sweep during weaning of VA ECMO, as weaning them
would create a right to left shunt.

QUICK READ SUMMARY

✓ For daily management of VA ECMO patients, monitor:
• Hemodynamics
• Rhythm
• Blood pressure
• Neurologic status
• Limb perfusion
• Bloodwork, including CBC, CMP, lactate, LDH, coagulation panel, ABG, pre- and
post-oxygenator blood gas values

✓ Management of the ECMO circuit includes:

• Careful assessment of flow, RPM, gas sweep, and FdO2
• Regular evaluation of gas tubing connections and oxygen tank
• Monitoring cannulas, ECMO tubing, and oxygenator

✓ Special circumstances and complications associated with VA ECMO include:

• Lower limb ischemia
• Differential cyanosis
• Low flow states

✓ When weaning a patient from VA ECMO:

• Optimize volume as appropriate
• Evaluate hemodynamics and gas exchange prior to decannulation
• Do NOT wean the FdO2 and sweep, as that would create a right to left shunt

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References
1. Extracorporeal Life Support Organization (ELSO) Guidelines for Cardiopulmonary Extracorporeal Life Support. Version
1.4. August 2017. Ann Arbor, MI. Available at: [Link]
All%20ECLS%20Version%201_4.pdf. Accessed 14 July 2021.

2. Su Y, Liu K, Zheng J-L, et al. Hemodynamic monitoring in patients with venoarterial extracorporeal membrane
oxygenation. Ann Transl Med. 2020;8(12). doi:10.21037/atm.2020.03.186

3. Pozzi M, Koffel C, Diaref C, et al. High rate of arterial complications in patients supported with extracorporeal life
support for drug intoxication-induced refractory cardiogenic shock or cardiac arrest. J Thorac Dis. 2017;9(7):1988-96.

4. Palanzo DA, Baer LD, El-Banayosy A, et al. Choosing a pump for extracorporeal membrane oxygenation in the USA:
Invited Editorial. Artificial Organs. 2014;38(1):1-4. doi:10.1111/aor.12215

5. Pang PYK, Wee GHL, Hoo AEE, et al. Therapeutic hypothermia in adult patients receiving extracorporeal life support:
early results of a randomized controlled study. J Cardiothorac Surg. 2016;11. doi:10.1186/s13019-016-0437-8

6. Cheng R, Hachamovitch R, Kittleson M, et al. Complications of extracorporeal membrane oxygenation for treatment of
cardiogenic shock and cardiac arrest: a meta-analysis of 1,866 adult patients. Ann Thorac Surg. 2014;97(2):610-6.

7. Atkinson TM, Ohman EM, O’Neill WW, et al. A practical approach to mechanical circulatory support in patients
undergoing percutaneous coronary intervention: an interventional perspective. JACC Cardiovasc Interv.
2016;9(9):871–83.

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18
PREVIOUS CHAPTER Chapter 18: VV ECMO NEXT CHAPTER

V V ECMO

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18.1
Introduction to
VV ECMO
Anthony J. Faugno, MD
Director, Medical Intensive Care Unit
Tufts Medical Center
Boston, MA
afaugno@[Link]

Haval Chweich, MD
Director, Cardiac Care Unit
Tufts Medical Center
Boston, MA
hchweich@[Link]

Navin K. Kapur, MD, FSCAI

Associate Professor, Department of Medicine
The Cardiovascular Center, Tufts Medical Center
Boston, MA
nkapur@[Link]
@navinkapur4

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Overview
VV ECMO supports native lung function when mechanical ventilation is either unable to achieve
adequate gas exchange to meet the body’s metabolic demands, or its intensity is considered injurious.
VV ECMO enables oxygen delivery and carbon dioxide removal as blood flows at high rates across a
polymethylpentene membrane lung with a countercurrent flow of oxygenated gas (100% or 95% O2).1
In select patients with end-stage lung disease, this application of support can provide a bridge to
transport allowing for physical rehabilitation. While randomized controlled trials have not demonstrated
a mortality benefit with this therapy in acute hypoxic respiratory failure, patient level meta-analyses
of available trial data suggest a mortality benefit.3-4 Multiple competing events may lead to mortality
while on VV ECMO, including but not limited to failure of lung recovery, multisystem organ failure, and
complications of extracorporeal support. The reported in-hospital mortality is approximately 40%.2
The deployment of VV ECMO should be considered when traditional evidence-based measures of
respiratory support have failed, including low tidal volume ventilation and prone mechanical ventilation
where possible.

Figure 1. VV ECMO Overview

The goal of VV ECMO is to supply sufficient oxygen delivery to avoid anaerobic cellular metabolism while allowing lung rest. The heart receives a
venous admixture of the deoxygenated native venous return and highly oxygenated blood returned to the venous circulation from the ECMO circuit.
This oxygenated venous admixture participates in gas exchange in the native lung, depending on the degree of lung injury, and is then delivered
systemically by the native cardiac output. This support can be provided in a variety of formats. (A) Femoral vein venous drainage and internal jugular
vein arterial limb is common. Alternative cannulation strategies can be deployed based on patient characteristics such as (B) bifemoral cannulation
where the arterial limb cannula sits at the cavoatrial junction above the venous limb cannula in the SVC, or (C) the bicaval dual lumen strategy which
utilizes a large dual lumen internal jugular cannula with IVC and SVC venous limbs and an arterial limb that directs flow toward the tricuspid valve,
with the intent of reducing recirculation. (D) A separate strategy of right atrial to pulmonary artery bypass has also been employed as VV ECMO,
utilizing a single IJ cannula, providing both respiratory support and single chamber cardiac support to the right ventricle.

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Procedural considerations
Oxygen delivery
In the case of total respiratory failure, the ability of the ECMO circuit to sufficiently oxygenate the blood in
a VV configuration is dependent on the circuit flowing at rates that capture approximately 60-80% of the
cardiac output. In this sense, oxygenation on ECMO is a “perfusion limited” process as it is in the lung, and as
a result, better systemic oxygenation can be achieved by increasing blood flow through the circuit to capture
a larger fraction of total cardiac output. Thus, cannula selection should be informed by the patient’s size (body
surface area) and considerations regarding native cardiac output. The adequacy of oxygen delivery (DO2) is
dependent on cardiac output and oxygen carrying capacity as well as variations in oxygen consumption (eg,
fever, poor sedation). While oxygen consumption (VO2) isn’t regularly measured in a clinical setting, lactate
production can serve as a surrogate for preservation of an aerobic DO2/VO2 relationship on ECMO.

This DO2/VO2 relationship is especially relevant when the severity of lung injury necessitates tolerance
of sub-physiologic oxygen saturation goals – sometimes as low as 80%. At times, there is greater
benefit to protecting the lungs than achieving traditional saturation targets. In this setting, serum lactate
levels can be trended for evidence of insufficient DO2. When lactate levels climb, indicating anaerobic
respiration, two factors should be optimized. The first factor is the oxygen carrying capacity, which is
optimized by transfusing red blood cells. The second is the effective blood flow, which is best achieved
by increasing the circuit blood flow (while minimizing recirculation). Revision of mechanical support
could be considered with an additional drainage cannula if circuit blood flow rates are insufficient,
although this is not without risk. Prior to adjusting or adding drainage cannulas due to poor circuit flow,
a thoughtful clinical evaluation for hypovolemia, hemorrhage, improper cannula positioning/kinking, or
tamponade physiology (pericardial tamponade or tension pneumothorax) should be performed.
A B
Carbon dioxide removal
Carbon dioxide removal occurs readily across the membrane lung, given that a large fraction of CO2 is
transported dissolved in the blood and isn’t reliant on binding to hemoglobin. With ECMO, the primary driver
of CO2 clearance is the gradient from the blood to the gas phase of the membrane, where CO2 is absent. The
gas flow through the membrane is conventionally known as the sweep flow, and it is effectively analogous
to the minute ventilation in the native lung. A faster sweep flow generates a larger gradient for CO2 diffusion,
removing CO2 from the body quite efficiently even at very low blood flow rates (0.5 L/min – 2 L/min). In the
setting of hypercarbia at the onset of ECMO therapy, care needs to be taken not to correct hypercarbia too
quickly, as large CO2 swings have been associated with cerebrovascular events in large registry reports.

Recirculation
The presence of drainage and return cannulas in the same vascular bed with VV ECMO introduces the
risk of recirculation phenomenon, where oxygenated blood from the return cannula is rapidly removed
from the body by the drainage cannula in a continuous loop – thus preventing systemic delivery of
oxygen.5 This can occur when cannulas are positioned too closely in the dual cannula configuration,
with improper placement (either depth or torque) in single vessel bicaval strategies, or when high circuit
flow rates discourage blood flow through the native cardiac circulation. Significant recirculation should
be suspected when the systemic oxygen saturation drops despite good flow, coupled with increase
in the pre-membranous oxygen saturation. Cannulas should be manipulated with caution under
echocardiographic or fluoroscopic guidance. Repositioning of a cannula is discouraged if patients appear
to be receiving adequate physiologic support. The radiographic appearance of cannula proximity should
not necessarily influence repositioning, as the multistage drainage cannula tends to provide drainage
from patent fenestrations most proximal to the pump head. From the femoral position, this drainage
tends to occur in the hepatic IVC where the hepatic parenchyma prevents vessel collapse.

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Table 1. Quick Reference Physiologic Calculations

NATIVE CARDIAC OUTPUT ON VV ECMO

(assumes no native lung function)

ECMO CaO2 × ECMO flow Venous CvO2 x cardiac output

O2 content = +
(ECMO flow + cardiac output) (ECMO flow + cardiac output)

OXYGEN CONTENT
SaO2
CaO2 = 1.36 × HgB × + 0.0031 × PaO2
100

OXYGEN DELIVERY
(cardiac output cannot be measured by Fick or thermodilution method on VV ECMO)

DO2 = cardiac output (CO) × oxygen content (CaO2)

RECIRCULATION PERCENTAGE
(where SpreO2 = pre oxygenator saturation; SpostO2 = post oxygenator saturation)

(SpreO2 – SvO2)
Recirculation % = × 100
(SpostO2 – SvO2)

Weaning of VV ECMO
Improvement in native lung compliance will be the first indication for considering the weaning of VV
ECMO. The other pre-requisites for weaning VV ECMO are hemodynamic stability, absence of high
work of breathing, and a PaO2 >225 mmHg during a 100% FiO2 challenge on the ventilator. Once the
patient is deemed appropriate for VV ECMO weaning, sweep gas flow is gradually reduced until it is
finally turned off. ECMO blood flow is not necessarily modified during the weaning trial, although this
practice is center dependent and may vary from patient to patient.7 During this phase, the patient is
technically “off ECMO” and can be decannulated after a 12-24 hour trial if gas exchange is stable on
protective lung ventilation without evidence of increased work of breathing.

Patient selection
Initiation of VV ECMO is often guided by institutional criteria for both inclusion and exclusion developed by
a multidisciplinary team. The use of VV ECMO is thought to be most beneficial when patients are suffering
only from single organ failure, generally within 7 to 10 days of mechanical ventilation. The indication
for therapy is driven either by the inability to oxygenate, as determined by the PaO2 /FiO2 ratio, or by the
inability to ventilate without harmful levels of positive pressure ventilation to correct respiratory acidosis
(pH <7.25). Indications and contraindications from previous trials are listed in Table 2 as a general guide.

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Table 2. General Indications and Contraindications for Respiratory ECMO Support

INDICATIONS

• PaO2 /FiO2 ratio <50 mmHg for >3 hours or PaO2 /FiO2 ratio <80 mmHg for >6 hours
despite optimization of ventilator management and use of adjunctive therapies
(inhaled vasodilators, recruitment maneuvers, prone ventilation)

• Respiratory acidosis pH <7.25 with a PaCO2 >60 for >6 hours

despite respiratory rate >35 and ventilator plateau pressure <32 cm H2O

• Persistent air leak from the lung impeding ventilation

• Refractory status asthmaticus

CONTRAINDICATIONS

Relative Absolute

• Mechanical ventilation ≥7 days • Uncontrolled hemorrhage

• BMI ≥45 kg/m2 • Unrecoverable neurologic injury

• Chronic respiratory failure unless transplant candidate • Limitations to vascular access (eg, thrombus, stenosis)

• Acute and chronic renal failure • Baseline moribund condition

• Heparin-induced thrombocytopenia

• Shock requiring high dose vasopressors

• Multisystem organ failure

References
1. Bartlett RH. Physiology of gas exchange during ECMO for respiratory failure. J Intensive Care Med. 2017;32(4):243-8.
doi: 10.1177/0885066616641383. Epub 2016 Apr 3. PMID: 27040797.

2. Extracorporeal Life Support Organization: ECMO and ECLS > Registry > Statistics > International Summary. Available
at: [Link]

3. Combes A, Hajage D, Capellier G, et al. Extracorporeal membrane oxygenation for severe acute respiratory distress
syndrome. N Engl J Med. 2018;378(21):1965-75. doi: 10.1056/NEJMoa1800385. PMID: 29791822.

4. Noah MA, Peek GJ, Finney SJ, et al. Referral to an extracorporeal membrane oxygenation center and mortality among
patients with severe 2009 influenza A(H1N1). JAMA. 2011 Oct 19;306(15):1659-68. doi: 10.1001/jama.2011.1471.
Epub 2011 Oct 5. PMID: 21976615.

5. Combes A, Peek GJ, Hajage D, et al. ECMO for severe ARDS: systematic review and individual patient data meta-
analysis. Intensive Care Med. 2020;46(11):2048-57. doi: 10.1007/s00134-020-06248-3. Epub 2020 Oct 6. PMID:
33021684; PMCID: PMC7537368.

6. Abrams D, Bacchetta M, Brodie D. Recirculation in venovenous extracorporeal membrane oxygenation. ASAIO J.

2015;61(2):115-21. doi: 10.1097/MAT.0000000000000179. PMID: 25423117.

7. Teijeiro-Paradis R, Cherkos Dawit T, Munshi L, et al. Liberation from venovenous extracorporeal membrane
oxygenation for respiratory failure: a scoping review. Chest. 2023;164(5):1184-203. doi: 10.1016/j.
chest.2023.06.018. Epub 2023 Jun 21. PMID: 37353070.

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18.2
Common Access
Strategies:
2-site vs 1-site
Peripheral Access
Rajiv Tayal MD, MPH, FSCAI Jagpreet Grewal, MD
Director, Cardiac Catheterization Laboratories Assistant Professor of Medicine
Valley Health System Advanced Heart Failure and
Clinical Assistant Professor of Medicine Transplant Cardiology
Icahn School of Medicine, Mt. Sinai Rutgers - Robert Wood Johnson
New York, NY University Hospital
tayara@[Link] New Brunswick, NJ
@rajtayalmd Jgrewal12@[Link]

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Introduction
Patients considered for VV ECMO support typically have a compromised respiratory status refractory
to mechanical ventilation and medical therapy. Importantly, the VV ECMO circuit is dependent on the
patient’s native cardiac output to maintain perfusion and prevent recirculation. A patient who has
reversible respiratory failure (eg, aspiration, viral/bacterial pneumonia, barotrauma, acute on chronic
interstitial pneumonitis) with acceptable unsupported cardiac output may be a suitable candidate for
VV ECMO. The presence of concomitant left ventricular dysfunction may instead require the use of VA
ECMO. Thus, an echocardiogram or hemodynamic assessment of cardiac function should be performed
prior to cannulation.

Cannulation strategies
Double cannulation
In the classic configuration, VV ECMO support may be achieved with two cannulas, as shown in Figure 1.
The first cannula is inserted into the right femoral vein and advanced to the junction of the inferior vena cava
(IVC) and right atrium. The second cannula is inserted into the right internal jugular vein (IJV) and advanced
to the right atrium.2 If internal jugular vein cannulation is not possible, bilateral femoral cannulations can be
utilized as a second-line strategy. This configuration, however, is less advantageous as it induces higher
levels of recirculation if the return cannula is not placed in front of the tricuspid valve
.

Figure 1. Classic Double Cannulation VV ECMO

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Single cannulation
Single access VV ECMO can be initiated with a single double lumen bicaval cannula. The single cannula
has three ports: proximal, middle, and distal. The distal port is positioned in the IVC and the proximal port
is located in the superior vena cava (SVC). The proximal port drains deoxygenated blood into the ECMO
circuit. The middle port is positioned in the right atrium facing the tricuspid valve and delivers oxygenated
blood from the ECMO circuit. Although more technically challenging, this technique offers the advantages
of avoiding femoral cannulation, facilitating proning, and allowing early mobilization and ambulation.

A B

Figure 2. Single Access VV ECMO

Preprocedural planning
VV ECMO can be placed bedside in the ICU or in the cardiac catheterization laboratory or operating
room. The following are key elements of preprocedural planning for VV ECMO:
• Obtain an echocardiogram prior to cannulation to assess cardiac function and rule out structural
abnormalities, such as patent foramen ovale (PFO) or significant tricuspid regurgitation (TR),
which may lead to inadequate mixing of ECMO flow.
• Evaluate vascular anatomy by ultrasound to identify pathology or devices that may preclude
cannula placement (eg, thrombus, IVC filter, stents, stenosis).
• Identify coagulopathy or contraindications to anticoagulation prior to cannulation.

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• Use the largest possible venous cannula to maximize flow and achieve target output.2
• Have echocardiography available at the bedside to help visualize guidewire position and possible
complications. If adequate visualization of the cardiac structures is not obtained by transthoracic
echocardiography (TTE), transesophageal echocardiography (TEE) should be used.1
• Have ultrasound readily available as it increases overall success and decreases the incidence of
complications associated with large-bore catheters. A single center retrospective study showed
a high degree of success with a low complication rate by intensivists using ultrasound and/or
fluoroscopic guidance.3
• Two operators are recommended to assist in handling wires and cannulas.
• Prep and drape the patient in sterile fashion and give appropriate sedation prior to initiation of the
procedure.
• Prep bilateral groins in case internal jugular access is not feasible.
• Place a central venous line and an arterial line for proper monitoring of hemodynamics along with
access to vasopressors and volume as needed throughout the procedure.

Cannulation techniques
Double site VV cannulation
1. Puncture the right internal jugular vein (IJV) with ultrasound guidance, preferably 4-5 cm away from
the clavicle.
2. Advance the guidewire to the IVC distal to the hepatic vein to prevent dislodgement of the wire.
3. It is imperative to confirm guidewire position with echocardiography or fluoroscopy to ensure that
the wire has not passed into the RV, coronary sinus, or across an unknown atrial septal defect
(ASD).
4. After the vascular puncture and insertion of the guidewire using the Seldinger technique, place
successive dilators over the guidewire to progressively enlarge the access site. While dilating it is
important to continuously visualize the guidewire for any secondary migration.
5. Once the area is dilated, advance the inflow cannula to the right atrium in front of the tricuspid
valve with echocardiographic or fluoroscopic guidance. This position assures optimal reinjection and
reduces recirculation.
6. Cannulate the right common femoral vein (CFV) using ultrasound guidance. The right CFV is
preferred over the left CFV due to typical vessel angulation.
7. Using the Seldinger technique, advance a long J-tip guidewire through the IVC to the SVC using
ultrasound guidance. Advancing the wire to the SVC avoids inadvertent migration into the renal or
hepatic veins or the right ventricle.
8. After serial dilations with visualization of the guidewire for secondary migration, advance the
cannula to the IVC-RA junction. If the cannula is too distal there is an increased risk of the tip
aspirating against the wall, causing injury to the right atrium and also increasing the possibility of
recirculation. To decrease recirculation, 15 cm between the two cannulas is usually required.
For double cannula configurations where IJ access cannot be obtained, VV ECMO support can be
performed via bilateral femoral cannulation. To mitigate recirculation, the tip of the drainage venous
cannula is placed in the IVC while the tip of the inflow cannula is positioned in the right atrium.

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Single bicaval VV cannulation

The single access technique provides the benefits of a single cannula with two lumens (inflow and
outflow). As described earlier, the double lumen cannula consists of three ports: the proximal and distal
ports serving as inflow ports draining deoxygenated blood, and the middle port serving as an outflow
port reinjecting oxygenated blood. Optimal positioning is vital to the functionality of the double lumen
single bicaval cannulation. It is important to follow these steps:
1. Access the internal jugular vein with ultrasound guidance as described earlier.
2. Advance a guidewire to the IVC with TEE or TTE guidance to ensure proper positioning and to
identify any migration into the right ventricle or other smaller branches.
3. After serial dilations to the desired cannula size, advance the cannula over a wire.
4. Confirm, with TTE or TEE guidance, that the distal tip is positioned in the IVC with the middle port
of the catheter positioned in the RA with the outflow injecting toward the tricuspid valve.

Post cannulation
1. After cannulation, connect the ECMO circuit paying particular attention to de-airing the circuit.
2. Following connection, remove the clamps and set the desired flow on the device console.
3. Suture cannulas into place to prevent dislodgement.
4. Perform echocardiogram and chest x-ray to confirm placement and rule out potential complications,
such as pneumothorax or tamponade.

QUICK READ SUMMARY

✓ VV ECMO is classically configured with double cannulation with 1 cannula inserted into
the right femoral vein and the other inserted into the right internal jugular vein. Bilateral
femoral cannulation may be a second-line strategy.

✓ VV ECMO may be initiated with a single double lumen bicaval cannula inserted through
the internal jugular vein, avoiding femoral access and allowing early mobilization.

✓ Key elements of pre-procedural planning include obtaining an echo prior to cannulation,

evaluating vasculature with ultrasound, and placing a central venous line and arterial
line for hemodynamic monitoring and procedural access.

✓ For double site VV cannulation it is imperative to confirm guidewire position with echo
or fluoro to prevent complications.

✓ Optimal positioning is also vital to the functionality of double lumen single bicaval
cannulation.

✓ Post cannulation, echo and chest x-ray are important for confirming placement and
ruling out potential complications.

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References
1. Shaheen A, Tanaka D, Cavarocchi NC, Hirose H. Veno-venous extracorporeal membrane oxygenation (VV ECMO):
indications, preprocedural considerations, and technique. J Card Surg. 2016;31(4):248-52.

2. Banfi C, Pozzi M, Siegenthaler N, et al. Veno-venous extracorporeal membrane oxygenation: cannulation techniques.
J Thorac Dis. 2016;8(12):3762-73.

3. Burns J, Cooper E, Salt G, et al. Retrospective observational review of percutaneous cannulation for extracorporeal
membrane oxygenation. ASAIO J. 2016;62(3):325-8.

4. Troianos CA, Hartman GS, Glas KE, et al. Guidelines for performing ultrasound guided vascular cannulation:
recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists.
J Am Soc Echocardiogr. 2011;24:1291-318.

5. Platts DG, Sedgwick JF, Burstow DJ, et al. The role of echocardiography in the management of patients supported
with extracorporeal membrane oxygenation. J Am Soc Echocardiogr. 2012;25(2):131-41.

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18.3
ECMO Daily
Management
James Lantry III, MD
Associate Director of Quality, Critical Care
INOVA Heart and Vascular Institute
Falls Church, VA
jlantrymd@[Link]
@EmCritDr

Mehul Desai, MD
System Chief Critical Care, Pulmonary, Allergy and Immunology
INOVA Heart and Vascular Institute
Falls Church, VA

Erik Osborn, MD
COL (Ret) MC USA
American College of Chest Physicians
Glenview, Illinois

Araba Ofosu-Somuah, MD
Cardiovascular Disease Fellow
INOVA Heart and Vascular Institute
Falls Church, VA

Theresa Ganoe, ACNP-BC

Critical Care Nurse Practitioner
INOVA Heart and Vascular Institute
Falls Church, VA

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Introduction
Extracorporeal membrane oxygenation (ECMO) affects the daily management of every organ system
of the ICU patient. Drug pharmacokinetics are altered due to circuit absorption and the increased
volume of distribution. A mixed picture of coagulopathy bleeding and thrombosis occurs as the circuit
activates clotting cascades and platelet function coupled with the need for systemic anticoagulation
to avoid circuit and cannula thrombosis. Bleeding is often an ongoing issue leading to periodic
blood product requirements and resuscitation needs. Additionally, exposure of blood to the artificial
surface of the ECMO circuit leads to a transient systemic inflammatory response that may compromise
hemodynamics, worsen existing kidney injury, and complicate ARDS. Increased metabolic demand
requires adjustment of nutritional goals and effects glomerular filtration rates. And finally, the often
prolonged times of VV ECMO runs frequently lead to worsening of existing ICU myopathy and stresses
the need for daily physical therapy and mobility trials.

Analgesia and sedation

The most recent clinical practice guidelines released by the Society of Critical Care Medicine describe, in
detail, that utilization of goal-directed analgesia and sedation for the ICU population results in better long-
term outcomes.1 The ECMO patient population is no different; the only caveat is that the ECMO circuit
can alter the pharmacokinetics and pharmacodynamics of many sedative and analgesic medications.
Additionally, the presence of multisystem organ failure and other clinical variables common in the ECMO
population can affect medication choices, requiring closer monitoring and adjustment. Box 1 summarizes
general guidelines and goals for managing analgesia and sedation in these patients.

BOX 1. ANALGESIA AND SEDATION MANAGEMENT GUIDELINES

• Optimize environment (adhere to “day and night” cycles, daily reorientation, use of
corrective devices such as eyeglasses and hearing aids when appropriate)
• Maximize sleep protocols when possible, minimizing lights, sounds, and disturbances
• Use objective scoring systems for sedatives (eg, RASS) and analgesia (eg, CPOT)
• Adhere to an algorithmic approach to both sedation and analgesia
• Assess for delirium at least twice a day (eg, CAM-ICU)
• Consider antipsychotic therapies with close monitoring of QTc
• Avoid medications that induce delirium (benzodiazepines, anticholinergics) unless clinically
necessary
• Overall, maintain sedation and analgesia with reliance on nonpharmacological measures as
primary therapy with escalation to the minimal effective dose of all other medications

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Analgesia
Pain increases proinflammatory cytokine levels and results in arteriolar constriction and tissue
hypoperfusion.2 If left improperly managed, pain can also lead to PTSD and chronic pain syndromes.3
Non-narcotic analgesics, such as acetaminophen and gabapentin, are first-line pain management
options. If these medications fail to resolve pain, narcotics are often the logical next choice. Due to
stacking of half-lives, intermittent dosing is preferred over IV infusions.

Fentanyl is often the first-line IV narcotic analgesic utilized in the ICU population. When used in
conjunction with ECMO, dose adjustments are imperative as Fentanyl and its derivatives are highly
lipophilic and nearly fully absorbed by the oxygenator within 48 hours of continuous administration.4,5
Therefore, initial bolus doses may be higher than expected to fully saturate the circuit, and upon
discontinuation of a Fentanyl infusion there will be prolonged effects due to a slow osmotic leeching
of the drug off the oxygenator into the circulating blood volume. Alternative IV analgesics include
morphine due to its hydrophilic nature and limited circuit absorption.4,5 However, histamine release
leading to hypotension and bronchospasm coupled with the sedative effects of its metabolites may limit
widespread use of morphine in the ECMO population.6 Hydromorphone, which has the hydrophilic
properties of morphine without the histamine release or metabolites, is a viable alternative in the ECMO
population.

Parenteral narcotics may also be considered for pain control, with oxycodone being a mainstay of
therapy. The only caveat is factoring in variable absorption rates in critically ill patients and peak effect
may not occur until 30 minutes after the drug is ingested.7

Regardless of the analgesic chosen, goal directed therapy is required to avoid excessive pain control and
limit
A side effects. Although self-assessment of painBis ideal, multiple pain scales exist to target analgesia
in patients unable to appropriately communicate. The two most popular scales are: 8

• Behavioral Pain Scale

• Critical Care Pain Observation Tool
With no data or research comparing the two scales in the ECMO population, appropriate utilization is
center specific as opposed to population dependent.

Sedation
Several sedative choices have been tested in the ECMO population:
• Propofol
• Dexmedetomidine
• Ketamine
• Benzodiazepines
Propofol—often the first choice for the ICU population—is extremely lipophilic and highly absorbed by
the ECMO oxygenator.9 The higher doses required in the ECMO population have led clinicians to avoid
its use out of fear of inducing propofol infusion syndrome or causing layering and obstruction of the
oxygenator.10,11 Despite these fears, propofol has a decent safety profile when dosing is adjusted to
account for altered pharmacokinetics in the ECMO population.9

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Dexmedetomidine is a selective alpha-2 receptor agonist with both sedative and analgesic properties
that can lower the need for IV narcotic therapy.12 An additional benefit with dexmedetomidine is the
ability to utilize an infusion in the non-mechanically ventilated ICU patient population as it causes less
respiratory depression and allows for easier arousal than alternative sedative agents. Use in the ECMO
population is again affected by drug absorption, into both the PVC tubing and the oxygenator of the
ECMO circuit, requiring dose adjustments including consideration of an initial loading bolus.13,14

Ketamine is an NMDA antagonist that has sedative, analgesic, and bronchodilator properties with
minimal effect on respiratory drive or hemodynamics.15 Ketamine use has been associated with
decreased narcotic requirements in the ICU population, although only at higher doses.16 Like other
sedative infusions, ketamine is lipophilic and absorbed into the oxygenator, and thus requires dose
adjustments in the ECMO population.

Infusions of benzodiazepines in the ICU population have fallen out of favor except for sedative
withdrawal or seizures. Numerous studies have shown that continuous infusions increase the incidence
of ICU delirium and subsequent poor long-term outcomes.1,17 Additionally, benzodiazepines are highly
lipophilic and absorption into the circuitry can be extensive leading to high levels of sequestration that
make proper dosing problematic long term.18

As with analgesic use, adhering to a protocolized sedative scale is ideal to avoid oversedation and limit
side effect profiles. There are two widely accepted scales in the ICU population:
• Richmond Agitation-Sedation scale (RASS)
• Sedation-Agitation scale (SAS)
Because there are no studies comparing the two scales in the ECMO population, center-specific
protocols often determine which scale is utilized.

Delirium monitoring
Delirium monitoring and management is vital in ECMO patients in the ICU. The best strategy entails
identifying delirium with the Confusion Assessment Method for the ICU (CAM-ICU) and making
environmental changes to lessen the impact of delirium.1,19 This includes:
• Adherence to day/night cycles
• Early mobilization
• Frequent orientation
• Use of auditory or visual aids
• Avoidance of loud noises or stimulation
In addition, avoid medications that increase the incidence of delirium, such as benzodiazepines17
and ideally transition off all sedative and analgesic infusions as soon as clinically feasible. Finally, an
ECMO specific intervention to avoid delirium is to extubate early with reliance on the ECMO circuit for
oxygenation and ventilation.20 The current literature does not support the routine use of antipsychotics,
but the minimal overall side effect profile supports the use of antipsychotics on an interim basis.1,21

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ECMO circuit management

Daily management and monitoring of VV ECMO patients is paramount to their survival. Patients depend
on the ability of ECMO to correct gas exchange abnormalities not maintained by conventional support
as well as to prevent ventilator-associated lung injury. It is important to preserve optimal blood flow
through the cannulas in an effort to match at least 60% of the patient’s cardiac output.22 Complications
can have a significant impact on morbidity and mortality; therefore early recognition of complications
drives the labor-intensive and time-consuming management of ECMO patients.22, 23 Table 1 summarizes
daily goals for managing and monitoring VV ECMO patients.

Table 1. Daily Management Goals for VV ECMO Circuit Health

1. Optimize anticoagulation • Heparin – most common

• Bivalirudin – alternative

2. Monitor clotting indicators • Delta P

• Plasma-free hemoglobin

• D-dimer

• Visual inspection

• PT/PTT fibrinogen, TEG

3. Circuit DIC • Acquired von Willebrand

• Systemic hyperfibrinolysis

• Bleeding and clotting complications

4. Cannula placement • Frequent x-rays

• Visual inspection

• Echocardiography

• Patient movement (eg, repositioning, bathing)

5. Circuit disruption • Entrainment of air to cause “air lock”

• Gaseous emboli

• Patient demise

• Complete circuit failure

• Ensure connections are fastened

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Optimizing anticoagulation and monitoring clotting indicators

The most common ECMO circuit complications occur when there are limitations in blood flow through
the circuit and providers need to be mindful of this in daily management and care. A potentially
dangerous complication is clotting of the circuit which impedes circulation through the oxygenator and
reduces gas exchange. Clotting can also cause an obstruction that impedes blood flow and injures red
blood cells and platelets resulting in hemolysis, and consequently can further potentiate complications
such as anemia, thrombocytopenia, and acute kidney injury due to acute tubular necrosis.23 ECMO
specialists should frequently monitor the circuit for clotting by direct visualization of the pre and post
pump windows of the oxygenator, following the cannulas to the insertion point, as well as any pertinent
laboratory values. The existence of clots can be detected by the presence of plasma-free Hgb or a
rising D-dimer. Serial prothrombin time (PT), PTT, and fibrinogen levels are also obtained to monitor for
evidence of hypercoagulability, coagulopathy, and/or disseminated intravascular coagulation (DIC), as
well as viscoelastic tests such as thromboelastography (TEG).23, 24, 25

Measuring Delta P is an excellent data point to aid intensivists in determining circuit health. Delta
P is the difference between the pressures on pre and post membrane outlets and provides the
transmembrane pressure gradient. An increase in the transmembrane pressure gradient coupled with
rising plasma-free Hgb levels could indicate clot formation within the oxygenator. The transmembrane
pressure gradient should remain less than 50 mmHg; if high, it requires proper anticoagulation or
replacement of the oxygenator.24, 23, 25 Furthermore, rapid rise throughout any shift could indicate
imminent pump failure and prompt intervention is required. Another indicator of pump failure is post
pump reduction of oxygen content in the post pump gas.23

Maximizing circuit life and being able to provide adequate ECMO circuit anticoagulation without
major bleeding events or thrombosis is challenging. Optimizing anticoagulation therapy is pivotal.
Anticoagulation is generally achieved using unfractionated heparin—commonly utilized exclusively
during ECMO due to its rapid onset of action, widespread availability, and familiarity to providers,
as well as the ability to reverse its action with protamine. Yet, heparin has innate limitations that
influence fluctuations in dose sensitivity as well as heparin-induced thrombocytopenia.25 Typically,
heparin infusions are employed as the sole agent because the role and safety of antiplatelet drugs in
the management of VV ECMO are unclear. However, antiplatelet agents may be used when additional
indications are present.25 Direct thrombin inhibitors, such as bivalirudin, offer advantages during ECMO
due to capabilities to attach to and inhibit both freely circulating and fibrin-bound thrombin and the
absence of HIT. Additionally, emerging data demonstrate superior balance between thrombosis and
hemorrhage and reliable pharmacokinetics with bivalirudin.25

Circuit DIC
As mentioned previously, the introduction of blood to the large surface of the ECMO circuit initiates
the intrinsic pathway of the coagulation cascade and induces an inflammatory response that can lead
to thrombotic complications as well as the potential for bleeding. This interaction between circulating
blood and the circuit’s artificial surfaces causes platelet activation and consumption of clotting
factors and results in a type of consumptive coagulopathy or “circuit DIC.”23,25 Under high shear stress
conditions typical to the ECMO circuit, high molecular weight von Willebrand factor (vWF) multimers
unfold, exposing their cleavage sites to ADAMTS13. Consequently, vWF will fall below the threshold in
which spontaneous bleeding occurs causing acquired von Willebrand syndrome. Moreover, the risk of
developing systemic hyperfibrinolysis secondary to fibrinolytic activation distinctive to the ECMO circuit
is significant and can lead to further systemic bleeding.23,25

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Cannula placement
To help minimize recirculation, confirm cannula location daily by either chest radiograph or point of
care ultrasound. Recirculation in VV ECMO hinders oxygenated blood flow and does not contribute
to systemic oxygen delivery, thus reducing the efficacy of ECMO therapy.22,23 In a properly positioned
VV ECMO circuit, deoxygenated blood is drained from the inferior vena cava (IVC), flows through the
oxygenator for gas exchange, returns to the superior vena cava, and is then pumped systemically by the
heart. If unwelcomed recirculation is occurring, a proportion of oxygenated blood is drained back into
the ECMO circuit rather than being pumped systemically, going from the return cannula directly to the
drainage cannula.22 Recirculation is affected by several factors including configuration and positioning
of the cannulas, ECMO blood flow, cannula size and pump speed, cardiac output, and intrathoracic/
intra-abdominal pressures.22,23 It is important to note that recirculation can occur in a dual lumen cannula
but occurs frequently when two single lumen cannulas are used and should be evaluated by CXR or
ultrasound if unexplained hypoxemia occurs.22

Right ventricular dysfunction or failure is not unknown to VV ECMO patients. Frequently, acute
respiratory distress syndrome is complicated by pulmonary hypertension and causes right ventricular
failure in nearly 10-25% of afflicted patients.24 Patients with severe ARDS who are referred for VV
ECMO have a higher incidence, up to 50%, of pulmonary hypertension and RV failure is already present
which leads to greater mortality.24 Because there is an associated higher mortality, patient management
is tailored to symptoms and drug treatment options. Some institutions perform routine transthoracic
echocardiograms (TTE) to assess right ventricular function as well as acute cor pulmonale which may
compromise LV filling.24 Occasionally, pulmonary artery catheters are placed to directly measure cardiac
chamber pressure and therapy is driven accordingly. Maintaining neutral to negative fluid balance is
typically achieved with diuretic use or renal replacement therapy.

Cannula dislodgement with loss of therapy is one of the most feared complications during ECMO support.
The highest risk factor is patient movement, either alone or with healthcare staff aiding in turns, coupled
with poor securement of cannulas. It is essential that staff be vigilant of cannula placement during daily
bathing, physical therapy, and repositioning. ECMO specialists must be present for patient movement
and must use multiple methods for securing cannulas. If the lines are secured and specialists are directly
managing the cannulas, patients with ECMO catheters can safely ambulate or be proned with no
increased risk.23

Circuit disruption
The entrainment of air due to a violation in the circuit pre-pump can lead to a catastrophic event such as
“airlock.” When airlock occurs the pump abruptly stops, which could cause patient demise or disastrous
neurological and cardiac events. The oxygenator is designed to trap air and has ports for air retrieval. Air
that cannot be expressed from the oxygenator could potentially cause an air embolism, increasing the
risk of neurologic complications from gaseous microemboli as well as cardiac arrest.23

Neurologic complications are often the most dreaded outcomes associated with the use of ECMO. As
described earlier, the massive inflammatory reaction responsible for elevated levels of anticoagulation
can lead to devastating intracranial bleeding and frequent neurological evaluations are vital given that
this carries a high mortality for these patients.23,26 Furthermore, studies have found that rapid correction
in PaCO2 during the early phase after initiation of VV ECMO is associated with intracranial bleeding.
Providers need to be mindful to provide ultra-lung protection ventilation strategy and solely focus on
adjusting the ECMO circuit for that reason. Frequent arterial blood gas sampling is key to successful
titration of FiO2 and sweep gases to avoid such complications in the early phase.27

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Management to reduce lung injury includes daily assessment of mechanical power, plateau and driving
pressures, as well as static and dynamic compliance to ensure ongoing ultra-lung-protective ventilation.
According to the recent ECMO to Rescue Lung Injury in Severe ARDS (EOLIA) trial, it may be prudent to
manipulate tidal volumes for a goal plateau airway pressure of ≤24 cmH2O in combination with PEEP ≥10
cmH2O; which would correspond to a driving pressure ≤14 cmH2O.22 Respirations should also be kept
low, ≤10 if possible. Providers must be aware that decreasing tidal volumes <4 mL/kg PBW may increase
atelectasis resulting in ventilation/perfusion mismatch and higher ECMO blood flow rates unless PEEP is
optimized.25 Higher blood flow rates can result in greater volume expansion, waning extravascular lung
water, generalized fluid overload, higher sedation requirements, and an inability to safely awaken patients
without compromising blood flow rates.22 Consequently, falling into this vicious cycle prolongs the duration
of ECMO support. Supporting patients with the minimum possible ECMO blood flow rates has advantages
and optimization of flow rates may allow more fluid restrictive and lung protective strategies.26

Institutions may employ protocol-driven weaning strategies to facilitate liberation from ECMO support.
However, protocol-driven modulation of blood flow rates is not commonplace and may result in
higher flows than physiologically necessary and this exposes patients to inherent risks.22 Traditional
approaches to VV ECMO weaning regard blood flow rates as a static variable and focus on reducing
sweep gas flow rates. While this approach is reasonable, it preserves flow rates when the patient’s
needs may be lower. The goal of weaning is to transition from near complete ECMO dependency to
some ECMO dependency, which is largely reliant upon oxygenation and decarboxylation. Once ECMO
blood flow rates are weaned to the lowest possible parameters, typically around 2-2.5 L/min, while
maintaining ultra-lung-protection, minimizing sedation, discontinuing neuromuscular blocking agents
(NMBA), and maintaining SpO2 ≥88%, the sweep gas may be “clamped” or turned off.22 If weaning is
successful, the intensity of mechanical ventilation may be upgraded from ultra-lung-protective to lung-
protective strategies.

Providers involved in the daily management of VV ECMO patients must watch for signs and symptoms
of infection. Infections occur in more than half of patients receiving ECMO support with nearly 10-21%
being nosocomial infections.23, 28, 29 The length of ECMO support is the greatest predictor of infectious
complications. Bloodstream infections are not an unexpected finding and have a prevalence of 3-18%
followed by lower respiratory tract infections.23 Bloodstream infections are largely circuit related. A
recent analysis found that the oxygenator membrane is a potential source of infection. Gram positive
bacteria such as coagulase-negative Staphylococcus and Candida were responsible for 72% of positive
findings in that study.30 A recent study found that prophylactic use of broad-spectrum antibiotics
accounted for an increased incidence of fungemia.23, 29

Another area of concern in daily management of ECMO patients is functional loss and long-term
complications. Severe critical illness often riddles patients with great impairments. ECMO survivors
are at an extremely high risk for the functional, psychological, and emotional impairments of “post-ICU
syndrome” and proper patient and family counseling should be initiated at the earliest time possible.
Furthermore, being mindful of patient selection in terms of adequate pre-morbid functional status
allows for meaningful functional recovery.23, 31

Detection and treatment of psychological trauma is pivotal in ECMO survivors. The prevalence of PTSD,
anxiety, and depression is higher in patients with longer ECMO support.32 Every effort should be made
to screen and appropriately treat mental health issues both in the hospital and following discharge.
Some institutions have dedicated follow-up clinics to provide a comprehensive approach to mental
health treatment. People with longer follow-up duration have far fewer difficulties than those who
did not attend therapy after hospitalization. Long term avoidance of mental health treatment has an
increased incidence of suicide among ECMO survivors with PTSD and severe depression.23,31,33

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Ventilator management
The initiation of VV ECMO allows for augmentation of oxygenation and highly efficient clearance of CO2.
The use of high tidal volumes exposes the lung parenchyma to significant parenchymal stress, resulting
in significant morbidity and mortality as evidenced by the ARDSNet trial.35 As a result, airway pressures
are progressively reduced following initiation of ECMO to obtain plateau pressures of 24 or less.36 This
may require reductions in tidal volumes to less than 4 cc/kg. Due to the heterogeneity of alveolar disease
in ARDS, excess volumes can cause significant increase in regional stress with small reductions in
functional alveoli.37

Terragni et al. demonstrated that reduction in the plateau pressure to 25-28 cmH2O produced less lung
injury, as evidenced by the lower cytokines production, compared to the group with plateau pressures
of 28-30 cmH2O.38 Classically a PEEP of 10-15 cmH2O is used to prevent intratidal collapse and prevent
worsening of the intrapulmonary shunt with reduction in total airway pressures. Excess PEEP should be
avoided due to risk of tidal hyperinflation. The ideal PEEP remains undefined, however a transpulmonary
pressure of 20-25 cmH2O theoretically mitigates injury to the lung. Obtaining accurate measurements is
difficult as pulmonary pressures are difficult to obtain in the presence of heterogenous disease. Optimal
FiO2 remains unclear, however in the first 24 hours FiO2 is reduced to 60%, with reductions below 40%
avoided due the potential for hypoxic pulmonary vasoconstriction.

Apnea is avoided as increased levels of oxygen would result in oxygen absorption and alveolar volume
loss. In addition to minimizing stress induced by the ventilator, intravascular volume status should be
closely monitored to avoid volume overload, and unless specific restrictions, prone positioning should
be considered following cannulation. Prior studies have demonstrated that a well-trained team can
successfully prone an ECMO patient without an increase in chest tube dislodgment, endotracheal tube
dislodgment, or disruption of ECMO flow.40

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GI and nutrition
Patients on extracorporeal support remain at extremely high risk for malnutrition. Once they have been
adequately resuscitated and a nutritional risk assessment has been completed, ECMO patients should
receive enteral nutrition within 24 hours with a hypocaloric (70-80% of the needs) and high protein
(2g/kg/day) strategy.41 The following variables demonstrate that patients are adequately resuscitated:
• Lactate is normal or normalizing
• Mean arterial pressure is above 65 mmHg
• Systolic pressure is >90 mmHg
• Intravascular volume is sufficient to achieve adequate perfusion

The quality of the evidence regarding nutrition in ECMO is low, but the evidence that exists clearly
shows a survival benefit when patients receive nutrition that meets their metabolic needs.42 The existing
guidelines for critically ill patients created by the European Society of Parenteral and Enteral Nutrition
and the American Society of Parenteral and Enteral Nutrition apply to critically ill ECMO patients. In
addition, there are 3 special considerations for ECMO patients:
• ECMO patients are among the most critically ill patients and will have the additional metabolic
stress of being on an extracorporeal circuit, so higher protein doses (2g/kg/day) have been shown
to improve outcomes.43
• The inflammatory response generated by continued exposure to the circuit tubing, membrane
lung, and centrifugal pump will increase their nutritional needs and thus increase their risk of
being malnourished.
• Extra attention to macro and micronutrient levels in ECMO patients is necessary, as some
evidence suggests that the ECMO circuit can deplete them.44 For example, administration of
500,000 IU of cholecalciferol within the first week in patients with significant deficiency may be
helpful in ECMO patients and is unlikely to cause harm.45
The use of enteral nutrition has been evaluated in six different studies including ARDS patients, mostly
prospective observational studies, and shown to be mostly well tolerated. Use of reverse Trendelenburg
position, or head of bed elevation 25-30 degrees is recommended, as well as careful monitoring for
vomiting and high gastric residual volumes.46 All patients on ECMO receive stress ulcer prophylaxis
with proton pump inhibitors. In the event of a small upper GI bleed, patients receive pantoprazole
intravenously every 12 hours and a lower anticoagulation dose. If bleeding is significant (requiring
more than one unit of packed red cells in 24 hours) then upper endoscopy is performed, and the
anticoagulation may be paused in patients supported with VV ECMO.

In summary, patients on ECMO should be enterally fed early once they have been resuscitated. If they
are not able to receive enteral feeding, then parenteral nutrition may be used after 5-7 days through
a separate line. ECMO patients who can be extubated may be able to receive oral nutrition. Nutrition
guidelines and the best evidence for management of adult critical care patients apply to ECMO patients
in most cases. ECMO patients remain at higher risk for malnutrition, will require more protein, and may
benefit from nutrient supplementation. Box 2 summarizes the GI and nutrition goals for this complex
patient population.

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BOX 2. KEY ASPECTS OF NUTRITION IN ECMO

• Start early enteral nutrition within 24 hours if patient resuscitated and adequately perfused;
hypocaloric (75% of the patient’s needs) strategy
• Advance toward goal in 24-48 hours
• High protein intake of up to 2g/kg/day
• Safe to feed in prone position (30° head elevation)
• Safe to feed when on low to moderate dose vasopressors if patient adequately resuscitated

Renal and volume management

Acute kidney injury (AKI) and renal failure are extremely common in ECMO patients, and they are both
linked to increased mortality. AKI is more common in VA ECMO than in VV ECMO and usually exists at the
time of ECMO initiation.50 The incidence of AKI reported in medical literature varies widely (26-85%), but
the pooled estimated incidence of AKI requiring renal replacement therapy (RRT) is 45%.50 Risk factors for
AKI in ECMO include:51,52
• Older age
• Higher APACHE II score
• Higher SOFA score
• Pre-existing comorbidities (eg, diabetes mellitus, cirrhosis)
• Delayed initiation of ECMO
• Longer duration of ECMO support
• Postcardiotomy shock
• Decreased LV ejection fraction
• Intraoperative transfusion
• High lactate
• Increased bilirubin
• High plasma free hemoglobin
• High neutrophil/lymphocyte ratio

Indications for RRT in ECMO patients are like those in other critically ill patients and include volume
overload refractory to medical therapy, acidosis, electrolyte abnormalities, toxin removal, and uremia. An
indication specific to patients on ECMO is the ability to remove volume slowly without disrupting ECMO
flow. Attempts at fluid removal with infusions of diuretics will often lead to access insufficiency that can
disrupt ECMO flow and put more stress on the blood cells. Equipoise exists regarding the timing of RRT,
although a large meta-analysis of 21,642 adults on ECMO support found an association between earlier
initiation of RRT and improved survival.53 Renal recovery in patients who require RRT while on ECMO
is less than 50% in most studies, and there is not a significant difference in renal recovery between
VV and VA ECMO. The mechanisms of AKI in ECMO patients listed in Table 2 are multifactorial and
complex, yet they provide insight into potential ways to attenuate AKI.

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Table 2. Key Mechanisms of AKI in ECMO Patients

PATIENT FACTORS ECMO CIRCUIT FACTORS

• Shock – hypoperfusion • Inflammatory response

• Hypoxia, hypercapnia • Shear stress on blood

• Nephrotoxins • Hemolysis and oxidative stress

• RAAS and ANP • Embolism

downregulation
• Deep coagulopathy
• Underlying disorder
• Bioincompatibility

• Continuous flow

Careful intravascular volume management improves outcomes in ECMO patients and requires a
multimodal approach. Robust evidence supports the correlation between less fluid administration and
fewer ICU and ventilator days. Multiple observational studies show that an increased cumulative fluid
balance increases mortality in critically ill patients.54,55 The ability to determine when an ECMO patient
who is being resuscitated would benefit more from a vasopressor versus a balanced crystalloid may
improve outcomes. The dynamic measurements of potential fluid responsiveness remain the most
validated, and include pulse pressure variation, stroke volume variation, passive leg raise, response to
fluid bolus, and use of lung, cardiac, and venous Doppler ultrasound. Although ECMO cannulas are
wire reinforced and can bend slowly without compromising flow, there is an understandable reluctance
to perform a passive leg raise in patients with femoral cannula. Measurement of changes in the left
ventricular outflow tract velocity time integral (VTI) during a Trendelenburg maneuver can predict fluid
responsiveness in ECMO.56 Table 3 describes some of the most validated methods of measuring fluid
responsiveness in patients.

Table 3. Validated Methods of Measuring Fluid Responsiveness in ECMO Patients

VENTILATED PATIENTS SPONTANEOUS BREATHING PATIENTS

• Pulse pressure variation > 12% • Passive leg raise – echo VTI

• Stroke volume variation > 2.5% • Fluid challenge – echo

• Passive leg raising – echo VTI • Clinical exam – feel legs

• Fluid challenge – echo • IVC collapse > 50%

measurements

If drainage insufficiency or decreased ECMO blood flow because of an excessively negative pressure
occurs, it is important to avoid reflexively giving additional fluids. The first step is to reduce ECMO blood
flow by decreasing the RPMs on the pump, and then check the cannula, circuit, and patient position. The
next step is to assess the patient’s fluid responsiveness before giving fluid. To avoid giving additional
unnecessary fluid to try and increase blood flow, investigate for correctible problems, and evaluate how
much ECMO blood flow the patient needs.57 If the patient needs a higher ECMO blood flow to perfuse
and oxygenate, then a fluid responsiveness evaluation is helpful before giving more fluid. Figure 1
identifies some potential causes of drainage insufficiency.

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Reduce pump speed

Check cannula and circuit
Position patient
Lung water will
decrease oxygenation
and slow recovery Assess fluid responsiveness
and consider fluid bolus

Evaluate and treat for:

• Agitation
• Bleeding
• Vasodilation
• Tension pneumothorax
Volume will • Cardiac tamponade
increase flow • Intra-abdominal hypertension
• Cannula clot or malposition

Figure 1. Drainage Insufficiency—

Place additional drainage cannula
ECMO Blood Flow Decreases

AKI is quite common in ECMO patients and is associated with decreased survival. A smaller cumulative
fluid balance leads to better outcomes in critically ill patients, and it is important to evaluate a patient’s
fluid responsiveness before giving more fluid. Adequate intravascular volume is necessary to achieve
sufficient ECMO blood flow, so prudent volume management is vital.

Physical therapy
Historically, VV ECMO cannulas have been inserted into the femoral veins leading to a constant supine
position which results in immobility. Typically, these patients are also deeply sedated. Consequently,
prolonged sedation and prolonged immobility may lead to several additional complications that result
in increased mortality, morbidity, and hospital length of stay. Furthermore, immobility and prolonged
sedation lead to complications such physical deconditioning, prolonged mechanical ventilation, and skin
breakdown.58-61 The use of alternate cannulation sites, including the internal jugular or subclavian veins,
has become possible with the introduction of bicaval dual lumen cannulas. The use of these alternative
sites takes away the need for strict supine positioning and promotes greater patient mobility.58 A
cannula in the groin, however, does not absolutely impede physical therapy.60

Despite alternatives in cannulation techniques, fear of adverse events such as decannulation, falls, and
bleeding from the insertion site, often causes hesitation in the initiation of physical therapy. To overcome
these concerns, it is prudent to have a multidisciplinary approach to performing physical therapy for
these patients. The multidisciplinary team is made up of anesthesiologists, surgeons, perfusionists,
physical therapists, nurses, respiratory therapists, and intensive care physicians (Figure 2).

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Physical
Therapist

Perfusionist Nurse

Surgeon Respiratory
Therapist

Anesthesiologist
PATIENT Intensive Care

SUCCESS
Physician

Figure 2. Multidisciplinary Team for Physical Therapy in ECMO Patients

Every member of the multidisciplinary team provides a unique perspective and contributes to patient success.

Advanced planning ensures that all needed support is available prior to beginning physical
therapy.58,59,62 Additionally it is important to perform a thorough screening on these patients that
includes establishing medical stability and assessment of hemodynamics.62 Screening also involves
assessing the stability of the ECMO circuit—as these flow devices are sensitive to gravity and changes
in angles—and ensuring that the cannulas are secure and stable. The patient’s functional and cognitive
readiness should also be a part of the screening process. Once the patient is deemed stable for physical
therapy, a detailed plan should be devised from a multidisciplinary approach34,62 (Box 3).

BOX 3. MULTIDISCIPLINARY SCREENING PRIOR TO PHYSICAL THERA-

PY IN ECMO PATIENTS
Assess all components prior to each session to determine patient's readiness for physical therapy:
• Establish medical stability (assess hemodynamics)
• Assess the stability of the ECMO circuit
• Assess patient’s functional readiness
• Assess patient’s cognitive readiness

It has been demonstrated that survival to hospital discharges is greater in patients who ambulate and
perform physical therapy.58 To reap the greatest benefit, it is recommended that physical therapy be
started as early as 2-5 days after cannulation and that it start with passive movement of the joints. This
helps maintain joint mobility, prevent muscular contractures, maintain the extensibility of soft tissue, and
preserve function with the goal of progression to more active movement. If patients cannot undergo
active physical therapy, in-bed positioning, such as sitting up in bed, can serve as a preventative activity.
In this patient population, independent feeding is also important.59

In conclusion, early mobilization leads to better outcomes in patients who require VV ECMO. A highly trained
multidisciplinary team and aggressive screening process is required to ensure success in these patients.

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22. Shekar K, Buscher H, Brodie D. Protocol-driven daily optimization of venovenous extracorporeal membrane
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27. Guennec LL, Cholet C, Huang F, et al. Ischemic and hemorrhagic brain injury during venoarterial extracorporeal
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28. Aubron C, Cheng AC, Pilcher D, et al. Infections acquired by adults who receive extracorporeal membrane
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29. Sun HY, Ko WJ, Tsai PR, et al. Infections occurring during extracorporeal membrane oxygenation use in adult patients.
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30. Biffi S, Di Bella S, Scaravilli V, et al. Infections during extracorporeal membrane oxygenation: epidemiology, risk
factors, pathogenesis and prevention. Int J Antimicrob Agents. 2017;50(1):9-16.

31. Schmidt M, Zoghieb E, Rozé H, et al. The PRESERVE mortality risk score and analysis of long-term outcomes
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32. Marasco SF, Lukas G, et al. Extra corporeal membrane oxygenation (ECMO) in the intensive care unit. St Vincent’s
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33. McDonald MD, Sandsmark DK, Palakshappa JA, et al. Long-term outcomes after extracorporeal life support for acute
respiratory failure. J Cardiothorac Vasc Anesth. 2019;33(1):72-9.

34. Ko YJ, Cho YH, Park YH, et al. Feasibility and safety of early physical therapy and active mobilization for patients on
extracorporeal membrane oxygenation. ASAIO J. 2015;61(5):564-8.

35. Acute Respiratory Distress Syndrome Network; Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal
volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.
N Engl J Med. 2000;342(18):1301-8.

36. Combes A, Hajage D, Capellier G, et al. Extracorporeal membrane oxygenation for severe acute respiratory distress
syndrome. N Engl J Med. 2018;378:1965-75.

37. Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol.
1970;28(5):596-608.

38. Terragni PP, Del Sorbo l, Mascia L, et al. Tidal volume lower than 6 ml/kg enhances lung protection: role of
extracorporeal carbon dioxide removal. Anesthesiology. 2009;111(4):826-35.

39. Araos J, Alegria L, Garcia P, et al. Near-apneic ventilation decreases lung injury and fibroproliferation in an acute
respiratory distress syndrome model with extracorporeal membrane oxygenation. Am J Respir Crit Care Med.
2019;199(5):603-12.

40. Lucchini A, Bambi S, Mattiussi E, et al. Prone position in acute respiratory distress syndrome patients: a retrospective
analysis of complications. Dimens Crit Care Nurs. 2020;39(1):39-46.

41. D’Alesio M, Martucci G, Arcadipane A, et al. Nutrition during extracorporeal life support: a review of
pathophysiological bases and application of guidelines. Artificial Organs. 2022:00:1-9.

42. Xu E, Tejada S, Solé-Lleonart C, et al. Evaluation of the quality of evidence supporting guideline recommendations for
the nutritional management of critically ill adults. Clin Nutr ESPEN. 2020;39:144-9.

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43. Pelekhaty SL, Galvagno SM Jr, Lantry JH, et al. Are current protein recommendations for the critically ill adequate for
patients on VV ECMO: experience from a high-volume center. J Parenter Enteral Nutr. 2020; 44(2):220-6.

44. Estensen K, Shekar K, Robins E, et al. Macro- and micronutrient disposition in an ex vivo model of extracorporeal
membrane oxygenation. Intensive Care Med Exp. 2014;2(1):29.

45. Nair P, Venkatesh B, Hoechter DJ, et al. Vitamin D status and supplementation in adult patients receiving
extracorporeal membrane oxygenation. Anaesth Intensive Care. 2018;46(6):589-95.

46. Al-Dorzi HM, Arabi YM. Enteral nutrition safety with advanced treatments; extracorporeal membrane oxygenation,
prone positioning, and infusion of neuromuscular blockers. Nutr Clin Prac. 2020;36(1):88-97.

47. Roth C, Schrutka L, Binder C et al. Liver function predicts survival in patients undergoing extracorporeal membrane
oxygenation following cardiac surgery. Crit Care. 2016:20:57.

48. Sparks BE, Cavarocchi NC, Hirose H. Extracorporeal membrane oxygenation with multiple-organ failure: can
molecular adsorbent recirculating system therapy improve survival? J Heart Lung Transplant. 2017;36(1):71-6.

49. Walayat S, Shoaib H, Asghar M, et al. Role of N-acetylcysteine in non-acetaminophen related acute liver failure, an
updated meta-analysis and systematic review. Ann Gastroenterol. 2021;34(2):235-40.

50. Thongprayoon C, Cheungpastiporn W, Lertjitbanjong P, et al. Incidence and impact of acute kidney injury in patients
receiving extracorporeal membrane oxygenation; a meta-analysis. J Clin Med. 2019;8:981.

51. Mou Z, Guan T, Chen L. Risk factors of acute kidney injury in ECMO patients: a systematic review and meta-analysis. J
Intensive Care Med. 2022;37(2):267-77.

52. Lepère V, Duceau B, Lebreton G, et al. Risk factors for developing severe acute kidney injury in adult patients with
refractory post cardiotomy cardiogenic shock receiving veno-arterial extracorporeal membrane oxygenation. Crit Care
Med. 2020;48(8):e715-21.

53. Han SS, Kim HJ, Lee SJ, et al. Effects of renal replacement therapy in patients receiving extracorporeal membrane
oxygenation: a meta-analysis. Ann Thorac Surg. 2015;100(4);1485-95.

54. Chiu L, Chuang L, Lin S, et al. Cumulative fluid balance during extracorporeal membrane oxygenation and mortality in
patients with acute respiratory distress syndrome. Membranes (Basel). 2021;11(8):567.

55. Schmidt M, Bailey M, Kelly J, at al. Impact of fluid balance on outcome of adult patients treated with extracorporeal
membrane oxygenation. Intensive Care Med. 2014;40(9):1256-66.

56. Luo J, Su Y, Dong L, et al. Trendelenburg maneuver predicts fluid responsiveness in patients on veno-arterial
extracorporeal membrane oxygenation. Ann Intensive Care. 2021;11(1):16.

57. Zakhary B, Vercaemst L, Mason P, et al. How I manage drainage insufficiency on extracorporeal membrane
oxygenation. Critical Care. 2020;24:151.

58. Boling B, Dennis DR, Tribble TA, et al. Safety of nurse-led ambulation for patients on venovenous extracorporeal
membrane oxygenation. Prog Transplant. 2016;26(2):112-6.

59. Polastri M, Loforte A, Dell’Amore A, Nava S. Physiotherapy for patients on awake extracorporeal membrane
oxygenation: a systematic review. Physiother Res Int. 2016;21(4):203-9.

60. Garcia JP, Kon ZN, Evans C, et al. Ambulatory veno-venous extracorporeal membrane oxygenation: innovation and
pitfalls. J Thorac Cardiovasc Surg. 2011;142(4):755-61.

61. Marhong JD, DeBacker J, Viau-Lapointe J, et al. Sedation and mobilization during venovenous extracorporeal
membrane oxygenation for acute respiratory failure: an international survey. Crit Care Med. 2017;45(11):1893-9.

62. Wells CL, Forrester J, Vogel J, et al. Safety and feasibility of early physical therapy for patients on extracorporeal
membrane oxygenator: University of Maryland Medical Center experience. Crit Care Med. 2018;46(1):53-9.

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PREVIOUS CHAPTER Chapter 19: ECMO Patient Management, Weaning, Troubleshooting, LV Unloading, and Closure NEXT CHAPTER

ECMO Patient
Management,
Weaning,
Troubleshooting,
LV Unloading,
and Closure

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19.1
Managing VA
ECMO in the ICU
Kari Gorder, MD
Cardiovascular Critical Care and Emergency Medicine
OhioHealth Riverside Methodist Hospital
Columbus, OH
[Link]@[Link]

Timothy D. Smith, MD, FSCAI

Interventional Cardiovascular and Critical Care Medicine
OhioHealth Riverside Methodist Hospital
Columbus, OH
Timothy.Smith3@[Link]

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Introduction
Successful outcomes for patients requiring veno-arterial extracorporeal membrane oxygenation (VA
ECMO) are contingent upon thoughtful patient selection, precise technical skills during cannulation,
and expert management in the intensive care unit (ICU) after cannulation. This chapter highlights some
of the keys to device and patient management as well as special considerations for the ICU patient
requiring VA ECMO support.

Device management
Device securement
After cannulation, cannulas should be adequately sutured into position and all tubing connections
should be banded securely with a tie gun. At the percutaneous access sites, an occlusive transparent
dressing (eg, Tegaderm) should be applied so that the access sites can be visually inspected by the
bedside nurse routinely. Care should be taken that no excess tension is created by the dressing material
that could transmit to the cannulae, including the reperfusion sheath, if present.

Anticoagulation
Although there is no clear consensus on the management of anticoagulation, most patients on VA
ECMO will require systemic anticoagulation. This is commonly achieved with unfractionated heparin, but
some centers choose to use a direct thrombin inhibitor.1 A variety of laboratory monitoring strategies
exist, including activated clotting time (ACT), aPTT, and anti-Xa tests. Although less conventional,
there is also some data to suggest that thromboelastography (TEG) can be safely used to guide
anticoagulation. In circumstances when bleeding complications pose a significant life threat to the
patient on VA ECMO or at centers that choose to avoid routine systemic anticoagulation, cessation of
anticoagulation for patients on VA ECMO may be feasible for short durations at higher flow rates.2

Circuit monitoring
Due to the high complexity of managing patients on VA ECMO, it is recommended that the circuit be
monitored routinely by bedside nursing staff as well as ECMO specialists or perfusionists. A full circuit
check should be performed every 12 hours and include:
• Access site assessment
• Evaluation for kinks in the tubing or turbulent flow
• Assessment for color change in the tubing
• Evaluation of the membrane oxygenator for clots or fibrin
We recommend that pre- and post-oxygenator ABGs are performed on an FdO2 of 100% daily or more
frequently as needed to assess for the presence of recirculation or impending oxygenator failure (Figure 1).
ECMO settings should be recorded hourly in the patient chart. We also recommend that the ECMO specialist
or perfusionist documents a pertinent device-related summary each shift. An example of what this summary
might contain, while not exhaustive, is shown in Box 1. The clinician and team should carefully review this
data for malignant trends.

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BOX 1. ECMO DOCUMENTATION EACH SHIFT

Pump speed and flow
Pint, Part, Pven, ΔP
Set temperature, patient temperature
SvO2, SpO2, PaO2
ACT and ACT goal range (or other anticoag test)
FdO2%
Sweep gas flow rate
Mechanical ventilator settings
Alarms or mechanical issues during shift
Physical appearance of oxygenator
Pertinent drips, patient events and plan of care

Figure 1. ECMO Circuit Monitoring

Note the similar appearance of the blood in both the drainage and return
cannulae in this patient with oxygenator failure, and the improvement after
changing to a new circuit.

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Patient management
General principles
For patients with cardiogenic shock requiring VA ECMO support, a strategy for decannulation must
be considered early on, ideally prior to cannulation in most circumstances. For some patients, primary
myocardial recovery is the principle (or only) option. For other patients, VA ECMO serves as a bridge
to temporary or durable ventricular assist device (VAD) placement or cardiac transplant. It cannot be
stressed enough that a multidisciplinary team with expertise in advanced heart failure management
must discuss an “exit strategy” early after a patient’s cannulation, ideally at a cardiac referral center with
high ECMO volume. Longer duration on VA ECMO is associated with increased mortality; after four days
on circuit, survival begins to decrease.3

ECMO-specific care
Patients on VA ECMO are by definition critically ill, and complications can and do arise. The most
common complications for patients on VA ECMO are bleeding, stroke, infection, leg ischemia, and
hemolysis. Diligent laboratory and patient monitoring are critical to early identification and mitigation of
these complications. A suggested ECMO-specific care schedule is presented in Box 2.

BOX 2. SUGGESTED ECMO-SPECIFIC MONITORING SCHEDULE

IN THE ICU*
Labs Patient Monitoring
ABG (patient) q4 or with changes Doppler extremity pulses q1h
CBC q6h Neuro exam q shift or per protocol
BMP/Mg/Phos q6h
CXR daily
Lactate q6h
Cardiac echo PRN
LDH/pfHgb daily
CK daily Goals
Flow > 3 lpm, Sweep > 0.1 lpm
LFTs daily
MAP > 65, CVP 8-10
INR daily
Hgb > 8-10, Plt > 50k
Coag monitoring per protocol
SaO2 > 90% (patient); SvO2 > 60%
Type & Screen q3days

*All goals and monitoring frequencies should be adjusted based on clinical acuity

Best-practice ICU care

Management of a patient on VA ECMO is ideally performed in an ICU with extensive experience caring
for patients on mechanical circulatory support devices. While ECMO is associated with its own set of
complications, quality ICU care is also integral to survival in these critically ill patients. The role of a
multidisciplinary Heart Team, with mechanical circulatory support and critical care experience, cannot
be understated. Box 3 includes some best-practice ICU concepts, frequently referred to as an “ICU
checklist,” which should be addressed for every patient on VA ECMO, if indicated or applicable.

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BOX 3. ICU CHECKLIST FOR VA ECMO PATIENTS

DVT prophylaxis
GI prophylaxis
Ventilator-associated pneumonia (VAP) prophylaxis
Spontaneous breathing trial (SBT)
Spontaneous awakening trial (SAT)
Bowel regimen
Delirium precautions
Review of lines, tubes, and drains
Review of active medications
PT/OT, social work planning and family engagement

Special considerations
Weaning
Efforts to liberate the patient from VA ECMO should be a result of dynamic patient assessment
and vigilant monitoring. Some conditions, such as viral cardiomyopathy, may lend themselves more
toward rapid recovery, compared to other disease states, such as dilated ischemic cardiomyopathy.
Major metabolic disturbances should be stabilized, oxygenation should be stable (ie, the native
cardiopulmonary circulation will suffice for oxygenation), and vasoactive medications should be weaned
or off (although many patients will require vasoactive medications to facilitate decannulation). Increasing
arterial line pulsatility may also portend myocardial recovery.

While ECMO weaning strategies vary, a common method involves decreasing ECMO flows to 1-1.5 L/min
and assessing echocardiographic function as well as using invasive hemodynamic monitoring to evaluate
a patient’s response to the decrease in support. A more objective method to assess readiness is an aortic
velocity-time interval (VTI) ≥10 cm/s or a lateral mitral annulus peak systolic velocity ≥6 cm/s. Care should
be taken to evaluate for both left and right ventricular recovery.1

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PITFALLS & PEARLS BASED ON THE AUTHORS’ EXPERIENCE AND

BEST PRACTICE STANDARDS
• Most patients on VA ECMO will benefit from an LV venting/offloading strategy.
• Superficial femoral artery reperfusion sheaths are standard of care for peripherally
cannulated patients and should also be considered bilaterally if there is an Impella® in
place (Figure 2).
• Right radial arterial ABG monitoring is integral to detecting the presence of differential
hypoxia.
• Ambulation is possible for femorally cannulated VA ECMO patients but should only be
attempted at high-volume centers with specially trained physical therapy staff.
• Extubating patients on VA ECMO is feasible, but patients often have disordered
breathing patterns and are more comfortable on mechanical ventilation.

Figure 2. Peripherally Cannulated VA ECMO With Impella for LV

Offloading (“ECpella”) With Bilateral SFA Reperfusion Sheaths

QUICK READ SUMMARY

✓ Ideally, prior to patient cannulation for VA ECMO, a multidisciplinary Heart Team should be
convened to discuss the strategies for liberation from mechanical circulatory support.

✓ The same evidence-based, best-practice principles of ICU management for general medical
patients apply to all patients on VA ECMO.

✓ Vigilance in patient monitoring, dynamic reassessment, and adherence to protocols will help
to mitigate some of the complications associated with VA ECMO in the ICU.

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References
1. Brogan TV, Lequier L, Lorusso R, MacLaren G, Peek G. Extracorporeal Life Support: The ELSO Red Book. 5th edition.
Ann Arbor, MI: Extracorporeal Life Support Organization; 2017.

2. Fina D, Matteucci M, Jiritano F, et al. Extracorporeal membrane oxygenation without systemic anticoagulation: a case-
series in challenging conditions. J Thorac Dis. 2020;12(5):2113-19.

3. Smith M, Vukomanovic A, Brodie D, et al. Duration of veno-arterial extracorporeal life support (VA ECMO) and
outcome: an analysis of the Extracorporeal Life Support Organization (ELSO) registry. Crit Care. 2017;21(1):45.

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19.2
Anticoagulation
& Transfusion
Strategies in ECMO
Emily Larnard, MD
Cardiology Fellow
Division of Cardiovascular Medicine
Beth Israel Deaconess Medical Center
Boston, MA

Bharath G. Rathakrishnan, MD, FSCAI

Interventional Cardiologist & Structural Heart Fellow
Division of Cardiovascular Medicine
Beth Israel Deaconess Medical Center
Boston, MA

Jeffrey A. Marbach, MBBS, MS, FRCPC, FSCAI

Interventional Cardiologist & Cardiac Intensivist
Division of Cardiology, Knight Cardiovascular Institute
Assistant Professor
Oregon Health & Sciences University
marbach@[Link]
@JAMarbach

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Overview
Extracorporeal membrane oxygenation (ECMO) is increasingly being utilized in the critical care
setting to provide temporary respiratory or cardiorespiratory support.1 Irrespective of the precise
indication for extracorporeal support, anticoagulation is commonly administered to prevent oxygenator
thrombosis, maintain patency of the circuit, and avoid thromboembolic complications.2 In addition to
the potential adverse thrombotic events, it has been estimated that bleeding will occur in up to 60%
of patients supported on ECMO, thereby demonstrating the delicate balance that must be achieved
between anticoagulation and hemostasis.3 In this chapter, we discuss the most frequently encountered
complications during extracorporeal support, as well as recommended anticoagulation and transfusion
targets aimed at minimizing these events.

Thrombotic & hemorrhagic complications

Among patients treated with ECMO, both thrombotic and hemorrhagic complications are associated
with significant morbidity and mortality.

Thrombotic complications
Complications related to thrombosis can occur in the extracorporeal circuit and within the patient’s
cardiovascular system (Figure 1). Thrombi can form anywhere along the circuit, but microthrombi of
the oxygenator are the most frequently encountered.4,5 The oxygenator should routinely be evaluated
for accumulating thrombus through visual inspection and frequent monitoring of the pressure gradient
across the oxygenator, as sudden oxygenator failure can occur requiring immediate replacement.
Systemic thromboembolism resulting in pulmonary embolism, deep venous thrombosis, and limb
ischemia is also commonly observed. In a systematic review and meta-analysis Cheng and colleagues
found that lower extremity ischemia was present in more than 15% of patients with 7-15% of patients
having compartment syndrome and/or requiring fasciotomy, and 5% requiring amputation.3

A B C D

Figure 1. ECMO Complications

(A) Massive pulmonary emboli status post pulmonary embolectomy; (B) microthrombi resulting in oxygenator failure; (C) ischemic lower extremity;
(D) common femoral artery pseudoaneurysm (arrow)

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Hemorrhagic complications
Hemorrhagic complications, which are the result of a combination of pharmacological anticoagulation,
acquired von Willebrand disease resulting in platelet dysfunction, and excessive coagulant
consumption, occur with greater frequency than thrombotic complications and portend similar morbidity
and mortality. In a report from the extracorporeal life support (ECLS) working group on thrombosis and
hemostasis, Mazzeffi et al. retrospectively analyzed adult patients treated with ECMO over a 3-year
period and found that the majority of patients (56%) had serious bleeding events.6 Moreover, there
was a trend toward decreased 90-day survival among patients who bled (46.7% vs. 64.9%) and the
adjusted odds ratio for mortality was 1.03 for each unit of red blood cells (RBCs) transfused.

Together these results demonstrate the importance of maintaining strict anticoagulation targets,
minimizing iatrogenic sources of bleeding, aggressive surveillance for both bleeding and thrombosis,
and careful consideration of transfusion goals.

Anticoagulation
As blood is circulated through the ECMO circuit and comes in contact with a non-endothelial surface
a pro-thrombotic state is triggered. Anticoagulation with close monitoring is thus required to avoid
thromboembolism in the patient and throughout the circuit. However, hemostasis also remains a
challenge for patients being managed with ECMO.

Unfractionated heparin
Unfractionated heparin (UFH) is the most commonly used anticoagulant in adult patients on ECMO.7
It is often preferred due to its immediate onset when administered intravenously as well as its easy
reversibility with protamine. UFH exerts its effect indirectly by binding to antithrombin. Binding of UFH
causes a conformational change in antithrombin and a 1,000 fold increase in antithrombin inhibition
of thrombin and other clotting factors.8 This prevents clot formation and prolongs clotting time. UFH
is metabolized both by the reticuloendothelial system and the kidneys.9 UFH can be monitored with
activated clotting time (ACT), activated partial thromboplastin time (aPTT), anti-Xa assay or viscoelastic
hemostatic assays (VHA). The Extracorporeal Life Support Organization (ELSO) does not recommend
a particular laboratory test, but rather recommends a tailored strategy for each patient based on their
broader clinical situation.10

Disadvantages of UFH use include varying pharmacokinetics, as heparin binds to several circulating
plasma proteins in addition to antithrombin. Heparin induced thrombocytopenia (HIT) can also occur
in 0.2 to 5% of adult patients.11 HIT occurs when platelet factor 4 binds to UFH and triggers formation
of antibodies against this complex. Binding of IgG triggers platelet activation and a prothrombotic
state resulting in thrombocytopenia along with arterial and venous thrombosis. The differential for
thrombocytopenia in ECMO patients is broad; the 4T score can be used to determine which patients
would most benefit from testing for HIT.12 Testing is done with both immunoassays and functional
assays, however an alternative anticoagulant should be used if HIT is suspected or confirmed.13

Direct thrombin inhibitors

The two commonly used direct thrombin inhibitors (DTIs) in ECMO are bivalirudin and argatroban.
DTIs bind directly to thrombin and, unlike UFH, do not bind to any other plasma proteins, making
DTI pharmacokinetics more predictable. DTI use is monitored with aPTT levels. Bivalirudin is given
intravenously with an onset of action within 2 to 4 minutes and a half-life of about 25 minutes. It is
metabolized primarily by proteolytic cleavage, however about 20% is cleared renally.14 Dosing may need
adjustment in the setting of renal dysfunction.15

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Disadvantages of DTIs include higher cost and lack of pharmacologic reversal agent, although the half-
life of these medications is short. Additionally, ECMO experience is more limited with DTIs and while
retrospective case series have evaluated the use of DTIs in ECMO compared to UFH, large prospective
randomized trials are lacking.16–22 Bivalirudin should be used with caution in low flow states such as
severe cardiac dysfunction due to the risk of intracardiac thrombus.23 Clotting can also occur in low
flow areas in the circuit when on bivalirudin, such as venous access sites or reperfusion cannulas.10
Resistance phenomenon has been reported both with bivalirudin24,25 and argatroban.26

Table 1. Anticoagulants

MECHANISM HALF-LIFE
ANTICOAGULANT METABOLISM ADVANTAGES DISADVANTAGES
OF ACTION (MINS)

UFH Binds to 60-90 • Reticuloendothelial • Inexpensive • Binds to plasma

antithrombin system • Antidote proteins
inhibiting • Renal clearance (protamine) • Heparin induced
thrombin and thrombocytopenia
• Many monitoring
Xa (HIT)
strategies

Bivalirudin Reversibly 25 • Proteolytic • Can be used in • No antidote

binds to cleavage HIT • Cost
thrombin • Renal clearance • Caution with
blood stasis
• Caution with renal
dysfunction

Argatroban Reversibly 45 • Hepatic clearance • Can be used in • No antidote

binds to HIT • Cost
thrombin • Caution with liver
dysfunction

Therapeutic monitoring
Activated clotting time
Activated clotting time (ACT) has been the most prominent method for monitoring ECMO anticoagulation
with UFH due to experience using ACT during cardiopulmonary bypass, as well as its availability as a
point of care test at most institutions.10 A whole blood sample is used to measure the time for initial fibrin
formation after the addition of coagulation activators. Several factors can impact ACT accuracy including
hemodilution, anemia, hypothermia, coagulation factor deficiencies, hypofibrinogenemia, platelet function,
and presence of GPIIb/IIIa antagonists.

Activated partial thromboplastin time

Activated partial thromboplastin time (aPTT) is widely available and is the standard monitoring test
for UFH. It is also the standard monitoring test for DTIs. A plasma sample is used to measure fibrin
formation. As this is a plasma-based test, results are not impacted by platelet count or anemia. Target
ranges can vary based on laboratory, reagent, and machine. In critically ill patients, nonspecific acute
phase reactants may impact the assumed linear relationship between UFH dose and aPTT, resulting in
wide variability in aPTT levels.10

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Anti-Xa assay
The anti-Xa assay is a direct measure of heparin inhibition, as it is a functional assay of the ability of
UFH to catalyze antithrombin inhibition of factor Xa. It is therefore not used for DTIs. Results can be
impacted by hyperlipidemia, hyperbilirubinemia, and high plasma-free hemoglobin.27

Viscoelastic hemostatic assays

Viscoelastic hemostatic assays (VHA), including TEG and ROTEM, measure the ability of a whole
blood sample to form a clot. These point of care assays provide a comprehensive assessment of
blood coagulability including time to initial fibrin formation, clot strength, speed of fibrin cross linking
and onset of fibrinolysis. VHAs are currently used to guide resuscitation in the setting of surgery or
trauma,29,30 however there is growing interest in their use to predict clotting and bleeding.31,32

Antithrombin monitoring
Antithrombin is produced by the liver. In ECMO patients with prolonged UFH exposure, antithrombin
can be consumed more quickly than it is produced. There is concern that low levels of antithrombin may
mitigate the effect of UFH leading to heparin resistance. However, there has not yet been convincing
data demonstrating benefit from replacing antithrombin with FFP or antithrombin concentrate.28 The
ELSO does not currently recommend routine antithrombin monitoring or supplementation.10

Table 2. Anticoagulant Monitoring

ANTICOAGULANT DOSING THERAPEUTIC RANGE MONITORING FREQUENCY

UFH Initiation at time of ECMO Initiation: ACT: > 250 Anti-Xa every 6 hours
cannulation: Bolus: 50-100 seconds
units/kg
Maintenance: Anti-Xa:
Maintenance: UFH 10 U/kg/hr 0.2-0.4 (for both VA
and VV ECMO)
Heparin rate adjusted based on
subsequent anti-Xa levels with Higher anti-Xa goals
infusions held for 30-60 minutes are targeted in patients
for supratherapeutic levels with other indications
for anticoagulation

Bivalirudin Dosing is dependent on renal aPTT: 50-70 seconds aPTT every 2 hours initially
function. Drip is initiated without
a bolus. aPTTs can subsequently be
spaced to every 8 hours after
CrCl>60: 0.08 mg/kg/hr 2 consecutive therapeutic
CrCl 30-60: 0.05 mg/kg/hr readings
CrCl <30: 0.02 mg/kg/hr
Requiring CRRT: 0.02 mg/kg/hr
Requiring intermittent HD: 0.01
mg/kg/hr

Argatroban Initiated without bolus aPTT: 50-70 seconds aPTT every 4 hours initially

0.5 mg/kg/min aPTTs can subsequently be

spaced to every 6 hours after
Dosing decreased for patients 2 consecutive therapeutic
with hepatic dysfunction (0.02- readings
0.1 mg/kg/min)

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Blood product replacement targets

Bleeding complications continue to affect a significant proportion of patients receiving ECMO support due
to the need for anticoagulation to prevent thrombus formation within the circuit and platelet dysfunction.33
These bleeding events and complications are exacerbated by the large size of arterial and venous cannulas
as well as the concurrent need for multiple additional central venous and arterial catheters to allow for
medication delivery as well as invasive hemodynamic monitoring in patients on ECMO.

Current guidelines by ELSO recommend maintaining hemoglobin levels between 12-14 g/dL.34 Higher
hemoglobin levels are targeted in part as a means of facilitating increased oxygen delivery to maintain
adequate oxygenation and to ensure a right atrial pressure of 5-10 mmHg to allow for appropriate
functioning of the venous drainage cannula. However, there is a growing recognition of the potential
harm associated with red blood cell (RBC) transfusions with potential risks including transfusion
reactions, introduction of infectious pathogens, as well as alloimmunization to other RBC antigens.35

Given prior trials demonstrating improved outcomes in critically-ill patients who received restrictive
transfusion strategies, there has been similar interest in targeting lower hemoglobin goals for patients
on ECMO.36 Voelker et al. performed a retrospective analysis of 18 patients on VV ECMO for ARDS and
found no evidence of increased mortality with a targeted hemoglobin transfusion threshold of 7 g/dL.37
Another retrospective study of 38 patients on VV ECMO also found no difference in survival and organ
recovery with the same targeted hemoglobin transfusion threshold of 7 g/dL.38 Further prospective
randomized trials are needed to assess whether lower hemoglobin transfusion thresholds can be safely
implemented for patients on VA and VV ECMO support.

Platelet and fibrinogen levels are also tightly monitored for patients on ECMO support to determine
the need for potential transfusion. ELSO guidelines recommend platelet transfusion to maintain levels
>75,000/mcL. Thrombocytopenia can occur as a result of direct platelet consumption by the ECMO
circuit and exposure to the plastic surfaces of the circuit, other medications, as well as the underlying
critical illness. A flow cytometry analysis of platelet function in patients on ECMO identified both
impaired platelet aggregation and decreased platelet activation.39 Platelet transfusions make up a
large portion of transfused blood products for patients on ECMO support.40 Fibrinogen levels are
also decreased while patients are on ECMO through similar mechanisms and contribute to excessive
bleeding. Guidelines recommend transfusion of cryoprecipitate when fibrinogen levels are less than
250 mg/dL.41 Some studies have suggested that maintenance of adequate fibrinogen levels is crucial
for reducing bleeding complications associated with ECMO.42 Frequent monitoring is needed to ensure
hemoglobin, platelet, and fibrinogen levels are at goal for patients receiving VV or VA ECMO support.

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QUICK READ SUMMARY

✓ Systemic thromboembolism resulting in pulmonary embolism, deep vein thrombosis, and

limb ischemia is commonly seen in patients requiring ECMO support. Thrombi can also
form anywhere along the ECMO circuit, with microthrombi of the oxygenator being most
frequently encountered.

✓ Hemorrhagic complications occur in the majority of patients receiving ECMO support. This
is driven by platelet and clotting factor consumption by the circuit, need for large bore
venous and arterial access, and frequent concomitant need for therapeutic anticoagulation.

✓ Unfractionated heparin is the most commonly used anticoagulant in adult patients on

ECMO. Direct thrombin inhibitors can be used as alternative agents.

✓ There are many strategies available for therapeutic anticoagulation monitoring during
ECMO, however activated clotting time (ACT) is often used given its wide availability as a
point of care test and historical experience using ACT during cardiopulmonary bypass.

✓ Current ELSO guidelines recommend maintaining a hemoglobin level of 12-14 g/dL, a

platelet level of greater than 75,000 platelets/mcL, and a fibrinogen level of greater than
250 mg/dL for patients receiving ECMO support.

References
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analysis of the Nationwide Inpatient Sample 1998-2009. J Thorac Cardiovasc Surg. 2014;148(2):416–21.e1.

2. Sklar MC, Sy E, Lequier L, et al. Anticoagulation practices during venovenous extracorporeal membrane oxygenation
for respiratory failure. A systematic review. Ann Am Thorac Soc. 2016;13(12):2242–50.

3. Cheng R, Hachamovitch R, Kittleson M, et al. Complications of extracorporeal membrane oxygenation for treatment of
cardiogenic shock and cardiac arrest: a meta-analysis of 1,866 adult patients. Ann Thorac Surg. 2014;97(2):610–6.

4. Lo Coco V, Lorusso R, Raffa GM, et al. Clinical complications during veno-arterial extracorporeal membrane
oxigenation in post-cardiotomy and non post-cardiotomy shock: still the achille’s heel. J Thorac Dis.
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5. Zanatta P, Forti A, Bosco E, et al. Microembolic signals and strategy to prevent gas embolism during extracorporeal
membrane oxygenation. J Cardiothorac Surg. 2010;5:5.

6. Mazzeffi M, Greenwood J, Tanaka K, et al. Bleeding, transfusion, and mortality on extracorporeal life support: ECLS
working group on thrombosis and hemostasis. Ann Thorac Surg. 2016;101(2):682–9.

7. Esper SA, Welsby IJ, Subramaniam K, et al. Adult extracorporeal membrane oxygenation: an international survey of
transfusion and anticoagulation techniques. Vox Sang. 2017;112(5):443–52.

8. Hirsh J, Dalen JE, Deykin D, Poller L. Heparin: mechanism of action, pharmacokinetics, dosing considerations,
monitoring, efficacy, and safety. Chest. 1992;102(4 Suppl):337S-351S.

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9. Hirsh J, Raschke R, Warkentin TE, et al. Heparin: mechanism of action, pharmacokinetics, dosing considerations,
monitoring, efficacy, and safety. Chest. 1995;108(4 Suppl):258S-275S.

10. McMichael ABV, Ryerson LM, Ratano D, et al. 2021 ELSO adult and pediatric anticoagulation guidelines. ASAIO J.
2022;68(3):303-10.

11. Hvas A-M, Favaloro EJ, Hellfritzsch M. Heparin-induced thrombocytopenia: pathophysiology, diagnosis and treatment.
Expert Rev Hematol. 2021;14(4):335–46.

12. Lo GK, Juhl D, Warkentin TE, et al. Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced
thrombocytopenia in two clinical settings. J Thromb Haemost. 2006;4(4):759–65.

13. Greinacher A. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373:252–61.

14. Robson R, White H, Aylward P, Frampton C. Bivalirudin pharmacokinetics and pharmacodynamics: effect of renal
function, dose, and gender. Clin Pharmacol Ther. 2002;71(6):433–9.

15. Swan SK, Hursting MJ. The pharmacokinetics and pharmacodynamics of argatroban: effects of age, gender, and
hepatic or renal dysfunction. Pharmacotherapy. 2000;20(3):318–29.

16. Ranucci M, Ballotta A, Kandil H, et al. Bivalirudin-based versus conventional heparin anticoagulation for
postcardiotomy extracorporeal membrane oxygenation. Crit Care. 2011;15(6):R275.

17. Netley J, Roy J, Greenlee J, et al. Bivalirudin anticoagulation dosing protocol for extracorporeal membrane oxygenation:
a retrospective review. J Extra Corpor Technol. 2018;50(3):161–6.

18. Pieri M, Agracheva N, Bonaveglio E, et al. Bivalirudin versus heparin as an anticoagulant during extracorporeal
membrane oxygenation: a case-control study. J Cardiothorac Vasc Anesth. 2013;27(1):30–4.

19. Sanfilippo F, Asmussen S, Maybauer DM, et al. Bivalirudin for alternative anticoagulation in extracorporeal membrane
oxygenation: a systematic review. J Intensive Care Med. 2017;32(5):312–9.

20. Young G, Yonekawa KE, Nakagawa P, Nugent DJ. Argatroban as an alternative to heparin in extracorporeal membrane
oxygenation circuits. Perfusion. 2004;19(5):283–8.

21. Sin JH, Lopez ND. Argatroban for heparin-induced thrombocytopenia during venovenous extracorporeal membrane
oxygenation with continuous venovenous hemofiltration. J Extra Corpor Technol. 2017;49(2):115–20.

22. Rivosecchi RM, Arakelians AR, Ryan J, et al. Comparison of anticoagulation strategies in patients requiring
venovenous extracorporeal membrane oxygenation: heparin versus bivalirudin. Crit Care Med. 2021;49(7):1129–36.

23. Ranucci M. Bivalirudin and post-cardiotomy ECMO: a word of caution. Crit Care. 2012;16(3):427.

24. Cardinale M, Ha M, Liu MH, Reardon DP. Direct thrombin inhibitor resistance and possible mechanisms. Hosp Pharm.
2016;51(11):922–7.

25. Kennedy DM, Alaniz C. Apparent argatroban resistance in a patient with elevated factor VIII levels. Ann
Pharmacother. 2013;47(7-8):e29.

26. Poyant JO, Gleason AM. Early identification of argatroban resistance and the consideration of factor VIII. J Pharm
Pract. 2021;34(2):329–31.

27. Ranucci M, Cotza M, Isgrò G, et al. Anti-factor Xa-based anticoagulation during extracorporeal membrane
oxygenation: potential problems and possible solutions. Semin Thromb Hemost. 2020;46(4):419–27.

28. Panigada M, Cucino A, Spinelli E, et al. A randomized controlled trial of antithrombin supplementation during
extracorporeal membrane oxygenation. Crit Care Med. 2020;48(11):1636–44.

29. Task Force on Patient Blood Management for Adult Cardiac Surgery of the European Association for Cardio-Thoracic
Surgery (EACTS) and the European Association of Cardiothoracic Anaesthesiology (EACTA), Boer C, Meesters
MI, Milojevic M, et al. 2017 EACTS/EACTA guidelines on patient blood management for adult cardiac surgery. J
Cardiothorac Vasc Anesth. 2018;32(1):88–120.

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30. Rossaint R, Bouillon B, Cerny V, et al. The European guideline on management of major bleeding and coagulopathy
following trauma: fourth edition. Crit Care. 2016;20:100.

31. Laine A, Niemi T, Suojaranta-Ylinen R, et al. Decreased maximum clot firmness in rotational thromboelastometry
(ROTEM®) is associated with bleeding during extracorporeal mechanical circulatory support. Perfusion.
2016;31(8):625–33.

32. Panigada M, E Iapichino G, Brioni M, et al. Thromboelastography-based anticoagulation management during

extracorporeal membrane oxygenation: a safety and feasibility pilot study. Ann Intensive Care. 2018;8(1):7.

33. Olson SR, Murphree CR, Zonies D, et al. Thrombosis and bleeding in extracorporeal membrane oxygenation (ECMO)
without anticoagulation: a systematic review. ASAIO J. 2021;67(3):290–6.

34. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support. Extracorporeal Life Support Organization, Version
1.4 August 2017. Ann Arbor, MI, USA. [Link]

35. Kim HS, Park S. Blood transfusion strategies in patients undergoing extracorporeal membrane oxygenation. Korean J
Crit Care Med. 2017;32(1):22–8.

36. Hébert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion
requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials
Group. N Engl J Med. 1999;340(6):409–17.

37. Voelker MT, Busch T, Bercker S, et al. Restrictive transfusion practice during extracorporeal membrane oxygenation
therapy for severe acute respiratory distress syndrome. Artif Organs. 2015;39(4):374–8.

38. Agerstrand CL, Burkart KM, Abrams DC, et al. Blood conservation in extracorporeal membrane oxygenation for acute
respiratory distress syndrome. Ann Thorac Surg. 2015;99(2):590–5.

39. Balle CM, Jeppesen AN, Christensen S, Hvas A-M. Platelet function during extracorporeal membrane oxygenation in
adult patients. Front Cardiovasc Med. 2019;6:114.

40. Jiritano F, Serraino GF, Ten Cate H, et al. Platelets and extra-corporeal membrane oxygenation in adult patients: a
systematic review and meta-analysis. Intensive Care Med. 2020;46(6):1154–69.

41. Cartwright B, Bruce HM, Kershaw G, et al. Hemostasis, coagulation and thrombin in venoarterial and venovenous
extracorporeal membrane oxygenation: the HECTIC study. Sci Rep. 2021;11:7975.

42. Doyle AJ, Hunt BJ. Current understanding of how extracorporeal membrane oxygenators activate haemostasis and
other blood components. Front Med. 2018;5:352.

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PREVIOUS CHAPTER Chapter 19.3: ECMO Complications NEXT CHAPTER

19.3
ECMO
Complications
James Lantry III, MD
Associate Director of Quality, Critical Care
INOVA Heart and Vascular Institute
Falls Church, VA
jlantrymd@[Link]
@EmCritDr

Mehul Desai, MD
System Chief Critical Care, Pulmonary, Allergy and Immunology
INOVA Heart and Vascular Institute
Falls Church, VA

Erik Osborn, MD
COL (Ret) MC USA
American College of Chest Physicians
Glenview, Illinois

Christopher A. King, MD, FSCAI

Medical director of the Transplant and Advanced Lung Disease Critical Care Program
INOVA Heart and Vascular Institute
Falls Church, VA

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Overview
The use of extracorporeal membrane oxygenation (ECMO) for both pulmonary and cardiac support has
increased over the past decade1 due to both increasing evidence and improved global access to ECMO
technology in critically ill patients. As the use of ECMO has increased, the incidence of complications has
remained quite variable between centers.2 In this chapter we summarize the most recent information
regarding ECMO complications, describing the site of complications (patient or ECMO circuit), whether
complications are iatrogenic, and whether they are associated with continued organ dysfunction.
According to the most recent data collected by the Extracorporeal Life Support Organization (ELSO),
the incidence of complications is extremely variable depending on the type of ECMO utilized and
the population in question.1 This chapter focuses on adult ECMO only and makes every effort to
differentiate between venovenous ECMO (VV ECMO) and venoarterial ECMO (VA ECMO). Table 1
summarizes ECMO complications.

Table 1. ECMO Complications Summary

PATIENT-RELATED MECHANICAL/CIRCUIT-RELATED
ECMO-RELATED COMPLICATIONS
COMPLICATIONS COMPLICATIONS

• Arrythmias • Pseudoaneurysm • “Circuit DIC”

• Acute pulmonary edema • Arterial dissection • Clot formation

• Hypotension • Retroperitoneal bleeding • Thrombus

• Infection (increased risk with • Recirculation burden • Embolus

central cannulation)
• Cannulation into wrong vessel • Hemolysis
• Increased risk of myopathy
• Nerve injury • Cannula dislodgement
• Delirium
• Hematoma formation • Entrainment of air “airlock”
• Acute MI
• Tamponade (central cannulation) • Circuit rupture
• Acute heart failure
• Increased risk of limb ischemia with • Pump failure
• Fluid overload large cannula

• Worsening cardiogenic shock • Fasciotomy or amputation risks

related to limb ischemia
• Stasis injury
• Pneumothorax
• Catastrophic cerebrovascular
complications

• Cardiac arrest

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The heart and lung machine was invented by Dr. John Gibbon, along with his wife Mary Gibbon, and
first used clinically in 1954 to perform cardiac surgery.3 This rudimentary device replicated the actions
of both the cardiac and pulmonary systems and facilitated what would be termed “open heart surgery.”
Due to direct exposure of blood to gas, after 2-3 hours extreme hemolysis and initiation/activation of the
inflammatory cascade resulted in fatal complications.4

Over the next decade, gas exchange membrane technology improved and the ability to utilize heart
and lung machines continuously for 24 hours became possible. In 1971, a variant of this technology
permitted Dr. J. Donald Hill to mechanically support a motorcycle crash victim with acute respiratory
distress syndrome (termed “shock-lung syndrome”) for 75 hours.5 This was the first documented use of
extracorporeal support for an adult patient in modern literature.

Since that first use of ECMO nearly 50 years ago, the technology utilized has dramatically improved
with more efficient gas exchange oxygenators as well as pumps that create a near frictionless means of
blood flow augmentation. Additionally, circuits can now be impregnated with anticoagulant materials,
further reducing the incidence of mechanical complications. Despite these advances in technology,
equipment-related issues remain the most prevalent complications in the ECMO population.1

Cannulation-related complications
ECMO cannulation carries the same risks as standard vascular access—vascular injury, bleeding, and
damage to surrounding structures (eg, nerve injury, pneumothorax).5 The major difference is that the
size of the ECMO cannula (13-32 Fr) is much larger than standard access catheters and there are few
options to replace the cannula once on ECMO. This means that care must be taken at the time of initial
cannulation to properly sterilize the site and adequately size the cannula for the desired flow.

The most common means to place an ECMO cannula is percutaneous via modified Seldinger technique
under ultrasound guidance.6 However, even with the use of ultrasound guidance and/or fluoroscopy,
the incidence of cannulation-related complications remains high. Per recent data, rates of puncture
site bleeding requiring blood transfusion are 5.7%, and vascular perforation rates are 1.9%.6 Other
studies have noted even higher rates with arterial cannulation, with 7-14% of patients experiencing a
pseudoaneurysm, dissection, or retroperitoneal bleeding.7

The alternative peripheral cannulation technique is an open surgical cutdown. This allows direct
visualization of the vessel, and facilitates proper sizing of ECMO cannulas, reduces risks of inadvertently
damaging the vessel wall or targeting the incorrect structure (eg, vein, artery, or nerve), but comes with
the trade-off of an increased risk of surgical site bleeding and infection.8 The placement of a purse string
suture with open technique can also facilitate more efficient vascular closure and better hemostasis after
decannulation.

Central cannulation is often used when patients are difficult to wean from cardiopulmonary bypass
or when adequate flows cannot be achieved with peripheral access. This cannulation technique can
optimize both the arterial and venous flow rates but comes with a significantly elevated risk of infection
and bleeding.8 Additionally, central cannulation requires that the patient be deeply sedated and
sedentary, increasing the risk of myopathy, delirium, and stasis injuries.

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Regardless of the means of cannulation, the formation of a hematoma remains a risk. A perivascular
hematoma can be both a source of blood loss and a nidus for infection.9 Deeper bleeds, such as
a retroperitoneal bleeds, can be a life-threatening complication if not properly recognized and
coagulopathy reversed.6 Bleeding with central cannulation can lead to a tamponade-like effect and
cardiac arrest.8 With proper cannulation technique the risk for hematoma formation can be lessened, but
never eliminated.

Arterial cannulation brings its own complication pattern due to a lack of redundancy in distal blood flow.
A large cannula can fully occlude the femoral artery, block distal limb perfusion, and lead to ischemic
changes in 10-70% of cases that may require surgical correction (eg, fasciotomy, amputation) if not
addressed in a timely manner.10-12 Timely (or obligate) placement of either a distal perfusion catheter
into the superficial femoral artery or a retrograde catheter into the dorsalis pedis or tibialis anterior
artery can alleviate this ischemic burden by bypassing the femoral artery obstruction.11-12 According to
the most recent ELSO registry, venous cannulation is associated with a 1.4% incidence of limb ischemia,
most likely due to thrombosis rather than embolization.1 Due to use of large drainage cannulas, patients
may experience phlegmasia cerulea dolens precipitating marked lower extremity swelling and possibly
resultant arterial ischemia.

Proper cannula placement is critical for proper gas exchange and cardiac augmentation in VV ECMO
and VA ECMO, respectively. When cannulas are placed too proximal to each other in the same vascular
structure (<10 cm) in VV ECMO, the incidence of recirculation, where arterialized blood is redirected
back to the drainage cannula, is increased significantly.14 Inadvertent placement of a cannula into
the incorrect vessel, common in morbidly obese patients with severe arterial calcifications and in
patients cannulated in emergency resuscitation scenarios, can be a life-threatening event with fatal
consequences.6 It is therefore advised to maximize radiographic and visual guidance during cannulation.
Even with an open technique, placement of a vascular cannula without direct fluoroscopic guidance
risks misplacement into a branching vessel (such as the hepatic vein with femoral vein cannulation) or
even the right atrium.

Both venous and arterial cannulation require use of a guidewire and misplacement of this wire can
cause arrythmias due to myocardial irritation or frank myocardial puncture and cardiac tamponade.13
Passage of the arterial wire can also cause dissection of the artery requiring emergency intervention.

Circuit-related complications
Malfunctions of the circuit tubing, oxygenator, and pump are among the most common complications
to affect the ECMO population, with clots forming in the VV ECMO circuitry at some point in 1 in
12 patients.1 When this clot starts to impede blood flow, such as across the oxygenator, the circuit
slowly loses efficiency in gas exchange. Additionally, this obstruction causes injury to red blood cells
and results in hemolysis. This hemolysis can lead to anemia as well as acute kidney injury due to
acute tubular necrosis caused by pigment and iron depositions.15 Oxygenator clots can be detected
by increased resistance across the oxygenator and an elevated pressure gradient coupled with rising
plasma-free hemoglobin levels and a decreased partial pressure of oxygen.

Although most commonly occurring along the oxygenator, a clot can occur at any point in the circuit
due to the baseline proinflammatory and procoagulant surfaces that exist at all areas of stasis or
turbulence.18 The presence of clots can first be detected by the presence of plasma-free hemoglobin or
a rising D-dimer level. Clots that occur in the arterial cannula may embolize and result in microvascular
complications or even lead to complete occlusion of cardiac or cerebral circulation.

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One of the most feared complications is cannula dislodgement with loss of ECMO functionality, air
entrainment, or massive blood loss.17 The highest risk for cannula dislodgement occurs with patient
movement, such as patient turning, coupled with poor securement of cannulas. This complication can
be easily prevented with close monitoring of cannula placement as well as use of multiple synergistic
methods to secure cannulas in place. Although a theoretical risk exists, no current evidence of cannula
dislodgement exists with prone positioning or with ambulation.19-21

Upwards of 1.1% of patients suffer a violation of the circuit pre-pump which entrains air due to the
overt negative pressure generated.1 This can lead to what is termed “airlock,” where the pump abruptly
stops functioning, often resulting in catastrophe.16 If air is able to make it past the pump, the oxygenator
is designed to trap this air with ports available to assist in removal. Any air that is able to make it past
the oxygenator runs the risk of causing air embolism. This can lead to neurologic complications resulting
from gaseous microemboli, or cardiac arrest as a result of massive air embolism.16

Infection-related complications
Infections rank second only to hemorrhage as the most common complication in the ECMO population,
occurring in 9-65% of patients depending on the study population, with nosocomial infections occurring
in 10-21% of patients.22-25,27-30 This is not an unexpected finding as patients on ECMO are often critically
ill, stationary for long periods of time, and have multiple portals of entry for infectious pathology (eg,
indwelling catheters, central access, surgical wounds). Couple that with the inability to remove vital
ECMO cannulas in the event of a bloodstream infection, and it becomes the perfect environment for
nosocomial infections. The incidence of bloodstream infections also increases with blood transfusions.25

Bloodstream infections are the most common source of nosocomial infection in the ECMO population,
with a prevalence of 3-18%, depending on the population.29-30 The next most prevalent source of
infection varies depending on the study, with lower respiratory tract (4-55%), urinary tract (1-2%),
and surgical site infections all being common.24, 30, 33 In addition to the standard sources of nosocomial
infections, cannula-related infections affect 17.7% of patients leading to bacteremia in 59.7% of cases
in a recent analysis.31 Another recent analysis evaluating the oxygenator membrane as a potential
source of infection demonstrated that 45% of oxygenators are colonized by bacteria, with gram-
positive bacteria being responsible for 72% of positive findings.35 According to a recent survey, 74% of
centers utilized antibiotic prophylaxis despite minimal evidence that this therapy reduces the incidence
of infection.32-33 Due to this broad use of antibiotics coupled with the presence of indwelling lines and
impaired immune function, ECMO patients are at increased risk of fungemia.25

Globally, the duration of ECMO support has been the greatest predictor of infectious complications,
followed by patient illness severity at ECMO onset (Sequential Organ Failure Assessment [SOFA] score),
use of VV ECMO as opposed to VA ECMO, development of a mechanical complication, and presence of
an autoimmune disease.24-26,30 Regardless of the source, the presence of an infection is an independent
risk factor for mortality in the ECMO population, with sepsis being the most lethal.27-28 Bloodstream
infections lead to a 3-fold increased risk of death.34

The presence of an infection will increase the length of time on ECMO, duration of mechanical
ventilation, time spent in the ICU, and time hospitalized.27 Infections can lead to mechanical
complications as well as activate the coagulation cascade, which leads to additional mechanical
dysfunction of the ECMO circuit and reduction in overall efficiency of gas exchange.26

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Neurologic-related complications
A neurologic complication is often the most dreaded outcome associated with the use of ECMO. In
the early era of ECMO use, the rudimentary circuitry created a massive inflammatory reaction and
required elevated levels of anticoagulation which often led to devastating intracranial bleeding episodes.
Modern circuitry and heightened awareness have decreased the incidence of neurologic complications
from 20% in a 2000-2004 data analysis down to 13% in 2011-2013.36 This incidence drops to 9%
with the elimination of events not felt to be ECMO-related, such as brain death and hypoxic ischemic
encephalopathy.38

Despite the use of modern circuitry, a recent systematic review found that intracranial hemorrhage (ICH)
was still the most common neurologic complication in the ECMO population, affecting approximately
5% of the ECMO population (2-21%) and leading to a median intrahospital mortality rate of 96%.36 This
was followed closely by acute ischemic stroke with an incidence of 5% (1-33%) and a median mortality
risk of 84%; epileptic seizure activity with an incidence of 2% (0.2-2%) and a median mortality rate of
40% (0-90%); as well as more nuanced complications such as nerve damage upon cannulation and
paraplegia resulting from spinal cord infarct, which has only been described with the concomitant use of
an intra-aortic balloon pump.38-39

Risk factors for each complication vary widely. Odds for ICH increase with the use of heparin, a
creatinine value greater than 2.6 mg/L, the use of hemodialysis, thrombocytopenia, decreased fibrinogen
levels, and longer duration of ECMO use or mechanical ventilation, younger age, pre-ECMO cardiac
arrest, and female gender.38, 40-41, 47 A recent observational study also determined that rapid changes in
both oxygenation (increase in PaO2 greater than 50 mmHg) or ventilation (drop in PaCO2 greater than
27 mmHg) can also increase the risk for an ICH.42 The key feature of all ICH risk factors is disruption
of the blood-brain barrier and extravasation of plasma and erythrocytes, often due to the disease
process itself (eg, sepsis, influenza) or the inflammatory response associated with the use of an artificial
membrane.47

The incidence of an acute ischemic stroke is increased by a serum lactic acid level greater than 10
mmol/L.38 There is also a linear relationship between time spent on VA ECMO and the development of a
thromboembolic stroke.43 Gaseous emboli are also a concern when utilizing VA ECMO, which can lead
to a pseudo-embolic event and poor outcome.46 Additionally, similar to ICH, a rapid decrease in PaCO2
may lead to a significant decrease in cerebral oxygenation and an ischemic insult.44

The one factor that makes neurologic injuries additionally devastating in the ECMO population is the
innate difficulty of obtaining and assessing a daily neurologic exam. The use of neuromuscular blockade
coupled with the deep levels of sedation utilized can often complicate the neurologic exam.45, 47 It is
imperative to use some clinical assessment, whether it is daily awakening, near-infrared spectroscopy
monitoring, or even continuous electroencephalogram.38, 42 Early detection is important, because
regardless of the neurologic complication, there is a higher likelihood of cognitive impairment and
decreased functionality, leading to prolonged hospital and long-term care facility stays, resulting in
elevated healthcare costs over time and increased general risk for mortality.37

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Hematological complications
Multiple reports suggest that due to the use of systemic anticoagulation coupled with vascular devices
and surgical wounds, bleeding complicates approximately 30% of ECMO cases.48 One of the critical
reasons for significant blood loss is the effect ECMO has upon hemostasis. The coagulation cascade
is activated by the blood-circuit barrier which can lead to thrombotic complications.47 In addition, the
interaction between the circulated blood and the circuit artificial surfaces can lead to platelet activation
and consumption of clotting factors which can lead to “circuit DIC”, a term used to explain the resultant
consumptive coagulopathy.47, 49-50 Acquired von Willebrand syndrome with spontaneous bleeding also
occurs in approximately 79% of patients.47 Additionally, there exists a significant risk of developing
systemic hyperfibrinolysis due to the fibrinolytic activation typical to the ECMO circuit, leading to further
systemic bleeding.51

Thrombosis is also a major risk among ECMO patients, related to cannula placement or the systemic
changes the ECMO circuit induces upon the clotting cascade. When this thrombosis impedes the
linear flow of red blood cells in the ECMO circuit, the shear stress can cause both hemolysis and
thrombocytopenia and lead to further blood loss.52 In addition to the shear stress from clot burden,
excessive negative pressure within the circuit can exacerbate the effect of hemolysis and contribute to
ongoing anemia. Prevention of ongoing hemolysis is crucial because excessive hemolysis, demonstrated
by plasma free hemoglobin greater than 50 mg/dL detected 24 hours after ECMO initiation,
independently predicts a greater than 3-fold increased risk for death.53

Functional loss and long-term complications

Severe critical illness can leave patients with functional, psychological, and emotional impairment long
after their critical illness resolves, a phenomenon sometimes referred to as the “post-ICU syndrome.”54
ECMO survivors are at high risk for post-ICU syndrome given their high acuity of illness, frequently
prolonged hospitalizations, relative immobilization, and need for sedation. Patients and families should
be counseled on the risk for a protracted recovery prior to initiation of ECMO support when possible.
Additionally, care should be taken to select ECMO candidates with adequate pre-morbid functional
status to make a meaningful functional recovery.

Data on the prevalence of critical illness polyneuropathy (CIPN) and myopathy (CIPM) following
ECMO support is lacking. It is likely that the incidence is reasonably high and increases with longer
hospitalizations. To combat development of CIPN/CIPM, clinicians should attempt to minimize sedatives
and mobilize patients as soon as feasible. Care should be taken to ensure adequate nutritional support
as well. Further research on incidence of, effective preventive and treatment strategies for, and long-
term sequelae of CIPN/CIPM are needed.

ECMO survivors may also suffer from psychological trauma including PTSD, anxiety, and depression.55-58
Efforts should be made to screen for and appropriately treat mental health issues both in the hospital
and following discharge. If possible, dedicated follow-up clinics should be established to provide
appropriate medical and psychological care to ECMO survivors.

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QUICK READ SUMMARY

✓ Utilization of extracorporeal membrane oxygenation (ECMO) is accompanied by a multitude of

complications. However, as this modality of treatment is reserved for only the most critically
ill, the risk of complications is often unavoidable.

✓ Regardless of the modality of support utilized, pulmonary and/or cardiac function is

mechanically augmented, and failure of this artificial circuitry is the most common
complication.

✓ Anticoagulation is utilized to reduce mechanical failure and results in an increased risk of

bleeding.

✓ This unique patient population is also fraught with neurologic, infectious, and thrombotic
complications.

References
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2. Zangrillo A, Landoni G, Biondi-Zoccai G, et al. A meta-analysis of complications and mortality of extracorporeal

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3. Gibbon JH. Application of a mechanical heart and lung apparatus to cardiac surgery. Minn Med. 1954;37(3):171.

4. Hill JD, O’Brien TG, Murray JJ, et al. Extracorporeal oxygenation for acute post-traumatic respiratory failure (shock-lung
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7. Pillai AK, Bhatti Z, Bosserman AJ, et al. Management of vascular complications of extracorporeal membrane
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8. Stulak JM, Dearani JA, Burkhart HM, et al. ECMO cannulation controversies and complications. Semin Cardiothorac
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9. Majunke N, Mangner N, Linke A, et al. Comparison of percutaneous closure versus surgical femoral cutdown for
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12. Bisdas T, Beutel G, Warnecke G, et al. Vascular complications in patients undergoing femoral cannulation for
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13. Vaquer S, de Haro C, Peruga P, et al. Systematic review and meta-analysis of complications and mortality of veno-
venous extracorporeal membrane oxygenation for refractory acute respiratory distress syndrome. Ann Intensive Care.
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15. Qian Q, Nath KA, Wu Y, et al. Hemolysis and acute kidney failure. Am J Kidney Dis. 2010;56(4):780–4. doi:10.1053/j.
ajkd.2010.03.025

16. Kumar A, Keshavamurthy S, Abraham JG, Toyoda Y. Massive air embolism caused by a central venous catheter during
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17. Bull T, Corley A, Smyth DJ, et al. Extracorporeal membrane oxygenation line-associated complications: in vitro testing
of cyanoacrylate tissue adhesive and securement devices to prevent infection and dislodgement. Intensive Care Med
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18. Thomas J, Kostousov V, Teruya J. Bleeding and thrombotic complications in the use of extracorporeal membrane
oxygenation. Semin Thromb Hemost. 2018;44(1):20-9.

19. Culbreth RE, Goodfellow LT. Complications of prone positioning during extracorporeal membrane oxygenation for
respiratory failure: a systematic review. Respir Care. 2016;61(2):249-54.

20. Abrams D, Garan AR, Brodie D. Awake and fully mobile patients on cardiac extracorporeal life support. Ann
Cardiothorac Surg. 2019;8(1):44-53.

21. Pasrija C, Mackowick KM, Raithel M, et al. Ambulation with femoral arterial cannulation can be safely performed on
venoarterial extracorporeal membrane oxygenation. Ann Thorac Surg. 2019;107(5):1389-94.

22. Burket JS, Bartlett RH, Vander Hyde K, Chenoweth CE. Nosocomial infections in adult patients undergoing
extracorporeal membrane oxygenation. Clin Infect Dis. 1999;28(4):828-33.

23. Grasselli G, Scaravilli V, Di Bella S, et al. Nosocomial infections during extracorporeal membrane oxygenation:
incidence, etiology, and impact on patients’ outcome. Crit Care Med. 2017;45(10):1726-33.

24. Pieri M, Agracheva N, Fumagalli L, et al. Infections occurring in adult patients receiving mechanical circulatory support:
the two-year experience of an Italian National Referral Tertiary Care Center. Med Intensiva. 2013;37(7):468-75.

25. Aubron C, Cheng AC, Pilcher D, et al. Infections acquired by adults who receive extracorporeal membrane
oxygenation: risk factors and outcome. Infect Control Hosp Epidemiol. 2013;34(1):24-30.

26. Sun HY, Ko WJ, Tsai PR, et al. Infections occurring during extracorporeal membrane oxygenation use in adult patients.
Thorac Cardiovasc Surg. 2010;140(5):1125-32.

27. Biffi S, Di Bella S, Scaravilli V, et al. Infections during extracorporeal membrane oxygenation: epidemiology, risk
factors, pathogenesis and prevention. Int J Antimicrob Agents. 2017;50(1):9-16.

28. Bizzarro MJ, Conrad SA, Kaufman DA, Rycus P. Infections acquired during extracorporeal membrane oxygenation in
neonates, children, and adults. Pediatr Crit Care Med. 2011;12(3):277–81.

29. Hsu MS, Chiu KM, Huang YT, et al. Risk factors for nosocomial infection during extracorporeal membrane
oxygenation. J Hosp Infect. 2009;73(3):210–6.

30. Schmidt M, Bréchot N, Hariri S, et al. Nosocomial infections in adult cardiogenic shock patients supported by
venoarterial extracorporeal membrane oxygenation. Clin Infect Dis. 2012;55(12):1633–41.

31. Allou N, Lo Pinto H, Persichini R, et al. Cannula-related infection in patients supported by peripheral ECMO: clinical
and microbiological characteristics. ASAIO J. 2019;65(2):180–6.

32. Kao LS, Fleming GM, Escamilla RJ, et al. Antimicrobial prophylaxis and infection surveillance in extracorporeal
membrane oxygenation patients: a multi-institutional survey of practice patterns. ASAIO J. 2011;57(3):231–8.

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33. O’Horo JC, Cawcutt KA, De Moraes AG, et al. The evidence base for prophylactic antibiotics in patients receiving
extracorporeal membrane oxygenation. ASAIO J. 2016;62(1):6-10.

34. Steiner CK, Stewart DL, Bond SJ, et al. Predictors of acquiring a nosocomial bloodstream infection on extracorporeal
membrane oxygenation. J Pediatr Surg. 2001;36(3):487-92.

35. Kuehn C, Orszag P, Burgwitz K, et al. Microbial adhesion on membrane oxygenators in patients requiring
extracorporeal life support detected by a universal rDNA PCR test. ASAIO J. 2013;59(4):368–73.

36. Sutter R, Tisljar K, Marsch S. Acute neurologic complications during extracorporeal membrane oxygenation: A
systematic review. Critical Care Medicine. 2018;46(9):1506-13.

37. Xie A, Lo P, Yan TD, Forrest P. Neurologic complications of extracorporeal membrane oxygenation: a review. J Cardiothorac
Vasc Anesth. 2017;31(5):1836-46.

38. Sutter R, Tisljar K, Marsch S. Acute neurologic complications during extracorporeal membrane oxygenation: a
systematic review. Crit Care Med. 2018;46(9):1506–13.

39. Samadi B, Nguyen D, Rudham S, Barnett Y. Spinal cord infarct during concomitant circulatory support with
intra-aortic balloon pump and veno- arterial extracorporeal membrane oxygenation. Critical Care Medicine.
2016;44(2):e101-5.

40. Kasirajan V, Smedira NG, McCarthy JF, et al. Risk factors for intracranial hemorrhage in adults on extracorporeal
membrane oxygenation. Eur J Cardiothorac Surg. 1999;15(4):508–14.

41. Omar HR, Mirsaeidi M, Mangar D, Camporesi EM. Duration of ECMO is an independent predictor of intracranial
hemorrhage occurring during ECMO support. ASAIO J. 2016;62(5):634–6.

42. Luyt CE, Bréchot N, Demondion P, et al. Brain injury during venovenous extracorporeal membrane oxygenation.
Intensive Care Med. 2016;42(5):897–907.

43. Rastan AJ, Dege A, Mohr M, et al. Early and late outcomes of 517 consecutive adult patients treated with
extracorporeal membrane oxygenation for refractory postcardiotomy cardiogenic shock. J Thorac Cardiovasc Surg
2010;139(2):302–11.

44. Muellenbach RM, Kilgenstein C, Kranke P, et al. Effects of venovenous extracorporeal membrane oxygenation on
cerebral oxygenation in hypercapnic ARDS. Perfusion. 2014;29(2):139–41.

45. Marhong JD, DeBacker J, Viau-Lapointe J, et al. Sedation and mobilization during venovenous extracorporeal
membrane oxygenation for acute respiratory failure: an international survey. Crit Care Med. 2017;45(11):1893‐9.

46. Risnes I, Wagner K, Nome T, et al. Cerebral outcome in adult patients treated with extracorporeal membrane
oxygenation. Ann Thorac Surg. 2006;81(4):1401-6.

47. Cavayas YA, Del Sorbo L, Fan E. Intracranial hemorrhage in adults on ECMO. Perfusion. 2018;33(1):42-50.

48. Aubron C, DePuydt J, Belon F, et al. Predictive factors of bleeding events in adults undergoing extracorporeal
membrane oxygenation. Ann Intensive Care. 2016;6(1):97.

49. Cheung PY, Sawicki G, Salas E, et al. The mechanisms of platelet dysfunction during extracorporeal membrane
oxygenation in critically ill neonates. Critical Care Medicine. 2000;28(7):2584–90.

50. Malfertheiner MV, Philipp A, Lubnow M, et al. Hemostatic Changes During Extracorporeal Membrane Oxygenation:
A Prospective Randomized Clinical Trial Comparing Three Different Extracorporeal Membrane Oxygenation Systems
Crit Care Med. 2016;44(4):747-54.

51. Doyle AJ, Hunt BJ. current understanding of how extracorporeal membrane oxygenators activate haemostasis and
other blood components. Front Med (Lausanne). 2018;5:352.

52. Thomas J, Kostousov V, Teruya J. Bleeding and thrombotic complications in the use of extracorporeal membrane
oxygenation. Semin Thromb Hemost. 2018;44(1):20-9.

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53. Omar HR, Mirsaeidi M, Socias S, et al. Plasma free hemoglobin is an independent predictor of mortality among
patients on extracorporeal membrane oxygenation support. PLoS One. 2015;10(4):e0124034.

54. Svenningsen H, Langhorn L, Agard AS, Dryer P. Post-ICU symptoms, consequences, and follow-up: an integrative
review. Nurs Crit Care. 2017;22(4):212-20.

55. Muller G, Flecher E, Lebreton G, et al. The ENCOURAGE mortality risk score and analysis of long-term outcomes after
VA-ECMO for acute myocardial infarction with cardiogenic shock. Intensive Care Med. 2016;42(3):370-8.

56. Schmidt M, Zoghieb E, Rozé H, et al. The PRESERVE mortality risk score and analysis of long-term outcomes
after extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. Intensive Care Med.
2013;39(10):1704-13.

57. von Bahr V, Kalzen H, Frenckner B, et al. Long-term pulmonary function and quality of life in adults after
extracorporeal membrane oxygenation for respiratory failure. Perfusion. 2019;34(1_suppl):49-57.

58. McDonald MD, Sandsmark DK, Palakshappa JA, et al. Long-term outcomes after extracorporeal life support for acute
respiratory failure. J Cardiothorac Vasc Anesth. 2019;33(1):72-9.

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PREVIOUS CHAPTER Chapter 19.4: Unloading the LV When Using ECMO NEXT CHAPTER

19.4
Unloading the LV
When Using ECMO
Allison G. Dupont, MD, FACC, FSCAI
Interventional Cardiologist
CCU Director
Medical Director ECMO Program
Northside Hospital Cardiovascular Institute
allison@[Link]

Jason J. Grady, NRP

System Manager, Emergency Cardiac Care
Northside Hospital System

Charlie Nix, RN
ECMO Coordinator
Northside Hospital System

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Introduction
Venoarterial extracorporeal membrane oxygenation (VA ECMO) is an effective method for circulatory
and oxygenation support of patients with refractory cardiogenic shock (CS). However, one pitfall
associated with its use in CS is a significant increase in afterload caused by retrograde perfusion of
the aorta. This increased afterload can precipitate left ventricular (LV) pressure and volume overload
and, if unrecognized or untreated, may cause LV distension leading to increased myocardial wall stress,
myocardial ischemia, pulmonary edema, ventricular arrhythmias, and sometimes intraventricular and
aortic root thrombosis.1

Pressure-volume loops
The relationship between LV pressure and volume is key to understanding the impact of VA ECMO on
LV loading conditions. This relationship is demonstrated visually by the pressure-volume (PV) loop. The
standard PV loop can be broken down into distinct phases, as described in Figure 1.

A Mitral valve opens

AàB Blood enters the LV, increasing its

volume to provide LV stroke volume;
as LV volume increases, LV pressure
increases slightly

B Mitral valve closes in preparation

for LV contraction at the completion
of LV filling, and diastole ends;
LVEDP is measured prior to the start
of LV contraction

BàC LV pressure rises sharply at the

start of systole, as LV contraction
begins before the aortic valve opens;
this cardiac cycle phase is called
isovolumetric contraction

C Aortic valve opens when LV

pressure exceeds aortic pressure,
and ventricular ejection occurs

CàD Blood ejected during this phase is

LV stroke volume

D Aortic valve closes as pressure in

the aorta and LV equalize following
LV ejection

DàA LV pressure drops as the LV relaxes

during the last phase of the cardiac
cycle prior to mitral valve re-opening

Figure 1. PV Loop Phases

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Cardiogenic shock and VA ECMO support

In CS, as the stroke volume decreases (Figure 2), volume remains in the LV (A) and left ventricular end-
diastolic pressure (LVEDP) rises (B). As CS progresses, the LV becomes less compliant and both stroke
volume and systolic pressure decrease (D). As LVEDP continues to rise and stroke volume continues
to decline, coronary artery perfusion is compromised leading to profound ischemia, myocardial
dysfunction, and sometimes death.

Figure 2. PV Loop Changes Secondary to Acute Cardiogenic Shock and VA ECMO Support

VA ECMO support augments mean arterial pressure (MAP) and increases systemic perfusion and tissue
oxygenation in patients with CS. However, it also results in an increase in afterload due to retrograde
perfusion of the aorta and does not inherently support (unload) the left ventricle, as shown in Figure 2.

Already compromised by progressive shock, the LV may not be able to generate sufficient pressure to
open the aortic valve in patients on VA ECMO support. This may be evidenced by absent pulsatility on
the arterial line waveform and/or by echocardiography. Peripheral VA ECMO utilizes an arterial cannula
which generates retrograde flow toward the aortic valve, increasing afterload and raising the pressure in
the aortic root. This, in turn, increases the afterload pressure on the aortic valve. As afterload continues
to increase, the aortic valve may remain closed, further increasing both LV volume and pressure, leading
to worsening LV dilation, increased myocardial wall stress, progressive myocardial ischemia, and often
pulmonary edema2 (Figure 3).

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Figure 3 (videos). Left Ventricular Distension Secondary to Increased Afterload with VA ECMO Support (Absent
LV Venting)

“Venting” versus “unloading”

Venting typically involves passive strategies to treat ventricular distension. These passive techniques
differ from active volume and pressure unloading interventions designed to reduce the pressure-volume
area of mechanical power expenditure of the ventricle to minimize myocardial oxygen consumption and
reduce hemodynamic forces that lead to ventricular remodeling.

Left ventricular unloading strategies

Strategies to vent and/or “unload” the LV during VA ECMO range from minimally invasive to open
surgical approaches. There have been no head-to-head randomized controlled trials demonstrating the
benefit of one unloading strategy over another, although there is retrospective data demonstrating a
mortality benefit with intra-aortic balloon pumps and percutaneous LVADs to unload the LV.6

Pharmacologic therapy
The least invasive method for LV venting is via inotropes. Milrinone and dobutamine improve
contractility, thereby increasing cardiac output. The benefits of inotropic therapy are that these agents
are low cost and do not require any additional invasive procedures. Limitations of this pharmacologic
approach, however, are significant. First, there is no direct unloading of the ventricle as “venting”
depends on intrinsic LV contractility (so that the LV can vent itself). Secondly, inotropes increase
myocardial oxygen demand, which is undesirable in patients with acute MI (see Figure 4A).

Intra-aortic balloon pump (IABP)

The IABP, the smallest bore device that can be used to vent the LV, indirectly provides LV venting by
reducing afterload. Although vascular complications may occur with these devices, the rate of these
complications is lower due to the small bore access. IABP has been shown in some retrospective analyses
to reduce mortality in VA ECMO as compared to patients who do not receive mechanical venting.6

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Impella®
Also known as a percutaneous left ventricular assist device (pLVAD), the Impella (Abiomed) directly
unloads the LV (Figure 4C). It produces axial flow from the LV into the ascending aorta, and in doing
so, directly decreases preload. By driving antegrade flow into the aortic root, it also minimizes the risk
of aortic root thrombus formation in VA ECMO patients. Some studies have shown that simultaneous
VA ECMO and Impella therapy (often referred to as ECpella™ or ECmella) is associated with improved
clinical outcomes in refractory cardiogenic shock.5 The use of Impella as an LV vent in VA ECMO
increases the risk of access site complications due to a second large bore arterial access site. As with
any patient treated with Impella, there is an increased risk of hemolysis, limb ischemia, bleeding,
and device malposition. In addition, ECpella use is associated with significantly higher device cost as
compared to the IABP venting strategy.

Figure 4. PV Loop Changes During Acute Cardiogenic Shock with Different Venting or Unloading Strategies

Percutaneous left atrial vent

Although a less commonly utilized strategy in the adult patient population, percutaneous left atrial
drainage is another option for LV venting. The different techniques for left atrial venting include
transseptal balloon septostomy, blade septostomy, or insertion of a left atrial drain. All of these
procedures require specialized training in transeptal technique. Depending on the size of the
septostomy, the interatrial defect may also sometimes require repair post-ECMO decannulation.
Some centers have also begun using LAVA ECMO (left atrial VA ECMO) to vent the left atrium directly
by placing a portion of the venous drainage cannula in the left atrium.7

Open surgical placement

The most invasive approach for venting the LV is the open surgical approach. In postcardiotomy patients
who have been unable to be weaned from cardiopulmonary bypass (CPB), a surgical vent is placed
into the LV via the right superior pulmonary vein or directly into the apex of the LV. Apical LV vents can
also be placed via a left anterolateral thoracotomy approach. All of these approaches provide direct
unloading of the LV which can be controlled by a C-clamp.

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QUICK READ SUMMARY

✓ Consider LV unloading in VA ECMO patients to minimize the detrimental effects of
increased afterload (eg, pulmonary edema, LV cavity thrombus, aortic root thrombosis)

✓ LV venting and unloading strategies include:

• Pharmacologic therapy (eg, milrinone, dobutamine)
• IABP
• Impella
• Percutaneous left atrial venting (eg, transseptal balloon septostomy, blade
septostomy, left atrial drain)
• Open surgical venting (eg, apical LV vent)

✓ Venting is a passive process which differs from active volume and pressure unloading.

✓ Consider the capabilities of ECMO operators and centers as well as patient-specific

factors when selecting an LV unloading strategy.

References
1. Grajeda Silvestri ER, Pino JE, Donath E, et al. Impella to unload the left ventricle in patients undergoing venoarterial
extracorporeal membrane oxygenation for cardiogenic shock: a systematic review and meta-analysis. J Card Surg.
2020;35(6):1237-42.

2. Rajagopal K. Left ventricular distension in veno-arterial extracorporeal membrane oxygenation: from mechanics to
therapies. ASAIO J. 2019;65(1):1-10.

3. Al-Fares AA, Randhawa VK, Englesakis M, et al. Optimal strategy and timing of left ventricular venting during veno-
arterial extracorporeal life support in cardiogenic shock: a systematic review and meta-analysis. Circ Heart Fail.
2019;12(11):e006486.

4. Cheng R, Hachamovitch R, Makkar R, et al. Lack of survival benefit found with use of intraaortic balloon pump in
extracorporeal membrane oxygenation: a pooled experience of 1517 patients. J Invasive Cardiol. 2015;27(10):453-8.

5. Patel SM, Lipinski J, Al-Kindi SG, et al. Simultaneous venoarterial extracorporeal membrane oxygenation and
percutaneous left ventricular decompression therapy with Impella is associated with improved outcomes in refractory
cardiogenic shock. ASAIO J. 2019;65(1):21-8.

6. Grandin EW, Nunez JI, Willar B, et al. Mechanical left ventricular unloading in patients undergoing venoarterial
extracorporeal membrane oxygenation. J Am Coll Cardiol. 2022;79(13):1239-50.

7. Lemor A, Basir MB, O'Neill BP, et al. Left atrial-veno-arterial extracorporeal membrane oxygenation: step-by-step
procedure and case example. Structural Heart. 2022;6(6).

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19.5
Weaning and
Decannulation
of VV and VA
ECMO
Ginger Jiang, MD
Cardiology Fellow
Beth Israel Deaconess Medical Center
Boston, MA

A. Reshad Garan, MD, MS

Section Chief
Advanced Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support
Beth Israel Deaconess Medical Center
Associate Professor of Medicine
Harvard Medical School
agaran@[Link]
@ReshadGaranMD

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Introduction
Weaning and preparation for decannulation of extracorporeal membrane oxygenation (ECMO), also
known as extracorporeal life support (ECLS), represent critical steps in the management of ECMO-
supported patients. Given the significant risks associated with prolonged time spent on ECMO, it is
important to regularly assess readiness for weaning. Strategies for stepwise weaning of ECMO and
assessment of stability during the weaning process vary across institutions. This chapter discusses
strategies for weaning and decannulation of veno-arterial (VA) and veno-venous (VV) ECMO, including
a review of predictors of successful weaning, hemodynamic and echocardiographic monitoring during
stepwise weaning, and risk and prevention of clotting.

Weaning and decannulation of VA ECMO

Assessing readiness
Assessment for readiness for ECMO weaning should be conducted on a regular basis given the risks
associated with prolonged ECMO utilization.1 The time to explant readiness for patients in cardiogenic
shock (CS) varies depending on the etiology of the initial decompensation, the speed of the recovery
process from CS, and the intention for support (ie, bridge to myocardial recovery vs. bridge to durable
left ventricular assist device [LVAD] or heart transplant [HT]).

Most clinicians focus on achieving the criteria shown in Box 1 prior to beginning a weaning trial. When
these criteria are met, performance of daily trials of ECMO flow reduction can identify the appropriate
timing of device explant to avoid unnecessarily prolonged periods of support which will expose the
patient to unnecessary risk.5 In situations where ECMO is used to bridge a patient to either LVAD or HT,
weaning trials may not be appropriate since ECMO explant will not occur prior to those surgeries.

BOX 1. CRITERIA TO BEGIN VA ECMO WEANING

• The cause of the initial decompensation has been treated or is resolving, for example,
coronary revascularization in the setting of acute myocardial infarction (AMI)
• Native cardiac output and markers of shock are improving, for example, appearance of
pulsatile arterial waveform, mean arterial pressure (MAP) >60 mmHg, improving markers
of end organ dysfunction, lactate clearance
• ECMO support requirement is minimal (eg, <2-2.5 L/min)
• Vasopressors and inotropes are at low doses2,3,4
• Markers of oxygenation and respiratory status are stable (eg, P:F is >150)

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Weaning and decannulation process

Predictors of successful weaning
Several observational studies have described predictors of successful weaning.3,6-10 Several studies
have found that a higher pulse pressure was associated with successful weaning.6,8 Multiple
echocardiographic parameters including LVEF, aortic velocity time integral (VTI), lateral mitral annulus
peak systolic velocity, and RVEF have been shown to predict successful weaning, and have been
incorporated into stepwise weaning protocols.6,7,10 Serum lactate and clearance have also been
associated with successful weaning.9 Age, sex, presence of comorbidities, and severity of illness on
initial presentation have not been shown to be predictors of successful weaning.11

Stepwise weaning trial

Weaning and decannulation protocols vary across institutions. Several studies have described specific
ECMO weaning protocols, though these studies tend to be limited to single institution experiences often
with small sample sizes.11 The guiding principle behind most commonly utilized weaning protocols is
the gradual reduction of flow and/or sweep rates (if VV configuration) with frequent interval assessment
of hemodynamic and respiratory stability. The rate at which ECMO flow is decreased should be
determined based on the clinical scenario at hand; weaning protocols typically describe decreasing flow
at rates of 0.5 L anywhere from every 2 to 24 hours though this may be altered in situations where a
high likelihood of successful wean is anticipated, for example from a rapidly reversible etiology of CS
(eg, calcium channel blocker overdose).1

The protocol used at our institution (Figure 1) includes the following steps once readiness to wean has
been determined:
1. Reduce ECMO flow by 0.5 L/min gradually until 2-2.5 L/min is reached.
2. Assess for stability with invasive hemodynamic and/or echocardiographic monitoring (see
“Assessment of stability during weaning trial” discussion below).
3. Ensure adequate anticoagulation prior to reduction of flows below 2 L/min (see “Risk of
thromboembolism and management of anticoagulation” discussion below).
4. A stepwise reduction of flow below 2-2.5 L/min (typically by 0.5 L/min increments) is implemented
with close monitoring of hemodynamic and/or echocardiographic parameters. If flows 0.5-1 L/
min are tolerated, then both the arterial and venous cannulas can be clamped to achieve transient
cessation of hemodynamic support. This stage should not last for more than several minutes and
adequate anticoagulation should be ensured prior to clamping.
5. Reassess at each stage of flow reduction for stability with invasive hemodynamic and/or
echocardiographic monitoring.
6. If this trial of flow reduction/cannula clamp is tolerated (from hemodynamic and respiratory
perspectives), return flows to 2-2.5 L/min or greater until decannulation can be pursued.

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REDUCE ECMO FLOW BY INTERVALS OF 0.5 L/MIN

Assess for stability with invasive hemodynamic and/or

echocardiographic monitoring

CI > 2.4 L/min/m², MAP > 60 mmHg, Markers of stability not met
PCWP < 18 mmHg, and CVP < 15 mmHg
OR
LVEF > 20%, TDSa > 6 cm/s, and aortic VTI >10 cm

Continue to reduce ECMO flow by intervals of

0.5 L/min with interval assessment of stability
until 2 L/min is reached

Increase anticoagulation prior to decreasing flow below

≤2 L/min

Continue to reduce ECMO flow in a stepwise fashion

Assess for stability with invasive hemodynamic

and/or echocardiographic monitoring

CI > 2.4 L/min/m², MAP > 60 mmHg, PCWP < 18 mmHg, Markers of
and CVP < 15 mmHg hemodynamic stability
not met
OR
OR
LVEF > 20%, TDSa > 6 cm/s, and aortic VTI >10 cm
SaO2 <90

Decannulate Increase flow to achieve stability and continue managing

active medical issues with plan to assess every 24 hours

ABG=arterial blood gas; CI=cardiac index; CVP=central venous pressure; ECMO=extracorporeal membrane oxygenation; LVEF=left ventricular
ejection fraction; MAP=mean arterial pressure; PCWP=pulmonary capillary wedge pressure; TDSa =lateral mitral annulus peak systolic velocity;
VTI=velocity time integral

Figure 1. Stepwise Approach to Weaning VA ECMO

Assessment of stability during weaning trial

Stability during a weaning attempt can be assessed via invasive hemodynamic monitoring (ie, with
pulmonary artery catheter) and/or echocardiography. When monitoring hemodynamics, a patient is
considered stable during weaning when the cardiac index remains >2.4 L/min/m2, MAP remains >60
mmHg, pulmonary capillary wedge pressure remains <18 mmHg, and central venous pressure remains
<15 mmHg with each flow rate reduction.12 Transthoracic echocardiography may also be utilized to
determine stability during stepwise weaning by repeating echocardiography following each flow rate
reduction. Parameters suggestive of a successful wean include LVEF >20%, lateral mitral annulus peak
systolic velocity >6 cm/s, and aortic VTI >10 cm as ECMO flows are reduced in a stepwise fashion.6

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Risk of thromboembolism and management of anticoagulation

The risk of thrombosis increases with lower circuit flow. Therefore, special consideration should be taken
to prevent clotting during the weaning process.13 At our institution, we typically use unfractionated
heparin with an anti-Xa monitoring protocol during ECMO support. However, as described above,
when flows are to be transiently reduced below 2-2.5 L/min to assess readiness for decannulation,
anticoagulation should be intensified (eg, we typically bolus heparin until an ACT ≥250 seconds). Even
if hemodynamic stability is maintained when flows are briefly reduced to 0 L/min by cannula clamping,
flows should be returned to ≥2-2.5 L/min until decannulation is performed to avoid risk of thrombosis.

Use of arteriovenous bridges for difficult to wean patients

In select patients, use of an arteriovenous (AV) bridge can be considered to facilitate the weaning
process while minimizing the risk of premature decannulation and thromboembolic complications of
the ECMO circuit. Use of this technique allows for a longer period of observation without hemodynamic
support before proceeding with decannulation and can be helpful when the ability to successfully
separate from ECMO is uncertain. The AV bridge incorporates a 30-50 cm long tube with Y-connects
into the ECMO circuit between the arterial and venous lines to effectively separate patient circulation
from the ECMO circuit.14,15 An adjustable Hoffman clamp may be placed on the AV bridge to control flow
rates throughout the circuit and bridge, and non-invasive flow meters may be utilized to measure blood
flow through the AV bridge. Support flow through the circuit is reduced in a stepwise fashion by 10-
15% increments with reassessment for stability via hemodynamics and/or echocardiography after each
reduction; meanwhile, the pump flow itself does not need to be altered. Patients may be monitored on
the weaning bridge to ensure stability while without hemodynamic support from the ECMO circuit prior
to decannulation. In patients who remain difficult to wean after optimal medical management, transfer
to a center with LVAD or HT capability is strongly encouraged.

Decannulation
Once a patient is deemed to be ready for separation from ECMO, the process of decannulation may
occur in an operating room or the cardiac catheterization laboratory. In the majority of instances at our
institution, decannulation is performed in the operating room with repair of the arteriotomy. However,
for lower risk cases, decannulation may be performed in the cardiac catheterization laboratory with
vascular surgery support readily available if necessary.

Weaning and decannulation of VV ECMO

Assessing readiness
As with VA ECMO, patients should be regularly assessed for readiness to wean from VV ECMO support.
Patients are ready to undergo a weaning trial once they achieve the criteria listed in Box 2. Once these
criteria are met, daily ECMO weaning trials should be conducted.

BOX 2. CRITERIA TO BEGIN VV ECMO WEANING

• Etiology of the initial decompensation is addressed or improving
• Improvement in pulmonary compliance (eg, P:F>150) and arterial saturation is observed
(eg, SaO2 ≥95 and PaO2 ≥55) with ECMO flow rate close to normal cardiac output
• Radiographic appearance of lung fields is improved
• Hemodynamic stability with minimal doses of vasopressors

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Weaning and decannulation process

Stepwise weaning trial
Weaning protocols for VV ECMO, like VA ECMO, vary from institution to institution. The following
stepwise approach to weaning is recommended in the 2017 ELSO guidelines (Figure 3).16
1. Reduce ECMO flow by 0.5 L/min gradually until 2 L/min is reached.
2. While maintaining 2 L/min of flow, perform stepwise reduction of sweep FiO2 while assessing for
interval stability with serial ABGs.
3. If gas exchange remains acceptable as sweep FiO2 is progressively reduced, sweep gas may be
clamped.
4. If SaO2 remains ≥95% and PaCO2 remains <50 after 60 minutes, decannulation should be pursued.
REDUCE ECMO FLOW BY INTERVALS OF 0.5 L/MIN
GRADUALLY UNTIL 2 L/MIN IS REACHED

Assess for stability with serial ABGs and

hemodynamic monitoring

SaO2 ≥95 and PaCO2 <50 Markers of stability not met

AND
Patient remains hemodynamically stable

While maintaining 2 L/min of flow,

perform stepwise reduction of sweep FiO2.
Assess for interval stability with serial ABGs.

SaO2 ≥95 and PaCO2 <50 Markers of stability not met

If gas exchange remains

acceptable as sweep FiO2 is
progressively reduced,
clamp sweep gas

SaO2 ≥95 and PaCO2 <50 after Markers of stability not met
60 minutes on the above settings

Decannulate Increase flow to achieve stability and continue managing

active medical issues with plan to assess every 24 hours

ABG=arterial blood gas; ECMO=extracorporeal membrane oxygenation; FiO2=fraction of inspired oxygen; PaCO2=partial pressure of carbon
dioxide; SaO2=oxygen saturation as measured by blood analysis

Figure 2. Stepwise Approach to Weaning VV ECMO

Decannulation
Decannulation of peripherally inserted VV cannulas may be performed at the bedside. For select high
risk patients, access cannulas may be left in place for up to 24 hours in case of the need for reinitiation
of ECMO support.

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QUICK READ SUMMARY

✓ Once key criteria for clinical improvement and stability are met, patients on VA and VV
ECMO should be assessed for weaning trials on a regular basis (eg, daily).

✓ Protocols for ECMO weaning vary across institutions and are often based upon small,
single-institution studies or expert recommendation.

✓ Weaning of VA ECMO is carried out by gradually reducing the ECMO flow rate
with frequent interval assessment of stability via invasive hemodynamic and/or
echocardiographic monitoring.

✓ Weaning of VV ECMO is conducted by gradually reducing pump flow, then sweep rate and
FiO2 with frequent interval assessment of oxygenation and ventilation via serial ABGs.

✓ Special consideration should be taken to avoid the risk of thromboembolism with lower
rates of flow through the circuit during the weaning process.

References
1. Guglin M, Zucker MJ, Bazan VM, et al. Venoarterial ECMO for adults: JACC Scientific Expert Panel. J Am Coll Cardiol.
2019;73(6):698-716. doi:10.1016/[Link].2018.11.038

2. Randhawa VK, Al-Fares A, Tong MZY, et al. A pragmatic approach to weaning temporary mechanical circulatory
support: a state-of-the-art review. JACC: Heart Failure. 2021;9(9):664-73. doi:10.1016/[Link].2021.05.011

3. Garan AR, Eckhardt C, Takeda K, et al. Predictors of survival and ability to wean from short-term mechanical
circulatory support device following acute myocardial infarction complicated by cardiogenic shock. Eur Heart J Acute
Cardiovasc Care. 2018;7(8):755-65. doi:10.1177/2048872617740834

4. Fried JA, Masoumi A, Takeda K, Brodie D. How I approach weaning from venoarterial ECMO. Crit Care.
2020;24(1):307, s13054-020-03010-03015. doi:10.1186/s13054-020-03010-5

5. Garan AR, Malick WA, Habal M, et al. Predictors of survival for patients with acute decompensated heart
failure requiring extra-corporeal membrane oxygenation therapy. ASAIO J. 2019;65(8):781-7. doi:10.1097/
mat.0000000000000898

6. Aissaoui N, Luyt CE, Leprince P, et al. Predictors of successful extracorporeal membrane oxygenation (ECMO)
weaning after assistance for refractory cardiogenic shock. Intensive Care Med. 2011;37(11):1738-45. doi:10.1007/
s00134-011-2358-2

7. Cavarocchi NC, Pitcher HT, Yang Q, et al. Weaning of extracorporeal membrane oxygenation using continuous
hemodynamic transesophageal echocardiography. J Thorac Cardiovasc Surg. 2013;146(6):1474-9. doi:10.1016/j.
jtcvs.2013.06.055

8. Pappalardo F, Pieri M, Arnaez Corada B, et al. Timing and strategy for weaning from venoarterial ECMO are complex
issues. J Cardiothorac Vasc Anesth. 2015;29(4):906-11. doi:10.1053/[Link].2014.12.011

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9. Li CL, Wang H, Jia M, et al. The early dynamic behavior of lactate is linked to mortality in postcardiotomy patients
with extracorporeal membrane oxygenation support: a retrospective observational study. J Thorac Cardiovasc Surg.
2015;149(5):1445-50. doi:10.1016/[Link].2014.11.052

10. Huang KC, Lin LY, Chen YS, et al. Three-dimensional echocardiography-derived right ventricular ejection fraction
correlates with success of decannulation and prognosis in patients stabilized by venoarterial extracorporeal life
support. J Am Soc Echocardiogr. 2018;31(2):169-79. doi:10.1016/[Link].2017.09.004

11. Ortuno S, Delmas C, Diehl JL, et al. Weaning from veno-arterial extra-corporeal membrane oxygenation: which
strategy to use? Ann Cardiothorac Surg. 2019;8(1): E1-8. doi:10.21037/acs.2018.08.05

12. Aziz TA, Singh G, Popjes E, et al. Initial experience with CentriMag extracorporal membrane oxygenation for support
of critically ill patients with refractory cardiogenic shock. J Heart Lung Transplant. 2010;29(1):66-71. doi:10.1016/j.
healun.2009.08.025

13. Oliver WC. Anticoagulation and coagulation management for ECMO. Semin Cardiothorac Vasc Anesth.
2009;13(3):154-75. doi:10.1177/1089253209347384

14. Babar Z, Sharma A, Ganushchak Y, et al. An arterio-venous bridge for gradual weaning from adult veno-arterial
extracorporeal life support. Perfusion. 2015;30(8):683-688. doi:10.1177/0267659115581197

15. Vida VL, Lo Rito M, Padalino MA, Stellin G. Extracorporeal membrane oxygenation: the simplified weaning bridge. J
Thorac Cardiovasc Surg. 2012;143(4): e27-8. doi:10.1016/[Link].2011.12.065

16. Extracorporeal Life Support Organization (ELSO) Guidelines for Adult Respiratory Failure. Published online August
2017.

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19.6
ECMO Access
Site Closure: OR,
Cath Lab, Bedside
Araba Ofosu-Somuah, MD
Interventional Cardiology Fellow
University of North Carolina
Chapel Hill, NC
abrucemensah@[Link]

Mehul Desai, MD
Director, Critical Care ECMO Services
Inova Heart and Vascular Institute

Ramesh Singh, MD
Surgical Director, Mechanical Circulatory Support
Inova Heart and Vascular Institute

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Introduction
Over the last several decades, the approach to ECMO arteriotomy closure has shifted in parallel with
emerging new technology. The primary method of achieving arterial and venous hemostasis remains
manual compression in many institutions; however, this approach requires continued compression
for long periods of time, is often limited by available resources, requires prolonged bedrest following
control of hemostasis, and may delay mobilization. In addition, the ability to achieve hemostasis may
be complicated by obesity, use of anticoagulant and antiplatelet therapies, and use of larger vascular
devices, particularly ECMO cannulas exceeding 17 Fr in outer diameter.

Vascular closure devices were initially introduced as alternatives to manual compression (Figure 1). Data
to date have shown earlier hemostasis, improved patient comfort, and earlier ambulation;1 however, this
has been counterbalanced by a potential for limb complications, device failure, and possible infection.2
For ECMO patients, where manual compression may be inadequate with removal of 17–25 Fr (or
larger) sheaths, which may have been indwelling for days to weeks, or in the event of injury to the
vessel during cannulation, surgical cutdown with open repair in the OR may be the preferred option for
arteriotomy and venotomy closure.

Figure 1. Perclose ProGlide™ Vascular Closure Device Used with ECMO Sheaths

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Surgical closure of arterial access

The primary approach to arterial closure in very large bore vascular procedures has historically been
surgical cutdown with open repair. The common femoral artery is exposed via a vertical or oblique
incision within the femoral triangle, followed by dissection through the skin and subcutaneous tissue
using electrocautery. The arteriotomy repair is performed with monofilament sutures (running or
interrupted) and if the vessel is mechanically damaged, an endarterectomy with either synthetic or
biologic patch repair is required.

Figure 2. Surgical Closure Following Femoral Access

Although surgical cutdown provides definitive repair, postoperative complications are seen more
frequently than in the percutaneous approach to ECMO decannulation and arteriotomy and venotomy
closure. The risk of complications rises especially in patients with diabetes and obesity. The incidence
of complications in the literature varies from 2.1% to 22.8%, resulting in the need for interventional
therapy and prolonged recovery periods.3,4,5 In addition to increased risk of infection, wound dehiscence,
and lymphatic leak, surgical removal of ECMO cannulas has also been associated with a higher
incidence of blood transfusions.

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Cath lab closure

Overview
With recent advancements in interventional cardiology, increasingly complex, large bore, procedures
are being performed percutaneously. Percutaneous (versus surgical) removal and arteriotomy/
venotomy closure of venoarterial extracorporeal membrane oxygenation (VA ECMO) catheters may be
associated with fewer complications including lower rates of infection, lymphatic leakage, bleeding,
and limb claudication, as well as earlier ambulation.5,7,8,9 Other literature suggests that success rates
and complications are similar to traditional open repair rates.7 Notably, the success of these closure
procedures relies heavily on optimal initial femoral access techniques. Currently, there are no established
guidelines regarding how large bore arterial access sites should be closed.

Many operators choose to use vascular closure devices rather than manual compression when
percutaneously removing VA ECMO catheters. Below we briefly introduce some of these vascular
closure devices (which primarily include suture-based and plug-based technologies) and techniques,
including pre-close technique with Perclose ProGlide, MANTA device closure, and hybrid techniques.

Pre-close technique
The pre-close technique is performed using the Perclose ProGlide™ vascular closure device (Abbot
Vascular, Santa Clara, CA). This device consists of a guidewire, plunger, handle, and sheath. It is
designed to deliver sutures to close large access sites in large vessels.10 It is a 6 Fr system that utilizes
a pair of polypropylene monofilament-loaded sutures to facilitate closure. It is designed to close arterial
access site sizes from 5 Fr up to 21 Fr.12

A video detailing Perclose ProGlide deployment

Relative contraindications to using can be found at [Link]
the Perclose suture device watch?v=MTcmYNZQl3M. For more information
about Perclose ProGlide and suture-based
• Common femoral artery wall femoral closure, refer to the Vascular Access,
calcification Management, and Closure Best Practices ebook
• Common femoral artery aneurysm (chapter 2, sections 11 and 12) available on the
• Arteriotomy outside the common SCAI website at [Link]
femoral artery and-closure.
• Extreme obesity
• Access vessel diameters <5 mm

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Figure 3. Perclose Positioning and Locking Down Perclose Sutures

Previously published studies have reported success rates from 70% to 100% with the pre-close
technique. The pre-placement of sutures via the pre-close technique is preferred to obtain the most
effective results from the Perclose system for large bore vascular access closure. Most of the failure
in insertion is observed in patients who are obese, patients with calcification in the common femoral
artery, and patients who have received larger introducer sheaths.8 There is uncertainty regarding
the safety of leaving exposed Perclose sutures in patients with VA ECMO devices left in place for
longer periods of time as the sutures may be a nidus for infection. However, multiple centers have
demonstrated success with this technique without infectious complications.13

Our Inova Heart and Vascular Institute experience with the Perclose device use via pre-close technique
in 51 VA ECMO patients (compared to 49 patients closed without pre-close Perclose insertion),
including many extracorporeal CPR patients, has demonstrated only 5 instances of device failure at
the time of bedside or OR device removal, all of which were subsequently successfully managed with
follow-on surgical repair or endovascular intervention. The use of pre-closure technique was associated
with fewer limb complications and bleeding events in comparison to patients undergoing open repair
(unpublished data). ICU length of stay, pseudoaneurysms, and distal embolization were not noted to
be statistically different. No patients in the pre-closure group suffered complications such as systemic
infection, loss of limb, or death due to use. Our single-center data suggest that the pre-close technique
with the Perclose ProGlide system is technically feasible, safe, and associated with a significantly lower
likelihood of limb complications and bleeding compared to surgical removal in the OR (6% versus
25%).14 Prospective studies will be required to determine the optimal use and implications on recovery.

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Percutaneous plug-based arteriotomy closure device

MANTA™ (Essential Medical Inc, Malvern, Pennsylvania) is a percutaneous plug-based arteriotomy
closure device that was recently approved by the FDA. This device consists of a sheath, closure unit,
introducer, and depth locator.11 MANTA was created to close arteriotomies from large bore vascular
devices. Hemostasis takes place through an “anchor-arteriotomy-collagen sandwich” complemented
by the coagulation-inducing properties of the collagen from the coagulation cascade. The collagen and
anchor are resorbable. A radiopaque stainless-steel suture lock remains as a landmark for subsequent
interventions. A single device can close an access site following a procedure with a device up to 25 Fr
in outer diameter.7,9 For more information about MANTA and other plug-based closure devices, refer to
Chapter 2, Section 13 the Vascular Access, Management, and Closure Best Practices eBook available on
the SCAI website at [Link]

One major concern with the MANTA device is how to accurately measure the depth of the device
insertion. Ultrasound and/or fluoroscopy is advised to estimate how deeply to insert the device.7,9 A
benefit of using the MANTA device is that this method does not require pre-closure at the time of initial
insertion, which can be beneficial under emergency circumstances.

Figure 4 (video). MANTA Deployment

(Courtesy of Teleflex Incorporated. ©2022 Teleflex Incorporated. All rights reserved.)

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Hybrid closure technique

The hybrid closure technique uses the suture-based Perclose system in conjunction with a plug-based
closure device. This technique may be used as a primary closure method, or it can be employed post-
hoc if the initial pre-close Perclose system does not succeed in achieving adequate hemostasis.12 For
further technical details pertaining to the hybrid closure technique, refer to Chapter 2, Section 13 the
Vascular Access, Management, and Closure Best Practices eBook available on the SCAI website at
[Link]

Figure 5. Hybrid Closure Approach with Angio-Seal and Perclose

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Bedside closure of arterial access

There are 3 methods performed at the bedside to achieve hemostasis following arterial access:
• Manual compression
• Assisted manual compression
• Bedside closure of pre-close Perclose sutures (as described above)

Manual compression
Manual compression remains the gold standard after smaller arteriotomies; however, it has been proven
to be more difficult after larger bore interventions such as ECMO. Nonetheless it is an essential skill,
particularly in the event of percutaneous closure device failure. It is important to employ good manual
compression technique, as described below.

1. Ensure that the ACT is less than 180 seconds.

2. Continuously monitor vital signs throughout the compression.
3. Flush the sheath prior to pulling.
4. Place fingers about 1 inch above the arteriotomy site and apply firm pressure. Standing on a stool
will help distribute body weight forward.
5. After adequate control is achieved, remove the sheath, taking care not to crush the sheath.
6. Ensure the patient is comfortable throughout by administering analgesia if indicated.
7. Monitor distal pulses every 2-3 minutes during compression. A diminished pulse is acceptable but
should not be obliterated completely. If the pulse is obliterated, gradually decrease the amount of
compression to the area.
8. The general rule is to apply 3 minutes of pressure per French size (eg, 51 minutes for a 17 Fr arterial
ECMO cannula).
9. Following hemostasis, prolonged multi-hour bed rest is indicated.12

Figure 6. Manual Compression

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Assisted manual compression

In some situations, hemostasis is best achieved with the aid of an extrinsic compression device, often
in conjunction with hemostatic pads. Hemostatic pads contain procoagulant coating to accelerate
coagulation and hemostasis and may result in shorter compression time with a lower incidence of
bleeding.12 FDA approved manual compression devices include FemoStop™ (St Jude Medical) and
C-clamp devices.12

FemoStop is currently the most commonly

used assisted compression device. It has a rigid
frame and a pneumatic dome that is inflated at
the arteriotomy site. A belt holds the frame in
place on the patient’s body. Once the dome is
positioned correctly over the arteriotomy site
(which is typically located cranial to the skin
access site, especially in obesity), it is inflated to
60-80 mmHg. The sheath can then be removed,
and the dome inflated to supra-systolic pressure.
The dome is then partially deflated after 3-5
minutes until the pedal pulses are palpable
again. Compression is maintained until adequate
hemostasis is achieved.12

Figure 7. FemoStop Manual Compression System

Figure 8 shows the CompressAR System C-clamp

style compression device. It consists of a stand
with an arm that puts manual pressure on the
arteriotomy site after the sheath is pulled.12

Figure 8. CompressAR System C-clamp Device

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QUICK READ SUMMARY

✓ The ideal approach to large bore ECMO vascular closure is highly dependent on patient
physical characteristics, site of access, cannula size, and duration of cannulation.

✓ The gold standard for decannulation remains open closure and repair.

✓ Percutaneous removal of VA ECMO catheters may be associated with fewer

complications and many operators choose to use vascular closure devices, such as
Perclose ProGlide or MANTA when percutaneously removing VA ECMO catheters.

✓ The use of pre-closure has demonstrated significant reduction in bleeding, surgical

complications, and earlier ambulation.

✓ User skill and comfort with devices and techniques as well as institutional expertise and
preference should be considered when selecting a closure technique.

✓ Further prospective studies are required to determine the ideal method for arterial
closure in patients undergoing large bore vascular access with ECMO.

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References
1. Danial P, Hajage D, Nguyen LS, et al. Percutaneous versus surgical femoro-femoral veno-arterial ECMO: a propensity
score matched study. Intensive Care Med. 2018;44(12):2153-61. doi:10.1007/s00134-018-5442-z.

2. Aziz F, Brehm CE, El-Banyosy A, et al. Arterial complications in patients undergoing extracorporeal membrane
oxygenation via femoral cannulation. 2014;28(1):178-83. doi:10.1016/[Link].2013.03.011

3. Morasch MD, Kibbe MR, Evans ME, et al. Percutaneous repair of abdominal aortic aneurysm. J Vasc Surg.
2004;40(1):12-6.

4. Thrumurthy SG, Karthikesalingam A, Patterson BO, et al. A systematic review of mid-term outcomes of thoracic
endovascular repair (TEVAR) of chronic type B aortic dissection. Eur J Vasc Endovasc Surg. 2011;42(5):632-47.

5. Aljabri B, Obrand DI, Montreuil B, et al. Early vascular complications after endovascular repair of aortoiliac aneurysms.
Ann Vasc Surg. 2001;15(6):608-14.

6. Lee WA, Brown MP, Nelson PR, et al. Midterm outcomes of femoral arteries after percutaneous endovascular aortic
repair using the preclose technique. J Vasc Surg. 2008;47(5):919-23. doi:10.1016/[Link].2007.12.029

7. Au SY, Fong KM, Ng WG, et al. Real-time ultrasound-guided bedside closure of arteriotomy wound using MANTA
closure device during venoarterial extracorporeal membrane oxygenation decannulation. Perfusion. 2021;36(2):118-
21. doi:10.1177/0267659120932429

8. Xu X, Liu Z, Han P, et al. Feasibility and safety of total percutaneous closure of femoral arterial access sites after veno-
arterial extracorporeal membrane oxygenation. Medicine. 2019;98(45):e17910. doi:10.1097/md.0000000000017910

9. Hassan MF, Lawrence M, Lee D, et al. Simplified percutaneous VA ECMO decannulation using the MANTA vascular
closure device: initial US experience. J Card Surg. 2020;35(1):217-21. doi:10.1111/jocs.14308

10. U.S. Food and Drug Administration. Abbott Perclose ProGlide suture-mediated closure system - P960043/S097.
FDA. Available at: [Link]
mediated-closure-system-p960043s097. Accessed on 10 June 2021.

11. U.S Food and Drug Administration. MANTA vascular closure device – P180025. FDA. Available at: [Link]
gov/medical-devices/recently-approved-devices/manta-vascular-closure-device-p180025. Accessed on 10 June
2021.

12. Shroff A, Pinto D. Vascular access, management, and closure: Best practices [eBook]. 2019. Society for
Cardiovascular Angiography & Interventions. [Link]

13. Lata K, Kaki A, Grines C, et al. Pre-close technique of percutaneous closure for delayed hemostasis of large bore
femoral sheaths. J Interv Cardiol. 2018;31(4):504-10. doi: 10.1111/joic.12490. Epub 2018 Feb 5. PMID: 29405431.

14. Chandel A, Desai M, Ryan LP, et al. Preclosure technique versus arterial cutdown after percutaneous cannulation for
venoarterial extracorporeal membrane oxygenation. JTCVS Tech. 2021;10:322-30.

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PREVIOUS SECTION SECTION 4: Selecting Devices and Device Combinations Based on Clinical Need NEXT SECTION

SECTION 4

Selecting Devices
and Device
Combinations
Based on
Clinical Need

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

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PREVIOUS CHAPTER Chapter 20: AMICS/Post PCI Shock NEXT CHAPTER

AMICS/Post PCI
Shock
Manu Kaushik, MD
Interventional Cardiologist
Bon Secours Mercy Health Physicians
St Mary’s Hospital
Richmond, VA
drmanukaushik@[Link]

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Overview
Cardiogenic shock (CS) is the most common cause of mortality after acute myocardial infarction (AMI)
and in the post percutaneous coronary intervention (PCI) setting. Despite large scale implementation
of early revascularization, mortality from AMI with CS (AMICS) is remarkably high at about 40% and
resistant to recent advances in pharmacotherapy and revascularization techniques. Post PCI coronary
ischemia with acute CS has similar pathophysiology to AMICS and often requires similar management.
Short-term mechanical circulatory support (MCS) devices appear to be an intuitive option to reduce
mortality in AMICS. In this chapter, we review the role of short-term mechanical circulatory support
devices in cardiogenic shock post-PCI and in AMICS with focus on the later.

CS is a state of reduced cardiac output in conjunction with evidence of systemic end organ
hypoperfusion that may progress to irreversible multiorgan dysfunction (MOD) without prompt and
appropriate management. Death in AMICS commonly occurs from mechanical complications of MI,
primary ventricular/pump failure, and subsequent or antecedent MOD. Cardiac power predicts mortality
in AMICS better than either cardiac output or blood pressure. Both cardiac output and blood pressure
play an important role in pathogenesis and prognosis of CS and an abnormality in either can be
associated with CS. Cardiac power in essence “captures” reduction in either cardiac output or systemic
perfusion pressure. Short-term MCS devices have been demonstrated to improve cardiac power by
increasing cardiac output, systemic blood pressure, or both and may have a positive physiologic impact
on hemodynamics in AMICS. Newer MCS devices demonstrate greater increments in cardiac output
compared to traditionally used intra-aortic balloon pump (IABP). Certain retrospective studies on real
world utilization of these devices have questioned the safety of these devices,2 a concern reaffirmed in
more recent randomized controlled trials.10,11 Nevertheless, recent RCTs also demonstrate reduction in
mortality with certain MCS devices.11

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Individual MCS devices and clinical data

Short-term MCS platforms currently available in the US include IABP, axial transvalvular ventricular
assist devices (Impella®), percutaneous short-term extracorporeal active decompression systems
(TandemHeart®), and extracorporeal membrane oxygenation (ECMO) systems. Table 1 describes how
each of these MCS devices impact hemodynamics.

Table 1. MCS Device Impact on Hemodynamic Parameters in Cardiogenic Shock

CIRCULATORY SUPPORT VENTRICULAR SUPPORT MYOCARDIAL PERFUSION

Arterial Oxygenation Ventricular Ventricular filling Coronary
perfusion and capability afterload pressure and perfusion
metabolite volume
clearance
Significantly No Reduced Reduced Improved
Impella 2.5®
improved
Impella CP®
Impella 5.0®
Impella 5.5®

IABP Improved No Reduced May be reduced Improved

Significantly Yes Increased May be reduced No change
TandemHeart LA RA improved
Significantly Yes Significantly Increased No change
VA ECMO improved increased

Impella RP®* — — Reduced* Reduced*

— Yes Reduced* Reduced*
TandemHeart RA PA*

* Right ventricle

MCS devices have been promoted to overcome the limitations of vasopressor and inotropic
pharmacotherapy in AMICS. Vasoactive drugs often have directly deleterious cardiac effects and one of
the potential benefits of MCS is the ability to wean use of those drugs. Unfortunately, there have been
limited randomized controlled trials to support therapeutic efficacy of currently available MCS devices.
Use of MCS devices has outpaced the evidence supporting the benefit. Some recent retrospective
studies on real-world use of these devices have questioned the safety of these devices2 thus
highlighting the importance of conducting adequately powered randomized trials to evaluate relative
safety and efficacy. Conduct of RCTs in this population is challenging. The appropriate target population
and endpoints are unclear. Investigator beliefs regarding the absence of equipoise or ability to provide
informed consent have stunted enrollment or led to premature trial discontinuation.

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IABP was the first device studied in a large randomized controlled trial in AMICS patients. IABP
SHOCK II was a multicenter randomized prospective trial evaluating benefit of IABP in 600 patients
with AMICS without cardiac arrest or mechanical complications. There was no difference in the IABP
group compared to optimal medical therapy in terms of 30-day mortality, length of intensive care stay,
renal function, time to hemodynamic stabilization, adverse events, or biochemical parameters.3 While
underpowered, it was the largest trial evaluating utility of any MCS device in the AMICS population and
following its publication, ESC guidelines downgraded the recommendation for use of IABP from 1a to
2b in patients with severe/refractory AMICS selectively.

More recently, 2 long-awaited randomized trials evaluated the use of other MCS devices in patients with
AMICS. The ECLS SHOCK trial10 compared the use of extracorporeal membrane oxygenation (ECMO)
in conjunction with standard care to standard care alone. ECLS Shock demonstrated no significant
survival benefit at 30 days. Interestingly, there was no difference in rates of resolution of lactic acidosis
and improvement in acute kidney injury between the 2 groups despite ECMO being deemed the best
MCS modality to improve tissue perfusion. The DanGer Shock trial11 evaluated the use of an Impella
microaxial pump in patients with AMICS, randomizing 360 patients to Impella in conjunction with
standard care or standard care alone. Post cardiac arrest patients who were comatose, as well as
those with predominantly right ventricular failure, were excluded. Impella use was associated with
improvement in 180-day survival with death from any cause occurring in 45.8% in the Impella group
and 58.5% in standard care. As expected, safety events were almost 4-fold higher in the Impella arm,
driven by bleeding and vascular complications. There was also a higher need for renal replacement
therapy in the Impella arm.

The divergent results between the 2 trials may be attributed primarily to 2 factors. ECLS Shock seems
to have included sicker patients, suggested by higher rates of pre-randomization resuscitation, higher
median lactate levels, and higher proportion of SCAI stage D and E patients, and in such patients benefit
of MCS may be attenuated due to futility. ECMO increases ventricular afterload, thereby increasing
myocardial oxygen demand, which may result in higher rates of myocardial injury and persistent
ventricular failure. Both trials found increased risk of vascular bleeding complications and vascular
complications. Further trials of MCS devices may be able to provide a better understanding of how to
mitigate the risk of MCS devices potentially involving smaller profile devices.

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Table 2. Key Trials Comparing MCS Devices in AMICS

NUMBER OF COMPARISON PRIMARY

TRIAL DESIGN RESULTS COMMENTS
PATIENTS ARMS OUTCOME

IABP-SHOCK II3 RCT 598 IABP vs All cause ND (p=0.96) No difference (ND) in
pharmacotherapy mortality ICU stay, lactate levels,
and early time to stabilization,
revascularization need for catecholamine
therapy or safety
outcomes

ISAR-SHOCK7 RCT 26 Impella 2.5 vs Change Change in CI ND in mortality. ND in

IABP in cardiac better with CI at 30 minutes or at
index (CI) Impella than 30 hours
IABP

IMPRESS7 RCT 48 Impella CP vs All cause ND (p=0.92) Critically ill; majority

IABP mortality with cardiac arrest.
Mortality close to 50%.
Higher safety events
with Impella.

Burkhoff et al.7 RCT 33 TandemHeart vs CI, PCWP, TandemHeart Only 70% of patients
IABP MAP superior had CS due to AMI; ND
in mortality

Thiele et al.7 RCT 41 TandemHeart vs Cardiac TandemHeart ND in mortality

IABP power superior
index

ECLS-SHOCK10 RCT 417 ECMO with All cause ND (p=0.81) No difference in

standard care vs. mortality recovery of biochemical
standard therapy at 30 days parameters with ECMO
alone

DanGer Shock11 RCT 355 Impella with All cause Impella arm Higher rate of safety
standard care mortality (45.8%) vs events in Impella arm
vs standard care at 180 standard (24% vs 6.2%); relative
alone days care group risk 4.74
(58.5%),
P=0.04

Babar et al.5 Prospective 406 Impella prior to Survival to 71% overall Higher survival than in
single arm PCI in AMICS discharge survival to previous similar cohorts
discharge

Schrage et al.8 Retrospective, 474 Impella vs IABP All cause ND Higher rate of bleeding
matched pair mortality in Impella arm
analysis

Lemor et al.9 Retrospective 6290 Impella (91%) vs In hospital Impella Likely significant
propensity ECMO(9%) mortality with lower indication bias
matched mortality
analysis (26.7%) vs
ECMO 43.3%
ND=No difference

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Invasive hemodynamic monitoring

Invasive hemodynamic monitoring with right heart catheterization (RHC) has not been demonstrated
to improve outcomes as a strategy in a randomized fashion. However, in observational studies of MCS
device patients, those undergoing invasive hemodynamic assessment with RHC fared better than those
without it.4 RHC can provide incremental information such as cardiac output, vascular resistance, filling
pressures, and right ventricular hemodynamics, thereby identifying the mechanism of underlying shock,
and excluding alternative etiologies of shock. While not prospectively validated, the information may
be used to guide the management of shock, the choice of MCS device, as well as decisions regarding
escalation and de-escalation of hemodynamic support (Figure 1).

Complete Likely futile Discuss goals of care

circulatory
arrest,
ongoing CPR
AMI with hemodynamic compromise
Invasive hemodynamics—CPO <0.6

Predominantly driven by Predominantly driven

low MAP (<65 mmHg) Both by low CO (<4 L/min)

LOW LOW
RAP • Fluids RAP
• Identify / treat hemorrhage / SIRS / sepsis
HIGH /
NORMAL • Treat acidosis HIGH / NORMAL

• Switch from propofol to benzo / sedative combination

SVR LVEDP

HIGH / NORMAL HIGH / NORMAL LOW

Consider Impella / TandemHeart Consider MCS with LV venting • Fluids

and wean pressors if feasible capability: Impella / TandemHeart • Inotropes/Vasopressors*
LOW • R/O PE/Pneumothorax
LOWPEEP
• Avoid high
• Consider RV failure
• Switch from propofol

• Continued shock
> 0.9 < 0.9 Consider adding
Consider ECMO • Increasing lactate PAPi
RV support
• Delta PCO2 >6

Figure 1. Hemodynamic Assessment of Patient with AMI or Post PCI Shock

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Patient selection for MCS in AMICS

Recent randomized trials indicate need for judicious use of MCS. Evidence on use of MCS devices in
AMICS is riddled with observational studies using heterogenous definitions of CS and often comparing
to previously examined cohorts. The IABP-SHOCK II trial showed up to 60% survival in AMICS.3 Some
recent focused strategic initiatives using stringent protocols, at specialized centers have demonstrated
survival rates to explant up to 70-75%,5 but have not been reproduced in a randomized trial. The scope
of further improvement in survival may be limited, as aggressive interventions may be futile in 25-30%
of patients1 due to significant anoxic brain injury or other medical comorbidities. Increased vascular
and bleeding complications, as shown by recent observational studies, further undermine the support
for frequent use of MCS devices. Hence, the prospects of treatment futility, as well as the likelihood of
complication, need to be weighed against potential benefit of MCS device use in individual patients.

Externally validated discriminatory tools such as IABP-SHOCK II risk score may help in identifying
patients at high risk of mortality, although using such tools in isolation to adjudicate the need for
MCS devices as a strategy has not been evaluated. SCAI CS classification may also be helpful in
identifying patients in whom MCS may be used cautiously or aggressively and in which cases it may
be futile (Figure 2). None of these strategies regarding MCS device utilization, however, has been
validated prospectively. Additionally, each patient should be carefully evaluated to rule out alternative
causes of shock by incorporating clinical assessment and laboratory data, and by performing bedside
echocardiogram and RHC if needed. Finally, in patients with CS with out of hospital cardiac arrest
(OHCA), outcomes are often determined by neurological recovery and if extensive anoxic brain injury or
irreversible MOD is suspected, it may be reasonable to forego MCS device placement.

STAGE E: Patient with complete circulatory collapse often resulting in Evaluate the impact

E
of MCS device
EXTREMIS refractory cardiac arrest with ongoing CPR; may include
ECMO-assisted CPR
intervention on outcome.
May defer if likely to be futile.

STAGE D: Patient with persistent hypotension and worsening

D
end organ perfusion despite inotropes, pressors, MCS, and
DETERIORATING treatment of underlying inciting cardiac pathology; patients
are in a “shock spiral”
MCS device may be considered.
When used as a part of strategic
initiatives, use may improve outcomes.
STAGE C: Patient with clinical signs of hypoperfusion –

CLASSIC C cold clammy skin, volume overloaded with extensive

rales and reduced urine output
Consider hemodynamic monitoring.
If used, cautiously weigh benefit
for MCS device against risk
STAGE B: Patient with relative hypotension or

B
of complications.
tachycardia without obvious hypoperfusion
BEGINNING
STAGE A: Patient with no obvious signs

AT RISK A and symptoms of CS, but at risk of

developing it

STAG E

Figure 2. Incorporating SCAI CS Classification12 in Decision Making for MCS Device Use

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Timing and choice of MCS devices in AMICS

Timing of MCS use
Timing of MCS device placement relative to timing of coronary revascularizations is often determined
by the degree of hemodynamic compromise, relative complexity of coronary disease requiring
intervention, accompanying problems such as cardiac arrest, and mechanical complications. The
National Cardiogenic Shock Initiative (NCSI) algorithm advocates for upfront left ventricle (LV) unloading
with Impella.4,5 In the DanGer Shock trial, a large majority of patients underwent revascularization after
initiation of ventricular unloading with Impella suggesting that the approach of unloading the ventricle
prior to revascularization in patients with cardiogenic shock is appropriate.11 Trials such as STEMI Door-
to-unload (DTU) are likely to provide insights into whether upfront ventricular unloading as a systemic
strategy has benefits that outweigh delays in revascularization.

Choice of MCS device

Choice of MCS device in AMICS should integrate patient dependent factors and shock phenotype, as
well as operator and institutional experience as illustrated in Figure 3.

PREEXISTING VARIABLES CONCOMITANT ISSUES

LV thrombus Cardiac arrest

Peripheral arterial disease Failure to oxygenate
Mechanical valves Mechanical complications of AMI
Severe aortic regurgitation or critical aortic stenosis

SHOCK PHENOTYPE INSTITUTIONAL/OPERATOR PREFERENCE

Left ventricular Device availability

Right ventricular Availability of perfusionist
Biventricular Transseptal experience

Figure 3. Factors Impacting Choice of MCS Device

Conditions associated with AMICS, such as cardiac arrest, sepsis/SIRS, and hypoperfusion-related brain
injury, often contribute to mortality that may not be modifiable by interventions predominantly aimed
at improving cardiac hemodynamics. Unlike cardiogenic shock from chronic heart failure, systemic
perfusion dysregulation is more acute in the setting of AMICS and post PCI, leading to increased
risk of acute as well as subacute MOD which may be a more significant contributor to mortality than
ventricular failure alone. Specific MCS devices differ in their ability to alter the pathogenesis of MOD,
ventricular failure, or myocardial perfusion. Understanding the primary underlying pathophysiologic
abnormality (Table 1) may help in selecting an MCS device based on desired hemodynamic impact.
No large, randomized trials have been performed comparing relative efficacy of various MCS devices
and available data comparing MCS devices is limited to small inadequately powered trials evaluating
hemodynamic rather than clinical outcomes, or retrospective registry analysis, which is impacted by
significant selection bias, as mentioned in Table 2.

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Data from the most contemporary randomized trials comparing MCS to prior standards of care seem to
support use of Impella as the first-line MCS device in appropriately selected patients with AMICS.11 Early
identification of shock and timely institution of MCS appears to be the key in optimizing outcomes. Lack
of need for a perfusion team, relatively easier access by interventional cardiologists, need for arterial
only access, and a requirement of lower degree on anticoagulation make Impella the preferred initial
mode of MCS. Indeed, addition of or escalation to ECMO or Impella RP may be considered in scenarios
of inadequate ventilation, persistent hypoperfusion, or evolution of LV shock phenotype to biventricular
shock phenotype. Finally, physiology guided early de-escalation of Impella may be the key to reduce need
for renal replacement therapy which may, in part, be needed due to potential hemolysis from the Impella
microaxial pump.

ECLS if persistent
hypoperfusion

Identification
of AMICS Heart Team discussion
Insertion of Coronary Comprehensive
TTE for microaxial flow hemodynamic and/or
RV function and revascularization
pump assessment Transfer to
assessment of hub shock center
cardiac anatomy

Impella RP
if biventricular dysfunction
develops

Figure 4. Treatment Algorithm Incorporating Evidence from Recent Randomized Trials

It is important to note that MCS device benefit has been demonstrated when used at high volume
institutions in conjunction with invasive hemodynamic monitoring, when patients are cared for by
multidisciplinary shock teams (including interventional cardiologists, heart failure cardiologists,
cardiothoracic surgeons, and intensive care physicians) making timely decisions regarding MCS device
introduction, escalation, and de-escalation. While NCSI is focused on Impella as the MCS device of
choice,5 similar initiatives have demonstrated improved survival regardless of the type of MCS device
used.6 However, based on the most contemporary data from DanGer Shock and ECLS Shock data, we
would favor use of Impella in majority of patient with AMICS. A device ‘agnostic’ approach guided by
shock phenotype and mechanism, while supported by some experts, has not been validated in recent
large, randomized trials evaluating the use of ECMO and Impella. Impella demonstrated incremental
improvement in survival compared to standard care whereas ECMO did not. This is probably related to the
ability of Impella to actively unload the ventricle compared to ECMO, which increases global ventricular
afterload, thus increasing the oxygen consumption and accentuating myocardial injury. If VA ECMO is
used as first-line therapy, often Impella may be needed for active LV venting if LV dilatation is observed.

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QUICK READ SUMMARY

✓ Short-term MCS platforms currently available in the US include IABP, Impella®,
TandemHeart®, and ECMO.

✓ RHC information may help guide shock management, choice of MCS device, as well as
escalation and de-escalation of hemodynamic support.

✓ IABP-SHOCK II risk score and SCAI CS classification may help identify patients in whom
MCS device use is appropriate.

✓ An approach to MCS device use guided by shock phenotype and mechanism, and used in
conjunction with management by an experienced multidisciplinary care team, may be key to
improving outcomes in AMICS patients.

References
1. Thiele H, Ohman EM, de Waha-Thiele S, et al. Management of cardiogenic shock complicating myocardial infarction:
an update 2019. Eur Heart J. 2019;40(32):2671-83. doi: 10.1093/eurheartj/ehz363. PMID: 31274157.

2. Dhruva SS, Ross JS, Mortazavi BJ, et al. Association of use of an intravascular microaxial left ventricular assist device
vs intra-aortic balloon pump with in-hospital mortality and major bleeding among patients with acute myocardial
infarction complicated by cardiogenic shock. JAMA. 2020;323(8):734-45. doi:10.1001/jama.2020.0254

3. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J
Med. 2012;367(14):1287-96. doi: 10.1056/NEJMoa1208410. Epub 2012 Aug 26. PMID: 22920912.

4. O’Neill WW, Grines C, Schreiber T, et al. Analysis of outcomes for 15,259 US patients with acute myocardial
infarction cardiogenic shock (AMICS) supported with the Impella device. Am Heart J. 2018;202:33-8. doi: 10.1016/j.
ahj.2018.03.024. Epub 2018 Apr 7. PMID: 29803984.

5. Basir MB. Final results from the National Cardiogenic Shock Initiative. Presented at: SCAI 2021. April 28, 2021.
Available at: [Link] Accessed Jul 22, 2021.

6. Taleb I, Koliopoulou AG, Tandar A, et al. Shock team approach in refractory cardiogenic shock requiring short-
term mechanical circulatory support: a proof of concept. Circulation. 2019;140(1):98-100. doi: 10.1161/
CIRCULATIONAHA.119.040654. Epub 2019 Jul 1. PMID: 31549877; PMCID: PMC6872455.

7. Thiele H, Jobs A, Ouweneel DM, et al. Percutaneous short-term active mechanical support devices in cardiogenic
shock: a systematic review and collaborative meta-analysis of randomized trials. Eur Heart J. 2017;38(47):3523-31.
doi: 10.1093/eurheartj/ehx363. PMID: 29020341.

8. Schrage B, Ibrahim K, Loehn T, et al. Impella support for acute myocardial infarction complicated by cardiogenic shock.
Circulation. 2019;139(10):1249-58. doi: 10.1161/CIRCULATIONAHA.118.036614. PMID: 30586755.

9. Lemor A, Hosseini Dehkordi SH, Basir MB, et al. Impella versus extracorporeal membrane oxygenation for
acute myocardial infarction cardiogenic shock. Cardiovasc Revasc Med. 2020;21(12):1465-71. doi: 10.1016/j.
carrev.2020.05.042. Epub 2020 May 30. PMID: 32605901.

10. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock. N Engl. J Med.
2023;389(14):1286-97.

11. Moller JE, Engstrom T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl. J Med. 2024;390(15):1382-93.

12. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update: a review
and incorporation of validation studies. Journal of the Society for Cardiovascular Angiography & Interventions.
2022;1(1):100008. [Link]

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PREVIOUS CHAPTER Chapter 21: Isolated RV Support: Impella RP® and TandemHeart® NEXT CHAPTER

Isolated RV
Support:
Impella RP and
®

TandemHeart
®

Mario Gramegna, MD Anna Mara Scandroglio, MD

Cardiac Intensive Care Unit Cardiac Surgery Intensive Care Unit
IRCCS San Raffaele Scientific Institute IRCCS San Raffaele Scientific Institute
Milan, Italy Milan, Italy
[Link]@[Link]
@MarioGramegnaMD Alaide Chieffo, MD
Interventional Cardiology Unit
Alessandro Beneduce, MD IRCCS San Raffaele Scientific Institute
Interventional Cardiology Unit Milan, Italy
IRCCS San Raffaele Scientific Institute
Milan, Italy

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Introduction
Management of acute isolated right ventricular failure (RVF) is a relevant clinical challenge. RVF
significantly increases short-term morbidity and mortality in various clinical scenarios. Medical
management is generally the first-line approach; however, in refractory cases that are unresponsive
to initial treatment of reversible causes, mechanical circulatory support (MCS) might specifically target
the failing right ventricle (RV). Choosing the most appropriate MCS device for the patient can be a
challenging decision and the choice should be carefully weighed on a case-by-case basis. This chapter
focuses on Impella RP® and TandemHeart® selection based on clinical needs in isolated RVF.

Isolated RVF pathogenesis

Isolated RVF may develop from a variety of causes. Pulmonary hypertension (PH) is the most common
cause of RVF, and it is often secondary to left-sided heart failure. RVF derives from a complex interplay
of pathogenetic mechanisms: contractile dysfunction, increased afterload, volume overload, and altered
ventricular interdependency (Figure 1).

EXTRINSIC
ARDS
COPD
Pulmonary embolism
AFTERLOAD Pulmonary hypertension

Left heart failure INTRINSIC

Pulmonary stenosis

Acute myocardial infarction

CONTRACTILITY Cardiomyopathies
Post-cardiotomy syndrome

Valvular heart disease

Congenital heart disease
PRELOAD
LVAD

ARDS=acute respiratory distress syndrome; COPD=chronic obstructive pulmonary disease; LVAD=left ventricular assist device

Figure 1. Pathogenesis of RVF (adapted from Akhmerov, Ramzy, 20216)

Right ventricular failure can be caused by several cardiac (intrinsic) or pulmonary (extrinsic) conditions and results from a complex interplay of
pathogenetic mechanisms

Mechanical circulatory support with RV assist devices (RVADs) should be considered when RVF
persists despite optimal medical treatment (OMT). Recent literature suggests that 42% to 75% of
patients with acute RVF may recover sufficient function to allow MCS device explantation. Therefore,
temporary percutaneous RVADs can be a valuable therapeutic option, but correct selection is essential
to maximize the possibility of myocardial recovery.1 Prompt etiology diagnosis, MCS device selection,
and timely implant of MCS are key to successfully managing a failing RV that is not responding to OMT.

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Diagnosing isolated RVF

Diagnosing acute isolated RVF is a major clinical challenge. Indeed, pure RVF is unusual to find in
clinical practice and most RVF is associated with some degree of left ventricular dysfunction. Clinical
presentation may not be straightforward, encompassing signs and symptoms of systemic venous
congestion and impaired cardiac output. Early diagnosis with laboratory, echocardiographic, and
hemodynamic parameters is a critical first step (Table 1). Invasive hemodynamic measures obtained
with a pulmonary artery catheter (PAC) are suggested to rapidly identify RVF and manage it correctly.
Furthermore, left ventricular dysfunction and severe pulmonary hypertension must be carefully ruled
out; otherwise, biventricular support or VA ECMO should be considered.2

Table 1. Diagnostic Features of Isolated RVF

LABORATORY FINDINGS

NT-proBNP 

Troponin 

Bilirubin, GGT, ALP, AST, ALT, PT  Liver dysfunction

Creatinine, urea  Kidney dysfunction

Lactate  Systemic hypoperfusion

ECHOCARDIOGRAPHIC CHARACTERISTICS

RV dilatation >42 mm basal

TAPSE <17 cm

S’-TDI <10 cm/s

FAC <35%

HEMODYNAMICS

RAP >15 mmHg

RAP/PCWP >0.63 RVF in AMI

>0.86 RVF after LVAD

PAPi (PASP-PADP/RAP) <1.0 RVF in AMI

<1.85 RVF after LVAD

(MPAP−RAP)×SV×0.0136 <15 mmHg•L RVF in AMI

<10 mmHg•L RVF after LVAD

PVR (MPAP-PCWP/CO) >3.6 WU RVF after LVAD

PA compliance (SV/PASP-PADP) <2.5 mL/mmHg RVF in chronic HF

AMI=acute myocardial infarction; CO=cardiac output; FAC=fractional area change; MPAP=mean pulmonary artery pressure; P2=pulmonic
component of the second heart sound; PA=pulmonary artery; PADP=pulmonary artery diastolic pressure; PAPi=pulmonary artery pulsatility
index; PASP=pulmonary artery systolic pressure; PCWP=pulmonary capillary wedge pressure; PV=pulmonary valve; PVR=pulmonary vascular
resistance; RAP=right atrial pressure; RV=right ventricle; RVF=right ventricular failure; RVSW=right ventricular stroke work; SV=stroke volume;
TAPSE=tricuspid annular plane systolic excursion; TDI=tissue-Doppler imaging; WU=Woods Units

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Managing isolated RVF

There are currently 2 temporary percutaneous RVADs specifically designed for patients with isolated
acute RVF:
• Impella RP (Abiomed Inc, Danvers, MA)
• TandemHeart RVAD (LivaNova, PLC, London, UK)
Table 2 describes the characteristics of these devices.

Table 2. Characteristics of Available Devices for MCS in Isolated RVF

IMPELLA RP TH-RVAD/ProtekDuo
General characteristics
Mechanism Axial-flow pump Centrifugal pump
Type Intracorporeal Paracorporeal
Inflow-outflow RA-PA RA-PA
Hemodynamics
RV support 2-4 L/min 2-4 L/min
CVP  

MPAP  

LVEDP  

MAP = =
Procedural and technical considerations
Implant timing 35 minutes 15 minutes
Vascular access site Single femoral access Double femoro-femoral
Double femoro-jugular
Single jugular (ProtekDuo)
Size of the cannula 23 Fr 21 Fr (TH-RVAD)
29-31 Fr (ProtekDuo)
Anticoagulation aPTT 45-60 seconds aPTT 60-80 seconds
Oxygenation/CO2 removal No Yes (optional)
Patient mobilization No Yes (ProtekDuo)
Maximal suggested support duration 14 days 28 days
Removal Bedside Bedside
Complications
Hemolysis ++ +
Thrombosis and limb ischemia + -
Hemorrhage + +
Infections + +
CVP=central venous pressure; LVEDP=left ventricular end-diastolic pressure; MAP=mean arterial pressure; MPAP=mean pulmonary artery
pressure; PA=pulmonary artery; RA=right atrium; RV=right ventricle; TH=TandemHeart

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The Impella RP is a microaxial flow intracorporeal pump that is placed percutaneously through the
femoral vein. The impeller delivers blood from the inferior vena cava (IVC) into the pulmonary artery
(PA). Impella RP cannot be used to oxygenate blood.3

The TandemHeart RVAD is a percutaneous centrifugal-flow extracorporeal pump. The inflow cannula is
typically placed into the right atrium via left femoral vein cannulation, and the outflow cannula is placed
into the main PA via right femoral vein cannulation.4 Alternatively, a single right internal jugular vein
access can be used to deploy the ProtekDuo® cannula.5 This is a dual-lumen coaxial cannula with its
distal tip in the PA, allowing patient ambulation. TandemHeart can be used with a blood oxygenator.

Both the Impella RP and TandemHeart RVAD directly bypass the RV by pumping blood into the PA. The
resulting hemodynamic effects are a marked reduction in central venous pressure (CVP) and an increase
in mean pulmonary artery pressure (mPAP), and thus left ventricle (LV) preload, with no effect on LV
afterload. In the setting of isolated RVF, these effects result in an increase in LV output and a reduction
in systemic venous congestion.

The most crucial target of percutaneous temporary RVADs is to reduce CVP to improve organ perfusion
and reverse the detrimental effect of high CVP. Given their recent introduction and lack of relevant
literature and evidence, no specific guidelines to optimize device selection and management exist to date.

Temporary percutaneous RVAD selection based on clinical need

The treatment strategy (eg, bridge to recovery or bridge to transplant) is important to define up front.
The implantation of a temporary percutaneous RVAD should be avoided if right ventricular recovery
is not expected and the patient is not a candidate for transplant. The timing of MCS implantation is
also crucial to prevent significant, potentially irreversible end-organ injury. Close hemodynamic and
laboratory monitoring, with particular attention to liver and kidney function, is essential. Frequent LV
function reassessment after RVAD implantation is mandatory because the increased LV preload could
lead to left ventricular failure necessitating LV support.

In the absence of studies establishing the superiority of a particular percutaneous RVAD in a specific
clinical setting, device selection should consider each patient’s hemodynamics and comorbidities
(hypoxemia, hemorrhagic diathesis), technical difficulties of the procedure (vascular access, special
anatomic considerations, IVC filters), and local expertise and resources (Figure 2).

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ISOLATED REFRACTORY RVF

Treatment objective

• Bridge-to-recovery
• Bridge-to-bridge • Bridge-to-transplant
• Bridge-to-decision • Destination therapy
• Bridge-to-transplant

Consider surgical RVAD

Consider percutaneous RVAD
(Impella RP or TandemHeart)

Contraindications to pRVAD
• Mechanical prosthesis
• Severe TV/PV disease Contraindications, expertise, and local resources Refer to MCS Center
• Thrombus in VC/RA/PA
• Severe irreversible PH

pRVAD device selection in specific situations

Concomitant conditions Technical issues

Respiratory failure High bleeding risk Femoral access issues Mobilization desired

TH RVAD Impella RP TH ProtekDuo

MCS=mechanical circulatory support; PA=pulmonary artery; PH=pulmonary hypertension; PV=pulmonary valve; RA=right atrium;
TH=TandemHeart; TV=tricuspid valve; VC=vena cava

Figure 2. Algorithm for pRVAD Device Selection in Refractory Isolated RVF

Selection of pRVAD in the clinical scenario of isolated RVF should be based on careful consideration of contraindications, local expertise, clinical
needs, specific patient comorbidities, and technical issues

Table 3 describes specific issues to consider when selecting a percutaneous RVAD.

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Table 3. Issues to Consider for pRVAD Selection

ISSUE CONSIDERATIONS

Vascular access • Venous connections must be carefully assessed before RVAD implantation

• Impella RP inevitably requires femoral venous access

• ProtekDuo cannula, requiring single internal jugular venous access, is preferred if

femoral venous access is limited by infection, thrombosis, reduced vessel caliber,
tortuosity, or IVC filters

Bleeding risk • Exposure of blood to the nonbiologic artificial surfaces of MCS circuits causes
a complex activation of the coagulation system, amplifying clotting factor
consumption, leading to increased bleeding

• This phenomenon is higher in TandemHeart due to a more significant blood-

circuit interaction

Respiratory failure/hypoxemia • If isolated RVF is associated with pulmonary failure and hypoxia, TandemHeart-
RVAD is preferable, as it allows blood oxygenation along with circulatory
support

Mobilization/ambulation • The ProtekDuo cannula, because of its internal jugular cannulation site, allows
greater mobilization and ambulation during support and is particularly useful if
prolonged support is expected

Contraindications The implantations of either device should be avoided if any of these conditions are
present:
• Mechanical prosthesis

• Severe tricuspid/pulmonary valve disease

• Thrombus in the right atrium, vena cava, or proximal pulmonary artery

• Severe irreversible pulmonary hypertension

Local expertise and availability • These are crucial aspects to consider

IVC=inferior vena cava; MCS=mechanical circulatory support; RVAD=right ventricular assist device; RVF=right ventricular failure

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References
1. Kapur NK, Esposito ML, Bader Y, et al. Mechanical circulatory support devices for acute right ventricular failure.
Circulation. 2017;136(3):314-26.

2. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and management of right-sided heart failure: a scientific
statement from the American Heart Association. Circulation. 2018; 137(20):e578-e622.

3. Anderson MB, Goldstein J, Milano C, et al. Benefits of a novel percutaneous ventricular assist device for right
heart failure: The prospective RECOVER RIGHT study of the Impella RP device. J Heart Lung Transplant.
2015;34(12):1549-60.

4. Kapur NK, Paruchuri V, Jagannathan A, et al. Mechanical circulatory support for right ventricular failure. JACC Heart Fail.
2013;1(2):127-34.

5. Aggarwal V, Einhorn BN, Cohen HA. Current status of percutaneous right ventricular assist devices: First-in-man use
of a novel dual lumen cannula. Catheter Cardiovasc Interv. 2016;88(3):390-6.

6. Akhmerov A, Ramzy D. Mechanical circulatory support in right ventricular failure. Interv Cardiol Clin. 2021;10(2):185-94.

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Biventricular
Support Without
ECMO
Kathryn Dawson, MD Kathleen Kearney, MD, FSCAI
Assistant Professor, Division of Cardiology Assistant Professor, Division of Cardiology
Montefiore Medical Center University of WashingtonSeattle, WA
Bronx, NY KaKearney@[Link]
kathrynldawson@[Link] @KateKearney4

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Overview
Mortality in cardiogenic shock (CS) remains high, with multiple studies demonstrating a survival to
discharge of less than 50% regardless of the etiology.1,2 Right ventricular (RV) failure in this population
is associated with a further increase in morbidity and mortality.3 The evolving landscape of mechanical
circulatory support (MCS) includes both left ventricular (LV) and RV specific devices, which may be
used either independently or together. Combined RV and LV percutaneous MCS offers an alternative to
extracorporeal membrane oxygenation (ECMO) when biventricular support is warranted but ECMO is
not available, contraindicated, or less desirable.

Strategic planning
Initial presentation with LV dysfunction
While LV MCS devices are often used as the initial intervention in CS, RV dysfunction and pulmonary
vascular resistance (PVR) have a significant adverse impact on adequate filling of the LV and performance
of percutaneous LV MCS devices. The SHOCK registry demonstrated that up to 40% of patients
presenting with presumed predominately LV cardiogenic shock also have concomitant RV failure.4 A
subset of patients will have RV dysfunction that may not have been evident at the acute presentation and
require adjunctive RV support. Escalation with a dedicated RV support device may be advantageous over
ECMO if it is likely that the devices will be weaned independently or if ECMO is not available. In addition,
this strategy does not raise systemic afterload, which may be a significant advantage over ECMO in certain
clinical presentations like acute myocardial infarction (AMI).

Primary RV failure
Patients presenting with predominant RV dysfunction, such as acute RV infarction, pulmonary
hypertension, or special cases of congenital heart disease, may warrant isolated RV support upfront. In
such cases where hypoxemia persists despite positive pressure ventilation, ECMO is typically pursued,
although an oxygenator may also be added to the TandemHeart family of devices in the absence of
ECMO. With primary RV dysfunction, left-sided support is sometimes required when LV dysfunction
ensues or is unmasked following RV rescue.

Determination at presentation
Clinical exam and even echocardiography are limited in identifying the degree of RV and LV contribution
to the dynamic process of CS. Incorporating invasive hemodynamic data is critical to decision-making
and is recommended before MCS implantation to guide intensive care unit management and support
escalation or possible explantation. There is limited data that survival is improved if biventricular support
is initiated during the same procedure rather than sequentially adding a second support device during a
later intervention, although this data is limited by survival bias.2

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Equipment and procedural considerations

The particular devices selected are determined by patients’ shock stage, etiology, phenotype and
desired device hemodynamic effects, anatomical considerations, opportunity for patient mobility, and
operator and center experience. Dedicated RV support devices include the Impella RP® (Abiomed,
Danvers, MA) and the TandemLife ProtekDuo (TandemLife, Pittsburgh, PA).

The ProtekDuo uses a centrifugal flow pump and only requires a single access due to the nested
cannula design, usually in the right internal jugular vein. Where available, this has largely replaced use
of an adapted TandemHeart setup, which requires a separate cannula placed in the right atrium and
pulmonary artery. In our experience, the ProtekDuo may also work well via the left subclavian vein;
however, in tall patients the length may not be adequate to position the outflow cannula distal to the
pulmonic valve. The 31 Fr ProtekDuo is best utilized for VV ECMO if an oxygenator is required.

The Impella RP is an RV support device with a coaxial pump placed via the femoral vein (or internal
jugular vein with the Impella RP Flex), and shunts blood from the right atrium to the pulmonary artery
across a dysfunctional RV. Either the Impella RP or ProtekDuo may be added independent of LV support
needs, particularly when the contribution of RV failure is not evident at initial presentation.

LV support devices discussed elsewhere in this e-book provide left-sided support and facilitate
varying degrees of afterload reduction for both the LV and RV. The main advantage of a more a la
carte approach for biventricular support is that virtually any device combination may be used based on
institutional preference, vascular access, and anticipated downstream needs of the patient.

While venoarterial extracorporeal membrane oxygenation (VA ECMO) is frequently used for patients
who require biventricular support, its availability and allocation vary across regions and institutions.
Resource allocation varies by site regarding need for trained perfusionists or nurse specialists, the
number of ECMO circuits available, and other support staff. Small caliber or diseased peripheral arteries
increase the risk of critical limb ischemia with the very large bore arterial cannula used for ECMO, which
may be occlusive and necessitate distal perfusion catheters (DPC). Smaller diameter LV support devices
may better accommodate these patients and not require DPC placement. The use of separate LV and
RV devices also allows for weaning to single ventricular support as needed during recovery and may
also allow for earlier mobilization by eliminating femoral access.

Hemodynamic considerations
Traditional hemodynamic definitions of CS focus on LV function, including a reduced systolic blood
pressure (SBP) <90 mmHg, elevated pulmonary capillary wedge pressure (PCWP), and reduced cardiac
index (CI) and cardiac power output (CPO). RV hemodynamic parameters that can predict the need for
RV support include the pulmonary artery pressure index (PAPi = [PASP-PADP]/RA), a CVP/PCWP ratio
>0.8, a CVP >15 mmHg, and right ventricular stroke work index <4 g/m/beat/m2 (RVSWI = (MAP-RAP) x
SVI).4,5,6 A PAPi <0.9 has been associated with the need for concurrent right ventricular support in patients
presenting with CS and is an important hemodynamic parameter in our practice for determining the
need for biventricular support. These metrics appear to perform differently depending on the underlying
etiology of shock presentation and the impact on long-term outcomes is not yet well understood.

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Case examples of biventricular support

Case 1

A 40-year-old male presented with fulminant myocarditis and cardiogenic shock. Invasive
hemodynamics demonstrated an elevated right atrial pressure of 14 mmHg and a PCWP of 32 mmHg
(ratio of 0.4). A PAPi of 0.78 was suggestive of significant RV dysfunction. A multidisciplinary shock call
was initiated. An Impella CP was placed in the right femoral artery and the moderate RV dysfunction
was initially managed with pharmacologic inotropic support. After initial improvement in hemodynamics,
the patient developed progressive shock physiology over several hours. Due to lack of available ECMO
circuits at our institution, we placed a ProtekDuo via the right IJ (Figure 1) and transferred to another
institution for transition to ECMO due to ongoing shock. The patient was ultimately successfully weaned
and decannulated and is now undergoing outpatient transplant evaluation for persistent ventricular
dysfunction and heart failure

Protek outflow
cannula in
pulmonary artery

Impella cannula in
left ventricle

Protek inflow
cannula in
Figure 1. Biventricular Hemodynamic Support with
right atrium ProtekDuo and Impella CP
ProtekDuo in the right ventricle via the right internal jugular vein and
Impella CP in the left ventricle via the right femoral artery; left IJ PA
catheter placed subsequent to ProtekDuo implantation

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Case 2

A 36-year-old female with newly diagnosed peripartum cardiomyopathy was admitted one month
postpartum with cardiogenic shock. Initial PAC hemodynamics demonstrated RA pressure of 12 mmHg,
PA 33/22/26 mmHg, PCWP 24 mmHg, Fick cardiac index of 1.5 L/min/m2 and a PAPi of 0.92. An
Impella 5.0 was placed via a surgical cutdown in the right axillary artery. Following Impella insertion the
patient developed recurrent suction events and hypotension with poor output from the Impella. Repeat
hemodynamic assessments demonstrated a PAPi of 0.25 consistent with severe RV dysfunction so
an Impella RP was placed via the right femoral vein. With optimization of volume status the patient
clinically improved, as did RV hemodynamics, such that the Impella RP was weaned and removed on
hospital day 6. The patient continued with Impella 5.0 support for 3 weeks as a bridge to orthotopic heart
transplantation and was ultimately discharged home after an unremarkable post-transplant course.

Impella 5.0

Impella RP
Figure 2. Biventricular Hemodynamic Support with
Impella RP and Impella 5.0
Impella RP in the right ventricle via the right femoral vein and
Impella 5.0 in the left ventricle via the right axillary artery

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QUICK READ SUMMARY

✓ Consider independent RV and LV support devices in biventricular failure when ECMO is

unavailable, or when weaning to a single ventricular support device may be facilitated by
initial biventricular support.

✓ Decision-making for escalation from single device to biventricular mechanical support

should include a multidisciplinary discussion to incorporate resource availability, device-
specific concerns, and patient hemodynamic needs.

✓ Up front evaluation of invasive hemodynamics and ongoing assessment is particularly

critical in patients where biventricular failure is implicated.

References
1. Mandawat A, Rao SV. Percutaneous mechanical circulatory support devices in cardiogenic shock. Circ Cardiovasc
Interv. 2018;10(5):e004337.

2. Kuchibhotla S, Esposito ML, Breton C, et al. Acute biventricular mechanical circulatory support for cardiogenic shock.
J Am Heart Assoc. 2017;6(10).

3. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll
Cardiol. 2019;73(13):1659-69.

4. Lala A, Guo Y, Xu J, et al. Right ventricular dysfunction in acute myocardial infarction complicated by cardiogenic
shock: a hemodynamic analysis of the should we emergently revascularize occluded coronaries for cardiogenic shock
(SHOCK) trial and registry. J Card Fail. 2018;24(3):148-56.

5. Saxena A, Garan AR, Kapur NK, et al. Value of hemodynamic monitoring in patients with cardiogenic shock
undergoing mechanical circulatory support. Circulation. 2020;141(14):1184-97.

6. Jain P, Thayer KL, Abraham et al. Right ventricular dysfunction is common and identifies patients at risk of dying in
cardiogenic shock. J Card Fail. 2021;27(10):1061-72. doi: 10.1016/[Link].2021.07.013. PMID: 34625126.

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PREVIOUS CHAPTER Chapter 23: Weaning of Mechanical Circulatory Support NEXT CHAPTER

Weaning of
Mechanical
Circulatory
Support
Waqas Ghumman, MD
Affiliated Clinical Assistant Professor of Medicine
University of Miami, JFK Campus
JFK Director of Heart Failure
Atlantis, FL
[Link]@[Link]

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Introduction
Weaning from a mechanical circulatory support (MCS) device can be a very challenging aspect of
patient care. No randomized controlled trials exist to provide formalized protocols for weaning of
MCS devices, so individual institutions typically create their own weaning strategies. These strategies
commonly include consensus-based principles such as achieving patient stability prior to weaning
attempts, performing a stepwise decrease in support, and evaluating for tolerance of weaning
hemodynamically, metabolically/biochemically, and symptomatically. Consistent with these principles,
the recently published AHA consensus guidelines for escalating and de-escalating mechanical
circulatory support further validate these strategies.7

Prior to weaning
Prior to initiating device weaning, most institutions take the following steps.
• Completely withdraw or minimize vasoactive drugs. See box for the recommended maximal
tolerated doses of vasoactive drugs for weaning described in the DanGer Shock trial.
• Maximize hemodynamics with MCS. Hemodynamic optimization includes evidence of adequate
left ventricular (LV) cardiac support as shown in Table 1.
• Correct organ dysfunction, particularly renal and hepatic dysfunction, prior to weaning.
Biochemical markers of organ resuscitation, as shown in Table 1, include lactate and mixed
venous oxygen saturation (SVO2).
• If possible, correct the cause of the insult to the myocardium prior to weaning. This may entail
revascularization in the setting of ischemia and/or correcting arrhythmic insults.
Once hemodynamics are optimized and organ function is restored, weaning should be considered.

Maximum Doses of Vasoactive Drugs Before Attempting MCS Weaning8

• Dobutamine 10 µg/kg/min
• Dopamine 10 µg/kg/min
• Milrinone 0.4 µg/kg/min
• Noradrenaline 0.15 µg/kg/min

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Table 1. Hemodynamic and Biochemical Markers Indicative of Readiness to Wean

HEMODYNAMIC MARKER VALUE INDICATIVE OR READINESS TO WEAN

Cardiac power output (CPO) CPO >0.6 watts without vasoactive agents
(CPO) = (CO x MAP)/451 in Watts or
CPO >0.8 watts with vasoactive agents

Cardiac index (CI) CI >2 L/min/m2

Pulmonary capillary wedge pressure (PWCP) PWCP <15 mmHg

Pulmonary artery pulsatility index (PAPi) PAPi >1.5

PAPi = (systolic PA pressure - diastolic PA pressure)/(CVP
or right atrial pressure)

Central venous pressure (CVP) CVP <15 mmHg

BIOCHEMICAL MARKER VALUE INDICATIVE OR READINESS TO WEAN

Lactate Lactate <2

Mixed venous oxygen saturation (SVO2) SVO2 >60

pH pH >7.3

Weaning strategy
A conscientious weaning strategy requires patience and diligence. Ideally, as the MCS device is being
downtitrated, continue to optimize hemodynamics, optimize organ function, and attain symptom
optimization.

With a continuous support device, such as TandemHeart®, Impella®, or VA ECMO, weaning is achieved
by decreasing device speed (rpms).
• With VA ECMO or TandemHeart, this is referred to as reducing degree of supported flow.
• With Impella, this is known as reducing performance level (P level), which ranges from P9 to P0.
Higher performance levels (eg, P9) indicate higher speed and a greater degree of cardiac support
as indicated by higher cardiac index.

At our institution, we ideally reduce the degree of support or P level by 0.5 L/min to 1 L/min no more
frequently than every 6 hours. There are numerous weaning protocols that reflect variability in clinical
practices and no randomized trials to establish best practices.

During each reduction in performance level or flow, we determine successful weaning by the patient’s
ability to maintain adequate LV function as noted by CPO >0.6 watts, CI >2 L/min/m2, PAPi >1.5, and
CVP <15 mmHg. We also recommend checking lactate and pH with each reduction in P level. If we
are not able to attain such hemodynamics, we increase hemodynamic support, allow more time for
recovery, and retry later. If such hemodynamic criteria are met with decreasing mechanical support,
we then continued to assess adequacy of organ perfusion by reassessing SVO2 on pulmonary artery
catheter and keeping it above 60 as well as assessing lactates and keeping them below 2.

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We also closely follow biochemical markers of organ injury, such as renal and hepatic function and
oxygen saturation. If SVO2, lactate, or biochemical markers indicate evidence of worsening organ
dysfunction, we then increase support again. If, however, hemodynamics are maintained and organ
function remains adequate, we assess the patient’s symptoms and continue to wean. Often patients
are intubated and sedated, and symptom assessment may be difficult, but if we are able, we assess
the patient’s pulmonary function for any evidence of congestion, and we assess urine output as we
wean MCS. When flows are the less than 2 liters there is risk of circuit thrombosis and we bolus with
IV anticoagulants to test for weaning readiness and then removal when anticoagulants are in an
acceptable range based on local practice. Alternatively, one may consider a circuit bypass during a
clamping trial to maintain circuit integrity.

During the process of weaning the patient from MCS, we may encounter varying levels of myocardial
recovery and restoration of pulsatile flow.

1. Optimize device setting/flow to achieve goals

Assess adequate cardiac support Assess right heart function Assess organ perfusion
• CPO >0.6-0.8 • PAPi >1.5 or at least >1 • SVO2 >60
• CI >2 • CVP <18 • Lactate <2
• API >1.45 • CVP/PCWP <0.6
• TAPSE >1.8
• RVSWI >5

2. Hold device setting until following criteria met before weaning

Optimize hemodynamics Optimize organ function Optimize symptoms

 CVP <15  Baseline liver function  Dyspnea
 PCWP <15  Baseline renal function  Edema
 CI >2  Anticoagulation  Walk distance
 CPO >0.8  Lactate < 2
 PAPi >1  SVO2 >60

3. With each setting or flow reduction, reassess steps 1 and 2 until flow <2L

4. Device explanatation trial

• Anticoagulation optimized or circuit bypass prior to flow <2L

• Evaluate restoration of pulsatility and pulse pressure >30
• Consider anatomic assessment of heart (echo for dilation of chambers or
worsening contractility)
• If hemodynamics hold, ventricular anatomy stays stable, and lactate stays
normal, proceed to explantation
• If not, re-establish support and consider a retrial later, referral to durable device
or transplant center, or consult hospice

Figure 1. Weaning Strategy

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Successful weaning scenario

In the most successful weaning scenario, we will be able to decrease Impella support to P2 or
TandemHeart or VA ECMO flow to 2 L/min or less while maintaining optimal hemodynamics, organ
function, and symptomatology. At this point, we make sure the patient is fully anticoagulated to prevent
device thrombosis or failure and we perform an echo ramp study to look for evidence of anatomic
preservation of function above and beyond the hemodynamic ramp already performed. We are assessing
whether the LV or RV dilate as well as whether LV and RV systolic function are maintained. We may also
assess for worsening valvular regurgitation as it may limit our ability to wean from the MCS device.

A successful echo ramp study would be one where, while decreasing device support, LV and RV
dimensions do not dilate and LV and RV function are maintained without worsening of valvular
regurgitation. If these conditions are met, we proceed with removing the support device once
anticoagulation is stopped and an adequate ACT or PTT is obtained. We consider this a case with
successful myocardial recovery.

Unsuccessful weaning scenario

In other cases, we may see no evidence of myocardial recovery and be unable to wean the MCS device
without hemodynamic compromise and/or organ dysfunction. In such a situation, we must consider
escalation of support with a device such as an Impella of 5.5®, CentriMag™, or higher-level temporary
support device, or consider palliative care if no other options are available. Alternatively, we may consider
transferring the patient to an advanced MCS center that may be able to evaluate the patient for a durable
left ventricular assist device (LVAD) and/or heart transplantation once support is re-established.

Other weaning scenarios

We may also encounter a situation in which myocardial recovery is inadequate. In such a case, we typically
continue support and/or frequent clinical reassessments. If we see signs of heart recovery, as described
above, we attempt weaning. If, however, after 48-72 hours we continue to see inadequate recovery, we
consider palliative care, device escalation, or transfer for evaluation for a durable LVAD/heart transplant.

QUICK READ SUMMARY

✓ No randomized controlled trials exist to provide formalized protocols for weaning of MCS
devices.

✓ Individual institutions typically create their own weaning strategies from consensus-based
principles.

✓ Weaning strategies commonly include:

• Achieving patient stability prior to weaning attempts

• Performing a stepwise decrease in support

• Evaluating for tolerance of weaning hemodynamically, metabolically/biochemically, and

symptomatically

✓ When attempting to wean from MCS, continue to optimize hemodynamics, optimize organ
function, and attain symptom optimization.

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References
1. Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am Heart Assoc. 2019;8(8):e011991. doi:10.1161/
JAHA.119.011991.

2. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from
the American Heart Association. Circulation. 2017;136(16):e232–e268.

3. Thayer K, Newman S, Ayouty M, et al. Abstract 15943: Phenotypes of cardiogenic shock associated with increasing
inhospital mortality: a report from the National Cardiogenic Shock Working Group Registry. Circulation. 2019;140.
doi: 10.1161/circ.140.suppl_1.15943.

4. Vallabhajosyula S, Dunlay SM, Prasad A, et al. Acute noncardiac organ failure in acute myocardial infarction with
cardiogenic shock. J Am Coll Cardiol. 2019;73(14):1781–91.

5. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll
Cardiol. 2019;73(13):1659-69. doi: 10.1016/[Link].2018.12.084.

6. Davila C, Morine K, Esposito M, et al. TCT-817 changes in right atrial pressure are associated with outcomes in
patients with cardiogenic shock receiving acute mechanical circulatory support devices: insights from the Cardiogenic
Shock Working Group. J Am Coll Cardiol. 2019;74(13 Suppl):B800. doi: 10.1016/[Link].2019.08.963.

7. Geller BJ, Sinha SS, Kapur NK, et al. Escalating and de-escalating temporary mechanical circulatory support in
cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2022;146(6):e50-e68.

8. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl J Med. 2024:390(15):1382-93.

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PREVIOUS CHAPTER Chapter 24: MCS Considerations in Acute Myocarditis, Chronic Decompensated HF, and AMI Cardiogenic Shock NEXT CHAPTER

MCS Considerations in
Acute Myocarditis,
Chronic
Decompensated
HF, and AMI
Cardiogenic Shock
Nathan W. Kong, MD John E. A. Blair, MD
Internal Medicine Resident Associate Professor of Medicine
Department of Medicine, University of Chicago Section of Cardiology, Department of
Chicago, IL Medicine, University of Chicago
[Link]@[Link] Chicago, IL
@nkong_med jblair2@[Link]
@JBlairMD
Viktoriya Kagan, APN-BC
Lead MCS Coordinator, APP Manager
Section of Cardiac Surgery, University of Chicago
Chicago, IL
[Link]@[Link]
@vkagan6

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PREVIOUS CHAPTER Chapter 24: MCS Considerations in Acute Myocarditis, Chronic Decompensated HF, and AMI Cardiogenic Shock NEXT CHAPTER

Introduction
Mechanical circulatory support (MCS) devices are invaluable tools to help support cardiorespiratory
function and prevent hemodynamic collapse and death. However, the decision to utilize MCS and
the choice of specific MCS device depends largely on the clinical scenario. In cardiogenic shock (CS),
MCS devices are often used as short-term “bridge” therapies to support hemodynamics while more
definitive therapies are pursued to treat the underlying cardiovascular dysfunction or to allow for
recovery of cardiovascular function.1 This chapter highlights principles emphasized in the most recent
guidelines on the escalation and de-escalation of MCS, including early use of full hemodynamic profiling,
multidisciplinary decision making, and separate pathways for ischemic and nonischemic etiologies of
cardiogenic shock.7

This chapter explores MCS considerations in 3 clinical scenarios:

• Acute myocarditis
• Chronic decompensated heart failure
• Acute myocardial infarction cardiogenic shock

MCS considerations in acute myocarditis

CASE 1

A 20-year-old male with a past medical history of asthma presented to the ED with shortness of breath
and pleuritic chest pain. He recently had an upper respiratory infection with fevers and malaise. His BP
was 88/63 mmHg, HR was 160 bpm, RR was 24 with 94% saturation on pulse oximetry on room air.
He appeared in distress, had jugular venous distention (JVD) to the angle of the mandible at 45 degrees,
and had cold extremities.

Laboratory data was significant for a lactate level of 3.3 mmol/L [normal <2.0 mmol/L], a creatinine of
2.4 mg/dL [baseline 0.4 mg/dL], a high sensitivity troponin T (hs-TnT) of 205 ng/L [normal <22 ng/L],
and a N-terminal pro B-type natriuretic peptide (NT-proBNP) of 19,314 pg/mL [normal <125 pg/mL].
He tested positive for COVID-19. His transthoracic echocardiogram (TTE) revealed a severely reduced
left ventricular ejection fraction (EF) of 15% with an end diastolic diameter of 4.6 cm (Figure 1A, 1B).

The patient was started on continuous parenteral inotropic support. Right heart catheterization (RHC)
showed a right atrial pressure (RAP) of 14 mmHg, a pulmonary capillary wedge pressure (PCWP) of 24
mmHg, and a Fick cardiac index (CI) of 1.3 L/min/m2. The patient was cannulated with VA ECMO with an
IABP, and high dose steroids were initiated (Figure 1C, 1D). He clinically improved over the subsequent 5
days and was decannulated from VA ECMO before eventual IABP removal. Seven days after admission, a
repeat TTE showed EF had improved to 50%, and he was discharged home 12 days after presentation.

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Figure 1. Case 1 Images

(A) Parasternal long-axis TEE at end diastole with near
normal LV end diastolic diameter of 4.6 cm attributed to
acute nature of LV dysfunction in this patient with low
EF. (B) Parasternal long-axis TTE at end systole with a
very similar diameter indicating severe LV dysfunction
observed in this patient. (C) Insertion site of VA ECMO
in the right femoral region. Swan-Ganz catheter placed
in the left femoral vein. (D) Distal end of VA ECMO
and Swan-Ganz catheter in the pulmonary artery as
well as the distal end of right-sided central line which
terminates in the superior vena cava.

Case 1 describes a hemodynamically unstable patient with acute onset CS likely from COVID-19 related
fulminant myocarditis. Patients with fulminant myocarditis face exceedingly high mortality rates (50-
70%), and are in danger of complete hemodynamic collapse without MCS.2 The choice of MCS should
be directed at the degree of hemodynamic support that is required. A small, single center case series
demonstrated efficacy of MCS in fulminant myocarditis with 8 of the 11 patients (73%) treated with
early MCS surviving to discharge.2

In a patient with acute cardiogenic shock from fulminant myocarditis and unknown transplant candidacy,
the use of short-term MCS has several functions. First, it can be used as a bridge to recovery. For example,
immunosuppressive medications (ie, high dose steroids as in Case 1) and intravenous immune globulin
therapy have been suggested to play a role in the treatment of types of myocarditis in addition to standard
guideline directed medical therapy (GDMT) for heart failure. MCS in the case of fulminant myocarditis
acute CS can also be used as a bridge to decision to allow for a multidisciplinary approach with advanced
HF consultation to adequately assess candidacy for long-term durable ventricular support devices or heart
transplantation should LV dysfunction persist after initial therapies. Ideally, an endomyocardial biopsy
in cases of suspected myocarditis should be performed prior to insertion of MCS given the difficulty of
working around cannula sites as well as the increased risk of bleeding from anticoagulation initiation
necessary for the MCS device. If there is no time to obtain an endomyocardial biopsy prior to MCS, then
empiric treatment for fulminant myocarditis may be considered.

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MCS considerations in chronic decompensated HF

CASE 2

A 69-year-old male with recently diagnosed non-ischemic cardiomyopathy with a reduced EF on

maximally tolerated GDMT presented after a syncopal event at home. His BP was 79/46 mmHg, HR
was 123 bpm, RR was 19 with 91% saturation on pulse oximetry on room air. He was lethargic and had
cold extremities. He was placed on continuous intravenous inotropic support and ultimately an IABP.
Due to concerns for continued cardiogenic shock with evidence of end-organ dysfunction, the patient
underwent urgent cannulation with VA ECMO. Five days after cannulation with VA ECMO, the patient
received an orthotopic heart transplantation with removal of VA ECMO and IABP. One month following
heart transplant, the patient was discharged to an acute rehabilitation facility.

Case 2 describes a patient with acute on chronic decompensated HF who presents in cardiogenic
shock. The discussion regarding MCS should be centered on stability and the role that MCS plays in the
long-term care for the patient. Clinicians should initiate a candid discussion with the patient and family
regarding prognosis and various options, including heart transplantation, durable long-term ventricular
support devices, or hospice care after recognition of the severity and reversibility of the shock state
(Figure 2). Candidacy for these various options should be decided upon in a multidisciplinary setting
with input from advanced heart failure, cardiothoracic surgery, and palliative care consultants.

If a patient is deemed to be a transplant candidate, the use of MCS affects the urgency status of
the patient’s listing with the Organ Procurement and Transplantation Network reserving the most
urgent status (ie, status 1) for a patient on VA ECMO. The need for rapid decision-making from the
patient, family, and clinicians has led many centers to create a dedicated “shock team,” whereby a
multidisciplinary team assembles over conference call immediately and is available 24 hours a day to
decide on the short-term support and immediate- and long-term plan.3

CRITICAL ACUTE CARDIOGENIC SHOCK;

UNKNOWN ADVANCED OPTIONS CANDIDACY

Short-term mechanical circulatory support

(eg, IABP, Impella, TandemHeart, VA ECMO)

Patient’s or
Bridge to recovery Bridge to decision family’s goals
of care

Recovery Advanced options candidate Hospice/palliative care

Bridge to candidacy Bridge to transplant

Long-term mechanical circulatory support Transplant

IABP=intra-aortic balloon pump; VA ECMO=venoarterial extracorporeal membrane oxygenation

Figure 2. Short-term MCS Decision Flow Chart and Potential Outcomes

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MCS considerations in AMI cardiogenic shock

CASE 3

A 48-year-old female with a history of hypertension and hyperlipidemia presented to the ED with
acute onset, crushing, substernal chest pain. Her BP was 100/85 mmHg and HR was 67 bpm. She
appeared uncomfortable. An ECG showed marked ST-segment elevations in aVR and V1 with diffuse
ST-segment depressions (Figure 3A). The patient was brought emergently to the catheterization suite
where a diagnostic angiogram was revealing for an acute 95% occlusion of the ostial left main coronary
artery (Figure 3B). The patient became profoundly hypotensive during the angiogram, requiring chest
compressions, an intravenous epinephrine bolus, and endotracheal intubation resulting in restoration
of spontaneous circulation. The decision was made to place an Impella CP® (Figure 3C) followed by
placement of a drug-eluting stent in the ostial left main (Figure 3D). Three days later, the Impella CP
was exchanged for an IABP, which was weaned over the subsequent days along with inotropic support.
Prior to discharge, a TTE showed an EF of 40%. The patient was initiated on GDMT and discharged
home 2 weeks after presentation.

Figure 3. Case 3 Images

(A) Electrocardiogram showing ST-segment
elevations in aVR and V1 with diffuse ST-segment
depressions in lateral and inferior leads. (B) Initial
coronary angiogram showing acute left main lesion
with TIMI 2 flow down the left anterior descending
artery. (C) Impella CP® in the left ventricle with
coronary wire in the left main and left anterior
descending artery. Automatic chest compressor
device (LUCAS©) in bottom of image. (D) Coronary
angiogram after revascularization with flow in the left
main, Impella CP in left ventricle.

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Case 3 describes a patient with an AMI complicated by CS (AMICS) and hemodynamic collapse. The
cornerstone of management for AMICS remains acute revascularization of the culprit lesion. However, it
has been suggested that in patients at risk of hemodynamic collapse due to severe CS, MCS should be
employed either before or immediately after revascularization.4 Despite this, multiple randomized control
trials have not shown significant benefit for the use of IABP in AMI presentations. The CRISP AMI
randomized trial found that in patients with anterior ST elevation MI, there was no difference in infarct
size with IABP plus primary PCI versus PCI alone.5 The IABP-SHOCK II trial showed no difference in
30-day mortality in all-comer AMICS patients randomized to IABP vs standard of care.4 In the recently
published DanGer Shock trial, patients with AMICS who received standard care plus a microaxial flow
pump had lower mortality at 180 days than those patients who received standard care alone.6

The DTU-STEMI trial is currently enrolling patients and aims to evaluate whether Impella CP insertion
prior to revascularization reduces infarct size and clinical events. Given the lack of high-quality data, it
remains clear that rapid revascularization of the culprit lesion remains the definitive treatment of choice
and should be pursued without delay. Should the patient be in critical CS and the risk of cardiovascular
collapse is exceptionally high, MCS as a bridge to definitive therapy should be considered. In cases
of AMICS from mechanical complications such as ventricular septal defect (VSD) or papillary muscle
rupture, Impella should be used with caution due to concerns of worsening VSD or device interactions
with the papillary muscles. Should MCS be necessary in these cases, VA ECMO with or without IABP or
TandemHeart would be preferred choices for MCS as a bridge to definitive treatment.

Table 1. Key Points from Case Studies

CASE AND DISEASE STATE KEY POINTS

• MCS is often appropriate to support hemodynamics and prevent cardiovascular

Case 1: collapse.
Acute myocarditis
• MCS is used as a bridge to recovery or bridge to decision for advanced options.
complicated by CS
• Patients with myocarditis can recover spontaneously or through medical therapy.

• MCS considerations should be made in the context of patient’s goals of care and
Case 2: advanced options candidacy.
Acute on chronic
decompensated HF • Consideration of MCS as a bridge to decision or transplant should be initiated early
and may need to be done urgently depending on the clinical scenario.

• Definitive treatment with revascularization should be pursued without delay.

• MCS should be considered in patients with extremely high risk of hemodynamic

Case 3: collapse as a bridge to revascularization.
AMI complicated by CS
• IABP does not appear to be beneficial in all patients with AMICS.

• The use and timing of Impella or VA ECMO for AMICS is still being studied.

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QUICK READ SUMMARY

✓ MCS is often appropriate in patients with acute myocarditis who present in critical CS as a
bridge to recovery or a bridge to decision.

✓ In patients with acute on chronic decompensated HF, MCS timing is often dependent on
hemodynamic status and input from a multidisciplinary team on the patient’s candidacy for
advanced options. MCS may be appropriate as a bridge to candidacy or a bridge to transplant.

✓ Prompt coronary revascularization of the culprit lesion is the standard of care for AMICS.
Despite the results of a recently published randomized trial, the debate surrounding the
efficacy and timing of MCS in AMICS and clinical trials continues. However, in select patients
with exceptionally high risk of cardiovascular collapse, MCS may be appropriate as a bridge to
revascularization.

References
1. Peura JL, Colvin-Adams M, Francis GS, et al. Recommendations for the use of mechanical circulatory support: device
strategies and patient selection. Circulation. 2012;126(22):2648-67. doi:doi:10.1161/CIR.0b013e3182769a54

2. Mody KP, Takayama H, Landes E, et al. Acute mechanical circulatory support for fulminant myocarditis complicated by
cardiogenic shock. J Cardiovasc Transl Res. 2014;7(2):156-64. doi:10.1007/s12265-013-9521-9

3. Taleb I, Koliopoulou AG, Tandar A, et al. Shock team approach in refractory cardiogenic shock requiring short-term
mechanical circulatory support. Circulation. 2019;140(1):98-100. doi:doi:10.1161/CIRCULATIONAHA.119.040654

4. Thiele H, Zeymer U, Neumann F-J, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N
Engl J Med. 2012;367(14):1287-96. doi:10.1056/NEJMoa1208410

5. Patel MR, Smalling RW, Thiele H, et al. Intra-aortic balloon counterpulsation and infarct size in patients with acute
anterior myocardial infarction without shock: the CRISP AMI randomized trial. JAMA. 2011;306(12):1329-37.
doi:10.1001/jama.2011.1280

6. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock.
N Engl J Med. 2024:390(15):1382-93.

7. Geller BJ, Sinha SS, Kapur NK, et al. Escalating and de-escalating temporary mechanical circulatory support in
cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2022;146(6):e50-e68.

Short-Term Mechanical Circulatory Support for Cardiogenic Shock 443

PREVIOUS SECTION SECTION 5: Future Innovations

SECTION 5

Future
Innovations

Short-Term Mechanical Circulatory Support for Cardiogenic Shock

25
PREVIOUS CHAPTER Chapter 25: Mechanical Circulatory Support Innovations and Future Directions

Mechanical
Circulatory Support
Innovations and
Future Directions
This chapter is currently under development and will be available in a future revision of this eBook.

Morgan H. Randall, MD, FSCAI Duane S. Pinto, MD, MPH, FSCAI

Clinical Assistant Professor of Medicine Chief, Interventional Cardiology
Interventional Cardiologist Division of Cardiology
University Cardiology Department of Medicine
University of Tennessee Medical Center Beth Israel Deaconess Medical Center
Knoxville, TN Associate Professor of Medicine
MRandall@[Link] Harvard Medical School
dpinto@[Link]
Ki Park, MD, MS, FSCAI @duanepinto
Interventional Cardiology
Division of Cardiology
Department of Medicine
Associate Professor of Medicine
University of Texas Southwestern
Dallas, TX
[Link]@[Link]
@cardioPCImom

Short-Term Mechanical Circulatory Support for Cardiogenic Shock