CLINICAL CARDIOLOGY TRAINING ELECTIVE

STUDENT MANUAL

Harvey®
The Cardiopulmonary Patient Simulator
Saving Lives Through Simulation Technology®

The Gordon Center

for Simulation and Innovation in Medical Education
University of Miami Miller School of Medicine
 CLINICAL CARDIOLOGY TRAINING ELECTIVE

STUDENT MANUAL

2023-24

Joseph B. Esterson, M.D.

Director, Cardiology Training Programs

Location: Tel: 305-243-6491

Post Office Box 016960 (D-41)
Miami, Florida 33101 1120 N.W. 14th Street Fax: 305-243-6136
Miami, Florida 33136 Web: [Link]
 TABLE OF CONTENTS

PAGE

INTRODUCTION 1

LEARNING GOALS – 4-week 3

LEARNING GOALS – 2-week 7

LEARNING OPPORTUNITIES

Bedside Skills Training Using “Harvey,” the Cardiopulmonary 9

Patient Simulator, and UMedic Computerized Programs

ECG and Arrhythmia Interpretation 11

UMedic MULTIMEDIA COMPUTER CURRICULUM IN CARDIOLOGY 13

READING ASSIGNMENTS 17

BEDSIDE MANEUVERS TO DIFFERENTIATE HEART MURMURS 19

DAILY ESSENTIAL ECG LEARNING GOALS 21

ECG PACKET READINGS – (2-week) 23

AXIS DIAGRAM 25

ECG 12-LEAD PEARLS 27

CORE ECG EXAMPLES – “Must Know” 33

ARRHYTHMIA PEARLS 51

CORE ARRHYTHMIA EXAMPLES – “Must Know” 57

ADDITIONAL ARRHYTHMIAS 65

ARRHYTHMIA WORKSHOP 71
 INTRODUCTION

A sincere welcome to the Clinical Cardiology Elective. The course is comprised of instructor-led large
group teaching, small group hands-on clinical skills sessions, and self-study opportunities. In lieu of
direct patient contact, simulation technology and e-learning are incorporated into the elective for
interactive self-learning and bedside skill acquisition using Harvey, the Cardiopulmonary Patient
Simulator, and the UMedic multimedia computer curriculum.

The elective focuses on the most essential aspects of cardiovascular medicine, including the
pathophysiology, diagnosis, and treatment of many common and complex cardiac diseases. It includes
the integration of the bedside evaluation with the current indications for non-invasive and invasive
diagnostic testing. The diagnosis and management of valvular heart disease, coronary heart disease,
hypertensive heart disease, congestive failure, and congenital lesions are covered by didactic lectures,
review of highly selected material during independent study and by group and individual sessions with
Harvey and UMedic.

Each student will read, interpret and review electrocardiograms and arrhythmias with faculty. Students
are expected to attend all scheduled lectures and sessions unless officially excused. At the end of the
course, students are assessed on their skills and cognitive knowledge.

We look forward to your participation in the course and sharing our enthusiasm for learning clinical
cardiology.

Joseph B. Esterson, M.D.

S. Barry Issenberg, M.D.
Ross J. Scalese, M.D.

THE GORDON CENTER FOR RESEARCH IN MEDICAL EDUCATION

1120 NW 14th Street / P O Box 016960 [D‐41], Miami, FL 33136
Dr. Joseph Esterson Donna Fye
jesterson@[Link] dfye@[Link]
305.243.6491 305.243.2724

1
SENIOR ELECTIVE LEARNING GOALS
4-week Rotation

BEDSIDE EXAMINATION OBJECTIVES

A. Each student should be able to demonstrate the skills to:
1. Assess the jugular venous pressure and pulse
2. Assess the carotid pulse for contour
3. Assess the peripheral arterial pulses
4. Evaluate the location and contour of the following precordial impulses:
a. A non-displaced apical impulse
b. Inferolaterally displaced apical impulse
c. Lower left parasternal impulse
d. Impulses arising in ectopic areas
5. Recognize and evaluate the following auscultatory events, the “Big 12”:
a. Second sound splitting g. Mitral regurgitation
b. Third heart sound h. Aortic regurgitation
c. Fourth heart sound i. Mitral stenosis
d. Systolic click j. Tricuspid regurgitation
e. Innocent murmur k. Pericardial friction rub
f. Aortic stenosis l. Continuous murmur

I. COGNITIVE LEARNING OBJECTIVES

A. The student should be able to explain the physiologic significance of the bedside
observations listed under I., and be able to list a reasonable differential diagnosis
based on the history and physical examination.
B. Pharmacology: State the mechanism of action, side effects, and toxicity of certain
cardiovascular pharmacologic agents, including ACE inhibitors, angiotensin II
receptor antagonists, antiarrhythmics, anticoagulants, antiplatelets, beta blockers,
calcium channel blockers, digitalis, diuretics, inotropic agents, nitrates, statins, and
thrombolytics.
C. Laboratory Data
1. Electrocardiography
a. Recognize the criteria for classical patterns on the scalar 12 leads
b. Recognize and explain the treatment of various ECG and arrhythmia
diagnoses
c. Electrophysiologic testing: list indications and limitations
2. Chest X-rays
a. Know the cardiac anatomy making up the normal PA and lateral views
b. Recognize chamber enlargement, abnormalities of the great vessels,
intracardiac calcification, and pericardial effusion
c. Recognize pulmonary blood flow patterns including pulmonary venous and
arterial hypertension, and increased vascularity
d. Be able to synthesize findings into diagnostic possibilities

3
SENIOR ELECTIVE LEARNING GOALS
4-week Rotation

3. Echocardiography – 2-D, Doppler

a. Recognize the normal echo patterns of the left ventricle, mitral valve,
aortic valve, and left atrium
b. Understand indications for diagnosis and management decisions
4. Exercise Electrocardiography:
Outline indications, contraindications, and limitations
5. Radionuclide Imaging: Outline indications and limitations of various scans
6. Cardiac Physiology/Catheterization
a. Know normal intracardiac pressures and oxygen saturations
b. Know the determinants of cardiac output
c. Recognize valvular gradients and valve areas
d. Understand basic angiographic coronary anatomy
e. Recognize mitral and aortic regurgitation angiographically
f. Understand shunt lesion detection
7. Magnetic Resonance/C.T. Imaging: State indications and limitations

D. Coronary Artery Disease – Outline and explain the following:

1. Risk factors for, and prevention of, CAD
2. Differential diagnosis of chest pain
3. Definitions and differences between stable and unstable angina, including
approach to therapy
4. Determinants of myocardial oxygen consumption (MVO2) (supply/demand)
5. Diagnosis, differential diagnosis, treatment, and common complications of acute
myocardial infarction
6. Standard of CCU orders and their rationale
7. Use of exercise testing
8. Indications for coronary angiography
9. Role of surgery in treatment of CAD
10. Role of interventional cardiology
11. Indications and contraindications for use of reperfusion drugs
12. Rehabilitation – (diet, exercise)

E. Systemic Hypertension
1. Know the causes of secondary hypertension, realizing that a relatively small
percentage of patients have secondary hypertension, but that certain historical
and bedside findings may be clues to such a diagnosis.
2. Know how to diagnose/establish hypertensive CV disease
3. Know the standard hypertensive work-up
4. Know the commonly used antihypertensive drugs, their mechanism of action, and
side effects
5. Know the natural history of hypertension including its common complications
6. Understand therapeutic approach to hypertensive crisis

4
SENIOR ELECTIVE LEARNING GOALS
4-week Rotation

F. Valvular Heart Disease

1. Isolated calcific aortic valve stenosis
2. Differentiate from aortic valve “sclerosis”
3. Understand the difference between acute vs. chronic valve disease
4. Understand the differences between mitral valve prolapse and other forms of
mitral regurgitation
5. Understand the differences physiologically and clinically between HOCM and
fixed LV outflow tract obstruction
6. Know the indications for surgical intervention

G. Congenital Heart Disease

1. Understand the clinical diagnosis of commonly seen entities
(ASD, Pulmonary Stenosis, Coarctation, VSD, PDA)

H. Pulmonary Hypertension
1. Understand the pathophysiology of the 5 major types
2. Understand the common bedside and laboratory features
3. Understand the concept of irreversible, fixed pulmonary vascular disease
(Eisenmenger’s Syndrome)

I. Congestive Heart Failure

1. Know the differential diagnosis of categories for acute and chronic heart failure
based on history, physical exam, and simple laboratory procedures
2. Know the standard regimens and their rationale for treatment, including beta
blockers, digitalis, diuretics, vasodilators, and ace inhibitors

J. Pericardial Disease
1. Know how to differentiate acute pericarditis from acute myocardial infarction
2. Know under which circumstances to suspect pericardial effusion and how to
document
3. Understand the concept of paradoxical pulse and how to measure
4. Understand the significance of rapid collapse in neck veins for constrictive
pericarditis

Please note that there will be course assessments on the last day of the rotation.
Careful attention to the above learning goals will result in satisfactory performance on
the exam and more importantly, improvement in medical knowledge and clinical ability.

5
SENIOR ELECTIVE LEARNING GOALS
2-week Rotation

I. BEDSIDE EXAMINATION OBJECTIVES

A. Each student should be able to demonstrate the skills to:
1. Assess the jugular venous pressure and pulse
2. Assess the carotid pulse for contour
3. Assess the peripheral arterial pulses
4. Evaluate the location and contour of the following precordial impulses:
a. A non-displaced apical impulse
b. Inferolaterally displaced apical impulse
c. Lower left parasternal impulse
d. Impulses arising in ectopic areas
5. Recognize and evaluate the following auscultatory events (“Big 12”):
a. Second sound splitting g. Mitral regurgitation
b. Third heart sound h. Aortic regurgitation
c. Fourth heart sound i. Mitral stenosis
d. Systolic click j. Tricuspid regurgitation
e. Innocent murmur k. Pericardial friction rub
f. Aortic stenosis l. Continuous murmur

II. COGNITIVE LEARNING OBJECTIVES

A. The student should be able to explain the physiologic significance of the bedside
observations listed under I, and be able to list a reasonable differential diagnosis based
on the history and physical examination.
B. Laboratory Data
1. Electrocardiography
a. Recognize the criteria for classical patterns on the scalar 12 leads
b. Recognize and explain the treatment of various ECG and arrhythmia diagnoses
c. Electrophysiologic testing: list indications and limitations

Please note that there will be course assessments on the last day of the rotation.
Careful attention to the above learning goals will result in satisfactory performance on
the exam and, more importantly, improvement in medical knowledge and clinical ability.

7
 BEDSIDE SKILLS TRAINING USING “HARVEY” AND “UMEDIC”

CARDIOPULMONARY PATIENT SIMULATOR (CPS) ROUNDS

These are classroom case discussions led by an attending physician with Harvey.

INDEPENDENT LEARNING SESSIONS

These sessions involve examining Harvey in conjunction with the UMedic programs to
enhance your bedside skills. Participation in the bedside skills sessions is mandatory. All
scheduled sessions must be completed during the course.

HARVEY, THE CARDIOPULMONARY PATIENT SIMULATOR

Examining Harvey with the UMedic programs provides a structured presentation of patient
cases for each disease state, including matched historical, physical, electrocardiographic,
radiologic, noninvasive, hemodynamic, therapeutic, pathologic, and epidemiologic information.
Harvey is used with the UMedic programs to teach and improve bedside diagnostic skills.

Harvey simulates the bedside findings of 48 disease states and 3 normal patient states.
Synchronized arterial (carotid, brachial, femoral) and jugular venous pulsations, precordial
movements, respiration, blood pressure, and auscultation in the four classic acoustic areas are
simulated. When appropriate, complex acoustic events vary with respiration.

The major cardiac conditions presented in Harvey that will be emphasized during the course:

Acute Inferior Myocardial Infarction Coarctation of the Aorta

Acute Anterior Myocardial Infarction Hypertension
Hypertrophic Obstructive Cardiomyopathy Acute Pericarditis
Mitral Valve Prolapse Innocent Murmur
Mitral Valve Prolapse, Isolated Click & Murmur Angina Pectoris
Mitral Regurgitation, Chronic Cardiomyopathy
Mitral Regurgitation, Mild Pulmonary Stenosis
Mitral Regurgitation, Acute Tetralogy of Fallot
Mitral Stenosis w/Severe Tricuspid Regurgitation Patent Ductus Arteriosus
Mitral Stenosis w/Mild Tricuspid Regurgitation Aortic Valve Sclerosis
Mitral Stenosis & Regurgitation Atrial Septal Defect
Aortic Regurgitation, Chronic Ventricular Septal Defect
Aortic Regurgitation, Acute Ventricular Aneurysm
Aortic Stenosis Primary Pulmonary Hypertension

9
 ECG AND ARRHYTHMIA INTERPRETATION

ECG LECTURES AND READING SESSIONS

The course is comprised of topical lectures with in-class review of the ECG tracings assigned
as homework. You are to read the assigned ECG tracings, notate your analysis and be
prepared to discuss your findings of the following in-class:

a. Rate, axis, and PR, QRS, QT intervals measurements

b. Rhythm
c. Abnormal findings and conclusions

During the course there are 2 review sessions scheduled for self-assessment: the ECG Mid-
Course Review and the Arrhythmia Mid-Course Review. These tracings are typical of those
covered in class to provide a realistic tool for you to personally assess your knowledge
acquisition.

ARRHYTHMIA LECTURES & WORKSHOP

Topical lectures will precede ECG sessions on supraventricular and ventricular arrhythmias
and heart block. The Arrhythmia Workshop exercise at the end of the syllabus is an interactive
review scheduled for the last week of the course. You will review the strips in advance and
prepare to discuss in class.

11
 UMedic Multimedia Computer Curriculum in Cardiology
4-week rotation

Studies have demonstrated that the bedside cardiovascular examination is accurate

and cost-effective. They have also demonstrated that these skills are sorely lacking in
medical students and house officers. One solution to for improve bedside diagnostic
skills is repetitive practice using simulation and computer technology in a
standardized curriculum.

The UMedic curriculum provides a system for learning cardiology bedside skills. This
educational system using simulation technology and Harvey, were developed by the
University of Miami Gordon Center for Research in Medical Education with cardiologists
from medical centers at Arizona, Duke, Emory, Florida, Illinois, Iowa, Rush and Mayo.
National multicenter studies of the UMedic system have demonstrated its
effectiveness and acceptance at all levels of the curriculum.

During the elective, course time is scheduled to fully review all assigned programs
together with Harvey, including the self-assessment components. Prior to using
Harvey, review the following pages on the “5 Finger” approach to Bedside
Diagnosis, hemodynamic curves, important murmurs and the key findings outline for
the first five programs. All physical findings should be reviewed using “Harvey” and
UMedic together (“H” Mode). You can increase your knowledge base by selecting the
additional discussion option for each possible answer in self-assessment questions of
the UMedic programs. Refer to the course schedule for the UMedic program
assignments.

While the UMedic curriculum is comprised of 20 programs, the post-course

assessment emphasizes the physical findings in the Essential Cardiac Auscultation
program and 5 programs: normal and the four valve lesions: AS, AR, MS, MR. For
each assigned program, you should be able to identify (1) the bedside finding,
(2) the underlying pathophysiology, and (3) its relation to specific diagnoses and
(4) the severity of the lesion.

13
 Orientation to Bedside Diagnosis

The Five Fingers of Clinical Diagnosis The Five Fingers of Physical Signs

ECG / X RAY VENOUS PULSE

PHYSICAL ARTERIAL
SIGNS NONINVASIVE PULSE
STUDIES PRECORDIAL
MOVEMENT
INVASIVE
PROCEDURES GENERAL AUSCULTATION
HISTORY APPEARANCE

Four Classic Left Heart Murmurs Essential Cardiac Auscultation - “The Big 12”

 2nd Sound Splitting  Aortic Stenosis

 Third Sound  Aortic Regurgitation
 Fourth Sound  Mitral Stenosis
 Systolic Clicks  Continuous Murmur
 Innocent Murmur  Tricuspid Regurgitation
 Mitral Regurgitation  Pericardial Rub

14
 UMedic Multimedia Computer Curriculum in Cardiology
4-week rotation

The following summarizes the key teaching points you will be responsible for mastering
after completing the first 5 programs. These items are discussed in detail during the
programs.

I. Normal

A. Identify a normal central venous pressure and jugular venous pulse wave form and
know it suggests there is no significant right heart disease.
B. Identify a normal split first heat sound and know its cause.
C. Identify the contour of a normal precordial impulse as early systolic.
D. Identify a 3rd heart sound and know its causes.
E. Identify physiological splitting of the 2nd heart sound and know its causes.

II. Aortic Stenosis

A. Identify the size and contour of the precordial pulse and know its cause and
differential diagnosis.
B. Know how the severity of Aortic Stenosis can be determined by the precordial
impulse.
C. Identify the murmur of Aortic Stenosis and determine its severity & etiology.
D. Identify the 4th heart sound and know its cause and relationship to severity.

III. Mitral Regurgitation

A. Identify the size and location and contour of the precordial impulse and know its
cause and differential diagnosis.
B. Identify severe mitral regurgitation on auscultation and know how its severity is
determined.

IV. Aortic Regurgitation

A. Identify the carotid pulse and know its differential diagnosis

B. Identify the size and location and contour of the precordial impulse and know its
cause.
C. Identify the murmur of Aortic Regurgitation.
D. Identify the Austin-Flint murmur and know its cause and association with the
severity of Aortic Regurgitation.

V. Mitral Stenosis

A. Identify the jugular venous pulse wave form and know is causes.
B. Identify the location and size and contour of the precordial impulses and know their
causes and differential diagnoses.
C. Identify the loud second heart sound and know its cause.
D. Identify the murmur of Mitral Stenosis & know how its severity is determined.
E. Identify right sided heart sounds and murmurs and know how they change with
respiration.

15
 CARDIOLOGY ELECTIVE READING ASSIGNMENTS
Lilly, Pathophysiology of Heart Disease unless otherwise noted

The following reading assignments are to be completed prior to each lecture in all
2‐ and 4‐week electives as noted below:

1. Electrocardiography and Arrhythmia Lectures: 6th Ed. 7th Ed.

Day 1 12‐21 12‐21

74‐90 79‐95
During the elective (to be announced) 91‐111 95‐116
268‐309 285‐328

2. CPS Rounds (Harvey Lectures):

Introduction to Bedside Skills: 26‐42 28‐45
Mitral Regurgitation: 198‐203 207‐213
Aortic Stenosis 204‐207 214‐217
HOCM 255‐262 272‐278
Aortic Regurgitation 207‐210 217‐219

3. Didactic Lectures:

2‐week elective:
Rx Supraventricular Arrhythmias 287‐309 305‐329

4‐week elective:
Acute Coronary Syndrome 162‐173 172‐183
CCU / Complications of MI 184‐190 193‐198
Echocardiography 48‐55 50‐57
Non‐invasive Imaging 66‐72 68‐75
Rx Supraventricular Arrhythmias 287‐309 305‐329
Stress testing 150‐152 158‐160
Treatment of Angina & CAD 134‐146 142‐154
Treatment Heart Failure 220‐235 232‐260

2021 JAN 29
17
 Bedside Maneuvers (short version) to
Differentiate Heart Murmurs (Revised 2014)
Arrows signify Loudness unless otherwise stated

Maneuvers Mitral Mitral Aortic Innocent Aortic Mitral Valve HOCM Tricuspid Pulmonic VSD
Stenosis Regurg. Stenosis Systolic Regurg. Prolapse Regurg. Stenosis
Murmur

     
Valsalva or
Stand
( Venous
Return, SV, Length 
Preload ) Loudness 

       
Squat or
Leg Raise
( VR,
Preload, Length  (Leg (or No
Loudness  Raise) Effect)
Afterload )

      
Hand Grip
( HR, CO,
Afterload, (or No Length 
Preload) Effect) Loudness 

    
Inspiration
( VR,
Preload – Rt.)


Sit Up, Lean
Forward
MR vs. AS: Hand grip MR vs. MVP: Squat, Leg raise
AS vs. HOCM: Valsalva, Stand, Squat MR vs. TR, AR vs. PR: Inspiration
HOCM vs. MVP: Hand grip 19
 ESSENTIAL ECG LEARNING GOALS
4TH YEAR STUDENT ELECTIVE IN CARDIOLOGY

ECG 1 ECG 2 ECG 3 ECG 4 ECG 5

Normal Atrial enlargement Non‐specific ST‐T abn. LVH LBBB
Early Repolarization First degree AVB Ischemic ST depression RVH RBBB
Sinus Arrhythmia Low Voltage Ischemic T inversion LVH and RVH with
Limb lead reversal Artifact Juvenile T pattern Ischemia
ECG 6 ECG 7 ECG 8 ECG 9 ECG 10
Hemiblocks Pericarditis Myocardial Infarction Review: Arrhythmias IA:
Bifascicular Block Myocardial Infarction BBB with Infarction Ischemia PAC
Hypertrophy Aberrancy
Conduction defects Ectopic atrial rhythm
Myocardial Atrial tachycardia
infarction with/without block
Pericarditis Multifocal atrial tach.
Wandering Atrial
Pacer
ECG 11 ECG 12 ECG 13 ECG 14 ECG 15
Arrhythmias IB: Arrhythmias IC: Review of Arrhythmias Arrhythmias II: Arrhythmias III:
Atrial fibrillation PSVT I A, B, C: PVC 2nd degree AVBlock
Atrial flutter • AVNRT Supraventricular Accel. vent. rhythm • Type I
PJC • AVRT Arrh. Vent. tachycardia • Type II
Junctional rhythm Pre‐excitation (WPW) Vent. fibrillation • Untypeable
Paced rhythms Complete AV Block
Review of AV
Dissoc’n
ECG 16 ECG 17 ECG 18
Review of Arrhythmias Electrolyte abnormal. Final Review and
II and III: Digitalis effect unusual tracings
Ventricular QT interval abnormal.
Arrhythm. CNS
Heart Blocks Electrical alternans
Pacing Hypothermia + other

NOTE: Not all ECG packets will be assigned as homework and reviewed in class
during the rotation.

During the 2‐week rotation, only certain tracings in the ECG packet are
assigned as homework. Refer to the list, ECG Packet Readings, for the
tracings assigned as homework each day.

08.14.2018 21
 2‐Week Cardiology Elective
ECG Packet Readings

Day ECG Packet # ECG’s to Interpret

1 1 All you can (finish tonight)

2 1, 2, 3, 4, 5, 6, 7, 9

2 3 1, 2, 3, 7, 9, 10
4 1, 2, 4, 5, 6, 7

3 5 1, 2, 4, 5, 7
6 1, 3, 6, 8, 9

4 7 1, 2, 3, 4, 5, 7, 9, 10 (in class)
8 1, 3, 4, 5, 6, 8, 9, 10

5 10 1, 2, 3, 4, 5, 6, 7, 8
11 1, 2, 3

6 11 4, 5, 6, 9, 10
12 1, 2, 3, 4, 5AB, 6, 8, 9, 10

7 14 1, 2, 3, 4, 5, 6, 8, 10 (in class)

8 15 1, 2, 3, 5, 6, 7, 8, 9, 10 (in class)

9 17 1, 3, 4, 5, 6, 8, 9, 10, 11 (in class)

18 1‐10 (in class)

2021 07 23
23
 Frontal QRS Axis
Extreme Axis Left Axis
-aVF (-90o)
(±180o to -90o) (-30o to -90o )
(-120o) -II -III (-60o)

(-150o) +aVR
+aVL (-30o)

±180o) -I
(±
±0o)
+I (±

(+150o) -aVL -aVR (+30o)

(+120o) +III +II (+60o)

Ri
Rightht Axis
A i +aVF (+90o) N
Normal l Axis
A i
(+90 to ±180o)
o (-30 to +90o)
o

Is QRS Axis Normal?

If not, is there Left or Right Axis Deviation?

Axis Lead I Lead II

Normall Positive
ii Positive
ii

Left Positive Negative

Right Negative (Positive or Neg.)

aVF Positive
25
 ECG 12‐LEAD PEARLS

I. ATRIAL ENLARGEMENT
A. RIGHT ATRIUM
• A tall, narrow, peaked P in lead 2 ‐ height > 2.5 mm
• Frequently associated with tall (> 1.5 mm) P in V1
B. LEFT ATRIUM
• Wide, notched P in lead 2; width  3 mm (0.12 sec), and/or
• Large ( 1 mm wide and deep) negative terminal deflection P in V1

II. VENTRICULAR HYPERTROPHY

A. LEFT VENTRICULAR HYPERTROPHY
• Voltage criteria
o R wave in aVL > 11 mm
o SV1 + RV5 or 6 > 35 mm
• Left atrial enlargement
• Axis horizontal or left
• Abnormal ST‐T pattern ‐ looks like a reversed check (“strain” or “secondary”)
• Delay in the intrinsicoid deflection over the left ventricle

B. RIGHT VENTRICULAR ENLARGEMENT

• Varies with the etiology of the RVH: suspect with right axis deviation

ETIOLOGY Pressure Overload Volume Overload Early Mitral Chronic

1. Pulmonary stenosis 1. Atrial septal defect Stenosis Lung Disease
2. Primary pulmonary 2. Anomalous venous
hypertension drainage
3. Secondary pulmonary 3. Pulmonary or
hypertension, e.g. tricuspid
repeated pulmonary regurgitation
emboli
‐ late mitral stenosis
‐ Eisenmengers

AXIS Mild: Vertical

Right Vertical or right Vertical or right Moderate: Abnormal LAD
Severe: Right (and superior)

ATRIUM Right atrial enlargement Right atrial Left atrial Right atrial enlargement
with normal sinus rhythm enlargement enlargement or
(except in mitral stenosis ‐ occasionally atrial fibrillation
Biatrial enlargement or
atrial fibrillation)
rSR’ R/S1 r/S
LEAD VI qR or R

2021 JUNE

27
III. CONDUCTION DISTURBANCES

A. RIGHT BUNDLE BRANCH BLOCK

• Septal depolarization unaffected
• Pre‐terminal delay with forces seen right and anteriorly, causing aVR and V1
to have RSR’ deflection;

• and the left ventricular leads (I, aVL, V6) usually show deep, delayed S wave

• Secondary ST‐T abnormalities with J depression and ST down, with T inverted in V1‐3
(similar to strain)
• Incomplete RBBB ‐ the QRS duration < .12 sec
• Complete RBBB ‐ QRS duration is  0.12 sec
• RSR’ in V1, and normal QRS duration is frequent normal finding in young individuals
with a vertical axis. It represents late crista supraventricularis depolarization
• It does not interfere with diagnosis of AMI (except True Posterior)

B. INCOMPLETE LEFT BUNDLE BRANCH BLOCK (controversial)

• Absence of normal septal 0.02 Q waves seen in all left ventricular leads
• QRS duration .10 to <0.12 sec
• A small R wave or no R wave seen in V1

C. COMPLETE LEFT BUNDLE BRANCH BLOCK

• Absence of normal 0.02 Q waves seen in I, V5‐6
• Delayed QRS (.12): delay (notched or slurred) is in the mid‐portion and seen as a positive
deflection on left‐ and negative deflection on right‐sided leads
• Secondary ST‐T abnormalities similar to strain in left‐sided leads with some J and ST
elevation in right‐sided leads
• There may be a small R or no R wave seen in lead VI
• The frontal plane axis may be normal or abnormally directed to the left
• Interferes with diagnosis of AMI

D. LEFT ANTERIOR HEMIBLOCK OR LEFT ANTERIOR FASICULAR BLOCK

• Frontal plane axis usually between ‐45° and ‐90° with an r/S deflection in
Lead II in the absence of other causes of LAD

E. LEFT POSTERIOR HEMIBLOCK OR LEFT POSTERIOR FASICULAR BLOCK

• Frontal plane axis usually +120o to 180o in the absence of other causes of RAD, when
Lead I has an r/S deflection

F. INTRAVENTRICULAR CONDUCTION DELAY

• QRS is 0.12 sec without the features of LBBB, RBBB, WPW

28
 G. WOLFF‐PARKINSON‐WHITE (WPW) (preexcitation)
Presence of an accessory conduction path is recognized by:
• Short PR interval
• Wide QRS due to initial delay = delta wave
• Secondary ST‐T abnormalities often (similar to BBB)

H. LOWN‐GANONG‐LEVINE (LGL) (preexcitation)

• Presence of a short A‐V node bypass pathway is recognized by the presence of a short PR
with P activity in normal direction
• Normal QRS + ST‐T (no Delta wave)
• History of tachyarrhythmias must be present

IV. ACUTE CORONARY SYNDROME PATTERNS

A. MYOCARDIAL ISCHEMIA
• ST‐segment depression ( 0.5mm) and/or T wave inversion ( 1mm) in  2 contiguous
ECG leads, in the presence of angina or anginal equivalent
• Serum markers of myocardial necrosis absent

B. NON‐ST ELEVATION MYOCARDIAL INFARCTION

(previously described as subendocardial, non‐transmural, non‐Q wave MI)
• Same as above for myocardial ischemia
• Q waves  0.03 sec may appear later (less common than with STEMI)
• Ultimately, serum markers of myocardial necrosis must be present to confirm

C. ST‐ELEVATION MYOCARDIAL INFARCTION

(previously described as transmural or Q‐wave myocardial infarction)
• Evolutionary Changes of Acute ST Elevation Myocardial Infarction:
1. Tall T waves (“Hyperacute T waves”):
• Minutes after onset of chest pain
• Transient finding
• Not often seen clinically as patients tend to present later in the course

2. ST‐segment elevation:
• Present early in the course of injury
• Decreases significantly in first 7‐12 hours after the onset of chest pain
• Usually convex upward combined with the tall T wave (“tombstone”) appearance
• Seen in leads facing the infarction (NOTE: ST depression in V1‐V3 may reflect
posterior ST elevation)
• Often associated with ST‐segment depression in leads opposite the site of injury
(reciprocal changes)

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 • Degree of ST‐segment elevation varies but typically:
o 1mm in 2 contiguous leads except V2‐3
o V2‐3: 2mm ‐ men;  1.5mm ‐ women
• Duration of ST elevation duration variable (hours ‐ 2 weeks; if >2 weeks suspect LV
aneurysm)

3. Appearance of abnormal Q waves (in 2 contiguous leads):

• Representative of myocardial necrosis
• Q wave duration of 0.03 sec. OR Q wave amplitude > 25% succeeding R wave
(does not apply to III, aVR, and V1 where Q waves may normally be deep and wide)
• A Q wave is abnormal even if duration < 0.03 sec in leads V2‐V3
• Over time pathologic Q waves may regress or disappear

4. Resolution of ST‐segment elevation with beginning of T wave inversion:

• T wave inversion begins as ST‐segment elevation decreases; occurs about same
timing as appearance of pathologic Q
• Changes differ from acute pericarditis in which the ST‐segment typically returns to
baseline before T wave inversion occurs.
• T wave changes are seen in more leads than the abnormal Q waves

5. Isoelectric ST‐segments with symmetric T wave inversion:

• ST‐segment elevation may fully resolve or remain slightly elevated with an upward
convexity followed by a negative T wave ‐ the latter is known as a “Coronary T
wave”

V. PATTERN RECOGNITION OF ST ELEVATION and Q WAVE MYOCARDIAL INFARCTION

A. ACUTE/EVOLVING ANTERIOR WALL MYOCARDIAL INFARCTION

• Abnormal Q waves (loss of R wave) V2‐4 (±V5‐V6)
• ST‐segment elevations in these leads with or without T wave inversions
OLD ANTERIOR WALL MYOCARDIAL INFARCTION
• Abnormal Q waves (loss of R wave) V2‐4

B. ACUTE/EVOLVING INFERIOR WALL MYOCARDIAL INFARCTION

• Abnormal Q waves ‐ leads 2, 3 aVF
• ST‐segment elevations in these leads with or without T wave inversions
OLD INFERIOR WALL MYOCARDIAL INFARCTION
• Abnormal Q waves, leads 2, 3, aVF

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C. ACUTE/EVOLVING ANTEROSEPTAL MYOCARDIAL INFARCTION
• ST‐segment elevation with or without T inversion ‐ V1, V2, ±V3
• Q waves in V1‐2, ±V3
OLD ANTEROSEPTAL MYOCARDIAL INFARCTION
• Q waves in V1‐2, ±V3

D. ACUTE/EVOLVING LATERAL MYOCARDIAL INFARCTION

• Abnormal Q’s seen in leads I, aVL, V5‐6
• High lateral infarcts may involve only leads I and aVL or aVL alone
• ST‐segment elevations in these leads with or without T wave inversions
OLD LATERAL MYOCARDIAL INFARCTION
• Abnormal Q’s seen in leads I, aVL, V5‐6

E. ACUTE/EVOLVING POSTERIOR WALL MYOCARDIAL INFARCTION

• Tall, slurred (sometimes broad) R waves in right precordial leads V1‐3 (r/s ratio >1 in V1)
• J and ST‐segment depression with tall, positive, wide, equal‐shouldered T waves (V1‐3)
• Almost always associated with acute inferior or lateral wall infarction
• Not associated usually with a Rt axis
OLD POSTERIOR WALL MYOCARDIAL INFARCTION
• Tall, slurred R waves in aVR and precordial leads V1‐3
• A positive equal‐shouldered T wave usually remain in V1
• Usually not associated with a Rt axis; if present consider RVH instead

F. ACUTE RIGHT VENTRICULAR INFARCTION

• Almost always associated with inferior or infero‐posterior infarction
• Can mimic acute anteroseptal MI
• ST elevation V3R‐V6R (most specific V4R), occasionally V1‐3

OLD RIGHT VENTRICULAR INFARCTION

• Cannot be recognized on the ECG

G. PERICARDITIS
• Initially produces diffuse ST‐segment elevation (concave upwards usually) with the ST‐
segment down in AVR and perhaps V1
• Frequently associated PR segment depression (seen best lead 2)  1 mm
• After acute phase, the ST’s return to the baseline and inverted T waves appear
• Finally T inversions disappear with normal appearing tracing

H. ANEURYSM (VENTRICULAR)
• Persistent ST‐segment elevations associated with evidence of transmural infarction (for
longer than 2 ‐ 3 weeks)

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VI. ELECTROLYTES

A. HYPOKALEMIA
• Generalized low amplitude T waves and ST depressions
• Prominent U waves that fuse with the low‐amplitude T waves
• Changes show in all leads, but are most prominent in V2‐4
• Later: T inversions, QRS widening, P changes, arrhythmias, AV block

B. HYPERKALEMIA
• Tall, narrow‐based, peaked (peaking is the most specific) T waves develop in most or all
leads except aVR, most noticeable in V2‐4
• Later: QRS widens, PR widens, P absent, sine wave pattern, arrhythmias

C. HYPOCALCEMIA
• Prolonged ST‐segments seen (causing a long QT interval)
• Mostly in standard leads

D. HYPERCALCEMIA
• Shortened ST‐segments (causing a short QT interval)
• Shows up best in standard leads

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 CARDIOLOGY ELECTIVE ECG EXAMPLES

CORE (“Must Know”)

1. Normal

2. Improper Technique - Limb Lead Reversal

3. Normal Variant - “Early Repolarization”

4. Acute Pericarditis

5. Complete Right Bundle Branch Block

6. Left Bundle Branch Block

7. Left Ventricular Hypertrophy with Secondary Repolarization changes

8. Right Ventricular Hypertrophy with Secondary Repolarization Changes

9. Ischemia ST Depressions ("Subendocardial Injury”)

10. Ischemic T Inversions (“Transmural Ischemia”)

11. Acute Inferior Posterior Myocardial Infarction (“Injury”)

12. Evolving Antero-Lateral Myocardial Infarction

13. Hyperkalemia

14. Hypokalemia

15. Wolff-Parkinson-White

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 ARRHYTHMIA PEARLS

Cardiac arrhythmias are among the most common problems encountered in the management of
heart disease. While most of our approach to anti-arrhythmic therapy is empirical, optimal therapy
depends on accurate diagnosis of the arrhythmia present. Although so-called bedside diagnosis
of arrhythmias may be possible in a limited number of cases, electrocardiograms are necessary
for their definitive diagnosis. A systematic approach to arrhythmia determination is necessary.
The first part of this paper will outline such a systematic approach.
To analyze an arrhythmia, certain general rules should be followed. Each of the following
determinations should be made in every case:

1. Analyze the P waves: what is depolarizing the atrium?

A. Shape and direction of the P

B. Rate of P
C. Regularity of P

2. Analyze the QRS complex: where is the origin of ventricular depolarization?

A. Shape: normal, aberrant or bizarre

Impulses arising in the ventricles (rather than supraventricular) are not transmitted
through normal conduction pathways. As a result, depolarization of ventricular
musculature usually occurs slowly with delay. The initial portion of the QRS, at least
in some leads, will differ from that of the normal QRS. Impulses arising from
supraventricular foci may depolarize the ventricle in normal fashion or, if they occur
too early, before complete repolarization has occurred, they will show some aberrancy
of conduction. This aberrancy affects the last 2/3 of the complex and is usually of
the right bundle branch block type. The initial 1/3 of the complex is identical to the
normal complex in all leads.
B. Rate
C. Regularity

3. Analyze the relationship between P wave and QRS complex, specifically P-R interval
length and constancy.

SPECIFIC CRITERIA:

SINUS RHYTHMS
1. P wave upright in lead I and II, inverted in aVR
2. P wave rates range between 40-60 and 160-180/minute
3. Supraventricular QRS with a constant PR interval

2021 JUNE
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SUPRAVENTRICULAR ARRHYTHMIAS

ATRIAL TACHYCARDIA (FOCAL)

1. P precedes QRS, upright (different than sinus P) or inverted lead II (PR ≥ .12)
2. Straight baseline exists between P’s if other complexes are eradicated
3. P rate is usually 100-180/minute, occasionally up to 250/minute
4. QRS shape is normal or aberrant
5. QRS rate may be the same as P or block can occur
Note: Atrial tachycardia with block is classically associated with digitalis toxicity; (P rate
usually 150-250).

MULTIFOCAL ATRIAL TACHYCARDIA

1. At least 3 different P morphologies in same lead, with isoelectric baseline
2. Irregularly irregular (varying PP, PR, RR intervals) - resembles Atrial Fib
3. Ventricular rate usually 100-150/min (up to 250)

JUNCTIONAL RHYTHMS
1. P wave inverted in lead II, upright in aVR (PR <.12)
2. Rate range: 35-60/minute Junctional Rhythm
60-130/minute Accelerated Junctional Rhythm
130-220/minute Junctional Tachycardia (rare in adults)
3. P may be before, after or lost in QRS
4. Supraventricular QRS

REENTRY SUPRAVENTRICULAR TACHYCARDIA (AVNRT AND AVRT)

1. Abrupt onset (initiated by PAC) and termination
2. Rate usually 140-220/min; there is 1:1 conduction
3. AVNRT: retrograde P usually hidden, might have “partial P” just after QRS
4. AVRT: retrograde P usually seen in ST segment (small)

ATRIAL FLUTTER
1. F wave rate is usually 250 to 350/minute (usually close to 300)
2. Undulating or saw-toothed baseline (especially leads II, III, aVF)
3. QRS shape normal or aberrant
4. QRS rate usually < P; most commonly 2:1 conduction, although it varies.

ATRIAL FIBRILLATION
1. Atrial fibrillatory waves, rapid (400-700); no definitive P waves seen
2. Ventricular response is irregularly irregular (unless AV block present)

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 HEART BLOCK

FIRST DEGREE ATRIOVENTRICULAR (A-V) BLOCK

1. Sinus impulse delay in reaching ventricle - pathology above or below His
2. P-R interval > 0.20 sec
3. Each P wave is followed by QRS complex.

SECOND DEGREE A-V BLOCK

1. One or more sinus impulses fail to activate the ventricles.
2. Two types:

Wenckebach - Mobitz - Type I Mobitz - Type II

 Lesion at A-V node: supra-Hisian  Lesion usually in bundle branch system: infra-
Hisian
 Associated with inferior wall MI, digitalis toxicity,
other drugs,  parasympathetic tone  Associated with anterior wall MI, chronic
conduction system lesions
 Described as reversible and transient;
ischemic if MI  Described as necrotic in nature
 Dropped QRS preceded by a progressive  Dropped QRS preceded by a fixed P-R
prolongation of P-R interval for at least 2 sequential beats
 Regular P-P intervals  Regular P-P intervals
 Less frequently 3° block  Commonly3° block
 Usually responds well to pharmacological  Usually non-responsive to pharmacological
intervention intervention - requires pacing

3. Untypeable second degree A-V block occurs when no two consecutive P waves are
conducted (i.e. 2:1 block / conduction) - cannot tell if Type I or Type II

ADVANCED A-V BLOCK

1. Occasional A-V capture by sinus P waves, with conduction 3:1 or higher

THIRD DEGREE A-V BLOCK

1. All of the sinus impulses fail to activate the ventricle.
2. No fixed relationship between P wave and QRS complex
3. Can occur as end result of Type I or Type II second degree A-V block
4. Regular P-P and R-R interval; atrial rate > ventricular rate
5. Following Wenckebach, the controlling rhythm is usually junctional. Following Mobitz II
block, the controlling rhythm is usually idioventricular.

Arrhythmias become potentially life-threatening under three conditions:

1. When they originate in the ventricles
2. When they result in critically slow ventricular rates
3. When they result in critically fast rates.

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VENTRICULAR ARRHYTHMIAS

PREMATURE VENTRICULAR CONTRACTIONS (PVCS): GENERAL CHARACTERISTICS

1. QRS complex is early, different from patient’s normal complex.
2. Interval between the preceding sinus beat and the PVC remains fixed or constant if the
PVCs are arising from the same focus.
3. Usually fully compensatory pause after the PVC.

IDIOVENTRICULAR RHYTHM
1. QRS complex different from patient's normal complex and wide.
2. QRS rate is 20-50/minute, often in 30's, but regular.
3. No associated P waves
4. Captures and fusions can occur

ACCELERATED VENTRICULAR RHYTHM (“SLOW VT”)

1. QRS complex different from patient's normal complex and wide.
2. QRS is regular, and rate is from 50-100 bpm.
3. No associated P waves
4. Captures and fusions can occur

VENTRICULAR TACHYCARDIA
1. 3 PVC’s or more in a row; ventricular rate >100/minute (usually 140-200/minute) and
fairly regular.
2. No associated P waves
3. Captures and fusions can occur
4. May occur de novo, or after increasing frequency of PVC’s.

TORSADE DE POINTES (see strip below)

1. Form of paroxysmal polymorphic VT which continuously (every 5-20 beats) changes
configuration and polarity, twisting around the isoelectric line.
2. Ventricular rate usually 200-250/minute; may  ventricular fibrillation
3. Associated with long Q-T interval (including Class IA and non-cardiac drugs,
hypokalemia, marked bradycardias, CNS, intrinsic heart disease, congenital)
4. Initiating PVC usually late in diastole and on summit of T wave
5. Majority end spontaneously and then recur

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 VENTRICULAR FIBRILLATION
1. Chaotic ventricular rhythm with no repetition of shape or form
2. Completely irregular, no rate discernible
3. Associated with absent carotid pulse

Terminology and Mechanisms of Some Clinically Occurring Arrhythmias

1. Aberration or aberrancy refers to transient intraventricular conduction abnormalities of

supraventricular impulses, resulting in a widened abnormal QRS complex. This is
usually due to heart rate change (transient slowing followed by a premature beat)
causing a refractory bundle. Since the right bundle branch has more refractoriness, the
wide QRS usually has a RBBB pattern - always check lead V1. The distinction
between supraventricular rhythms demonstrating aberrancy and ventricular rhythms is,
of course, of considerable clinical importance.

2. Escape beats occur when there is a pause or delay in the dominant mechanism,
allowing a lower pacemaker to step in and save the day. In a sense, they are “post-
mature beats”. Can occur with sinus bradyarrythmias and AV block. They can be single

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 or become a continuous escape rhythm. In the first case, with sinus bradycardia, the
marked beat is a ventricular escape. In the second case, with sinus slowing, a junctional
escape rhythm takes over.

3. Fusion beats arise when stimuli originating from two different foci concurrently
depolarize the ventricles. The resultant complex is a fusion or “combination” of the two
morphologies. A similar phenomenon is Capture beats, which are narrow-QRS
captures by conducted supraventricular impulses, which occur between the wide
ventricular tachycardia QRS’s. The presence of fusions and captures strongly supports
the diagnosis of ventricular tachycardia. The top 3 strips are continuous. Sinus rhythm
at a rate of 75/minute is overtaken by an accelerated ventricular rhythm at a slightly
faster rate. The third, fourth and fifth beats are fusion beats. In the middle of the bottom
strip, the sinus rhythm accelerates and recaptures the ventricle. The sixth beat in this
th
strip is a fusion beat. The lowest separate strip exhibits a capture beat - it is the 10 beat
in the middle of the wide QRS tachycardia, which spontaneously aborts, followed by
sinus tachycardia. It’s presence strongly suggests the diagnosis of ventricular
tachycardia.

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 CARDIOLOGY ELECTIVE ARRHYTHMIA EXAMPLES
CORE (“Must” Know)

1. Sinus Rhythm
2. Sinus Tachycardia
3. Sinus Bradycardia
4. Sinus Arrhythmia

5. PAC’S
6. AV Nodal Reentry Tachycardia (AVNRT)
7. Atrial Flutter (3:1 conduction)
8. Atrial Fibrillation

9. PJC’S
10. Junctional Rhythm with atrial activation before ventricular
11. Junctional Rhythm with no visible atrial activation
12. Junctional Rhythm with atrial activation after ventricular

13. 1st Degree AV Block

14. 2nd Degree AV Block Type I
15. 2nd Degree AV Block Type 2
16. 2nd degree AV Block Untypable 2/1
17. Complete (3rd degree) AV Block

18. PVC’S
19. Idioventricular Rhythm (Sinus Arrhythmia and Complete AV Block)
20. Ventricular Tachycardia (with a Sinus Capture)
21. Ventricular Fibrillation
22. Artificial (Electronic) Ventricular Pacer

04/05/05 (JBE)

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 CARDIOLOGY ELECTIVE - ADDITIONAL ARRHYTHMIAS

1. Sinus Arrest

2. Sinus Block

3. Wandering Atrial Pacemaker

4. PACs with Aberrancy

5. PACs non-conducted

6. Atrial Tachycardia

7. Atrial Tachycardia with 2:1 Block

8. Atrial Fibrillation with Aberrantly Conducted Beats

9. Multifocal Atrial Tachycardia

10. Ventricular Escape Beat

11. Ventricular Parasystole

12. Accelerated Ventricular Rhythm

13. Torsade de Pointes

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 2020 04 23

ARRHYTHMIA WORKSHOP INSTRUCTIONS

The Arrhythmia Workshop exercise is comprised of 40 rhythm strips that you are to review on
your own and write down the most likely diagnosis, in your opinion.

1. Review each strip on your own, and write down the most likely diagnosis (some are
controversial).

2. Suggestion: allow several hours over at least 2 evenings so you have time to review the
strips thoughtfully.

3. After you have completed the exercise on your own, you may review your answers with
your colleagues. [Hint: the answer is not the goal, knowledge is].

4. Refer to the course schedule for the date and time the workshop will be reviewed in
class. Be prepared to discuss your most likely diagnosis.

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 ARRHYTHMIA WORKSHOP

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