RIGHT HEART FAILURE

MECHANISM’S, DIAGNOSIS AND MANAGEMENT

DR DANISH GULZAR
During embryonic development, the right ventricle is formed
from the secondary heart field into a crescent-shaped, thin-
walled structure.
It is the most anterior heart chamber, sitting just beneath the
sternum.
Goor and Lillehi (1977) Proposed three part description of RV.
They described the RV as being composed of:
1) the inlet -including the tricuspid valve, chordae-tendineae,
and papillary muscles;
2) the trabeculated free wall and apical myocardium;
3) the outlet -including the infundibulum or conus and the
pulmonary valve.
Structural and functional comparison of RV & LV
 RV CARDIODYNAMICS
RV contraction is sequential and "peristaltic": inlet -› trabecular myocardium -> infundibulum (~ 25-50
ms apart). As RV fails, this normal "peristaltic" movement is lost (i.e., more “LV-like").

Three separate mechanisms of RV contraction: 1) free wall inward movement ("bellows"- like effect), 2)
contraction of longitudinal fibers (shortens long axis TV annulus toward apex), 3) traction of free wall
from septal LV attachments.

Shortening of RV is much greater longitudinally (80%) than radially (20%).

Twisting and rotational movements do not contribute as significantly to RV ejection as compared to LV

(Major mechanism) - disadvantage with increased load
 TORRENT-GUASP HELICAL MODEL
This helical orientation of Fibers in septum provides
Torsional movement that are
transmitted to RV cause
it to have peristaltic contraction.
LV and RV blood ejection primarily occurs via twisting (due to oblique septal fiber orientation)

Ventricular septum longitudinal/twisting motion due to the oblique fiber orientation -(MOST
IMPORTANT TO RV FUNCTION)

RV free wall: transverse motion.

LV CONTRIBUTION TO RV CONTRACTILITY
Pathophysiology of Right Ventricular Failure
The pathophysiological mechanisms of right ventricular failure can be conceptualized as acute or
chronic abnormalities of right ventricular load (preload or afterload) or myocardial function
(contractility [inotropy] and active relaxation [lusitropy]), though in clinical states of right ventricular
failure, these mechanisms frequently coexist .
Mechanical mechanism for right heart failure…
MOLECULAR MECHANISMS FOR RIGHT HEART FAILURE…
 Optimising RV contractility

Lower RV preload
Reduces septal flattening/shift and may improve septal function. (Haddad F et al. Circulation. 2008)
 Determinants of RV function

"RV failure occurs under two general conditions: excessive RV afterload and LV septal dysfunction..
[Link] afterload (impedance)Vascular ResistanceVascular Compliance (blood storage capacity of the vessels)Wave reflections due to blood pulsatility
Inertance of blood during RV ejection

[Link] contractility (systolic function)

[Link] coupling of RV contractility to RV afterload

[Link] constraint/RV-LV diastolic interaction

 RV Function and Acute Afterload

"PVR" = "RV afterload" for clinical care.

However, total RV impedance encompasses all resistive, capacitive, inertial and pulse-reflective properties of the pulmonary
vasculature (e.g., between 1/3 to 1/2 of hydraulic power in main PA is contained in pulsatile components of flow, in turn
dependent primarily on first 5 orders of main PA bifurcations).

•Models of the intact pulmonary vasculature integrating all these passive and dynamic impedance components have yet to be
developed for routine clinical use and thus challenge assessment of RV-PA coupling.
Compliance is independent of resistance in systemic circulation which different in pulmonary circulation
 Measures of intrinsic RV FUNCTION

GOLD STANDARD
Pressure-Volume Relations

Load Independent Measures of Contractility

End-Systolic Elastance (EFs)

Total or 'Lumped' Afterload

Effective Arterial Elastance (ЕA)

Coupling of Right Ventricle to Pulmonary Load

Ratio of elastances (EES/EA)
RV PRESSURE VOLUME LOOP
CONTRACTILITY ON PV LOOPS
END SYSTOLIC ELASTANCE
LUMPED AFTER-LOAD ON PV LOOP
RV-PA COUPLING
 NORMAL RV AND INCRESED LOAD

Ees increases
to match Ea
Ees/Ea is
preserved
RV-PA coupling
is preserved
FAILED RV AND INCREASED LOAD
CHRONICALY LOADED RV RESPONDS ACUTELY TO CHANGES IN AFTERLOAD

RV function is determined by the coupling of RV

contractility to RV afterload
RELATIONSHIP OF PCWP AND LV FUNCTION ON PULMONARY COMPLIANCE AND RV FUNCTION
 EFFECT OF PCWP ON RV PV-LOOP

Elevated PCWP lowers

compliance - PA Pulse pressure
increases.
RV Afterload is higher than you
would predict from PVR alone.
 RV LOOP UNDER HIGH RESISTIVE LOAD

Increases in PVR (resistive load) also lead to a

further decrease in compliance - increase in
pulsatile loading rise in pressure throughout
ejecting including mid to late systolic rise in PA
pressure…
MECHANISM OF PH AND RV DYSFUNCTION IN PATIENTS WITH LHF

Isolated post-capillary PH or Combined post-capillary and pre-

capillary PH (CpcPH).

Pulmonary vascular remodeling of distal arteries/arterioles (and or

veins).

Vasoconstriction due to endothelial dysfunction

Decreased Nitric Oxide (or lack of response to it)
Overproduction of Endothelin (ET-1)
Engorged lymphatics/edema compressing distal arteriolesElevation
in PAWP lower compliance and raise PVR.
Impact of increased PAWP due to both HErEF AND HEpEF on RV afterload
 AT RISK RV

EVERY RV THAT IS COUPLED WITH HEART HAVING HFrEF OR HFpEF.

Underlying heart failure syndrome may impair the RV (free wall) contractility (and
relaxation) directly.
IMPACT OF RV FUNCTION ON SURVIVAL IN PATIENTS WITH LEFT HEART SYNDROME

Ghio S et al. JAm Coll Cardiol. 2001

 LOW PAC vs HIGH PVR impact on RV DYSFUNCTION
Dupont. M et al study circulation 2012
 Agressive LV unloading too worsen RV FUNCTION
LV pre-load reduction leads to not only leftward septal shift (altered geometry), but
also a dramatic reduction in septal function.
EXAMPLE LVAD PATIENTS
1. Increased preload to RV
2. Reduced lv contribution due to septal dysfunction.
3. Impairs normal moblity of heart inside chest walll
 Summery

RV depends on the LV function for a significant portion of its function.

RV function is determined by coupling of RV contractility to afterload.

LHF leads to significant increases in RV afterload

LV pathology puts the RV "at risk
 DIAGNOSIS

Symptoms of right heart failure: dyspnea, early satiety, abdominal fullness, lower-
extremity edema, right-upper-quadrant tenderness, exercise intolerance, fatigue.

Associated conditions: coronary artery disease, left heart failure or valvular disease,
chronic lung disease, venous thrombosis or embolism, connective tissue disease, human
immunodeficiency virus infection.

Social history: tobacco use, illicit drug use, history of illicit or prescribed anorexigen use.

Family history: pulmonary arterial hypertension, left heart failure, sudden cardiac death,
ARVC.
ON EXAMINATION

Elevated jugular venous pressure, right ventricular heave, loud second component

of second heart sound (P2), tricuspid regurgitation murmur, enlarged and pulsatile

liver, hepatojugular reflux, ascites, lower-extremity edema.

Serum biomarker:

Elevated brain natriuretic peptide level

Electrocardiogram:

Right atrial dilatation, right ventricular hypertrophy, right-axis deviation

 ASSESSMENT OF RV FUNCTION

CHALLANGES

[Link] complex geometry (e.g., infundibulum accounts for

25-30% of RV volume),
2) obscuring, heavily trabeculated RV endocardial surface,
3) RV retrosternal position (echocardiography),
4) (sometimes marked) load dependence of virtually all
commonly used RV echocardiographic function indices
MEASUREMENT OF RV FUNCTION AND CONTRACTILITY
 RV STROKE WORK INDEX
IMPORTANT MEASURED PARAMETER FOR RV SYSTOLIC FUNCTION.

RVSWI (mmHg x ml/m2)= {[mean PAP (mmHg) - CVP (mmHg)] x SV

(mi)] / BSA (m2)= [mean PAP (mmHg) - CVP (mmHg)] x [CI (I/m/m2) /
HR
RVSWI < 300 mmlg x ml/m2 independently predicts risk of RV
failure.
ECHOCARDIOGRAPHIC MEASURES
 ECCENTRICITY INDEX

Leftward septal displacement is quantified by means of the eccentricity index, the ratio
of the anteroposterior dimension (D1) to the septolateral dimension (D2). If D1 is equal to
D2, there is no septal displacement and no evidence of right ventricular overload (Panel
B, left image). Two examples of right ventricular overload, in which D1 exceeds D2, are
shown, one indicating mild septal displacement and the other indicating severe
displacement

Flattening of the inter- ventricular septum during diastole indicates volume overload, whereas
flattening in systole is seen in pressure overload states.
 INVASIVE HEMODYANAMIC ASSESSMENT

Integration of hemodynamic variables yields more specific insight into RV function.

RAP/LAP > 0.63 (and more strongly RAP/LAP > 1) suggests predominant right heart
dysfunction and/or failure - "Kormos index" in predicting RV failure.

Reduced stroke volume index + elevated RAP more specific for RV dysfunction
and/or failure that reduced stroke volume index alone.

Exercise hemodynamic can be helpful:

1) unmask RV physiologic reserve via the relative change in RAP/LAP ratio from
rest to exercise to determine physiologic reserve and

2) probe malleability of PVR which should fall with exercise (e.g., Group 2 PH -
sharp increase in PAP, sharp increase in RAP and RAP/LAP ratio, elevated exercise
PVR).
HEMODYANAMIC PARAMETERS ASSOCIATED WITH RV FUNCTION AND THRESHOLDS FOR CLINICAL EVENTS

ACC/AHA KAPUR et al (2017)

 CPET
Reduction in peak V02 per se is not specific for RV dysfunction.
VE/VCO2 > 34 tend to have echocardiographic larger RVs, greater functional TR, lower
RVFAC, lower TAPSE with inverse correlation between TAPSE.
Exaggerated rise in VE/CO2 may be signature of RV dysfunction in Group II PH.
 TAPSE:PASP ratio
TAPSE:PASP ratio, which has been shown to be at least moderately correlated with the reference
standard of right ven- tricular–pulmonary arterial coupling which can be calculated by echo.
TAPSE/PASP CORRELLATION WITH MORTALITY IN HEART FAILURE
 CARDIAC MRI
GOLD STANDARD FOR MEASUERING RVEF, STOKE VOLUME, RV SIZE AND
MASS.

Another advantage of cardiac MRI over echocardiography is tissue characterization.

Contrast-enhanced cardiac MRI allows quantification of right ventricular septal and free-wall
fibrosis, which is characterized as either replacement ([Link] scar) or interstitial
(dynamic and modifiable).
Assessment for right ventricular free-wall morphologic features, motion, and fibro-fatty
replacement aids the diagnostic evaluation in patients with suspected ARVC.
Also provides information about the shunts leading to RV volume overload.
 TREATMENT OF RV FAILURE

"Pharmacologic and mechanical interventions targeting isolated acute and chronic RVF have not been investigated. Specific therapies
promoting stabilization and recovery of RV function are lacking. (AHA 2018)
ISOLATED RHF TREATMEN( Hadad et al circulation 2008)
IMPORTANCE OF PRELOAD
Patients who are in shock because of an acute increase in right ventricular afterload (due
to acute pulmonary embolism) or an acute reduction in contractility (due to a right
ventricular infarct) may benefit from volume loading to augment right ventricular stroke
volume and increase transpulmonary blood transit.
However, all patients with acute right ventricular failure require aggressive volume
loading is incorrect and may be harmful.
Patients with right ventricular infarction have a variable response to volume loading.
Patients who initially have relative volume depletion and right ventricular infarction are
likely to benefit from volume loading.
However, volume loading in patients with normal intravascular volume may compromise
cardiac output through increased pericardial constraint and a decrease in the left
ventricular transmural filling pressure.
Invasive hemodynamic monitoring may be beneficial to assess the response to preload
alteration in such patients.

Those with chronic right ventricular failure benefit from volume removal and
decongestion.

Normalization of the preload can reduce tricuspid valve annular dilatation and tricuspid
regurgitation, right ventricular wall stress, and septal deformation.

Volume reduction is most commonly accomplished with intra- venous diuretics, though
ultrafiltration may be necessary in some cases.
Afterload Reduction
For patients with elevated right ventricular after load and right
ventricular failure, reducing afterload is beneficial.

Cronically elevated right ventricular afterload and right ventricular

failure, afterload reduction can also be therapeutic.

In patients with pulmonary arterial hypertension, clinical trials have

established the long-term benefit of pharmacotherapy targeted toward
afterload reduction.

Pharmacologic pulmonary vasodilator therapy currently focuses on

three pathways: endothelin antagonists, augmented signaling in the
prostacyclin pathway, and the nitric oxide pathway.
For pulmonary hypertension due to lung disease ILD, a recent
clinical trial showed improved exercise capacity in patients treated
with inhaled treprostinil.

In patients with pulmonary hypertension due to chronic

thromboembolic disease, surgical pulmonary endarterectomy or (in
inoperable patients) percutaneous balloon pulmonary angioplasty
should be considered, alongside anticoagulation therapy.

Adjunctive pharmacologic therapies aimed at afterload reduction

are also used.
For patients with acute right ventricular failure and chronically elevated
precapillary right ventricular afterload, inhaled pulmonary vasodilators
(nitric oxide or epoprostenol) can provide immediate improvement.

For intractable right ventricular failure in this clinical context, lung or heart–
lung transplantation may be considered in selected patients.

Direct pulmonary vasodilators have largely not proved beneficial in patients

with pulmonary hypertension due to left heart disease, may not provide the
desired reduction in afterload, and may even be harmful.
Reduction of left atrial pressure administration of systemic vasodilators
such as nitroprusside, implantation of ventricular assist devices, and heart
transplantation may both increase pulmonary vascular compliance and
reduce pulmonary vascular resistance.

Volume removal in patients who have hypervolemia with right ventricular

failure and left heart disease will improve right ventricular afterload, as well
as preload.

High prevalence of sleep-disordered breathing among patients with

pulmonary hypertension (including pulmonary arterial hypertension), both
diagnosis and treatment are important, with opportunities to alleviate
associated hypoxemia, reduce afterload, and perhaps limit right ventricular
ischemia
Augmentation of Contractility

Initial efforts should focus on addressing the underlying cause of disease while
augmenting right ventricular contractility to support cardiac output.

Urgent reperfusion therapy is warranted in patients with acute right ventricular

myocardial infarction.

For patients with certain types of inflammatory heart disease and right ventricular
failure, immunosuppression may be beneficial.
While the underlying cause is being determined, inotropic or vasodilator support
may be necessary to maintain cardiac output.
Dobutamine increases cardiac output and stroke volume in patients with right

ventricular myocardial infarction and those with pulmonary hypertension.

Milrinone may be used, with careful attention to avoid excess systemic vasodilatation and
hypotension. The latter may lead to right ventricular ischemia and reduction in left ventricular
contractility.

The evidence for using digoxin in patients with right ventricular failure is mixed.

For patients with acutely decompensated right ventricular failure and shock who do not have a
response to pharmacologic therapy, there has been a recent proliferation of temporary mechanical
support devices to help augment blood flow from the systemic to pulmonary circulation, but should
be avoided in patients with severe PAH

Extracorporeal membrane oxygenation may be used in severe cases.

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