Acute Right Ventricular Infarction:

Insights for the Interventional Era

James A. Goldstein, MD, FACC
Abstract: Acute right ventricular infarction is associated
with higher in-hospital morbidity and mortality related to
life-threatening hemodynamic compromise and arrhyth-
mias during acute occlusion and abruptly with reperfusion,
complications which have implications for interventional
management. Acute right coronary artery occlusion proxi-
mal to the right ventricular (RV) branches results in de-
pressed RV systolic function, leading to diminished trans-
pulmonary delivery of left ventricular preload and resulting
in low-output hypotension. Under these conditions, RV
pressure generation and output are dependent on left ven-
tricularseptal contraction via paradoxical septal motion.
With culprit lesions distal to the right atrial (RA) branches,
augmented RA contractility enhances RV performance and
cardiac output, whereas proximal occlusions induce RA
ischemia, which exacerbates hemodynamic compromise.
Hypotension may respond to volume resuscitation and res-
toration of a physiologic rhythm. Refractory cases usually
respond to parenteral inotropes, though in some cases
mechanical support is required. The right ventricle is rela-
tively resistant to infarction and usually recovers even after
prolonged occlusion. Acute percutaneous mechanical reper-
fusion enhances recovery of RV performance and improves
the clinical course and survival of patients with right ven-
tricular infarction. (Curr Probl Cardiol 2012;37:533-557.)
T
hus it may be said that the purpose of the right ventricle is to pump
blood to the lungs, not to nourish them.
Sir William Harvey
De Motu Cordis 1628
2012 James Goldstein. Published by
Elsevier Inc. All rights reserved.
Curr Probl Cardiol 2012;37:533-557.
0146-2806/$ see front matter
http://dx.doi.org/10.1016/j.cpcardiol.2012.05.001
Curr Probl Cardiol, December 2012 533
Nearly 50% of patients with acute ST elevation inferior myocardial
infarction (IMI) suffer concomitant right ventricular infarction (RVI),
which is associated with higher in-hospital morbidity and mortality
related to profound hemodynamic and electrophysiologic complica-
tions.
1-6
Given that the vast majority of patients with IMI now undergo
emergency percutaneous revascularization, their care is typically in the
hands of interventional cardiologists. Over the past decade, there have
been signicant advances in the pathophysiology and therapy of RVI that
are relevant to the acute management of patients undergoing primary
percutaneous coronary intervention. This article reviews the pathophysi-
ology, hemodynamics, natural history, and management of patients with
IMI complicated by RVI, highlighting key areas in which recent advances
may impact catheterization laboratory management of these acutely ill
patients, including:
1. The differences between the right and left ventricles with respect to
structure, function, and metabolism that inuence their disparate
responses to ischemia and reperfusion.
2. The relationship between the site of right coronary artery (RCA)
occlusion and the presence and magnitude of right heart ischemia and
intraprocedural complications.
3. The pathophysiologic mechanisms leading to hemodynamic compro-
mise and their relevance to pharmacologic and mechanical interven-
tions.
4. Bradyarrhythmias and tachyarrhythmias complicating management
during acute occlusion and reperfusion.
5. The concept that right ventricular (RV) infarction is actually a
misnomer, for even severe acute ischemic RV dysfunction is nearly
always reversible.
6. The benets of mechanical reperfusion therapy on hemodynamics and
clinical outcome, even after prolonged occlusion and in patients with
severe shock.
Background
Based on early experiments of RV performance, it was felt for many
years that RV contraction was unimportant in the circulation and that,
despite loss of RV contraction, pulmonary ow could be generated by a
passive gradient from a distended venous system and active right atrial
(RA) contraction.
7
However, recognition of the profound hemodynamic
effects of RV systolic dysfunction became evident during the 1970s with
the description of severe RVI, resulting in severe right heart failure, clear
534 Curr Probl Cardiol, December 2012
lungs, and low-output hypotension despite intact global left ventricular
(LV) systolic function.
6
Nearly 50% of patients with acute ST elevation
IMI manifest RV involvement by noninvasive studies;
1,4
however, only
half of those with any evidence of RVI develop hemodynamic compli-
cations. Although the magnitude of hemodynamic derangements is
related to the extent of RV free wall (FW) (RVFW) contraction
abnormalities,
1
some patients tolerate severe RV systolic dysfunction
without compromise, whereas others develop life-threatening low output,
thereby emphasizing that additional factors modulate the clinical expres-
sion of RVI. Importantly, the term RV infarction is to an extent a
misnomer. For, in most cases, acute RV ischemic dysfunction appears to
represent viable myocardium, which recovers over time, especially after
successful reperfusion and even after prolonged occlusion.
8-10
Robert O. Bonow: Right ventricular infarction develops very frequently in
patients with inferior ST-segment elevation MI, but often escapes detection.
Recognition of its clinical manifestations, complications, and management of
is essential for optimal patient outcomes.
RV Mechanics and Oxygen Supply and Demand
The right and left ventricles differ markedly in their anatomy, mechan-
ics, loading conditions, and metabolism; therefore, it should not be
surprising that they have strikingly different oxygen supply and demand
characteristics
11-13
and thus manifest disparate responses to ischemic
insults. The left ventricle is a thick-walled pressure pump. In contrast, the
pyramidal-shaped right ventricle with its thin crescentic FW is designed
as a volume pump, ejecting into the lower resistance pulmonary circula-
tion. RV systolic pressure and ow are generated by RVFW shortening
and contraction toward the septum from apex to outow tract.
12
The
septum is an integral architectural and mechanical component of the RV
chamber, and, even under physiologic conditions, LV-septal contraction
contributes to RV performance. The right ventricle has a more favorable
oxygen supply demand prole than the left ventricle. RV oxygen demand
is lower owing to lesser myocardial mass, preload, and afterload.
11,14
RV
perfusion also is more favorable because of dual anatomic supply system
from left coronary branches. Also, the RVFW is thinner, develops lower
systolic intramyocardial pressure, and faces less diastolic intracavitary
pressure, and lower coronary resistance favors acute collateral develop-
ment to the RCA.
13
In summary, lower RV oxygen demands represent the
most important factor in protecting its myocardium from irreversible
Curr Probl Cardiol, December 2012 535
ischemic damage after coronary occlusion. The ability to extract more
oxygen during times of stress in addition to both systolic and diastolic
coronary ow provides a greater reserve of nutrients and oxygen during
ischemia. All of these factors may work in concert to prevent irreversible
ischemic damage to the right ventricle.
Patterns of Coronary Compromise Resulting in RVI
Signicant RVI nearly always occurs in association with acute trans-
mural inferiorposterior LV myocardial infarction (MI), and the RCA is
always the culprit vessel,
15,16
typically a proximal occlusion compromis-
ing ow to one or more of the major RV branches (Figs 1 and 2). In
contrast, distal RCA occlusions or circumex culprits that spare RV
branch perfusion rarely compromise RV performance. Occasionally,
isolated RVI may develop from occlusion of a nondominant RCA or
selective compromise of RV branches during percutaneous interventions.
Fig 1. Patient with proximal right coronary artery (RCA; right panel, arrow) compromising the
right ventricular (RV) branches and resulting in severe right ventricular infarction (RVI), indicated
on echo as severe RV free wall (RVFW) dysfunction and depressed global RV performance at
end systole and marked RV dilation at end diastole. RA right atrium. (Color version of gure
is available online.)
536 Curr Probl Cardiol, December 2012
Robert O. Bonow: The distinction between proximal and distal occlusion of
the right coronary artery is important with respect to likelihood of severe RV
dysfunction and its consequences.
At necropsy, RVI inscribes a tripartite signature consisting of LV
inferiorposterior wall, septal, and posterior RVFW necrosis contiguous
with the septum.
17
However, it is important to emphasize that these
autopsy patterns do not reect the vast majority of patients who survive
acute RVI, for even in the absence of reperfusion of the infarct-related
artery, most patients with severe ischemic RV dysfunction manifest
spontaneous early hemodynamic improvement and later recovery of RV
function.
8-10
In fact, chronic right heart failure attributable to RVI is rare.
Fig 2. Patient with proximal RCA occlusion (arrow) complicated by third-degree atrioventricular
block.
16
(Color version of gure is available online.)
Curr Probl Cardiol, December 2012 537
Thus, the term RV infarction is to an extent a misnomer, as in most
cases, acute RV ischemic dysfunction appears to represent predominantly
viable myocardium. These responses are in marked contrast to the effects
of ischemia and reperfusion on the left ventricle.
18-20
Effects of Ischemia on RV Systolic and
Diastolic Function
Proximal RCA occlusion compromises RVFW perfusion, resulting in
RVFW dyskinesis and depressed global RV performance reected in the
RV waveform by a sluggish, depressed, and systolic waveform (Figs 3
Fig 3. Hemodynamic recordings from a patient with right atrial pressure W pattern, timed to
electrocardiography (A) and RV pressures (B, C). Peaks of W are formed by prominent A waves
with associated sharp X systolic descent, followed by a comparatively blunted Y descent.
Peak RV systolic pressure is depressed, RV relaxation is prolonged, and there is a dip and rapid
rise in RV diastolic pressure.
21
538 Curr Probl Cardiol, December 2012
and 4).
8,15,21-23
RV systolic dysfunction diminishes transpulmonary
delivery of LV preload, leading to decreased cardiac output despite intact
LV contractility. Biventricular diastolic dysfunction contributes to hemo-
dynamic compromise.
21-25
The ischemic right ventricle is stiff and dilated
early in diastole, which impedes inow leading to rapid diastolic pressure
elevation.
Septal-mediated diastolic ventricular interactions intensied by an
acutely crowded pericardium underly the unique hemodynamic signature
of severe RVI.
1,21-26
The right and left ventricles are composed of the
same interlacing muscle bers that encircle the heart, the greater disten-
sibility of the right ventricle reects a necessary functional difference of
2 pumps in series having equal stroke outputs but coupled to markedly
different vascular loads. Diastolic ventricular interaction is present on a
moment-to-moment and beat-to-beat basis, especially during respiration;
however, ventricular interaction is most apparent with acute changes in
ventricular volume. Acute RV dilatation and elevated diastolic pressure
shift the interventricular septum toward the volume-deprived LV, further
impairing LV compliance and lling. Abrupt RV dilatation within the
noncompliant pericardium elevates intrapericardial pressure, the resultant
constraint further intensifying septal-mediated diastolic ventricular inter-
Fig 4. Right atrial M pressure pattern timed to electrocardiogram (A) and RV pressure (B). M
pattern comprises a depressed A wave, X descent before a small C wave, a prominent X
descent, a small V wave, and a blunted Y descent. Peak RV systolic pressure is depressed and
bid (arrow) with delayed relaxation and an elevated end-diastolic pressure. (All pressures are
measured in mm Hg).
21
Curr Probl Cardiol, December 2012 539
actions and thereby impairing both RV and LV compliance and lling
(Fig 5). These effects contribute to the pattern of equalized diastolic
pressures and RV dip-and-plateau characteristic of RVI.
21-25
Determinants of RV Performance in Severe RVI
Importance of Systolic Ventricular Interactions
Despite the absence of RVFW motion, an active albeit depressed RV
systolic waveform is generated by systolic interactions mediated by
primary septal contraction and through mechanical displacement of the
septum into the RV cavity associated with paradoxical septal motion
(Figs 1 and 6).
8,15,23-25
In the left ventricle, acute ischemia results in
regional dyskinesis; such dyssynergic segments are stretched in early
isovolumic systole by neighboring contracting segments through regional
intraventricular interactions that dissipate the functional work of these
neighboring regions.
27
The ischemic dyskinetic RVFW behaves similarly
and must be stretched to the maximal extent of its systolic lengthening
through interventricular interactions before providing a stable buttress on
which actively contracting segments can generate effective stroke work,
thereby impose a mechanical disadvantage that reduce contributions to
cardiac performance.
11,23-25
The compensatory contributions of LV-
Fig 5. Hemodynamic recordings from experimental animal study demonstrating that RVI induces
elevated and equalized diastolic lling pressures, a pattern that resolves after pericardiot-
omy.
26
(Color version of gure is available online.)
540 Curr Probl Cardiol, December 2012
septal contraction are emphasized by the deleterious effects of LV-septal
dysfunction, which exacerbates hemodynamic compromise associated
with RVI.
25
In contrast, inotropic stimulation enhances LV-septal con-
traction and thereby augments RV performance through augmented
compensatory systolic interactions.
Compensatory Role of Augmented RA Contraction
The hemodynamic benets of augmented atrial contraction to perfor-
mance of the ischemic LV are well documented.
28
Similarly, augmented
RA booster pump transport is an important compensatory mechanism that
optimizes RV performance and cardiac output.
21,23,24
When RVI devel-
Fig 6. Diagram of diastolic and systolic ventricular interactions mediated by the septum. Acute
RV dysfunction (bottom right panel) shifts the septum toward the preload-deprived left ventricular
(LV). In systole (bottom right panel), the septum bulges paradoxically into the RV, contributing
to RV pressure generation. (Color version of gure is available online.)
Curr Probl Cardiol, December 2012 541
ops from occlusions compromising RV, but sparing RA branches, RV
diastolic dysfunction imposes increased preload and afterload on the right
atrium, resulting in enhanced RA contractility that augments RV lling
and performance. This is reected in the RA waveform as a W pattern
characterized by a rapid upstroke and increased peak A wave amplitude,
sharp X descent reecting enhanced atrial relaxation, and blunted Y
descent owing to pandiastolic RV dysfunction (Fig 3).
Deleterious Impact of RA Ischemia
Conversely, more proximal RCA occlusions compromising atrial as
well as RV branches result in ischemic depression of atrial function,
which compromises RV performance and cardiac output.
21,23,24
RA
ischemia manifests hemodynamically as more severely elevated mean RA
pressure and inscribes an M pattern in the RA waveform characterized
by depressed A wave and X descent, as well as blunted Y descent (Fig 4).
Ischemic atrial involvement is not rare, with autopsy studies documenting
atrial infarction in up to 20% of cases of ventricular infarction, with RA
involvement 5 times commoner than left.
29,30
Under conditions of acute
RV dysfunction, loss of augmented RA transport because of ischemic
depression of atrial contractility or atrioventricular (AV) dyssynchrony
precipitates more severe hemodynamic compromise.
21,23,24
RA dysfunc-
tion decreases RV lling, which impairs global RV systolic performance,
thereby resulting in further decrements in LV preload and cardiac output.
Impaired RA contraction diminishes atrial relaxation; thus, RA ischemia
impedes venous return and right heart lling owing to loss of atrial
suction associated with atrial relaxation during the X descent.
Natural History of Ischemic RV Dysfunction
Although RVI may result in profound acute hemodynamic effects,
arrhythmias and higher in-hospital mortality, many patients spontane-
ously improve within 3-10 days regardless of the patency status of the
infarct-related artery.
8
Furthermore, global RV performance typically
recovers, with normalization within 3-12 months.
9,10
Moreover, chronic
unilateral right heart failure secondary to RVI is rare. This favorable
natural history of RV performance is in marked contrast to the effects of
coronary occlusion on segmental and global LV function.
18-20
Observa-
tions from experimental animal studies conrm spontaneous recovery of
RV function despite chronic RCA occlusion attributable to the more
favorable oxygen supply demand characteristics of the RV in general and
the benecial effects of collaterals in particular.
31,32
Similarly, in patients
with chronic proximal RCA occlusion, RV function is typically main-
542 Curr Probl Cardiol, December 2012
tained at rest and augments appropriately during stress.
10
The relative
resistance of the RVFW to infarction is undoubtedly attributable to more
favorable oxygen supply demand characteristics. Preinfarction angina
appears to reduce the risk of developing RVI, possibly because of
preconditioning.
13
Effects of Reperfusion on Ischemic RV Dysfunction
Although RV function may recover despite persistent RCA occlusion,
acute RV ischemia contributes to early morbidity and mortality. Further-
more, spontaneous recovery of RV contractile function and hemodynam-
ics may be slow. The benecial effects of successful reperfusion in
patients with predominant LV infarction are well documented. Observa-
tions in experimental animals
32
and in humans
8,33-35
now demonstrate the
benecial effects of reperfusion on recovery of RV performance. In
patients, successful mechanical reperfusion of the RCA including the
major RV branches leads to immediate improvement in and later
complete recovery of RVFW function and global RV performance (Fig
7). Reperfusion-mediated recovery of RV performance is associated with
excellent clinical outcome (Fig 8). In contrast, failure to restore ow to
the major RV branches was associated with lack of recovery of RV
performance and refractory hemodynamic compromise leading to high
in-hospital mortality, even if ow was restored in the main RCA.
Findings now also demonstrate that successful mechanical reperfusion
leads to superior late survival of patients with shock because of predom-
inant RVI versus those with LV shock.
35
Although evidence suggests that patients with IMI benet from timely
thrombolytic reperfusion, the specic short- and long-term responses of
those with RVI have not been adequately evaluated. Some studies
suggested that RV function improves after brinolytic therapy only in
patients in whom RCA patency is achieved,
36-38
whereas others report
little benet.
39,40
More recent prospective reports demonstrate that
successful thrombolysis imparts survival benet in those with RV
involvement and that failure to restore infarct-related artery patency is
associated with persistent RV dysfunction and increased mortality.
40
Unfortunately, patients with RVI appear to be particularly resistant to
brinolytic recanalization owing to proximal RCA occlusion with exten-
sive clot burden, which together with impaired coronary delivery of
brinolytic agents is attributable to hypotension.
40
There also appears to
be a higher incidence of reocclusion after thrombolysis of the RCA.
It is important to consider separately RVI in the elderly patients. Early
reports suggested elderly patients with RVI suffer 50% in-hospital
Curr Probl Cardiol, December 2012 543
mortality and that hemodynamic compromise in such cases is irreversible.
However, recent studies now document the majority of elderly RVI
patients undergoing successful mechanical reperfusion survive, including
those with hemodynamic compromise.
34
Although RVI typically presents with relatively preserved left ventric-
ular ejection fraction, such patients virtually always suffer LV inferior
posterior septal infarction. Given that systolic performance of the isch-
emic right ventricle is dependent on LV-septal contractile contributions,
it would not be surprising that concomitant-depressed LV function would
further exacerbate hemodynamic compromise in patients with acute RVI.
Although there are little data addressing the subset of RVI patients with
global LV dysfunction, 1 recent report demonstrates that the combination
of extensive RV myocardial infarction and depressed left ventricular
ejection fraction is associated with poor outcomes.
5
It might be expected
to occur either from acute occlusion of a wrap-around dominant RCA,
Fig 7. Echocardiographic images from a patient with acute inferior myocardial infarction and
RV ischemia undergoing successful angioplasty. End-diastolic and end-systolic images obtained
at baseline show severe RV dilatation with reduced LV diastolic size. At end systole, there was
RVFW dyskinesis (arrows), intact LV function, and compensatory paradoxical septal motion.
One hour after angioplasty, there was striking recovery of RVFW contraction (arrows), resulting
in marked improvement in global RV performance and markedly RV size and increased LV
preload. At 1 day, there was further improvement in RV function (arrows), which at 1 month was
normal. RV denotes right ventricle, and LV denotes left ventricle.
8
544 Curr Probl Cardiol, December 2012
or in those with acute IMI-RVI but previous anteriorseptal MI. De-
pressed LV global function would be precited to exacerbate hemody-
namic compromise both because of direct loss of LV stroke work as well
as loss of compensatory LV-septal contractile contributions to RV
systolic performance.
Rhythm Disorders and Reexes
Associated with RVI
Bradyarrhythmias and Hypotension
High-grade AV block and bradycardia hypotension without AV block
commonly complicate IMI and have been attributed predominantly to the
effects of AV nodal ischemia and cardioinhibitory (Bezold-Jarisch)
reexes arising from stimulation of vagal afferents in the ischemic LV
inferoposterior wall.
41-44
Patients with acute RVI are at increased risk for
both high-grade AV block and bradycardia hypotension without AV
block.
2,44
Recent ndings now document that during acute coronary
occlusion, bradycardia hypotension and AV block are far more common
in patients with proximal RCA lesions (Fig 2) inducing RV and LV
inferiorposterior ischemia, compared with more distal occlusions com-
promising LV perfusion but sparing the RV branches.
16
These observa-
Fig 8. Bar graphs demonstrating benets of successful reperfusion versus reperfusion failure with
respect to reduced arrhythmias, sustained hypotension, and in-hospital survival.
8
(Color version
of gure is available online.)
Curr Probl Cardiol, December 2012 545
tions suggest that the ischemic right heart may elicit cardioinhibitory-
vasodilator reexes. In patients with IMI, whose rhythm and blood
pressure were stable during occlusion, similar bradycardic-hypotensive
reexes may be elicited during reperfusion
16,45
and also appear to be
more common with proximal lesions (Fig 9).
Robert O. Bonow: The predisposition to bradycardiac and atrioventricular
block in patients with right ventricular infarction has important implications
regarding use of beta blockers acutely in the management of inferior MI.
Fig 9. Patient with proximal RCA (left panel, arrow) compromising the RV branches (right panel,
solid arrow) as well as the LV and atrioventricular nodal branches (right panel, open arrow),
who developed profound reperfusion-induced bradycardia-hypotension. During occlusion,
there was sinus rhythm with normal blood pressure. Reperfusion by primary percutaneous
transluminal coronary angioplasty resulted in abrupt but transient sinus bradycardia with
profound hypotension.
16
(Color version of gure is available online.)
546 Curr Probl Cardiol, December 2012
Ventricular Arrhythmias
Patients with RVI are prone to malignant ventricular arrhythmias,
5,46
which should not be unexpected given that the ischemic RV is often
massively dilated.
46
Autonomic denervation in the peri-infarct area may
also play a role.
47
In patients with RVI, ventricular tachyarrhythmias may
develop in a trimodal pattern, either during acute occlusion, abruptly with
reperfusion, or later.
46
However, successful mechanical reperfusion
dramatically reduces the incidence of malignant ventricular arrhyth-
mias,
8,46
presumably through improvement in RV function, which lessens
late ventricular arrhythmias. Occasionally, RVI may be complicated by
recurrent malignant arrhythmias and in some cases intractable electrical
storm (Fig 10), possibly because of sustained severe RV dilatation.
46
Mechanical Complications Associated with RVI
Patients with acute RVI may suffer additional mechanical complica-
tions of acute infarction that may compound hemodynamic compromise
and confound the clinical-hemodynamic picture. Ventricular septal rup-
ture is a particularly disastrous complication, adding substantial overload
stress to the ischemic RV, precipitating pulmonary edema, elevating
pulmonary pressures and resistance, and exacerbating low output.
48
Fig 10. Patient with acute RVI who developed intractable ventricular arrhythmias 36 hours after
otherwise successful mechanical reperfusion. The patient had sustained marked RV dilatation
and dysfunction.
Curr Probl Cardiol, December 2012 547
Surgical repair is imperative, but may be technically difcult owing to
extensive necrosis involving the LV inferiorposterior FW, septum, and
apex. Catheter closure of such defects may be possible. Severe right heart
dilatation and diastolic pressure elevation associated with RVI may
stretch open a patent foramen ovale, precipitating acute right-to-left
shunting manifest as systemic hypoxemia or paradoxical emboli.
49
Although patent foramen ovale complications typically abate after suc-
cessful mechanical reperfusions, as right heart pressures diminish with
recovery of RV performance, rarely some may require percutaneous
closure.
50
Severe tricuspid regurgitation may also complicate RVI,
developing as a result of primary papillary muscle ischemic dysfunction
or rupture as well as secondary functional regurgitation attributable to
severe RV and tricuspid valve annular dilatation.
51
Clinical Presentations and Evaluation
RVI is often silent because only 25% of patients develop clinically
evident hemodynamic manifestations.
1
Patients with severe RVI but
preserved global LV function may be hemodynamically compensated,
manifesting by elevated jugular venous pressure but clear lungs, with
normal systemic arterial pressure and intact perfusion. When RVI leads to
more severe hemodynamic compromise, systemic hypotension and hy-
poperfusion result. Patients with IMI may initially present without
evidence of hemodynamic compromise, but subsequently develop hypo-
tension precipitated by preload reduction attributable to nitroglycerin
52
or
associated with bradyarrhythmias.
16
When RVI develops in the setting of
global LV dysfunction, the picture may be dominated by low output and
pulmonary congestion, with right heart failure.
Noninvasive and Hemodynamic Evaluation
Although ST-segment elevation and loss of R wave in the right-sided
electrocardiography leads (V
3R
and V
4R
) are sensitive indicators of the
presence of RVI,
53,54
they are neither predictive of the magnitude of RV
dysfunction nor its hemodynamic impact. Echocardiography is the most
effective tool for delineation of the presence and severity of RV dilatation
and depression of global RV performance. Echo also delineates the extent
of reversed septal curvature, which conrms the presence of signicant
adverse diastolic interactions, the degree of paradoxical septal motion
indicative of compensatory systolic interactions, and the presence of
severe RA enlargement, which may indicate concomitant ischemic RA
dysfunction and/or tricuspid regurgitation.
548 Curr Probl Cardiol, December 2012
Invasive hemodynamic assessment of the extent and severity of right
heart ischemic involvement has been extensively discussed.
Robert O. Bonow: Echocardiography has an essential role in the manage-
ment of patients with suspected right ventricular infarction.
Differential Diagnosis of RVI
Important clinical entities to consider in patients who present with acute
low-output hypotension, clear lungs, and disproportionate right heart
failure include cardiac tamponade, acute pulmonary embolism, severe
pulmonary hypertension, right heart mass obstruction, and acute severe
tricuspid regurgitation; entities, including constrictive pericarditis or
restrictive cardiomyopathy, present similar picture but are not acute
processes (Table 1). The general clinical presentation of chest pain with
acute IMI, together with echocardiographic documentation of RV dilata-
tion and dysfunction, effectively exclude tamponade, constriction, and
restriction. Acute massive pulmonary embolism may also mimic severe
RVI, and because the unprepared right ventricle cannot acutely generate
elevated RV systolic pressures (50-55 mm Hg), severe pulmonary
hypertension may be absent. In such cases, absence of inferior LV MI by
electrocardiography and echocardiography points to embolism, easily
conrmed by computed tomography or invasive angiography. Severe
pulmonary hypertension with RV decompensation may mimic severe
RVI, but delineation of markedly elevated posteroanterior systolic pres-
sures by Doppler or invasive hemodynamic monitoring excludes RVI, in
which RV pressure generation is depressed. Acute primary tricuspid
regurgitation should be evident by echocardiography, typically because of
infective endocarditis with obvious vegetations.
TABLE 1. Differential diagnosis of hypotension with disproportionate right heart failure
Right ventricular infarction
Cardiac tamponade
Acute pulmonary embolus
Acute tricuspid regurgitation
Pulmonary hypertension with RV failure
Acute MI with LV failure
Right heart mass obstruction
Constriction/restriction
RV, right ventricular; LV, left ventricular; MI, myocardial infarction.
Curr Probl Cardiol, December 2012 549
Therapy
Therapeutic options for management of right heart ischemia (Table 2)
follow directly from the pathophysiology discussed. Treatment modalities
include (1) restoration of physiologic rhythm, (2) optimization of ven-
tricular preload, (3) optimization of oxygen supply and demand, (4)
parenteral inotropic support for persistent hemodynamic compromise, (5)
reperfusion, and (6) mechanical support with intra-aortic balloon coun-
terpulsation and RV assist devices.
Physiologic Rhythm
Patients with RVI are particularly prone to bradyarrhythmias. The
depressed ischemic right ventricle has a relatively xed stroke volume, as
does the preload-deprived left ventricle. Therefore, biventricular output is
exquisitely heart rate dependent, and bradycardia even in the absence of
AV dyssynchrony may be deleterious to patients with RVI. For similar
reasons, chronotropic competence is critical in patients with RVI.
However, not only are such patients notoriously prone to reex-mediated
frank bradycardia, they often manifest a relative inability to increase sinus
rate in response to low output owing to excess vagal tone, ischemia, or
pharmacologic agents. Given that the ischemic right ventricle is depen-
dent on atrial transport, the loss of RA contraction because of AV
dyssynchrony further exacerbates difculties with RV lling and contrib-
utes to hemodynamic compromise.
8,21,23
Although atropine may restore
physiologic rhythm in some patients, temporary pacing is often required.
Although ventricular pacing alone may sufce, especially if the bradyar-
rhythmias are intermittent, some patients require AV sequential pacing.
55
However, transvenous pacing can be difcult because of issues with
ventricular sensing, presumably related to diminished generation of
endomyocardial potentials in the ischemic right ventricle. Manipulating
catheters within the dilated ischemic RV may also induce ventricular
TABLE 2. Treatment strategies for right ventricular infarction
Optimize oxygen supply demand
Establish physiologic rhythm
Optimize preload
Inotropes for persistent low-output hypotension
Mechanical support for refractory hypotension
Intra-aortic balloon pump
Right ventricular assist device
Reperfusion: primary mechanical
550 Curr Probl Cardiol, December 2012
arrhythmias.
46
Intravenous aminophylline may restore sinus rhythm in the
adverse effects of some patients with atropine-resistant AV block, a
response likely reecting reversal of ischemia-induced adenosine elabo-
ration.
56,57
Optimization of Preload
In patients with RVI, the dilated noncompliant right ventricle is
exquisitely preload dependent, as is the left ventricle, which is stiff but
preload deprived. Therefore, any factor that reduces ventricular preload
tends to be detrimental. Accordingly, vasodilators and diuretics are
contraindicated. Although experimental animal studies of RVI demon-
strate hemodynamic benet from volume loading,
26
clinical studies have
reported variable responses to volume challenge.
58-60
These conicting
results may reect a spectrum of initial volume status in patients with
acute RVI, with those patients who are relatively volume depleted
beneting, and those who are more replete manifesting a at response to
uid resuscitation. Nevertheless, an initial volume challenge is appropri-
ate for patients manifesting low output without pulmonary congestion,
particularly if the estimated central venous pressure is 15 mm Hg. For
those unresponsive to an initial trail of uids, determination of lling
pressures and subsequent hemodynamically monitored volume challenge
may be appropriate. Caution should be exercised to avoid excessive
volume administration above and beyond that documented to augment
output, as the right heart chambers may operate on a descending limb
of the Starling curve, resulting in further depression of RV pump
performance as well as inducing severe systemic venous congestion.
Abnormalities of volume retention and impaired diuresis may be related
in part to impaired responses of atrial natriuretic factor.
61
Robert O. Bonow: This discussion underscores the importance of judicious
use of volume expansion in patients with right ventricular infarction.
Anti-ischemic Therapies
Treatment of RVI should focus on optimizing oxygen supply and
demand to optimize recovery of both LV and RV function and LV
function. However, most anti-ischemic agents exert hemodynamic effects
that may be deleterious in patients with RVI. Specially, -blockers and
some calcium-channel blockers may reduce heart rate and depress
conduction, thereby increasing the risk of bradyarrhythmias and heart
Curr Probl Cardiol, December 2012 551
block in these chronotropically dependent patients. The vasodilator
properties of nitrates and calcium-channel blockers may precipitate
hypotension. In general, these drugs should be avoided in patients with
RVI.
Robert O. Bonow. The potential for harm with use of these drugs highlights
the importance of identifying patients with ischemic right ventricular dysfunc-
tion associated with inferior MI.
Reperfusion Therapy
The benecial effects of successful reperfusion on RV function and
clinical outcome, as well as the demonstrated efcacy and advantages of
primary angioplasty versus thrombolysis in patients with acute right heart
ischemic dysfunction, have been discussed.
Inotropic Stimulation
Parenteral inotropic support is usually effective in stabilizing hemody-
namically compromised patients not fully responsive to volume resusci-
tation and restoration of physiologic rhythm.
8,24,58
The mechanisms by
which inotropic stimulation improves low output and hypotension in
patients with acute RVI have not been well studied. However, experi-
mental animal investigations suggest that inotropic stimulation enhances
RV performance by increasing LV-septal contraction, which thereby
augments septal-mediated systolic ventricular interactions.
24
Although an
inotropic agent such as dobutamine that has the least deleterious effects
on afterload, oxygen consumption, and arrhythmias is the preferred initial
drug of choice, patients with severe hypotension may require agents with
pressor effects (such as dopamine) for prompt restoration of adequate
coronary perfusion pressure. The inodilator agents, such as milrinone,
have not been studied in patients with RVI, but their vasodilator
properties could exacerbate hypotension.
Mechanical Assist Devices
The ischemic RV nearly always recovers over time (if the patient can
survive the acute hemodynamic compromise), but in some cases recovery
may be slow and in others RV shock may be refractory to initial medical
management. In such patients, temporary mechanical hemodynamic
support may provide a bridge-to-recovery. Anecdotally, intra-aortic
balloon pumping (IABP) may be benecial, although there is little
552 Curr Probl Cardiol, December 2012
research to shed light on the mechanisms by which IABP exerts salutary
effects in acute RV shock. It is unlikely that IABP directly improves RV
performance, but rather functions by stabilizing mean aortic pressure and
thereby improving coronary perfusion pressure in severely hypotensive
patients. Because RV myocardial blood ow is dependent on perfusion
pressure, balloon pumping may, therefore, also improve RV perfusion
and thereby benet RV function, particularly if the RCA has been
recanalized or if there is collateral supply to an occluded vessel. IABP
may also potentially improve LV performance in those patients with
hypotension and depressed LV function. Because performance of the
dysfunctional right ventricle is largely dependent on LV septal contrac-
tion, RV performance may also benet. In RVI shock cases refractory to
IABP, temporary mechanical support with a ventricular assist device may
be life saving. Recent reports suggest percutaneous RV assist devices can
improve hemodynamics in patients with refractory life-threatening low
output, thereby providing the reperfused right ventricle a bridge to
recovery.
62,63
Conclusions
Acute RCA occlusion proximal to the RV branches results in RVFW
dysfunction. The ischemic dyskinetic RVFW exerts mechanically disad-
vantageous effects on biventricular performance. Depressed RV systolic
function leads to a diminished transpulmonary delivery of LV preload,
resulting in reduced cardiac output. The ischemic right ventricle is stiff,
dilated, and volume dependent, resulting in pandiastolic RV dysfunction
and septally mediated alterations in LV compliance, exacerbated by
elevated intrapericardial pressure. Under these conditions, RV pressure
generation and output are dependent on LV-septal contraction and
paradoxical septal motion. Culprit lesions distal to the RA branches
augment RA contractility and enhance RV lling and performance.
Bradyarrhythmias limit the output generated by the rate-dependent
ventricles. Ventricular arrhythmias are common, but do not impact
short-term outcomes if mechanical reperfusion is prompt. Patients with
RVI and hemodynamic instability often respond to volume resuscitation
and restoration of a physiologic rhythm. Vasodilators and diuretics should
generally be avoided. In some patients, parenteral inotropes are required.
The right ventricle is relatively resistant to infarction and usually recovers
even after prolonged occlusion. However, prompt reperfusion enhances
recovery of RV performance and improves the clinical course and
survival of patients with ischemic RV dysfunction.
Curr Probl Cardiol, December 2012 553
Robert O. Bonow. Dr Goldstein has provided a lucid discussion of the
clinical scenarios associated with right ventricular infarction. Prompt identi-
cation of patients with this condition and recognition of its unique manage-
ment challenges are essential for optimal patient outcome.
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