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150.e4 PART III Coronary Artery Disease
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95. Cotter G, Kaluski E, Milovanov O, et al. LINCS: L-NAME (a
NO synthase inhibitor) in the treatment of refractory
cardiogenic shock: a prospective randomized study. Eur Heart J.
2003;24:1287.
96. Dzavik V, Cotter G, Reynolds HR, et al. Effect of nitric oxide
synthase inhibition on hemodynamics and outcome of patients
with persistent cardiogenic shock complicating acute
myocardial infarction: a phase II dose-ranging study. Eur Heart
J. 2007;28:1009.
97. The TRIUMPH Investigators. Effect of tilarginine acetate in
patients with acute myocardial infarction and cardiogenic
shock. The TRIUMPH randomized controlled trial. JAMA.
2007;297:1657.
98. Fox KA, Steg PG, Eagle KA, et al. Decline in rates of death and
heart failure in acute coronary syndromes, 1999-2006. JAMA.
2007;297:1892.
99. Webb JG, Sanborn TA, Sleeper LA, et al. Percutaneous coronary
intervention for cardiogenic shock in the SHOCK Trial
Registry. Am Heart J. 2001;141:964.
100. Sleeper LA, Ramanathan K, Picard MH, et al. Functional
capacity and quality of life following emergency
revascularization for cardiogenic shock complicating acute
myocardial infarction. J Am Coll Cardiol. 2005;46:266.
101. Singh M, White J, Hasdai D, et al. Long-term outcome and its
predictors among patients with ST-segment elevation
myocardial infarction complicated by shock. J Am Coll Cardiol.
2007;50:1752.
OUTLINE
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Historical Perspective, 151
Coronary Circulation and the Right Ventricle, 151
Ventricular Interdependence, 152
Clinical Presentation, 152
Diagnosis, 153
Electrocardiographic Diagnosis, 153
ST Segment, 153
Q Waves in Right Ventricular Infarction, 154
Bundle Branch Block, 154
Atrioventricular Block, 155
Arrhythmia, 155
Prognostic Implications, 155
Echocardiography, 155
Cardiovascular Magnetic Resonance Imaging, 155
14
Right Ventricular Infarction
Jonathan D. Moreno, David L. Brown
Treatment, 155
Volume Resuscitation, 155
Electrical Stabilization, 156
Reperfusion Therapy, 157
Inotropic Support, 157
Right Ventricular Assist Devices, 157
Hemodynamic Monitoring, 157
Pulmonary Vasodilator Therapy, 157
Preload and Afterload Reduction, 157
Complications, 158
Prognosis, 158
Conclusion, 159
Infarction of the right ventricle is now known to be a common
clinical event, occurring in one-third of patients with inferior
myocardial infarction (MI).
confers a worse prognosis in patients with inferior wall MI.2
Because of the requirement for different treatment strategies in
right ventricular myocardial infarction (RVMI), prompt recognition and appropriate treatment require a thorough understanding
of the unique anatomy and pathophysiology of the RV.
1–3
Right ventricular (RV) infarction
HISTORICAL PERSPECTIVE
In 1930, Sanders4 reported the first clinical description of RVMI.
During the following 4 decades, RVMI received attention mainly
in autopsy series.5 At that time, any shock syndrome was considered the result of MI.
from open pericardium dog models in which destruction of the
right ventricle was not associated with shock.
of surgical procedures that bypassed the right ventricle, such as
the Glenn and Fontan procedures, furthered the belief that the
right ventricle is mainly a volume conduit contributing little to
cardiac output.
In 1974, Cohn and coworkers12 first called attention to RVMI
as a unique clinical and hemodynamic syndrome characterized,
in its extreme form, by shock, distended neck veins, and clear
lung fields. During the ensuing 2 decades of intense investigation
into the syndrome, the crucial role of ventricular interdependence
through the pericardium and the septum was recognized.
10,11
6,7
This view was buttressed by evidence
8,9
The development
13–16
Today, a rational approach to therapy of RVMI based on an
understanding of its pathophysiology is possible.
CORONARY CIRCULATION AND THE
RIGHT VENTRICLE
In the 85% of patients with right dominant coronary circulation,
the RV receives its blood supply almost exclusively from the
right coronary artery (RCA), with the septum and part of the
posterior wall supplied by the posterior descending artery and
the anterior and lateral RV walls supplied by acute marginal
branches of the RCA.
artery supplies a small portion of the anterior wall of the right
ventricle. In left dominant circulation, the left circumflex coronary
artery supplies the posterior descending artery, and a nondominant RCA supplies the acute marginal branches. Isolated RV
infarct without any LV involvement can occur with occlusion
of a nondominant RCA.
The angiographic hallmark of RVMI is thrombotic occlusion
of the RCA proximal to the origin of the acute marginal branches.
Angiographic flow studies suggest that the status of RV branch
perfusion is the critical determinant of RV ischemic dysfunction.19
Proximal RCA occlusions typically limit RV branch perfusion
in contrast to distal RCA occlusions.
Not every case of proximal RCA occlusion results in RV
infarction.18 This relative protection of the right ventricle from
infarction is thought to be a consequence of its lower oxygen
17,18
The left anterior descending (LAD)
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mm Hg
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demand, its continued perfusion during systole, and the potential
presence of collaterals from the LAD coronary artery, which,
because of the lower systolic pressure on the right side, are more
capable of supplying blood in the direction of the right ventricle
than in the reverse direction. The LAD collaterals to the RV are
mainly through the moderator band artery, a branch of the first
septal perforator.20 Prior severe stenosis or occlusions of the
LAD coronary artery can limit the development of collaterals
to the right ventricle with an acute RCA occlusion increasing
the degree of acute ischemic RV dysfunction.
21
VENTRICULAR INTERDEPENDENCE
The concept of ventricular interdependence in RVMI is central
to understanding the pathogenesis of the resultant low cardiac
output state. Ventricular interdependence is mediated through
the common pericardium and shared septum. The septum is an
integral component—both physically and functionally—to the
RV and even under physiologic conditions, septal contraction
contributes to RV performance.22 In RVMI, acute RV dilation
15,16,23
occurs.
the LV, the pericardial pressure abruptly increases, leading to
impaired LV filling. In animal models with the pericardium
removed, it is difficult to induce hypotension with RVMI.8 When
the pericardium is left intact,
with the full syndrome, as originally described by Cohn and
coworkers.12 Incision of the pericardium leads to improvement
in cardiac output, pressure equalization, and an increase in RV
systolic pressure.
The increase in right-sided diastolic pressure that occurs in
RVMI leads to a reversal of the normal left-to-right transseptal
diastolic gradient.25 On echocardiography, the septum can be
seen to flatten and encroach on the LV diastolic dimension.
During systole, the septum can be seen to move paradoxically
toward the RV, at times in a piston-like manner.
Except in rare cases of isolated RVMI,
LVMI accompanies RVMI. The pericardial constraint and alterations in septal geometry lead to reduced LV filling; cardiac output
is diminished further by the decrease in LV systolic function.
Development of shock syndrome with isolated RV infarction26
proves, however, that LV systolic dysfunction is not necessary
for the development of shock. Echocardiographic assessment in
cases of hemodynamically severe RVMI has confirmed that shock
may be present with preserved LV systolic function.
The hemodynamic hallmarks of RV infarction (Box 14.1) are
a decrease in cardiac output, elevation of right atrial pressure
BOX 14.1 Hemodynamic Findings in Cases
of Right Ventricular Myocardial Infarction
Elevated right atrial pressure (>10 mm Hg)
Right atrial pressure/pulmonary wedge pressure ratio >0.8
Noncompliant jugular venous pattern (prominent y descent)
Dip and plateau right ventricular diastolic pressure pattern
Depressed and delayed (often bifid) right ventricular systolic pressure
Decreased cardiac output
Hypotension
Because the RV shares a relatively fixed space with
16,24
however, RVMI is associated
16
16
26,27
some degree of
16
(>10 mm Hg), elevation of RV diastolic pressure, and decrease
in RV systolic pressure.
28–30
There is diastolic equalization of RV
and LV pressures, as in cardiac tamponade and the ratio between
right atrial and pulmonary capillary wedge pressure increases.
This ratio, which normally is less than 0.65, is usually greater
than 0.8 in RVMI.28 RV tracing reveals a delayed, depressed, and
often bifid peak, indicating systolic RV failure.16 RV diastolic
failure is also manifested by a dip and plateau pattern on the
RV pressure tracing. In most studies, hemodynamic tracings
showed a blunted x descent with a prominent y descent, suggesting
decreased compliance of the RV, as seen in pericardial constriction
(Fig. 14.1).
18,28–32
Although the hemodynamic criteria for RVMI
are usually present on admission, volume loading may increase
the identification of these abnormalities in some patients.
29
CLINICAL PRESENTATION
Clinically significant RVMI usually occurs in patients with
concomitant inferoposterior infarction of the LV, and many of
the symptoms overlap. Necropsy studies suggest that RVMI occurs
almost exclusively in patients with transmural posteroseptal MI.33
The size of the LV infarct does not correlate with RV infarct size.
The size of the RV infarct influences the severity of RV dysfunction
and presentation, however.21 What is unique to RVMI is the
occurrence of a syndrome of RV diastolic and systolic failure
that, in its extreme form, is characterized by a triad of signs:
hypotension that can progress to cardiogenic shock, elevated
neck veins, and clear lung fields.
When RVMI is hemodynamically significant, the physical
examination is a sensitive method of detection. Dell’Italia and
colleagues34 found elevated jugular venous pressure to be 88%
sensitive, with a specificity of 69% for inferior wall MI with RV
involvement. Kussmaul sign, an inspiratory increase in the jugular
venous pressure, was found to be 100% sensitive and specific
in the same series; Bellamy and coworkers35 found it to have a
sensitivity of 59% and a specificity of 89%. Other associated
findings include a high frequency of bradycardia, atrioventricular
(AV) block, and atrial arrhythmias, including supraventricular
tachycardias and atrial fibrillation or flutter. A right-sided fourth
ECG
200
Radial artery
100
0
Right atrial
40
pressure
20
mm Hg
0
Fig. 14.1 Hemodynamic tracings in right ventricular myocardial
infarction (RVMI). Noncompliant pattern of RVMI, with elevated
right atrial pressure, a deep y descent in the atrial tracing, dip
and plateau diastolic pattern in the right ventricle and relatively
low pulmonary artery pressure. (From Lorrell B, Leinbach RC,
Pohost GM, et al. Right ventricular infarction: clinical diagnosis
and differentiation from cardiac tamponade and pericardial
constriction. Am J Cardiol. 1979;43:465–471.)
4,12,18,34
Right ventricular
pressure
Pulmonary artery
pressure
CHAPTER 14 Right Ventricular Infarction 153
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BOX 14.2 Differential Diagnosis of Right
Ventricular Myocardial Infarction and Quick
Decision Supports
Cardiac tamponade (rule out with echocardiography)
Tension pneumothorax
Acute pulmonary embolism (PE; suggested by echo findings of 60/60 sign,
McConnell sign—confirm with computed tomography PE protocol)
Acute tricuspid regurgitation (rule out with echocardiography, assess for
endocarditis and vegetations)
Pulmonary hypertension with right ventricular failure
Right heart mass obstruction (rule out with echocardiography, other imaging
techniques)
Constriction/restriction (rule out with clinical presentation and history—most
often not an acute process)
Right ventricular variant takotsubo cardiomyopathy (consider if coronary arteries
are normal on angiography)
heart sound was described in 11 of 16 patients in one series,
with 4 of 16 having a right-sided third heart sound.36 Tricuspid
regurgitation may be audible. Pericardial friction rubs may be
heard because infarction in the thin RV is usually transmural.
32
The differential diagnosis includes tension pneumothorax,
cardiac tamponade, constrictive pericarditis, pulmonary embolism,
and, rarely, atypical RV-variant takotsubo cardiomyopathy.37
When the full triad (hypotension, elevated neck veins, clear lungs)
is present and ST segment elevations are observed in inferior
leads, the diagnosis is straightforward. A potential pitfall is the
occurrence of isolated RV branch infarction, which may manifest
with the full clinical picture of RVMI but without evidence of
MI on the standard 12-lead electrocardiogram (ECG)26 or with
ECG evidence of a presumed anterior infarct. Harnett et al.38
recently presented a case series of two isolated RV branch MIs
that were initially missed on angiography owing to an ECG
pattern consistent with an anterior STEMI. Given the anatomic
location, an isolated RVMI can mimic the clinical and ECG
picture of an anterior LVMI. Consequently, anterior ST elevation
in the precordial leads without reciprocal changes and lack of
significant left coronary disease should prompt careful attention
to the RV branch at time of angiography (Box 14.2).
Pulmonary embolism (PE) occasionally mimics RVMI and
may predispose to occult RVMI.
39
Conversely, RVMI with secondary thrombus formation in the RV can lead to PE. Dyspnea is
usually more severe in PE; RV systolic pressure, pulmonary artery
pressure, and pulmonary vascular resistance are usually higher
with PE than with RVMI. Cardiac tamponade may be acute and
may manifest with a similar triad of elevated neck veins, hypotension, and clear lungs; it can be distinguished easily at the bedside
with echocardiography, however. Pulsus paradoxus, a hallmark
of tamponade, is unusual in RVMI, which tends to more closely
resemble pericardial constriction.
32
DIAGNOSIS
Electrocardiographic Diagnosis
ST Segment. The ECG remains the most useful tool for the
diagnosis of RVMI.40 The hallmark of acute RV ischemia is ST
segment elevation in the right precordial leads, a finding first
reported in 1976 by Erhardt and coworkers,41 who used lead CR
located in the fifth intercostal space at the right midclavicular
line.42 The importance of obtaining right-sided chest leads on
presentation in patients with suspected acute MI, particularly
with evidence of inferior wall involvement, cannot be overemphasized (Fig. 14.2).
Several studies have documented that ST segment elevation
of 0.05 mV or greater (0.5 mm when using standard settings of
10 mm/mV) in lead V4R in the setting of inferior MI is sensitive
and specific for RV involvement, as documented by postmortem
examination42 or by radionuclide,
hemodynamic,40 or angiographic studies.
40,43,44
echocardiographic,43
32,44
Infrequently, ST
segment elevation in V5R or V6R occurs in the absence of elevation
in V4R.
40,43
Zehender and colleagues
2,40
confirmed the utility of
0.1-mV ST segment elevation in any of the right precordial leads
(V
) in a series of 200 patients, showing a sensitivity of 89%
4R-V6R
and a specificity of 83%.
The ECG findings in RVMI of right precordial ST segment
elevations are the result of a rightward and anteriorly directed
vector. Andersen and coworkers45 showed that ST segment elevation in lead III exceeding that in lead II (i.e., ST segment vector
directed rightward) is reasonably sensitive (68%) in diagnosing
RVMI. This criterion had a specificity of only 11% and a positive
predictive value of 58% in Zehender’s series of 200 patients with
inferior MI but had a sensitivity of 95%.
40
Certain special situations with variant ECG findings that may
cause confusion warrant mention. Geft and colleagues46 described
five patients with ST segment elevations in leads V1 to V5 who
on catheterization were shown to have RCA occlusion and acute
RVMI. All five patients had minimal or absent ST segment elevations in the inferior leads. The authors speculate that in the
usual cases of RVMI, ST segment elevations in leads V1 to V5
are blocked by the dominant electrical forces of inferoposterior
MI, resulting in isoelectric or even depressed ST segments in
the left precordium. When these forces are absent, because of
isolated RVMI
38,47
or with minimal posterior involvement, as
may be seen in a patient with a codominant circulation,46 ST
segment elevation in the left precordial leads mimicking anterior
wall MI may be seen. A distinguishing characteristic in RV
infarction may be that the ST segment elevations are highest in
leads V1 or V2 and decrease toward lead V5, a pattern opposite
that usually seen in anterior MI.
46
If septal involvement can mimic RVMI, a left lateral wall
infarction or a large true posterior infarction can be expected
to cancel right precordial ST segment elevations. Such cases of
false-negative findings have been described.
48,49
Most studies of right precordial lead ST segment elevation
have been limited to patients with evidence of inferior wall MI.
In anterior MI, ST segment elevation in the right precordial leads
has also been documented and has been found to be predictive of proximal LAD occlusion before the first septal branch,
suggesting that the right precordial lead ST segment elevations
are the result of a septal current of injury.50 A distinguishing
characteristic in cases of LAD occlusion is that the ST segment
elevation has a leftward axis in contrast to the rightward ST
segment in RV infarction, as emphasized by Hurst.51 Other
154 PART III Coronary Artery Disease
A
B
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aVR
I
II
I
I
II
aVL
aVF
aVR V1 V4
aVL
V1 V4
V3 V6
V2
V5
V5V2
(V4R)
(V5R)
III
II
Fig. 14.2 (A) 12-Lead electrocardiogram from a 63-year-old man with chest discomfort after
running on a treadmill, demonstrating ST elevation in lead III greater than in lead II; ST depression
in leads I and aVL; and ST elevation in lead aVF greater than ST depression in lead V
are suggestive of a right ventricular myocardial infarction. (B) 12-Lead electrocardiogram from
the patient in (A) using right-sided precordial leads, demonstrating ST segment elevation in leads
V
to V6R, consistent with a right ventricular myocardial infarction. (From Nagam MR, Vinson
3R
DR, Levis JT. ECG diagnosis: right ventricular myocardial infarction. Perm J. 2017;21:16–105.)
aVF
causes of right precordial ST segment elevation in the absence
of RVMI include pericardial disease, left anterior hemiblock,
and PE.
52
The time course of ST segment elevation in RVMI warrants
emphasis. Braat and colleagues43 reported that ST segment elevations in lead V4R resolve within 10 hours after the onset of chest
pain in half of patients. Similar findings were reported by Klein
V3 (V3R)
leads (as a QS or a QR pattern) was 100% specific and 78%
sensitive. The high specificity (>90%) of Q waves was confirmed
in Zehender’s series of 200 patients with inferior wall MI.40 Early
in the course of infarction, Q waves are still absent and the
sensitivity is low, particularly for patients presenting early. In
patients admitted late (>12 hours after the onset of symptoms),
the sensitivity increases to 95%.
V6 (V6R)
. Findings
2
and colleagues.48 Thus, it is important to obtain a right-sided
ECG soon after the patient’s presentation.
Bundle Branch Block. RVMI, especially when extensive, has
been shown to be associated with an incomplete and often
Q Waves in Right Ventricular Infarction. Because patients may
present after the ST segments have returned to baseline, criteria
using Q waves in the right precordial leads have been sought.
In normal subjects, an rS pattern is always present in V3R and
usually (>90%) in V4R. In one series53 of patients with autopsydocumented RV infarction, the presence of a Q wave in these
transient right bundle branch block. The block is postulated to
occur distally. Because there may also be precordial ST segment
elevation in RV infarction, the right bundle branch block may
be difficult to detect in lead V1. Kataoka and coworkers54 pointed
to a cove-shaped ST-T elevation in lead V1 as suggestive of an
underlying right bundle branch block.
CHAPTER 14 Right Ventricular Infarction 155
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Atrioventricular Block. Significant AV block is more common
in inferior wall MI with RV involvement.55 The presence of ST
segment elevation in V4R was shown to predict the development
of high-grade AV block, with 48% of patients in one series
developing AV block during the first 3 days of infarction compared
with only 13% without evidence of RVMI.56 After AV block
develops in the setting of RV infarction, it has important implications for therapy. Because cardiac output depends on preload
and right atrial function, RV pacing alone may be inadequate
to improve hemodynamics.
Arrhythmia. Atrial arrhythmias are common in RVMI. Because
of the propensity for low cardiac output and preload dependence, these arrhythmias are poorly tolerated and should be
treated aggressively. Early cardioversion and antidysrhythmic
therapy for atrial fibrillation are recommended.52 One study of
patients with RVMI did not reveal an increase in ventricular
arrhythmias compared with patients with inferior MI without
RV involvement.
57
Prognostic Implications. ECG findings for RV infarction have
marked prognostic implications, even in the absence of hemodynamic abnormalities. In the series of 200 patients by Zehender
and associates,58 ST segment elevation in lead V4R was shown
on multiple logistic regression analyses to be the strongest predictor of in-hospital morbidity and mortality. Patients with inferior
MI and ST segment elevation in V4R had a mortality rate of 31%
compared with 6% for patients without such evidence of RV
involvement. Similarly, major complications (ventricular fibrillation, sustained ventricular tachycardia, cardiogenic shock, cardiac
rupture, high-grade AV block, reinfarction) were markedly more
common (64% vs. 28%; P < .001) in patients with ECG evidence
of RV involvement. In one series, the presence of AV block in
RV infarction was found to be associated with a mortality rate
of 41%, whereas the mortality rate for patients with inferior
wall infarction with RV infarction but without AV block and for
patients with inferior MI with AV block but without RV infarction
was only 11% to 14%.
59
Echocardiography
Two-dimensional echocardiography is a fast, widely available,
and inexpensive tool for assessment of RV function. It is also
sensitive (80% to 90%) and specific (>90%) in the detection of hemodynamically significant RV infarction.
echocardiographic findings in RVMI include RV dilation, RV
hypokinesis, abnormal (paradoxic) septal motion, septal flattening,63 and reduced septal thickening (Video 14.1). Tissue Doppler
imaging has also revealed that peak systolic velocity (S′
peak early diastolic velocity (E′
) are significantly reduced in
TDI
RVMI.64 Kidawa et al.64 also utilized 3D echo to estimate RV
ejection fraction (RVEF); while this performed no better than
TDI in the diagnosis of RVMI, they found that an RVEF less
than 51% has adequate specificity and sensitivity for RV infarct
(Box 14.3).
Echocardiography is particularly useful in assessment of RVMI
because it also provides information on LV function, associated
valvular regurgitation, and possible alternative or concomitant
60–63
TDI
Key
) and
BOX 14.3 Echocardiographic Findings
in Cases of Right Ventricular (RV)
Myocardial Infarction
RV free wall dilatation and wall motion abnormalities (hypokinesis, akinesis)
Flattened interventricular septum (D-shaped septum) and paradoxic movement
Reduced septal wall thickening
Reduced tissue Doppler peak systolic velocity (S’), and early peak diastolic
velocity (E’)
Reduced RV ejection fraction (<51%)
64
BOX 14.4 Treatment Strategies for Right
Ventricular Myocardial Infarction
Volume resuscitation (goal: right atrial pressure 14 mm Hg)
Electrical stabilization and synchrony (may need atrial and ventricular sequential
pacing)
Reperfusion therapy (early, primary percutaneous coronary intervention
preferred)
Inotropic support for persistent hypotension with low output (dobutamine,
dopamine, norepinephrine)
Right ventricular assist devices (Impella RP, intraaortic balloon pump, Tandem
Heart)
Invasive hemodynamic monitoring
diagnoses such as cardiac tamponade. Echocardiography may also
detect important complications, such as thrombus formation or
pericardial effusion. Two-dimensional contrast echocardiography
may help detect right-to-left shunting through a patent foramen
ovale.65 While echocardiography remains an indispensable tool
for assessment of RV function, it remains technically challenging
owing to the complex shape and structure of the RV, the need
for multiple acoustic windows for complete visualization, and
the transient nature of some echocardiographic abnormalities.
66
Cardiovascular Magnetic Resonance Imaging
Late enhancement cardiovascular magnetic resonance imaging
(MRI) has greater sensitivity at detecting RVMI than ECG,
physical examination, or echocardiography. Late enhancement
cardiovascular MRI findings of injury of the RV in the acute
phase persist for 13 months, suggesting that this imaging modality
can predict the extent of irreversible RV injury in the acute
67
phase.
TREATMENT
The goals of treatment for RV infarction are volume resuscitation
to maintain arterial pressure, electrical stabilization, revascularization, and, if needed, mechanical or pharmacologic support and
invasive hemodynamic monitoring. Box 14.4 summarizes treat-
ment strategies for patients with RVMI.
Volume Resuscitation
Volume resuscitation in RVMI requires balancing the need for
adequate RV preload and impaired LV diastolic filling. A key
metric in the decision algorithm of volume resuscitation is
involvement of the septum. The RV is preload dependent and,
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in the setting of ischemia with decreased diastolic compliance,
it may benefit from an augmentation in preload. If hypovolemia
is present, there may be a marked improvement with saline
administration. When marked RV dilation has already occurred,
however, further increases in RV preload do not result in an
increase in RV stroke volume and may impair LV filling further
through increased septal shift in combination with pericardial
constraint.14 Cardiac output and arterial blood pressure may not
increase. In various studies,
pressure to 10 to 14 mm Hg was followed by an improvement
in stroke volume and RV stroke work index, but further augmentation was associated with no improvement or even a decrease in
stroke volume.
60–63
The optimal pulmonary capillary wedge
pressure corresponding to maximum LV stroke work index was
16 mm Hg.71 Given these narrow constraints, invasive hemodynamic monitoring is usually necessary to guide therapy.
Excessive volume loading can lead to elevation in pericardial
pressure and shift the interventricular septum leftward, leading
to impaired LV filling and a subsequent low-output state. In
addition, LV septal involvement further impairs RV force generation. These patients tend to present with hypotension and low
cardiac output and are more refractory to volume infusion. This
subset of patients may benefit most from inotropic support.66
Fig. 14.3 summarizes the detrimental effects of excessive volume
loading.
68–70
an increase in mean right atrial
Electrical Stabilization
Acute RVMI is often associated with bradyarrhythmias, including
high-degree AV block, bradycardia, and AV dyssynchrony.
The mechanisms underlying bradycardia include excessive vagal
tone, reflex-mediated bradycardia (e.g., Bezold-Harisch reflex),
pharmacologic therapy (e.g.. β-blockers, calcium channel blockers), and AV node ischemia.22 Bradyarrhythmias and hypotension
are far more common with proximal RCA lesions and can also
be induced in a relatively stable patient upon successful reperfu-
73,74
sion.
Given a relatively fixed stroke volume of the ischemic
RV, cardiac output in the preload-dependent LV is extremely
sensitive to heart rate; maintaining chronotropic competence is
therefore essential. Low-output RV failure can also be exacerbated
by the loss of right atrial systole. Thus, while RV pacing may be
of benefit, some patients require dual chamber pacing to restore
AV synchrony.75 Sequential pacing may have a marked salutary
effect on cardiac output
52,75
and can lead to significant improvement and recovery from shock in patients refractory to RV pacing
alone.52 The clinician should be aware that, in practice, pacing
can be complicated by improper placement of temporary pacing
wires owing to right-sided chamber dilation, tricuspid regurgitation, and initiation of ventricular arrhythmias.22 Further issues
of impaired ventricular sensing and sustained impulse generation
are common in the ischemic RV. A higher pacing threshold should
14,56,72
Normal
ED
RV LV
Fig. 14.3 Excessive right ventricular (RV) volume loading. Two physiologic concepts explaining
the detrimental effects of excessive volume loading. Normal ventricle: At end systole (ES), the
RV free wall moves toward the septum. Pericardial restraining effects (above, before volume
loading; below, after excessive volume loading): RV dilatation, as a result of excessive volume
loading, can lead to the elevation of intrapericardial pressure, increase in pericardial constraint
(red arrow), and change of geometry due to interventricular septum shift. These changes contribute
to the low-output state by decreasing left ventricular (LV) distensibility, preload, and ventricular
elastance. Role of the interventricular septum (pure RV infarction, RV infarction with septal
ischemia): At ES, the RV free wall moves toward the septum. At end diastole (ED), the RV dilates
during diastole and the septum reverse curves toward the volume-reduced LV. At ES, the septum
thickens but moves paradoxically into the RV, displacing the RV volume despite RV free wall
dyskinesis. Septal ischemia depresses septal contraction and global LV function, resulting in LV
dilatation. The septum stops thickening and there is increased systolic septal displacement into
the RV. Pansystolic septal thinning and more extensive paradoxical displacement are associated
with further depression of RV performance. (From Inohara T, et al. The challenges in the management of right ventricular infarction. Eur Heart J Acute Cardiovasc Care. 2013;2[3]:226–234.)
Pericardial restraining Pure RV infarction
Before
AfterES
ED
ES
RV infarction with
septal ischemia
ED
ES
CHAPTER 14 Right Ventricular Infarction 157
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be anticipated.
59,76
Caution should be employed when placing a
pacing wire in an area of infarction because the risk of rupture
may be increased. If transvenous pacing fails, transcutaneous
external pacing may be successful.
77
Reperfusion Therapy
Proximal RCA occlusion can compromise both right atrial and
RV branch perfusion, which can lead to both RV dysfunction
and impaired atrial contraction. Thus patients with proximal
RCA lesions are more unstable than those without.
66,78
Given
the adverse prognosis of RVMI, establishing reperfusion by
primary percutaneous coronary intervention (PCI) or thrombolytic therapy is particularly important in these patients.
Meta-analyses have shown that PCI results in superior outcomes
compared with thrombolysis when performed rapidly by an
experienced team.79 PCI should be the reperfusion modality of
choice where available. If PCI is unavailable, thrombolysis is an
appropriate alternative therapy that has been shown to reduce
mortality.
2,80
Radionuclide studies have confirmed a marked
reduction in the extent of RVMI in patients who achieved early
reperfusion.
71,81
Other studies have suggested that complete RCA
revascularization, especially when complicated by ventricular
reperfusion arrhythmias, was associated with a better progno-
82,83
sis.
Thrombolytic therapy is relatively ineffective in the presence
of cardiogenic shock, however. In the presence of shock not
responsive to volume replacement and inotropic therapy, primary
PCI is the preferable approach even if the patient requires transfer
to another facility.
Inotropic Support
Dobutamine and dopamine have been evaluated in the setting
of severe RVMI (defined by right atrial pressure >13 mm Hg)
and have consistently been found to increase RV stroke work
and cardiac output, while volume loading and nitroprusside
were generally ineffective.69 Dobutamine, which also has arteriolar
vasodilating effects, usually does not increase mean arterial
pressure significantly and has the least deleterious effect on
afterload and oxygen consumption.22 Dopamine (by activating
dopaminergic and α-adrenergic receptors) and norepinephrine
increase mean arterial pressure; they should be used when patients
are severely hypotensive and require pressor support in addition
to inotropy.14 After the systolic blood pressure increases to greater
than 90 mm Hg, dobutamine may be used, alone or in combination with dopamine or norepinephrine.
The use of milrinone,84 a phosphodiesterase inhibitor, has
been shown to be beneficial in chronic right heart failure, increasing myocardial contractility. While milrinone has the advantage
of reducing pulmonary vascular resistance and unloading the
right ventricle, it may exacerbate hypotension.22 Its use in RVMI
has not been systematically evaluated.
Right Ventricular Assist Devices
Recent reports of the use of percutaneous RV assist devices in
patients with shock complicating RVMI are encouraging. There
are currently three such devices in clinical practice: the Tandem
Heart (CardiacAssist), the Impella RP (Abiomed), and the
intraaortic balloon pump (IABP). For the Tandem Heart, two
21F cannulae are placed via both femoral veins, one in the right
atrium and the other in the pulmonary artery with assist pumping
using an extracorporeal centrifugal pump. The Impella RP utilizes
a 22F catheter placed through the femoral vein and is positioned
with the inlet valve in the RV and the outlet in the pulmonary
artery (Video 14.2). It can deliver flow rates up to 4 L/min and
can be placed for up to 14 days. It is indicated for acute right
heart failure or decompensation. Data from the RECOVERRIGHT trial indicate marked, immediate hemodynamic improvement with an average duration of use of 3 days. The overall
survival at 30 days was 73.3%85 (Fig. 14.4). Last, an IABP has
recently been shown to improve hemodynamics in patients with
cardiac shock secondary to RVMI.86 The mechanism of beneficial
effect for a left-sided device remains incompletely understood
but likely stabilizes mean arterial pressure and improves coronary
perfusion. Other postulated mechanisms include improved LV
function through LV septal contraction. Thus, the temporary
use of such invasive RV assistance is now a promising tool as a
“bridge to recovery”; in all devices, the unloading of the RV
reduces RV dilation and pericardial pressure while improving
LV filling in the setting of shock from RVMI.
87,88
Hemodynamic Monitoring
In a patient with hemodynamic instability in the setting of RVMI,
the use of a pulmonary artery catheter often helps guide therapy.
Extra caution should be employed in the placement of the catheter
because a higher incidence of ventricular arrhythmias, including
ventricular fibrillation, has been described in the setting of RVMI
(4% vs. 0.3% in patients without RV infarction).89 Flotation of
the catheter under fluoroscopic guidance by a cardiologist or
other intensivist may help minimize the risk.
Pulmonary Vasodilator Therapy
The use of selective pulmonary vasodilators might be expected
to provide afterload reduction for the failing RV without concurrent systemic vasodilation and hypotension, potentially resulting
in improved cardiac output. Inhaled nitric oxide acts as a selective
pulmonary vasodilator, producing smooth muscle cell relaxation
and vasodilation in the pulmonary circulation without systemic
vasodilation owing to its active binding to hemoglobin and
inactivation in circulating erythrocytes.
90
A few studies91 have
examined pulmonary vasodilator therapy with cautiously
optimistic results, but further study and validation of these agents
in RVMI is necessary.
Preload and Afterload Reduction
The RV is sensitive to preload, particularly in the setting of
RVMI. Hypotension provoked by nitroglycerin, morphine sulfate,
or diuretics in patients with an acute inferior MI should alert
the clinician to the possibility of a preload-sensitive state, such
as RVMI. The routine use of these agents should be discouraged
in patients with acute inferior MI until RV involvement is ruled
out. Sodium nitroprusside may result in marked afterload reduction which, if ineffective in increasing right-sided output, results
in systemic hypotension.69 In some clinical situations, such as
combined right and left heart failure with severe LV dysfunction
or when fluid administration has been overzealous, the cautious
158 PART III Coronary Artery Disease
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Fig. 14.4 Placement of the percutaneous right ventricular (RV) Impella right side percutaneous
device (Abiomed). (A) Tracking the right-sided percutaneous device over an 0.018 stiff guidewire
through the right ventricular outflow tract into the main pulmonary artery. The procedure was
performed under general anesthesia with transesophageal echocardiography guidance. (B) Final
position of the RV support device, with the device inflow located below the right atrial inferior
vena cava junction (arrow) and the device outflow located in the main pulmonary artery (arrowhead).
Note the relationship of the device outflow to the pulmonary artery pulmonary artery catheter,
a simple method to confirm device position on plain chest radiography. (From Margey R, et al.
First experience with implantation of a percutaneous right ventricular Impella right side percutaneous
support device as a bridge to recovery in acute right ventricular infarction complicated by cardiogenic
shock in the United States. Circ Cardiovasc Interv. 2013;6[3]:e37–e38.)
BOX 14.5 Complications of Right
Ventricular Myocardial Infarction
Atrioventricular block
Atrial tachyarrhythmias
Tricuspid regurgitation
Right-to-left shunting
Right ventricular thrombus
Pulmonary embolism
Paradoxical embolism
Septal rupture
Free wall rupture
use of vasodilators may be attempted.14 Invasive hemodynamic
monitoring should be used and right atrial pressure should be
maintained at greater than 10 mm Hg.
COMPLICATIONS
Patients with inferior wall MI and accompanying RVMI have a
much higher rate of complications than patients with inferior
wall MI without RV involvement, accounting for part of the
adverse prognostic implications of RVMI (Box 14.5). These
include AV block, atrial arrhythmias, profound hypotension and
bradycardia, and pericarditis. The cardiac intensivist should also
be aware of several less common complications.
Patent foramen ovale (PFO) is present in 25% of the population. In the setting of RVMI and elevated right-sided pressures,
right-to-left shunting may occur, resulting in hypoxemia.
Maneuvers that reduce LV pressures, such as afterload reduction,
65,92–95
exacerbate this shunting. Percutaneous closure of the patent
foramen may be necessary in extreme cases.
4
As in LVMI, RVMI may predispose to thrombus formation
in the infarcted ventricle with possible pulmonary embolism.
In the presence of a PFO, paradoxical embolization may lead to
systemic emboli. Thrombus has been identified in the RV of
patients with RVMI (3 of 33; 9%) and in patients without RV
infarction with posterior wall MI (4 of 106; 4%).
96
Severe tricuspid regurgitation secondary to papillary muscle
necrosis or severe RV dilation has been described in the setting
of RVMI. In extreme cases, refractory heart failure has necessitated
valve replacement.97 Other complications include septal rupture,95
RV free wall rupture,97 and pericarditis, which is common in
RV infarction because of the thinness of the RV wall.
Last, ventricular septal rupture in the setting of acute RVMI
can be particularly disastrous, precipitating pulmonary edema,
increased pulmonary pressures and resistance, and further decreasing cardiac output. Surgical repair is mandatory in most cases
but is associated with significant mortality and morbidity.
22,98
PROGNOSIS
RVMI is associated with markedly increased complication and
mortality rates.39 The reduction in mortality by reperfusion
therapy is dramatic. Aggressive reperfusion therapy is indicated to maximize survival in the absence of severe mitigating
circumstances.
After RVMI, RV function generally improves.99 Long-term
prognosis is determined, however, by residual LV rather than
RV function, with similar posthospital courses for patients with
CHAPTER 14 Right Ventricular Infarction 159
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and without RVMI.39 A strong correlation exists between the
outcome of RVMI and age.
substantially increases the risk of death and major complications
in elderly patients.
33,100
In acute inferior MI, RV infarction
33
CONCLUSION
RVMI occurs mainly in the setting of inferior wall MI with
proximal RCA occlusion. RV involvement in inferior MI has
a marked adverse effect on complication rate and prognosis.
Patients with RVMI benefit, however, from reperfusion therapy.
Complications such as hypotension, AV block, and atrial tachyarrhythmias should be treated aggressively. Although the short-term
prognosis in RV infarction is poor, if the patient survives the
acute illness, the long-term prognosis is good.
Acknowledgment
We acknowledge the contributions of Dr. Anil J. Mani to this
chapter in the previous edition.
The full reference list for this chapter is available at
ExpertConsult.com.
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