Professional Documents
Culture Documents
Clifford R. Greyson, MD
Right ventricular failure may be defined as the inability of the tion may occur abruptly and catastrophically because of unique
right ventricle of the heart to provide adequate blood flow through aspects of right ventricular physiology. This review will focus on
the pulmonary circulation at a normal central venous pressure. the pathophysiology of acute right ventricular failure in the critical
Critical care specialists encounter right ventricular failure rou- care setting and summarize the limited management options
tinely in their practice, but until recently right ventricular failure available. (Crit Care Med 2008; 36[Suppl.]:S57–S65)
as a primary clinical entity received scant consideration. Indeed, KEY WORDS: right ventricle; pulmonary hypertension; Frank-
there is still not a single published practice guideline focused on Starling relation; contractile dysfunction; hypoxic pulmonary va-
right ventricular failure. Right ventricular failure is usually due to soconstriction; coronary ischemia; ventricular wall stress; central
a combination of right ventricular pressure overload and contrac- venous pressure; heart failure; cor pulmonale
tile abnormalities of the right ventricular free wall. Decompensa-
I n contrast to the left ventricle hypertension, and consequent right acutely decompensated left heart fail-
(LV) of the heart, the right ventri- ventricular dysfunction is seen rou- ure). Ultimately, many of these patients
cle (RV) receives little attention. tinely in critically ill patients (2). Sepsis end up in critical care units, where RV
Pulmonary disease specialists con- may cause right heart failure directly by failure may be the primary manifestation
centrate on disorders of the pulmonary inducing RV dysfunction (3). Pulmo- of their disease or a major complicating
circulation that affect right heart func- nary embolism is far more common factor in the management of their under-
tion directly but tend not to study disor- than generally appreciated, with an es- lying conditions. Altogether, RV failure is
ders of right heart function per se. At the timated 600,000 cases in the United estimated to account for 3% of all acute
same time, cardiovascular disease spe- States each year, and causes ⬎50,000 heart failure admissions and confers
cialists interested in heart failure have deaths annually, largely due to acute RV worse mortality rates than acutely de-
largely ignored the right heart as a dis- failure (4). RV failure occurs in the set- compensated left heart failure (12).
tinct area of investigation. Indeed, Amer- ting of idiopathic dilated cardiomyopa- While the function of the RV has long
ican Heart Association/American College thy, probably as a consequence of the been recognized, awareness of its impor-
of Cardiology practice guidelines for same mechanism causing LV dysfunc- tance has waxed and waned over the
management of heart failure barely men- tion and also as a consequence of pul- years. The importance of the RV was first
tion the RV and provide no guidance for monary hypertension secondary to ele- recognized by William Harvey in 1616
management of either acute or chronic vated left-sided filling pressures in (13), but in 1943 Starr et al. (14) con-
RV failure (1). Not a single professional ischemic LV cardiomyopathy (5). RV cluded that the RV functioned only as a
society has published a practice guideline failure may be an independent risk fac- passive conduit, since there were “no in-
concentrating on RV failure. tor for morbidity and mortality in pa- crements of venous pressure” following
Nevertheless, right heart failure re- tients with left heart failure (6). RV electrocautery ablation of the RV free wall
mains a major public health problem. failure is still a leading cause of death in dogs. A resurgence of interest in the
Respiratory failure causing hypoxic pul- and morbidity early after cardiac trans- RV followed reports by Cohn and col-
monary vasoconstriction, pulmonary plant (7) and following several other leagues (15) in 1974 that RV infarction
cardiothoracic procedures (8). Primary was common and difficult to manage,
pulmonary hypertension, while rela- that RV involvement in inferior myocar-
From the Department of Veterans Affairs Medical tively rare with only 300 new cases an- dial infarction conferred an eight-fold in-
Center and the University of Colorado Health Sciences nually in the United States, is difficult crease in mortality (16), that RV dysfunc-
Center, Denver, CO. to manage and results in RV failure (9). tion in acute pulmonary embolism is a
Supported, in part, by the Department of Veterans
Affairs and by grant R01 HL068606 from the National
By some estimates, 1 in 2000 of the predictor of mortality independent of sys-
Institutes of Health/National Heart, Lung, and Blood 10 –15 million people with chronic ob- temic hemodynamics (17), and that RV
Institute, Bethesda, MD. structive pulmonary disease will de- dysfunction is an independent predictor
Dr. Greyson has applied for a patent for protease velop RV failure, accounting for several of poor outcome in left heart failure (6).
inhibition for prevention or treatment of heart failure.
thousand new cases per year (10). Cor- Why have investigators only recently
For information regarding this article, E-mail:
clifford.greyson@uchsc.edu onary ischemia may cause RV failure, rediscovered the clinical importance of
Copyright © 2007 by the Society of Critical Care both directly (as in RV myocardial in- the RV of the heart? Limited understand-
Medicine and Lippincott Williams & Wilkins farction) (11) and indirectly (as in acute ing of the physiology of the RV by clini-
DOI: 10.1097/01.CCM.0000296265.52518.70 ventricular septal defect or from cians who view the RV merely as a weak
RV Response to a Primary
Reduction in Contractility
Pulmonary vascular resistance is nor-
mally ⱕ10% of systemic vascular resis-
Figure 2. Main figure from the seminal investigation by Arthur Guyton and colleagues (39) showing tance, and mean pulmonary artery pres-
the limits of right (RT.) ventricle (RV) contractile function in the setting of increasing pulmonary sure is normally not much higher than
artery (PUL. ART.) outflow obstruction, with the resulting abrupt and catastrophic collapse in systemic
15 mm Hg. If LV filling pressure is low
hemodynamics once RV compensatory mechanisms are exhausted. The original figure legend reads
“Effect of increasing pulmonary arterial constriction on the mean pressures at different points in the
and pulmonary vascular resistance is nor-
circulatory system.” mal, active contraction of the RV, or even
the interventricular septum, is not nec-
essary to maintain cardiac output. For
tion, is probably not the only contributor example, to maintain a cardiac output of
to altered RV contractile function during 6 L/min with a normal left atrial pressure
acute pressure overload and may not play of 8 mm Hg requires a mean pulmonary
a significant role in right heart failure artery pressure of only 14 mm Hg; with
from pulmonary hypertension in a major- no contribution from the RV at all, this
ity of stable patients (46). While homeo- can be developed entirely by a modest
metric autoregulation and increased ad- increase in central venous pressure.
renergic tone both up-regulate RV Thus, a reduction in RV contractility
contractility during acute pressure over- may not by itself result in RV failure, and
load, there is evidence that pressure over- even very severe isolated RV ischemia
load down-regulates RV contractility dur- may be well tolerated because elevated
ing (47) and following (48, 49) acute RV central venous pressure provides suffi-
pressure overload even in the absence of cient driving force to maintain flow
ischemia. The mechanism of the down- across the pulmonary circulation. This
ward regulation is not known; however, was demonstrated in a report by Brooks
the severity of this element of contractile and colleagues (43), in which complete
dysfunction is directly related to end- right coronary occlusion had essentially
Figure 3. Illustration of the downward spiral of systolic wall stress and is exacerbated by no impact on RV developed pressure, car-
right ventricle (RV) function that ensues once RV end-systolic RV dilation, presumably be- diac output, or left ventricular developed
compensatory mechanisms are exhausted in the cause end-systolic RV dilation results in pressure, when pulmonary artery pres-
face of rising RV systolic pressure stress. With the RV wall thinning, increased RV radius of sure was normal. Congenital heart dis-
RV teetering on the edge of compensation, even a curvature, and increased wall stress at ease corrective procedures, such as the
small additional increment in pulmonary outflow the same RV systolic pressure (49). Fontan procedure, exploit this low-
resistance, or a small decrement in RV contrac- Shortly after acute RV pressure over- resistance state of the normal pulmonary
tile function, can precipitate an abrupt decline in
load ensues, ultrastructural changes con- circulation, bypassing the RV entirely
function through a feed-forward mechanism in-
sisting of focal myocyte necrosis can be (56).
volving decreased systemic pressure, decreased
RV coronary perfusion, RV ischemia, RV contrac- identified in the RV free wall (50). While However, in the setting of increased
tile dysfunction, and further reduction in cardiac some of these are potentially due to direct pulmonary vascular resistance or ele-
output. The decline is irreversible if pulmonary mechanical disruption of myofibrils or vated left atrial filling pressure, central
vascular impedance is not reduced or RV contrac- focal adrenergic overstimulation, the venous pressure may not be sufficient to
tility is not increased. possible contribution of activation of pro- maintain pulmonary arterial flow and RV