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2016 ; 20
(1
): 266
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The right ventricle: interaction with the pulmonary circulation
#MMPMID27613549
Pinsky MR
Crit Care
2016[Sep]; 20
(1
): 266
PMID27613549
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The primary role of the right ventricle (RV) is to deliver all the blood it
receives per beat into the pulmonary circulation without causing right atrial
pressure to rise. To the extent that it also does not impede left ventricular
(LV) filling, cardiac output responsiveness to increased metabolic demand is
optimized. Since cardiac output is a function of metabolic demand of the body,
during stress and exercise states the flow to the RV can vary widely. Also,
instantaneous venous return varies widely for a constant cardiac output as
ventilatory efforts alter the dynamic pressure gradient for venous return.
Normally, blood flow varies with minimal changes in pulmonary arterial pressure.
Similarly, RV filling normally occurs with minimal increases in right atrial
pressure. When pulmonary vascular reserve is compromised RV ejection may also be
compromised, increasing right atrial pressure and limiting maximal cardiac
output. Acute increases in RV outflow resistance, as may occur with acute
pulmonary embolism, will cause acute RV dilation and, by ventricular
interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to
acute cardiogenic shock and death. Treatments include reversing the causes of
pulmonary hypertension and sustaining mean arterial pressure higher than
pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary
hypertension induces progressive RV hypertrophy to match RV contractility to the
increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is
associated with a sustained increase in right atrial pressure, impaired LV
filling, and decreased exercise tolerance. Treatment focuses on pharmacologic
therapies to selectively reduce pulmonary vasomotor tone and diuretics to
minimize excessive RV dilation. Owning to the irreversible nature of most forms
of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds
the adaptive increase in RV systolic elastance, due to RV dilation, progressive
pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If
associated with cardiogenic shock, it can effectively be treated only by
artificial ventricular support or lung transplantation. Knowing how the RV adapts
to these stresses, its sign posts, and treatment options will greatly improve the
bedside clinician's ability to diagnose and treat RV dysfunction.
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