Circulation, Vol 63, 87-95, Copyright © 1981 by American Heart Association
GJ Vlahakes, K Turley and JI Hoffman
Acute right ventricular (RV) hypertension and failure occur clinically. In
this study we examined the mechanism of RV failure. Adult dogs were studied
acutely under anesthesia; dogs were instrumented for measurement of
pressures and right coronary artery blood flow. Myocardial blood flow and
cardiac output were determined with radionuclide-labeled microspheres, and
the presence of ischemia was determined by biochemical analysis of
ventricular biopsies. RV hypertension was produced by constricting the
pulmonary artery and was increased until RV failure occurred, as evidenced
by decreased aortic pressure and cardiac output and increased RV
end-diastolic pressure. With increasing RV systolic pressure, RV myocardial
blood flow failed to increase in proportion to demand. At the onset of RV
failure, there was no reactive hyperemia of right coronary flow compared
with control, indicating the absence of further coronary vascular reserve;
biochemical analysis demonstrated that the RV free wall was ischemic; the
LV free wall was not. Infusion of phenylephrine raised aortic pressure and
hence, myocardial perfusion pressure; RV failure reversed as shown by
decreased RV end-diastolic pressure and increased cardiac output and RV
systolic pressure; reactive hyperemia of right coronary flow was restored
and the biochemical indexes of ischemia were reversed, demonstrating that
ischemia is the cause of failure in acute RV hypertension.
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The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations
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