Regional myocardial blood flow and coronary vasodilator reserve during acute right ventricular failure due to pressure overload in swine

Abstract

Right ventricular (RV) failure due to acute RV pressure overload has been attributed to the inability of RV myocardial blood flow to increase following maximal RV coronary vasodilatation, which may occur with mild to moderate RV systolic hypertension, such that further increments in RV systolic pressure by way of decreasing RV coronary driving pressure hamper RV myocardial perfusion. To test this hypothesis, myocardial blood flow (15-μm-diameter tracer microspheres) was studied during adenosine infusion (3 μmole · kg⁻¹ · min⁻¹) instituted before and during acute RV failure in 10 closed-chest ketamine anesthetized young pigs. Acute RV failure, characterized by 10 mm Hg increase in RV end-diastolic pressure, 15 mm Hg drop in mean aortic pressure and 30% drop in cardiac output, was produced by partial constriction of the main pulmonary artery upon inflation of a previously implanted cuff. Acute RV failure was accompanied by a significant increase in myocardial blood flow in the RV free wall (91%) and right side of the septum (44%) while left ventricular myocardial blood flow was unaltered. Adenosine infusion during acute RV failure resulted in a significant increase in ventricular myocardial blood flow despite a significant drop in mean aortic pressure while RV end-diastolic and RV systolic pressures were further increased. Thus, the concept of maximal RV coronary vasodilatation during acute RV failure was not supported by these data. RV myocardial blood flow with adenosine infusion during acute RV failure (3.8 ml.min⁻¹ · g⁻¹) was, however, only 67% of that observed without RV failure (5.7 ml.min⁻¹ · g⁻¹). Also, during acute RV failure + adenosine, RV endo:epi flow ratio decreased markedly. We believe these differences were due to a combination of factors, namely, decreased diastolic duration for RV perfusion consequent upon prolongation of RV systole due to RV pressure overload, and higher back pressure opposing the diastolic RV perfusion because of significantly elevated preload.