Effect of cardiotonic and vasoactive drugs on transmural flow distribution and ventricular volume in the fibrillating heart on cardiopulmonary bypass.

Subendocardial hemorrhagic necrosis in an important cause of death following cardiopulmonary bypass. The transmural distribution of flow across the left ventricle (LV), septum (SP), and right ventricle (RV) is a complex interaction of vascular resistance and myocardial compressive resistance. We studied the change in transmural blood flow in LV, SP, and RV, and left ventricular volume, following administration of cardiotonic and vasoactive drugs in the fibrillating heart. The drugs studied included calcium with and without ATP-induced vasodilation, isoproterenol, epinephrine, angiotensin, and ouabain. Calcium produced underperfusion of LV subendocardium with or without previous ATP vasodilation. Isoproterenol also caused underperfusion of LV subendocardium. Both calcium and isoproterenol decreased ventricular volume. Angiotensin increased resistance in the subepicardium and increased flow in the subendocardium, with no change in ventricular volume. Epinephrine and ouabain caused no consistent changes in transmural flow. The decreased ventricular volume produced by calcium and isoproterenol restricts flow in the subendocardium because of increased compressive resistance. Increased subendocardial flow with angiotensin indicates that subepicardial vasodilation in the fibrillating heart causes epicardial "steal," which contributes to subendocardial ischemia.