Effects of increased arterial pressure and positive inotropic agents on the severity of myocardial ischemia in the acutely depressed heart

Abstract

Recently it has been established that factors that affect myocardial oxygen consumption also influence the magnitude and extent of ischemic injury. In the nonfailing heart when mean arterial pressure was increased, the extent of ischemic injury decreased and, after isoproterenol or digitalis administration, ischemic injury increased. However, agents such as digitalis and catecholamines can have differing effects on myocardial oxygen consumption, depending on the initial contractile state and heart size. Moreover, since many patients with acute myocardial infarction have an associated depression of left ventricular function, the relevance of the earlier findings to the failing heart must be considered. The present study was undertaken to examine the effects of systemic arterial hypertension, digitalis and isoproterenol on the extent of myocardial ischemic injury after acute pharmacologic depression of the dog heart. Following card̄iac depression in 22 experiments, when mean arterial pressure was increased from 110 to 145 mm Hg, mean S-T segment elevation increased from 3.6 to 4.7 mv ( P < 0.05). In 6 acutely depressed left ventricles, ouabain (0.03 mg per body weight kg) resulted in a decrease in mean S-T elevation from 4.2 to 1.5 mv ( P < 0.01), whereas the average left atrial pressure decreased from 25.3 to 11.1 mm Hg. In 3 of 10 studies, administration of isoproterenol in small doses produced a positive inotropic and chronotropic effect on the depressed heart but failed to increase the extent of ischemic injury. These studies indicate that the effects of hemodynamic and pharmacologic interventions can depend on the prior functional status of the left ventricle. Thus, in contrast to findings in the nonfailing heart, in the presence of acute experimental cardiac depression, elevation of systemic arterial blood pressure to above normal levels after coronary occlusion can result in the extension of ischemic injury, whereas digitalis can decrease the extent of myocardial ischemic injury.