Isoproterenol and cardiovascular performance

The effects of isoproterenol on cardiac dynamics and myocardial metabolism have been studied in thirty-seven human subjects and in ten dogs. The responses of subjects with valvular or ischemic heart disease were similar to those of control subjects. Left ventricular mean volume tended to decrease without any change in systolic mean pressure, indicating a decrease in mean afterload to contraction. Initial load (left ventricular end diastolic volume and pressure) tended to decrease or remain unchanged. Stroke volume was maintained despite tachycardia by increased ventricular emptying. An increased rate of ejection implied a similar directional change in fiber shortening rate. There was an inverse relation between "afterload" and systolic ejection rate. Myocardial oxygen consumption increased far out of proportion to pressure time. This was considered to be related to induced change in other mechanical factors, especially the rate of fiber shortening. Myocardial aerobic efficiency was unchanged and anaerobic metabolism was absent or insignificant. Isoproterenol acted both as a primary and a secondary coronary vasodilator, with rise in coronary venous oxygen saturation. Exercise produced significantly different effects on afterload, efficiency, pressure-energy ratio and coronary vasomotion. Isoproterenol action is mediated not only by a direct increase in chronotropism and inotropism, but also by a decrease in afterload to contraction, these effects offsetting the decrease in initial load (Starling mechanism).