Control of myocardial oxygen consumption: Physiologic and clinical considerations

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The basal oxygen consumption of the heart is small, approximately 20 percent of that of the contracting organ. Oxygen cost of depolarization is approximately 0.5 percent of the total oxygen consumed by the normally working heart. There is a far greater oxygen cost of “pressure work” as opposed to “flow work,” and a close relation between the area beneath the left ventricular pressure curve, that is, the tension-time index, and myocardial oxygen consumption. Also, the contractile state of the heart, as reflected in the maximal velocity of isotonic shortening, is a major determinant of myocardial oxygen consumption. Thus, velocity of contraction shares the role of important determinant of myocardial oxygen consumption with developed tension and heart rate. Although the precise costs of activation and maintenance of the active state of the myocardium have not yet been clearly defined, it is likely that they are relatively low. In studies on isolated papillary muscles, oxygen consumption was found to be a function of the tension that is developed and the velocity of shortening of the unloaded muscle. Shortening against a load requires oxygen above and beyond that required for the development of tension. Almost the entire increase in myocardial oxygen consumption produced by the administration of catecholamines results from the increased contractile activity produced rather than from a direct stimulating effect of the catecholamines on myocardial metabolism. Severe valvular regurgitation does not increase myocardial consumption significantly when myocardial tension is held constant. Congestive heart failure is associated with depression of myocardial contractility, but this cannot be attributed to any reduction of high energy phosphate stores in muscles that are utilized normally. A technique for reducing myocardial oxygen requirements by stimulating the carotid sinus nerves is described and its application to the treatment of angina pectoris demonstrated. It is also shown that following coronary occlusion, interventions that increase myocardial oxygen consumption appear to increase the size of the infarction, whereas those that decrease myocardial oxygen consumption reduce the size of the infarction.