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.

Control of myocardial oxygen consumption: physiologic and clinical considerations.

Pharmacokinetic changes in patients receiving extracorporeal membrane oxygenation

The AVCO balloon pump has been employed in treating 40 patients with cardiogenic shock from acute myocardial infarction (CS-MI). All patients were given a trial of medical therapy with hemodynamic monitoring. The time from the development of shock to institution of intraaortic balloon pumping (IABP) was less than 24 hours in all but nine patients. Prior to IABP the mean hemodynamic values were: cardiac index (CI) 1.7 liters/min/m2; mean arterial pressure (MAP) 66 mm Hg; pulmonary artery wedge pressure (PAW) 22 mm Hg. After 24-48 hours of IABP the CI and MAP had increased 0.8 liters/min/m2 and 8 mm Hg, respectively, and the PAW had decreased 4.8 mm Hg. During IABP the shock syndrome was reversed in 31 patients. Four of 25 patients treated with IABP alone survived to be discharged, but two have died from subsequent infarctions. Because of the persistent high mortality, 15 patients judged unable to survive off IABP have undergone emergency surgical procedures with IABP continuing during preoperative angiogra...

Clinical and Hemodynamic Results of Intraaortic Balloon Pumping and Surgery for Cardiogenic Shock

Clinical features, predisposing factors, precipitating events, laboratory and hemodynamic observations, pathologic findings, prognostic indicators and the results of therapy are surveyed for 73 patients in whom shock developed after acute myocardial infarction. The incidence of shock was 15 percent, and the mortality 86 percent. It was not possible to differentiate patients with shock from those with acute infarction alone on the basis of age, anamnestic data, delay before hospitalization or anatomic location of infarction. No precipitating cause for shock other than acute infarction itself was consistently present. Hypovolemia, anemia, arrhythmia and drugs could not be incriminated as important factors in the genesis of shock. Extensive myocardial damage, coronary atherosclerosis and left ventricular hypertrophy were found at postmortem examination in most patients who died, but similar findings were noted in a group of patients in the coronary care unit who died without evidence of shock during the period of the study. Delay in onset of shock in many cases suggested progression of cardiac damage after the initial clinical event. Hemodynamic studies in 19 patients showed that cardiac index was less than half of the normal index, stroke volume index about a third of normal, and peripheral resistance generally increased. We conclude that patients who have the highest risk can be identified from various clinical and hemodynamic observations. It is appropriate to consider such patients for unconventional therapy.

Shock after acute myocardial infarction: A clinical and hemodynamic profile

Background— Enhanced external counterpulsation (EECP) is a noninvasive, pneumatic technique that provides beneficial effects for patients with chronic, symptomatic angina pectoris. However, the physiological effects of EECP have not been studied directly. We examined intracoronary and left ventricular hemodynamics in the cardiac catheterization laboratory during EECP. Methods and Results— Ten patients referred for diagnostic evaluation underwent left heart catheterization and coronary angiography from the radial artery. At baseline and then during EECP, central aortic pressure, intracoronary pressure, and intracoronary Doppler flow velocity were measured using a coronary catheter, a sensor-tipped high-fidelity pressure guidewire, and a Doppler flow guidewire, respectively. Similar to changes in aortic pressure, EECP resulted in a dramatic increase in diastolic (71±10 mm Hg at baseline to 137±21 mm Hg during EECP; +93%; P<0.0001) and mean intracoronary pressures (88±9 to 102±16 mm Hg; +16%; P=0.006) with a...

http://www.counterpulsation.co.za/files/J2002---Michaels---Left-Ventricular-Systolic-Unloading-and-A.pdf

Left Ventricular Systolic Unloading and Augmentation of Intracoronary Pressure and Doppler Flow During Enhanced External Counterpulsation

IT is now generally accepted that blood flow is unaffected by depulsation, 1-4 but there is considerable evidence that tissue function is impaired by nonpulsatile perfusion. 5-7 Although there have been many interesting studies of the effects of depulsation on renal function, their results have been contradictory. Further, because extracorporeal pumping mechanisms have been used to achieve nonpulsatile flow and because of the possible limitations imposed by the preparations used, their applicability to the intact organism is uncertain. In our laboratory, we have designed a depulsation model that uses a passive, electronically controlled, pulse-shaping device installed in series with the aorta. The device is energized by the heart, rather than by an extracorporeal pump, and allows the autoregulatory mechanisms to retain their integrity. In studies 4 of the systemic-physiologic effects of total and regional depulsation, we found a significant rise of 9.6% in mean aortic pressure and peripheral resistance when the

The Physiologic Role of Pulsatile and Nonpulsatile Blood Flow: II. Effects on Renal Function

The effect of counterpulsation upon hemodynamics and myocardial oxygen consumption was studied in 14 dogs. With properly synchronized counterpulsation, a reduction in mean systolic pressure, tension-time index, left ventricular work, and myocardial oxygen consumption was observed, with no change in effective cardiac output. The reduction in myocardial qO2, however, did not parallel the fall in tension-time index. Mechanical efficiency fell and the oxygen cost of pressure generation by the left ventricle rose. Premature triggering of the pump systole resulted in an actual increase in myocardial qO2, despite a fall in tension-time index. The influence of counterpulsation upon the energy requirements of the left ventricle is briefly discussed.

Soroff Hs

Papers

The Physiologic Role of Pulsatile and Nonpulsatile Blood Flow: II. Effects on Renal Function

Assisted Circulation II. Effects of Counterpulsation on Left Ventricular Oxygen Consumption and Hemodynamics

Support of the systemic circulation and left ventricular assist by synchronous pulsation of extramural pressure.

Assisted circulation. I. An improved method for counterpulsation.

Support of the systemic circulation and left ventricular assist by synchronous pulsation of extramural pressure.