Depressed postoperative cardiac performance. Prevention by adequate myocardial protection during cardiopulmonary bypass.

Abstract

Depressed postoperative myocardial performance (low output syndrome) requiring inotropic drugs or balloon counterpulsation is due to subendocardial ischemic damage. Before July, 1972, we needed inotropic drugs in 30 to 52 per cent of 189 patients undergoing coronary revascularization or aortic or mitral valve replacement in whom we used ischemic arrest, profound topical hypothermia, and ventricular fibrillation. The mortality rate ranged from 10 to 17 per cent. Our experimental studies show that morbidity and death in such cases are caused by ischemic injury to the heart resulting from inadequate myocardial protection during bypass. Based on these experimental studies, we have, since July, 1972, employed the following principles clinically: (1) Maintain beating empty heart whenever possible; (2) maintain adequate coronary perfusion pressure (less than 80 mm. Hg); (3) avoid extreme hemodilution; (4) avoid ventricular fibrillation; (5) avoid prolonged hypothermic arrest, limiting ischemic periods to less than 15 minutes; (6) repay myocardial ischemic oxygen debt with total (vented) bypass; and (7) optimize DPTI/TTI (supply/demand ratio) pre- and postoperatively. These principles were followed in 189 consecutive operations, and postoperative inotropic drugs were needed in only 12. The principles were violated in 4 of the 12 patients (6 per cent), and 5 others had identifiable causes of myocardial depression; low output syndrome was unexplained in only 3 patients (1.7 per cent).