Dose-dependent depression of cardiac function and metabolism by halothane in swine (Sus scrofa).

Halothane depresses myocardial blood flow and metabolism in the dog, but no studies in man have been published. However, the coronary circulation of the pig is remarkably similar to that of man. The authors investigated the effects of halothane-nitrous oxide anesthesia on cardiac function and metabolism in piglets. Thermodilution cardiac output, catheter-tip-manometer measurement of left ventricular function, electro-magnetic flowmeter measurement of coronary blood flow, and blood and tissue measurements of gases and metabolites were made during 0.04 (control), 0.46 (low concentration), and 1.04 (high concentration) per cent halothane vaporized in nitrous oxide, 60 per cent: oxygen, 40 per cent. Compared with control, the low concentration decreased cardiac output (CO) by 10 per cent, left ventricular systolic pressure (LVSP) by 30 per cent, peak contractile element velocity (Vmax by 34 percent, coronary blood flow (CBF) by 36 per cent, and cardiac oxygen uptake (V02) by 55 per cent. Compared with control, the high concentration decreased CO by 32 per cent, LVSP and Vmax by 53 per cent, CBF by 63 per cent and V02 by 62 per cent. This indicates that the dose-related depression in left ventricular function produced by halothane was accompanied by equivalent decreases in coronary blood flow and oxygen comsumption. There was minimal evidence of anaerobic metabolism in these depressed ventricles. Tissue levels of the high-energy phosplates, adenosinetriphosphate and creatine phosphate, and glycogen were unchanged. It is concluded that changes in cardiac oxygenation and metabolism in the pig during halothane anesthesia result from the changes in ventricular function.