Dose-dependent Depression of Cardiac Function and Metabolism by Halothane in Swine (Sus scrofa)

Abstract

Halothane depresses myocardial blood flow and metabolism in the dog, but since the coronary circulation of the pig is remarkably similar to that of man, the effects of halothane-nitrous oxide anesthesia on cardiac function and metabolism was investigated in piglets. Thermodilution cardiac output, catheter-tip-manometer measurement of left ventricular function, electromagnetic 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) percent halothane vaporized in nitrous oxide, 60%: O2, 40%. Compared with control, the low concentration decreased cardiac output (CO) by 10%, left ventricular systolic pressure (LVSP) by 30%, peak contractile element velocity (Vmax) by 34%, coronary blood flow (CBF) by 36%, and cardiac O2 uptake (.ovrhdot.VO2) by 55%. Compared with control, the high concentration decreased CO by 32%, LVSP and Vmax by 53%, CBF by 63% and .ovrhdot.VO2 by 62%. The dose-related depression in left ventricular function produced by halothane was probably accompanied by equivalent decreases in coronary blood flow and O2 consumption. There was minimal evidence of anaerobic metabolism in these depressed ventricles. Tissue levels of the high-energy phosphates, ATP and creatine phosphate; and glycogen were unchanged. Changes in cardiac oxygenation and metabolism in the pig during halothane anesthesia result from the changes in ventricular function.