Effects of halothane on coronary and systemic circulations, myocardial metabolism and blood flow distribution within the canine heart.

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Abstract
Myocardial metabolism, blood flow distribution within the heart, and coronary and systemic circulations were observed during halothane anesthesia using 15 mongrel dogs. PaO2 [arterial O2 tension] and PaCO2 [arterial CO2 tension] were maintained near 100 and 40 torr, respectively. As arterial halothane content increased, most parameters of systemic circulation were depressed significantly. Coronary blood flow was reduced in parallel with myocardial O2 consumption (MVO2) (r = +0.89, P < 0.001). Myocardial contractility decreased significantly as anesthesia deepened. MVO2 and myocardial CO2 production were reduced as arterial halothane concentration rose. Arterial-coronary venous difference in blood O2 content remained unchanged even in deep stage. Lactate and pyruvate were continuously taken up by the myocardium, although the amounts of uptake were reduced as anesthesia progressed. Calculated excess lactate and redox potential did not show any signs of myocardial hypoxia even in deep halothane anesthesia. Among major hemodynamic parameters, left ventricular dp/dt max [maximal change in pressure with change in time] showed the closest correlation with MVO2. Microsphere injection method was used to observe blood flow distribution within the heart. Halothane did not influence the distribution significantly and I/O [gamma emission compared in endocardial and epicardial layers] ratio of the left ventricular free wall remained near 1.0.

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