Effect of Arterial Hypoxia on Myocardial Oxygen Consumption

Abstract

To evaluate the effect of arterial hypoxia on myocardial oxygen consumption (MVO₂) under controlled conditions of stable or decreased contractility and tension, 18 anesthetized, adrenergically blocked dogs on right heart bypass were studied. Heart rate, cardiac output, pH, and Pco₂ were constant. In 9 dogs, progressive decreases in arterial oxygen content were associated with progressive significant increases in MVO₂ to a peak of 1.5 ± 0.5 ml/min 100 g^-1 left ventricle (P 200 mm Hg). Progressive decreases occurred in mean aortic pressure (P < 0.001) and tension-time index (P < 0.001) with no significant change in mean ejection rate, left ventricular dP/dt, or left ventricular end-diastolic pressure. Quantitatively similar increases in MVO₂ with controlled hemodynamics were found when coronary flow was held constant (5 dogs), after catecholamine depletion with reserpine (2 dogs), and in the beating, empty ventricle (2 dogs). Thus, arterial hypoxia results in (1) an increase in MVO₂ despite no change or a decrease in the magnitude of the hemodynamic parameters correlated with MV₂ and (2) a decrease in myocardial efficiency.