Effect of arterial hypoxia on myocardial oxygen consumption.

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" left ventricle (P < 0.005) above the control level at an arterial oxygen content of 7-9 ml/100 ml blood (Po2 = 30 mm Hg). This value represents a 19% increase from a control MVO2 of 7.9 ml/min 100 g1 left ventricle (arterial oxygen content 15-18 ml/100 ml blood, Po2 > 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 MV02 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 MVO2 and (2) a decrease in myocardial efficiency.