ACUTE RESPIRATORY-ACIDOSIS DECREASES LEFT-VENTRICULAR CONTRACTILITY BUT INCREASES CARDIAC-OUTPUT IN DOGS

To understand the cardiovascular response to respiratory acidosis, we measured hemodynamics, left ventricular pressure, and left ventricular volume (three ultrasonic crystal pairs) during eucapnia and respiratory acidosis in 10 fentanyl-anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope (E(max)) and intercept (V0) of the left ventricular end-systolic pressure-volume relation determined by combining end-systolic points from a vena caval occlusion and from brief aortic cross-clamping. Respiratory acidosis (pH 7.09, P(CO2) 92 mm Hg) reduced contractility by a decrease in E(max) (11.4 to 9.2 mm Hg/ml, p < 0.01) with no change in V0. Despite this, cardiac output increased (1.7 to 2.1 l/min, p < 0.01), and heart rate increased (96 to 121 beats/min, p < 0.05), with no change in blood pressure. Systemic vascular resistance fell by 26% (p < 0.01). During eucapnia, propranolol reduced E(max) (11.4 to 4.6 mm Hg/ml, p < 0.01) with no change in V0. After propranolol treatment, respiratory acidosis further reduced E(max) (4.6 to 3.6 mm Hg/ml, p < 0.05) and increased end-systolic volume more than before propranolol (p < 0.001). Now cardiac output did not increase even though heart rate increased (81 to 106 beats/min, p < 0.001) and systemic vascular resistance fell by 20% (p < 0.01). We conclude that the effect of respiratory acidosis on the circulation is to increase venous return (equals cardiac output) in the face of decreased left ventricular contractility. The β-adrenergic response to respiratory acidosis substantially ameliorated the increase in end-systolic volume and supported the increase in venous return but did not alter the associated tachycardia or vasodilation. Respiratory acidosis, like propranolol treatment, decreases contractility by decreasing E(max).