Cardiovascular responses to metabolic acidosis

Abstract

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po₂, and Pco₂ were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.