Primary hypocapnia: a cause of metabolic acidosis

Abstract

In the presence of severe, sustained hypocapnia produced in dogs by mechanical hyperventilation, a bicarbonate deficit has been observed. The development of this deficit was progressive and did not terminate at pH compensation. The consequence of this progressive deficit was metabolic acidosis. Simultaneous with the increasing bicarbonate deficit, a rise in lactic and pyruvic acids was observed. Most of the bicarbonate deficit could be accounted for by the rise in the organic acids. In a series of experiments in which pH and pCO2 have been independently controlled, the rise in lactic and pyruvic acids was only associated with reduced pCO2. No rise in lactic and pyruvic acids occurred during hypoxia unless associated with hypocapnia. The rise in lactic and pyruvic acids plays a major role in the compensation for respiratory alkalosis. This process of compensation, although homeostatic in regard to pH, may be considered a pathologic state characterized by a progressive bicarbonate deficit. This deficit may be extensive enough to result in metabolic acidosis. Note: (With the Technical Assistance of J. Sellner, C. Pfeffer, and D. Larson) Submitted on November 29, 1961