Cardiovascular response to acute hypocapnia due to overbreathing

Abstract

Anesthetized dogs were maintained by artificial respiration at a fixed rate and depth. The composition of inspired CO₂ was varied while O₂ content was maintained at control levels. Cardiac output was measured by the indicator-dilution technique. Acute reduction of end-expiratory CO₂ levels below the normal value caused a decrease in blood pressure, pulse pressure, stroke volume, and cardiac output, no essential change in heart rate and an increase in total peripheral resistance. Mean systemic blood pressure and net vascular resistance were less with hypocapnia than they were at the same cardiac output at normal CO₂ levels. However, the over-all vascular resistance was greater with hypocapnia than it was in the same animal at normal CO₂ levels and control output values. Analysis of these data leads to the conclusion that the hypocapnia produced by overbreathing causes some degree of net vasodilation. The hypotension associated with hyperventilation appears to result in these experiments from the drop in cardiac output and to a lesser degree the relatively less than normal compensatory increase in total peripheral resistance.