Effects of Halothane Anesthesia on Rate of Canine Oxygen Consumption

Abstract

In dogs anesthetized with halothane, increase in halothane concentration from 0. 8 to 2. 5% (mean expired) was accompanied by a 17% reduction in O2 consumption (VO2) and a halving of cardiac output (Q) and arterial pressure. Repayment of an O2 debt was not observed with return to 0. 8% halothane. Values of VO2 at 0. 8% halothane were reduced by measures that reduced Q and arterial pressure (vagal and paired pulse stimulation). Conversely, VO2 at 1. 7% halothane was increased by maneuvers that increased Q ana arterial pressure (digitalis and blood or dextran administration). Change in myocardial VO2 alone is believed to be insufficient to account for the observed changes in whole-body VO2. Accordingly, the reductions in VO2 observed with increased halothane concentration may represent indirect effects mediated by halothane-induced changes in the circulation although direct metabolic depressant effects of halothane per se were not ruled out.