Comparison of cardiorespiratory responses to sudden progressive hypoxia in an animal model with and without respiratory failure.

Abstract

The aim of this study was to compare the hemodynamic and oxygen transport responses to sudden, acute progressive hypoxia in normal control conditions (six healthy dogs) and in subacute respiratory failure (six dogs with naturally occurring distemper). The latter were used to simulate respiratory failure from viral pneumonitis in man. Acute progressive hypoxia was induced by rebreathing through a respirometer while hemodynamic and oxygen transport variables were rapidly and repeatedly measured. The immediate effects of hypoxia were decreased PaO2 and oxygen delivery. In the middle period of hypoxia, defined as periods 4, 5, and 6 of eight equally spaced time periods, cardiac index, stroke volume, and oxygen extraction increased; these occurred as compensatory responses. Oxygen consumption (VO2) remained relatively stable until late in both control and distemper dogs. Initially, physiologic compensations in distemper dogs were found to be partially exhausted and overall to be shorter in duration and of lesser magnitude when compared with the healthy control animals. Failure to maintain near normal VO2 toward the end of the hypoxic episode indicated the progression of decompensation, imminent circulatory deterioration, and death.