Oxygen Toxicity. Effects of Oxygen Breathing at Increased Ambient Pressure Upon pCO2 of Subcutaneous Gas Depots in Men, Dogs, Rabbits and Cats

Abstract

Gesell proposed 30 years ago that failure of hemoglobin (hgb.) reduction during inhalation of O2 at high partial pressure might contribute to the development of O2 convulsions by causing a severe CO2 autointoxication. Since that time repeated reports of the occurrence of extremely large elevations of the pCO2 in subcutaneous or peritoneal depots in small animals have been published pointing to an important role of CO2 retention in O2 poisoning. Our studies in men, dogs, rabbits and cats indicate that no appreciable elevation of depot pCO2 can be demonstrated until after the onset of O2 convulsions and that the subsequent gradual rise in depot pCO2 is due primarily to pulmonary damage and respiratory failure, not to decreased hgb. reduction. The absence of an immediate, gross rise in depot pCO2 is in agreement with our previous findings that diminished hgb. reduction during oxygen inhalation at 3.5 atms. causes only a 2 to 3 mm. Hg increase in the internal jugular pCO2 of normal men. The sources of error inherent in the tissue depot method as employed by previous workers indicate that the reported early and extreme elevations of depot pCO2 do not represent levels of pCO2 within the tissues. We conclude that these reports can no longer be considered as supporting interference with CO2 transport from the tissues to the lungs as a contributory factor in O2 poisoning. The late rise in tissue pCO2 which follows interference with the pulmonary gas exchange appears to be a result, rather than a cause, of O2 toxicity.