Nitrous oxide intensifies the pulmonary arterial pressure response to venous injection of carbon dioxide in the dog.

To determine the effect of nitrous oxide on the body's response to venous carbon dioxide (CO2) embolization, the authors compared changes in mean pulmonary arterial pressure (MPAP) following intravenous injections of CO2 in pentobarbital-anesthetized dogs breathing 100 per cent oxygen (O2) or nitrous oxide--oxygen, 79:21 per cent (N2O). When CO2 was infused intravenously in seven dogs at a rate of 3 ml/kg/min the volume of injected CO2 needed to increase MPAP to 40 per cent above control during breathing of O2 was approximately 5.5 times the volume necessary during inhalation of N2O. In a second group of eight dogs, breathing N2O, compared with O2 or air, resulted in a significantly greater increase and duration of increase in MPAP following a bolus injection of CO2 of 20, 40 or 80 ml. The data suggest that breathing nitrous oxide intensifies and prolongs the effect of CO2 bubbles in blood. While the magnitude of insult following intravenous injection of CO2 is about 6.5 times less than that for a similar volume of air, avoidance of nitrous oxide should be considered in management of patients in whom CO2 embolism is possible.