Cardiopulmonary responses to experimental venous carbon dioxide embolism

Background: Although the low-flow CO₂ insufflation rate used to initiate pneumoperitoneum may reduce the severity of potential venous embolism, its safety is not established. Methods: Anesthetized pigs were ventilated with room air at a fixed minute ventilation. After 1 h of baseline, they were intravenously infused with CO₂ at the rate of 0.3, 0.75, or 1.2 ml/kg/min for 2 h (n = 5 for each group), followed by 1 h of recovery. Results: All animals experienced pulmonary hypertension, depressed stroke volume, hypoxemia, hypercarbia, and acidemia during intravenous CO₂ infusion. They had systemic hypertension at the low rate and hypotension at the highest rate of infusion. End-tidal CO₂ levels briefly decreased, then increased in all cases. In the highest rate group, three of the five animals (60%) died at 50, 65, and 100 min of infusion. These three animals had severe hypotension and hypoxemia, with visible coronary gas embolism. There was no patent foramen ovale at necropsy in any animals. Conclusions: The low-flow insufflation rate exceeds the fatal rate of continuous intravenous CO₂ infusion. End-tidal CO₂ levels were increased in venous CO₂ embolism, not decreased as seen in venous air embolism. Severe hypoxemia and hypotension are predictors of potentially fatal cases.