Mayer K L, Ho H S, Mathiesen K A, Wolfe B M
Department of Surgery, University of California Davis Medical Center, Sacramento 95817-2214, USA.
Surg Endosc. 1998 Aug;12(8):1025-30. doi: 10.1007/s004649900773.
Although the low-flow CO2 insufflation rate used to initiate pneumoperitoneum may reduce the severity of potential venous embolism, its safety is not established.
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.
All animals experienced pulmonary hypertension, depressed stroke volume, hypoxemia, hypercarbia, and acidemia during intravenous CO2 infusion. They had systemic hypertension at the low rate of 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.
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.
