The effect of insufflation pressure on CO₂ pneumoperitoneum and embolism in piglets

We conducted this study to investigate the effect of insufflation pressure on the pathophysiology of CO₂ pneumoperitoneum and embolism in an infant model. Twenty anesthetized piglets had stepwise intraperitoneal insufflation with CO₂ for 15 min at pressures ranging from 5 to 20 mm Hg. The piglets were ventilated to baseline normocarbia (ET_CO2 = 30 mm Hg, Pa_CO2 = 38 mm Hg) before beginning each insufflation. CO₂ was then insufflated IV in 15 of these piglets at the same pressures. There was no reduction of blood pressure or cardiac output with intraperitoneal insufflation, but the stroke volume declined significantly (* P < 0.05) from (mean ± SE) 10.6 ± 1.3 mL to 8.5 ± 1.3* mL and from 10.0 ± 1.4 mL to 7.2 ± 1.2* mL at 15 and 20 mm Hg insufflation pressure, respectively. Abdominal insufflation at 5, 10, 15, and 20 mm Hg caused an increase in ET_CO2 to 31.7 ± 0.8 mm Hg, 35.6 ± 1.2* mm Hg, 37.5 ± 1.5* mm Hg, and 40.1 ± 1.8* mm Hg and in Pa_CO2 to 41.1 ± 1.3* mm Hg, 44.2 ± 1.4* mm Hg, 49.9 ± 1.8* mm Hg, and 53.0 ± 2.1* mm Hg, respectively. In contrast, the ET_CO2 decreased to 19.4 ± 1.5* mm Hg, 20.4 ± 1.4 mm Hg, 15.2 ± 2.1* mm Hg, and 10.6 ± 2.0* mm Hg with IV insufflation using the same pressures. IV insufflation caused marked hypotension and mortality. As the insufflation pressure increased, the mortality increased (0 in 15, 1 in 15, 1 in 14, and 6 in 13* at 5, 10, 15, and 20 mm Hg;* P < 0.05 vs 0 in 15, 1 in 15, and 1 in 14). This study suggests that although intraperitoneal insufflation up to 20 mm Hg may be tolerated hemodynamically, the lowest possible pressure should be used to reduce hypercarbia. A low insufflation pressure may also prevent mortality from CO₂ embolism.