Metabolic and Hemodynamic Effects of CO2 Pneumoperitoneum in a Controlled Hemorrhage Model.

摘要

Background: Intracavity infusion of fibrin sealant-based agents, as a novel modality to control internal bleeding, is associated with an increase of pneumoperitoneum (PP) pressure. The safe limit of such increase has not been well defined in hypovolemic subjects. The purpose of this study was to evaluate the hemodynamic and metabolic effects of increasing PP pressure and to define the limits of carbon dioxide (CO2) insufflation in a controlled hemorrhage rat model. Methods: Ninety male rats (474 + or - 6 g, 37 degrees + or - 1 Degrees C) were anesthetized, and mechanically ventilated. Animals were randomly distributed among 14 groups (n = 6 8) with an increasing amount of blood loss (0, 10, 15, and 17.5 mL/kg) and 15 minutes of CO2 insufflation at 0, 5, 10, and 15 mm Hg starting 15 minutes after hemorrhage, followed by desufflation. Mean arterial pressure (MAP), heart rate, and survival were recorded and arterial and venous blood samples were collected at baseline, at 15 minutes after hemorrhage, after insufflation, and after desufflation procedures to determine arterial blood gases and lactic acid levels. Results: In nonhemorrhaged animals, increasing PP pressure up to 15 mm Hg produced only transient changes in MAP and no increase in lactate level. A moderate hemorrhage (10 mL/kg) limited the safe abdominal pressure to 10 mm Hg with metabolic changes that were restored 15 minutes after desufflation. Higher PP pressure (15 mm Hg) at this hemorrhage level produced a significant decline in MAP (42%, p less than 0.001) and progressive metabolic acidosis with a 2.1-fold increase ( p less than 0.01) in lactate level. The more severe hemorrhage (15 mL/kg) further reduced the limits of PP pressure such that 10 and 15 mm Hg resulted in a progressive decline of blood pressures (52% and 54%, respectively; p less than 0.001) and severe metabolic acidosis as manifested by 3.3- and 3.1-fold rises in lactate levels, respectively.