Pathogenesis CO 2 Pneumoperitoneum-Induced Metabolic Hypoxemia in a Rabbit Model

Abstract

Study Objective To investigate the effects of carbon dioxide (CO 2) pneumoperitoneum-induced changes in blood gases, acid-base balance, and oxygen homeostasis in rabbits. Design Prospective, randomized, controlled study (Canadian Task Force classification I). Setting University training and teaching center. Subjects Twenty-six adult female New Zealand white rabbits. Interventions Anesthesia and pneumoperitoneum. Measurements and Main Results In anesthetized rabbits arterial blood gases, acid-base balance, oxygenation values, and lactate concentrations were assayed during 2 hours. Spontaneous breathing, superficial and optimal ventilation without pneumoperitoneum, and with pneumoperitoneum at low (6 mm Hg) and higher (10 mm Hg) insufflation pressures were compared. The CO 2 pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis. Carboxemia with increasing end-tidal CO 2 and partial pressure of CO 2 (p< 0.001), acidosis with decreasing pH (p< 0.001), and base deficiency with decreasing actual base excess (p< 0.001), standard base excess and standard bicarbonate and acid excess with increasing hydrogen bicarbonate (p<0.05 and <0.01) were found. Desaturation (p <0.01) with decreasing oxyhemoglobin p <0.05) and hemoglobin oxygen affinity (p <0.01) were also found. Carboxemia with acidosis was more pronounced with higher (p <0.01) than with lower (p >0.05) intraperitoneal pressures, and also with spontaneous breathing (p <0.05) and superficial ventilation (p< 0.001) than with optimal ventilation, resulting in metabolic hypoxemia. Conclusion In superficially ventilated and spontaneously breathing rabbits, CO 2 pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis, resulting in metabolic hypoxemia. With optimal ventilation and low intraperitoneal pressure carboxemia, respiratory acidosis, and changes in oxygen metabolism were minimal.