Pathogenesis of CO(2) pneumoperitoneum-induced metabolic hypoxemia in a rabbit model

To investigate the effects of carbon dioxide (CO(2)) pneumoperitoneum-induced changes in blood gases, acid-base balance, and oxygen homeostasis in rabbits.

Prospective, randomized, controlled study (Canadian Task Force classification I).

University training and teaching center.

Twenty-six adult female New Zealand white rabbits.

Anesthesia and pneumoperitoneum.

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.

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.