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

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. INTERVENTION: 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.

Reduction of CO(2)-pneumoperitoneum-induced metabolic hypoxaemia by the addition of small amounts of O(2) to the CO(2) in a rabbit ventilated model. A preliminary study.

BACKGROUND: CO(2)-pneumoperitoneum used in endoscopic surgery induces system effects by CO(2) absorption. This study investigated the effect of the addition of O(2) to CO(2)-pneumoperitoneum, upon CO(2) absorption. METHODS: The effect of a pneumoperitoneum using 100% CO(2) or 94% CO(2) + 6% O(2) upon arterial blood gases, acid base and O(2) homeostasis was evaluated. In series A suboptimal ventilation and a pneumoperitoneum pressure (PP) of 10 mmHg was used. In series B adequate ventilation and PP of 6 mmHg was used. RESULTS: CO(2)-pneumoperitoneum profoundly affected blood gases and acid base homeostasis i.e. increasing pCO(2), HCO(3)(P < 0.001) and lactate concentrations (P < 0.05) and decreasing pH, actual base excess and standard bicarbonate (P < 0.001), resulting in metabolic hypoxaemia with desaturation, lower pO(2) (P < 0.001) and O(2)Hb (P < 0.05). These effects were more pronounced with higher PP and suboptimal ventilation. CONCLUSION: CO(2)-pneumoperitoneum profoundly affected blood gases and acid base homeostasis resulting in metabolic hypoxaemia. The addition of 6% of O(2) to the CO(2)-pneumoperitoneum prevented these effects to a large extent. If these preliminary data are confirmed in the human, the addition of a few percent of O(2) to CO(2) could become important for endoscopic surgery of long duration, especially in obese patients with limited cardiorespiratory adaptation and steep Trendelenburg.