Comparative cardiopulmonary effects of carbon dioxide versus helium pneumoperitoneum

The recent surge in enthusiasm for laparoscopic surgery has created concern that abdominal insufflation with carbon dioxide produces a respiratory acidosis. This may be because of both transperitoneal gas absorption and impaired ventilation with increased dead space from elevated intraabdominal pressure. To examine the relative contributions of these factors, we developed an animal model of surgical pneumoperitoneum that evaluated the cardiorespiratory effects of abdominal insufflation. Helium was chosen as an alternative to CO2 because it is both chemically and biologically inert. Carbon dioxide absorption during CO2 pneumoperitoneum caused arterial PCO2 to increase from 41.3 +/- 3.0 to a maximum of 58.3 +/- 4.0 mm Hg, with pH descending from 7.46 +/- 0.02 to a nadir of 7.31 +/- 0.02 (p < 0.05). Pulmonary artery pressure increased to twice baseline levels during CO2 insufflation (p < 0.05). Helium did not cause hypercarbia, acidemia, or pulmonary hypertension despite insufflation under identical conditions. These results indicate that transperitoneal absorption of CO2, not increased dead space, is responsible for the respiratory acidosis observed. Helium merits further study as an agent to induce pneumoperitoneum, especially when concerns of underlying acidosis or impaired gas exchange are present.