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Abstract
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.
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Article info
Publication history
Accepted:
February 1,
1992
Identification
Copyright
© 1993 Published by Elsevier Inc.
