Intraperitoneal and Retroperitoneal Carbon Dioxide Insufflation Evoke Different Effects on Caval Vein Pressure Gradients in Humans

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Abstract
Background: The authors hypothesized that intraperitoneal and retroperitoneal carbon dioxide insufflation during surgical procedures evoke markedly different effects on the venous low-pressure system, induce different inferior caval vein pressure gradients at similar insufflation pressures, and may provide evidence for the Starling resistor concept of abdominal venous return. Methods: Intra- and extrathoracic caval vein pressures were measured using micromanometers during carbon dioxide insufflation at six cavity pressures (baseline and 10, 15, 20, and 24 mmHg and desufflation) in 20 anesthetized patients undergoing laparoscopic (supine, n = 8) or left (n = 6) or right (n = 6) retroperitoneoscopic (prone position) surgery. Intracavital, esophageal, and gastric pressures also were assessed. Data were analyzed for insufflation pressure-dependent and group effects by one-way and two-way analysis of variance for repeated measurements, respectively, followed by the Newman-Keuls post hoc test (P < 0.05). Results: Intraperitoneal, unlike retroperitoneal, insufflation markedly increased, in an insufflation pressure-dependent fashion, the inferior-to-superior caval vein pressure gradient (P < 0.00001) at the level of the diaphragm. In contrast to what was observed with retroperitoneal insufflation, transmural intrathoracic caval vein pressure increased at 10 mmHg insufflation pressure, but the increase flattened with an insufflation pressure of more than 10 mmHg, and pressure decreased with an inflation pressure of 20 mmHg (P = 0.0397). These data are consistent with a zone 2 or 3 abdominal vascular condition during intraperitoneal and a zone 3 abdominal vascular condition during retroperitoneal insufflation. Conclusions: Intraperitoneal but not retroperitoneal carbon dioxide insufflation evokes a transition of the abdominal venous compartment from a zone 3 to a zone 2 condition, presumably impairing venous return, supporting the Starling resistor concept of abdominal venous return in humans.

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