• E C Rackow, M E Astiz, C E Mecher, and M H Weil.
• Department of Medicine, St. Vincent's Hospital, New York, NY 10011.
• Crit. Care Med. 1994 Jan 1;22(1):121-5.

ObjectiveTo test the hypothesis that decreases in blood flow during septic shock lead to increases in the venous-arterial PCO2 difference in a rat model of sepsis.DesignProspective, randomized, controlled experimental study.SettingResearch laboratory.SubjectsFifteen Sprague-Dawley rats.InterventionsSevere sepsis was induced by cecal ligation and perforation. Ten animals were randomized to no treatment or fluid infusion to maintain the cardiac output at baseline values. An additional five rats served as sham-operated controls.Measurements And Main ResultsHemodynamic measurements, arterial and central venous blood gases were obtained at baseline, and then at 3 hrs and 6 hrs after abdominal surgery. In the five septic rats that did not receive volume infusion, cardiac output decreased from 331 +/- 32 to 172 +/- 9 mL/min/kg (p < .001). This decrease in cardiac output was associated with an increase of 13 +/- 2 torr (1.7 +/- 0.2 kPa) in the venous-arterial PCO2 difference (p < .001). Furthermore, the venous-arterial PCO2 gradient correlated linearly with the cardiac output in the same animals (r2 = .52, p < .001). In the septic animals that received volume infusion and in sham animals, cardiac output and the venous-arterial PCO2 remained unchanged from baseline at 6 hrs.ConclusionWe conclude that the increase in the venous-arterial PCO2 gradient in severe sepsis appears to be related to reductions in cardiac output.

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