• A Heino, J Hartikainen, M E Merasto, E Alhava, and J Takala.
• Department of Surgery, Kuopio University Hospital, Finland.
• Intensive Care Med. 1998 Jun 1; 24 (6): 599604599-604.

ObjectiveWe evaluated the response of mixed venous-arterial carbon dioxide (pCO2) to severe intestinal ischaemia produced by gradual occlusion of the superior mesenteric artery (SMA).DesignProspective, controlled, experimental study.SettingAnimal research laboratory.SubjectsTwelve domestic pigs.InterventionsSMA blood flow was reduced by 40%, 70% and 100% from the baseline at 60-min intervals.Measurements And Main ResultsHaemodynamics were monitored continuously and blood gas values were determined at 30-min intervals. During the SMA occlusion we observed the development of intramucosal acidosis, increased splanchnic oxygen extraction and an increased portal venous-arterial lactate gradient indicative of splanchnic hypoperfusion and intestinal ischaemia. Intramucosal-arterial (p < 0.001), intramucosal-portal venous (p < 0.01) and portal venousarterial (p < 0.01) pCO2 gradients increased during the SMA occlusion, whereas the mixed venous-arterial pCO2 gradient remained unchanged. The mixed venous-arterial pCO2 gradient did not correlate with the intramucosal-arterial pCO2 gradient (r = 0.13), portal venous-arterial lactate gradient (r = 0.10) or splanchnic oxygen extraction (r = 0.14). The portal venous-arterial pCO2 gradient correlated with the portal venous-arterial lactate gradient (r = 0.75, p < 0.001) and splanchnic oxygen extraction (r = 0.79, p < 0.001), but not with the intramucosal-arterial pCO2 gradient (r = 0.35).ConclusionDespite clear evidence of severe splanchnic hypoperfusion, as shown by regional hypercarbia and lactate production, the mixed venous-arterial pCO2 gradient did not reflect splanchnic hypoperfusion.

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