OBJECTIVE: We evaluated the response of mixed venous-arterial carbon dioxide (pCO2) to severe intestinal ischaemia produced by gradual occlusion of the superior mesenteric artery (SMA). DESIGN: Prospective, controlled, experimental study. SETTING: Animal research laboratory. SUBJECTS: Twelve domestic pigs. INTERVENTIONS: SMA blood flow was reduced by 40%, 70% and 100% from the baseline at 60-min intervals. MEASUREMENTS AND MAIN RESULTS: Haemodynamics 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). CONCLUSION: Despite 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.
OBJECTIVE: We evaluated the response of mixed venous-arterial carbon dioxide (pCO2) to severe intestinal ischaemia produced by gradual occlusion of the superior mesenteric artery (SMA). DESIGN: Prospective, controlled, experimental study. SETTING: Animal research laboratory. SUBJECTS: Twelve domestic pigs. INTERVENTIONS: SMA blood flow was reduced by 40%, 70% and 100% from the baseline at 60-min intervals. MEASUREMENTS AND MAIN RESULTS: Haemodynamics 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). CONCLUSION: Despite 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.
Authors: G Gutierrez; F Palizas; G Doglio; N Wainsztein; A Gallesio; J Pacin; A Dubin; E Schiavi; M Jorge; J Pusajo Journal: Lancet Date: 1992-01-25 Impact factor: 79.321
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Authors: Rafael Knuesel; Stephan M Jakob; Lukas Brander; Hendrik Bracht; Andreas Siegenthaler; Jukka Takala Journal: Intensive Care Med Date: 2003-09-17 Impact factor: 17.440