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Recent reports indicate the possible role of bladder CO 2  as a marker of low perfusion states. To test this hypothesis, shock was induced in six beagle dogs with 1 mg/kg of  E. coli  lipopolysaccharide, gastric CO 2  (CO 2 -G) was measured with a continuous monitor, and a pulmonary catheter was inserted in the bladder to measure CO 2  (CO 2 -B). Levels of CO 2 -B were found to be lower than those of CO 2 -G, with a mean difference of 36.8 mmHg ( P  < 0.001), and correlation between both measurements was poor ( r   2  = 0.16). Even when the correlation between CO 2 -G and ΔCO 2 -G was narrow ( r   2  = 0.86), this was not the case for the relationship between CO 2 -B and ΔCO 2 -B ( r   2  = 0.29). Finally, the correlation between CO 2 -G and base deficit was good ( r   2  = 0.45), which was not the case with the CO 2 -B correlation ( r   2  = 0.03). In our experience, bladder CO 2  does not correlate to hemodynamic parameters and does not substitute gastric CO 2  for detection of low perfusion states.

Bladder Mucosal CO2Compared with Gastric Mucosal CO2as a Marker for Low Perfusion States in Septic Shock

Bladder Mucosal CO₂Compared with Gastric Mucosal CO₂as a Marker for Low Perfusion States in Septic Shock