Continuous intramucosal PCO2 measurement allows the early detection of intestinal malperfusion.

OBJECTIVES

The intestinal metabolic and histologic changes that occur in the gastrointestinal tract with ischemia and that form the basis of intramucosal pH and PCO2 alterations have not been well established. Recent evidence suggests that apart from technical problems with gastric tonometry, some methodologic misconceptions in the interpretation of intramucosal pH and PCO2 exist. The present study was designed to demonstrate the effects of impaired mesenteric perfusion with specific consideration to the induced intramucosal PCO2 changes using a new technique, the continuous fiberoptic CO2 sensor, and a new concept of interpretation.

DESIGN

Randomized, controlled intervention trial.

SETTING

University animal laboratory.

SUBJECTS

Twelve anesthetized female pigs, weighing 67+/-6 kg.

INTERVENTIONS

The pigs were assigned to control and stenosis groups. In the stenosis group, blood flow in the superior mesenteric artery was reduced by 70% from baseline for 180 mins, followed by 120 mins of reperfusion. Serum lactate concentration, pH, PCO2, PO2, and bicarbonate concentration (cHCO3-) were determined in arterial, superior mesenteric venous, portal venous, hepatic venous, and pulmonary arterial blood. In the lumen of the ileum, intramucosal PCO2 was continuously determined by a fiberoptic CO2 sensor. At the end of the experiment, the gut was examined for histologic changes.

MEASUREMENTS AND MAIN RESULTS

During mesenterial hypoperfusion, a sudden and significant increase in intramucosal PCO2 was observed. This increase was paralleled by increases in superior mesenteric venous PCO2 and portal venous PCO2 (p < .05) and a concomitant decrease in intramucosal pH, superior mesenteric venous pH, and portal venous pH. Arterial and mixed venous PCO2 and pH did not change. cHCO3- did not change in local or systemic blood samples.

CONCLUSIONS

Compromised mesenteric blood flow causes significant metabolic and histologic changes. These local changes could not be detected by arterial or mixed venous lactate concentrations, pH, and PCO2 determinations. Under closed-system conditions, mesenteric CO2 accumulation causes an impairment of the CO2-HCO3- buffer, resulting in an unchanged cHCO3-. With impaired mesenteric perfusion, only intramucosal PCO2 alterations occur and an intramucosal pH calculation based on systemic cHCO3-changes is not necessarily correct. Therefore, the only parameter of importance is the intraluminal measurement of intramucosal PCO2 that can reflect isolated mesenteric changes. Thus, we recommended abolishing the terms "intramucosal pH measurement" and "gastric tonometry" and propose using the definition "intramucosal PCO2 measurement."