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 o f intramucosal pH and Pco(2) alterations have not been well establishe d. Recent evidence suggests that apart from technical problems with ga stric tonometry, some methodologic misconceptions in the interpretatio n of intramucosal pH and Pco(2) exist. The present study was designed to demonstrate the effects of impaired mesenteric perfusion with speci fic consideration to the induced intramucosal Pco(2) changes using a n ew technique, the continuous fiberoptic CO2 sensor, and a new concept of interpretation. Design: Randomized, controlled intervention trial. Setting: University animal laboratory. Subjects: Twelve anesthetized f emale pigs, weighing 67 +/- 6 kg. Interventions: The pigs were assigne d to control and stenosis groups. In the stenosis group, blood flow in the superior mesenteric artery was reduced by 70% from baseline for 1 80 mins, followed by 120 mins of reperfusion. Serum lactate concentrat ion, PR, Pco(2), Po-2, and bicarbonate concentration (cHCO(3)(-)) were determined in arterial, superior mesenteric venous, portal venous, he patic venous, and pulmonary arterial blood. In the lumen of the ileum, intramucosal Pco(2) was continuously determined by a fiberoptic CO2 s ensor. At the end of the experiment, the gut was examined for histolog ic changes. Measurements and Main Results: During mesenterial hypoperf usion, a sudden and significant increase in intramucosal Pco(2) was ob served. This increase was paralleled by increases in superior mesenter ic venous Pco(2) and portal venous Pco(2) (p<.05) and a concomitant de crease in intramucosal pH, superior mesenteric venous pH, and portal v enous pH. Arterial and mixed venous Pco(2) and pH did not change. cHCO (3)(-) did not change in local or systemic blood samples. Conclusions: Compromised mesenteric blood flow causes significant metabolic and hi stologic changes. These local changes could not be detected by arteria l or mixed venous lactate concentrations, pH, and Pco(2) determination s. Under closed-system conditions, mesenteric CO2 accumulation causes an impairment of the CO2-HCO3- buffer, resulting in an unchanged cHCO( 3)(-) With impaired mesenteric perfusion, only intramucosal Pco(2) alt erations occur and an intramucosal pH calculation based on systemic cH CO(3)(-) changes is not necessarily correct. Therefore, the only param eter of importance is the intraluminal measurement of intramucosal Pco (2) that can reflect isolated mesenteric changes. Thus, we recommended abolishing the terms ''intramucosal pH measurement'' and ''gastric to nometry'' and propose using the definition ''intramucosal Pco(2) measu rement.'' (Crit Care Med 1998; 26:1550-1557).