Effect of gastric feeding on intragastric P(CO2) tonometry in healthy volunteers.

PURPOSE

The tonometric detection of a high intragastric regional P(CO2) (PrCO2) reflecting an elevated intramucosal P(CO2) can be helpful to diagnose mucosal ischemia, if acid secretion is suppressed to avoid intragastric CO2 production through buffering of acid by bicarbonate in the stomach. It is recommended to perform tonometry in the fasting state, but this may hamper feeding of the critically ill. On the other hand, postfeeding tonometry could serve as a diagnostic stress test because feeding increases mucosal blood flow demand, provided that the meal itself does not hamper diffusion of CO2 from mucosa to tonometer balloon and does not generate intragastric CO2, independently from intramucosal P(CO2). We therefore studied the effect of a standard meal on intragastric PrCO2 tonometry in healthy volunteers with suppression of meal-stimulated gastric acid secretion and, presumably, with an adequate mucosal blood flow reserve.

MATERIAL AND METHODS

The gastric juice pH and tonometric PrCO2 were measured in 14 human volunteers, after gastric acid secretion suppression by either ranitidine (100-mg bolus, followed by 25 mg/h i.v., n = 7) or by ranitidine plus pirenzepine (10-mg bolus, followed by 3 mg/h i.v., n=7) to suppress any residual meal-stimulated gastric acid secretion, before and at 30-minute intervals until 120 minutes after oral ingestion of a standard liquid test meal (Pulmocare [Abbott, the Netherlands]; 500 mL, 750 kcal, P(CO2) 5 mm Hg, pH 7.50).

RESULTS

The gastric juice pH, which was >4.0 in all individuals throughout the study, and the PrCO2 did not depend on the regimen for gastric acid secretion suppression, and therefore the data were pooled. The PrCO2 (median [range]) after feeding was 69% (56% to 170%) of baseline (42 [37-51] mm Hg) from 0 to 30 minutes (P < .001), 85% (72% to 167%) of baseline from 30 to 60 (P < .05), 97% (57% to 193%) from 60 to 90 minutes, and 112% (97% to 189%) of baseline from 90 to 120 minutes with a rise above baseline in 10 of 14 patients. In vitro, the liquid test meal generated CO2 after adding bicarbonate but not after hydrochloric acid.

CONCLUSION

We recommend intragastric tonometry to be performed in the fasting state and discourage tonometry after feeding as a stress test, because a single test meal changes tonometric PrCO2 in a time-dependent manner until 2 hours after gastric feeding of healthy volunteers. The fall in PrCO2 directly after feeding can be attributed to dilution, whereas a rise above baseline in some patients may have been caused, as supported by CO2 production after adding bicarbonate to the test meal in vitro, by CO2 production through buffering of meal-derived acid by gastric bicarbonate, in the absence of stimulated gastric acid secretion by feeding.