Objective: To determine if intraluminal production of CO2 leads to underestimation of gastric intramural pH (pHi) by tonometry.
Design: Nonrandomized controlled study.
Patients: Healthy volunteers.
Interventions: NG tonometers were placed in healthy volunteers. Some of the volunteers (n = 11) were pretreated with ranitidine to prevent secretion of protons into the gastric lumen. Others (n = 13) were untreated (i.e., gastric acid secretion was uninhibited).
Measurements and Main Results: Gastric pHi was calculated from the arterial (HCO3) and the tonometrically determined intraluminal Pco2 using the Henderson-Hasselbalch equation. Intraluminal Pco2 was significantly higher in the control group (54 +/- 14 torr [7.2 +/- 1.9 kPa]) than in the ranitidine-treated group (42 +/- 4 torr [5.6 +/- 0.4 kPa], p = .02). Mean gastric luminal pH was 1.9 +/- 0.6 in the control group as compared with 6.7 +/- 0.7 in volunteers treated with ranitidine (p < .01). Mean calculated gastric pHi was 7.30 +/- 0.11 in the untreated group and 7.39 +/- 0.03 in the ranitidine-treated group (p < .03).
Conclusions: These data suggest that intraluminal production of CO2 from the titration of gastric HCO-3 by secreted H+ can result in the underestimation of gastric pHi by tonometry. This phenomenon can be eliminated by H2-receptor blockade. (Crit Care Med 1991; 19:271)
(C) Williams & Wilkins 1991. All Rights Reserved.