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)
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