Objective: To determine the effect of enteral tube feedings on the measurement of gastric intramucosal pH.
Design: Interventional study.
Setting: Two intensive care units of a university-affiliated teaching hospital.
Patients: Twenty hemodynamically stable patients undergoing mechanical ventilation, with a nasogastric tonometer in situ, in whom enteral feeding was initiated.
Interventions: The baseline fasting gastric intramucosal pH and gastric fluid pH were determined in the study population. The patients then received enteral feedings for 2 hrs, after which the gastric intramucosal pH and gastric fluid pH measurements were repeated. The tube feedings were then withheld for 2 hrs. The data set was repeated 1 and 2 hrs after the feedings had been stopped. Finally, tube feedings were retarded and the data set was repeated after 4 hrs. All patients received a histamine-2 (H2)-receptor antagonist-blocking agent during the study. To investigate the possibility that a direct reaction between gastric fluid and enteral feedings may generate CO2, 30-mL aliquots of gastric fluid from an independent sample of 14 patients (seven receiving cimetidine) were mixed with 60 mL of enteral feeding in an airtight container; the PCO2 of the gastric fluid before and after adding enteral feeding was measured tonometrically.
Measurements and main results: The mean +/- SD gastric intramucosal pH decreased from 7.40 +/- 0.08 to 7.33 +/- 0.12 (p < .005), and from 7.38 +/- 0.07 to 7.31 +/- 0.1 (p < .005) after the first and second feeding challenges, respectively. The gastric intramucosal pH returned to the baseline value after 1 hr of fasting. The mean in vitro PCO2 of the gastric fluid increased from 11.9 +/- 3.0 to 16.2 +/- 2.0 torr (1.6 +/- 0.4 to 2.1 +/- 0.27 kPa) (p = .003) after the addition of tube feedings in the samples from those patients who were not receiving H2 receptor antagonists, but did not change significantly in those samples from the patients who were receiving H2 receptor antagonists.
Conclusions: Enteral feeding stimulates the secretion of hydrogen ions, which are then buffered by ionized bicarbonate secreted by the nonparietal gastric cells generating CO2. In addition, the enzymatic digestion of nutrients in the stomach may also generate CO2. The increased intraluminal CO2 following enteral feeding results in a spuriously low gastric intramucosal pH reading. Our data suggest that tube feedings should be temporarily discontinued for at least 1 hr when measuring the gastric intramucosal pH. These data should, however, be used with caution when extrapolating to hemodynamically unstable patients. Furthermore, the consequences of frequent interruptions of enteral feeding need to be weighed against the possible benefits derived from the use of this monitoring tool.