Gastric tonometry was developed in the late 1950s as a method of measure arterial PCO2 in mechanically ventilated children with poliomyelitis. Clinical studies showed that arterial PCO2 could be estimated with reasonable accuracy, but that gastric PCO2 surpassed arterial PCO2 during severe shock. Although not recognized at the time, it is precisely this property that makes tonometry a useful monitor of regional anaerobic metabolism. For all practical purposes, the concept of tonometry was forgotten until Fiddi§.D.iGie.§D §.LqL (1982) advanced the notion that the pH of the gut mucosa could be calculated using this method. This hypothesis was based on the following assumptions: free CO2 diffusion in tissue; luminal fluid PCO2 is in equilibrium with mucosal PCO2; intestinal mucosal bicarbonate concentration [HCO3-] is similar to arterial bicarbonate concentration. Making these assumptions, it is possible to estimate the intramucosal pH (pHi) from the Henderson-Hasselbalch equation:
The assumptions that underlie the calculation of pHi are applicable to many clinical conditions. Total intestinal ischemia is a notable exception. In this condition mucosal bicarbonate may be lower than arterial bicarbonate. The presence of systemic acidosis also complicates the interpretation of pHi. A low mucosal pH in concert with a low arterial pH does not imply local tissue hypoxia, but most likely reflects generalized tissue acidosis. Given these potential difficulties in the interpretation of pHi, the use of the difference between tonometric and arterial PCO2 (the PCO2 gap) is recommended.
Saline tonometry is a labor-intensive technique (Table 1) and its successful use requires the close co-operation of physicians, nurses, and laboratory personnel.
Table 1 Steps required in the measurement of gastric pHi with the saline balloon system
There are ample opportunities to introduce errors at any point during the measurement process, including the following:
1. inaccurate timing of partially equilibrated samples;
2. the introduction of air in the saline sample;
3. erroneous saline PCO2 measurements by the blood gas analyzer;
4. high gastric luminal acidity, whose buffering by exogenous or endogenous bicarbonate may elevate tonometer PCO2.
The last is a common source of error and many investigators recommend the use of H2-receptor antagonists in patients in whom tonometry is used. The idea is to maintain a relatively alkalotic gastric luminal pH and prevent the spurious generation of CO 2 in the stomach by exogenous or endogenous icarbonate. The use of sucralfate has been suggested as an alternative to H2-receptor blockers. Improvements in tonometer technology now permit the measurement of mucosal PCO2 using air instead of saline.
Was this article helpful?