A new algorithm for the determination of intramucosal pH and mucosal plasma lactate concentration

The conventional calculation of gastric intramucosal pH (pHi) makes the invalid assumption that mucosal and arterial plasma bicarbonate concentrations are identical. Mucosal bicarbonate concentrations exceed arterial during aerobic O₂–CO₂ exchange, causing underestimation of intramucosal pH. Conversely, because of locally reduced bicarbonate concentrations, the conventional calculation significantly overestimates intra-mucosal pH in regional mucosal lactic acidosis, as shown by direct intramucosal pH measurement in animal models of splanchnic ischaemia. Accurate pHi calculation is important since mucosal acidosis is the probable cause of loss of barrier function in gut ischaemia.

We devised an algorithm eliminating arterial bicarbonate from the calculation by: (i) determining the aerobic and anaerobic components of the arterial-mucosal pCO₂ gap using an equation for the Dill nomogram: (ii) introducing a factor quantifying the fall in base excess (BE) which accompanies anaerobic pCO₂ elevation (determined in vitro by anaerobic addition of lactic acid to blood): (iii) applying the Siggaard-Andersen algorithm to derive mucosal end-capillary pH from the calculated mucosal BE.

The pHi was estimated by the new and conventional algorithms tor mucosal pCO₂ values ranging from normal to those associated with severe intramucosal acidosis, assuming [Hb]= 15 g%, SaO₂ = 97%, arterial pCO₂ = 40 mmHg, BE = 0 meq/l and plasma (lactate) =1.5 mmol/l.

Results

See table.

Conclusion

The new pHi values appear valid, exceeding conventional in mild aerobic mucosal acidosis, and in severe acidosis closely resembling directly measured pHi during mesenteric ischaemia. Lactate estimations provide additional information about the gut wall redox state. The algorithm requires experimental evaluation.

Table