- Meeting abstract
- Open Access
A new algorithm for the determination of intramucosal pH and mucosal plasma lactate concentration
© Current Science Ltd 1997
- Published: 1 March 1997
- Lactic Acidosis
- Base Excess
- Bicarbonate Concentration
- pCO2 Elevation
- 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.
Mucosal pCO2 (mmHg)
Mucosal plasma [lactate] (mmol/l)