Gastric Intramural Pco2 During Peritonitis and Shock

Changes in p i CO 2 reflect splanchnic mucosal ischaemia more reliably than changes in pH i during haemorrhagic shock

“…In the state of hypoperfusion, anaerobic metabolism is induced and tissular bicarbonate at first is utilised to buffer the protons. Therefore, splanchnic mucosal arterial bicarbonate results will be much lower than arterial bicarbonate influencing the calculation of pH i [10,27]. In addition, in patients already treated, the administration of sodium bicarbonate in the presence of decreased gastric mucosal blood flow might cause a significant difference between intestinal tissular and systemic HCO 3 - [28].…”

Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry

“…It is difficult to follow this concept in an organ that is supposedly underperfused at the time when tonometry is supposed to be most beneficial, and when bicarbonate would be expected to be consumed as a buffer. Despite these arguments, direct measurement of pHi has shown good correlation with tonometrically derived pHi [20,21]. However, derivation of pHi seems to add nothing to the information obtained from the PiCO 2 − PaCO 2 gap.…”

Advantage of buffered solutions or automated capnometry in air-filled balloons for use in gastric tonometry

“…Arterial [HCO 3 -] has been found not to equal intracellular [HCO 3 -] under various conditions, resulting in inaccurate calculation of pHi [3][4][5]. Against this background, the evaluation of the gastric intramucosal pCO 2 as an independent variable, without calculating pHi, has been recommended.…”