Lack of effect of ranitidine on gastric luminal pH and mucosal PCO2 during the first day in the ICU.

Background: Histamine(2) (H(2))-blocking agents can attenuate intragastric CO(2)-production by reducing gastric acid secretion and preventing the interaction between H(+) and bicarbonate. However, gastric acid production may be impaired in acute circulatory failure due to poor mucosal perfusion, and H(2)-blockade could further impair mucosal perfusion.

Methods: Forty patients with acute circulatory and/or respiratory failure, age 61 +/- 16 years (mean +/- SD), APACHE II score 21 +/- 7, and SOFA score 8 +/- 3, received randomly either ranitidine, 50 mg (R) or placebo (P) every 8 h. Gastric intraluminal pH (gpH; antimony probe with external reference electrode) and mucosal pCO(2) (prCO(2), semicontinuous air-tonometry) were measured during 24 h, and blood gases were taken at 6-h intervals.

Results: Gastric intraluminal pH was 4.3 +/- 2.4 in P and 5.1 +/- 1.6 in R (NS). Mean prCO(2) was 6.8 +/- 2.7 kPa in P and 7.4 +/- 2.1 kPa in R, and mucosal-arterial pCO(2) gradient (Delta pCO(2)) was 2.2 +/- 2.9 kPa and 2.4 +/- 2.4 kPa, respectively (NS). Within-patient variabilities of gpH and prCO(2) were not influenced by ranitidine. A posthoc analysis revealed that non-survival in R was associated with a low mucosal pHi after 24 h (P = 0.002). This was explained by a low arterial pH but not by differences in gpH or prCO(2).

Conclusions: In acute respiratory and circulatory failure, H(2) blockade has an inconsistent impact on gpH and does not reduce variabilities of gpH or prCO(2).