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  • Poster presentation
  • Open Access

Contribution of perfusion-related, metabolic and respiratory components to gastric mucosal acidosis in acute cardiorespiratory failure

  • 1,
  • 2,
  • 2 and
  • 1
Critical Care200610 (Suppl 1) :P238

  • Published:


  • Metabolic Acidosis
  • Sofa Score
  • Arterial pCO2
  • Microcirculatory Perfusion
  • Cardiorespiratory Failure


Local mucosal acidosis in acute circulatory and respiratory failure is influenced by three main components: local perfusion and metabolism (mucosal-arterial pCO2 gradient), systemic metabolic acidosis (arterial bicarbonate), and respiration (arterial pCO2). The aim of this study was to determine the effect of primary resuscitation on these components of gastric mucosal pH in surviving and nonsurviving patients admitted to the ICU.

Patients and methods

One hundred and three patients with acute respiratory or circulatory failure (age 63 ± 15 years [mean ± SD], APACHE II score 20 ± 6, SOFA score 8 ± 3) were studied during the first 24 hours after ICU admission. Gastric air tonometers were inserted and arterial blood gases for the calculation of pHi and DpCO2 were taken ≥ 4 times daily. The effects of bicarbonate, and arterial and mucosal pCO2 on pHi were calculated using the Hendersson-Hasselbach equation.


The pHi increased from 7.27 ± 0.14 at admission to 7.30 ± 0.12 after 24 hours (P < 0.005). Twenty-three patients died in hospital. In nonsurvivors, ΔpCO2 contributed more to pHi at admission than in survivors (0.04 ± 0.10 vs -0.02 ± 0.09, P = 0.023) and this effect persisted for 24 hours. Arterial bicarbonate altered pHi at admission twice as much as (nonsurvivors: ΔpCO2 0.08 ± 0.10 vs survivors: 0.03 ± 0.09, P = 0.006) but this effect decreased during the first 24 hours (in nonsurvivors to 0.04 ± 0.10 and in survivors to 0.01 ± 0.09, P < 0.001 both). In nonsurvivors, hypocapnia increased pHi both at admission and after 24 hours (P = 0.013 both).


Persistent inadequate gastric mucosal perfusion (increased ΔpCO2) during primary resuscitation is associated with increased mortality. Arterial bicarbonate contributes more to gastric mucosal acidosis than the ΔpCO2 at admission, and increases in both survivors and nonsurvivors. The severity of mucosal acidosis is partially masked by hyperventilation. These results support the concept that inadequate microcirculatory perfusion may persist despite normalization of systemic hemodynamics and that this contributes to poor outcome.

Authors’ Affiliations

University Hospital – Inselspital, Bern, Switzerland
University Hospital Kuopio, Finland


© BioMed Central Ltd 2006