Tonometry revisited: Perfusion-related, metabolic, and respiratory components of gastric mucosal acidosis in acute cardiorespiratory failure

Mucosal pH (pHi) is influenced by local perfusion and metabolism (mucosal-arterial pCO2 gradient, ΔpCO2), systemic metabolic acidosis (arterial bicarbonate), and respiration (arterial pCO2). We determined these components of pHi and their relation to outcome during the first 24 h of intensive care. We studied 103 patients with acute respiratory or circulatory failure (age, 63 ± 2 [mean ± SEM]; Acute Physiology and Chronic Health Evaluation II score, 20 ± 1; Sequential Organ Failure Assessment score, 8 ± 0). pHi, and the effects of bicarbonate and arterial and mucosal pCO2 on pHi, were assessed at admission, 6, and 24 h. pHi was reduced (at admission, 7.27 ± 0.01) due to low arterial bicarbonate and increased ΔpCO2. Low pHi (<7.32) at admission (n = 58; mortality, 29% vs. 13% in those with pHi ≥7.32 at admission; P = 0.061) was associated with an increased ΔpCO2 in 59% of patients (mortality, 47% vs. 4% for patients with low pHi and normal ΔpCO2; P = 0.0003). An increased versus normal ΔpCO2, regardless of pHi, was associated with increased mortality at admission (51% vs. 5%; P < 0.0001; n = 39) and at 6 h (34% vs. 13%; P = 0.016; n = 45). A delayed normalization or persistently low pHi (n = 47) or high ΔpCO2 (n = 25) was associated with high mortality (low pHi [34%] vs. high ΔpCO2 [60%]; P = 0.046). In nonsurvivors, hypocapnia increased pHi at baseline, 6, and 24 h (all P ≤ 0.001). In patients with initially normal pHi or ΔpCO2, outcome was not related to subsequent changes in pHi or ΔpCO2. Increased ΔpCO2 during early resuscitation suggests poor tissue perfusion and is associated with high mortality. Arterial bicarbonate contributes more to pHi than the ΔpCO2 but is not associated with mortality. Hyperventilation partly masks mucosal acidosis. Inadequate tissue perfusion may persist despite stable hemodynamics and contributes to poor outcome.