Pulmonary lactate release in patients with acute lung injury is not attributable to lung tissue hypoxia

OBJECTIVE:To determine whether pulmonary lactate production in patients with acute lung injury is attributable to lung tissue hypoxia. DESIGN:Prospective, controlled, clinical study. SETTING:A multidisciplinary university intensive care unit in a general hospital. PATIENTS:Seventy consecutive critically ill patients requiring mechanical ventilation and invasive hemodynamic monitoring. Of these patients, 18 had no acute lung injury (no ALI); 33 had acute lung injury (ALI) (Lung Injury Score [LIS] ≤2.5); and 19 had acute respiratory distress syndrome (ARDS) (LIS >2.5). INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:After hemodynamic measurements, lactate and pyruvate concentrations were assessed in simultaneously drawn arterial (a) and mixed venous (v) blood samples. Pulmonary lactate release was calculated as the product of transpulmonary a-v lactate difference (L[a-v]) times the cardiac index. Two indices of anaerobic metabolism of the lung, i.e., the transpulmonary a-v difference of lactate pyruvate ratio (L/P[a-v]) and excess lactate formation across the lungs (XL), were calculated. L(a-v) and pulmonary lactate release were higher in patients with ARDS than in the other groups (p < .001), and they were also higher in patients with ALI compared with patients with no ALI (p < .001). In patients with ALI and ARDS (n = 52), pulmonary lactate release correlated significantly with LIS (r = .14, p < .01) and venous admixture (r = .13, p < .01). When all patients were lumped together (n = 70), pulmonary lactate release directly correlated with LIS (r = .30, p < .001), venous admixture (r = .26, p < .001), and P(A-a)O2 (r = .14, p < .01). Neither L/P(a-v) nor XL was significantly different among the three groups. CONCLUSION:The lungs of patients with ALI produce lactate that is proportional to the severity of lung injury. This lactate production does not seem to be attributable to lung tissue hypoxia.