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 wi th acute lung injury is attributable to lung tissue hypoxia, Design: Prospective, controlled, clinical study. Setting: A multidisciplinary university intensive care unit in a general ho spital. 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] less than or equal to 2.5); and 19 had acute respiratory distre ss 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 calculate d as the product of transpulmonary a-v lactate difference (L[a-v]) times th e 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 exc ess lactate formation across the lungs (XL), were calculated. L(a-v) and pu lmonary 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 = 5 2), pulmonary lactate release correlated significantly with LIS (r(2) = .14 , p < .01) and venous admixture (r(2) = .13, p < .01), When all patients we re lumped together (n = 70), pulmonary lactate release directly correlated with LIS (r(2) = .30, p < .001), venous admixture (r(2) = .26, p < .001), a nd P(A-a)O-2 (r(2) = .14, p < .01). Neither VP(a-v) nor XL was significantl y different among the three groups. Conclusion: The lungs of patients with ALI produce lactate that is proporti onal to the severity of lung injury. This lactate production does not seem to be attributable to lung tissue hypoxia.