Objective: The role of plasma B-type natriuretic peptide (BNP) in critically ill patients with acute pulmonary edema is controversial. We postulated that a low BNP level would exclude cardiac dysfunction as the principal cause of pulmonary edema and therefore help in the diagnosis of acute lung injury.
Design: A retrospective derivation cohort was followed by a prospective validation cohort of consecutive patients with acute pulmonary edema admitted to three intensive care units. BNP was measured within 24 hrs from onset. Critical care experts blinded to BNP results integrated clinical data with the course of disease and response to therapy and served as the reference standard.
Setting: Three intensive care units at the tertiary center.
Patients: Consecutive critically ill patients with acute pulmonary edema.
Measurements and Main Results: In a derivation cohort of 84 patients, a BNP threshold of ≤250 pg/mL had a specificity of 87% and sensitivity of 48% for the diagnosis of acute lung injury. High specificity of BNP (90%, likelihood ratio of 3.9) was confirmed in a validation cohort of 120 consecutive patients, 52 (43%) of whom had acute lung injury. Notably, 32% of patients with acute lung injury had concomitant cardiac dysfunction. The median time from the onset of pulmonary edema to BNP testing was 3 hrs. The accuracy of BNP (area under receiver operator curve, 0.71) was comparable with pulmonary artery occlusion pressure (area under receiver operator curve, 0.66) and superior to ejection fraction (area under receiver operator curve, 0.60) in subgroups of patients in whom these tests were performed. The accuracy of BNP improved when patients with renal insufficiency were excluded (area under receiver operator curve, 0.82).
Conclusion: When measured early after the onset of acute pulmonary edema, a BNP level of <250 pg/mL supports the diagnosis of acute lung injury. The high rate of cardiac and renal dysfunction in critically ill patients limits the discriminative role of BNP. No level of BNP could completely exclude cardiac dysfunction.
From the Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine (RR, NEV, CED, RDH, OG); Department of Internal Medicine, Division of Cardiovascular Diseases (ASJ); and the Department of Laboratory Medicine and Pathology (ASJ, GGK), Mayo Clinic College of Medicine, Rochester, MN.
Supported, in part, by NHLBI K23 HL78743-01A1 and a grant from the National Blood Foundation.
The authors do not have any financial interests to disclose.