• Rimki Rana, Nicholas E Vlahakis, Craig E Daniels, Allan S Jaffe, George G Klee, Rolf D Hubmayr, and Ognjen Gajic.
• Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
• Crit. Care Med. 2006 Jul 1;34(7):1941-6.

ObjectiveThe 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.DesignA 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.SettingThree intensive care units at the tertiary center.PatientsConsecutive critically ill patients with acute pulmonary edema.InterventionsNone.Measurements And Main ResultsIn a derivation cohort of 84 patients, a BNP threshold of ConclusionWhen 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.

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