B-type natriuretic peptide (BNP) is a 32-amino-acid polypeptide cardiac neurohormone specifically secreted from the ventricles in response to volume expansion and pressure overload. BNP was originally identified in extracts of porcine brain. It is present in minute amounts in human brain, but the clinically important source originates in the cardiac ventricles. The levels of B-type natriuretic peptide are elevated in patients with left ventricular dysfunction and the levels correlate with both the severity of symptoms and the prognosis.

The presenting features of acute cardiogenic and noncardiogenic pulmonary edema are similar and can be clinically difficult to distinguish. Common causes of cardiogenic pulmonary edema include cardiac ischemia with or without myocardial infarction, exacerbation of chronic systolic or diastolic heart failure, and dysfunction of the mitral or aortic valve. Volume overload should also be considered. A typical history of paroxysmal nocturnal dyspnea or orthopnea suggests cardiogenic pulmonary edema. However, a silent myocardial infarction or occult diastolic dysfunction may also manifest as acute pulmonary edema, with few clues provided by the history.