BNP is produced by cardiac myocytes in response to stretch which occurs in impaired diastolic or systolic function. BNP may play an important role in acute cardiac failure. BNP assays can supplement clinical judgment when the cause of a patients dyspnoea is uncertain. Results should be interpreted in the context of all available clinical data. The role of BNP in chronic heart failure is, however, well established for diagnosing, staging and risk stratifying patients.
BNP has reasonable sensitivity and therefore can be used to rule out heart failure as a cause of a patients breathlessness (in a primary care setting for example) but it is not very specific and therefore not useful for ruling the diagnosis in. BNP rises due to sepsis, renal or liver failure, hypoxia, myocardial ischaemia, tachycardia as well as many other reasons. In hyperacute or flash pulmonary oedema or acute mitral regurgitation the BNP level may not be elevated initially.
NT-proBNP is useful in differentiating between respiratory and cardiac disease in infants. It may be a good cardiac marker. May be useful for pneumonia prognostication. Can help risk assess PEs, although troponin is probably more sensitive so it's generally not considered useful. It is a marker of secondary myocardial injury.
Interestingly: *Low risk patients do not need specific right ventricular (RV) functional assessment but where RV dilatation has been identified on CT or Echo in patients otherwise suitable for outpatient management, consider measuring BNP, NT-proBNP and hsTnI or hsTnT. Elevated biomarkers should prompt inpatient admission for observation. Incidental elevated troponin requires senior review and consideration of an alternative cause to the elevated troponin.
Probably adding noise to an already uncertain baseline. Sensitive but not specific.