What Is the Role of BNP in Diagnosis and Management of Acutely Decompensated Heart Failure?


A 76-year-old woman with a history of chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), and atrial fibrillation presents with shortness of breath. She is tachypneic, her pulse is 105 beats per minute, and her blood pressure is 105/60 mm/Hg. She is obese and has an immeasurable venous pressure with decreased breath sounds in both lung bases, and irregular and distant heart sounds. What is the role of brain (or B-type) natriuretic peptide (BNP) in the diagnosis and management of this patient?


Each year, more than 1 million patients are admitted to hospitals with acutely decompensated heart failure (ADHF). Although many of these patients carry a pre-admission diagnosis of CHF, their common presenting symptoms are not specific for ADHF, which leads to delays in diagnosis and therapy initiation, and increased diagnostic costs and potentially worse outcomes. Clinical risk scores from NHANES and the Framingham heart study have limited sensitivity, missing nearly 20% of patients.1,2 Moreover, these scores are underused by clinicians who depend heavily on clinical gestalt.3

Once ADHF is diagnosed, ongoing bedside assessment of volume status is a difficult and inexact science. The physiologic goal is achievement of normal left ventricular end diastolic volume; however, surrogate measures of this status, including weight change, venous pressure, and pulmonary and cardiac auscultatory findings, have significant limitations. After discharge, patients have high and heterogeneous risks of readmission, death, and other adverse events. Identifying patients with the highest risk might allow for intensive strategies to improve outcomes.

BNP is a neurohormone released from the ventricular cells in response to increased cardiac filling pressures. Plasma measurements of BNP have been shown to reflect volume status, to predict risk at admission and discharge, and to serve as a treatment guide in a variety of clinical settings.4 This simple laboratory test increasingly has been used to diagnose and manage ADHF; its utility and limitations deserve critical review.

KEY Points

  • BNP levels can augment clinical judgment regarding the presence of heart failure in dyspneic patients.
  • Atrial fibrillation and chronic kidney disease independently increase BNP levels, while obesity decreases BNP levels.
  • Daily BNP measurements should not be used to guide diuretic therapy in heart failure inpatients.
  • Admission and discharge BNP levels can predict adverse outcomes, but it is unclear how to act upon these data.

Additional Reading

  • Heart Failure Society of America. HFSA 2010 comprehensive heart failure practice guideline. J Card Fail. 2010;16(6):e1-194.
  • Jessup M, Abraham WT, Casey DE, et al. 2009 Focused Update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults. Circulation. 2009;119(14):1977-2016.
  • Green SM, Green JA, Januzzi JL Jr. Natriuretic peptide testing for the heart failure therapy guidance in the inpatient and outpatient setting. Am J Ther. 2009;16(2):171-177.

Review of the Data

CHF diagnosis. Since introduction of the rapid BNP assay, several trials have evaluated its clinical utility in determining whether ADHF is the cause of a patient’s dyspnea. The largest of these trials, the Breathing Not Properly Multinational Study, conducted by McCullough et al, enrolled nearly 1,600 patients who presented with the primary complaint of dyspnea.5 After reviewing conventional clinical information, ED physicians were asked to determine the likelihood that ADHF was the etiology of a patient’s dyspnea. These likelihoods were classified as low (<20%), intermediate (20%-80%), or high (>80%). The admission BNP was recorded but was not available for the ED physician decisions.


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