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American Journal of Critical Care. 2006;15: 614-616
Copyright © 2006 by the American Association of Critical-Care Nurses.
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Brain Natriuretic Peptide, Clinical Reasoning, and Congestive Heart Failure

By Hussam Ammar, MD, Ashok Kumar Malani, MD, FRCS, Chakshu Gupta, MD and Dennis C. Dobyan, MD. From Heartland Regional Medical Center, St. Joseph, Mo.

Corresponding author: Chakshu Gupta, MD, Heartland Regional Medical Center, 5325 Faraon St, St. Joseph, MO 64506 (e-mail: chakgupta @yahoo.com).

Dyspnea is a sensation of the need to breathe or difficult or labored breathing. It leads to 2.5 million visits to healthcare providers annually in the United States.1 A number of abnormalities can cause dyspnea, and determining the etiology will allow institution of timely therapy and avoidance of unnecessary diagnostic tests.

Brain natriuretic peptide (BNP) is a neurohormone secreted by the left ventricle in response to pressure and volume overload. It produces natriuresis, a decrease in systemic vascular resistance, and a reduction in cardiac filling pressure. After publication of the results of the Breathing Not Properly Multinational Study,2 BNP levels have increasingly been used to evaluate patients who have dyspnea; many physicians associate elevated BNP levels with congestive heart failure (CHF).3

We present a case study of an elderly woman with a known history of CHF who came to the emergency department because of dyspnea. She had markedly elevated BNP levels, and the working diagnosis was exacerbation of CHF until further investigation revealed a pulmonary embolism. This case highlights the importance of excluding other causes before attributing signs and symptoms and elevated BNP levels to CHF.


   Case Report
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An 86-year-old woman came to the emergency department because she had shortness of breath, chest tightness, and rapid heart rate. Physical examination revealed blood pressure 134/76 mm Hg, heart rate 73/min, and respirations 33/min. She had jugular venous distention; a chest auscultation revealed bilateral wheezing. The patient’s oxygen saturation on room air was 76%. Her medical history included CHF, paroxysmal atrial fibrillation, hypertension, diabetes mellitus, and chronic renal failure.

The patient’s risk for pulmonary embolism was low according to modified Wells criteria. Blood was obtained for laboratory evaluation, and electrocardiography (ECG) revealed an s1q3 pattern (see FigureGo). Plain radiographs showed evidence of cardiomegaly and mild pulmonary congestion. Laboratory results included a markedly elevated level of BNP of 1200 pg/mL, elevated levels of serum urea nitrogen and creatinine, and normal levels of cardiac enzymes. Values on arterial blood gas analysis were pH 7.44, PCO2 39 mmHg, PO2 45 mm Hg, and alveolar-arterial difference in partial pressure of oxygen 56 mm Hg. The working diagnosis was CHF and the patient was given 80 mg of intravenous furosemide. However, her condition did not improve; she required more than 16 L/min of oxygen to maintain oxygen saturation at 90%.


Figure 1
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  		Electrocardiogram shows an s1q3 pattern.

 
The patient’s condition was reevaluated. A closer examination of the ECGs raised the possibility of pulmonary embolism. Modified Wells criteria for pulmonary embolism increased to intermediate probability because the patient was not responding to treatment. Administration of intravenous unfractionated heparin was started, and a ventilation-perfusion scan was performed. The scan showed 2 large segmental defects with ventilation-perfusion mismatch. A 2-dimensional echocardiogram revealed enlargement of the right ventricle and left ventricular hypertrophy. The patient’s left ventricular function and ejection fractions were normal. Her condition steadily improved with anticoagulation. Warfarin therapy was started, and she was discharged to home.


   Discussion
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This case is an example of "shortcuts in reasoning."3 In this case, the shortcut led to undue emphasis on the markedly elevated BNP levels and history of CHF in an elderly patient. Other possible causes were ignored, and CHF was diagnosed as the cause of the patient’s dyspnea.

Studies in emergency departments indicate that as BNP levels increase, the likelihood of CHF generally increases, especially at BNP levels greater than 1000 pg/mL.4 Of note, however, is the fact that no BNP level is absolutely predictive of CHF.1 Sepsis and pulmonary embolism should always be excluded when BNP levels are greater than 1000 pg/mL.4 This step may be difficult in patients with chronic symptomatic heart failure in whom dyspnea develops because of a pulmonary embolism. In this situation, a high BNP value can be misleading.5

The negative predictive value of BNP levels less than 100 pg/mL is 98%, and at these levels CHF can be ruled out.2,4 According to the European task force, because of the high negative predictive value, assays of BNP levels are best used as a "rule out" test. Levels greater than 400 pg/mL are moderately predictive of CHF, and levels greater than 1000 pg/mL are substantially predictive of CHF.4 With BNP levels between 400 and 1000 pg/mL, a variety of conditions, including CHF, asymptomatic left ventricular dysfunction, chronic pulmonary hypertension, unstable myocardial infarction, atrial fibrillation, pulmonary embolism, left ventricular hypertrophy, lung cancer, and even old age must be considered. Interestingly, 40% of participants in the Breathing Not Properly study had BNP values in this range at least 40% of the time.2 BNP levels are also higher in patients with renal failure independent of the presence or absence of CHF. In such patients, a BNP level less than 200 pg/mL should be used to exclude CHF if the estimated glomerular filtration rate is less than 60 mL/min.6

A known history of CHF, presence of abdomino-jugular reflux, and presence of a third heart sound are strongly predictive of CHF; conversely, the absence of pulmonary rales, pedal edema, and elevated jugular venous pressure have a strong negative predictive value. Evidence of pulmonary edema is reportedly the most useful radiological finding in CHF. Other useful findings include cardiomegaly and pleural effusion.1

The most useful ECG finding for predicting CHF is the presence of atrial fibrillation. A pattern on ECGs that was noted but ignored in our patient is the s1q3 pattern. Although this pattern remains controversial, some investigators7 believe it indicates pulmonary embolism. Echocardiography is considered the gold standard for the diagnosis of left ventricular dysfunction, but the procedure is not always readily available.2 According to estimates,8 in 20% to 50% of patients with diastolic heart failure, echocardiograms show normal left ventricular systolic function.

The diagnosis of congestive heart failure is best based on a combination of clinical features, thorough physical examination, radiological and laboratory data, and exclusion of other conditions.1 Although BNP values are an important part of this evaluation, they should be interpreted within the context of the entire clinical findings. Shortcuts in reasoning during evaluation of patients with dyspnea can have undesirable consequences.


   Summary
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 Case Report
 Discussion
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BNP levels may be elevated in conditions other than CHF. At levels less than 100 pg/mL, CHF is unlikely. At levels greater than 100 pg/mL, a diagnosis of CHF should be made only after other conditions such as pulmonary embolism, asymptomatic left ventricular dysfunction, chronic pulmonary hypertension, unstable myocardial infarction, atrial fibrillation, left ventricular hypertrophy, lung cancer, and advanced age have been excluded.

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.


   REFERENCES
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  1. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA. 2005;294:1944–1956.[Abstract/Free Full Text]
  2. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161–167.[Abstract/Free Full Text]
  3. Redelmeier DA. Improving patient care: the cognitive psychology of missed diagnoses. Ann Intern Med. 2005;142:115–120.[Abstract/Free Full Text]
  4. Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med. 2004;11:686–691.[Medline]
  5. Schwam E. Rapid measurement of B-type natriuretic peptides reduced time to discharge and treatment costs in patients with acute dyspnea. ACP J Club. January-February 2005;142:A14.[Medline]
  6. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med. 2004;350:647–654.[Abstract/Free Full Text]
  7. Costantini M, Bossone E, Renna R, et al. Electrocardiographic features in critical pulmonary embolism: results from baseline and continuous electrocardiographic monitoring. Ital Heart J. 2004;5:214–216.[Medline]
  8. Aurigemma GP, Gaasch WH. Diastolic heart failure. N Engl J Med. 2004;351:1097–1105.[Free Full Text]



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