Mrs. A. is a 72-year-old female who was diagnosed with hypertension 25 years ago and is currently being treated with furosemide (Lasix) 20 mg per day and enalapril (Vasotec) 5 mg twice a day. She was brought to the ED by her daughter with a complaint of shortness of breath. Mrs. A. reports that she has had progressive fatigue and difficulty breathing for the last 5 days. She also notes that she could not sleep the previous evening because she "couldn't get enough air" and needed to sit up in the chair to feel comfortable. In addition, she tells the NP that her ankles and feet are getting very swollen and she has gained 6 pounds during the last 7 days.

Upon exam, Mrs. A. has some difficulty ambulating around the room and getting on to the exam table. She is in moderate respiratory distress, gasping for air with each respiratory cycle. Her temperature is 98.6[degrees] F (37[degrees] C), pulse 86 and regular, respiratory rate 28 with an oxygen saturation rate of 92% on room air, and BP is 160/90. Mild cyanosis is noted in the perioral area and nail beds. Respiratory exam revealed bilateral breath sounds with scattered crackles and occasional expiratory wheezes throughout the posterior thorax. Cardiac assessment revealed a mitral systolic murmur 4/6 and jugular venous distension. Mrs. A. reported tenderness in her right upper quadrant on palpation of her abdomen and mild hepatomegaly was noted. Pitting edema (3+) was noted on her lower extremities bilaterally.

After completing Mrs. A.'s history and physical exam, the NP ordered several tests to assist in the differential diagnosis. A complete blood cell (CBC) count, complete metabolic profile (CMP), urinalysis (UA), ECG, chest X-ray (CXR), echocardiogram, and B-type Natriuretic Peptide (BNP) were requested. In the management of this patient with severe shortness of breath, the NP considered conditions in which there is circulatory congestion secondary to abnormal salt and water retention but intact cardiac structure and function (such as renal failure), noncardiac causes of pulmonary edema (such as acute respiratory distress syndrome), acute presentation of chronic lung disease, respiratory or kidney infection, and heart failure secondary to chronic hypertension. The results of Mrs. A.'s history and physical exam encouraged the NP to focus on heart failure as the pathophysiologic cause for her distress.

Heart failure

Heart failure is a progressive, chronic disorder that results after acute damage such as myocardial ischemia or infarction, or as a result of chronic diseases such as uncontrolled hypertension. Heart failure occurs when there is a loss of functioning cardiac myocytes and a disruption of the ability of the myocardium to contract normally. In heart failure, a variety of compensatory mechanisms are activated. These include the adrenergic nervous system, the renin-angiotensin-aldosterone system, and the cytokine system. Initially, these systems are able to restore cardiovascular contractility. However, over a period of time continual activation of these systems can lead to a decrease in pumping ability, secondary end organ damage, left ventricular remodeling, and subsequent cardiac decompensation.1

BNP and NT-proBNP

BNP and the N-terminal portion of its precursor form (NT-proBNP) are cardiac neurohormones produced by the ventricular myocardium. The hormone is called brain natriuretic peptide because it was originally isolated from the porcine brain. In humans BNP levels are higher in the heart than in the brain.2 The production of BNP and NT-proBNP increases in response to ventricular volume expansion and pressure overload. They are markers of ventricular dysfunction and useful in diagnosing and monitoring the severity of heart failure. They are particularly useful in the ED setting, but may be ordered by primary care providers as well.3,4 Results for BNP and NT-proBNP are not interchangeable. BNP is more commonly used in clinical practice than NT-proBNP. The normal reference range for BNP is less than 100 pg/mL or less than 100 ng/L. Values increase with age, weight, and are higher in women than men.5 BNP levels higher than 400 correlate with heart failure.2 The severity of heart failure is directly correlated to the level of BNP. That is, the higher the BNP level, the greater the severity of heart failure. BNP levels increase in heart failure, decreased left ventricular ejection fraction, and diastolic dysfunction. BNP may also be increased in patients with stroke, severe sepsis or shock, subarachnoid hemorrhage, or renal impairment. It should be noted that elevated BNP will not differentiate between ventricular systolic or ventricular diastolic dysfunction.5

Studies reveal that BNP is a marker that is highly sensitive and specific.6 A single measurement of BNP at anytime during the progression of heart failure is a clinically useful tool for risk stratification. The greater value of BNP is in repeated measurement to monitor the progression of disease and in evaluating the response to medical therapy.7 For patients who present to the ED or other outpatient settings in acute dyspnea, BNP measurement is an extremely valuable tool in differentiating cardiac from noncardiac causes of the respiratory distress. Several studies have shown that concentrations of BNP were substantially higher in patients with acute heart failure when compared with those who had dyspnea due to other causes.6-8

Conclusion

Mrs. A. was provided oxygen therapy and other comfort measures in the ED while awaiting the results of her diagnostic tests. Her CBC, CMP, and UA were normal. However, her CXR and echocardiogram revealed cardiomyopathy. Her BNP was 2,020 pg/mL. Mrs. A. was admitted to the hospital for treatment of her heart failure and alleviation of her acute dypsnea.

Measurement of BNP is a valuable tool for diagnosing heart failure in emergency and other outpatient settings, especially when one of the patient's presenting symptoms is dyspnea. Additionally, serial BNP measurements may be useful in assessing the efficacy of medical therapy in patients with heart failure; however, ongoing clinical trials are still needed to determine the value of serial BNP measurements in guiding therapy for heart failure patients.9

Because increased levels of BNP may be indicative of a higher risk of mortality due to heart failure, NPs should strive to obtain this valuable information in appropriate patients.

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