1. McCarron, Kim RN, CRNP, MS
  2. Labovitz, Benjamin

Article Content

Mary Hartley, 82, comes to your ED with noticeable fatigue and breathlessness. She has 3+ pretibial edema and an oxygen saturation value of 86% on room air. Her initial brain natriuretic peptide (BNP) level, which is drawn within 30 minutes of admission, is 3,266 pg/mL. Eighteen hours later after furosemide, a beta-blocker, and an angiotensin-converting enzyme (ACE) inhibitor are prescribed and oxygen is administered, her BNP level continues to rise at 3,405 pg/mL. One day later, with continued therapy, her BNP level drops to 2,462 pg/mL and 2 days later, it has dropped to 1,050 pg/mL and her symptoms have markedly improved. Mrs. Hartley's heart failure is classified as New York Heart Association (NYHA) Class IV and biventricular pacing is prescribed to assist her failing myocardial pump.


If you practice in an ED or cardiac area, many of your patients will have BNP values drawn. I'll help you understand what this diagnostic test reveals about your patient's condition.


Nature's diuretic

In practical terms, natriuresis is the elimination of sodium and water from the renal tubules, and for this reason BNP can be considered nature's diuretic. Natriuresis also causes arteriolar and venous vasodilation, with the effect of lowering BP. BNP reduces output from the sympathetic nervous system and the renin-angiotension-aldosterone system, moderating heart rate and cardiac afterload. It has a bonus effect of endothelial protection and inhibits ventricular remodeling, lessening the harmful structural changes that result in hypertrophy of cardiac muscle.


BNP is present in minute quantities in a healthy person, but levels rise significantly in response to cardiac chamber stretch. When the ventricles become distended due to volume overload, BNP production is stimulated. Type A receptors, present in large blood vessels and kidney and adrenal tissue, respond to rising levels of BNP and through assorted mechanisms work to promote homeostasis. It's important to note that age and gender are influencing factors. BNP levels increase in both genders as a person ages, and women secrete higher plasma levels of BNP. BNP levels are lower in obese individuals and among patients who are prescribed diuretics, ACE inhibitors, digoxin, or vasodilators.


Determining heart failure

Current heart failure practice guidelines support drawing BNP levels for patients who arrive at the urgent care setting and for whom the clinical diagnosis of heart failure is uncertain. Heart failure patients typically present with fatigue, dyspnea, decreased oxygen saturation, and weight gain as fluid is retained in body tissues. This constellation of symptoms may indicate left ventricular systolic or diastolic dysfunction or right ventricular pressure overload states such as pulmonary embolism, cor pulmonale, or primary pulmonary hypertension. Also, conditions that cause extracellular fluid volume expansion, such as renal failure and liver cirrhosis, will result in elevated levels of natriuretic hormones.


In addition to differentiating heart failure from other disorders, BNP assessment is used as a prognostic marker in cardiac patients. After a patient is diagnosed with heart failure, it's staged functionally according to the NYHA Heart Failure Classification. BNP levels correlate with NYHA Classes I to IV, increasing as the level of heart function declines (see Relationship of BNP to heart failure). Researchers are monitoring levels and collecting data on hospitalization rates, length of stay, and mortality. A systematic review of studies reveals that the relative risk of death increases by 35% for every 100 pg/mL increase in BNP concentration.


Optimal measurement of BNP is within 2 to 4 hours after the onset of acute symptoms; BNP is detectable from 5 to 5,000 pg/mL. If the patient's serum level is less than 100 pg/mL, conditions other than heart failure are explored as the cause of dyspnea. A value that exceeds 100 pg/mL is suggestive of heart failure. Rapid assessment is crucial to guiding therapy. An assay may be drawn for the active hormone, BNP, or the lab may measure the inactive peptide, NT-proBNP. Be aware that there are subtle differences between the two, but clinically both provide important information about the condition of the heart. After heart failure treatment is initiated, cyclical BNP levels may demonstrate the effectiveness of therapy.


What you need to do

If your patient is scheduled to have her BNP levels drawn, explain the purpose of the test. Evaluate patient outcomes and monitor appropriately for heart failure. Explain to your patient the need for possible follow-up tests and medication therapy.


It's important to stress that BNP as a diagnostic test compliments, but doesn't substitute for, careful physical assessment. Obtaining a complete history is crucial; however, in the acutely ill patient this may not be feasible. Observing breathing patterns and accessory muscle use, auscultating absent breath sounds or adventitious sounds, measuring jugular venous pressure, listening for the third heart sound (S3), and assessing for peripheral edema are all assessments that should be performed for the patient experiencing symptoms of heart failure. In addition, the echocardiogram is regarded as the gold standard for assessment of heart failure. Echocardiography has a greater sensitivity and specificity than BNP measurement and combined they provide crucial information about heart function.


A tool in the arsenal

An increased BNP level signals cardiac distress because it primes the system to reduce volume overload. Measurement is relatively easy and cost effective while supplying the healthcare provider with information about the severity of a patient's heart failure. And the use of BNP in monitoring the effectiveness of treatment and planning for discharge are tools that can be utilized when formulating the care plan.


Learn more about it


Agruss JC, Garrett K. New markers for CVD. Nurse Pract. 2005;30(11):26, 29-31.


Fischbach F. A Manual of Laboratory and Diagnostic Tests. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004:362-364.


Ford CM, Pruitt R, Parker V, Reimels E. CHF: effects of cardiac rehabilitation and brain natriuretic peptide. Nurse Pract. 2004; 29(3):36-39.


Kinkade E, Frazier SK. BNP assays: predicting the future of CHF patients. Nurse Pract. 2006;31(13):36-41.


Sikaris K. BNP-considering a heartfelt message. Heart Lung Circ. 2004;13(suppl 3):S31-S37.