What BNP level indicates heart failure?

BNP above 100 pg/mL suggests possible heart failure, and levels above 400 pg/mL make heart failure very likely (positive predictive value >95% in the appropriate clinical setting). For NT-proBNP, age-stratified cutoffs are used: >450 pg/mL for age 900 pg/mL for age 50–75, and >1,800 pg/mL for age >75. The 'grey zone' between these values requires clinical correlation. BNP and NT-proBNP have excellent negative predictive value — levels below the cutoff effectively rule out heart failure in dyspneic patients.

What is a dangerous BNP level?

BNP levels above 400 pg/mL strongly suggest significant heart failure and warrant urgent evaluation and treatment. Levels above 900–1,000 pg/mL indicate severe heart failure and are associated with high short-term mortality and hospitalization risk. For NT-proBNP, values exceeding 5,000–10,000 pg/mL are seen in acute decompensated heart failure and carry a poor prognosis. However, absolute numbers must always be interpreted alongside the clinical picture.

What is the difference between BNP and NT-proBNP?

Both are released when the proBNP precursor is cleaved in response to ventricular wall stress. BNP is the active hormone (32 amino acids, half-life ~20 minutes, cleared by NPR-C receptors and neprilysin). NT-proBNP is the inactive N-terminal fragment (76 amino acids, half-life ~120 minutes, cleared primarily by the kidneys). Because NT-proBNP is more affected by renal function, its levels are higher and require age-adjusted cutoffs. The two tests are equally effective for heart failure diagnosis but are not interchangeable — they use different cutoffs and assays.

Can BNP be elevated without heart failure?

Yes. BNP can be elevated in many conditions besides heart failure, including: pulmonary embolism, pulmonary hypertension, acute coronary syndromes, atrial fibrillation, valvular heart disease, renal failure (especially NT-proBNP), sepsis, critical illness, advanced age, and anemia. Conversely, BNP can be falsely low in obesity (adipose tissue expresses natriuretic peptide clearance receptors) and in flash pulmonary edema before peptides have had time to rise.

What does a BNP of 500 mean?

A BNP of 500 pg/mL is significantly elevated and, in a patient with dyspnea, strongly suggests heart failure as the cause (the Breathing Not Properly study showed 95% probability of heart failure at this level). However, clinical context matters — renal insufficiency, pulmonary embolism, sepsis, and other conditions can also produce this level. A BNP of 500 should prompt echocardiography, chest X-ray, and clinical assessment. Serial measurements are useful: a BNP that decreases with treatment confirms response; a rising BNP suggests worsening failure.

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BNP Levels — Normal Range & Heart Failure

Complete reference on BNP and NT-proBNP levels for heart failure diagnosis, interpretation thresholds, and causes of elevation beyond cardiac disease.

⚡ Quick Answer — BNP Decision Thresholds

BNP <100 pg/mL → Heart failure unlikely

BNP 100–400 pg/mL → Grey zone — correlate clinically

BNP >400 pg/mL → Heart failure likely

NT-proBNP uses age-stratified cutoffs. BNP has excellent negative predictive value — a normal BNP effectively rules out heart failure in dyspneic patients.

What Is BNP?

B-type natriuretic peptide (BNP) is a cardiac neurohormone secreted primarily by the ventricular myocardium in response to increased wall stress from volume overload or pressure overload. It is synthesized as a prohormone (proBNP, 108 amino acids) which is cleaved into the biologically active BNP (32 amino acids) and the inactive N-terminal fragment, NT-proBNP (76 amino acids).

BNP promotes natriuresis (sodium excretion), diuresis, and vasodilation — counteracting the renin-angiotensin-aldosterone system (RAAS). It acts as the body's defense mechanism against volume overload. In clinical practice, BNP and NT-proBNP are used primarily for the diagnosis and management of heart failure, particularly in the emergency department evaluation of acute dyspnea.

The landmark Breathing Not Properly Multinational Study (Maisel et al., NEJM 2002) established BNP as a powerful diagnostic tool for heart failure, demonstrating that a BNP cutoff of 100 pg/mL had 90% sensitivity and 76% specificity for the diagnosis of congestive heart failure in patients presenting with acute dyspnea.

Normal BNP and NT-proBNP Ranges

BNP Interpretation Thresholds

BNP Level (pg/mL)	Interpretation	Likelihood of HF
<100	Normal / HF unlikely	Low (<2%)
100–400	Grey zone — possible HF	Intermediate
>400	Heart failure likely	High (>95%)

NT-proBNP Age-Stratified Cutoffs (Heart Failure Diagnosis)

Age Group	Rule-Out Cutoff (pg/mL)	Rule-In Cutoff (pg/mL)	SI (pmol/L rule-in)
All ages (acute)	<300	See age-specific below	—
<50 years	<300	>450	>53
50–75 years	<300	>900	>106
>75 years	<300	>1,800	>212
Chronic HF (outpatient): >125 pg/mL (<75y) or >450 pg/mL (>75y) suggests HF

BNP thresholds from Maisel et al., NEJM 2002. NT-proBNP age-stratified cutoffs from Januzzi et al., Eur Heart J 2006 (ICON study). ESC/AHA guidelines recommend these thresholds. 1 pg/mL BNP ≈ 0.289 pmol/L; 1 pg/mL NT-proBNP ≈ 0.118 pmol/L.

What Does a High BNP Mean?

Elevated BNP or NT-proBNP reflects increased myocardial wall stress. While heart failure is the primary diagnostic target, multiple conditions can raise natriuretic peptides:

Cardiac Causes

Heart failure — both HFrEF (reduced ejection fraction) and HFpEF (preserved ejection fraction). BNP correlates with NYHA functional class and prognosis.
Acute coronary syndromes — myocardial ischemia and infarction cause transient BNP elevation, which has independent prognostic significance.
Atrial fibrillation / flutter — atrial stretch and rapid rates elevate BNP even without ventricular dysfunction.
Valvular heart disease — aortic stenosis, mitral regurgitation, and other significant valvular lesions.
Hypertrophic cardiomyopathy — from diastolic dysfunction and outflow obstruction.
Myocarditis / Takotsubo cardiomyopathy — acute myocardial inflammation or stress cardiomyopathy.

Non-Cardiac Causes

Pulmonary embolism — right ventricular strain elevates BNP; higher BNP in PE is associated with worse outcomes.
Pulmonary hypertension — right-sided heart strain from any cause.
Renal failure — impaired clearance (especially NT-proBNP) and chronic volume overload. CKD patients may have chronically elevated baselines.
Sepsis / critical illness — cytokine-mediated BNP release and septic cardiomyopathy.
Advanced age — BNP and NT-proBNP increase with age, even in healthy individuals. Women tend to have higher levels than men.
Anemia — compensatory high-output state increases wall stress.

Symptoms Associated with Elevated BNP

Symptoms reflect the underlying cause. In heart failure: dyspnea (on exertion and at rest), orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, fatigue, weight gain (fluid retention), jugular venous distension, and pulmonary crackles. BNP levels correlate with severity — NYHA Class IV patients typically have BNP >900 pg/mL.

What Does a Low BNP Mean?

A low BNP (<100 pg/mL) in a dyspneic patient is most useful as a rule-out test — it makes heart failure very unlikely (negative predictive value >98%). However, two important caveats exist:

Obesity — BNP is paradoxically lower in obese patients. Adipose tissue expresses natriuretic peptide clearance receptors (NPR-C), leading to increased BNP clearance. Some guidelines suggest using a lower cutoff (e.g., BNP <50 pg/mL) in obese patients. NT-proBNP is less affected.
Flash pulmonary edema — in very acute onset (e.g., hypertensive crisis with pulmonary edema), BNP may not have had time to rise when blood is drawn in the first 1–2 hours.
Early or mild heart failure — NYHA Class I patients may have near-normal BNP levels.
Constrictive pericarditis — BNP may be lower than expected for the degree of congestion, as ventricular wall stress is less pronounced.

Sacubitril/valsartan (Entresto) inhibits neprilysin, which degrades BNP — resulting in elevated BNP but decreased NT-proBNP. In patients on this medication, NT-proBNP should be used for monitoring, not BNP.

Related Tests & Calculators

Echocardiography — the gold standard for evaluating cardiac structure and function after BNP raises suspicion for heart failure.
Troponin — to evaluate for acute myocardial injury/infarction alongside BNP.
Chest X-ray — for pulmonary congestion, cardiomegaly, and pleural effusions.
Renal function (BUN, creatinine, eGFR) — to assess cardiorenal syndrome and BNP clearance.
NT-proBNP — alternative natriuretic peptide test; preferred in patients on sacubitril/valsartan and for renal-adjusted interpretation.
SOFA Score — SOFA Calculator — for critically ill patients where BNP elevation may indicate septic cardiomyopathy.
Framingham Risk Score — Framingham Calculator — cardiovascular risk assessment.

About This Test

Clinical Pearls

🔑 Key Points for Clinicians

BNP for rule-out, not just rule-in: The greatest clinical utility of BNP is its negative predictive value. A BNP <100 pg/mL (or NT-proBNP <300 pg/mL) in an acutely dyspneic patient makes heart failure extremely unlikely (NPV >98%).
Serial monitoring: In admitted heart failure patients, a decrease in BNP >30% from admission predicts better outcomes. A rising BNP despite treatment suggests inadequate response or worsening failure.
Obesity adjustment: Consider halving the BNP cutoff (i.e., using 50 pg/mL) in patients with BMI >35, as false negatives are more common. NT-proBNP is less affected by BMI.
Sacubitril/valsartan caveat: This drug inhibits BNP degradation, raising BNP levels. Use NT-proBNP (not BNP) for monitoring in patients on this medication.
Renal failure: Baseline BNP/NT-proBNP is chronically elevated in CKD/ESRD due to volume expansion and reduced clearance. Use higher cutoffs or trend values rather than single measurements.
BNP in PE: Elevated BNP in pulmonary embolism indicates right ventricular strain and is associated with higher mortality — it adds prognostic information but is not diagnostic for PE.

Specimen and Assay Notes

BNP is measured from EDTA plasma; NT-proBNP can be measured from serum, EDTA, or heparinized plasma. BNP is unstable and degrades in vitro — specimens should be processed within 4 hours. NT-proBNP is more stable (can be stored at room temperature for up to 72 hours). Different assays are not interchangeable — BNP and NT-proBNP values from different manufacturers may vary, so serial monitoring should use the same platform.

References

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(3):161-167.
Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study. Am J Cardiol. 2005;95(8):948-954.
Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032.
McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599-3726.
Daniels LB, Maisel AS. Natriuretic peptides in heart failure diagnosis and management. UpToDate. Accessed January 2025.
Januzzi JL Jr, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients (ICON study). Eur Heart J. 2006;27(3):330-337.
Wang TJ, Larson MG, Levy D, et al. Impact of obesity on plasma natriuretic peptide levels. Circulation. 2004;109(5):594-600.

References last verified: February 2026