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  • For Educational Purposes Only: This content is intended for educational reference and should not be used for clinical decision-making.
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The clinical content and references are curated and reviewed by myself; however, AI was used to assist in organizing, paraphrasing, and formatting the information presented.
Quick Reference
  • Primary Use: Diagnosis and assessment of heart failure; differentiation of cardiac vs non-cardiac dyspnea
  • Released From: Cardiac ventricles in response to wall stretch and volume overload
  • Rule-Out (Acute): BNP <100 pg/mL or NT-proBNP <300 pg/mL makes acute heart failure unlikely
  • Rule-Out (Outpatient): BNP <35 pg/mL or NT-proBNP <125 pg/mL effectively excludes chronic HF
  • Sample Type: Serum or plasma (venous blood)
  • Key Point: Higher in elderly and females; multiple non-HF causes can elevate levels

Test Description

What is BNP?

Brain natriuretic peptide (BNP) and its N-terminal fragment (NT-proBNP) are neurohormones secreted primarily by the cardiac ventricles. Despite the name "brain natriuretic peptide," BNP is predominantly produced in the heart.

Why is BNP Released?

BNP is released in response to cardiac stress:

  • Ventricular wall stretch
  • Pressure overload (increased afterload)
  • Volume overload (increased preload)

How BNP is Produced

When ventricular myocytes are stretched, the following process occurs:

  • Precursor release: The prohormone proBNP is released
  • Cleavage: proBNP is cleaved into two fragments:
    • BNP: Biologically active hormone
    • NT-proBNP: Inactive N-terminal fragment
  • Circulation: Both fragments are released into the bloodstream
BNP vs NT-proBNP: BNP has a shorter half-life (~20 minutes) compared to NT-proBNP (~120 minutes), making NT-proBNP more stable for measurement. NT-proBNP levels are generally higher than BNP due to longer half-life and accumulation.

Physiological Actions

BNP acts as a compensatory mechanism in heart failure:

  • Promotes natriuresis (sodium excretion) and diuresis
  • Causes vasodilation
  • Inhibits the renin-angiotensin-aldosterone system (RAAS)
  • Reduces sympathetic nervous system activity
  • Overall effect: Reduces blood volume and pressure, countering heart failure pathophysiology
Normal Reference Ranges

Important Note: Reference ranges vary by assay, age, sex, and clinical context. Always use institution-specific values.

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TestAcute HF Rule-OutChronic HF Rule-OutElevated Range
BNP< 100 pg/mL< 35 pg/mL> 400 pg/mL moderate-severe HF
NT-proBNP< 300 pg/mL< 125 pg/mL> 900 pg/mL moderate-severe HF

Age-Stratified NT-proBNP Cutoffs for Acute HF:

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Age GroupRule-OutDiagnostic
< 50 years< 300 pg/mL> 450 pg/mL
50–75 years< 300 pg/mL> 900 pg/mL
> 75 years< 300 pg/mL> 1800 pg/mL
Age and Gender Influence: NT-proBNP increases significantly with age and is higher in females. Older adults (≥80 years) can have median values 5-10× higher than younger adults even without heart failure.
Clinical Significance

Primary Clinical Uses:

  • Diagnosis of Heart Failure: Differentiating cardiac from non-cardiac causes of dyspnea in acute settings
  • Risk Stratification: Higher BNP/NT-proBNP correlates with worse prognosis in HF patients
  • Monitoring Therapy: Serial measurements help assess response to HF treatment
  • Screening: Identifying asymptomatic LV dysfunction in high-risk populations

Cardiac Causes of Elevation

  • Acute decompensated heart failure (HFrEF or HFpEF)
  • Acute coronary syndrome / myocardial infarction
  • Pulmonary hypertension (right ventricular strain)
  • Valvular heart disease (AS, AR, MR)
  • Atrial fibrillation (due to atrial stretch)
  • Myocarditis or pericarditis
  • Cardiomyopathy (dilated, hypertrophic, restrictive)

Non-Cardiac Causes of Elevation

  • Renal Failure: Reduced clearance; chronic elevation common in CKD/ESRD
  • Pulmonary Embolism: Right heart strain
  • Severe Sepsis/Septic Shock: Myocardial depression and volume shifts
  • Liver Cirrhosis: Volume overload and cardiac dysfunction
  • Stroke/Subarachnoid Hemorrhage: Neurogenic cardiac dysfunction
  • Advanced Age: Baseline elevation even without HF
Obesity Paradox: BNP and NT-proBNP are lower in obese patients due to increased clearance by adipocyte natriuretic peptide receptors. Consider using lower thresholds or clinical judgment in obese patients.
Interpretation Guidelines

Acute Dyspnea in the Emergency Department:

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BNP LevelNT-proBNP LevelInterpretation
< 100 pg/mL< 300 pg/mLHeart failure unlikely (high NPV)
100–400 pg/mL300–900 pg/mLGray zone; correlate with clinical findings
> 400 pg/mL> 900 pg/mLHeart failure likely

Outpatient/Chronic Setting:

  • BNP <35 pg/mL or NT-proBNP <125 pg/mL: Effectively rules out chronic HF
  • Values above these thresholds warrant echocardiographic assessment

Prognostic Stratification in Known HF:

  • Higher baseline BNP/NT-proBNP correlates with increased mortality and hospitalization
  • Failure of BNP/NT-proBNP to decrease with therapy suggests poor response
  • Serial monitoring can guide medication titration
Clinical Pearl: BNP/NT-proBNP has excellent negative predictive value for heart failure. A low value in an acutely dyspneic patient makes HF very unlikely; look for alternative diagnoses (pneumonia, COPD, PE, etc.).
Interfering Factors & Limitations
  • Age: Baseline increases with age; use age-adjusted cutoffs
  • Gender: Females have ~50% higher baseline NT-proBNP than males
  • Renal Dysfunction: Chronic elevation due to decreased clearance
  • Obesity: Falsely low BNP/NT-proBNP; may need to adjust thresholds downward
  • Atrial Fibrillation: Often elevated due to atrial stretch even without HF
  • Nesiritide Therapy: Synthetic BNP; interferes with BNP assays (NT-proBNP unaffected)
Not Specific to HF: BNP/NT-proBNP indicates ventricular wall stress but does not specify the cause. PE, renal failure, sepsis, and many other conditions can elevate levels.
Clinical Pearls
Excellent Rule-Out Test: The greatest utility of BNP/NT-proBNP is its high negative predictive value. A normal value in an acutely dyspneic patient makes heart failure very unlikely.
Adjust for Age: NT-proBNP increases dramatically with age. An 80-year-old with NT-proBNP of 500 pg/mL may be at baseline, whereas a 40-year-old with the same value likely has significant pathology.
Obesity Lowers BNP: Obese patients have falsely reassuring BNP/NT-proBNP levels. Don't rule out HF based solely on a "normal" BNP in an obese patient with clinical signs of HF.
CKD: CKD patients often have chronically elevated BNP/NT-proBNP. Establishing a baseline value in stable CKD patients helps interpret acute changes.
Trend Matters: In patients with known HF, the trend (rising or falling) is often more important than the absolute value.
PE Causes Elevation: Pulmonary embolism causes right heart strain and elevates BNP/NT-proBNP. Always consider PE if clinical presentation is atypical for HF.
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. NEJM, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult. Medscape.
  4. Nickson, C. Critical Care Compendium. Life in the Fast Lane.
  5. Farkas, Josh MD. (2015). EMCrit Project.
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