BNP & NT-proBNP
The heart failure blood test — produced when the heart wall is under stretch
BNP is released when ventricular walls stretch under pressure or volume overload. A normal BNP makes significant heart failure extremely unlikely — it's one of the most powerful negative predictors in cardiology.
Brain natriuretic peptide (BNP) is a cardiac hormone from ventricular myocytes, released when wall tension rises. It causes vasodilation, natriuresis, and diuresis — a compensatory mechanism to reduce preload. NT-proBNP is the inactive N-terminal cleavage fragment with a longer half-life, making it more stable for testing. Both rise proportionally to cardiac wall stress.
Reference Ranges
How clinicians interpret BNP / NT-proBNP results — from optimal to concerning.
⚠ Reference ranges vary by laboratory and assay. Always interpret your result in context of your laboratory's own reference intervals and your clinical presentation.
What raises BNP / NT-proBNP
Any elevated filling pressure stretches ventricles — HFpEF, HFrEF, ischaemic cardiomyopathy all drive BNP release.
Massive PE causes acute right ventricular pressure overload — BNP and troponin both rise and predict 30-day mortality.
NT-proBNP is renally cleared — CKD raises NT-proBNP independent of cardiac function. Use BNP or higher cut-offs in CKD.
AF causes atrial wall stress — BNP rises even without HF, complicating interpretation.
Cytokine-driven ventricular dysfunction in sepsis elevates BNP — predicts ICU mortality.
What lowers BNP / NT-proBNP
Diuretics, ACEi, beta-blockers, SGLT2i all reduce BNP by lowering filling pressures. Serial BNP guides drug titration.
Adipose tissue clears BNP via NPR-C receptors — obese patients with HF may have lower BNP than lean patients with equivalent disease.
Sacubitril inhibits BNP degradation — BNP rises but NT-proBNP falls. Always use NT-proBNP in patients on sacubitril/valsartan.
Conditions this biomarker signals
When BNP / NT-proBNP is outside normal range, these are the most clinically significant possibilities.
BNP > 500 or NT-proBNP > 2,000 in dyspnoea supports acute HF with > 90% sensitivity.
Persistently elevated NT-proBNP despite optimal therapy = target for additional treatment (CRT, LVAD).
BNP + troponin both elevated = submassive PE — thrombolysis or catheter-directed therapy consideration.
Which tests measure this biomarker
BNP / NT-proBNP may be included in or ordered alongside these panels.
Use for acute monitoring. Do NOT use BNP in patients on sacubitril — levels are falsely elevated.
More analytically stable. Renally cleared — use age-adjusted cut-offs. Preferred in sacubitril patients.
How the heart uses BNP to fight its own failure
BNP is the heart's endogenous counter-regulatory response to rising wall tension. As ventricular tension rises, myocytes release pre-pro-BNP, cleaved into active BNP and the inactive NT-proBNP fragment. Active BNP binds NPR-A receptors in kidney and vasculature, causing vasodilation and natriuresis — physiologically unloading the failing ventricle. This is why sacubitril (neprilysin inhibitor) — which prevents BNP breakdown — is now first-line in HFrEF: it amplifies the heart's own protective response. A normal BNP (< 35 pg/mL) has a > 98% NPV for excluding HF as a cause of dyspnoea.
A normal BNP virtually excludes heart failure
BNP < 35 pg/mL or NT-proBNP < 125 pg/mL has a negative predictive value of > 98% for excluding heart failure as cause of acute dyspnoea. This allows rapid, safe exclusion of HF in the ED and redirects investigation toward PE, pneumonia, or COPD.
The obesity paradox: obese patients have lower BNP
Adipocytes express NPR-C (clearance receptor) for natriuretic peptides — obese patients clear BNP faster, resulting in lower levels for the same cardiac dysfunction. A BNP of 80 pg/mL in an obese patient may represent HF that would generate 300 pg/mL in a lean patient — the standard cut-offs underperform in obesity.
Sacubitril raises BNP but lowers NT-proBNP
Sacubitril inhibits neprilysin (the enzyme that degrades BNP), elevating BNP levels independent of cardiac function. NT-proBNP is not a neprilysin substrate and continues to reflect true filling pressures. In patients on sacubitril/valsartan (Entresto), always use NT-proBNP for monitoring.
Clinical use — when and why this is ordered
How clinicians use BNP / NT-proBNP in practice — the real-world scenarios where it changes decisions.
Emergency dyspnoea triage
First-line ED test for acute breathlessness — distinguishes cardiac from respiratory cause. BNP result within 30 minutes of draw.
HF treatment monitoring
NT-proBNP-guided therapy (target 30% reduction from baseline) reduces HF hospitalisation. Guides titration of diuretics, ACEi, beta-blockers.
Post-MI risk stratification
BNP at 24–72h post-MI predicts 1-year mortality independently of LVEF — high BNP = priority for ACEi/beta-blocker initiation.
Pre-operative cardiac risk
Pre-op NT-proBNP > 300 pg/mL is associated with 5-fold increased 30-day cardiovascular mortality after non-cardiac surgery (ESC/ESA guidelines).