Heart failure

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Heart failure is a clinical syndrome caused by structural or functional cardiac abnormality. Symptoms alone are non-specific; natriuretic peptide triage and echocardiography establish likelihood, phenotype and cause.

HFrEF is LVEF 40% or lower, HFmrEF 41–49%, and HFpEF 50% or higher in contemporary use. Treatment evidence and NICE strength differ between phenotypes.

Optimisation means reaching maximum tolerated evidence-based therapy, not necessarily target doses in every patient. Introduce therapies promptly but tailor order, interval and dose to congestion, BP, pulse, renal function, frailty and preference.

Every diagnosis should trigger aetiology work-up: ischaemia, hypertension, valve disease, arrhythmia, toxins, cardiomyopathy, endocrine disease, infiltrative disease and congenital causes may require specific treatment.

Key points

In untreated suspected heart failure, NT-proBNP above 2000 ng/L requires urgent specialist assessment and transthoracic echo within 2 weeks; 400–2000 ng/L requires both within 6 weeks.
NT-proBNP below 400 ng/L makes heart failure less likely in an untreated person, but obesity and HF medicines can lower it; seek specialist advice if concern persists.
Echocardiography must identify LVEF phenotype, valves, chamber size, diastolic function and alternative structural disease; do not diagnose solely from a natriuretic peptide.
For HFrEF, 2025 NICE recommends four foundational classes: ACE inhibitor, evidence-based beta-blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor, introduced in a sequence and tempo tailored to the person.
If symptoms persist on maximum tolerated four-pillar treatment, consider replacing the ACE inhibitor with sacubitril/valsartan; seek specialist advice before starting ARNI in primary care.
Use a loop diuretic at the lowest dose that maintains euvolaemia; it relieves congestion but is not a substitute for disease-modifying therapy.
NICE now advises considering an MRA plus SGLT2 inhibitor in HFpEF and considering the four HFrEF classes in HFmrEF, with phenotype/comorbidity review.
Check renal function and electrolytes before and 1–2 weeks after starting or increasing ACEi/ARB/ARNI/MRA, then every 3–6 months at stable maximum tolerated dose.
Refer for ICD/CRT assessment when LVEF remains 35% or lower despite optimised therapy; QRS duration, LBBB morphology, NYHA class and ischaemic substrate determine the device.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Ischaemic myocardial damage

Prior infarction, repeated ischaemia or hibernating myocardium can reduce contractile mass and promote scar-based remodelling. Coronary disease may also cause acute decompensation through infarction or ischaemic valve dysfunction.

Pressure and volume overload

Longstanding hypertension, stenotic valves, regurgitant valves and congenital shunts impose chronic mechanical load. Compensatory hypertrophy or dilatation eventually becomes maladaptive, raising filling pressure and reducing reserve.

Primary myocardial disease

Inherited cardiomyopathy, myocarditis, toxins and infiltrative disorders directly impair myocytes or ventricular compliance. The resulting phenotype may be reduced, mildly reduced or preserved ejection fraction.

Rhythm and systemic drivers

Persistent tachyarrhythmia, bradycardia, endocrine disease, severe anaemia and renal disease can cause or amplify heart failure. Identifying these contributors is important because some are reversible.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pump or filling abnormality
Structural or functional disease impairs ventricular contraction, relaxation or both. Stroke volume falls, filling pressure rises, or these changes become apparent only when circulatory demand increases.
2
Neurohormonal activation
Reduced effective perfusion activates sympathetic, renin–angiotensin–aldosterone and vasopressin pathways. Faster heart rate, vasoconstriction and fluid retention initially defend blood pressure and organ flow.
3
Maladaptive loading
Continued sodium retention increases preload, while vasoconstriction increases afterload. These responses raise myocardial oxygen demand and filling pressures, turning short-term compensation into progressive congestion and dysfunction.
4
Cardiac remodelling
Chronic wall stress drives hypertrophy, chamber dilatation, fibrosis and functional valve regurgitation. Geometry and electrical conduction deteriorate, further reducing mechanical efficiency and creating arrhythmic substrate.
5
Organ congestion and hypoperfusion
Left-sided pressure produces pulmonary congestion, while right-sided pressure causes peripheral and abdominal fluid accumulation. Advanced low output compromises renal, cerebral, hepatic and coronary perfusion.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical symptoms

Exertional breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, ankle swelling, abdominal distension and reduced exercise tolerance.

Supporting signs

Raised JVP, pulmonary crackles, peripheral oedema, displaced apex, S3, tachycardia, cool peripheries, hepatomegaly or a causative murmur.

Acute pulmonary oedemaRed flag

Severe breathlessness at rest, hypoxia, widespread crackles, pink frothy sputum or inability to lie flat requires emergency treatment.

Low-output stateRed flag

Hypotension, confusion, cold/clammy skin, oliguria, rising lactate or narrow pulse pressure suggests cardiogenic shock and needs critical-care/shock-team escalation.

Precipitant requiring urgent treatmentRed flag

ACS, rapid AF or ventricular arrhythmia, infection, hypertensive emergency, pulmonary embolism, acute severe valve disease, renal failure or medication toxicity can destabilise heart failure.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Clinical assessment, observations and 12-lead ECGFirst step
Why
Assess severity and identify ischaemia, AF, conduction disease, QRS width or a pacing/device clue.
Interpretation and limitations
A completely normal ECG makes major systolic dysfunction less likely but does not exclude HFpEF; acute ischaemia or unstable rhythm requires an emergency pathway.
02
NT-proBNP
Why
Triage untreated suspected chronic heart failure to echocardiography and specialist assessment.
Interpretation and limitations
Above 2000 ng/L: both within 2 weeks; 400–2000 ng/L: both within 6 weeks; below 400 ng/L: HF less likely, consider alternatives and discuss persistent concern.
03
Transthoracic echocardiography
Why
Measure LVEF, assess regional wall motion, diastolic function, valves, RV, chambers and shunts.
Interpretation and limitations
Phenotype guides therapy; severe valve disease, marked LV dysfunction, pulmonary hypertension or RV failure changes urgency and referral.
04
Bloods and urine
Why
FBC, U&E/eGFR, LFT, TFT, HbA1c, lipids, urinalysis; add iron studies (ferritin and transferrin saturation) and tests directed by suspected cause.
Interpretation and limitations
Find anaemia, renal/endocrine disease and treatment constraints. In HFrEF with Hb below 150 g/L, consider IV iron when TSAT is below 20% or ferritin below 100 ng/mL.
05
Chest X-ray
Why
Assess pulmonary congestion, pleural effusions, cardiomegaly and lung alternatives.
Interpretation and limitations
A normal film does not exclude chronic heart failure.
06
Cause-directed imaging/testing
Why
CTCA/angiography or functional testing for CAD; CMR for myocarditis, infiltrative or genetic cardiomyopathy; ambulatory ECG for intermittent rhythm; spirometry if lung disease suspected.
Interpretation and limitations
Treatable aetiology changes prognosis and may prompt revascularisation, valve intervention, immunological or inherited-cardiac referral.
07
Functional and congestion baseline
Why
NYHA class, weight, BP, pulse, oxygen saturation and, where useful, 6-minute walk or CPET.
Interpretation and limitations
Provides an objective reference for response and identifies advanced-HF features.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Chronic lung disease

COPD, asthma or interstitial lung disease can cause exertional breathlessness and low oxygen saturation. Wheeze, pulmonary-function abnormalities and lung-imaging findings may predominate, but pulmonary disease and heart failure commonly coexist.

Pulmonary embolism

Acute dyspnoea, chest pain, hypoxaemia and raised natriuretic peptide may resemble decompensated heart failure. Sudden onset, venous thromboembolic risk and right-heart strain direct pulmonary vascular imaging.

Renal, hepatic or venous oedema

Kidney failure, cirrhosis and chronic venous insufficiency can each cause peripheral swelling. Urine, renal and liver findings or local venous changes may support an alternative or additional cause; coexisting cardiac congestion still needs assessment.

Anaemia or deconditioning

Reduced oxygen-carrying capacity, frailty and inactivity commonly cause fatigue and exertional breathlessness. Blood count and functional assessment may support these explanations, although any can coexist with heart failure.

Obesity and sleep-disordered breathing

Obesity, reduced fitness and sleep apnoea cause breathlessness, oedema and fatigue while potentially suppressing natriuretic peptide concentrations. Sleep history and objective cardiac evidence help avoid misclassification.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DiagnosisNatriuretic-peptide triageFirst stepSymptoms/signs suggest chronic heart failure and the patient is not already diagnosed.

1Measure NT-proBNP; do not use it to distinguish HFrEF from HFpEF.
2If above 2000 ng/L, arrange urgent specialist assessment and TTE within 2 weeks; if 400–2000 ng/L, arrange both within 6 weeks.
3AlternativeIf below 400 ng/L in an untreated person, review alternative causes; obesity, diuretics, ACEi/ARB/ARNI, beta-blockers and MRAs can reduce peptide concentration, so discuss persistent concern with a HF specialist.
4At specialist assessment establish phenotype, cause, severity, comorbidities and the person's goals.

02HFrEFBuild the four foundational therapiesConfirmed HFrEF without a contraindication to treatment.

1Offer an ACE inhibitor, a beta-blocker licensed for heart failure, an MRA and an SGLT2 inhibitor; choose order, spacing and dose increments according to BP, pulse, renal function, potassium, congestion and frailty.
2Do not withhold a beta-blocker solely because of age, peripheral vascular disease, erectile dysfunction, diabetes, interstitial lung disease or COPD without reversibility; start only once clinically stable.
3Use a loop diuretic for congestion and titrate up or down to the lowest dose maintaining euvolaemia.
4Reassess after starts and increments; maximise tolerated doses rather than waiting for one class to reach target before introducing every other pillar.

03AlternativeIntolerance or persistent HFrEF symptomsAlternativeACE inhibitor cannot be used, or symptoms persist despite maximum tolerated four-pillar treatment.

1ACE-inhibitor intolerance other than angioedema: offer ARNI with beta-blocker, MRA and SGLT2 inhibitor. Previous ACEi/ARB angioedema or ARNI intolerance: use beta-blocker, MRA and SGLT2 inhibitor and consider an ARB.
2Persistent symptoms on maximum tolerated ACEi plus the other pillars: consider switching ACEi to ARNI, with at least a 36-hour ACEi washout.
3Specialist options include ivabradine within NICE technology-appraisal criteria, hydralazine plus nitrate when ACEi/ARNI/ARB cannot be used, and digoxin for worsening or severe HFrEF despite optimised therapy.
4Check ferritin, TSAT and Hb; in eligible iron-deficient HFrEF consider IV iron using a licensed product-specific deficit calculation.

04EscalationDevices and advanced heart-failure referralEscalationPersistent LVEF 35% or lower, conduction delay, malignant arrhythmia, recurrent admission or advanced symptoms despite optimised treatment.

1Refer for ICD/CRT assessment under NICE TA314; QRS duration, LBBB morphology, NYHA class, ischaemic risk and pacing need determine ICD, CRT-D or CRT-P.
2EscalationSeek advanced-HF/transplant-centre advice for refractory NYHA III–IV symptoms, repeated admissions, escalating diuretics, intolerance of disease-modifying therapy from hypotension/renal dysfunction, inotrope dependence or end-organ dysfunction.
3Give anticipatory care, vaccination, self-management advice and an individualised rescue-diuretic plan where the HF team supports one.
4Review clinically stable patients at least every 6 months; after a clinical or medicine change, review within days to 2 weeks.

Key medicines and prescribing safety7 treatments · regimens, roles and cautions

NICE first foundational renin–angiotensin drug for HFrEF when tolerated.

Ramipril — licensed symptomatic-heart-failure example

Start 1.25 mg by mouth once daily in a diuretic-treated, stabilised patient; double at 1–2-week intervals to a maximum 10 mg/day, preferably in 2 divided doses for heart failure.

Check BP, creatinine/eGFR and potassium before and 1–2 weeks after every start/increment. Avoid in pregnancy, previous ACE-inhibitor angioedema, bilateral renal artery stenosis and with sacubitril/valsartan; cough and hyperkalaemia may limit use.

Evidence-based HFrEF beta-blocker; start when clinically stable and euvolaemic.

Bisoprolol — licensed stable chronic-HF example

1.25 mg once daily for week 1; 2.5 mg once daily week 2; 3.75 mg once daily week 3; 5 mg once daily weeks 4–7; 7.5 mg once daily weeks 8–11; then 10 mg once daily maintenance/maximum, only as tolerated.

Pretreatment ECG. Do not use with heart rate below 50 beats/min or unpaced second/third-degree AV block. Monitor pulse, BP, congestion and bronchospasm; slow or pause titration if decompensation occurs and never stop abruptly without a clinical reason.

MRA foundational therapy in HFrEF; NICE also says consider an MRA in HFmrEF and HFpEF.

Spironolactone — licensed severe-HF example

Start 25 mg by mouth once daily when potassium is 5.0 mmol/L or lower and creatinine is 2.5 mg/dL (about 221 micromol/L) or lower; increase to 50 mg once daily if tolerated, or reduce to 25 mg on alternate days if not.

Avoid significant hyperkalaemia, Addison disease and combination with another potassium-sparing diuretic. Monitor potassium/renal function closely; gynaecomastia can occur. Specialist/renal input is needed with advanced CKD.

SGLT2 inhibitor foundational therapy in HFrEF and considered by NICE in HFmrEF/HFpEF, with or without diabetes.

Dapagliflozin — licensed chronic-HF example

10 mg by mouth once daily; no HF dose titration. The cited current SmPC advises not initiating below eGFR 15 mL/min/1.73 m².

Assess volume status and renal function; counsel genital infection and euglycaemic DKA symptoms. Interrupt during hospitalisation for major surgery or acute serious illness, monitor blood ketones and restart only once ketones are normal and the patient is stable.

Replacement for ACEi in persistent symptomatic HFrEF on maximum tolerated pillars, or alternative when ACEi intolerance is not angioedema; seek specialist advice before primary-care initiation.

Sacubitril/valsartan — licensed ARNI example

Usually 49/51 mg by mouth twice daily, doubled after 2–4 weeks to target 97/103 mg twice daily. Use 24/26 mg twice daily with no/low prior ACEi/ARB exposure, eGFR below 60, or systolic BP 100–110 mmHg, with slower 3–4-week titration.

Stop ACEi for at least 36 hours first; never combine with ACEi or another ARB. Do not initiate if systolic BP is below 100 mmHg or potassium above 5.4 mmol/L. Contraindicated with prior ACEi/ARB angioedema, pregnancy and severe hepatic impairment; monitor BP, renal function and potassium.

Rapid relief of pulmonary/peripheral congestion; no proven substitute for disease-modifying therapy.

Furosemide — licensed oedema example

A common oral start is 40 mg in the morning; licensed maintenance examples are 20 mg daily or 40 mg on alternate days, while resistant oedema may require 80 mg daily or specialist-divided/higher dosing. In HF, titrate individually to euvolaemia rather than applying one fixed dose.

Monitor weight, BP, renal function, sodium, potassium and magnesium; avoid over-diuresis, hypotension and gout exacerbation. Acute pulmonary oedema requires hospital treatment rather than unsupervised oral escalation.

Consider in HFrEF when Hb is below 150 g/L and TSAT below 20% or ferritin below 100 ng/mL.

Intravenous iron — NICE requirement with product-specific dosing

No universal fixed dose: calculate iron deficit from body weight and Hb using the selected SmPC. Ferric carboxymaltose is commonly limited to a single dose of 15 mg/kg by injection or 20 mg/kg by infusion and no more than 1000 mg in a week; re-dose only after reassessment.

Use a setting able to manage hypersensitivity; monitor during administration and for at least 30 minutes afterwards. Ferric carboxymaltose can cause hypophosphataemia; repeat phosphate in at-risk or repeated high-dose patients.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute pulmonary oedema

A rapid rise in left-sided filling pressure drives fluid into alveoli, causing severe hypoxaemia and respiratory distress. It requires emergency treatment and investigation of an acute precipitant.

Cardiogenic shock

Severe pump failure can no longer sustain organ perfusion, producing hypotension, cold peripheries, confusion, oliguria and rising lactate. Without rapid escalation, multiorgan failure may follow.

Cardiorenal and hepatic dysfunction

Low forward flow and venous congestion reduce kidney filtration and congest the liver. Organ dysfunction then restricts treatment tolerance, promotes fluid retention and worsens prognosis.

Atrial and ventricular arrhythmia

Chamber stretch, fibrosis, ischaemia and electrolyte disturbance promote atrial fibrillation and ventricular arrhythmia. These may worsen output, cause thromboembolism or lead to sudden cardiac death.

Frailty and recurrent admission

Persistent congestion and low output drive exercise intolerance, muscle wasting, falls and loss of independence. Repeated decompensation often marks advanced disease and a need to revisit goals and specialist options.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Before ACEi/ARB/ARNI/MRA: BP, renal function and electrolytes; repeat 1–2 weeks after starting, 1–2 weeks after each dose increase, every 3–6 months at stable maximum tolerated dose, and whenever renal function may be compromised.
If creatinine rises by more than 50% or potassium exceeds 5.5 mmol/L, follow local HF/renal guidance urgently and review nephrotoxins, potassium supplements and interacting medicines rather than reflexively abandoning all therapy.
At eGFR 45 mL/min/1.73 m² or lower use lower starting doses/smaller increments; below 30 liaise with renal and HF specialists.
Before beta-blocker obtain ECG; after each increment check pulse, BP and clinical congestion. Avoid initiation during unstable decompensation.
For diuretics use daily weights during active titration and monitor U&E/eGFR after changes; teach the patient their target weight and escalation plan.
For SGLT2 inhibitors review volume status, renal function, genital infection and DKA risk; pause for acute serious illness/major surgery with blood-ketone monitoring.
Review stable HF at least every 6 months, including functional capacity, fluid status, rhythm, cognition/nutrition, medicine optimisation, vaccination and advance-care priorities.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Peptide level is a referral tool, not the phenotype

NT-proBNP determines urgency but cannot distinguish HFrEF from HFpEF and can be raised by age, renal dysfunction and AF.

Four pillars are classes, not one rigid sequence

NICE explicitly asks clinicians to tailor order, timing and dose to the individual; clinically useful doses across classes are preferable to a prolonged one-drug-at-a-time delay.

Congestion and perfusion are separate questions

A patient can be oedematous yet intravascularly vulnerable. Reassess JVP, weight, BP, renal function and symptoms rather than chasing ankle oedema alone.

Recovered EF is not necessarily cured

Relapse after withdrawing HFrEF treatment is common in recovered dilated cardiomyopathy; continued therapy is usually appropriate unless a specialist-led reason exists.

Iron deficiency is functional

NICE eligibility uses TSAT/ferritin plus Hb and does not require microcytosis. Oral iron is not an equivalent evidence-based substitute for the IV-HF pathway.

Device referral is phenotype-based

LVEF 35% or lower opens assessment, but QRS width/morphology, NYHA class, ischaemic risk and pacing needs decide ICD versus CRT-P/CRT-D.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing or excluding HF from NT-proBNP alone without echocardiography and aetiology review.
02
Waiting to maximise one drug before introducing every other foundational HFrEF class.
03
Starting a beta-blocker during unstable, congested decompensation or stopping it abruptly without assessment.
04
Combining an ACE inhibitor with sacubitril/valsartan or omitting the 36-hour washout.
05
Treating oedema with escalating loop diuretic while overlooking disease-modifying therapy, renal injury or a precipitant.
06
Applying a fixed IV-iron dose without the selected product's weight/Hb calculation and safety monitoring.