Heart Failure
A complete, readable guide to what heart failure means, how patients present, how the diagnosis is confirmed, and how acute and chronic heart failure are treated.
Definition, causes and typesHeart failure causes low output, raised filling pressure, or both.
What is heart failure?
Heart failure is a clinical syndrome in which a structural or functional cardiac problem prevents effective filling or pumping. The result is inadequate blood flow, abnormally high intracardiac pressure, or both.
Raised left-sided pressure causes pulmonary congestion and breathlessness. Raised right-sided pressure causes systemic venous congestion, which may produce swollen legs, liver enlargement and ascites. Reduced cardiac output causes fatigue, poor exercise tolerance and, in severe cases, organ hypoperfusion.
Symptoms and signs alone are not enough for a secure diagnosis. Clinical heart failure requires objective evidence of cardiac dysfunction or congestion, such as abnormal echocardiography, raised natriuretic peptides or documented raised filling pressures.
How heart failure develops
When stroke volume falls, the body activates the sympathetic nervous system and renin–angiotensin–aldosterone system. Faster heart rate, vasoconstriction and salt-and-water retention can temporarily support blood pressure and organ perfusion.
Persistent activation eventually becomes harmful. Greater afterload, fluid retention and wall stress drive congestion and ventricular remodelling through ventricular dilatation, hypertrophy and fibrosis.
Arginine vasopressin, also called antidiuretic hormone, increases water retention. In advanced heart failure, disproportionate water retention can dilute serum sodium and cause hyponatraemia.
Causes and risk factors
Common cardiac causes include coronary artery disease, previous myocardial infarction, longstanding hypertension, valve disease and cardiomyopathy. Congenital heart disease, myocarditis, persistent tachyarrhythmias, pericardial disease and severe bradyarrhythmias are additional causes.
Alcohol, cocaine, some chemotherapy medicines and other toxins can damage myocardium. Diabetes, obesity, chronic kidney disease, thyroid disease and iron overload may contribute directly or increase cardiovascular risk.
Why coronary artery disease matters
Reduced coronary blood flow and myocardial infarction can permanently damage heart muscle. The injured left ventricle contracts less effectively, making ischaemic heart disease the most common cause of reduced-ejection-fraction heart failure in many populations.
High-output heart failure
Less commonly, the heart pumps a normal or increased volume but still cannot meet an abnormally high demand. Severe anaemia, thyrotoxicosis, large arteriovenous shunts and beriberi are classic high-output causes.
Common causes of sudden deterioration
- Acute coronary syndrome, severe hypertension or acute valve failure.
- Atrial fibrillation or another rapid or slow arrhythmia.
- Infection, anaemia, thyroid dysfunction or pulmonary embolism.
- Missed medication, excess dietary salt, kidney injury or excessive intravenous fluid.
- Myocarditis, pregnancy-related cardiomyopathy or medicines that retain sodium.
Ways to classify heart failure
Left-sided versus right-sided
Left-sided failure mainly produces pulmonary congestion; right-sided failure mainly produces systemic venous congestion. Both commonly coexist.
Acute versus chronic
Acute heart failure develops rapidly; chronic heart failure develops or persists over time.
Low-output failure
Cardiac output is inadequate, particularly during exertion. Most conventional heart failure is low-output failure.
High-output failure
Cardiac output may be high but remains insufficient for greatly increased demand, as in severe anaemia or thyrotoxicosis.
Cor pulmonale
Cor pulmonale describes right ventricular structural change and failure caused by pulmonary hypertension arising from lung or pulmonary vascular disease. Chronic obstructive pulmonary disease, interstitial lung disease and recurrent pulmonary emboli are important causes.
Functional severity
The New York Heart Association (NYHA) classification describes symptom-related limitation of physical activity.
| Class | Functional limitation |
|---|---|
| I | Ordinary activity causes no undue symptoms. |
| II | Ordinary activity causes symptoms, but rest is comfortable. |
| III | Less-than-ordinary activity causes symptoms; rest is comfortable. |
| IV | Symptoms occur at rest and worsen with any activity. |
Symptoms and clinical signsBreathlessness and swelling reflect pulmonary or systemic congestion.
Symptoms and clinical signs
Ask about exertional breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced exercise tolerance and ankle swelling. Rapid weight gain, nocturnal cough and frothy sputum provide additional clues.
Left-sided heart failure
Raised left-sided filling pressure is transmitted backward into the pulmonary veins. Fluid then enters the lung interstitium and alveoli, producing breathlessness, orthopnoea and inspiratory basal crackles.
Right-sided heart failure
Raised right-sided pressure is transmitted into the systemic veins. Examination may reveal an elevated jugular venous pressure, dependent oedema, hepatomegaly and ascites.
Orthopnoea and paroxysmal nocturnal dyspnoea
Orthopnoea is breathlessness when lying flat that improves on sitting up. Paroxysmal nocturnal dyspnoea is waking from sleep with severe breathlessness and needing to sit or stand for relief.
Lying flat returns more venous blood from the legs and abdomen to the chest. A failing left ventricle cannot handle the increased preload, so pulmonary venous pressure rises and breathlessness worsens.
Congestion
Raised jugular venous pressure, a positive hepatojugular reflux, crackles, oedema, ascites, pleural effusions and rapid weight gain.
Low cardiac output
Fatigue, cool extremities, confusion, narrow pulse pressure, reduced urine output and exercise intolerance.
Third and fourth heart sounds
Third heart sound
A third heart sound occurs just after the second heart sound during rapid ventricular filling. In an older adult, a new third heart sound suggests volume overload or ventricular systolic dysfunction.
Fourth heart sound
A fourth heart sound occurs immediately before the first heart sound when atrial contraction forces blood into a stiff, poorly compliant ventricle.
Acute pulmonary oedema
Acute pulmonary oedema is a medical emergency caused by a rapid rise in pulmonary capillary pressure. Patients are often distressed, tachypnoeic and unable to lie flat.
Classic presentation
Alveolar fluid severely impairs gas exchange. Severe breathlessness, widespread crackles, hypoxaemia and pink frothy sputum form the classic presentation.
Cardiogenic shock
Hypotension plus hypoperfusion
Cardiogenic shock occurs when cardiac pump failure causes inadequate tissue perfusion. Hypotension is accompanied by evidence such as cold extremities, altered consciousness, oliguria or raised lactate.
Investigations and diagnosisNatriuretic peptides screen; echocardiography defines structure and function.
A practical diagnostic approach
- Suspect heart failure: recognise typical symptoms, signs and risk factors.
- Assess stability: identify pulmonary oedema, acute coronary syndrome or shock immediately.
- Request initial tests: electrocardiogram (ECG), chest X-ray, blood tests and natriuretic peptides.
- Perform echocardiography: confirm structural or functional abnormality and measure ejection fraction.
- Find the cause: assess for ischaemia, valve disease, hypertension, arrhythmia or cardiomyopathy.
Initial blood tests commonly include full blood count, electrolytes, renal function, liver function, glucose, thyroid function and iron studies. Troponin is appropriate when acute myocardial injury is suspected.
No single symptom, examination sign or test confirms every case. Diagnosis combines the clinical picture with objective evidence and actively considers alternative explanations for breathlessness or oedema.
Natriuretic peptides
Why levels rise
Ventricular pressure or volume overload stretches myocardial cells, which release B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). These hormones promote sodium excretion and vasodilation.
Why a low level is useful
Natriuretic peptides are particularly valuable as rule-out tests. A low result makes clinically important heart failure less likely, although strong clinical suspicion still requires assessment.
Age, atrial fibrillation, kidney disease, pulmonary hypertension, pulmonary embolism and severe systemic illness may raise results. Obesity and established treatment may produce lower-than-expected results.
Echocardiography
What the scan answers
Echocardiography measures left ventricular ejection fraction and evaluates chamber size, wall thickness, regional wall motion, right ventricular function and valve disease. It may also provide evidence of raised filling pressure.
A regional wall-motion abnormality may suggest previous myocardial infarction. Severe valve disease, ventricular hypertrophy, dilated chambers or right ventricular dysfunction may reveal the underlying cause.
Classification by ejection fraction
Ejection fraction is the percentage of blood ejected from the left ventricle during each contraction. It helps classify heart failure and guide treatment, but does not replace symptoms, signs and objective evidence.
| Category | Left ventricular ejection fraction | What else is required? |
|---|---|---|
| Reduced | 40% or lower | Clinical heart failure |
| Mildly reduced | 41%–49% | Evidence supporting raised filling pressure |
| Preserved | 50% or higher | Objective evidence of raised filling pressure |
| Improved | Previously 40% or lower, now above 40% | At least a 10-point absolute increase |
Heart failure with reduced ejection fraction (HFrEF)
The left ventricle has impaired systolic contraction. A left ventricular ejection fraction of exactly 40% belongs in the reduced category.
Heart failure with preserved ejection fraction (HFpEF)
The ventricle often contracts normally but relaxes poorly and fills at abnormally high pressure. Symptoms plus an ejection fraction of 50% or higher are not enough without objective evidence of raised filling pressure.
Ejection fraction is a continuum and can change with time or treatment. Current international definitions therefore emphasise the patient’s phenotype, cause and disease trajectory rather than relying on one isolated percentage.
Chest radiography
A chest X-ray can show pulmonary congestion, heart enlargement, pleural effusions or an alternative lung diagnosis. A normal chest X-ray does not exclude chronic heart failure.
Cardiomegaly
On an upright posterior–anterior chest radiograph, cardiomegaly is present when the maximal cardiac width exceeds half the internal thoracic width.
Kerley B lines
Kerley B lines are short horizontal peripheral lines near the lung bases. They represent thickened interlobular septa caused by interstitial fluid.
A quick chest X-ray pattern
- Alveolar oedema: bilateral perihilar “bat-wing” shadowing may appear in severe pulmonary oedema.
- Interstitial oedema: Kerley B lines, peribronchial cuffing and fluid in the fissures may be visible.
- Vascular redistribution: upper-lobe vessels become unusually prominent as pulmonary venous pressure rises.
- Pleural fluid: blunted costophrenic angles or larger pleural effusions may accompany congestion.
Additional testing and important alternatives
An ECG may reveal previous myocardial infarction, left ventricular hypertrophy, atrial fibrillation, tachyarrhythmia or conduction disease. A completely normal ECG makes major left ventricular systolic dysfunction less likely but does not exclude heart failure.
Cardiac magnetic resonance imaging helps characterise myocarditis, infiltrative disease, scar and cardiomyopathy when echocardiography is insufficient. Stress imaging or coronary angiography may be used when ischaemia is suspected, while right-heart catheterisation is reserved for selected cases with diagnostic uncertainty or advanced disease.
Important alternative explanations for breathlessness or oedema include chronic lung disease, pulmonary embolism, anaemia, obesity, physical deconditioning, kidney disease, cirrhosis and chronic venous insufficiency.
Treatment, monitoring and complicationsRelieve congestion, add disease-modifying therapy, then monitor closely.
Goals of treatment
Management aims to relieve congestion, improve symptoms, prevent hospital admission, slow disease progression and improve survival. Every plan should also treat the underlying cause and correct reversible precipitants.
The most useful approach combines disease-modifying treatment, symptom control, management of comorbidities, education, planned monitoring and timely referral for devices or advanced care.
Acute pulmonary oedema and decompensated heart failure
Begin with airway, breathing and circulation assessment while treating the precipitating cause. Sit the patient upright, stop unnecessary intravenous fluid and monitor oxygen saturation, blood pressure, cardiac rhythm, urine output and renal function.
Search promptly for acute coronary syndrome, hypertensive emergency, arrhythmia, infection, pulmonary embolism, acute valve failure, myocarditis, medication problems and worsening kidney function.
Immediate decongestion
Intravenous loop diuretics are used promptly when significant fluid overload is present. Oxygen is given for hypoxaemia rather than automatically, and non-invasive ventilation may be required for severe respiratory distress.
Congested with adequate pressure
Use intravenous loop diuresis. Intravenous vasodilators may be considered in selected patients without systemic hypotension.
Hypoperfusion or shock
Urgent specialist care may require inotropic or vasopressor support and temporary mechanical circulatory support.
Chronic reduced-ejection-fraction treatment
Modern treatment aims to establish four foundational medicine classes early, using tolerated doses and monitoring blood pressure, kidney function and potassium.
Renin–angiotensin system treatment
An angiotensin receptor–neprilysin inhibitor (ARNI) is preferred in many suitable patients. An angiotensin-converting enzyme inhibitor or angiotensin receptor blocker is used when appropriate.
Evidence-based beta-blocker
Bisoprolol, carvedilol or sustained-release metoprolol is introduced when the patient is clinically compensated, then increased as tolerated.
Mineralocorticoid receptor antagonist
Spironolactone or eplerenone reduces adverse outcomes but requires potassium and renal-function monitoring.
Sodium–glucose cotransporter 2 inhibitor
Dapagliflozin or empagliflozin improves outcomes even when the patient does not have diabetes, unless contraindicated.
The four foundational classes
Starting low doses of all four core classes is usually more valuable than maximising only one or two while leaving the others absent.
Where loop diuretics fit
Loop diuretics such as furosemide relieve breathlessness and oedema by removing excess fluid. They are essential for congestion but are not a substitute for disease-modifying therapy.
Selected patients may also benefit from hydralazine with isosorbide dinitrate, ivabradine, intravenous iron, digoxin or other specialist-directed treatment. Anticoagulation is used for a separate indication such as atrial fibrillation or venous thromboembolism, not simply because heart failure is present.
Preserved and mildly reduced ejection fraction
Sodium–glucose cotransporter 2 inhibitors reduce heart-failure events across preserved and mildly reduced ejection fractions. Diuretics treat congestion, and a mineralocorticoid receptor antagonist may be considered in suitable patients with appropriate renal function and potassium monitoring.
Heart failure with preserved ejection fraction is a multisystem syndrome rather than one uniform disease. Management targets hypertension, obesity, diabetes, atrial fibrillation, sleep apnoea, coronary disease and chronic kidney disease.
Devices, procedures and advanced care
Implantable cardioverter-defibrillator (ICD)
Selected patients with persistently reduced ejection fraction receive an ICD to reduce sudden arrhythmic death.
Cardiac resynchronisation therapy (CRT)
Selected symptomatic patients with reduced ejection fraction and electrical dyssynchrony benefit from coordinated biventricular pacing.
Correcting the cause
Revascularisation, valve intervention or arrhythmia treatment may be needed when a reversible cardiac cause is identified.
Advanced heart failure
Specialist teams assess suitable patients for mechanical circulatory support, transplantation and integrated palliative care.
Self-care, monitoring and follow-up
- Track breathlessness, swelling, exercise tolerance and sudden weight change.
- Review blood pressure, pulse, kidney function, sodium and potassium.
- Use regular physical activity or cardiac rehabilitation when clinically stable.
- Stop smoking and avoid excess alcohol; individualise salt and fluid advice.
- Review vaccination, iron deficiency, diabetes, kidney disease and sleep apnoea.
- Avoid stopping disease-modifying treatment solely because ejection fraction improves.
Medication changes should be followed by checks for symptoms, congestion, postural dizziness, heart rate, blood pressure, renal function and electrolytes. A sudden increase in weight may indicate fluid accumulation, but trends are more useful than one isolated measurement.
Complications and prognostic clues
Heart failure may cause recurrent pulmonary oedema, arrhythmias, thromboembolism, kidney or liver dysfunction, sudden cardiac death and cardiogenic shock.
Hyponatraemia in advanced disease
Low serum sodium often reflects intense neurohormonal activation, water retention and advanced circulatory dysfunction. Persistent hyponatraemia is therefore an adverse prognostic marker rather than simple evidence of dietary sodium deficiency.
Other adverse features include recurrent admissions, worsening renal function, persistent hypotension, escalating diuretic requirements, high natriuretic peptide levels and severe functional limitation.
Test yourself
A breathless patient has an ejection fraction of 55% but no evidence of raised filling pressure. Is preserved-ejection-fraction heart failure confirmed?
Answer: No. Symptoms and preserved ejection fraction are insufficient without objective evidence of raised filling pressure.
Which medicines relieve congestion without independently improving survival?
Answer: Loop diuretics relieve congestion and symptoms but are not one of the four foundational survival-improving classes.
Does a raised B-type natriuretic peptide level confirm heart failure?
Answer: No. A raised result supports the diagnosis but may also occur with kidney disease, atrial fibrillation, pulmonary hypertension and other illnesses.
References
- American Heart Association, American College of Cardiology and Heart Failure Society of America: 2022 Guideline for the Management of Heart Failure.
- American College of Cardiology: 2024 Expert Consensus Decision Pathway for Heart Failure With Reduced Ejection Fraction.
- American College of Cardiology: 2026 Expert Consensus Decision Pathway for Heart Failure With Preserved Ejection Fraction.
- European Society of Cardiology: 2023 Focused Update on Acute and Chronic Heart Failure.
- National Institute for Health and Care Excellence: Chronic Heart Failure in Adults—Diagnosis and Management, updated 2025.
- National Institute for Health and Care Excellence: Acute Heart Failure—Diagnosis and Management.
- American Heart Association, American College of Cardiology, European Society of Cardiology and World Heart Federation: Second Universal Definition of Heart Failure, 2026.
- National Heart, Lung, and Blood Institute: Heart Failure.
- National Health Service: Heart Failure—Symptoms, Tests, Treatment and Living With Heart Failure, reviewed 2026.
- American Heart Association: What Is Heart Failure?.