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Q3 LONG ANSWER 10M ★ High-yield

Discuss the aetiology, classification, clinical features, investigations and management of heart failure.

General Medicine · Final Professional

Definition

Heart failure is a clinical syndrome in which structural or functional cardiac abnormality causes reduced cardiac output and/or elevated intracardiac pressures at rest or during stress, producing the characteristic symptoms (breathlessness, fatigue, ankle swelling) and signs (raised JVP, pulmonary crackles, peripheral oedema).

Classification BY Ejection Fraction

TypeLV ejection fractionComment
HFrEF — reduced≤ 40%Systolic failure; the best-studied, with the strongest evidence base
HFmrEF — mildly reduced41–49%Intermediate; treated broadly as HFrEF
HFpEF — preserved≥ 50% with structural or functional abnormality and raised natriuretic peptidesDiastolic failure — impaired relaxation and filling; commoner in elderly women, hypertensives, diabetics and the obese; treatment options are far more limited

Other classifications: acute versus chronic; left versus right sided; high output (anaemia, thyrotoxicosis, beriberi, arteriovenous fistula, Paget's disease, pregnancy) versus low output.

Aetiology

  • Coronary artery disease — the commonest cause worldwide
  • Hypertension — the commonest cause of HFpEF
  • Valvular heart disease — RHEUMATIC HEART DISEASE remains a major cause in India
  • Cardiomyopathies — dilated, hypertrophic, restrictive; peripartum cardiomyopathy
  • Myocarditis — viral, diphtheritic, Chagas disease
  • Arrhythmias — persistent tachycardia causing tachycardia-mediated cardiomyopathy; atrial fibrillation
  • Toxins — alcohol, anthracyclines, trastuzumab, cocaine
  • Nutritional — thiamine deficiency (wet beriberi), selenium deficiency
  • Endocrine — thyrotoxicosis, hypothyroidism, acromegaly, phaeochromocytoma, diabetes
  • Infiltrative — amyloidosis, sarcoidosis, haemochromatosis
  • Congenital heart disease; pericardial disease; cor pulmonale

Precipitants of decompensation — the "FAILURE" list: Forgotten medication (non-adherence — the commonest), Arrhythmia and Anaemia, Ischaemia and Infection, Lifestyle (salt and fluid excess, alcohol), Upregulation (thyrotoxicosis, pregnancy), Renal failure, Embolism (pulmonary) and Endocarditis. Also drugs — NSAIDs, calcium channel blockers (verapamil, diltiazem), pioglitazone, steroids.

Clinical Features

LEFT heart failure (pulmonary congestion)RIGHT heart failure (systemic congestion)
Exertional dyspnoea; ORTHOPNOEA; PAROXYSMAL NOCTURNAL DYSPNOEAPeripheral pitting oedema (ankles, sacrum)
Fatigue, reduced exercise toleranceRAISED JVP
Cough with frothy pink sputum (pulmonary oedema)Tender hepatomegaly, hepatojugular reflux, pulsatile liver in tricuspid regurgitation
Nocturia; cardiac cachexia in advanced diseaseAscites, pleural effusion
Bibasal crepitations, wheeze ("cardiac asthma")Anorexia, nausea, right hypochondrial discomfort (hepatic congestion)
Displaced apex, S3 GALLOP (the most specific sign), functional mitral regurgitationRight ventricular heave, tricuspid regurgitation murmur
Tachycardia, pulsus alternans, low pulse pressureFacial oedema, jaundice in severe congestion

Congestive cardiac failure denotes both together — most commonly right failure secondary to left.

NYHA functional classification (used for prognosis and treatment decisions): I — no limitation; II — slight limitation with ordinary activity; III — marked limitation with less than ordinary activity; IV — symptoms at rest.

Investigations

  • Natriuretic peptides (BNP or NT-proBNP) — the key initial test. A normal level makes heart failure very unlikely (high negative predictive value), making it valuable for ruling out. Levels rise with age, renal impairment and atrial fibrillation, and are lower in obesity.
  • ECHOCARDIOGRAPHY — the central diagnostic investigation: ejection fraction, chamber sizes, wall motion abnormalities, valve function, diastolic parameters, pulmonary pressures and pericardium.
  • ECG — rarely normal in heart failure; shows previous infarction, LVH, arrhythmia, conduction disease (a broad QRS raises the question of cardiac resynchronisation therapy).
  • Chest X-ray: cardiomegaly (cardiothoracic ratio > 50%), upper lobe blood diversion, Kerley B lines, perihilar "bat's wing" alveolar oedema, pleural effusions.
  • Bloods: CBC (anaemia — both a cause and a consequence), renal function and electrolytes, liver function, thyroid function, glucose and HbA1c, lipids, iron studies (ferritin and transferrin saturation — iron deficiency is common and treatable).
  • Further: coronary angiography or CT coronary angiography for ischaemic aetiology; cardiac MRI for cardiomyopathy, infiltration and viability; endomyocardial biopsy in selected cases.

Management

ACUTE HEART FAILURE / PULMONARY OEDEMA — an emergency

  • Sit the patient upright; high-flow oxygen if hypoxic.
  • Intravenous loop diuretic (furosemide) — the mainstay for congestion.
  • Nitrates (intravenous or sublingual) if the blood pressure permits — they reduce preload and afterload and are particularly valuable in hypertensive pulmonary oedema.
  • Non-invasive ventilation (CPAP or BiPAP) — reduces work of breathing and the need for intubation.
  • Morphine — used sparingly; evidence of benefit is weak and it may worsen outcomes.
  • Identify and treat the precipitant — ischaemia, arrhythmia, infection, non-adherence.
  • Inotropes and vasopressors only for cardiogenic shock with hypoperfusion; mechanical support in specialist centres.
  • Monitor urine output, weight, renal function and electrolytes.

CHRONIC HFrEF — the "four pillars" of disease-modifying therapy

All four should be started early, at low doses, and titrated up — the evidence supports rapid sequential or simultaneous initiation rather than the older stepwise approach over months:

1. ACE inhibitor or ARB — or preferably ARNI (sacubitril/valsartan), which is superior to an ACE inhibitor in reducing mortality and hospitalisation

2. Beta-blocker — bisoprolol, carvedilol or metoprolol succinate. Start low, go slow, and never start during acute decompensation

3. Mineralocorticoid receptor antagonist — spironolactone or eplerenone; monitor potassium and renal function

4. SGLT2 inhibitor — dapagliflozin or empagliflozin; benefit is independent of diabetes, and this is the most important recent addition to heart failure therapy

Additional therapy: loop diuretics for symptom control (they improve symptoms but not survival); ivabradine for persistent tachycardia in sinus rhythm; hydralazine with nitrate (particularly in those intolerant of ACE inhibitors); digoxin for symptom control and rate control in atrial fibrillation; intravenous iron for iron deficiency; vericiguat in selected patients.

Device therapy: implantable cardioverter-defibrillator (ICD) for primary prevention of sudden death in persistent severe LV dysfunction; cardiac resynchronisation therapy (CRT) for LV dysfunction with a broad QRS (especially LBBB).

Advanced heart failure: left ventricular assist device and cardiac transplantation; and, where these are not options, palliative care with symptom control and advance care planning — an area consistently neglected.

HFpEF: treat hypertension, atrial fibrillation, obesity, diabetes and ischaemia; diuretics for congestion; SGLT2 inhibitors are the first class shown to improve outcomes in this group.

Non-pharmacological for all: salt restriction, fluid restriction in advanced disease, daily weight monitoring with a written action plan, alcohol and smoking cessation, vaccination (influenza and pneumococcal), supervised exercise and cardiac rehabilitation, and structured education with self-management support.

DANGER / REMEMBER

Never start or increase a beta-blocker in a patient who is acutely decompensated and congested — it will worsen the failure. Beta-blockers are started when the patient is euvolaemic and stable, at low dose, and titrated slowly. Conversely, do not stop a beta-blocker abruptly in a stable patient admitted for another reason. Also avoid verapamil, diltiazem, NSAIDs, pioglitazone and most antiarrhythmics in HFrEF — all worsen outcomes.

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  3. Q3Discuss the aetiology, classification, clinical features, investigations and management of heart failure. ★
  4. Q4Discuss the classification, causes, clinical features, complications and management of systemic hypertension. ★
  5. Q5Discuss the aetiology, clinical features, investigations and management of valvular heart disease. ★
  6. SN1Write a short note on chronic rheumatic heart disease.
  7. SN2Write a short note on chronic coronary syndrome (stable angina) and non-invasive testing for myocardial ischaemia.
  8. SN3Write a short note on the cardiomyopathies.
  9. SN4Write a short note on pericardial disease — acute pericarditis, pericardial effusion, tamponade and constrictive pericarditis.
  10. SN5Write a short note on atrial fibrillation, including digoxin therapy and toxicity.
  11. SN6Write a short note on supraventricular tachyarrhythmias and antiarrhythmic drugs.
  12. SN7Write a short note on bradyarrhythmias and complete heart block.
  13. SN8Write a short note on cardiac arrest and cardiopulmonary resuscitation.
  14. SN9Write a short note on the jugular venous pressure.
  15. SN10Write a short note on cyanosis.
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