What Is Heart Failure?
Heart failure (HF) is a clinical syndrome in which the heart cannot pump enough blood to meet the body's needs, or can only do so at abnormally elevated filling pressures. It affects more than 64 million people worldwide and is the leading cause of hospitalisation in adults over 65. "Congestive heart failure" is an older term still commonly used when fluid backs up into the lungs or body tissues.
Heart failure is categorised by ejection fraction (EF) — the percentage of blood the left ventricle pumps out with each beat (normal ≥55%). HF with reduced EF (HFrEF, EF <40%) and HF with preserved EF (HFpEF, EF ≥50%) have different underlying mechanisms and slightly different treatments.
Symptoms to Recognise
- Breathlessness — initially on exertion, progressing to rest or lying flat (orthopnoea)
- Paroxysmal nocturnal dyspnoea — waking suddenly at night gasping for air
- Persistent fatigue and weakness — reduced cardiac output limits oxygen delivery to muscles
- Ankle and leg swelling — fluid retention (oedema) from impaired venous return
- Rapid or irregular heartbeat
- Reduced ability to exercise — a key functional marker tracked in clinical visits
- Persistent cough or wheeze — sometimes producing pink, foamy mucus
- Sudden weight gain — 2 kg or more in 2–3 days signals fluid accumulation; patients are taught to weigh daily
The Four Stages (ACC/AHA Classification)
- Stage A — High risk but no structural heart disease or symptoms. Includes patients with hypertension, diabetes, or family history of cardiomyopathy.
- Stage B — Structural heart disease (e.g. reduced EF, prior MI) but no HF symptoms yet. Intervention at this stage can prevent progression.
- Stage C — Structural heart disease with current or prior HF symptoms. The largest treatment group.
- Stage D — Advanced, refractory HF despite optimal therapy. Requires specialised interventions: intravenous inotropes, mechanical circulatory support, transplant evaluation, or palliative care.
NYHA Functional Classes
The New York Heart Association (NYHA) classes describe symptom severity:
- Class I — No symptoms with ordinary activity
- Class II — Slight limitation; comfortable at rest but symptoms with moderate exertion
- Class III — Marked limitation; comfortable at rest but symptoms with minimal activity
- Class IV — Symptoms at rest; unable to carry on any activity without discomfort
Common Causes
Coronary artery disease and prior heart attack cause about two-thirds of HFrEF cases. Other causes include:
- Long-standing, poorly controlled hypertension (most common cause of HFpEF)
- Dilated cardiomyopathy (genetic or idiopathic)
- Valvular heart disease (aortic stenosis, mitral regurgitation)
- Diabetes
- Viral myocarditis
- Chemotherapy-related cardiac toxicity (e.g. anthracyclines, trastuzumab)
- Atrial fibrillation — sustained rapid rate leads to tachycardia-induced cardiomyopathy
- Alcohol-related cardiomyopathy
Diagnosis
Diagnosis requires symptoms, signs, and objective evidence of cardiac dysfunction. Key investigations:
- Echocardiogram — gold standard for measuring EF and assessing valve function and wall motion
- BNP / NT-proBNP — natriuretic peptides rise when the ventricle is under stress; levels help confirm diagnosis and guide treatment intensity
- ECG — may reveal prior MI, left bundle branch block, or arrhythmia
- Chest X-ray — pulmonary oedema (bilateral haziness), cardiomegaly, pleural effusions
- Blood tests — full blood count, renal function, electrolytes, thyroid function (hypothyroidism can cause HF), iron studies
Treatment: Medications That Save Lives
For HFrEF, four drug classes are the foundation of modern therapy — often called the "four pillars":
- ACE inhibitors / ARBs / ARNI (e.g. sacubitril/valsartan, ramipril) — block the renin-angiotensin system, reduce afterload, improve EF
- Beta-blockers (e.g. carvedilol, bisoprolol, metoprolol succinate) — reduce heart rate and oxygen demand, prevent sudden cardiac death
- Mineralocorticoid receptor antagonists (e.g. spironolactone, eplerenone) — block aldosterone, reduce fluid retention, improve survival
- SGLT2 inhibitors (e.g. dapagliflozin, empagliflozin) — originally diabetes drugs, now proven to reduce HF hospitalisations and cardiovascular death in both HFrEF and HFpEF
- Diuretics (e.g. furosemide) — relieve congestion and breathlessness; do not improve survival but dramatically improve quality of life
Device Therapy
- ICD (implantable cardioverter-defibrillator) — prevents sudden cardiac death from ventricular arrhythmias; indicated in EF ≤35% on optimal therapy
- CRT (cardiac resynchronisation therapy) — biventricular pacemaker for patients with left bundle branch block and EF ≤35%; improves EF, symptoms, and survival
- LVAD (left ventricular assist device) — mechanical pump implanted in Stage D HF as a bridge to transplant or destination therapy
Self-Management and Lifestyle
- Weigh yourself every morning; contact your care team if you gain >2 kg in 48 hours
- Limit sodium to <2,000 mg/day to reduce fluid retention
- Fluid restriction (typically 1.5–2 L/day) in advanced cases
- Supervised cardiac rehabilitation programmes improve exercise capacity and quality of life
- Abstain from alcohol (alcohol worsens cardiomyopathy and interacts with medications)
- Influenza and pneumococcal vaccinations reduce hospitalisation risk