Heart Failure — Causes, Symptoms, Staging & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Heart failure (HF) is a clinical syndrome in which the heart is unable to pump enough blood to meet the body's metabolic demands at normal filling pressures, resulting in symptoms of breathlessness, fluid retention, and fatigue. It affects approximately 64 million people worldwide and carries a 5-year mortality rate exceeding 50% — higher than many common cancers. Heart failure is classified by left ventricular ejection fraction (LVEF): HFrEF (heart failure with reduced EF — LVEF below 40%, sometimes called 'systolic heart failure'); HFmrEF (heart failure with mildly reduced EF — LVEF 40-49%); and HFpEF (heart failure with preserved EF — LVEF 50% or above, sometimes called 'diastolic heart failure'). HFpEF now accounts for more than 50% of all heart failure cases globally, more common in older women with hypertension, diabetes, and atrial fibrillation. The distinction is important because evidence-based pharmacological treatments differ significantly between HFrEF and HFpEF.

Coronary artery disease (ischaemic cardiomyopathy — from myocardial infarction causing regional wall motion abnormality) is the most common cause of HFrEF, accounting for approximately 60-70% of cases. Other causes of HFrEF: dilated cardiomyopathy (idiopathic, familial/genetic — titin mutations in 25%; viral myocarditis, peripartum cardiomyopathy, alcohol cardiomyopathy, chemotherapy-induced — doxorubicin, trastuzumab, tyrosine kinase inhibitors). HFpEF causes: hypertension-related concentric left ventricular hypertrophy (most common), diabetes mellitus, obesity, atrial fibrillation, and chronic kidney disease. Valvular heart disease: aortic stenosis (pressure overload), mitral regurgitation (volume overload). Arrhythmias: sustained tachyarrhythmias (tachycardia-mediated cardiomyopathy — reversible with rate control or ablation). Right heart failure: pulmonary arterial hypertension, right ventricular MI. Precipitants of acute decompensation in stable chronic HF: non-compliance with medications/diet, arrhythmias (AF with rapid ventricular rate), infection (pneumonia, UTI), anaemia, uncontrolled hypertension, renal impairment, and NSAIDs (cause fluid retention and worsen HF).

Cardinal symptoms: dyspnoea (breathlessness) — initially on exertion, progressing to dyspnoea at rest; orthopnoea (breathlessness lying flat — patients sleep on multiple pillows); paroxysmal nocturnal dyspnoea (awakening from sleep gasping, relieved by sitting upright); and peripheral oedema (ankle and leg swelling — from venous congestion). Additional features: fatigue and reduced exercise tolerance, persistent cough (especially with lying flat), nocturia, ascites (in severe right heart failure), cardiac cachexia (weight loss from poor appetite and increased catabolism). Clinical signs: elevated JVP (jugular venous pressure), bilateral basal lung crepitations (pulmonary oedema), S3 gallop rhythm, mitral regurgitation murmur, ankle oedema. NYHA Classification: Class I (no symptoms at ordinary activity); Class II (slight limitation); Class III (marked limitation — comfortable only at rest); Class IV (unable to carry out any activity without symptoms; symptoms at rest).

BNP/NT-proBNP: natriuretic peptides are the most important biomarkers for heart failure diagnosis and monitoring. Elevated NT-proBNP (above 125 pg/mL in chronic HF; above 300 pg/mL in acute HF) has high sensitivity for HF. Very elevated levels (above 1000 pg/mL in acute) predict high risk. Normal NT-proBNP effectively excludes heart failure as a cause of dyspnoea. Echocardiography (transthoracic echo — TTE) is the cornerstone diagnostic test: measures LVEF (normal above 50-55%), wall motion abnormalities (ischaemia), left ventricular hypertrophy, valvular disease, right ventricular function, and filling pressures. Chest X-ray: cardiomegaly (cardiothoracic ratio above 0.5), pulmonary vascular congestion, Kerley B lines (interstitial oedema), pleural effusions. 12-lead ECG: identifies atrial fibrillation, LBBB (left bundle branch block — indicates CRT candidate), evidence of prior MI. Cardiac MRI: gold standard for myocardial viability, cardiomyopathy characterisation, and tissue characterisation with late gadolinium enhancement. Coronary angiography or CT coronary angiography to evaluate for ischaemic aetiology. Blood tests: FBC (anaemia), U&E (renal function — critical for medication titration), TFTs (hypothyroidism/hyperthyroidism), LFTs, HbA1c, fasting lipids, iron studies (iron deficiency is common in HF — IV iron replacement improves symptoms).

HFrEF (LVEF below 40%) — the 'fantastic four' disease-modifying therapies proven to reduce mortality: (1) ACE inhibitor/ARB (or sacubitril/valsartan — angiotensin receptor neprilysin inhibitor, ARNI — superior to ACE inhibitor in HFrEF, PARADIGM-HF trial, 20% additional mortality reduction); (2) beta-blocker (bisoprolol, carvedilol, metoprolol succinate — proven mortality benefit only in stable patients; start low, titrate slowly); (3) mineralocorticoid receptor antagonist/MRA (spironolactone or eplerenone — additional 15-20% mortality reduction); (4) SGLT2 inhibitors (dapagliflozin or empagliflozin — 25-35% reduction in HF hospitalisation and CV death — DAPA-HF and EMPEROR-Reduced trials). Loop diuretics (furosemide, bumetanide) for symptomatic congestion relief — do not reduce mortality but are essential for symptom management. HFpEF: SGLT2 inhibitors (dapagliflozin — DELIVER trial; empagliflozin — EMPEROR-Preserved) reduce HF hospitalisation by 20-25% — the first evidence-based pharmacological therapies for HFpEF. Device therapy: ICD (implantable cardioverter-defibrillator) for primary prevention of sudden cardiac death in HFrEF with LVEF below 35% despite optimal medical therapy; CRT (cardiac resynchronisation therapy) for HFrEF with LBBB and QRS above 130 ms — reduces symptoms, hospitalisation, and mortality. Advanced HF: LVAD (left ventricular assist device) as bridge to transplant or destination therapy; cardiac transplantation is the gold standard for end-stage HF with 10-year survival around 50%.

Acute decompensated heart failure (ADHF) — sudden fluid overload requiring hospitalisation — carries 5–10% in-hospital mortality and 20–30% 90-day readmission rates. Sudden cardiac death from ventricular arrhythmias (VT/VF) accounts for 40–50% of deaths in HFrEF — primary prevention ICD is indicated when EF remains below 35% despite 3 months of optimal medical therapy. Cardiorenal syndrome (mutual deterioration of heart and kidneys) complicates aggressive diuresis, reducing eGFR and limiting the use of renin-angiotensin-aldosterone system blockers that improve prognosis. Atrial fibrillation complicates 40–50% of heart failure cases, worsening haemodynamics and increasing stroke risk. Hepatic congestion from right heart failure causes cardiac hepatopathy and, in severe cases, cardiac cirrhosis. Cardiac cachexia — progressive muscle wasting from neurohormonal activation, inflammation, and gut oedema causing malabsorption — occurs in advanced HF and is an independent predictor of poor prognosis.

Prevent HF by aggressive management of its risk factors: treat hypertension to target below 130/80 mmHg; control diabetes (SGLT2 inhibitors reduce HF hospitalisation by 35% even in diabetics without established HF); manage dyslipidaemia; achieve and maintain healthy weight; engage in regular aerobic exercise; abstain from tobacco and limit alcohol; and treat AF rhythm or rate appropriately. Cardiac rehabilitation improves exercise tolerance, quality of life, and reduces hospitalisation. Daily weight monitoring: patients should weigh daily — weight gain of 2 kg in 2 days or 3 kg in 1 week indicates fluid retention requiring urgent review and diuretic adjustment. Salt restriction below 2g/day reduces fluid retention. Fluid restriction (1.5-2L/day) for severe HF with hyponatraemia. Influenza, pneumococcal, and COVID-19 vaccination recommended for all HF patients. Avoid NSAIDs (cause fluid retention and acute kidney injury), most calcium channel blockers (except amlodipine in HFrEF), and Class I antiarrhythmics.

Call emergency services (999/911) immediately for: sudden severe breathlessness at rest (acute pulmonary oedema — a medical emergency); pink frothy sputum; severe leg swelling appearing rapidly over hours; chest pain with breathlessness; or loss of consciousness. Seek urgent medical assessment (same day) for: weight gain of 2 kg in 2 days; increased ankle swelling; worsening breathlessness over days; persistent new irregular heartbeat. All patients with new symptoms of breathlessness, ankle swelling, and exercise intolerance should have NT-proBNP measured promptly — if elevated, refer to cardiology for echocardiography. HF is best managed in a dedicated HF specialist clinic with regular review of medications, volume status, renal function, and device therapy.