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

Heart failure (HF) is a complex clinical syndrome in which the heart is unable to pump sufficient blood to meet the body's demands, or can only do so at abnormally elevated filling pressures. It affects approximately 64 million people globally and carries a 5-year mortality of approximately 50%, comparable to many cancers. Heart failure is classified by ejection fraction: HFrEF (heart failure with reduced ejection fraction, EF below 40%) and HFpEF (preserved EF, above 50%). The NYHA classification (I–IV) grades symptom severity from no limitation to symptoms at rest. The NYHA classification provides functional staging: Class I (no limitation, ordinary physical activity causes no symptoms); Class II (slight limitation — comfortable at rest, but ordinary activity causes symptoms); Class III (marked limitation — comfortable only at rest, less than ordinary activity causes symptoms); Class IV (symptoms at rest, any activity causes discomfort). The MAGGIC and CHARM risk models predict mortality and guide prognosis discussions. Heart failure with mid-range ejection fraction (HFmrEF, EF 40–49%) is now recognized as a distinct entity bridging HFrEF and HFpEF.

Coronary artery disease (ischemic cardiomyopathy after MI) and hypertension are the two most common causes in developed nations. Other causes include dilated cardiomyopathy (idiopathic, genetic, alcoholic, peripartum), valvular heart disease (aortic stenosis, mitral regurgitation), hypertrophic cardiomyopathy, cardiac arrhythmias (especially atrial fibrillation), chemotherapy-related cardiotoxicity, and constrictive pericarditis. Risk factors include hypertension, diabetes, obesity, sleep apnea, renal impairment, smoking, and excessive alcohol use. Viral myocarditis is an increasingly recognized cause in young patients. Viral myocarditis — caused by Coxsackievirus B, adenovirus, parvovirus B19, SARS-CoV-2 — is an increasingly recognized cause of dilated cardiomyopathy in young patients. Takotsubo (stress) cardiomyopathy causes acute transient apical ballooning (apical dysfunction) triggered by intense emotional or physical stress, predominantly in postmenopausal women — 90% recover fully within weeks. Selenium deficiency (Keshan disease) is an important cause in endemic areas and is treated with selenium supplementation.

Classic symptoms include dyspnea (shortness of breath) on exertion progressing to orthopnea (dyspnea lying flat requiring extra pillows) and paroxysmal nocturnal dyspnea (sudden waking from sleep with breathlessness). Bilateral ankle swelling (peripheral edema), fatigue, exercise intolerance, rapid weight gain from fluid retention (more than 2 kg in 3 days signals decompensation), and abdominal bloating from ascites or hepatic congestion are common. Physical signs include elevated jugular venous pressure, third heart sound (S3 gallop), bibasal crackles, and peripheral pitting edema. NYHA Class III–IV patients are breathless with minimal activity or at rest. Cheyne-Stokes respiration — periodic cycles of apnoea followed by hyperpnoea — occurs during sleep in advanced HF from prolonged circulation time causing oscillating arterial CO2 levels, contributing to sleep-disordered breathing and nocturnal arrhythmias. Cardiac cachexia — weight loss exceeding 5% of non-oedematous body weight — indicates advanced HF with significantly worse prognosis.

Echocardiography is the cornerstone investigation, measuring ejection fraction, assessing cardiac structure, and identifying valvular disease or wall motion abnormalities. BNP (B-type natriuretic peptide) or NT-proBNP blood levels are elevated in heart failure — normal levels effectively rule out HF (high negative predictive value). ECG may show LV hypertrophy, bundle branch block, or arrhythmia. Chest X-ray shows cardiomegaly, pulmonary edema (Kerley B lines, bilateral perihilar shadowing), and pleural effusions. Blood tests include renal function, electrolytes, thyroid function (hypothyroidism causes dilated cardiomyopathy), iron studies, and CBC. Cardiac MRI provides the most detailed assessment of myocardial structure and fibrosis. Cardiac biomarkers: troponin is often mildly elevated in chronic HF reflecting ongoing myocardial stress and injury — significantly elevated troponin suggests ACS as a precipitant. Radionuclide ventriculography (MUGA scan) provides accurate LVEF measurement as an alternative to echocardiography when echo windows are poor. Right heart catheterisation (Swan-Ganz) measures pulmonary capillary wedge pressure (PCWP — elevated in left heart failure) and pulmonary artery pressures, guiding treatment in refractory or uncertain HF.

For HFrEF (EF below 40%), the four pillars of disease-modifying therapy are: ACE inhibitors or ARBs (or ARNI — sacubitril/valsartan — now preferred first-line), beta-blockers (bisoprolol, carvedilol, metoprolol succinate), mineralocorticoid receptor antagonists (spironolactone, eplerenone), and SGLT2 inhibitors (dapagliflozin, empagliflozin) — together reducing mortality by up to 60%. Loop diuretics (furosemide) relieve fluid congestion symptoms but do not reduce mortality. ICD (implantable cardioverter-defibrillator) is indicated for EF below 35% to prevent sudden cardiac death. CRT (cardiac resynchronization therapy) improves outcomes in bundle branch block with EF below 35%. Heart transplantation or LVAD (left ventricular assist device) is considered for end-stage disease. Sodium restriction below 2 g/day and fluid restriction to 1.5–2 L/day in symptomatic patients reduce hospitalisation. Mineralocorticoid receptor antagonist spironolactone should be avoided if eGFR below 30 or potassium above 5.0 mmol/L due to hyperkalaemia risk. For advanced HF refractory to medical therapy: inotropes (dobutamine, dopamine) as bridge to transplant; LVAD (HeartMate 3 — magnetically levitated centrifugal pump) as destination therapy for non-transplant candidates; orthotopic heart transplantation (gold standard — 10-year survival approximately 50%).

Acute decompensated heart failure (ADHF) — sudden worsening of heart failure requiring emergency hospitalization — carries 5–10% in-hospital mortality. Sudden cardiac death from ventricular arrhythmia accounts for up to 50% of heart failure deaths. Atrial fibrillation is extremely common in HF, increasing stroke risk and worsening cardiac function. Cardiorenal syndrome — worsening renal function during treatment — complicates diuretic management. Cardiac cachexia (severe muscle wasting) affects advanced HF patients. Frequent hospitalizations cause enormous healthcare burden and significantly impair patients' quality of life and independence.

Manage all cardiovascular risk factors aggressively — hypertension and diabetes are the two most preventable causes of heart failure. After MI, immediate and sustained ACE inhibitor and beta-blocker therapy reduces the risk of developing heart failure. Daily weight monitoring at home: if weight increases more than 2 kg in 2 days, contact your heart failure nurse or doctor for diuretic adjustment before hospitalization becomes necessary. Restrict fluid intake to 1.5–2 L per day and sodium to below 2 g per day in symptomatic HF. Alcohol abstinence in alcoholic cardiomyopathy can partially reverse LV dysfunction. Cardiac rehabilitation is beneficial and safe in stable heart failure.

Call 999 or go to A&E immediately for: severe breathlessness at rest or waking you from sleep, rapidly worsening breathlessness, coughing up pink frothy sputum (acute pulmonary oedema), chest pain, loss of consciousness, or extremely rapid or irregular heartbeat. Contact your heart failure nurse or GP urgently for: weight gain of more than 2 kg over 2 days (a sensitive early sign of fluid accumulation — adjust diuretics per your heart failure action plan), increasing breathlessness that is worse than your usual baseline, needing more pillows at night to breathe comfortably, new or significantly worsening ankle swelling, or reduced urine output despite taking diuretics. Do not wait for your next scheduled appointment if symptoms change — the majority of heart failure hospitalisations are preventable with early intervention. All patients with heart failure should have a written personalised action plan specifying what to do and who to call when warning signs appear, with out-of-hours contact details for their heart failure team.