Heart Failure

Heart failure is a multifaceted clinical syndrome characterized by cardinal symptoms (e.g., breathlessness, ankle swelling, and fatigue) and signs (e.g., elevated jugular venous pressure, pulmonary crackles, and peripheral oedema). It is not a single pathological diagnosis but the end-stage of various cardiovascular diseases, most commonly ischaemic heart disease and hypertension. The European Society of Cardiology (ESC) and NICE classify HF based on Left Ventricular Ejection Fraction (LVEF). Heart Failure with Reduced Ejection Fraction (HFrEF) is defined as LVEF <40%. Heart Failure with Preserved Ejection Fraction (HFpEF) is LVEF >50% with evidence of diastolic dysfunction. Heart Failure with Mildly Reduced Ejection Fraction (HFmrEF) sits in between (41-49%). Management has evolved significantly with the introduction of SGLT2 inhibitors. The New York Heart Association (NYHA) classification (I-IV) is used to grade functional severity. Prognosis remains poor, with a 5-year survival rate of approximately 50%, highlighting the need for aggressive pharmacological and device therapy (ICD/CRT) where indicated.

The pathophysiology of chronic heart failure is rooted in the body's compensatory mechanisms for low cardiac output, which eventually become maladaptive. When the heart's pumping capacity fails, the Sympathetic Nervous System (SNS) is activated, increasing heart rate and contractility (via catecholamines). Simultaneously, the Renin-Angiotensin-Aldosterone System (RAAS) is triggered by reduced renal perfusion. Angiotensin II causes vasoconstriction and stimulates Aldosterone release, leading to sodium and water retention. While these mechanisms maintain perfusion in the short term, the chronic increase in afterload (vasoconstriction) and preload (fluid retention) leads to ventricular wall stress, hypertrophy, and fibrosis—a process known as ventricular remodelling. Natriuretic peptides (BNP and ANP) are released from the stretched myocardium to counteract RAAS through vasodilation and natriuresis, but their effect is eventually overwhelmed. Molecular changes include altered calcium handling and myocyte apoptosis.

Patients typically present with triad of dyspnoea (on exertion or at rest), orthopnoea (breathlessness lying flat, relieved by pillows), and paroxysmal nocturnal dyspnoea (PND). Signs of left-sided failure include bibasal fine inspiratory crackles and a gallop rhythm (S3). Right-sided failure presents with raised JVP (with hepatojugular reflux), hepatomegaly (tender if acute), and pitting peripheral oedema (ankles, or sacral in bedbound patients). Complications are frequent: atrial fibrillation (due to atrial stretch), ventricular arrhythmias, cardiorenal syndrome, and hepatic congestion ('cardiac cirrhosis'). Iron deficiency is found in 50% of HF patients and worsens exercise tolerance regardless of anaemia status. Patients are often classified by the NYHA system: I (no limitation), II (slight limitation), III (marked limitation), IV (symptoms at rest).

1. First-line Bloods: NT-proBNP (If >2000 ng/L urgent specialist assessment <2 weeks; if 400-2000 ng/L assessment <6 weeks). FBC (anaemia), U&Es (renal function), LFTs, TFTs, HbA1c, Lipids.
2. Imaging: 12-lead ECG (rarely normal in HF), Chest X-ray (Alveolar oedema-Bat's wings, Kerley B lines, Cardiomegaly, Effusions, Upper lobe diversion).
3. Gold Standard: Transthoracic Echocardiogram (TTE) to assess LVEF and valvular function.
4. Advanced: Cardiac MRI for aetiology (e.g., infiltrative diseases like amyloid).

Acute Management: Oxygen (if hypoxic), IV Loop Diuretics (Furosemide 40-80mg), CPAP (for pulmonary oedema), Nitrates (if hypertensive). Stop CCBs (Diltiazem/Verapamil).
Chronic Management (HFrEF):
1. First-line: ACE inhibitors (e.g., Ramipril) AND Beta-blockers (e.g., Bisoprolol/Carvedilol).
2. Second-line: Mineraloid Receptor Antagonist (MRA) like Spironolactone or Eplerenone.
3. Third-line: Replace ACEi with ARNI (Sacubitril-Valsartan) if still symptomatic.
4. SGLT2 inhibitors (Dapagliflozin or Empagliflozin) for ALL HFrEF patients regardless of diabetes status.
5. Symptomatic: Furosemide or Bumetanide.
6. Non-pharmacological: Cardiac Resynchronisation Therapy (CRT) if QRS >130ms; ICD if high sudden death risk; annual flu/pneumococcal vaccines.