1. Definition

• Heart failure is a clinical syndrome in which the heart’s ability to pump blood effectively is impaired, causing characteristic symptoms (e.g., dyspnoea, fatigue) and signs (e.g., oedema, raised jugular venous pressure).
• It can result from many disorders and often involves complex changes affecting multiple organ systems (e.g., renal, hepatic, musculoskeletal, endocrine).

2. Key Classifications

1. By Ejection Fraction (EF)
   • HFpEF (Heart Failure with Preserved Ejection Fraction): EF ≥ 50%.
     • Main problem is diastolic dysfunction (ventricular relaxation/filling impairment).
     • Often associated with hypertension, age, obesity, diabetes, and renal disease.
   • HFmrEF (Heart Failure with Mid-Range Ejection Fraction): EF typically 40–49%.
   • HFrEF (Heart Failure with Reduced Ejection Fraction): EF < 40%.
     • Main problem is systolic dysfunction (impaired contractility). Often secondary to ischaemic heart disease.
2. By Anatomical Location
   • Left-Sided Heart Failure: Often due to ischaemia, hypertension, dilated or restrictive cardiomyopathy, or myocardial infarction.
     • Reduced forward perfusion and pulmonary congestion predominate.
   • Right-Sided Heart Failure: Most commonly secondary to left-sided failure; can also be due to lung disease (cor pulmonale) or left-to-right shunts.
     • Systemic congestion (jugular venous distension, peripheral oedema, hepatic enlargement) predominates.
   • Biventricular / Congestive Cardiac Failure: Evidence of both left- and right-sided dysfunction.
3. By Time Course
   • Chronic (Long-standing, progressive)
   • Acute (Sudden) or Acute-on-Chronic
4. By AHA/ACC Stages (Disease Progression)
   • Stage A: High risk (e.g., hypertension, diabetes, obesity, ischaemic heart disease) but no structural heart disease or symptoms
   • Stage B: Structural heart disease (e.g., left ventricular hypertrophy, previous MI) without symptoms
   • Stage C: Structural heart disease with current or prior symptoms (clinical heart failure)
   • Stage D: Refractory heart failure requiring advanced interventions (transplant, mechanical support, palliative care)

3. Epidemiology

• Prevalence in Europe ~1% of adults.
• Incidence rises with age; mean age of diagnosis ~76 years.
• 5-year survival ~50%, worse than many cancers.
• Frequent cause of hospitalisation in those over 65, accounting for ~5% of admissions in the UK.

4. Aetiology

• Ischaemic heart disease: Most common overall cause of HF (particularly HFrEF).
• Hypertension: A leading cause of LV hypertrophy (common risk factor for HFpEF).
• Valvular disease (e.g., mitral regurgitation).
• Arrhythmias (e.g., atrial fibrillation).
• Congenital abnormalities (e.g., septal defects).
• Non-cardiac factors that increase demand or reduce oxygen carrying capacity, such as severe anaemia, endocrine disorders (thyrotoxicosis), and infection.

5. Pathogenesis

1. HFrEF (Reduced EF)
   • Systolic dysfunction due to myocardial injury or scarring (e.g., past MI).
   • Scar tissue cannot contract, lowering stroke volume.
   • Over time, neurohormonal mechanisms (sympathetic drive, RAAS) initially compensate but ultimately exacerbate the failure process.
2. HFpEF (Preserved EF)
   • Diastolic dysfunction often from LV hypertrophy (e.g., chronic hypertension).
   • The stiff LV wall is poor at relaxing; end-diastolic pressure rises, reducing filling and output.
   • May also involve subclinical myocardial fibrosis and microvascular changes.
3. Left vs. Right Heart Failure
   • Left-Sided Failure: Pulmonary congestion, dyspnoea, orthopnoea, and decreased forward perfusion (leading to RAAS activation).
   • Right-Sided Failure: Usually secondary to left-sided failure; leads to systemic venous congestion (JVP elevation, peripheral oedema, ‘nutmeg’ liver).

6. Clinical Features

• General Symptoms: Fatigue, dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, oedema, reduced exercise tolerance.
• Left-Sided: Pulmonary symptoms predominate (e.g., crackles on auscultation, pulmonary oedema, cough, possible hemosiderin-laden macrophages ‘heart-failure cells’ in alveoli if chronic congestion).
• Right-Sided: Jugular venous distension, peripheral oedema, hepatic congestion (painful hepatomegaly, ‘nutmeg liver’), ascites.
• NYHA Functional Classification:
  • I: No limitation
  • II: Mild limitation (breathless with inclines)
  • III: Moderate limitation (symptoms with minimal exertion, though comfortable at rest)
  • IV: Severe limitation (symptoms at rest)

7. Diagnosis

• History & Physical Examination: Hallmark symptoms and signs (e.g., raised JVP, crepitations, peripheral oedema).
• ECG: May show LV hypertrophy, ischaemic changes, Q waves, or arrhythmias (e.g., AF).
  • A normal ECG makes HF unlikely.
• Chest X-Ray: Pulmonary vascular congestion, cardiomegaly, Kerley B lines, pleural effusions.
• Blood Tests:
  • BNP or NT-proBNP (natriuretic peptides) elevated in HF.
  • FBC (exclude anaemia as a cause of dyspnoea), U&E (renal function), LFTs, thyroid function, lipids, glucose.
• Echocardiography: Key imaging modality to measure ejection fraction, assess valve disease, chamber sizes, wall thickness, and diastolic function.
• Additional: Cardiac MRI for detailed anatomy and to assess infiltrative disease; angiography if ischaemic aetiology suspected.

8. Management of Chronic Heart Failure

1. Lifestyle Modifications
   • Smoking cessation, moderate alcohol intake (complete abstinence in alcohol-related cardiomyopathy), weight management, and regular structured exercise.
   • Flu and pneumococcal vaccinations.
   • Fluid and salt restriction in advanced disease.
2. Pharmacological
   • HFpEF: No proven mortality-reducing treatment.
     • Focus on controlling BP, addressing comorbidities (e.g., strict glycaemic control), and using diuretics for volume overload.
   • HFrEF:
     • First-line: ACE inhibitors (or ARBs if ACE-intolerant) + Beta-blockers.
     • Diuretics (thiazide or loop) for symptom relief (fluid overload).
     • Aldosterone antagonists (e.g., spironolactone) can be added in certain cases.
     • Digoxin in patients with AF or in advanced HF for additional symptom control.
   • Avoid negative inotropes (e.g., verapamil) in HFrEF.
3. Device Therapy (HFrEF)
   • Cardiac Resynchronisation Therapy (CRT) if there is evidence of dyssynchrony (wide QRS).
   • Implantable Cardioverter Defibrillator (ICD) if high risk of lethal arrhythmias or LVEF <40% with persistent risk factors.
4. Surgical Interventions
   • Valve repair/replacement (e.g., severe mitral regurgitation).
   • Coronary artery bypass grafting for significant ischaemic disease.
   • Left ventricular assist device (LVAD) as bridge to transplant or destination therapy in end-stage HF.
   • Heart transplant in select patients (gold standard, but limited by age, comorbidity, and donor availability).

9. Prognosis

• Many patients require ongoing monitoring and may benefit from palliative care approaches if severely symptomatic (NYHA III–IV).

• Overall poor prognosis, with ~35% mortality in the first year of diagnosis and ~50% mortality at 5 years.

1. Definition

• A sudden or rapid onset of heart failure symptoms and signs.
• It can be de novo (no prior cardiac history) or acute-on-chronic (an exacerbation in someone with known heart failure).

2. Epidemiology

• Patients often in their mid-70s.
• ~30% have no previous history of cardiac dysfunction at presentation.
• Common comorbidities: ischaemic heart disease, diabetes, CKD, COPD, atrial fibrillation.

3. Aetiology

1. De Novo Acute HF
   • Myocardial infarction
   • Acute severe valvular dysfunction (e.g., chordae rupture → acute MR)
   • Arrhythmia (ventricular tachycardia, AF with rapid rate)
   • Cardiac tamponade
2. Acute-on-Chronic HF
   • Triggering factors: non-compliance with medication, negatively inotropic drugs (e.g., some calcium channel blockers, NSAIDs), infection, anaemia, uncontrolled hypertension, or thyroid dysfunction.

4. Clinical Features

• Fatigue, cough, and acute breathlessness (often with orthopnoea).
• Physical exam: Tachycardia, raised respiratory rate, possible hypertension (though BP can be normal or low), third heart sound (S3), peripheral oedema, raised JVP.
• Pulmonary oedema (common in acute left-sided failure) → hypoxia, inspiratory crackles on auscultation, frothy sputum.
• If severe and associated with very low BP, may develop cardiogenic shock (SBP <90 mmHg, poor urine output, confusion, elevated lactate).

5. Diagnosis

• Clinical: Focus on identifying fluid status (e.g., ‘wet vs dry’) and perfusion status (‘warm vs cold’).
• ECG: Often shows tachycardia or arrhythmia but is non-specific.
• Chest X-Ray: Pulmonary oedema, Kerley B lines, cardiomegaly.
• Echocardiography: Particularly urgent in new-onset acute HF to find the underlying cause (e.g., acute valvular lesion, LV dysfunction).

6. Management

1. Immediate Measures
   • Move to a high-dependency or coronary care unit for close monitoring.
   • Positioning: Sit the patient upright to improve ventilation-perfusion matching.
   • Oxygen: Only if O₂ saturation <94%.
   • IV Loop Diuretics (e.g., furosemide) to relieve fluid overload.
   • IV Vasodilators (e.g., glyceryl trinitrate) to reduce preload and afterload if BP allows.
   • IV Morphine in selected patients for venodilation and stress reduction (though use is more cautious in modern practice).
   • Non-invasive ventilation (CPAP) if significant pulmonary oedema and hypoxia.
   • Inotropes (if evidence of low perfusion and a reversible cause is identified, e.g., cardiogenic shock).
2. Supportive Care
   • Stop inappropriate medications (e.g., NSAIDs) that worsen HF.
   • Monitor urine output, daily weight, and renal function (U&Es) closely.
   • Restrict fluid intake (~1.5 L/day).
   • Invasive ventilation if respiratory failure or severe distress not improving with initial measures.
3. Transition to Chronic HF Therapy
   • Once haemodynamically stable, initiate or reintroduce standard chronic HF therapies (ACE inhibitors, beta-blockers, etc.). Introducing them too early in unstable patients can worsen renal function and hypotension.

7. Prognosis

• Varies widely depending on the cause and speed of management. Prompt treatment of acute decompensation can significantly improve outcomes.
• Patients remain at risk for future exacerbations and must receive appropriate follow-up and optimisation of chronic HF management.