💡 Key Point: Heart failure (HF) is a clinical syndrome of symptoms/signs due to structural or functional cardiac abnormality → impaired ventricular filling or ejection.  
⚡ It is a major cause of morbidity and mortality, but effective guideline-based therapy can improve survival and quality of life.
📖 About Heart Failure
- Acute HF: Rapid onset or worsening of symptoms (e.g. pulmonary oedema, cardiogenic shock). Often needs urgent hospital management.
- Chronic HF: Long-standing, stable or progressively worsening symptoms, usually managed in the community with optimisation of guideline-directed therapy.
💡 Key Point: Heart failure can be predominantly left-sided (pulmonary congestion due to LV dysfunction) or right-sided (systemic venous congestion due to RV dysfunction).  
Often both sides eventually fail, but early recognition of the dominant pattern helps with diagnosis and management.
🧬 Pathophysiology
- HFrEF: LV systolic dysfunction (EF <40%) → impaired contractility → ↓ stroke volume.
- HFmrEF: Mid-range EF (40–49%), overlapping features.
- HFpEF: EF ≥50% → diastolic dysfunction, stiff LV, impaired filling despite normal contractility.
- Neurohormonal activation (RAAS, SNS, ADH) → fluid retention, vasoconstriction, cardiac remodelling.
📖 Types
- Left Heart Failure: Failure of the LV to pump blood forward → ↑ left atrial pressure → pulmonary venous congestion → pulmonary oedema and breathlessness.
- Right Heart Failure: Failure of the RV to pump into pulmonary circulation → ↑ systemic venous pressure → peripheral oedema, ascites, hepatomegaly.
- Most cases of R-sided failure are secondary to L-sided failure, but isolated RV failure can occur (e.g. cor pulmonale, RV infarct, pulmonary hypertension).
🩺 Clinical Features
- Breathlessness (exertional → orthopnoea → PND → rest dyspnoea).
- Fatigue, reduced exercise tolerance.
- Peripheral oedema, ascites, hepatomegaly.
- Signs: elevated JVP, displaced apex, third heart sound (S3 gallop), pulmonary crepitations, ankle oedema.
- Acute HF: Pulmonary oedema, hypoxia, pink frothy sputum, tachycardia, cool peripheries.
🔎 Diagnosis
- Clinical syndrome: Symptoms + signs suggestive of HF.
- BNP/NT-proBNP: Sensitive test; normal level rules out HF. High levels prompt urgent echocardiography.
- ECG: AF, LVH, Q waves, conduction delay → may support HF diagnosis.
- Echocardiography: Gold standard → assesses EF, chamber size, wall motion, valves.
- CXR: Cardiomegaly, pulmonary venous congestion, Kerley B lines, pleural effusion.
- Bloods: FBC, U&E, LFT, TFT, glucose, lipids; troponin if ACS suspected.
📊 Classification of HF
| Type | EF Criteria | Typical Features | 
|---|
| HFrEF | EF <40% | Systolic dysfunction, most evidence-based therapies apply here. | 
| HFmrEF | EF 40–49% | Intermediate group, may benefit from HFrEF therapies. | 
| HFpEF | EF ≥50% | Diastolic dysfunction, preserved systolic function. Often elderly, hypertensive, female. | 
🚑 Acute HF – Management (ABCDE)
- 🫁 Oxygen: If hypoxic, titrate to SpO₂ > 94%.
- 💊 IV diuretics: Furosemide 40–80 mg IV bolus (higher in chronic users).
- 🪑 Sit upright to improve ventilation.
- 💊 Nitrates: If hypertensive and not hypotensive, GTN infusion reduces preload/afterload.
- ⚡ Inotropes/vasopressors: Dobutamine, noradrenaline in cardiogenic shock.
- 💉 Consider CPAP/NIV if severe pulmonary oedema.
- 🚨 Identify and treat precipitant: ACS, arrhythmia, infection, PE, poor compliance.
💊 Chronic HF – Guideline-Directed Therapy (HFrEF)
- Stepwise drug therapy:
- ACEi (or ARB if intolerant) + beta-blocker (bisoprolol, carvedilol, nebivolol) ➝ titrate to max tolerated.
- Add MRA (spironolactone/eplerenone) if still symptomatic.
- SGLT2 inhibitors (dapagliflozin, empagliflozin) – now class I recommendation (ESC 2021).
- ARNI (sacubitril/valsartan) in place of ACEi if EF remains <35% and symptomatic.
- Other: Ivabradine (if sinus rhythm HR ≥75 despite max beta-blocker), hydralazine/nitrates (esp. Afro-Caribbean patients), digoxin (AF, symptoms).
 
- Devices:
- CRT (cardiac resynchronisation) – EF ≤35%, broad QRS.
- ICD – for secondary prevention (post-VF/VT) or primary prevention in selected HFrEF.
 
- Advanced: LVAD, transplant in refractory cases.
💊 Chronic HF – HFpEF
- No disease-modifying therapy proven.
- Focus on treating comorbidities: HTN, AF, IHD, obesity, diabetes.
- Diuretics for symptom control (congestion relief).
- SGLT2 inhibitors show emerging benefit (EMPEROR-Preserved trial).
⚡ Complications
- Arrhythmias (AF, VT/VF).
- Thromboembolism (esp. in AF).
- Progressive renal dysfunction.
- Sudden cardiac death.
📚 Prognosis
- 5-year mortality for HFrEF ≈ 50% (worse than many cancers).
- Timely initiation of guideline therapies improves both survival and quality of life.
- HFpEF prognosis is comparable but with fewer therapeutic options.
📝 Teaching Pearls
🔍 BNP normal virtually excludes HF (high negative predictive value).  
💡 Always distinguish HFpEF vs HFrEF → management pathways differ.  
⚠️ In acute pulmonary oedema: sit up, O₂, IV furosemide, GTN (if BP allows), treat trigger.  
📚 References
- ESC Heart Failure Guidelines 2021
- NICE NG106: Chronic Heart Failure (2018, updated 2022)
- Ponikowski P et al, Eur Heart J 2021
💓 Case 1 — Heart Failure with Reduced Ejection Fraction (HFrEF)
A 68-year-old man with a history of myocardial infarction presents with progressive exertional breathlessness, orthopnoea, and ankle swelling. Examination reveals bibasal crackles, pitting oedema, and an S3 heart sound. 💡 HFrEF typically follows ischaemic damage or dilated cardiomyopathy, with impaired systolic function (LVEF <40%). Management includes loop diuretics for symptom relief, plus disease-modifying agents such as ACE inhibitors/ARNI, beta-blockers, and mineralocorticoid antagonists, alongside cardiac rehabilitation.
💓 Case 2 — Heart Failure with Preserved Ejection Fraction (HFpEF)
A 75-year-old hypertensive woman with longstanding diabetes reports exertional breathlessness and fatigue. Echocardiography shows normal LV systolic function but concentric hypertrophy and impaired diastolic filling. 💡 HFpEF results from stiff ventricles that cannot relax properly, leading to raised filling pressures. Management focuses on controlling blood pressure, treating comorbidities (e.g. AF, diabetes), optimising diuretics for symptoms, and lifestyle modification, as no therapy yet convincingly reduces mortality.
💓 Case 3 — Acute Decompensated Heart Failure
A 60-year-old man with chronic HFrEF presents acutely with severe dyspnoea, frothy pink sputum, and orthopnoea after missing his medications. Examination reveals tachypnoea, raised JVP, widespread crackles, and pulmonary oedema on CXR. 💡 Acute decompensation can be triggered by infection, arrhythmia, or poor adherence. It requires urgent IV loop diuretics, oxygen, and consideration of nitrates or non-invasive ventilation. Once stabilised, optimising long-term guideline-directed therapy is essential to prevent recurrence.