Cardiology:Heart Failure

🫀 Heart Failure (HF) is a clinical syndrome caused by structural or functional cardiac abnormalities that impair ventricular filling, ejection or both. It results in symptoms such as breathlessness, fatigue and exercise intolerance, often accompanied by signs of pulmonary or systemic congestion. Heart failure may develop gradually or present acutely with pulmonary oedema, hypotension or cardiogenic shock. Important: Heart failure does not necessarily mean that the left ventricular ejection fraction is reduced. Patients may have severe heart failure despite a normal or near-normal ejection fraction. ⚠️ Clinical priorities: Confirm the diagnosis, identify the underlying cause, assess congestion and perfusion, treat reversible precipitants and introduce evidence-based treatment.

2.01 🫀 Understanding Heart Failure

The heart must generate sufficient cardiac output to meet the metabolic requirements of the body while maintaining normal or near-normal filling pressures.

• Cardiac output: Cardiac output = heart rate × stroke volume; Normal resting cardiac output is approximately 4–8 litres/minute, depending on body size and physiological conditions; Stroke volume depends on preload, afterload and myocardial contractility; Heart failure may result from impaired contraction, abnormal relaxation, excessive loading conditions or structural abnormalities.
• Two major haemodynamic problems: Reduced forward flow: Inadequate cardiac output may cause fatigue, renal hypoperfusion, confusion and reduced exercise tolerance; Increased filling pressures: Elevated cardiac pressures cause pulmonary congestion, peripheral oedema, ascites and orthopnoea.

💡 Clinical Pearl: Many symptoms of heart failure result from increased cardiac filling pressures rather than reduced cardiac output alone. A patient with preserved cardiac output may still develop severe pulmonary oedema if left atrial pressure rises sufficiently.

2.02 ⚖️ Classification of Heart Failure

• Heart Failure with Reduced Ejection Fraction (HFrEF): NICE classification: LVEF ≤40%; Usually involves impaired left ventricular systolic function; Common causes include previous myocardial infarction, dilated cardiomyopathy and myocarditis; Benefits substantially from disease-modifying pharmacological treatment.
• Heart Failure with Mildly Reduced Ejection Fraction (HFmrEF): NICE classification: LVEF 41–49%; May represent partially recovered systolic dysfunction or a phenotype between HFrEF and HFpEF; Patients often benefit from treatments used for reduced ejection fraction.
• Heart Failure with Preserved Ejection Fraction (HFpEF): NICE classification: LVEF ≥50%; Usually involves increased ventricular stiffness, impaired relaxation or abnormal ventricular-vascular coupling; Common in older adults with hypertension, obesity, diabetes, atrial fibrillation and chronic kidney disease; Diagnosis requires symptoms or signs of heart failure plus objective evidence supporting elevated filling pressures or cardiac structural or functional abnormalities.
• Heart Failure with Improved Ejection Fraction (HFimpEF): Previously documented LVEF ≤40%, with subsequent improvement by at least 10 percentage points to more than 40%; Recovery may follow treatment of cardiomyopathy, tachyarrhythmia or myocardial ischaemia; Improved EF does not necessarily indicate permanent recovery; Continue disease-modifying treatment unless there is a compelling reason to change it.

📌 2026 Guideline Update: NICE retains the categories HFrEF ≤40%, HFmrEF 41–49% and HFpEF ≥50%. The 2026 ESC guidelines simplify classification to HFrEF with LVEF below 50% and HFpEF with LVEF ≥50%. For UK prescribing and examinations, recognise both systems and follow current NICE recommendations where appropriate.

2.03 📊 New York Heart Association (NYHA) Classification

• Class I: No limitation of ordinary physical activity.
• Class II: Comfortable at rest, but ordinary activity produces breathlessness, fatigue or palpitations.
• Class III: Comfortable at rest, but less-than-ordinary activity produces symptoms.
• Class IV: Symptoms occur at rest, and any physical activity increases discomfort.

NYHA classification assesses functional limitation, not ejection fraction. It is subjective but valuable for describing symptom burden, monitoring treatment response and selecting some specialist interventions.

2.04 🔬 Pathophysiology of Heart Failure

Heart failure initiates a series of compensatory mechanisms intended to maintain cardiac output and blood pressure. Initially beneficial, these adaptations become harmful when chronically activated.

• Frank-Starling mechanism: Increased venous return stretches ventricular myocardial fibres; Within physiological limits, greater fibre stretch increases contractile force; In failing ventricles, further increases in preload produce relatively little improvement in stroke volume; Excessive preload increases ventricular filling pressures and congestion.
• Sympathetic nervous system activation: Reduced effective arterial perfusion activates sympathetic responses; Noradrenaline increases heart rate, contractility and peripheral vascular resistance; Persistent activation increases myocardial oxygen demand and promotes arrhythmias; Chronic catecholamine stimulation contributes to myocardial injury and adverse ventricular remodelling.
• Renin-angiotensin-aldosterone system (RAAS): Reduced renal perfusion stimulates renin release; Angiotensin II causes vasoconstriction and increases afterload; Aldosterone promotes sodium and water retention; Persistent activation contributes to myocardial fibrosis, ventricular remodelling and progressive dysfunction.
• Vasopressin (ADH): Promotes renal water retention; Can contribute to dilutional hyponatraemia; Severe hyponatraemia is associated with advanced disease and adverse prognosis.
• Natriuretic peptides: BNP and NT-proBNP increase in response to myocardial wall stress; BNP promotes natriuresis, diuresis and vasodilatation; The natriuretic peptide system counteracts RAAS and sympathetic activation; Despite this response, progressive heart failure often produces persistent sodium and water retention.
• Ventricular remodelling: Chronic pressure overload promotes concentric hypertrophy; Chronic volume overload or myocardial injury may produce ventricular dilatation; Myocyte loss, interstitial fibrosis and altered ventricular geometry impair cardiac function; Mitral regurgitation may develop as a consequence of ventricular dilatation and papillary muscle displacement.

💡 MRCP Pearl: ACE inhibitors, beta blockers, MRAs and ARNIs modify the maladaptive neurohormonal response. Their benefit extends beyond reducing symptoms: they can slow or reverse remodelling and reduce mortality in selected heart failure populations.

2.05 🧬 Causes of Heart Failure

• Ischaemic heart disease: Previous myocardial infarction; Extensive coronary artery disease; Chronic ischaemic myocardial dysfunction; Acute myocardial infarction causing severe LV dysfunction.
• Hypertension: Chronic pressure overload produces LV hypertrophy; Myocardial fibrosis and impaired relaxation may cause HFpEF; Advanced disease can eventually cause systolic dysfunction.
• Valvular heart disease: Aortic stenosis causes pressure overload; Aortic regurgitation causes LV volume overload; Mitral regurgitation causes left atrial and ventricular volume overload; Mitral stenosis produces increased left atrial and pulmonary venous pressure.
• Cardiomyopathies: Dilated cardiomyopathy; Hypertrophic cardiomyopathy; Restrictive cardiomyopathy; Arrhythmogenic cardiomyopathy; Inherited or familial cardiomyopathies; Peripartum cardiomyopathy; Takotsubo syndrome.
• Inflammatory and infiltrative disease: Myocarditis; Cardiac amyloidosis; Cardiac sarcoidosis; Haemochromatosis; Fabry disease.
• Arrhythmias: Atrial fibrillation with rapid ventricular response; Persistent supraventricular tachycardia; High burden of ventricular ectopic beats; Severe bradyarrhythmias.
• Toxic, endocrine and metabolic causes: Excess alcohol consumption; Anthracycline chemotherapy; Trastuzumab-associated cardiac dysfunction; Thyrotoxicosis or severe hypothyroidism; Thiamine deficiency; Severe chronic anaemia.

💡 Clinical Pearl: Every new diagnosis of heart failure should trigger a search for its cause. Identifying coronary disease, valve pathology, uncontrolled tachyarrhythmia or a specific cardiomyopathy may reveal a treatable or reversible mechanism.

2.06 🫁 Left-Sided Heart Failure

Left ventricular dysfunction increases LV end-diastolic pressure, which is transmitted backwards to the left atrium and pulmonary veins.

• Symptoms: Exertional breathlessness. Orthopnoea; Paroxysmal nocturnal dyspnoea (PND); Nocturnal cough. Reduced exercise tolerance; Fatigue. Occasionally pink frothy sputum in severe pulmonary oedema.
• Signs: Tachycardia; Basal inspiratory crackles; Third heart sound (S3), particularly in volume-overloaded dilated ventricles; Displaced apex beat in LV dilatation; Functional mitral regurgitation; Hypoxaemia in acute pulmonary oedema.
• Why does orthopnoea occur?: Lying flat redistributes blood from the lower limbs and splanchnic circulation towards the thorax; Venous return increases; A failing LV cannot accommodate the additional preload without a substantial rise in filling pressure; Pulmonary venous congestion develops, producing breathlessness.
• Why does PND occur?: Redistribution of peripheral oedema fluid occurs during sleep; Increased venous return and pulmonary congestion develop; Patients awaken after a period of sleep with severe breathlessness and frequently sit upright for relief.

2.07 🩺 Right-Sided Heart Failure

Right ventricular dysfunction causes increased systemic venous pressure and impaired pulmonary blood flow.

• Symptoms: Dependent oedema; Abdominal distension; Early satiety; Right upper quadrant discomfort; Fatigue and reduced exercise tolerance.
• Signs: Raised jugular venous pressure (JVP); Peripheral pitting oedema; Congestive hepatomegaly; Ascites; Tricuspid regurgitation; Right ventricular heave; Pleural effusions.
• Important causes: Left-sided heart failure causing pulmonary hypertension; Pulmonary arterial hypertension; Chronic thromboembolic pulmonary hypertension; Chronic lung disease; Right ventricular myocardial infarction; Tricuspid or pulmonary valve disease; Right ventricular cardiomyopathy.

💡 Clinical Pearl: Right heart failure commonly develops secondary to left heart disease, but isolated right ventricular failure should prompt consideration of pulmonary hypertension, pulmonary embolic disease, RV infarction and primary RV pathology.

2.08 🩺 Examination of a Patient with Heart Failure

• General examination: Assess respiratory distress, ability to speak and posture; Look for cyanosis, pallor, muscle wasting and frailty; Assess peripheral temperature and capillary refill; Look for peripheral oedema, including sacral oedema in bedbound patients.
• Pulse and blood pressure: Tachycardia suggests sympathetic activation or another precipitant; An irregularly irregular pulse suggests atrial fibrillation; Hypotension may indicate advanced LV dysfunction or shock; Postural hypotension may occur with medication or volume depletion; A narrow pulse pressure may suggest low stroke volume.
• Jugular venous pressure: An elevated JVP indicates raised right atrial pressure; Assess with the patient appropriately reclined and the neck relaxed; Observe the internal jugular venous pulsation and estimate its height above the sternal angle; The abdominojugular reflux may reveal elevated filling pressures; A prominent V wave suggests significant tricuspid regurgitation.
• Cardiac examination: Displaced apex beat suggests ventricular enlargement; S3 occurs during rapid early diastolic filling and may indicate increased filling pressures in HFrEF; S4 may occur with a stiff ventricle in sinus rhythm, such as hypertensive heart disease; A pansystolic murmur may indicate functional mitral or tricuspid regurgitation; Consider aortic stenosis when there is an ejection systolic murmur and slow-rising carotid pulse.
• Respiratory examination: Basal crackles suggest pulmonary congestion but are not specific; Pleural effusions may produce reduced breath sounds and stony dullness; Wheeze may occur in pulmonary oedema and has historically been termed cardiac asthma; The absence of crackles does not exclude chronic heart failure.
• Abdominal examination: Congestive hepatomegaly. Ascites; Hepatic tenderness in acute congestion; Abdominojugular reflux.

💡 MRCP Examination Pearl: An elevated JVP is a useful sign of systemic congestion. An S3 supports ventricular dysfunction but is less sensitive. Always interpret these findings with the history, echocardiography and natriuretic peptides.

2.09 🧪 Investigations in Suspected Heart Failure

• Blood investigations: FBC: Anaemia or infection; U&E and creatinine: Renal impairment and electrolyte disturbance; LFTs: Congestive hepatopathy or alternative liver disease; TSH: Thyroid dysfunction; HbA1c: Diabetes mellitus.
• Continued: Serum calcium: Metabolic abnormalities; Lipid profile: Cardiovascular risk assessment; Ferritin and transferrin saturation: Iron deficiency; CRP and infection investigations where clinically indicated; Troponin if ACS, myocarditis or acute myocardial injury is suspected.
• 12-lead ECG: Previous myocardial infarction or pathological Q waves; Atrial fibrillation; Left bundle branch block; Left ventricular hypertrophy; Conduction abnormalities; Tachyarrhythmias or bradyarrhythmias.

A completely normal ECG makes significant LV systolic dysfunction less likely, although it does not exclude HFpEF.

• Chest X-ray: Cardiomegaly; Upper-lobe venous diversion; Interstitial pulmonary oedema; Kerley B lines; Perihilar or alveolar shadowing; Pleural effusions.

A normal chest X-ray does not exclude heart failure, especially HFpEF or previously treated chronic heart failure.

2.10 🧪 NT-proBNP and BNP

Natriuretic peptides are released in response to myocardial wall stress and provide important diagnostic and prognostic information.

• Chronic suspected heart failure — NICE pathway: NT-proBNP below 400 ng/L: Heart failure is less likely in an untreated patient, although not excluded; NT-proBNP 400–2,000 ng/L: Refer for specialist assessment and echocardiography within 6 weeks; NT-proBNP above 2,000 ng/L: Refer urgently for specialist assessment and echocardiography within 2 weeks.
• Acute suspected heart failure: BNP below 100 ng/L makes new acute heart failure unlikely; NT-proBNP below 300 ng/L makes new acute heart failure unlikely; These acute thresholds differ from the outpatient chronic heart failure pathway.
• Factors increasing natriuretic peptides: Increasing age. Atrial fibrillation. Chronic kidney disease. Pulmonary embolism. Sepsis and critical illness. Pulmonary hypertension.
• Factors reducing natriuretic peptides: Obesity. Established heart failure therapy. Some patients with HFpEF may have relatively low levels, particularly with obesity.

💡 MRCP Pearl: NT-proBNP is not a measurement of ejection fraction. A patient with HFpEF, AF and CKD may have markedly elevated NT-proBNP despite preserved LV systolic function. The chronic and acute NT-proBNP thresholds serve different clinical purposes and should not be interchanged.

2.11 🫀 Echocardiography in Heart Failure

Transthoracic echocardiography is central to confirming cardiac structural or functional abnormalities and identifying the heart failure phenotype.

• Important measurements: LV ejection fraction. LV chamber dimensions; Regional wall motion abnormalities; LV hypertrophy. Left atrial size; Right ventricular size and function; Valvular stenosis and regurgitation; Estimated pulmonary artery pressure where measurable; Diastolic function and filling pressure indices.
• Left ventricular ejection fraction: EF = (end-diastolic volume − end-systolic volume) ÷ end-diastolic volume × 100%; An EF of 30% indicates that 30% of the end-diastolic LV volume is ejected with each contraction; EF is influenced by loading conditions and ventricular geometry; It is not a direct measurement of total cardiac output or intrinsic myocardial contractility.
• Diastolic dysfunction: Impaired relaxation may reduce early ventricular filling; Increased ventricular stiffness causes a disproportionate rise in pressure for a given filling volume; Important measurements include tissue Doppler e', E/e' ratio, left atrial size and tricuspid regurgitation velocity; No single echocardiographic measurement reliably establishes HFpEF in every patient.
• Other investigations: Cardiac MRI: Useful for cardiomyopathy, myocarditis, scar, infiltrative disease and uncertain echocardiographic findings; Coronary CT or angiography: Consider when ischaemic aetiology is suspected and investigation would change management; Ambulatory ECG: Detects AF, tachycardia burden and other arrhythmias; Cardiopulmonary exercise testing: May clarify exercise limitation and assess advanced heart failure; Right-heart catheterisation: Reserved for selected patients with complex haemodynamics, pulmonary hypertension or advanced disease.

2.12 🩺 Diagnosing HFpEF

HFpEF is not simply breathlessness with a normal ejection fraction. Objective evidence of cardiac dysfunction or elevated filling pressures is required.

• Common clinical context: Older age. Longstanding hypertension. Obesity. Type 2 diabetes. Atrial fibrillation. Chronic kidney disease. Left ventricular hypertrophy.
• Supporting findings: Symptoms and signs of heart failure. Preserved LVEF; Elevated natriuretic peptides, although levels can be low in obesity; Left atrial enlargement. LV hypertrophy; Abnormal diastolic function measurements; Evidence of elevated filling pressures.
• Important alternative diagnoses: Obesity-related breathlessness; COPD or interstitial lung disease; Anaemia. Deconditioning; Pulmonary hypertension; Severe valvular disease; Cardiac amyloidosis.

💡 Clinical Pearl: HFpEF is particularly important in geriatric medicine. Frailty, AF, CKD and multiple comorbidities are common, making diagnostic interpretation and treatment tolerability more challenging.

2.13 🚨 Acute Decompensated Heart Failure

Acute decompensated heart failure occurs when new or worsening cardiac dysfunction produces clinically significant congestion, impaired perfusion or both.

• Common precipitating factors: Acute coronary syndrome; Atrial fibrillation with rapid ventricular response; Uncontrolled hypertension; Infection or sepsis; Medication non-adherence.
• Continued: Excess sodium or fluid intake in susceptible patients; Renal dysfunction; Acute valvular dysfunction; Pulmonary embolism; Anaemia or thyrotoxicosis; NSAIDs or other fluid-retaining medications.

2.14 🩺 Haemodynamic Profiles in Acute Heart Failure

Patients can be classified clinically according to congestion (wet or dry) and peripheral perfusion (warm or cold).

• Warm and wet: Congestion with relatively preserved perfusion; Commonest acute decompensated presentation; Diuretics are usually central to treatment.
• Cold and wet: Congestion with impaired systemic perfusion; May have hypotension, cold extremities, oliguria and raised lactate; Requires urgent senior assessment and consideration of cardiogenic shock.
• Cold and dry: Reduced perfusion without obvious congestion; May reflect overdiuresis, inadequate preload or severe low-output failure; Requires careful haemodynamic assessment rather than automatic fluid administration.
• Warm and dry: Adequate perfusion without clinically significant congestion; Usually the desired state in stable chronic heart failure.

💡 MRCP Pearl: A patient with warm, oedematous extremities and preserved blood pressure usually has a different immediate treatment requirement from a patient with cold extremities, hypotension and a rising lactate. The second patient may have cardiogenic shock.

2.15 🚑 Acute Pulmonary Oedema

Acute cardiogenic pulmonary oedema results from a rapid increase in pulmonary capillary hydrostatic pressure, causing fluid accumulation within the pulmonary interstitium and alveoli.

• Clinical features: Sudden severe breathlessness. Orthopnoea. Tachypnoea and increased work of breathing. Hypoxaemia. Widespread crackles. Diaphoresis and distress. Occasionally pink frothy sputum.
• Immediate management — ABCDE: Assess airway, breathing, circulation and conscious level. Sit the patient upright when tolerated with legs dependent. Continuous pulse oximetry and cardiac monitoring. Obtain IV access. Record ECG and look for ACS or arrhythmia. Administer oxygen for hypoxaemia, using appropriate saturation targets. Check blood gas when respiratory failure, acidosis or poor perfusion is suspected. Obtain urgent senior medical and cardiology input.
• IV loop diuretics: Give IV furosemide for congestive acute heart failure. A commonly used initial dose in a diuretic-naive adult is 20–40 mg IV, adjusted to the clinical situation. Patients already taking loop diuretics may require larger IV doses. Monitor urine output, blood pressure, renal function and electrolytes. Escalate diuretic treatment according to clinical response.
• Non-invasive ventilation:CPAP or bilevel ventilation can reduce work of breathing and improve oxygenation. NICE does not recommend routine NIV in all cases of cardiogenic pulmonary oedema. Consider it promptly in patients with severe dyspnoea and acidaemia, or an inadequate response to initial treatment. Intubation may be required for persistent respiratory failure, exhaustion or reduced consciousness.
• Nitrates: Not recommended routinely for all patients with acute heart failure. May be appropriate in selected patients with severe hypertension, concomitant myocardial ischaemia or regurgitant valve disease. Require careful blood pressure monitoring.
• Other considerations: Do not routinely give morphine. Treat ACS, arrhythmia or hypertensive emergency when present. Assess for acute valvular lesions and mechanical complications. Consider critical care when oxygenation or haemodynamics remain unstable.

⚠️ Important: Not all acute pulmonary oedema results from large total-body fluid overload. Sudden hypertensive pulmonary oedema may be driven by rapid pressure elevation and fluid redistribution. These patients may require different haemodynamic management from those with marked peripheral oedema.

2.16 💉 Diuretics in Heart Failure

Diuretics relieve congestion by increasing renal sodium and water excretion.

• Loop diuretics: Furosemide. Bumetanide. Act on the Na-K-2Cl cotransporter in the thick ascending limb of Henle. Effective for pulmonary and peripheral congestion. Can cause hypokalaemia, hyponatraemia, dehydration and renal dysfunction.
• Thiazide-type diuretics: Metolazone may be used by specialists for resistant congestion. Produces sequential nephron blockade when combined with a loop diuretic. Can cause profound electrolyte depletion and volume loss. Requires close biochemical and fluid-balance monitoring.
• Practical assessment of response: Daily weight. Urine output. Assess Oedema and JVP; Breathlessness and oxygen requirements; Creatinine, sodium and potassium; Fluid balance and haemodynamic stability.
• Diuretic resistance: May result from impaired renal delivery of diuretic, intestinal oedema, reduced GFR or compensatory sodium reabsorption. Check adherence and medication interactions, including NSAIDs. Consider increased IV loop diuretic dosing. Sequential nephron blockade may be necessary under specialist supervision. Ultrafiltration is not routine and may be considered in confirmed resistant congestion

💡 Clinical Pearl: Diuretics improve congestion and symptoms, whereas foundational HFrEF treatments modify disease progression and improve outcomes. A patient who becomes euvolaemic on furosemide alone has not necessarily received adequate long-term heart failure treatment.

2.17 💊 Chronic HFrEF — The Four Foundational Drug Classes

The four foundational treatment classes are:

• 1. ACE inhibitor: Reduces RAAS-mediated vasoconstriction, sodium retention and remodelling.
• 2. Evidence-based beta blocker: Reduces adverse sympathetic activation and improves long-term ventricular function.
• 3. Mineralocorticoid receptor antagonist (MRA): Reduces aldosterone-mediated sodium retention, fibrosis and remodelling.
• 4. SGLT2 inhibitor: Reduces heart failure hospitalisation and cardiovascular events through renal and other cardiometabolic mechanisms.
• NICE treatment approach: Offer all four classes to eligible patients with HFrEF. Do not necessarily wait for one drug to reach maximum dose before introducing another class. Choose the sequence and starting doses according to blood pressure, renal function, potassium, frailty and clinical stability. If symptoms persist despite maximally tolerated treatment, consider switching the ACE inhibitor to sacubitril/valsartan. When ACE inhibitor intolerance other than angioedema occurs, NICE supports using an ARNI with the other foundational classes. If ACE inhibitor-associated angioedema occurs, avoid ACE inhibitor and ARNI therapy and consider an ARB where clinically appropriate.

💡 Teaching Pearl: Combining different disease-modifying mechanisms is more effective than relying on one treatment class. Modern HFrEF care aims for early introduction of all suitable foundational therapies, followed by careful dose optimisation.

2.18 💊 ACE Inhibitors and ARBs

• Mechanism: ACE inhibitors reduce formation of angiotensin II. They reduce vasoconstriction and aldosterone secretion. They lower ventricular loading conditions. They reduce adverse myocardial remodelling.
• Common drugs: Ramipril. Enalapril. Lisinopril. Candesartan, an ARB alternative.
• Benefits: Reduced mortality in HFrEF. Reduced hospitalisation. Improvement in symptoms and ventricular remodelling.
• Adverse effects: Hypotension. Hyperkalaemia. Creatinine rise. Dry cough with ACE inhibitors. Angioedema, a potentially serious complication.
• Monitoring: Measure renal function and potassium before treatment. Repeat 1–2 weeks after initiation or dose increase. Monitor blood pressure and postural symptoms. Once stable, repeat renal function and electrolytes every 3–6 months.

2.19 💊 Beta Blockers

Beta blockers reduce chronic sympathetic stimulation and are associated with improved survival in appropriate patients with HFrEF.

• Evidence-based agents: Bisoprolol. Carvedilol. Metoprolol succinate modified-release. Nebivolol in selected patients.
• Mechanism: Reduce heart rate. Reduce myocardial oxygen demand. Reduce arrhythmogenic sympathetic effects. Allow improved ventricular filling time. Promote favourable long-term remodelling.
• Prescribing principles: Start at a low dose and increase gradually. Check ECG, heart rate and blood pressure. Introduce when haemodynamically stable rather than during active cardiogenic shock. Do not automatically withhold treatment solely because of COPD, peripheral vascular disease or older age. Avoid in clinically significant bradycardia or unpaced second- or third-degree AV block.

💡 Clinical Pearl: Beta blockers initially reduce contractility, but improve outcomes with sustained treatment. This explains why initiation during severe acute haemodynamic instability can be harmful despite their long-term benefits.

2.20 💊 Mineralocorticoid Receptor Antagonists

• Drugs: Spironolactone. Eplerenone.
• Mechanism: Block aldosterone receptors. Reduce sodium retention. Reduce myocardial fibrosis and remodelling. Improve outcomes in HFrEF.
• Adverse effects: Hyperkalaemia. Renal dysfunction. Gynaecomastia with spironolactone. Menstrual or sexual adverse effects with spironolactone. Eplerenone is more selective for the mineralocorticoid receptor and causes fewer endocrine adverse effects.
• Monitoring: Check potassium and renal function before treatment. Repeat 1–2 weeks after initiation and dose increases. Use caution with renal impairment or baseline hyperkalaemia. Avoid unnecessary potassium supplements and potassium-containing salt substitutes.

2.21 💊 SGLT2 Inhibitors

Sodium-glucose cotransporter-2 inhibitors were initially developed for diabetes but provide important benefits in heart failure, including in patients without diabetes.

• Drugs Dapagliflozin 10 mg daily. Empagliflozin 10 mg daily.
• Mechanisms: Inhibit sodium-glucose reabsorption in the proximal renal tubule. Promote glucose and sodium excretion. Produce modest osmotic diuresis and natriuresis. Influence renal haemodynamics and cardiometabolic pathways. Reduce heart failure admissions across the ejection fraction spectrum.
• Adverse effects and cautions: Genital mycotic infections. Volume depletion in susceptible patients. Transient early reduction in eGFR. Rare euglycaemic diabetic ketoacidosis. Check kidney function and drug-specific initiation criteria. Provide advice about temporary interruption during severe acute illness, prolonged fasting or major surgery. Not routinely prescribed for heart failure in type 1 diabetes.

💡 MRCP Pearl: SGLT2 inhibitors provide heart failure benefits independent of glucose lowering. An important prescribing complication is euglycaemic DKA, which can occur despite a normal or only mildly elevated blood glucose concentration.

2.22 💊 Sacubitril/Valsartan (ARNI)

Sacubitril/valsartan combines an angiotensin receptor blocker with inhibition of neprilysin.

• Mechanism: Sacubitril inhibits neprilysin, reducing breakdown of endogenous natriuretic peptides. Valsartan blocks angiotensin II AT1 receptors. The combination promotes natriuresis and vasodilatation and reduces maladaptive remodelling.
• Benefits: Reduces heart failure hospitalisation in appropriate patients with HFrEF. Reduces cardiovascular mortality compared with ACE inhibitor treatment in selected populations. May improve symptoms and ventricular remodelling.
• Important cautions: Do not prescribe together with an ACE inhibitor. Allow at least 36 hours after stopping an ACE inhibitor before starting sacubitril/valsartan. Contraindicated with a history of ACE inhibitor- or ARNI-related angioedema. Monitor blood pressure, potassium and renal function. May cause symptomatic hypotension. Should not be combined with another ARB.

💡 Clinical Pearl: Neprilysin inhibition increases beneficial endogenous vasoactive peptides. Concurrent ACE inhibition increases the risk of angioedema, which is why the 36-hour washout is essential.

2.23 💊 Management of HFmrEF

Under NICE classification, HFmrEF describes an ejection fraction of 41–49%.

• NICE 2025 treatment: Consider an ACE inhibitor; Consider an evidence-based beta blocker; Consider an MRA; Consider an SGLT2 inhibitor; Use a loop diuretic when symptomatic congestion is present; Use an ARB when ACE inhibitor intolerance makes this appropriate.

Decisions should reflect the underlying mechanism, comorbidities, blood pressure, renal function and individual treatment tolerance.

2.24 💊 Management of HFpEF

Treatment focuses on reducing heart failure events, relieving congestion, managing comorbidities and identifying the underlying cardiac abnormality.

• Recommended treatment approach: SGLT2 inhibitor: Consider dapagliflozin or empagliflozin, including in suitable patients without diabetes; MRA: NICE 2025 recommends considering an MRA, with careful monitoring of renal function and potassium; Loop diuretics: Use when fluid retention or congestion is present; Hypertension: Treat appropriately to reduce pressure overload and cardiovascular risk; Atrial fibrillation: Assess rate or rhythm control and anticoagulation requirements; Coronary disease: Investigate and manage when present; Obesity: Encourage appropriate weight management and exercise; Diabetes and CKD: Optimise treatment; Valvular disease: Consider intervention when clinically indicated.

💡 Clinical Pearl: Patients with HFpEF can be highly sensitive to both excessive fluid loading and excessive diuresis. A stiff ventricle requires adequate filling, but small increases in volume can cause large increases in filling pressure.

2.25 🩺 Heart Failure and Atrial Fibrillation

Atrial fibrillation and heart failure frequently coexist and can worsen each other.

• Why AF worsens heart failure: Loss of organised atrial contraction reduces ventricular filling; Rapid ventricular rates shorten diastole; Persistent tachycardia can cause tachycardia-mediated cardiomyopathy; Irregular ventricular filling can reduce effective cardiac output.
• Management: Determine whether AF is causing haemodynamic instability; Consider urgent electrical cardioversion for life-threatening instability caused by AF; Use appropriate rate control in stable patients; Beta blockers are often useful when tolerated; Digoxin may be helpful in selected patients with HFrEF; Consider rhythm-control strategies, including catheter ablation, when clinically appropriate; Assess stroke risk and anticoagulation using established AF guidance.
• Important caution: Verapamil and diltiazem are generally avoided in HFrEF because of negative inotropic effects; Anticoagulation is not routinely indicated solely because LVEF is reduced in a patient in sinus rhythm.

2.26 🫀 Cardiac Devices

• Implantable Cardioverter Defibrillator (ICD): Detects and treats life-threatening ventricular arrhythmias; Reduces sudden arrhythmic death in selected patients; Used for secondary prevention following certain sustained ventricular arrhythmias; May be appropriate for primary prevention in selected patients with persistently reduced EF despite optimal treatment; Patient selection depends on LV function, symptoms, arrhythmic risk, life expectancy and comorbidity.
• Cardiac Resynchronisation Therapy (CRT): Coordinates ventricular contraction using appropriately positioned pacing leads; Particularly beneficial in selected patients with LV systolic dysfunction and electrical dyssynchrony; Greatest benefit is often seen with broad QRS complexes and left bundle branch block; Can improve symptoms, LV function and hospitalisation outcomes; CRT-P provides pacing alone; CRT-D combines resynchronisation and defibrillation.

NICE TA314 provides detailed device-selection criteria based on LVEF, NYHA class, QRS duration and bundle branch block morphology.

💡 MRCP Pearl: ICD therapy primarily prevents sudden arrhythmic death, whereas CRT addresses ventricular electrical dyssynchrony. They have different mechanisms and indications, although some patients require a combined device.

2.27 🧬 Specialist and Advanced Heart Failure Treatment

• Ivabradine: Can reduce sinus rate in selected symptomatic HFrEF patients with elevated heart rate despite optimised therapy. Requires sinus rhythm and appropriate specialist assessment.
• Digoxin: May be useful for worsening or severe HFrEF despite optimised treatment and for ventricular rate control in selected AF patients.
• Hydralazine with nitrate: May be considered in selected patients who cannot tolerate RAAS-blocking therapies or in specific specialist populations.
• Intravenous iron: Consider in eligible patients with HFrEF and iron deficiency.
• Valve intervention: May be appropriate for severe aortic or mitral valve disease.
• Revascularisation: Consider when appropriate in selected patients with ischaemic cardiomyopathy.
• Ventricular assist devices: Mechanical circulatory support for carefully selected advanced cases.
• Cardiac transplantation: Consider for suitable patients with advanced heart failure despite optimal therapy.

2.28 🩸 Iron Deficiency in Heart Failure

Iron deficiency is common in heart failure and may impair exercise capacity even without classical anaemia.

• Mechanisms: Reduced dietary intake or gastrointestinal absorption. Chronic inflammation and altered iron handling. Blood loss. Functional iron deficiency, where iron stores are present but unavailable for effective cellular use.
• NICE 2025 assessment: Check haemoglobin. Check ferritin. Check transferrin saturation (TSAT).
• IV iron treatment: In HFrEF, NICE advises considering IV iron when haemoglobin is below 150 g/L and iron deficiency is present; Iron deficiency is defined for this recommendation by TSAT below 20% or ferritin below 100 ng/mL; Preparations include iron sucrose, ferric carboxymaltose and ferric derisomaltose; Benefits include improvement in exercise tolerance and quality of life in eligible patients; Investigate the underlying cause of iron deficiency, particularly possible gastrointestinal blood loss.

💡 MRCP Pearl: A normal haemoglobin does not exclude iron deficiency. Ferritin can be elevated as an acute-phase reactant, making transferrin saturation especially useful in inflammatory conditions.

2.29 🩺 Heart Failure and Renal Dysfunction

Heart failure and renal disease frequently coexist. The interaction between cardiac dysfunction and worsening renal function is termed cardiorenal syndrome.

• Mechanisms: Reduced renal perfusion; Renal venous congestion; RAAS activation; Neurohormonal sodium retention; Pre-existing CKD; Medication-related haemodynamic changes.
• Management principles: Assess whether the patient is congested, euvolaemic or intravascularly depleted; Persistent renal venous congestion may itself worsen kidney function; Do not automatically discontinue diuretics because of a modest creatinine rise in a patient who remains severely congested; Monitor potassium, creatinine and volume status carefully during RAAS inhibition; NICE recommends considering lower starting doses and smaller titration steps when eGFR is 45 mL/min/1.73 m² or lower; Consider renal specialist collaboration when eGFR is below 30 mL/min/1.73 m².

💡 Clinical Pearl: A deteriorating creatinine does not automatically indicate overdiuresis. In a patient with raised JVP, oedema and persistent congestion, high renal venous pressure may contribute substantially to impaired renal filtration.

2.30 🧪 Hyponatraemia and Electrolyte Disorders

• Hyponatraemia: Often results from increased vasopressin-mediated water retention. May occur alongside marked fluid overload. Can also result from diuretics or other causes of sodium loss. Associated with more advanced heart failure and worse outcomes. Treatment depends on volume status, symptoms, severity and chronicity.
• Hypokalaemia: Commonly caused by loop or thiazide-type diuretics. May provoke ventricular arrhythmias. Increases sensitivity to digoxin toxicity.
• Hyperkalaemia: May result from renal dysfunction, ACE inhibitors, ARBs, ARNIs or MRAs. Can cause life-threatening conduction abnormalities. Requires careful biochemical monitoring and assessment of medication combinations.

2.31 🧬 Cardiac Amyloidosis

Cardiac amyloidosis is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins within myocardial tissue.

• Important types: ATTR amyloidosis: Transthyretin-related disease, including wild-type disease in older adults; AL amyloidosis: Associated with monoclonal immunoglobulin light chains and requires urgent specialist evaluation.
• Clinical clues: HFpEF or progressive heart failure in an older adult; Disproportionate ventricular wall thickening; Low-voltage ECG relative to ventricular wall thickness, although this is not universal; Conduction disease; Atrial fibrillation; Orthostatic hypotension; Carpal tunnel syndrome; Peripheral neuropathy or autonomic dysfunction.
• Investigations: Echocardiography and strain imaging. Cardiac MRI. Serum free light chains plus serum and urine immunofixation to exclude AL amyloidosis. Bone scintigraphy with an appropriate tracer where ATTR is suspected. Specialist assessment for confirmation and amyloid subtype.

💡 MRCP Pearl: An older patient with HFpEF, thick ventricular walls, conduction disease and bilateral carpal tunnel syndrome should prompt consideration of ATTR cardiac amyloidosis. Excluding AL amyloidosis is essential because it requires different and potentially urgent treatment.

2.32 ⚠️ Cardiogenic Shock

Cardiogenic shock is a state of inadequate systemic tissue perfusion caused primarily by severe cardiac dysfunction.

• Clinical findings: Hypotension or need for circulatory support. Cold extremities. Oliguria. Confusion or reduced consciousness. Raised lactate. Acidosis. Possible pulmonary oedema or systemic congestion.
• Causes: Extensive acute myocardial infarction. Severe decompensated cardiomyopathy. Fulminant myocarditis. Severe ventricular arrhythmias. Acute mechanical complications of MI. Acute severe valve dysfunction.
• Management: Immediate critical care and cardiology assessment. Identify and reverse the precipitating cause. Urgent coronary reperfusion if ACS is responsible. Bedside echocardiography. Careful fluid and haemodynamic assessment. Vasopressors or inotropes when indicated in monitored critical care. Consider specialist mechanical circulatory support in selected patients.

⚠️ Clinical Pearl: Cardiogenic shock may occur without marked hypotension, particularly in patients with pre-existing hypertension or compensatory vasoconstriction. Evidence of impaired organ perfusion is central to the diagnosis.

2.33 💊 Common Drugs and Adult Doses

These are typical adult starting doses and commonly used target or maintenance doses. They are educational examples, not substitutes for the BNF, prescribing information or local protocols.

⚠️ Prescribing Safety: ACE inhibitors, ARNIs, ARBs and MRAs require potassium and renal monitoring. Beta blockers require heart-rate and haemodynamic assessment. SGLT2 inhibitors require consideration of renal function, acute illness and ketoacidosis risk. Sacubitril/valsartan must not be given concurrently with an ACE inhibitor. Observe the required 36-hour washout when switching from an ACE inhibitor.

2.34 🚫 Medications That Can Worsen Heart Failure

• NSAIDs: Promote sodium retention, impair renal perfusion and reduce diuretic effectiveness.
• Verapamil and diltiazem: Negative inotropic effects may worsen HFrEF.
• Pioglitazone: Can cause fluid retention and aggravate heart failure.
• Systemic corticosteroids: Some regimens may worsen fluid retention, depending on dose and mineralocorticoid activity.
• Excessive IV fluids: May precipitate pulmonary oedema in susceptible patients.
• Excess alcohol: Can cause or worsen cardiomyopathy.
• Certain antiarrhythmics: May worsen systolic function or provoke arrhythmias.
• Some cancer treatments: Can cause cardiomyopathy and require specialist monitoring.

2.35 🧑‍⚕️ Heart Failure in Older Adults

Heart failure is common in older adults and frequently coexists with frailty, cognitive impairment, CKD and multiple long-term conditions.

• Important clinical considerations: HFpEF is common; Breathlessness may present as reduced mobility or functional deterioration; Fatigue, anorexia and falls may dominate the presentation; Delirium may be precipitated by hypoxia, infection, electrolyte disturbance or poor perfusion; Peripheral oedema may have multiple causes, including venous insufficiency and immobility; Orthostatic hypotension is common with vasodilators and diuretics; Renal impairment increases the risk of drug accumulation and electrolyte disturbance; Medication burden may compromise adherence.
• Practical approach: Establish the cause and subtype of heart failure; Assess frailty, functional status, cognition and falls risk; Use evidence-based treatments where beneficial and tolerable; Start low and titrate thoughtfully, avoiding unnecessary therapeutic inertia; Consider treatment burden and patient priorities; Ensure clear follow-up and monitoring arrangements.

💡 Geriatric Medicine Pearl: Chronological age alone is not a reason to withhold effective heart failure treatment. However, frailty, postural hypotension, renal dysfunction, life expectancy and patient preferences influence the balance of benefit and harm.

2.36 🏃 Rehabilitation and Long-Term Management

• Offer suitable patients a personalised, exercise-based cardiac rehabilitation programme; Support smoking cessation; Encourage a healthy, balanced diet.
• Advise against excessive alcohol consumption; Individualise sodium and fluid advice; routine severe restriction is not appropriate for every patient; Monitor weight and symptoms where helpful.
• Discuss vaccination in accordance with current national recommendations; Screen for depression and anxiety; Review medication adherence and practical barriers.
• Provide clear instructions for deterioration.
• Patient self-monitoring: Increasing breathlessness. Worsening orthopnoea; New or increasing peripheral oedema; Rapid weight gain consistent with fluid retention; Reduced urine output. Dizziness or symptomatic hypotension.

2.37 🏥 Discharge Planning After Acute Heart Failure

• Before discharge: Confirm clinical stability and adequate decongestion; Identify the underlying cause and precipitating factors; Document ejection fraction and relevant echocardiographic findings; Review renal function and electrolytes; Optimise medication as far as clinically appropriate; Provide a clear medication and monitoring plan; Explain red flags and who to contact with worsening symptoms; Assess mobility, cognition, frailty and support at home; Arrange heart failure specialist follow-up.

NICE recommends clinical assessment by a member of the specialist heart failure team within 2 weeks after discharge following an acute heart failure admission.

2.38 🕊️ Advanced Heart Failure and Palliative Care

Advanced heart failure may involve persistent symptoms despite optimal treatment, repeated hospital admissions, progressive end-organ dysfunction and increasing dependence.

• Features suggesting advanced disease: Persistent NYHA III–IV symptoms; Repeated decompensations; Recurrent hypotension; Progressive renal dysfunction; Inability to tolerate disease-modifying therapies; Severe frailty or cachexia; Frequent arrhythmias or device therapies.
• Management principles: Assess whether advanced therapies are appropriate; Continue proportionate treatments that improve symptoms or outcomes; Address breathlessness, oedema, fatigue and anxiety; Discuss prognosis and treatment preferences sensitively; Consider advance care planning where appropriate; Review hospital admission preferences and resuscitation decisions; Discuss ICD deactivation when clinically appropriate and consistent with the patient's wishes; Involve palliative care alongside active cardiac management when beneficial.

💡 Clinical Pearl: Palliative care is not synonymous with stopping heart failure treatment. Diuretics, selected cardiac medicines and other interventions may provide meaningful symptom relief even when care priorities become predominantly comfort-focused.

2.39 📉 Prognosis

Prognosis varies considerably according to the underlying disease, response to treatment, comorbidities and frequency of decompensation.

• Factors associated with poorer prognosis: Advanced NYHA class; Repeated hospitalisation; Low blood pressure with poor perfusion; Persistent congestion; Renal dysfunction.
• Continued: Hyponatraemia; Elevated NT-proBNP; Severe right ventricular dysfunction; Significant arrhythmia burden; Cardiac cachexia and frailty.

Ejection fraction alone does not determine prognosis. Patients with HFpEF may experience substantial morbidity, recurrent admissions and mortality, particularly with advanced age and multimorbidity.

2.40 ✅ Key MRCP and Clinical Pearls

• 1. Heart failure is a clinical syndrome, not an echocardiographic measurement.
• 2. Normal ejection fraction does not exclude heart failure.
• 3. Elevated filling pressures explain many symptoms of HFpEF.
• 4. Orthopnoea results partly from redistribution of blood towards the thorax when supine.
• 5. An S3 suggests increased ventricular filling pressures, particularly in dilated HFrEF.
• 6. A raised JVP is an important sign of systemic venous congestion.
• 7. NT-proBNP is influenced by age, AF, renal function, obesity and treatment.
• 8. NICE chronic HF and acute HF use different NT-proBNP thresholds.
• 9. Diuretics relieve congestion but do not replace disease-modifying treatment.
• 10. HFrEF management should include the four foundational drug classes when appropriate.
• 11. SGLT2 inhibitors benefit heart failure patients even without diabetes.
• 12. Sacubitril/valsartan must not be combined with an ACE inhibitor.
• 13. Severe bradycardia, high-grade AV block and shock are important beta-blocker contraindications or precautions.
• 14. Renal dysfunction during decongestion does not automatically mean the patient is dehydrated.
• 15. Severe pulmonary oedema may be precipitated by acute hypertension without major total-body fluid overload.
• 16. A new diagnosis of heart failure requires an aetiological assessment.
• 17. Atrial fibrillation can both cause and result from heart failure.
• 18. Consider cardiac amyloidosis in an older adult with unexplained ventricular thickening and HFpEF.
• 19. Iron deficiency may worsen heart failure symptoms even without conventional anaemia.
• 20. Frailty changes treatment planning but does not automatically remove the benefits of evidence-based therapy.

2.41 🧑‍⚕️ Teaching Commentary

Heart failure is best understood as a syndrome of abnormal cardiac structure or function leading to inadequate forward flow, elevated filling pressures or both. Systolic dysfunction commonly involves impaired contraction and ventricular dilatation, while HFpEF frequently reflects a stiff ventricle that develops high filling pressures despite preserved ejection fraction. The neurohormonal response initially maintains blood pressure and perfusion, but chronic sympathetic and RAAS activation contribute to sodium retention, fibrosis and adverse ventricular remodelling. This explains why modern treatments target neurohormonal mechanisms rather than simply removing excess fluid. In acute presentations, the immediate clinical task is to establish whether the patient is congested, poorly perfused or both, while identifying reversible precipitants such as ACS, arrhythmia, infection or valve dysfunction. IV diuretics are central to the treatment of congestive decompensation, while respiratory support and specialist haemodynamic interventions may be needed in severe cases. Long-term treatment should be individualised according to ejection fraction, aetiology, renal function, blood pressure and comorbidity. The objective is not only to improve breathlessness and oedema but also to reduce hospitalisation, prevent progressive ventricular dysfunction and improve survival. For medical students and MRCP candidates, the most important distinction is between relief of congestion, treatment of the underlying disease and pharmacological modification of the processes that drive heart failure progression.

2.42 📌 NICE and European Guidelines

• NICE NG106: Chronic Heart Failure in Adults — diagnosis, HFrEF, HFmrEF, HFpEF and long-term management; NICE CG187: Acute Heart Failure — acute assessment, IV diuretics, respiratory support and discharge; NICE TA314: ICD and CRT — implantable defibrillators and cardiac resynchronisation therapy.
• NICE TA388: Sacubitril/Valsartan — ARNI treatment in HFrEF; NICE TA902: Dapagliflozin — heart failure with mildly reduced or preserved ejection fraction; NICE TA929: Empagliflozin — chronic heart failure with preserved or mildly reduced ejection fraction.
• ESC 2026 Heart Failure Guidelines — European heart failure classification, diagnosis and treatment.