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Heart Failure with preserved and reduced EF

🫀 Heart failure (HF) is a clinical syndrome (symptoms + signs) caused by a structural/functional cardiac problem leading to reduced cardiac output and/or raised filling pressures. 🎯 Exam focus: confirm HF → define the phenotype by EF (HFrEF vs HFpEF) → treat congestion + start disease-modifying therapy early → manage comorbidities and triggers.

🔎 Core definitions (EF-based)

🔻 HFrEF (reduced EF): LVEF ≤40% + clinical HF.
🟠 HFmrEF (mildly reduced EF): LVEF 41–49% + clinical HF.
🟢 HFpEF (preserved EF): LVEF ≥50% + clinical HF and evidence of raised filling pressures/diastolic dysfunction (often LA enlargement, LVH, raised E/e’).
📈 HFimpEF (improved EF): previous LVEF ≤40% that has improved to >40% — continue HFrEF therapy (benefit persists).

🧠 Pathophysiology: why HFrEF and HFpEF behave differently

🔻 HFrEF: primary problem is impaired contractility (often post-MI or dilated cardiomyopathy) → ↓ stroke volume → compensatory SNS/RAAS activation → salt/water retention, vasoconstriction, and adverse remodelling (LV dilatation).
🟢 HFpEF: primary problem is impaired relaxation + increased stiffness (often long-standing HTN, ageing, obesity, diabetes) → normal EF but high filling pressures → pulmonary congestion on exertion, AF susceptibility, and exercise intolerance.
⚠️ Both phenotypes share: congestion, neurohormonal activation, inflammation, and high comorbidity burden — but disease-modifying evidence is strongest in HFrEF.

🧩 Causes of Heart Failure (HF) — exam-friendly table

Cause category	Typical examples	Clues / why it matters (high-yield)
🫀 Ischaemic heart disease (IHD)	Prior MI, chronic CAD, hibernating myocardium	Most common cause of HFrEF in the UK; ECG Q waves/old infarct, angina history, regional wall motion abnormalities on echo → consider revascularisation if appropriate.
📈 Hypertension	Long-standing uncontrolled BP	Pressure overload → LVH → diastolic dysfunction (HFpEF) ± later systolic failure; echo shows concentric LVH/LA enlargement; BP control is disease-modifying for HFpEF trajectory.
🚪 Valvular heart disease	AS, AR, MR, MS	Murmurs + echo severity; AS/HTN = pressure overload, AR/MR = volume overload; valve intervention can reverse symptoms and prevent progression.
🧬 Cardiomyopathies	Dilated (familial/idiopathic), hypertrophic, restrictive	Dilated → HFrEF; hypertrophic/restrictive → often HFpEF physiology; think genetics, myocarditis history, alcohol/chemo; cardiac MRI helps phenotype (fibrosis/infiltration).
⚡ Arrhythmia-related HF	AF (loss of atrial kick), rapid AF, SVT, frequent ectopy; tachycardia-induced cardiomyopathy	Rate/rhythm control can markedly improve EF if tachycardia-driven; always check ECG/Holter in “unexplained” HF or fluctuating symptoms.
🦠 Myocarditis	Viral, autoimmune, post-infective	Often younger patient, chest pain/viral prodrome, troponin rise; MRI shows inflammation; some progress to dilated cardiomyopathy.
🧫 Infiltrative / storage disease	Amyloidosis, sarcoid, haemochromatosis	Often HFpEF pattern + thick “sparkly” myocardium, low-voltage ECG (amyloid), conduction disease; specific therapies exist so don’t miss (MRI + targeted blood tests).
🫁 Pulmonary causes (right HF)	Cor pulmonale (COPD/ILD), pulmonary HTN, chronic thromboembolic disease	Raised JVP, peripheral oedema with relatively “clear” lungs; echo RV strain/pulmonary pressures; treat lung disease and consider pulmonary HTN/CTEPH pathways.
🧱 Pericardial disease	Constrictive pericarditis, tamponade	“HF signs with preserved EF”: raised JVP, hepatomegaly/ascites; tamponade = hypotension + tachycardia + raised JVP; echo is key and treatment is procedural.
🧠 Endocrine / metabolic	Thyrotoxicosis, hypothyroidism, diabetes, severe renal failure	Can precipitate or mimic HF via fluid retention and altered vascular tone; TFTs, HbA1c, renal function are part of standard HF workup.
🩸 High-output states	Severe anaemia, sepsis, AV fistula, pregnancy, beriberi (thiamine deficiency), Paget’s	Warm peripheries, bounding pulse, wide pulse pressure; the heart “can’t keep up” despite high CO — treat the driver (e.g., anaemia/sepsis).
🍷 Toxins / drugs / iatrogenic	Alcohol, cocaine; anthracyclines, trastuzumab; radiotherapy; NSAIDs (fluid retention), some CCBs	Medication history is mandatory; stopping/avoiding offending agents can prevent deterioration; chemo-related cardiomyopathy needs cardio-oncology follow-up.
🧷 Congenital / structural	ASD/VSD, coarctation, complex congenital lesions	May present later with pulmonary HTN/right HF or LV failure; murmurs, fixed split S2, echo diagnosis; specialist congenital heart disease input.

🧠 Teaching pearl: In exams, lead with IHD + hypertension + valve disease first, then add the “missable but treatable” causes (tachycardia-induced cardiomyopathy, myocarditis, amyloid/iron overload, pericardial disease, thyroid disease, high-output states). A great closing line is: “I would also look for triggers (infection, ACS, AF with RVR, PE, anaemia, thyroid disease, drugs like NSAIDs) and treat them in parallel.”

📊 HFrEF vs HFpEF (high-yield comparison table)

Feature	🔻 HFrEF (≤40%)	🟢 HFpEF (≥50%)
Typical patient	More often male; ischaemic heart disease; dilated LV	More often older, female; HTN, obesity, diabetes; AF common
Core mechanism	↓ contractility → ↓ forward flow + remodelling	Stiff LV → ↑ filling pressures (esp. with exertion) despite preserved EF
Echo pattern	Low EF, LV dilatation, global/regional wall motion abnormality	Normal EF, concentric LVH, LA enlargement, diastolic dysfunction indices
Symptoms	Very similar: dyspnoea, orthopnoea/PND, fatigue, reduced exercise tolerance, ankle oedema
Signs	S3, displaced apex, signs of congestion	S4 may be present; often HTN; signs of congestion; AF common
Prognostic levers	Strong mortality-reducing GDMT available	Focus on congestion + comorbidity control; SGLT2 inhibitors reduce HF admissions

🩺 Presentation (OSCE structure)

🫁 Breathlessness: exertional dyspnoea → orthopnoea → PND (ask “how many pillows?”).
💧 Congestion: ankle oedema, weight gain, abdominal distension/ascites, nocturia.
🧠 Low output: fatigue, poor exercise tolerance, dizziness, cool peripheries (advanced).
🎧 Key exam findings: raised JVP, bibasal crackles, pleural effusions, pitting oedema, hepatomegaly, displaced apex, murmurs (valve disease), S3 (HFrEF), AF.

🧪 Investigations (UK exam-friendly “what + why”)

📈 ECG: rarely normal in true HF; look for AF, prior MI, LVH, bundle branch block.
🩸 Natriuretic peptides (BNP/NT-proBNP): ventricular stretch marker; excellent rule-out test if low.
🖼️ CXR: cardiomegaly, upper lobe diversion, Kerley B lines, alveolar oedema, pleural effusions.
🫀 Echocardiography (gold standard): confirms EF phenotype, valves, RV function, pulmonary pressures, pericardium, diastolic indices.
🧪 Bloods to look for causes/complications: FBC, U&E (baseline + drug safety), LFTs, TFTs, HbA1c, lipids, ferritin/TSAT (iron deficiency), troponin if ACS suspected.

🧠 Teaching point: HF symptoms are non-specific. The diagnostic “anchor” is usually raised natriuretic peptide + echo confirmation. Obesity can lower BNP/NT-proBNP (false reassurance), while AF/CKD/age can raise them without HF — interpret in context.

💊 Management principles (applies to all HF phenotypes)

🧯 Treat congestion: loop diuretic for fluid overload (symptom relief; not a mortality drug).
🔍 Find and treat the cause: IHD, HTN, valve disease, tachycardia-induced cardiomyopathy, toxins, myocarditis.
🧩 Fix triggers: infection, ACS, AF with RVR, PE, anaemia, thyrotoxicosis, poor adherence, NSAIDs.
🧑‍⚕️ Educate: daily weights, salt/fluid advice when appropriate, vaccination, exercise/rehab, sick-day rules (esp. diuretics/SGLT2i), when to seek help.

🔻 HFrEF (≤40%): disease-modifying therapy (the “4 pillars”)

✅ HFrEF is where you win lives: combine disease-modifying drugs early (as tolerated), then uptitrate. 🎯 Typical “pillar” set: ACEi/ARB or ARNI + beta-blocker + MRA + SGLT2 inhibitor.

🧱 ACEi (or ARB if intolerant): reduces RAAS-driven remodelling and mortality; monitor BP, creatinine, K⁺.
🧠 Beta-blocker (HF-licensed): bisoprolol/carvedilol/metoprolol succinate; start when euvolaemic; slow uptitration.
🧂 MRA: spironolactone/eplerenone; mortality benefit; monitor K⁺ and renal function closely.
🧪 SGLT2 inhibitor: dapagliflozin/empagliflozin; reduces HF hospitalisation and CV events even without diabetes; watch volume status and genital infections.
💧 Loop diuretic: for congestion (symptom control); adjust to weights and renal function.
➕ Selected add-ons (specialist-led): ARNI switch if symptomatic despite ACEi/ARB; ivabradine (sinus rhythm HR ≥70 despite BB); hydralazine/isosorbide dinitrate if RAAS drugs not tolerated; iron (IV) if deficient; devices (ICD/CRT) based on EF/QRS/LBBB and symptoms.

🟢 HFpEF (≥50%): what actually helps

🧠 HFpEF is often “comorbidity-driven HF”: you improve symptoms and admissions by controlling BP, volume status, AF, ischaemia, obesity, diabetes, sleep apnoea. SGLT2 inhibitors have clear outcome benefit for HFpEF/HFmrEF (especially reducing HF admissions).

💧 Diuretics for congestion: cornerstone for symptom relief (careful with preload dependence).
🩺 Blood pressure optimisation: treat HTN aggressively (reduces LVH and filling pressures).
🫀 AF management: rate/rhythm strategy + anticoagulation when indicated; AF is a major driver of HFpEF decompensation.
🍩 Weight + metabolic health: obesity and insulin resistance worsen diastolic stiffness; weight loss/exercise improves functional capacity.
🧪 SGLT2 inhibitors: recommended option for HFpEF/HFmrEF to reduce HF events (UK appraisal-supported).
🧩 Consider specialist therapies: MRAs/ARNI may help selected patients (benefits vary); decisions usually MDT/heart failure clinic-led.

⚖️ HFrEF vs HFpEF: “what you say in exams”

🎤 HFrEF: “I will start disease-modifying therapy early (4 pillars) and uptitrate to target doses, plus diuretics for congestion.”
🎤 HFpEF: “I will treat congestion with diuretics and aggressively manage comorbidities (HTN, AF, obesity, diabetes), consider SGLT2 inhibitor, and arrange HF clinic follow-up.”

🚨 Acute decompensated HF (quick OSCE line)

🫁 Sit up, oxygen only if hypoxic, monitor, IV access, treat pulmonary oedema (IV loop diuretic ± nitrates if hypertensive), treat trigger (ACS/AF/sepsis), early senior/CCO input if unstable.

📚 References (UK + core)

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