🫀 HK-MLE Heart Failure — 50 High-Yield MCQs

SECTION A — GDMT (Questions 1–15)

• A) Add spironolactone 25 mg OD
• B) Switch ramipril to sacubitril/valsartan 97/103 mg BD
• C) Add dapagliflozin 10 mg OD
• D) Add digoxin 125 mcg OD
• E) Increase bisoprolol to 20 mg OD

• A) MRA (spironolactone) reduces mortality in HFrEF (RALES trial, 30% reduction) and should also be added, but ARNI delivers the greatest incremental benefit when switching from ACEi.
• C) SGLT2i (dapagliflozin, DAPA-HF) reduces the composite outcome by 26% in HFrEF and is a 4th pillar, but the question asks for the single most important step — ARNI transition first when ACEi is already on board.
• D) Digoxin reduces HF hospitalisations only (DIG trial) with no mortality benefit; not a priority step.
• E) Bisoprolol at 10 mg already achieves near-target dose; doubling beta-blocker above target offers no additional mortality benefit.

• A) ACE inhibitor rebound — rechallenge lisinopril
• B) Angioedema due to bradykinin accumulation from dual neprilysin + ACEi — stop sacubitril/valsartan, do NOT restart ACEi
• C) Allergic reaction to valsartan — switch to an ARB monotherapy
• D) Volume overload worsening — increase furosemide
• E) Hereditary angioedema flare — give C1-esterase inhibitor

• A) Rebound ACEi effect is not a recognised entity; the bradykinin pathway explains this.
• C) Valsartan as an ARB rarely causes angioedema because ARBs do not elevate bradykinin; the culprit is the neprilysin inhibitor component combined with residual ACEi.
• D) Facial/lip oedema in this setting is angioedema, not volume overload; increasing diuretics is dangerous and irrelevant.
• E) Hereditary angioedema (C1-inhibitor deficiency) is possible but far less likely in this clinical scenario; the drug timing makes bradykinin-mediated angioedema the correct diagnosis.

• A) Carvedilol — switch to metoprolol succinate
• B) Eplerenone — reduce to 12.5 mg OD or hold if K⁺ >5.5 mmol/L; recheck electrolytes
• C) Enalapril — switch to losartan
• D) All three drugs — discontinue all GDMT
• E) None — start patiromer and continue all drugs unchanged

• A) Carvedilol does not cause hyperkalaemia; switching beta-blockers does not address this problem.
• C) ACEi contributes to hyperkalaemia, but in the context of an MRA also on board, the MRA is typically the most modifiable agent; switching to an ARB does not eliminate the risk.
• D) Discontinuing all GDMT significantly worsens prognosis; targeted dose reduction of the offending agent is the standard approach.
• E) Patiromer (potassium binder) is an option to enable GDMT continuation but is not first-line before trying dose reduction; monotherapy dose reduction comes first.

• A) Dapagliflozin and empagliflozin are Class I, LOE A for HFrEF only
• B) SGLT2 inhibitors are Class I, LOE A for HFmrEF (EF 41–49%) AND HFpEF (EF ≥50%) to reduce HF hospitalisation or CV death
• C) SGLT2 inhibitors should only be initiated after 3 months of stable ACEi/ARB therapy
• D) SGLT2 inhibitors are contraindicated in CKD stage 3b (eGFR 30–44 mL/min)
• E) Canagliflozin is the preferred SGLT2 inhibitor for HFpEF based on DELIVER trial data

• A) The recommendation now extends beyond HFrEF; this was the older 2021 position.
• C) There is no mandatory waiting period before SGLT2i initiation; they can and should be initiated promptly, including during hospitalisation.
• D) Current guidance supports use of dapagliflozin down to eGFR ≥25 mL/min and empagliflozin ≥20 mL/min for HF; eGFR 30–44 is not a contraindication.
• E) Canagliflozin has no Class I HF indication; dapagliflozin (DELIVER) and empagliflozin (EMPEROR-Preserved) are the evidence-based agents.

• A) Add ivabradine (since HR >75 bpm and on ARNI)
• B) Start carvedilol at a low dose (3.125 mg BD) and up-titrate
• C) Start digoxin to reduce HR
• D) Refer for ICD implantation first before adding beta-blocker
• E) Add hydralazine-nitrate combination

• A) Ivabradine (SHIFT trial) is indicated when HR ≥75 bpm on maximally tolerated beta-blocker in sinus rhythm — it is not a substitute for initiating a beta-blocker first.
• C) Digoxin does not reduce mortality and does not replace the evidence-based role of beta-blockers.
• D) ICD eligibility is reassessed after ≥3 months of optimal GDMT, as EF may improve; ICD should not delay initiating beta-blocker.
• E) Hydralazine/isosorbide dinitrate is a mortality-reducing alternative in patients intolerant of both ACEi and ARB/ARNI (or in self-identified Black patients per A-HeFT), not here.

• A) Atenolol
• B) Metoprolol tartrate (immediate-release)
• C) Metoprolol succinate (extended-release)
• D) Propranolol
• E) Nebivolol (for patients under 70 years)

• A) Atenolol has never been shown to reduce mortality in HFrEF in an RCT.
• B) Metoprolol tartrate (immediate-release) was NOT the drug in MERIT-HF; the extended-release succinate form was; this is a classic HK-MLE trap.
• D) Propranolol has no mortality RCT data in HFrEF.
• E) Nebivolol (SENIORS trial) showed benefit but was limited to patients ≥70 years and did not show all-cause mortality reduction as the primary endpoint; it is not first-line.

• A) Stop spironolactone permanently; MRA contraindicated
• B) Switch spironolactone to eplerenone 25–50 mg OD
• C) Add tamoxifen to manage the breast tenderness
• D) Reduce spironolactone to 12.5 mg OD
• E) Switch to finerenone (non-steroidal MRA)

• A) MRA has a 30% mortality reduction in HFrEF (RALES) and should not be permanently stopped for a manageable side effect.
• C) Tamoxifen is not indicated; addressing the cause by switching to a selective MRA is correct.
• D) Dose reduction may reduce the side effect but does not eliminate it and may reduce efficacy.
• E) Finerenone is a non-steroidal MRA with compelling evidence in CKD/T2DM (FIDELIO, FIGARO) but is not yet approved with the same evidence base as spironolactone/eplerenone for HFrEF; eplerenone is the established switch.

• A) Increase bisoprolol to 10 mg (target dose)
• B) Add ivabradine 5 mg BD
• C) Add digoxin 125 mcg OD
• D) Add hydralazine 25 mg TDS
• E) Add amiodarone 100 mg OD

• A) "Maximally tolerated" bisoprolol is already defined; increasing further risks symptomatic hypotension and is not achievable in this patient.
• C) Digoxin can reduce hospitalisation but does not add mortality benefit beyond the 4-pillar GDMT already on board.
• D) Hydralazine monotherapy has no mortality evidence; it is used in combination with nitrates as an ACEi/ARB substitute.
• E) Amiodarone is reserved for arrhythmia management, not routine HFrEF GDMT, and has significant toxicity.

• A) Implantable cardioverter-defibrillator (ICD) alone
• B) Cardiac resynchronisation therapy with defibrillator (CRT-D)
• C) Heart transplantation listing
• D) Left ventricular assist device (LVAD)
• E) Right heart catheterisation

• A) ICD alone without CRT misses the benefit of resynchronisation; CRT-D provides both cardiac resynchronisation and defibrillation.
• C) Transplantation is reserved for Stage D refractory HF after maximal medical and device therapy fails; premature here.
• D) LVAD is for Stage D end-stage HF as bridge to transplant or destination therapy; not indicated at this stage.
• E) Right heart catheterisation guides haemodynamic management in refractory/uncertain cases but is not the next therapeutic step here.

• A) ACEi is absolutely contraindicated below systolic BP 110 mmHg
• B) Start at the lowest available dose (e.g., ramipril 1.25 mg OD) and up-titrate as tolerated
• C) Use an ARB instead, as ARBs carry less risk of hypotension
• D) Wait until systolic BP exceeds 120 mmHg before initiating
• E) Start at target dose immediately to achieve faster benefit

• A) Absolute contraindication is bilateral renal artery stenosis, pregnancy, angioedema, or K⁺ >5.5 mmol/L; SBP 100 mmHg alone is not absolute.
• C) ARBs carry equivalent first-dose hypotension risk; no advantage over ACEi in this regard.
• D) Delaying GDMT initiation worsens outcomes; low-dose initiation is the safe approach.
• E) Starting at target dose risks severe first-dose hypotension; low-and-slow up-titration is standard.

• A) Direct inhibition of aldosterone synthesis
• B) Neprilysin inhibition → ↑ BNP, ANP, cGMP → natriuresis, vasodilation, anti-fibrotic effects
• C) Inhibition of the sympathetic nervous system via central beta-blockade
• D) Inhibition of HCN4 channels reducing sinus node automaticity
• E) Blockade of mineralocorticoid receptors in myocardial fibroblasts

• A) Aldosterone synthesis inhibition is the mechanism of MRAs, not ARNI.
• C) Central beta-blockade describes metoprolol's CNS effects; sacubitril has no direct SNS inhibitory action.
• D) HCN4 inhibition is the mechanism of ivabradine (I-funny current blockade); unrelated to neprilysin.
• E) MR blockade is the mechanism of spironolactone/eplerenone; valsartan blocks AT1 receptors, not MR.

• A) Start ACEi first, wait 4 weeks, then add beta-blocker, then MRA, then SGLT2i sequentially
• B) Initiate all 4 pillars simultaneously (ARNI, beta-blocker, MRA, SGLT2i) aiming for 4-drug GDMT within 3 months
• C) Start SGLT2i and beta-blocker only; add others later
• D) Wait 3 months to see if EF improves spontaneously before starting GDMT
• E) Start at target doses immediately for fastest mortality reduction

• A) The old sequential approach (ACEi → BB → MRA → SGLT2i) is obsolete; simultaneous initiation is now endorsed.
• C) Omitting ARNI and MRA loses two mortality-reducing pillars; incomplete GDMT.
• D) Delaying therapy for "spontaneous recovery" is not guideline-endorsed; GDMT itself promotes reverse remodelling.
• E) Low starting doses with up-titration are necessary to avoid hypotension, renal dysfunction, and hyperkalaemia.

• A) Stop sacubitril/valsartan immediately and switch to hydralazine/nitrate
• B) Withhold until eGFR stabilises, then restart at lower dose; check for reversible causes (dehydration, NSAIDs)
• C) Add furosemide 20 mg to improve renal perfusion
• D) Start haemodialysis
• E) Add amlodipine for additional afterload reduction

• A) Permanent discontinuation is premature; the mortality benefit of ARNI in HFrEF is too great to abandon without first addressing reversible causes.
• C) Adding furosemide in a patient likely volume-depleted worsens renal function further.
• D) Haemodialysis is not warranted for a functional/haemodynamic reduction in eGFR; no signs of uraemia.
• E) Amlodipine does not improve intrarenal haemodynamics in RAAS-associated AKI.

• A) Continue at the current dose
• B) Reduce carvedilol dose by 50% but do not stop
• C) Stop carvedilol abruptly and do not restart
• D) Increase carvedilol dose to maximise HR control
• E) Replace carvedilol with metoprolol tartrate for acute use

• A) Continuing the full dose in haemodynamically compromised decompensation is dangerous due to negative inotropy.
• C) Abrupt discontinuation precipitates rebound tachycardia and worsening myocardial ischaemia.
• D) Increasing dose during decompensation is contraindicated.
• E) Metoprolol tartrate has no mortality evidence in HFrEF and should not be substituted for the evidence-based agents.

• A) It is first-line GDMT equivalent to ACEi in all patients with HFrEF
• B) It is a mortality-reducing alternative in HFrEF patients intolerant of both ACEi and ARB/ARNI
• C) H-ISDN reduces mortality in HFpEF
• D) H-ISDN should be added to ARNI as a 5th drug in refractory HFrEF
• E) H-ISDN is primarily used for rate control in atrial fibrillation with HF

• A) ACEi has superior efficacy to H-ISDN (V-HeFT II showed enalapril superior to H-ISDN); H-ISDN is not first-line.
• C) No mortality benefit has been demonstrated for H-ISDN in HFpEF.
• D) There is no evidence for adding H-ISDN as a 5th drug on top of complete GDMT.
• E) H-ISDN has no role in rate control; it acts as a preload/afterload reducer.

SECTION B — ACUTE DECOMPENSATED HEART FAILURE & LMNOP (Questions 16–27)

• A) IV furosemide 40 mg and IV morphine 2 mg
• B) High-flow oxygen, IV furosemide 40–80 mg, and IV nitrates (glyceryl trinitrate infusion)
• C) IV dobutamine infusion
• D) IV adrenaline and defibrillation
• E) Oral torsemide and sublingual nitrate only

• A) Morphine in ADHF increases mortality risk (ADHERE registry: increased need for mechanical ventilation), it is no longer routinely recommended — a classic HK-MLE trap.
• C) Dobutamine is for the "cold and wet" (low-output) ADHF phenotype; IV inotropes are inappropriate in hypertensive pulmonary oedema where the problem is vasoconstriction, not low output.
• D) Adrenaline/defibrillation is for cardiac arrest; this patient has a pulse with a BP of 192 mmHg.
• E) Oral torsemide has inadequate bioavailability in gut oedema during decompensation; IV route is essential.

• A) Lasix, Morphine, Nitrates, Oxygen, Positioning — Morphine is most controversial
• B) Lasix, Milrinone, Nitrates, Oxygen, Positioning — Milrinone is most controversial
• C) Loop diuretics, Morphine, Nesiritide, Oxygen, Positioning — Nesiritide is most controversial
• D) Lasix, Morphine, Nitrates, Oxygen, Positioning — Nitrates are most controversial
• E) Lasix, Metoprolol, Nitrates, Oxygen, Positioning — Metoprolol is most controversial

• B) Milrinone is not part of LMNOP; it is a phosphodiesterase inhibitor used in cardiogenic shock.
• C) Nesiritide (recombinant BNP) was not proven to reduce mortality in ASCEND-HF and is not part of standard LMNOP.
• D) Nitrates are well-established and not controversial; their vasodilatory benefit in hypertensive APO is robust.
• E) Metoprolol is not in LMNOP; beta-blockers are dose-reduced or held in decompensated HF.

• A) "Warm and wet" — IV diuretics
• B) "Cold and dry" (true hypovolaemia) — cautious IV fluid challenge
• C) "Cold and wet" (cardiogenic shock with congestion) — vasopressors ± inotropes, consider mechanical support
• D) "Cold and wet" — immediate IV high-dose morphine
• E) "Warm and dry" — reassurance and discharge

• A) "Warm and wet" (congested, good perfusion) is managed with diuretics/vasodilators; this patient is hypoperfused with cold peripheries — wrong phenotype identification.
• B) Clear lung bases might suggest hypovolaemia, but the context of known HFrEF with severely depressed EF and hypotension makes cardiogenic shock more likely; blind fluid boluses worsen pulmonary congestion.
• D) Morphine is contraindicated in cardiogenic shock; it causes vasodilation and can worsen hypotension.
• E) "Warm and dry" is the compensated euvolaemic state; this patient has signs of organ hypoperfusion.

• A) Add thiazide diuretic (metolazone) for sequential nephron blockade
• B) Switch to peritoneal dialysis
• C) Add spironolactone 100 mg
• D) Reduce IV furosemide dose
• E) Add vasopressin antagonist (tolvaptan)

• B) Peritoneal dialysis is reserved for end-stage renal failure or refractory volume overload; not first-line for diuretic resistance.
• C) Spironolactone is a weak diuretic in this context and acts at the collecting duct only; less effective than thiazide combination.
• D) Reducing dose worsens diuresis further.
• E) Tolvaptan (ADH2 receptor antagonist) corrects hyponatraemia and has modest diuretic effect but did not reduce mortality in EVEREST trial; it is not first-line for diuretic resistance.

• A) Daily serum albumin
• B) Daily weight (target 0.5–1 kg loss/day), renal function, and electrolytes
• C) Continuous ECG monitoring only
• D) Daily urinary protein
• E) Weekly echocardiography

• A) Albumin is relevant for oedema management but not the primary monitoring parameter during diuresis.
• C) Continuous ECG is important for arrhythmia but does not guide diuretic titration.
• D) Urinary protein is for CKD monitoring; not relevant to acute diuresis titration.
• E) Weekly echo is appropriate for outpatient reassessment; daily monitoring parameters guide inpatient diuresis.

• A) Intubation and mechanical ventilation (IMV)
• B) Non-invasive ventilation (BiPAP/CPAP)
• C) High-flow nasal cannula only
• D) Inhaled salbutamol
• E) IV hydrocortisone for presumed bronchospasm

• A) IMV is reserved for failure of NIV or haemodynamic collapse; it carries higher complication rates and is not first-line.
• C) High-flow nasal cannula (HFNC) is appropriate in certain settings but lacks the same positive pressure preload benefit as BiPAP/CPAP in APO.
• D) Salbutamol is for bronchospasm; cardiogenic pulmonary oedema does not respond to bronchodilators.
• E) Hydrocortisone has no role; this is not asthma.

• A) Only after 6 months of outpatient stability
• B) Before discharge and intensive follow-up in the first 6 weeks after hospitalisation
• C) Not recommended for elderly patients >70 years
• D) SGLT2i should be held for 3 months before re-initiation
• E) Beta-blockers should be started within 24 hours of diuresis regardless of volume status

• A) Waiting 6 months is dangerous; the highest mortality risk is in the first 90 days post-discharge.
• C) Age is not a contraindication to GDMT; benefit extends to patients >70 years.
• D) SGLT2i can be initiated or continued during hospitalisation for ADHF and before discharge.
• E) Beta-blockers should be initiated or continued once the patient is no longer acutely decompensated (euvolaemic), not during fluid overload.

• A) Aortic valve stenosis
• B) Rapid ventricular filling in a volume-overloaded, dilated, poorly compliant ventricle — indicates elevated filling pressure
• C) Pericardial rub from pericarditis
• D) Mitral valve prolapse
• E) Pacemaker spike artefact

• A) Aortic stenosis produces a harsh ejection systolic murmur; the S3 is unrelated to AS.
• C) Pericardial rub is a friction sound with three components; heard over the left sternal edge, not a gallop rhythm.
• D) Mitral valve prolapse produces a mid-systolic click ± late systolic murmur; no gallop.
• E) A pacemaker spike is an electrical artefact on ECG, not an auscultatory finding.

• A) Upper lobe diversion
• B) Kerley B lines
• C) Bilateral hilar ("bat-wing") opacities
• D) Hyperinflation with flattened diaphragms
• E) Cardiomegaly (CTR >50%)

• A) Upper lobe diversion (cephalisation of pulmonary vasculature) is a classic early sign of elevated pulmonary venous pressure in HF.
• B) Kerley B lines (short horizontal lines at the lung bases) indicate interstitial oedema from elevated capillary pressure.
• C) Bilateral perihilar opacification is the "bat-wing" pattern of alveolar oedema.
• E) Cardiomegaly (CTR >0.5 on PA CXR) is a common finding in dilated cardiomyopathy and chronic HF.

• A) Hypothyroidism
• B) Non-adherence to sodium restriction or diuretic medication
• C) Pulmonary embolism
• D) New-onset hypothermia
• E) Vitamin D deficiency

• A) Hypothyroidism can precipitate HF decompensation but is much less common than medication/dietary non-adherence.
• C) PE is an important and often fatal precipitant but is less common than dietary/medication-related triggers.
• D) Hypothermia can cause myocardial depression but is uncommon in the HK climate.
• E) Vitamin D deficiency has been associated with cardiovascular risk but is not a recognised common precipitant of acute decompensation.

• A) Continue bisoprolol at current dose
• B) Stop bisoprolol immediately
• C) Switch to carvedilol IV formulation
• D) Double the dose for better HR control
• E) Add digoxin and stop bisoprolol

• B) Abrupt bisoprolol withdrawal causes rebound sympathetic activation, tachycardia, and can worsen ischaemia.
• C) No IV formulation of carvedilol exists; metoprolol has an IV form but is not evidence-based for HFrEF.
• D) Doubling during decompensation risks worsening hypotension and further negative inotropy.
• E) Adding digoxin is not indicated simply because of hospitalisation, and replacing bisoprolol with digoxin removes a mortality-reducing drug.

• A) Dobutamine is the preferred first-line vasopressor for systemic hypotension in cardiogenic shock
• B) Noradrenaline is the preferred vasopressor to maintain MAP, with dobutamine added as inotrope for low output
• C) High-dose dopamine is preferred over noradrenaline based on SOAP II trial data
• D) Adrenaline alone is the safest inotrope/vasopressor in cardiogenic shock
• E) Levosimendan is first-line in all cardiogenic shock presentations

• A) Dobutamine is primarily an inotrope; as a vasopressor for systemic hypotension it is inadequate and can worsen hypotension further.
• C) The SOAP II trial showed dopamine had higher arrhythmia rates than noradrenaline in cardiogenic shock; dopamine is no longer preferred.
• D) Adrenaline causes lactic acidosis and excessive HR increases, impairing cardiac filling; it is reserved as last resort.
• E) Levosimendan (calcium sensitiser) is useful in certain low-output states but is not first-line in all presentations; evidence is less robust than dobutamine.

SECTION C — DIAGNOSIS, BNP, AND INVESTIGATIONS (Questions 28–37)

• A) HFrEF — start standard 4-pillar GDMT
• B) HFpEF — SGLT2 inhibitor (Class I) + diuretics for symptoms + treat comorbidities
• C) Normal ageing cardiac changes — reassure
• D) Cardiac amyloidosis — endomyocardial biopsy
• E) Hypertrophic obstructive cardiomyopathy — consider myomectomy

• A) EF 60% rules out HFrEF (EF ≤40%); 4-pillar GDMT is for reduced EF.
• C) This patient has objective evidence of diastolic dysfunction and elevated BNP; normal ageing does not explain BNP 310 or E/e' 16.
• D) Cardiac amyloidosis should be in the differential in elderly patients with concentric LVH, but biopsy is not the first step — ECG (low voltage), bone scintigraphy (ATTR), or serum/urine electrophoresis (AL) should be checked first.
• E) HOCM causes asymmetric septal hypertrophy with dynamic outflow obstruction; not typical here.

• A) BNP has a longer half-life than NT-proBNP
• B) NT-proBNP has a half-life of 60–120 minutes vs BNP's half-life of ~20 minutes; NT-proBNP does not accurately reflect acute haemodynamic change
• C) BNP levels are falsely elevated in obesity; NT-proBNP is not affected
• D) NT-proBNP has a longer half-life (1–2 hours vs 20 min for BNP), making it more stable but slower to reflect rapid haemodynamic change; both are falsely low in obesity
• E) BNP is the preferred marker for HFpEF diagnosis and NT-proBNP is only for HFrEF

• A) Incorrect — BNP has the shorter half-life.
• B) Partially correct description but incompletely states that NT-proBNP's longer half-life also allows it to serve as a reliable prognostic marker; both are clinically useful.
• C) Obesity lowers both BNP and NT-proBNP; the statement that NT-proBNP is unaffected is wrong.
• E) Both BNP and NT-proBNP are validated markers across HFrEF, HFmrEF, and HFpEF.

• A) NT-proBNP >125 pg/mL is diagnostic of heart failure in all age groups
• B) For patients >75 years, NT-proBNP >1,800 pg/mL is used for the "rule-in" threshold; age-adjusted cut-offs are critical
• C) NT-proBNP level cannot be used in patients with atrial fibrillation
• D) NT-proBNP >300 pg/mL rules out non-cardiac dyspnoea
• E) Renal failure falsely lowers NT-proBNP

• A) The 125 pg/mL threshold is the rule-out cut-off, not diagnostic; diagnostic accuracy requires clinical context.
• C) AF raises BNP/NT-proBNP independent of HF, but it does not invalidate the test — clinical context must guide interpretation.
• D) NT-proBNP >300 pg/mL increases probability of HF but cannot definitively rule out non-cardiac causes without clinical correlation.
• E) Renal failure elevates NT-proBNP (reduced renal clearance); higher cut-offs may be needed in CKD.

• A) Left ventricular ejection fraction
• B) E/e' ratio (ratio of mitral inflow velocity E to tissue Doppler annular velocity e')
• C) Left ventricular end-systolic volume
• D) Tricuspid regurgitation pressure gradient alone
• E) Fractional shortening

• A) LVEF is preserved by definition in HFpEF; assessing EF does not diagnose or grade diastolic dysfunction.
• C) LV end-systolic volume assesses systolic dimensions; not the primary diastolic parameter.
• D) TR gradient is used to estimate RVSP; while useful for pulmonary hypertension assessment, it is not the primary diastolic parameter.
• E) Fractional shortening is a systolic function metric derived from M-mode.

• A) Child-Pugh score
• B) NYHA Functional Classification
• C) TIMI risk score
• D) Wells criteria
• E) Duke criteria

• A) Child-Pugh score assesses hepatic cirrhosis severity; irrelevant here.
• C) TIMI score assesses ischaemic risk in ACS; not HF staging.
• D) Wells criteria assess DVT/PE probability.
• E) Duke criteria are for infective endocarditis diagnosis.

• A) Stage A (at risk for HF)
• B) Stage B (pre-HF with structural changes)
• C) Stage C (symptomatic HF)
• D) Stage D (refractory HF)
• E) NYHA Class I

• B) Stage B (pre-HF) requires structural cardiac change (e.g., LVH, reduced EF, prior MI) without symptoms; this patient has risk factors only.
• C) Stage C requires symptomatic HF with structural disease.
• D) Stage D is refractory end-stage HF despite optimal therapy.
• E) NYHA Class I (no limitation despite ordinary activity) is a symptom severity classification, not a structural staging system; NYHA and ACC/AHA stages are complementary but distinct.

• A) HFpEF (EF ≥50%)
• B) HFmrEF (EF 41–49%)
• C) HFrEF (EF ≤40%)
• D) Normal EF — no treatment needed
• E) Borderline EF — no evidence-based treatment

• A) HFpEF requires EF ≥50%; 38% is below this threshold.
• B) HFmrEF is EF 41–49%; 38% falls below this range.
• D/E) EF 38% with symptoms and CXR changes is definitive HFrEF requiring GDMT; describing it as "borderline" or "normal" is incorrect.

• A) This confirms acute heart failure — treat immediately
• B) A BNP <100 pg/mL effectively rules out acute heart failure as the cause of dyspnoea
• C) BNP is unreliable in dyspnoea assessment
• D) BNP 38 is elevated in the context of obesity — confirm with echo
• E) BNP must be paired with troponin to interpret dyspnoea

• A) BNP 38 does not confirm HF; it effectively rules it out.
• C) BNP has well-validated diagnostic and prognostic utility across HF phenotypes.
• D) Obesity lowers BNP; in an obese patient with BNP 38, HF is even less likely — not more.
• E) Troponin is a complementary cardiac marker for myocardial injury, not a prerequisite for BNP interpretation.

• A) Paroxysmal nocturnal dyspnoea (PND)
• B) Orthopnoea
• C) Peripheral oedema
• D) Third heart sound (S3 gallop)
• E) Raised JVP

• A) PND is highly specific for HF (pulmonary venous congestion relieved by sitting upright); few other conditions produce classic nocturnal awakening with dyspnoea relieved within 20–30 min.
• B) Orthopnoea is also highly specific for elevated left heart filling pressure; it distinguishes cardiac from most respiratory causes of exertional dyspnoea.
• D) S3 gallop in adults (>35 years) is highly specific for elevated filling pressures and significantly predicts adverse outcomes in HF.
• E) Elevated JVP is highly specific for elevated right heart filling pressure in HF; hepatojugular reflux increases specificity further.

• A) Jugular venous distension, Ascites, Liver congestion (hepatomegaly/tender), Edema (peripheral)
• B) Jaundice, Aortic stenosis, Left axis deviation, Ejection fraction
• C) JVP, Amyloid, LBABB, Ecg changes
• D) Jugular venous pulsation, Atrial fibrillation, Lung fibrosis, Eosinophilia
• E) JVP, Aortography, Liver scan, Echo

• B–E) These combinations incorrectly match elements that do not constitute the JALE mnemonic and mix unrelated clinical findings.

SECTION D — HFpEF (Questions 38–42)

• A) Digoxin 125 mcg OD
• B) Spironolactone 25 mg OD
• C) Empagliflozin 10 mg OD
• D) Sacubitril/valsartan 97/103 mg BD
• E) Carvedilol 6.25 mg BD

• A) Digoxin failed to show benefit in HFpEF and is not recommended.
• B) Spironolactone (TOPCAT trial) showed neutral primary outcome in HFpEF; it does not carry a Class I recommendation for HFpEF (Class IIb at best).
• D) Sacubitril/valsartan (PARAGON-HF) showed a trend but did not meet its primary endpoint in HFpEF; it is approved in some jurisdictions for HFpEF but is not Class I, LOE A.
• E) Beta-blockers are not indicated in HFpEF (where heart rate reduction may actually worsen filling) unless there is a co-existing indication (AF rate control, ischaemic heart disease).

• A) Excessive calcium efflux from sarcoplasmic reticulum causing prolonged systolic calcium exposure
• B) Reduced reuptake of cytosolic calcium into the sarcoplasmic reticulum (SR) by SERCA2a, causing impaired myocardial relaxation
• C) Complete loss of titin protein from sarcomeres
• D) Overexpression of beta-myosin heavy chain causing hypercontractility
• E) Mitochondrial ATP overproduction causing calcium toxicity

• A) Excessive calcium release from SR would impair systole, not relaxation; it is reduced reuptake that causes diastolic dysfunction.
• C) Titin abnormalities contribute to increased resting stiffness but reduced titin does not fully explain impaired relaxation.
• D) Beta-myosin heavy chain overexpression (re-expression of foetal isoforms) impairs systolic efficiency; it describes HFrEF remodelling more than diastolic dysfunction.
• E) Mitochondrial ATP overproduction is not a recognised pathological mechanism.

• A) Oral iron supplementation only
• B) Red cell transfusion to Hb >120 g/L
• C) IV ferric carboxymaltose (or ferric derisomaltose) to reduce HF hospitalisation
• D) Erythropoietin-stimulating agents
• E) No iron replacement — wait for cardiac improvement first

• A) Oral iron has poor bioavailability in HF patients (gut congestion, hepcidin upregulation); IV formulation is required.
• B) Transfusion is reserved for severe symptomatic anaemia; it does not correct the underlying iron deficiency or improve HF outcomes.
• D) ESAs are not recommended for iron deficiency anaemia in HF; they increase thromboembolic risk.
• E) Iron deficiency is independently associated with worse HF outcomes regardless of anaemia; waiting delays benefit.

• A) Beta-blockers cause excessive bradycardia in HFpEF patients
• B) In HFpEF, cardiac output is largely heart rate-dependent; excessive beta-blockade reduces HR, impairs CO augmentation, and worsens exercise tolerance
• C) Beta-blockers increase aldosterone levels in HFpEF
• D) Beta-blockers are metabolised differently in HFpEF patients
• E) HFpEF patients have fewer beta-receptors

• A) Excessive bradycardia is a risk, but the mechanism underlying harm is specifically the loss of chronotropic reserve needed in a stroke volume-limited heart.
• C) Beta-blockers do not directly raise aldosterone; this pathway is inaccurate.
• D) No significant pharmacokinetic difference between HFrEF and HFpEF for beta-blocker metabolism.
• E) Beta-receptor density changes are not the primary mechanistic explanation.

• A) AF causes paradoxical increase in afterload in HFpEF
• B) Loss of atrial systole removes the 20–25% "atrial kick" that fills a stiff, poorly compliant LV — critically impaired in HFpEF
• C) AF causes immediate valvular regurgitation in HFpEF
• D) AF is uniquely proarrhythmic in HFpEF due to ion channel differences
• E) AF abolishes ventricular contractility in HFpEF

• A) AF does not directly increase LV afterload; heart rate increase reduces diastolic filling time but does not change systemic vascular resistance acutely.
• C) AF does not cause valvular changes directly.
• D) Ion channel differences between HF phenotypes are not the primary mechanism of haemodynamic decompensation with AF.
• E) Ventricular contractility (EF) is preserved in HFpEF by definition; AF does not abolish it.

SECTION E — PATHOPHYSIOLOGY & NEUROHORMONAL ACTIVATION (Questions 43–46)

• A) Decreased aldosterone → natriuresis → reduced preload
• B) Angiotensin II → vasoconstriction, aldosterone release, sodium retention, myocardial hypertrophy/fibrosis, and inflammatory cytokine upregulation → progressive remodelling
• C) Renin directly causes myocardial necrosis
• D) Aldosterone inhibits sympathetic nervous system activation
• E) Angiotensin II directly causes potassium wasting by acting on the loop of Henle

• A) RAAS activation in HF increases aldosterone, promoting sodium and water retention — the opposite of natriuresis.
• C) Renin does not directly cause myocardial necrosis; it cleaves angiotensinogen to angiotensin I.
• D) Aldosterone promotes SNS activation through permissive mechanisms; it does not inhibit it.
• E) Angiotensin II acts primarily on the proximal tubule to increase sodium-hydrogen exchange; aldosterone acts on the collecting duct for potassium excretion.

• A) Concentric hypertrophy with preserved cavity geometry
• B) Eccentric hypertrophy with LV chamber dilation, wall thinning, spherical geometry, and reduced EF
• C) Isolated right ventricular hypertrophy without LV involvement
• D) Fibrosis only without chamber dilation
• E) Pericardial calcification

• A) Concentric hypertrophy (sarcomere replication in parallel, normal cavity) is the pattern of pressure overload (hypertension, AS) and is associated with HFpEF rather than HFrEF.
• C) Isolated RV hypertrophy describes cor pulmonale from chronic pulmonary hypertension.
• D) Interstitial fibrosis accompanies remodelling but alone does not describe the chamber geometry changes in HFrEF.
• E) Pericardial calcification is a feature of constrictive pericarditis.

• A) IL-4
• B) Tumour necrosis factor-alpha (TNF-α / cachexin)
• C) TGF-β (transforming growth factor beta)
• D) IL-13
• E) Erythropoietin

• A) IL-4 is an anti-inflammatory/Th2 cytokine; not implicated in cardiac cachexia.
• C) TGF-β drives fibrosis in cardiac remodelling but is not the primary mediator of systemic wasting.
• D) IL-13 is associated with airway hyperreactivity; not cardiac cachexia.
• E) Erythropoietin is a haematopoietic growth factor; its deficiency contributes to anaemia in HF but it is not a wasting cytokine.

• A) In advanced HFrEF, stroke volume continues to increase linearly with increased preload (ascending limb only)
• B) The Frank-Starling curve shifts downward and right in HFrEF; at high filling pressures, further preload increase fails to augment stroke volume and worsens pulmonary oedema
• C) The failing heart operates on the ascending limb of the Frank-Starling curve exclusively
• D) Frank-Starling mechanism is irrelevant in the setting of beta-blocker therapy
• E) Preload reduction with nitrates reduces the failing heart's stroke volume proportionally

• A) The relationship is not linear in the failing heart; the curve reaches its blunted plateau at lower preloads than normal.
• C) The failing heart operates on the plateau/descending limb in decompensation, not the ascending limb.
• D) Beta-blockers affect chronotropy and inotropy; they modify but do not abolish the Frank-Starling relationship.
• E) Preload reduction in a congested, volume-overloaded heart decreases filling pressure and actually improves stroke volume (operating closer to the optimal point on the blunted curve) — the basis for vasodilator therapy in APO.

SECTION F — HIGH-OUTPUT HEART FAILURE & CARDIAC CACHEXIA (Questions 47–48)

• A) HFpEF — start SGLT2 inhibitor
• B) High-output heart failure — investigate for cause (anaemia, thiamine deficiency/beriberi, AV fistula, hyperthyroidism, Paget's disease, liver cirrhosis)
• C) HFrEF — start 4-pillar GDMT
• D) Dilated cardiomyopathy due to alcohol — alcohol cessation only
• E) Sepsis with high-output haemodynamics — blood cultures

• A) HFpEF has preserved EF but normal (not elevated) cardiac output; bounding pulses and warm peripheries point to high-output state.
• C) EF 65% and elevated CO are not HFrEF features; standard GDMT does not address the high-output cause.
• D) Alcoholic cardiomyopathy typically causes a dilated cardiomyopathy with reduced EF; high-output in this context points to thiamine deficiency (wet beriberi) complicating the alcohol history — a critical HKMLE trap.
• E) Sepsis can cause high-output haemodynamics acutely but the chronic nature and oedema here point to a non-infective cause.

• A) A minor complication of diuretic therapy reversible with potassium supplementation
• B) Unintentional non-oedematous weight loss >6% of total body weight over 6–12 months in chronic HF; carries poor prognosis with median survival <1 year
• C) Weight loss secondary to fluid overload responding to diuresis
• D) A reversible syndrome seen only in HFrEF with EF <20%
• E) Cardiac cachexia is synonymous with cardiac sarcopaenia and treated with anabolic steroids

• A) Diuresis-related weight loss is fluid loss (oedema), not muscle/fat wasting; correction of potassium does not address cachexia.
• C) Oedema-related weight loss from diuresis is a distinct process from true cachexia; the definition specifically excludes oedematous weight.
• D) Cardiac cachexia can occur across EF categories in advanced HF; no EF threshold is specified in the definition.
• E) Cardiac cachexia and sarcopaenia overlap but are distinct entities; anabolic steroids are not guideline-endorsed therapy for cardiac cachexia.

SECTION G — SPECIAL TOPICS & TRAP QUESTIONS (Questions 49–50)

• A) ACEi + MRA + SGLT2i
• B) ARNI + MRA + SGLT2i
• C) ACEi + beta-blocker only; defer MRA and SGLT2i due to CKD and hyperkalaemia
• D) SGLT2i + beta-blocker; hold ACEi/ARNI and MRA until K⁺ <5.0 mmol/L and eGFR stabilises; add patiromer if needed to enable ACEi
• E) Digoxin + diuretics only; all other drugs contraindicated in CKD

• A) Adding MRA when K⁺ is already 5.8 risks life-threatening hyperkalaemia; both ACEi and MRA together in advanced CKD are relatively contraindicated until K⁺ is corrected.
• B) ARNI + MRA in K⁺ 5.8/eGFR 25 is dangerous; dual blockade raises potassium further.
• C) Deferring both MRA and SGLT2i is overly conservative; SGLT2i can be safely used at eGFR 25 and has renal protective effects.
• E) Digoxin-only management misses all mortality-reducing therapies and is inappropriate in modern practice.

• A) HF progression despite GDMT — escalate diuretics
• B) Amiodarone pulmonary toxicity — stop amiodarone, consider corticosteroids; plus amiodarone-induced hypothyroidism worsening HF
• C) New malignancy — urgent bronchoscopy
• D) Sarcoidosis — start prednisolone
• E) Community-acquired pneumonia — start antibiotics

• A) A new bilateral CT pattern with restrictive spirometry is not consistent with isolated HF progression; echo shows stable EF; a drug-related cause must be considered before escalating diuretics.
• C) Bilateral interstitial changes without mass lesion in an amiodarone user strongly suggest drug toxicity before malignancy.
• D) Sarcoidosis is possible but amiodarone history makes drug toxicity the leading diagnosis; sarcoidosis should only be considered after excluding APT.
• E) Community-acquired pneumonia is typically unilateral or lobar, febrile, with elevated CRP/WBC; chronic bilateral interstitial change over 6 months is not consistent.

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