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1. HFrEF is defined as LVEF {{c1::≤40%}} #CutOff #HF
2. HFmrEF is defined as LVEF {{c1::41-49%}} (mildly reduced) #CutOff #HF
3. HFpEF is defined as LVEF {{c1::≥50%}} #CutOff #HF
4. HFimpEF = previously HFrEF, now LVEF >40% after GDMT — GDMT should be {{c1::CONTINUED (do NOT stop)}} per 2022 AHA/ACC/HFSA guidelines #Management #HKMLEtrap
5. ACC/AHA Stage B = structural disease but {{c1::NO symptoms}} — this is NOT yet heart failure #CutOff #HF
6. Haemodynamic profile "Wet + Cold" corresponds to {{c1::cardiogenic shock}} (congestion + hypoperfusion) #Management #HF
7. Haemodynamic profile "Wet + Warm" is the {{c1::most common}} decompensated HF profile #HF

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1. The #1 cause of HFrEF in developed countries is {{c1::ischaemic heart disease (IHD)}} #HF
2. The #1 cause of HFpEF in Chinese patients is {{c1::hypertension}} #HF
3. Tachycardia-induced cardiomyopathy from untreated AF is {{c1::reversible}} — treat the AF #Management #HKMLEtrap
4. Mnemonic for causes of HF: "I HAVE CADS" = {{c1::Ischaemia, Hypertension, Arrhythmia, Valve disease, Endocrine/metabolic, Cardiomyopathy, Alcohol/toxic, Drugs, Systemic/infiltrative}} #HF

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1. BNP >{{c1::100 pg/mL}} supports HF diagnosis; <{{c1::35 pg/mL}} excludes HF #CutOff #Investigation
2. NT-proBNP >{{c1::125 pg/mL}} (outpatient) or >{{c1::300 pg/mL}} (acute) supports HF #CutOff #Investigation
3. In patients on ARNI (sacubitril/valsartan), monitor {{c1::NT-proBNP}} (not BNP) because neprilysin inhibition falsely elevates BNP #Investigation #HKMLEtrap
4. Cornerstone investigation to determine HFrEF vs HFpEF and guide GDMT eligibility is {{c1::echocardiogram}} #Investigation #NextBestStep
5. Cardiothoracic ratio >{{c1::0.5}} on CXR indicates cardiomegaly #CutOff #Investigation
6. CXR features of acute pulmonary oedema (APO): cardiomegaly, {{c1::upper lobe diversion, Kerley B lines, bat-wing oedema, pleural effusion}} #Investigation
7. ECG finding of LBBB with QRS >{{c1::130ms}} in HFrEF with EF ≤35% = potential CRT candidate #CutOff #Investigation
8. VO2 max <{{c1::12 mL/kg/min}} on beta-blocker (or <14 if not on BB) = consider heart transplant listing (Seattle HF criteria) #CutOff #Investigation
9. MRA is contraindicated if eGFR <{{c1::30}} #Contraindication #Management
10. SGLT2i can be used in HFrEF down to eGFR {{c1::20}} #CutOff #Management
11. Iron deficiency is present in {{c1::30-50%}} of HF patients — IV iron improves outcomes #Management #HF
12. ECG finding in digoxin toxicity with hypokalaemia: {{c1::bidirectional VT, inverted T waves, Salvador Dali moustache scooping}} #Investigation #Complication

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1. First step in APO management: {{c1::sit patient upright}} (reduces preload) #Management #NextBestStep
2. First-line NIV in acute pulmonary oedema (APO) is {{c1::CPAP}} (not BiPAP) #Management #HKMLEtrap #NextBestStep
3. BiPAP is reserved for APO with concurrent {{c1::hypercapnia (Type 2 respiratory failure)}} #Management #HKMLEtrap
4. IV furosemide dose in APO (not on diuretic): {{c1::40-80 mg IV bolus}}; if already on oral diuretic: {{c1::2.5x usual oral dose}} #Management
5. IV GTN infusion (10-200 mcg/min) is indicated in APO if SBP {{c1::>90 mmHg}} — reduces preload AND afterload #Management #CutOff
6. GTN is contraindicated in APO if SBP {{c1::<90 mmHg}} (cardiogenic shock) #Contraindication
7. In cardiogenic shock (SBP <90): {{c1::DO NOT give vasodilators; give dobutamine ± noradrenaline, call ICU}} #Management #NextBestStep
8. ESC 2021 has downgraded morphine in APO from routine to {{c1::"consider with caution"}} — associated with worse outcomes in observational data #Management #HKMLEtrap
9. Mnemonic for APO management "LMNOP" = {{c1::Lasix (furosemide) IV, Morphine IV (cautious), Nitrates IV, Oxygen (high-flow/CPAP), Position upright}} #Management

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1. Definition of cardiogenic shock: SBP <90 mmHg + signs of hypoperfusion + lactate {{c1::>2}} despite adequate preload #CutOff #Management
2. First-line vasopressor in cardiogenic shock is {{c1::noradrenaline}} #Management #NextBestStep
3. First-line inotrope in cardiogenic shock is {{c1::dobutamine}} (β1 agonist — reduces PCWP, increases CO) #Management
4. Levosimendan mechanism: {{c1::calcium sensitiser + K-ATP channel opener}} → inotropy + vasodilation without increasing myocardial O2 demand #Management
5. In cardiogenic shock, primary PCI is indicated if cause is {{c1::ACS-related}} #Management #NextBestStep

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1. The four pillars of HFrEF GDMT ("BAMS") are {{c1::Beta-blocker, ARNI/ACEi/ARB, MRA, SGLT2 inhibitor}} #Management
2. The three evidence-based beta-blockers proven to reduce mortality in HFrEF are {{c1::bisoprolol (CIBIS-II), carvedilol (COPERNICUS), metoprolol succinate CR/XL (MERIT-HF)}} #Management #HKMLEtrap
3. Atenolol and metoprolol tartrate are {{c1::NOT proven}} to reduce mortality in HFrEF #Management #HKMLEtrap
4. Sacubitril/valsartan (ARNI) vs enalapril in PARADIGM-HF: {{c1::20%}} reduction in CV death/HF hospitalisation #Management
5. Before starting ARNI, ACEi must be stopped and a washout of {{c1::36 hours}} observed (bilateral angioedema risk) #Contraindication #HKMLEtrap
6. You CAN switch directly from {{c1::ARB to ARNI}} without a washout period #Management #HKMLEtrap
7. SGLT2 inhibitors (dapagliflozin/empagliflozin) are Class 1A in HFrEF {{c1::regardless of presence of diabetes}} (2022 AHA/ACC/HFSA) #Management #HKMLEtrap
8. Fixed target dose for dapagliflozin and empagliflozin in HF is {{c1::10 mg OD}} #Management #CutOff
9. Spironolactone is contraindicated if K+ >{{c1::5.0}} or eGFR <{{c1::30}} #Contraindication #CutOff
10. Beta-blockers are CONTRAINDICATED in {{c1::acutely decompensated HF}} (new initiation) #Contraindication #HKMLEtrap
11. If a patient on beta-blocker presents with decompensated HF: {{c1::CONTINUE (or halve dose) — do NOT abruptly stop}} #Management #HKMLEtrap
12. Combining ACEi + ARB + MRA (triple RAAS blockade) has {{c1::no added mortality benefit}} but significantly increases hyperkalaemia risk — DO NOT combine #Contraindication #HKMLEtrap
13. Digoxin target serum level in HF: {{c1::0.5-0.9 ng/mL}} #CutOff #Management
14. Digoxin reduces HF hospitalisations but has {{c1::NO mortality benefit}} (DIG trial) #Management
15. Ivabradine indication in HFrEF: sinus rhythm with HR {{c1::≥70}} despite maximally tolerated beta-blocker #Management #CutOff
16. Ivabradine is contraindicated in {{c1::atrial fibrillation}} (works on HCN channel — sinus only) #Contraindication
17. ACEi creatinine rise of up to {{c1::30%}} is acceptable after initiation — reflects reduced intraglomerular pressure (beneficial) #CutOff #HKMLEtrap
18. Furosemide has {{c1::no proven mortality benefit}} in HF — symptom relief only #Management #HKMLEtrap
19. NSAIDs in HF cause {{c1::fluid retention, reduced diuretic efficacy, increased K+, and worsened HF}} — DO NOT use #Contraindication #HKMLEtrap
20. H-ISDN (hydralazine + isosorbide dinitrate) is used if patient is {{c1::intolerant of ACEi/ARB/ARNI, OR as add-on in Black patients}} #Management
21. ACEi/ARB/ARNI are {{c1::CONTRAINDICATED in pregnancy}} — use hydralazine + nitrates instead #Contraindication

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1. Mnemonic for HFpEF treatment "SUDAF" = {{c1::SGLT2i, Underlying cause treatment, Diuretics (symptom relief), AF management, Finerenone/MRA}} #Management
2. ACEi, ARBs, and beta-blockers have {{c1::NO proven mortality benefit}} in HFpEF #Management #HKMLEtrap
3. SGLT2i in HFpEF has Class {{c1::2a}} (not Class 1) recommendation per 2022 guidelines (EMPEROR-Preserved, DELIVER trials) #Management #CutOff

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1. ICD is indicated for primary prevention if LVEF {{c1::≤35%}} + NYHA Class II-III + life expectancy >1 year + ≥3 months optimal GDMT #CutOff #Management
2. You must wait {{c1::at least 3 months}} of optimised GDMT before reassessing LVEF for ICD eligibility #Management #HKMLEtrap
3. CRT indication: LVEF ≤35% + NYHA II-IV + LBBB with QRS {{c1::≥150ms}} (Class 1A) or QRS 120-149ms (Class 2a) on optimal GDMT #CutOff #Management
4. CRT-D = {{c1::CRT + ICD combined}} — preferred when patient has indications for both #Management
5. Mnemonic for CRT criteria: "CRT = {{c1::QRS ≥150ms, LBBB, EF ≤35%, NYHA Class II-IV}}" #Management

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1. AF occurs in {{c1::30-40%}} of HF patients #Complication #CutOff
2. Sudden cardiac death accounts for {{c1::~50%}} of HF mortality — mostly due to VT/VF, prevented by ICD #Complication
3. Cardiorenal Syndrome Type 1: {{c1::acute HF → AKI}} #Complication
4. Cardiorenal Syndrome Type 2: {{c1::chronic HF → progressive CKD}} #Complication
5. Cardiac cachexia is defined by BMI loss >{{c1::6%}} with muscle wasting and anorexia — indicates poor prognosis #Complication #CutOff
6. Digoxin toxicity is dramatically worsened by {{c1::hypokalaemia}} (K+ competes with digoxin at Na/K-ATPase) — target K+ 4.0-5.0 mmol/L #Complication #HKMLEtrap

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1. 5-year mortality after HF diagnosis is {{c1::~50%}} (comparable to many cancers) #CutOff #HF
2. 1-year mortality after hospitalisation for HF is {{c1::~25%}} #CutOff #HF
3. Poor prognostic mnemonic "BAD HEART" = {{c1::BNP elevated, Anaemia/Arrhythmia, Diabetes/Dilated LV/Decreased EF (<20%), Hypotension (SBP<100)/Hospitalisation frequency, eGFR<30, Age>75/Advanced NYHA, RV dysfunction/Raised troponin, Tachycardia/Thinning myocardium}} #Complication

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1. Patient on HFrEF medications with K+ 5.6: first drug to reduce/stop is {{c1::spironolactone}} (NOT ACEi first) #NextBestStep #HKMLEtrap
2. If K+ >{{c1::6.0}} in HF: urgent management as hyperkalaemia emergency #CutOff #HKMLEtrap
3. HFimpEF — TRED-HF trial showed {{c1::40% relapse rate}} within 6 months of stopping GDMT #Management #HKMLEtrap
4. SGLT2i should be withheld during {{c1::acute illness, surgery, or prolonged fasting}} ("sick day rules") to prevent euglycaemic DKA #Contraindication #HKMLEtrap
5. Metformin is {{c1::no longer contraindicated}} in HF — safe to use #Management #HKMLEtrap
6. ARNI on monitoring: BNP rises (false elevation from neprilysin inhibition) → use {{c1::NT-proBNP}} for monitoring #Investigation #HKMLEtrap
7. First-line NIV in APO is {{c1::CPAP}} — SpO2 may be normal on CXR despite pulmonary oedema before O2 desaturation occurs #Management #HKMLEtrap

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1. Alert threshold for daily weight monitoring in HF: {{c1::>2 kg in 2 days}} → contact doctor or go to A&E #Management #CutOff
2. Fluid restriction (1.5-2 L/day) is indicated in {{c1::severe HF or hyponatraemia}} — NOT routinely required in mild-moderate HF #Management #CutOff
3. Salt restriction target in HF: {{c1::<2-3 g NaCl/day}} #Management #CutOff
4. Vaccination mandatory in all HF patients: {{c1::annual influenza + pneumococcal vaccine}} #Management
5. Only proven therapy to improve VO2 max in HFpEF is {{c1::supervised exercise rehabilitation}} #Management

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1. Heart failure is {{c1::NOT a statutory notifiable disease}} in Hong Kong #HKMLEtrap
2. Advise patients with NYHA Class III-IV or recent syncopal/ICD shock to {{c1::stop driving}} and notify the Transport Department (HK Road Traffic Ordinance Cap. 374) #Management
3. ICD deactivation at end-of-life in Stage D HF is {{c1::ethically permissible and does NOT constitute euthanasia}} (withdrawal of life-sustaining treatment) #Management

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HKMLE Module 1B — Heart Failure: MCQ Bank

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HARDEST QUESTION IDENTIFIED

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5 VARIATIONS ON QUESTION 9 — ICD TIMING IN HFrEF

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HKMLE MODULE 1C: ARRHYTHMIAS + CARDIAC EMERGENCIES

ACE-Level Comprehensive Study Note

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📌 QUICK SUMMARY

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SECTION 1: ATRIAL FIBRILLATION (AF)

1A. Definition

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1B. Classification

"PPLP-F" = Paroxysmal, Persistent, Long-standing, Permanent, First-detected

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1C. Aetiology / Causes

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1D. Pathophysiology (Step-by-Step)

STEP 1: Triggers (ectopic foci, especially from pulmonary veins)
    ↓
STEP 2: Rapid firing from pulmonary vein sleeves → disorganised atrial activation
    ↓
STEP 3: Multiple re-entrant wavelets propagate chaotically across atria
    ↓
STEP 4: AV node bombarded with ~400-600 impulses/min → random conduction
    ↓
STEP 5: Irregularly irregular ventricular response (typically 100-160 bpm if uncontrolled)
    ↓
STEP 6: Loss of atrial contraction → blood stasis in left atrial appendage → thrombus → stroke
    ↓
STEP 7: Tachycardia-induced cardiomyopathy if sustained high rate

• Pulmonary vein ostia have sleeves of atrial myocardium with short refractory periods — primary source of AF triggers
• Structural remodelling (fibrosis) creates heterogeneous conduction = AF substrate
• "AF begets AF" — every AF episode remodels the atria, making future AF more likely
• Loss of atrial kick reduces cardiac output by ~15-20% (critical in stiff LV/HFpEF patients)
• Braunwald's Heart Disease, p. 693

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1E. Risk Factors

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1F. Symptoms

Many patients are asymptomatic — AF found incidentally on pulse check or ECG!

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1G. Signs

1. Pulse: State "the pulse is irregularly irregular" — feel for ≥30 seconds
2. Apex-radial deficit: Simultaneously count apex (auscultation) and radial — state the difference
3. Assess haemodynamic stability: BP, GCS, signs of shock
4. Look for cause: Thyroid, mitral facies, peripheral stigmata of IE
5. Assess for complications: Neurological deficit (embolic stroke), HF signs
6. Always state: "I would examine the JVP and listen for a mitral murmur"

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1H. Investigations

• Rate 130 bpm, no distinct P waves, fibrillatory baseline between complexes, RR intervals completely irregular, narrow QRS complexes
• Interpretation: "AF with rapid ventricular response at 130 bpm — narrow complex confirms no aberrant conduction; no delta waves to suggest WPW"

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1I. Management

FLOWCHART: Overall AF Management Framework (2024 ESC: "CARE")

C — Comorbidities first (HTN, OSA, obesity, alcohol, thyroid)
A — Avoid stroke (anticoagulation based on CHA₂DS₂-VASc)
R — Rate or Rhythm control
E — Evaluation and Reassessment (ongoing)

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STEP 1: HAEMODYNAMIC ASSESSMENT — Is the patient UNSTABLE?

AF WITH HAEMODYNAMIC INSTABILITY?
(SBP <90 mmHg / pulmonary oedema / syncope / ongoing ACS / ischaemia)
    ↓ YES
Immediate DC cardioversion (synchronised 200J biphasic)
    ↓ NO
Proceed to rate/rhythm control decision

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STEP 2: ACUTE RATE CONTROL

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STEP 3: ANTICOAGULATION — CHA₂DS₂-VASc SCORE

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STEP 4: ANTICOAGULATION — DRUG CHOICE

• HA Drug Formulary: Apixaban and dabigatran are Restricted drugs for AF anticoagulation, requiring specialist (cardiologist/haematologist) initiation in most clusters
• Warfarin is General List — any doctor can prescribe
• INR monitoring clinics available at all HA specialist outpatient departments
• HAS-BLED score must be documented before initiating anticoagulation in HA

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HAS-BLED SCORE (Bleeding Risk)

Score ≥3 = high bleeding risk → does NOT contraindicate anticoagulation — instead, identify and correct modifiable bleeding risks (control BP, review NSAIDs, address alcohol)

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STEP 5: RHYTHM CONTROL — CARDIOVERSION

AF duration <48 hours?
    → YES: Can cardiovert immediately (DC or pharmacological)
           + anticoagulate for ≥4 weeks AFTER cardioversion
    → NO (or duration unknown):
           Option A: Anticoagulate ≥3 weeks THEN cardiovert
           Option B: TOE to exclude LA thrombus, then cardiovert immediately
                     + anticoagulate ≥4 weeks after

• Flecainide 200-300 mg oral ("pill in the pocket") — only if NO structural heart disease
• Propafenone 450-600 mg oral — similar cautions to flecainide
• Amiodarone IV — preferred if structural heart disease or HFrEF
• Vernakalant IV — atrial-selective; not widely available in HK HA

• Synchronised DC cardioversion (synchronised to R wave — prevents triggering VF)
• Start at 200J biphasic (monophasic: 360J)
• Sedate/anaesthetise first (propofol / midazolam)

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STEP 6: LONG-TERM RHYTHM CONTROL DRUGS

• Class 1A for symptomatic paroxysmal AF after failed antiarrhythmic drugs
• Class 1A for AF + HFrEF to improve LVEF (CASTLE-AF trial)
• HK: Performed at QMH, QEH, PWH, PYNEH

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1J. AF with RAPID VENTRICULAR RESPONSE (RVR)

Emergency Management Verbal Script:

"I would immediately:
1. Place the patient upright, O2 if SpO2 <90%
2. IV access, cardiac monitor, pulse oximetry
3. 12-lead ECG — confirm AF with RVR, check QRS width,
   look for delta waves (WPW!)
4. If haemodynamically UNSTABLE (SBP <90, pulmonary oedema, ACS):
   → Synchronised DC cardioversion 200J biphasic IMMEDIATELY
5. If haemodynamically STABLE:
   → IV metoprolol 2.5-5 mg over 2 min (repeat x3 to max 15 mg)
   OR IV diltiazem (NOT if HFrEF)
   OR IV digoxin 0.25 mg over 20 min (if HFrEF or BB/CCB contraindicated)
6. Bloods: TFT, U&E, Mg²⁺, FBC, troponin
7. Consider cause: sepsis, thyrotoxicosis, PE"

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1K. AF in WPW SYNDROME

• Accessory pathway (Bundle of Kent) bypasses AV node
• Resting ECG: Short PR (<120ms) + delta wave + wide QRS
• In AF: Rapid impulses can bypass AV node via accessory pathway at 300+ bpm → VF → cardiac arrest

ECG in AF + WPW:

• Broad, irregular complexes (not narrow — accessory pathway conducts wide)
• Irregularly irregular
• Rate can exceed 200-300 bpm
• "Bizarrely irregular wide-complex tachycardia" = WPW + AF until proven otherwise

Management of AF + WPW:

HAEMODYNAMICALLY UNSTABLE?
    → IMMEDIATE synchronised DC cardioversion

HAEMODYNAMICALLY STABLE?
    → IV PROCAINAMIDE (drug of choice) or
    → IV FLECAINIDE (slows accessory pathway)
    → Or synchronised DC cardioversion

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SECTION 2: SUPRAVENTRICULAR TACHYCARDIA (SVT)

2A. Definition and Types

AVNRT is the most common SVT (~60%) — typically young women with episodic palpitations.

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2B. Pathophysiology — AVNRT (Beginner-Friendly)

Normal: Fast pathway (fast conduction, long refractory period)
         Slow pathway (slow conduction, short refractory period)

Trigger (PAC): Arrives when fast pathway is refractory
    ↓
Conducts DOWN slow pathway → reaches ventricles late
    ↓
Fast pathway now recovered → conducts BACK UP fast pathway → reaches atria
    ↓
Re-entrant circuit established → AVNRT
    ↓
Result: Atria and ventricles depolarise almost simultaneously
        P wave buried in/just after QRS → very short RP interval

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2C. Symptoms and Signs

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2D. Management

STEP 1: Assess Haemodynamic Stability

UNSTABLE (SBP <90, pulmonary oedema, altered consciousness, severe chest pain)?
    → IMMEDIATE synchronised DC cardioversion
STABLE?
    → Vagal manoeuvres → Adenosine → Verapamil/beta-blocker

STEP 2: Vagal Manoeuvres

• Modified Valsalva (2019 REVERT trial) — now first-line: Lie supine, strain for 15s, then raise legs 45°, then return to sitting — ~43% conversion rate (vs 17% for standard Valsalva)
• Carotid sinus massage (one side only, avoid if carotid bruit — risk of plaque dislodgement causing stroke)
• Ice water immersion (paediatrics)
• Breath-holding with straining

STEP 3: Adenosine

• Severe asthma / COPD (bronchospasm)
• 2nd/3rd degree AV block
• WPW syndrome (see above — fatal risk)
• Sick sinus syndrome
• Transplanted heart (enhanced sensitivity — use 1/4 dose)

• Dipyridamole (antiplatelet) blocks adenosine breakdown → potentiates effect → use HALF dose adenosine
• Theophylline / caffeine → block adenosine receptors → use larger dose

STEP 4: Second-Line Drug Options

STEP 5: Long-Term Prevention

• Catheter ablation — curative, first-line choice for recurrent symptomatic SVT (>95% success rate for AVNRT)
• Daily oral beta-blocker or verapamil — if patient declines ablation
• "Pill in the pocket" diltiazem or beta-blocker — for infrequent episodes

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SECTION 3: VENTRICULAR TACHYCARDIA (VT)

3A. Definition and Classification

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3B. ECG Features of VT

1. AV dissociation (P waves unrelated to QRS) — pathognomonic of VT
2. QRS >160ms
3. Concordance in V1-V6 (all positive or all negative)
4. Fusion beats (simultaneous atrial + ventricular depolarisation — narrow QRS)
5. Capture beats (normal narrow complex intermittently — atrial impulse captures ventricle)
6. Northwest axis (negative in I AND aVF)
7. RBBB morphology with R:S <1 in V6 or LBBB with positive deflection in aVR

• Monomorphic VT in post-MI patients: scar creates fixed re-entrant circuit around infarct zone
• Polymorphic VT / TdP: triggered activity from early afterdepolarisations (EADs) — occur when QT is prolonged
• ICD treats VT by delivering internal shock OR anti-tachycardia pacing (ATP)

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3C. Causes

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3D. Causes of Long QT / Torsades de Pointes

• QTc >450ms (male) or >470ms (female) = prolonged
• QTc >500ms = high TdP risk — review all QT-prolonging medications
• Normal QTc = QT ÷ √RR interval (Bazett formula)

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3E. Management

EMERGENCY MANAGEMENT FLOWCHART:

BROAD COMPLEX TACHYCARDIA
    ↓
Pulse present?
    ↓ NO → Treat as VF → CPR + defibrillate (unsynchronised 200J)
    ↓ YES
Haemodynamically UNSTABLE?
(SBP <90 / pulmonary oedema / ACS / altered consciousness)
    ↓ YES → Synchronised DC cardioversion (200J biphasic)
    ↓ NO → Stable VT
Monomorphic or polymorphic?
    ↓
MONOMORPHIC stable VT:
    → Amiodarone 150 mg IV over 10 min (then 1 mg/min x6h, then 0.5 mg/min x18h)
    → Lidocaine 1-1.5 mg/kg IV bolus (alternative — especially post-MI VT)
    → If fails → synchronised DC cardioversion
POLYMORPHIC VT (normal QT):
    → Treat ischaemia, correct electrolytes
    → Amiodarone 150 mg IV
TORSADES de POINTES (long QT):
    → IV MAGNESIUM SULPHATE 2g IV over 5-15 min (STOP ALL QT-PROLONGING DRUGS)
    → Correct K+ to 4.5-5.0 mmol/L
    → Overdrive pacing / isoprenaline to shorten QT
    → Do NOT use amiodarone (worsens QT)

VERBAL EMERGENCY ORDERS (OSCE):

"I would immediately:
1. Call for help / crash team
2. O2 15L/min non-rebreather, IV access x2
3. Cardiac monitor, 12-lead ECG, pulse oximetry
4. Assess pulse and haemodynamic stability
5. If pulseless: commence CPR immediately, prepare defibrillator
6. If pulse present and unstable: synchronised DC cardioversion 200J
7. If pulse present and stable monomorphic VT:
   Amiodarone 150 mg IV over 10 min, continuous infusion
8. Bloods: U&E, Mg²⁺, troponin, ABG, drug levels
9. Identify and correct precipitant (ischaemia, hypokalaemia, drug toxicity)"

• Synchronised (cardioversion): for VT with pulse, AF, SVT — delivers shock timed to R wave to avoid triggering VF
• Unsynchronised (defibrillation): for VF and pulseless VT — no R wave to synchronise to
• If VT with pulse deteriorates to pulseless → immediately switch to unsynchronised

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SECTION 4: VENTRICULAR FIBRILLATION (VF)

4A. Definition

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4B. ALS Algorithm — Full Cardiac Arrest

ADULT ALS FLOWCHART:

CARDIAC ARREST
    ↓
CALL FOR HELP + START CPR (30:2, 100-120 compressions/min, 5-6 cm depth)
    ↓
Attach defibrillator → ASSESS RHYTHM
    ↓
┌──────────────────────┬─────────────────────────────────┐
│   SHOCKABLE          │       NON-SHOCKABLE             │
│   (VF / pulseless VT)│       (PEA / Asystole)          │
└──────────────────────┴─────────────────────────────────┘
    ↓                              ↓
1 SHOCK: 200J biphasic         CONTINUE CPR 2 min
    ↓                              ↓
CPR 2 MINUTES                  ADRENALINE 1 mg IV every 3-5 min
    ↓                              ↓
REASSESS RHYTHM                Identify and treat reversible causes
    ↓
If still shockable:
  After 3rd shock:
  ADRENALINE 1 mg IV (every 3-5 min thereafter)
  AMIODARONE 300 mg IV bolus
    ↓
After 5th shock:
  AMIODARONE 150 mg IV (second dose)
    ↓
CONTINUE 2 min CPR cycles + reassess

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4C. Post-Resuscitation Care (ROSC — Return of Spontaneous Circulation)

• Post-ROSC patients are transferred to ICU/CCU for targeted temperature management
• OHCA (out-of-hospital cardiac arrest) in HK: Activated AED programme at Mass Transit Railway (MTR) stations, airports, government buildings
• Primary PCI available 24/7 at QMH, QEH, PWH, PYNEH, TMH, PMH for post-VF STEMI

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SECTION 5: BRADYARRHYTHMIAS

5A. Classification

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5B. ECG Interpretation Box

• PR interval 280ms, all P waves followed by QRS, normal QRS width
• Interpretation: "1st degree AV block — benign, no treatment needed; may be due to vagal tone, inferior MI, digoxin"

• PR intervals: 160ms → 200ms → 240ms → P wave not conducted → cycle repeats
• Interpretation: "2nd degree AV block Mobitz I (Wenckebach) — progressive PR lengthening with grouped beating; usually at AV node level; generally benign; may occur in inferior STEMI"

• Fixed PR interval 180ms, then suddenly a P wave is not followed by QRS (no PR lengthening)
• Interpretation: "2nd degree AV block Mobitz II — unpredictable complete block; below AV node (His-Purkinje); high risk of progressing to complete heart block; requires pacing"

• P rate 75 bpm, QRS rate 38 bpm, no consistent PR relationship
• Wide QRS escape at 38 bpm
• Interpretation: "Complete AV block with ventricular escape rhythm — haemodynamic instability expected; requires emergency pacing; if anterior MI → permanent pacemaker"

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5C. Causes

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5D. Acute Management of Bradycardia

Emergency Verbal Orders:

"I would immediately:
1. O2, IV access, cardiac monitor
2. 12-lead ECG — identify type of block
3. Assess haemodynamic stability:
   Signs of shock? (pallor, cold peripheries, BP, altered GCS)
4. If SYMPTOMATIC/UNSTABLE (SBP <90, syncope, heart failure, ischaemia):
   ATROPINE 0.5 mg IV — repeat every 3-5 min to max 3 mg
   (Works for sinus bradycardia + Mobitz I — NOT effective for Mobitz II or complete block)
5. If no response to atropine OR Mobitz II/Complete block:
   TRANSCUTANEOUS PACING (external pads — temporising measure)
   Or ISOPRENALINE infusion (2-10 mcg/min) while awaiting pacing
6. Call cardiology for TRANSVENOUS PACING or PPM insertion
7. Identify and reverse cause: stop offending drugs, K+, thyroid"

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5E. Indications for Permanent Pacemaker (PPM)

• Symptomatic sinus node dysfunction (sick sinus syndrome)
• 3rd degree / complete AV block (symptomatic)
• Mobitz II 2nd degree AV block (regardless of symptoms — high risk of progression)
• Symptomatic 2:1 AV block
• Complete heart block post-anterior MI (even if asymptomatic — indicates large infranodal disease)
• Complete heart block in Inferior MI that persists >2 weeks

• Asymptomatic Mobitz I (Wenckebach) at infranodal level (HV ≥100ms on EP study)
• Asymptomatic 1st degree AV block with symptoms likely due to "pacemaker syndrome" from long PR

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SECTION 6: CARDIAC EMERGENCIES

6A. CARDIAC TAMPONADE

Definition

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Aetiology

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Pathophysiology

Fluid accumulates in pericardial sac (pericardium is non-compliant once ~150-200 mL acute)
    ↓
Intrapericardial pressure rises → compresses cardiac chambers
    ↓
Right atrium compressed first (lowest pressure) → then right ventricle → then left
    ↓
Ventricular filling impaired → reduced stroke volume → low cardiac output
    ↓
Compensatory: tachycardia, peripheral vasoconstriction, SNS activation
    ↓
PULSUS PARADOXUS:
    On inspiration: intrathoracic pressure ↓ → RV fills more → IVS shifts LEFT
    → LV compressed → LV output falls → systolic BP drops >10 mmHg on inspiration
    ↓
Beck's Triad: Hypotension + JVP elevation + Muffled heart sounds

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Clinical Features

• Hypotension (SBP <90 mmHg)
• Elevated JVP (engorged neck veins)
• Muffled heart sounds

• Pulsus paradoxus (SBP drop >10 mmHg on inspiration)
• Tachycardia
• Kussmaul's sign (JVP RISES on inspiration — paradoxical — also seen in constrictive pericarditis)

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Investigations

• Low voltage QRS throughout all leads, QRS complex axis alternates +/- 10-15° with each beat, sinus tachycardia 115 bpm
• Interpretation: "Low voltage + electrical alternans in a tachycardic patient = cardiac tamponade until proven otherwise — arrange urgent bedside echocardiography"

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Management

HAEMODYNAMIC INSTABILITY?
    ↓ YES → Emergency pericardiocentesis
             (subxiphoid approach, needle at 45° towards left shoulder)
             ECHO-guided preferred; connect to ECG lead — ST elevation if myocardium touched
    ↓ STABLE → Urgent echocardiography + cardiology review
                IV fluids (cautious — maintain preload while awaiting drainage)

DEFINITIVE:
    Pericardiocentesis (needle drainage)
    Surgical pericardial window (if recurrent / loculated / malignant)
    Treat underlying cause

"I would immediately:
1. IV fluids cautiously (maintain preload — do NOT diurese)
2. O2, monitoring
3. Bedside echocardiography (POCUS) — confirm effusion and tamponade physiology
4. Cardiology emergency referral
5. Prepare for pericardiocentesis
6. AVOID: beta-blockers, vasodilators, diuretics (all reduce preload → cardiac arrest)
7. If pulseless: CPR + immediate pericardiocentesis (needle decompression)"

1. Assess BP — note SBP on inspiration vs expiration (pulsus paradoxus ≥10 mmHg)
2. Assess JVP — elevated; rises further on inspiration (Kussmaul's sign)
3. Auscultate — muffled heart sounds
4. Assess peripheries — cool, clammy (low output)
5. State: "I would arrange urgent bedside echocardiography and call cardiology"

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6B. AORTIC DISSECTION

Definition

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Classification

Mnemonic: "Stanford A = Ascending = Awful = Acute surgery" "Stanford B = Below = Better with Blood pressure control"

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Aetiology

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Clinical Features

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Investigations

• Mediastinum 9.2 cm on PA film, aortic knuckle poorly defined, left pleural effusion
• Interpretation: "Widened mediastinum and left pleural effusion in a patient with sudden-onset tearing back pain = aortic dissection until excluded by CT aortogram"

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Management

TYPE A — Emergency Surgery

"I would immediately:
1. Call vascular/cardiothoracic surgery EMERGENCY
2. Large bore IV x2, send blood for crossmatch (6 units), FBC, coag, U&E, troponin, D-dimer
3. O2, analgesia (IV morphine — reduces sympathetic drive)
4. Target SBP 100-120 mmHg using IV labetalol or esmolol
   (reduce shear stress on dissection — BEFORE nitroprusside)
5. NEVER give thrombolytics (will cause haemopericardium → tamponade → death)
6. Urgent CT aortogram (if haemodynamically stable enough)
7. Transfer to cardiac surgery
8. If tamponade develops: very cautious pericardiocentesis — enough to stabilise,
   not full drainage (can worsen by decompressing tamponade before surgery)"

TYPE B — Medical Management

Target: SBP 100-120 mmHg + HR <60 bpm
Drug: IV LABETALOL (alpha+beta block) or IV ESMOLOL (beta blocker)
If further BP reduction needed: add IV sodium nitroprusside or IV nicardipine
   (NEVER use nitroprusside without beta-blocker — reflex tachycardia increases wall stress)
Monitor: Urine output, limb pulses, neuro assessment (spinal ischaemia)
Complications requiring surgery: malperfusion, expansion, rupture

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SECTION 7: COMPLICATIONS OVERVIEW

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SECTION 8: PROGNOSIS

• S — Stabilise in ICU
• H — Hypothermia/TTM (32-36°C x24h)
• O — Oxygenation controlled (avoid hyperoxia — target SpO2 94-98%)
• C — Coronary angiography (if ischaemia suspected)
• K — K+/Mg²⁺ correction

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❓ COMMON EXAM QUESTION BOX

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⚠️ DRUG TRAPS TABLE

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📊 NOTABLE TRIALS TABLE

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🧠 MASTER MNEMONICS TABLE

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🔗 CROSS-MODULE LINKS

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• Cardiac arrest / AED use: The Hong Kong Good Samaritan Ordinance (effective 2021) protects laypersons who use an AED in good faith from civil liability — actively promotes bystander defibrillation
• Driving with arrhythmias: HK Road Traffic Ordinance (Cap. 374) — patients with uncontrolled VT, complete heart block, or recent ICD shock should not drive; notify Transport Department; same for recent syncope
• ICD deactivation: Ethically permissible in end-of-life (Stage D HF or terminal illness); does NOT constitute euthanasia (withdrawal of life-sustaining treatment); discuss with patient + family using ACP framework
• Notifiable diseases: Cardiac arrhythmias are NOT notifiable diseases in HK. However sudden unexplained death may trigger Coroner notification (Coroners Ordinance Cap. 504)
• Aortic dissection as occupational hazard: If post-traumatic (industrial accident), occupational disease reporting may apply

• Chagas disease (rare cause of cardiomyopathy + arrhythmias in imported cases) — notify if identified
• If cardiac death is sudden and unexpected → Coroner's Court notification required

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1. AF is classified as paroxysmal when episodes last {{c1::<7 days and self-terminate}} #CutOff #AF
2. AF is classified as persistent when episodes last {{c1::>7 days and require cardioversion}} #CutOff #AF
3. AF is classified as permanent when {{c1::rate control is accepted and no further cardioversion is attempted}} #CutOff #AF
4. Paroxysmal AF {{c1::still carries the same stroke risk}} as persistent or permanent AF — anticoagulate based on CHA₂DS₂-VASc #HKMLEtrap #AF
5. The primary source of AF triggers is {{c1::ectopic foci from pulmonary vein sleeves}} #AF
6. Loss of atrial kick in AF reduces cardiac output by {{c1::~15-20%}} — critical in HFpEF patients #AF

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1. Next best investigation to confirm AF is {{c1::12-lead ECG}} showing absent P waves and irregularly irregular RR intervals #NextBestStep #Investigation #AF
2. Gold standard investigation to exclude LA appendage thrombus before cardioversion is {{c1::transoesophageal echocardiography (TOE)}} #Investigation #AF
3. In AF, TFTs should be requested to exclude {{c1::thyrotoxicosis}} as a reversible precipitant #Investigation #AF
4. Monitoring with {{c1::Holter monitor or 7-day ECG}} is used to document paroxysmal AF when resting ECG is normal #Investigation #AF

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1. Initial resting heart rate target in AF rate control is {{c1::<110 bpm}} (lenient); strict target is {{c1::<80 bpm}} for symptomatic patients #CutOff #Management #AF
2. First-line oral agent for rate control in AF is {{c1::bisoprolol}} #Management #AF
3. Rate control agent of choice in AF with HFrEF is {{c1::digoxin}} (or amiodarone) — NOT diltiazem or verapamil #Management #HKMLEtrap #AF
4. Diltiazem and verapamil are contraindicated for rate control in AF with {{c1::HFrEF}} (negative inotropy worsens LV function) #Contraindication #HKMLEtrap #AF
5. IV metoprolol dose for acute AF rate control is {{c1::2.5-5 mg IV over 2 min, repeat up to 3 times (max 15 mg)}} #Management #AF
6. IV digoxin dose for acute AF rate control is {{c1::0.25 mg IV over 20 min}} #Management #AF

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1. Next best step in AF with haemodynamic instability (SBP <90, pulmonary oedema, ACS) is {{c1::immediate synchronised DC cardioversion at 200J biphasic}} #NextBestStep #Emergency #AF
2. Electrical cardioversion for AF uses a {{c1::synchronised}} shock (timed to R wave) to avoid triggering VF #Management #HKMLEtrap #AF

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1. In the CHA₂DS₂-VASc score, Age ≥75 scores {{c1::2 points}} #CutOff #AF
2. In the CHA₂DS₂-VASc score, prior Stroke/TIA/thromboembolism scores {{c1::2 points}} #CutOff #AF
3. In the CHA₂DS₂-VASc score, female sex scores {{c1::1 point}} #CutOff #AF
4. CHA₂DS₂-VASc score ≥{{c1::2}} in males OR ≥{{c1::3}} in females → anticoagulate #CutOff #AF
5. CHA₂DS₂-VASc score of 1 in male AF patient → {{c1::consider anticoagulation}} (discuss with patient) #Management #AF
6. All persons aged ≥75 with AF have CHA₂DS₂-VASc ≥2 and are {{c1::candidates for anticoagulation regardless of AF type (paroxysmal/persistent/permanent)}} #CutOff #HKMLEtrap #AF

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1. Preferred anticoagulants in non-valvular AF are {{c1::DOACs (apixaban, dabigatran, rivaroxaban, edoxaban)}} over warfarin #Management #AF
2. Warfarin (not DOAC) is mandatory in AF with {{c1::mechanical prosthetic heart valves}} or {{c1::moderate-to-severe rheumatic mitral stenosis}} #Contraindication #HKMLEtrap #AF
3. INR target for warfarin in non-valvular AF is {{c1::2.0-3.0}} #CutOff #AF
4. Apixaban dose reduction to 2.5 mg BD applies if patient meets ≥2 of: age ≥80, weight ≤60 kg, creatinine {{c1::≥133 µmol/L}} #CutOff #Management #AF
5. Dabigatran is contraindicated if eGFR <{{c1::30 mL/min}} #Contraindication #AF
6. HK HA preferred first-line DOAC for AF is {{c1::apixaban or dabigatran}} (superior safety in Asian patients) #Management #AF
7. Reversal agent for apixaban and rivaroxaban is {{c1::andexanet alfa}} #Management #AF
8. Reversal agent for dabigatran is {{c1::idarucizumab}} #Management #AF

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1. HAS-BLED score ≥3 indicates high bleeding risk but does {{c1::NOT contraindicate anticoagulation}} — correct modifiable risks instead #HKMLEtrap #AF
2. In HAS-BLED, "L" stands for {{c1::Labile INR (TTR <60% on warfarin)}} #CutOff #AF
3. In HAS-BLED, "E" (elderly) is defined as age >{{c1::65}} years #CutOff #AF

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1. AF duration <48 hours → can cardiovert immediately AND must anticoagulate for {{c1::≥4 weeks}} AFTER cardioversion #CutOff #Management #AF
2. AF duration >48 hours or unknown → must either anticoagulate for {{c1::≥3 weeks}} before cardioversion OR perform {{c1::TOE to exclude LA thrombus}} first #Management #HKMLEtrap #AF
3. After successful cardioversion for AF >48h, anticoagulate for at least {{c1::4 weeks}} due to atrial stunning #CutOff #HKMLEtrap #AF
4. Pharmacological cardioversion agent for AF with NO structural heart disease is {{c1::flecainide (200-300 mg oral "pill in the pocket")}} or propafenone #Management #AF
5. Pharmacological cardioversion agent for AF WITH structural heart disease or HFrEF is {{c1::amiodarone IV}} #Management #HKMLEtrap #AF
6. Flecainide is absolutely contraindicated in AF with {{c1::structural heart disease (post-MI, LVH, HF)}} — pro-arrhythmic (CAST trial) #Contraindication #HKMLEtrap #AF
7. Dronedarone is contraindicated in {{c1::HFrEF}} (ANDROMEDA trial — increased mortality) and in {{c1::permanent AF}} #Contraindication #HKMLEtrap #AF
8. Before using sotalol for AF rhythm control, check {{c1::QTc}} — avoid if QTc >500ms #Contraindication #AF
9. Catheter ablation (pulmonary vein isolation) is Class 1A for AF + HFrEF to improve LVEF — based on the {{c1::CASTLE-AF}} trial #Management #AF

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1. Resting ECG features of WPW syndrome: {{c1::short PR (<120ms), delta wave, wide QRS}} #Investigation #WPW
2. In AF + WPW, impulses can bypass the AV node and conduct at {{c1::300+ bpm}} → VF → cardiac arrest #HKMLEtrap #WPW
3. ECG appearance of AF + WPW: {{c1::bizarrely irregular wide-complex tachycardia}} (broad, irregular, rate >200 bpm) #Investigation #WPW
4. Drug of choice for haemodynamically stable AF + WPW is {{c1::IV procainamide}} (or IV flecainide) #Management #WPW #NextBestStep
5. Next best step in haemodynamically unstable AF + WPW is {{c1::immediate synchronised DC cardioversion}} #NextBestStep #Emergency #WPW
6. Adenosine is contraindicated in AF + WPW because it {{c1::blocks the AV node, forcing ALL conduction down the accessory pathway → VF}} #Contraindication #HKMLEtrap #WPW
7. Verapamil is contraindicated in AF + WPW because it {{c1::blocks the AV node, accelerating accessory pathway conduction → VF}} #Contraindication #HKMLEtrap #WPW
8. Digoxin is contraindicated in AF + WPW because it {{c1::shortens the accessory pathway refractory period, increasing conduction rate → VF}} #Contraindication #HKMLEtrap #WPW
9. Mnemonic for forbidden drugs in AF + WPW: "AVoiD DruGs" = {{c1::Adenosine, Verapamil, Diltiazem, Digoxin}} #Contraindication #WPW

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1. The most common type of SVT (~60%) is {{c1::AVNRT (AV Nodal Re-entrant Tachycardia)}} — typically young women #Management #SVT
2. ECG feature of AVNRT: P waves are {{c1::buried in or just after the QRS}} with a very short RP interval #Investigation #SVT
3. ECG feature of atrial flutter: {{c1::sawtooth flutter waves at 300 bpm, typically with 2:1 block giving ventricular rate ~150 bpm}} #Investigation #SVT
4. First-line vagal manoeuvre for SVT (2019 REVERT trial evidence) is {{c1::Modified Valsalva (strain 15s then immediately raise legs 45°, then sit up)}} — converts ~43% #Management #NextBestStep #SVT
5. Carotid sinus massage is contraindicated if {{c1::carotid bruit is present}} (risk of plaque dislodgement and stroke) #Contraindication #SVT
6. First drug for stable SVT after failed vagal manoeuvres is {{c1::adenosine 6 mg IV rapid bolus}} with immediate 20 mL saline flush #Management #NextBestStep #SVT
7. If adenosine 6 mg fails, next doses are {{c1::12 mg → 12 mg}} (allow 1-2 min between doses) #Management #SVT
8. Adenosine is contraindicated in {{c1::severe asthma/COPD, 2nd/3rd degree AV block, WPW syndrome, sick sinus syndrome}} #Contraindication #SVT
9. Dipyridamole (antiplatelet) blocks adenosine breakdown → {{c1::use HALF dose adenosine}} (potentiation) #HKMLEtrap #Management #SVT
10. Theophylline and caffeine block adenosine receptors → may need {{c1::larger adenosine dose}} #HKMLEtrap #Management #SVT
11. Never give IV verapamil AND IV/oral beta-blocker simultaneously — risk of {{c1::severe bradycardia, hypotension, and complete AV block}} #Contraindication #HKMLEtrap #SVT
12. Curative treatment for recurrent symptomatic SVT (>95% success) is {{c1::catheter ablation (radiofrequency)}} #Management #SVT

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1. VT is defined as ≥{{c1::3 consecutive ventricular beats at rate ≥100 bpm}} #CutOff #VT
2. Sustained VT is defined as lasting {{c1::≥30 seconds}} or requiring intervention #CutOff #VT
3. Pathognomonic ECG finding of VT (vs SVT with aberrancy) is {{c1::AV dissociation}} (P waves unrelated to QRS) #Investigation #HKMLEtrap #VT
4. Other ECG criteria favouring VT include: QRS >{{c1::160ms}}, concordance in V1-V6, fusion beats, capture beats, northwest axis #Investigation #VT
5. Torsades de Pointes (TdP) is a polymorphic VT associated with {{c1::prolonged QT interval}} — QRS twists around the isoelectric baseline #Investigation #VT
6. First-line drug for stable monomorphic VT is {{c1::amiodarone 150 mg IV over 10 min}} (then 1 mg/min x6h, then 0.5 mg/min x18h) #Management #NextBestStep #VT
7. Alternative drug for stable monomorphic VT (especially post-MI) is {{c1::lidocaine 1-1.5 mg/kg IV bolus}} #Management #VT
8. Treatment for Torsades de Pointes is {{c1::IV magnesium sulphate 2g IV over 5-15 min}} + stop all QT-prolonging drugs #Management #NextBestStep #VT
9. Amiodarone is contraindicated in Torsades de Pointes because it {{c1::prolongs QT and worsens TdP}} #Contraindication #HKMLEtrap #VT
10. K+ target in patients with TdP/long QT is {{c1::4.5-5.0 mmol/L}} #CutOff #Management #VT
11. QTc >{{c1::450ms}} (male) or >{{c1::470ms}} (female) = prolonged QT #CutOff #VT
12. QTc >{{c1::500ms}} = high TdP risk — review all QT-prolonging medications #CutOff #HKMLEtrap #VT
13. Mnemonic for QT-prolonging drugs "MATES": {{c1::Macrolides, Antipsychotics, Tricyclics, E-drugs (ondansetron/methadone/antifungals), Sotalol/quinidine}} #Contraindication #VT
14. Next best step in haemodynamically unstable VT with pulse is {{c1::synchronised DC cardioversion 200J biphasic}} #NextBestStep #Emergency #VT
15. Next best step in pulseless VT is {{c1::immediate unsynchronised defibrillation 200J}} (treat same as VF) #NextBestStep #Emergency #VT
16. Synchronised shock is used for VT with pulse / AF / SVT; unsynchronised shock is used for {{c1::VF and pulseless VT}} (no R wave to synchronise to) #HKMLEtrap #Management

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1. VF is always {{c1::pulseless}} — always a cardiac arrest #Emergency #VF
2. CPR compression rate is {{c1::100-120/min}} at depth {{c1::5-6 cm}} in a 30:2 ratio #Management #Emergency
3. First shock energy in ALS for shockable rhythm is {{c1::200J biphasic}} #Management #Emergency
4. After the 3rd shock in ALS, give {{c1::adrenaline 1 mg IV}} (then every 3-5 min) AND {{c1::amiodarone 300 mg IV bolus}} #Management #Emergency
5. After the 5th shock in ALS, give a second dose of amiodarone {{c1::150 mg IV}} #Management #Emergency
6. For non-shockable rhythms (PEA/asystole), adrenaline is given {{c1::as soon as IV access obtained, then every 3-5 min}} #Management #Emergency
7. Mnemonic for reversible causes in cardiac arrest: "4H + 4T" = {{c1::Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia/Hypoglycaemia/Hypothermia, Hydrogen ions + Thromboembolism, Tension pneumothorax, Tamponade, Toxins}} #Management #Emergency
8. Post-ROSC targeted temperature management (TTM) target is {{c1::32-36°C for 24 hours}} in comatose patients #Management #CutOff
9. Post-ROSC ventilation targets: SpO2 {{c1::94-98%}} and PaCO2 {{c1::35-45 mmHg}} #Management #CutOff
10. Post-ROSC MAP target is ≥{{c1::65 mmHg}} #Management #CutOff
11. After ROSC in suspected ischaemic VF/VT, next best step is {{c1::urgent coronary angiography ± primary PCI}} #NextBestStep #Management

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1. PR interval >{{c1::200ms (>5 small squares)}} = 1st degree AV block — benign, no treatment needed #CutOff #Investigation
2. ECG of Mobitz I (Wenckebach): {{c1::progressive PR lengthening until a QRS is dropped, then cycle repeats}} #Investigation
3. ECG of Mobitz II: {{c1::fixed PR interval with sudden dropped QRS (no PR lengthening before the dropped beat)}} #Investigation #HKMLEtrap
4. Mobitz II 2nd degree AV block requires pacing {{c1::regardless of symptoms}} — high risk of progression to complete block #Management #HKMLEtrap
5. Complete (3rd degree) AV block ECG: {{c1::complete dissociation of P waves and QRS complexes}} (P rate and QRS rate are independent) #Investigation
6. First drug for symptomatic bradycardia is {{c1::atropine 0.5 mg IV, repeat every 3-5 min to max 3 mg}} #Management #NextBestStep
7. Atropine is ineffective (and may worsen) {{c1::Mobitz II and 3rd degree AV block}} — these are infranodal (sub-nodal) in origin #Contraindication #HKMLEtrap
8. If atropine fails in symptomatic bradycardia, next step is {{c1::transcutaneous pacing (external)}} or isoprenaline infusion while awaiting transvenous pacing #NextBestStep #Management
9. Complete AV block in inferior STEMI is usually {{c1::transient}} (AV nodal, due to vagal tone/RCA ischaemia) — resolves with reperfusion; PPM not always needed #HKMLEtrap #Management
10. Complete AV block in anterior STEMI indicates {{c1::massive bilateral bundle branch disease}} — PPM almost always required #Management #HKMLEtrap
11. Mnemonic for causes of bradycardia "HIS DEAD": {{c1::Hyperkalaemia/Hypothyroid, Inferior MI, Surgery/Sarcoidosis, Drugs, Endocarditis, Anterior MI, Degenerative (Lev/Lenègre)}} #Management
12. Class I pacing indication: Mobitz II 2nd degree AV block requires {{c1::permanent pacemaker (PPM) regardless of symptoms)}} #Management #CutOff
13. Class I pacing indication: Complete 3rd degree AV block {{c1::with symptoms}} requires PPM #Management #CutOff
14. Complete heart block persisting >{{c1::2 weeks}} after inferior MI requires PPM #CutOff #Management

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1. Beck's Triad = {{c1::hypotension + elevated JVP + muffled heart sounds}} #Investigation #Diagnosis
2. Pulsus paradoxus = SBP drop >{{c1::10 mmHg}} on inspiration — hallmark of tamponade #CutOff #Investigation
3. ECG finding pathognomonic of cardiac tamponade is {{c1::electrical alternans}} (alternating QRS amplitude) + low voltage #Investigation
4. Gold standard investigation for cardiac tamponade is {{c1::echocardiogram}} — shows pericardial effusion and RA/RV diastolic collapse #Investigation #NextBestStep
5. CXR finding in cardiac tamponade: {{c1::"water bottle" globular enlarged cardiac silhouette}} (if >250 mL) — may be normal in acute tamponade #Investigation
6. Next best step in haemodynamically unstable cardiac tamponade is {{c1::emergency pericardiocentesis (subxiphoid approach)}} #NextBestStep #Emergency
7. Pericardiocentesis approach: needle at {{c1::45° towards the left shoulder}} via subxiphoid route; ECG-guided — ST elevation indicates myocardium contact #Management
8. Diuretics and vasodilators are absolutely contraindicated in cardiac tamponade because they {{c1::reduce preload, precipitating cardiac arrest}} #Contraindication #HKMLEtrap
9. IV fluids in cardiac tamponade serve to {{c1::maintain preload as a bridge to pericardiocentesis}} — give cautiously #Management
10. Kussmaul's sign (JVP rises on inspiration) is seen in {{c1::cardiac tamponade AND constrictive pericarditis}} #Investigation
11. Mnemonic for cardiac tamponade causes "TRAUMA CATS": {{c1::Trauma, Renal failure, Aortic dissection, Uraemia, Malignancy, Autoimmune, Cardiac surgery, Anticoagulation, TB, Sepsis}} #Management

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1. Stanford Type A aortic dissection involves {{c1::the ascending aorta}} (regardless of origin) → emergency surgery #Management #Emergency
2. Stanford Type B aortic dissection involves {{c1::the descending aorta only (distal to left subclavian)}} → medical management #Management
3. DeBakey Type I dissection extends from {{c1::ascending aorta through the arch to the descending aorta}} #CutOff
4. DeBakey Type III = Stanford {{c1::Type B}} (descending only) #CutOff
5. #1 modifiable risk factor for aortic dissection is {{c1::hypertension}} (~70% of cases) #Management
6. Classic pain of aortic dissection is {{c1::sudden-onset tearing/ripping pain, maximal at onset, radiating to the back}} — differentiates from MI #Investigation #Diagnosis
7. BP differential >{{c1::20 mmHg}} between arms suggests subclavian involvement in aortic dissection #CutOff #Investigation
8. Gold standard investigation for aortic dissection is {{c1::CT aortogram}} #Investigation #NextBestStep
9. Low D-dimer has {{c1::high negative predictive value}} for ruling out aortic dissection #Investigation
10. Thrombolytics are absolutely contraindicated in aortic dissection because they cause {{c1::haemorrhage into the false lumen → haemopericardium → tamponade → death}} #Contraindication #HKMLEtrap #Emergency
11. BP target in acute aortic dissection is SBP {{c1::100-120 mmHg}} + HR <{{c1::60 bpm}} #CutOff #Management
12. First-line drug for BP control in aortic dissection is {{c1::IV labetalol or IV esmolol (beta-blocker first)}} #Management #NextBestStep
13. In aortic dissection, vasodilator (nitroprusside) must NEVER be given without a beta-blocker because {{c1::reflex tachycardia increases aortic wall stress and propagates the dissection}} #Contraindication #HKMLEtrap
14. In Type A dissection with cardiac tamponade, pericardiocentesis should be {{c1::cautious and minimal (just enough to stabilise)}} — aggressive drainage before surgery can worsen dissection #HKMLEtrap #Management
15. ACEi/ARB/ARNI are contraindicated in aortic dissection during pregnancy — use {{c1::hydralazine + IV labetalol/nicardipine}} for BP control #Contraindication
16. Mnemonic "Stanford A = {{c1::Ascending = Awful = Acute surgery}}" #Management

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1. EAST-AFNET 4 trial showed that {{c1::early rhythm control}} (within 1 year of AF diagnosis) reduced CV outcomes — 2020 paradigm shift #Management #AF
2. AFFIRM trial showed {{c1::no mortality difference}} between rate control and rhythm control strategies in AF #Management #AF
3. RACE II trial showed lenient rate control (<{{c1::110 bpm}}) is non-inferior to strict rate control (<80 bpm) in AF outcomes #CutOff #Management #AF
4. CAST trial showed flecainide/encainide increased mortality in {{c1::structural heart disease post-MI}} — no antiarrhythmic should be used empirically post-MI #HKMLEtrap #Management
5. ARISTOTLE trial: apixaban vs warfarin in AF — apixaban reduced {{c1::stroke, mortality, AND major bleeding}} #Management #AF
6. REVERT trial: Modified Valsalva converts SVT in {{c1::~43%}} vs ~17% for standard Valsalva #Management #SVT
7. MADIT-II: ICD in post-MI patients with EF ≤30% reduced total mortality by {{c1::31%}} #Management
8. HK Good Samaritan Ordinance (effective 2021) protects laypersons using an AED in good faith from {{c1::civil liability}} #Management
9. Patients with uncontrolled VT, complete heart block, recent ICD shock, or recent syncope should be advised {{c1::not to drive}} and to notify the Transport Department (Cap. 374) #Management

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HKMLE Module 1C — Arrhythmias + Cardiac Emergencies: MCQ Bank

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HARDEST QUESTION IDENTIFIED

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5 VARIATIONS ON QUESTION 3 — AF + WPW / FORBIDDEN DRUGS

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HKMLE MODULE 1D: VALVULAR + PERICARDIAL + CARDIOMYOPATHIES + INFECTIVE ENDOCARDITIS

ACE-Level Comprehensive Study Note

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📌 QUICK SUMMARY TABLE

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PART 1: VALVULAR HEART DISEASE

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SECTION 1: AORTIC STENOSIS (AS)

Definition

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Classification

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Aetiology / Causes

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Pathophysiology

Valve orifice narrows → Resistance to LV outflow ↑
    ↓
LV must generate higher pressure to eject blood → Pressure overload
    ↓
CONCENTRIC LV HYPERTROPHY (LVH) — thicker walls, normal/small cavity
    ↓
LVH initially compensates (increased wall stress distribution)
    ↓
LATE DECOMPENSATION:
    → Diastolic dysfunction (stiff LV → requires atrial kick → loss of AF = acute decompensation)
    → Coronary insufficiency (increased O2 demand by hypertrophied muscle, reduced diastolic time)
    → Subendocardial ischaemia → angina (even without CAD)
    → Eventually: LV dilatation, systolic failure, low output
    ↓
SYMPTOMS APPEAR: SAD (Syncope, Angina, Dyspnoea) — median survival ↓ precipitously

• LVH causes increased O2 demand AND impaired coronary flow reserve (compressed subendocardial vessels) → angina without obstructive CAD
• Baroreceptor malfunction during Valsalva/exertion → syncope (peripheral vasodilation + fixed low output)
• Paradoxical splitting of S2 (A2 delayed by prolonged ejection — occurs AFTER P2)
• Gallavardin phenomenon: AS murmur radiates to apex, mimicking MR — distinguished by its musical quality and radiation to carotids

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Risk Factors

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Symptoms — "SAD"

SAD = the 3 D's — once symptoms develop, mortality escalates dramatically. Any symptom = indication for surgery.

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Signs

1. General: Dyspnoea at rest? Cachexia?
2. Pulse: Slow-rising carotid — describe character ("pulsus parvus et tardus")
3. BP both arms: Check pulse pressure (<40 mmHg = severe)
4. JVP: Note a-wave prominence (RVH from pulmonary hypertension late)
5. Apex beat: Palpate — sustained, non-displaced (heaving)
6. Thrill: Palpate 2nd right intercostal space and suprasternal notch
7. Auscultation: Position patient sitting forward — ejection systolic murmur peaking mid-systole, S2 quality, ejection click
8. Carotid transmission: Place stethoscope over carotids
9. State: "I would perform dynamic auscultation (standing/squatting) and arrange echocardiogram" Examiner make-or-break: Describe the pulse character before the murmur — this differentiates AS from other ejection systolic murmurs.

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Investigations

• AVA 0.75 cm², mean gradient 52 mmHg, peak velocity 4.6 m/s, LVEF 55%, concentric LVH
• Interpretation: "Severe aortic stenosis with preserved LV function — symptomatic patient → indication for valve replacement; TAVI vs SAVR decision based on surgical risk"

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Management

Indications for Intervention (Class I):

TAVI vs SAVR Decision:

Patient identified for AVR
    ↓
Assess surgical risk (STS score, EuroSCORE II)
    ↓
High surgical risk (STS ≥8% or EuroSCORE II ≥8%) → TAVI preferred
    ↓
Intermediate risk (STS 4-8%) → Heart Team decision (TAVI or SAVR)
    ↓
Low surgical risk (STS <4%, age <70, no anatomical barriers) → SAVR preferred
    ↓
Anatomical barriers to TAVI? (unfavourable iliofemoral access, severe AR, bicuspid) → SAVR

• TAVI in HK: Performed at QMH, QEH, PWH, Grantham Hospital
• "Heart Team" approach: interventional cardiologist + cardiac surgeon + structural heart disease specialist
• Pre-TAVI: CT aortogram (256-slice), coronary angiogram mandatory
• Post-TAVI: Dual antiplatelet for 3-6 months (aspirin + clopidogrel), then aspirin lifelong
• SAVR mechanical valve: Warfarin INR 2.5-3.5 (aortic), 3.0-4.0 (mitral) lifelong
• SAVR bioprosthetic: Anticoagulation 3 months post-op only, then aspirin

Medical Management (Pre-surgery / Inoperable):

• NO proven medical therapy slows AS progression
• Statin trials (SALTIRE, SEAS) showed no benefit in preventing AS progression
• Treat HF symptoms cautiously (diuretics) — avoid vasodilators (reduce preload → syncope)
• AVOID nitrates, ACEi, ARB, CCB in severe symptomatic AS — cause hypotension
• Treat AF urgently (atrial kick critical in stiff LV)

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SECTION 2: AORTIC REGURGITATION (AR)

Definition

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Aetiology

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Pathophysiology

CHRONIC AR:
Gradual volume overload → LV dilates (eccentric hypertrophy)
    ↓
Large stroke volume ejected = wide pulse pressure
    ↓
Compensation maintained for years (asymptomatic)
    ↓
Eventually: LV systolic dysfunction → symptoms
    ↓
Intervention needed BEFORE irreversible LV dysfunction

ACUTE AR (emergency — endocarditis, dissection):
Sudden regurgitant volume → normal-sized LV cannot accommodate
    ↓
↑↑ LV end-diastolic pressure → pulmonary oedema
    ↓
Low forward output → cardiogenic shock
    ↓
Premature mitral valve closure (LV pressure exceeds LA pressure)
    ↓
EMERGENCY surgery often required

• In chronic AR: LV compensates by eccentric hypertrophy (Frank-Starling) — cavity dilates but wall tension is maintained
• Wide pulse pressure (systolic BP high, diastolic BP low) — high stroke volume + blood runs back into aorta
• Peripheral vascular signs are ALL manifestations of high stroke volume + wide pulse pressure

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Symptoms

• Chronic AR: Palpitations (bounding pulse awareness), exertional dyspnoea, orthopnoea, PND, fatigue
• Acute AR: Acute pulmonary oedema, cardiogenic shock — NO time for compensation

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Signs

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Investigations

• Echo (TTE/TOE): Regurgitant severity (colour flow, EROA, vena contracta), LV size (LVESD/LVEDD), LVEF, aortic root diameter — MOST IMPORTANT for surgical timing
• ECG: LVH, volume overload pattern
• CXR: Cardiomegaly (cardiothoracic ratio >0.5), dilated aortic root/knuckle
• CT aortogram: If aortic dissection suspected or aortic root >45mm

• Severe AR on colour flow, LVESD 55mm, LVEF 48%, aortic root 4.5 cm, moderate LVH
• Interpretation: "Severe AR with borderline LV dysfunction (EF approaching 50%) and dilated LV — surgical indication present even though minimally symptomatic"

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Surgical Indications

• Vasodilators (nifedipine, ACEi/ARB) reduce afterload — used in chronic severe AR when surgery not feasible or as bridge
• Rate control — faster HR reduces diastolic filling time, less regurgitant time
• Acute severe AR: vasodilators (nitroprusside) + dobutamine as bridge to emergency surgery
• AVOID beta-blockers in severe AR — bradycardia prolongs diastole, worsening regurgitation

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SECTION 3: MITRAL STENOSIS (MS)

Definition

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Aetiology

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Pathophysiology

Rheumatic fever → Mitral leaflet inflammation → Scarring → Commissural fusion
    ↓
Mitral valve orifice narrows → Obstruction to LA→LV flow
    ↓
LA pressure ↑ → LA dilatation
    ↓
Pulmonary venous pressure ↑ → Pulmonary hypertension
    ↓
RV pressure overload → RV hypertrophy → RV failure (raised JVP, oedema, ascites)
    ↓
LA dilatation → AF (30-40% of MS patients)
    ↓
AF → Loss of atrial kick → Acute deterioration + Thrombus in LAA → Stroke
    ↓
Exercise / Tachycardia → Shorter diastolic filling time → Acute pulmonary oedema

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Symptoms

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Signs

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Investigations

• Absent P waves, irregularly irregular QRS, right axis deviation, R:S >1 in V1
• Interpretation: "AF with right axis deviation indicating right ventricular hypertrophy — suggests established pulmonary hypertension from severe MS"

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Management

Indications for Intervention:

• Leaflet mobility (1-4 points)
• Leaflet thickening (1-4 points)
• Calcification (1-4 points)
• Subvalvular thickening (1-4 points)

• Rate control for AF: Beta-blockers, digoxin, diltiazem
• Anticoagulation: Warfarin (INR 2-3) for AF + MS — DOACs are CONTRAINDICATED (moderate-severe rheumatic MS = valvular AF)
• Diuretics: Symptom relief (reduce pulmonary congestion)
• Rheumatic fever prophylaxis: Benzathine penicillin (see Section 5)

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SECTION 4: MITRAL REGURGITATION (MR)

Definition

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Aetiology

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Acute vs Chronic MR Pathophysiology

Sudden large regurgitant volume into non-dilated LA
    ↓
↑↑ LA pressure → acute pulmonary oedema
    ↓
Normal-sized LA cannot buffer the volume
    ↓
Forward output ↓↓ → cardiogenic shock
    ↓
Emergency surgery needed

Gradual regurgitation → LA dilates (accommodates volume)
    ↓
LV volume overload → eccentric hypertrophy → LV dilates
    ↓
Compensation maintained for years
    ↓
LVEF may appear falsely normal/high (easy ejection into low-resistance LA)
    ↓
Decompensation: EF falls, LV cannot compensate
    ↓
Surgical threshold: symptoms OR EF <60% OR LVESD >45mm

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Symptoms

• Chronic: Exertional dyspnoea, fatigue, palpitations (AF from LA dilatation)
• Acute: Sudden severe dyspnoea, pulmonary oedema, haemoptysis, cardiogenic shock
• MVP-specific: Atypical chest pain, palpitations, anxiety

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Signs

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Investigations

• Echo (TTE/TOE): Severity, mechanism (leaflet prolapse, flail leaflet, functional), LVEF, LVESD, LA size, PHT
• Exercise echo: If symptoms unclear
• TOE: Better visualisation of leaflets, pre-surgical planning

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Surgical Indications

• Mitral valve repair (not replacement) is the gold standard where possible — performed at QMH, QEH, PWH
• Transcatheter mitral repair (MitraClip) available at selected HA centres for high surgical risk patients with severe functional or degenerative MR
• Pre-operative: TOE mandatory; coronary angiogram if age >40 or risk factors

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SECTION 5: RHEUMATIC HEART DISEASE (RHD)

Definition

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Jones Criteria (2015 AHA Revision)

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Secondary Prophylaxis

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PART 2: PERICARDIAL DISEASE

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SECTION 6: ACUTE PERICARDITIS

Definition

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Aetiology

• Subacute onset, weight loss, night sweats, fever
• Effusion + haemorrhagic fluid on pericardiocentesis
• Chinese/immigrant patient with TB risk factors → Consider TB pericarditis; send pericardial fluid for AFB, PCR, culture + biopsy

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Clinical Features

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ECG Changes

Stage 1 (hours-days): Diffuse saddle-shaped ST elevation (concave up) + PR depression
    ↓
Stage 2 (days): ST returns to baseline, PR still depressed
    ↓
Stage 3 (days-weeks): Diffuse T-wave inversions (ST now isoelectric)
    ↓
Stage 4 (weeks): ECG normalises

• Diffuse concave-up ST elevation in I, II, III, aVL, aVF, V2-V6; PR segment depression in II and V4-V6; PR elevation in aVR; no reciprocal changes; no Q waves
• Interpretation: "Diffuse saddle-shaped ST elevation with PR depression in multiple leads — consistent with acute pericarditis Stage 1; no regional distribution or reciprocal changes to suggest STEMI"

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Investigations

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Management

• Fever >38°C
• Purulent/TB/malignant aetiology suspected
• Troponin elevated (myopericarditis)
• Effusion >20mm
• Haemodynamic compromise
• Immunosuppressed / oral anticoagulation

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SECTION 7: CARDIAC TAMPONADE

Key Points for Module 1D Context

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SECTION 8: CONSTRICTIVE PERICARDITIS

Definition

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Aetiology

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Clinical Features

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Constrictive Pericarditis vs Cardiac Tamponade vs Restrictive CMP

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Investigations

• CXR (lateral): Pericardial calcification (eggshell appearance)
• Echo: Normal LV function, biatrial enlargement, thickened pericardium, septal bounce (septal shift with respiration), dilated IVC
• CT/MRI: Pericardial thickening >3mm (CT) — MRI distinguishes constrictive from restrictive CMP
• Right heart catheterisation (RHCS): "Dip-and-plateau" (square root sign) — hallmark of constriction: rapid early diastolic fall, then abrupt rise and plateau; equalisation of RVEDP, LVEDP, PAOP within 5 mmHg of each other

• RVEDP 18 mmHg = LVEDP 19 mmHg = PAOP 18 mmHg; dip-and-plateau pattern on RV pressure waveform
• Interpretation: "Equalisation of diastolic filling pressures within 5 mmHg + square root sign = diagnostic of constrictive pericarditis"

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Management

• Curative: Pericardiectomy (surgical stripping of pericardium) — indicated in symptomatic constriction
• Pre-operative management: Diuretics for congestion
• TB constrictive pericarditis: Full antitubercular treatment first (2HRZE + 4HR); corticosteroids may reduce progression to constriction (prednisolone during initial treatment)
• Post-surgery: Improvement may be delayed 3-6 months as myocardium recovers

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PART 3: CARDIOMYOPATHIES

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SECTION 9: DILATED CARDIOMYOPATHY (DCM)

Definition

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Aetiology

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Pathophysiology

Myocardial injury → Loss of cardiomyocytes + fibrosis
    ↓
LV dilates (eccentric remodelling) → decreased contractility
    ↓
LVEF ↓ → neurohormonal activation (same as HFrEF Module 1B)
    ↓
Progressive dilation → functional MR (papillary muscle displacement)
    ↓
Arrhythmia substrate (fibrosis) → VT/VF + SCD risk
    ↓
Mural thrombus (dilated LV, stasis) → emboli

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Management

• 4 pillars: Beta-blocker + ACEi/ARB/ARNI + MRA + SGLT2i
• ICD: If LVEF ≤35% after ≥3 months GDMT
• CRT: If LVEF ≤35% + LBBB + QRS ≥150ms
• Anticoagulation: If LVEF very low (<25%) or mural thrombus detected on echo
• Genetic testing: Offer to all first-degree relatives
• Alcohol DCM: Strict alcohol cessation — LVEF may improve significantly
• Tachycardia DCM: Rate control (or rhythm control if AF) — LVEF may fully recover
• Peripartum CMP: Bromocriptine (prolactin inhibition) + standard HF therapy (avoid RAAS in breastfeeding)
• End-stage (Stage D): LVAD as bridge to transplant; cardiac transplant

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SECTION 10: HYPERTROPHIC CARDIOMYOPATHY (HCM)

Definition

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Genetics

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Pathophysiology

Sarcomere gene mutation → Disorganised, hypertrophied myocytes ("myofibre disarray")
    ↓
ASYMMETRIC SEPTAL HYPERTROPHY (ASH) — usually septum > posterior wall
    ↓
LVOT OBSTRUCTION (in 70% — "obstructive HCM"):
    Narrow LVOT → Venturi effect → draws anterior mitral leaflet into LVOT
    (SAM — systolic anterior motion of mitral valve)
    → Dynamic LVOT obstruction + MR
    ↓
Diastolic dysfunction (stiff LV) → elevated filling pressures → dyspnoea
    ↓
Microvascular ischaemia (small vessel disease) → angina, fibrosis
    ↓
Arrhythmia substrate (myofibre disarray + fibrosis) → VT/VF/SCD
    ↓
Obstructed outflow + limited filling → exercise syncope

• LVOT obstruction is DYNAMIC — worsens with: decreased preload (dehydration, standing, Valsalva), decreased afterload (vasodilators), increased contractility (sympathetic stimulation, digoxin)
• Murmur INCREASES with Valsalva (decreases preload → worsens obstruction) — classic exam point
• Murmur DECREASES with squatting (increases preload → reduces obstruction)
• SAM (systolic anterior motion) of anterior mitral leaflet is the mechanism of LVOT obstruction in most cases

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Symptoms

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Signs

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Investigations

• Asymmetric septal hypertrophy (IVS 20mm, posterior wall 10mm), SAM of anterior mitral leaflet, resting LVOT gradient 65 mmHg, moderate MR
• Interpretation: "Obstructive HCM with severe resting LVOT obstruction — symptoms + LVOT gradient ≥50 mmHg = intervention indicated (septal reduction therapy)"

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Management

Medical:

Drugs to AVOID in HCM with LVOT obstruction:

Septal Reduction Therapy (for severe obstructive HCM + symptoms despite max medications):

ICD Implantation for SCD Prevention:

• HCM management at HA: Dedicated HCM clinics at QMH and QEH
• Genetic testing and cascade family screening available at Clinical Genetics Service
• ICD implantation at QMH, QEH, PWH, PYNEH
• Alcohol septal ablation and surgical myectomy available at QMH/QEH
• Mavacamten: Pending HA Drug Formulary approval (available privately in HK as of 2024)

• HCM and driving: Competitive athletes with HCM should be restricted from competitive sports (HK Sports Medicine Federation guidelines)
• Patients with ICD or recent syncope from HCM: refer to Transport Department for driving assessment (Cap. 374)
• HCM in competitive athletes in HK: Pre-participation screening required for professional athletes; echo + ECG at least once

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SECTION 11: RESTRICTIVE CARDIOMYOPATHY (RCM)

Definition

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Aetiology

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Features Distinguishing RCM from Constrictive Pericarditis:

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Management

• Amyloidosis (ATTR): Tafamidis (ATTRvx + ATTRwt) — ATTR-ACT trial: 30% mortality reduction; now standard of care
• Haemochromatosis: Venesection (reduces iron load, may improve cardiac function if early)
• Sarcoidosis: Corticosteroids; ICD if VT/heart block
• Symptomatic: Diuretics carefully (preload dependent); anticoagulation if AF or EF very low

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SECTION 12: ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY (ARVC)

Definition

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Genetics

• Desmoplakin (DSP), Plakophilin-2 (PKP2), Desmoglein-2 (DSG2) — desmosome proteins (~50% of cases)
• Autosomal dominant (variable penetrance)
• Naxos disease: Autosomal recessive ARVC + palmoplantar keratoderma + woolly hair (plakoglobin mutation)

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Pathophysiology

Desmosome mutation → Defective cell-cell adhesion in RV myocardium
    ↓
Apoptosis + fibrofatty replacement (RV free wall → "fatty replacement")
    ↓
RV dilatation + aneurysms + regional wall motion abnormalities
    ↓
Arrhythmia substrate (re-entry around fibrofatty scars) → VT originating from RV
    ↓
VT is LBBB morphology (originating in RV — right-sided conduction → LBBB pattern on ECG)
    ↓
Exercise triggers VT → SCD in young athletes

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ECG Features

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Clinical Features

• Young athlete with exercise-induced palpitations/syncope/VT
• VT with LBBB morphology (RV origin)
• Family history of SCD or ARVC

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Diagnosis — Task Force Criteria

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Management

• ICD: Recommended for all ARVC patients with sustained VT or VF; consider for high-risk features
• Beta-blockers: Reduce VT burden
• Sotalol/amiodarone: Antiarrhythmic therapy
• Catheter ablation: For recurrent VT (not curative — disease progresses)
• Exercise restriction: All ARVC patients should avoid competitive/endurance sports
• Genetic counselling + cascade screening: First-degree relatives

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PART 4: INFECTIVE ENDOCARDITIS (IE)

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SECTION 13: INFECTIVE ENDOCARDITIS

Definition

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Classification

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Aetiology — Microorganisms

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Modified Duke Criteria

Diagnosis Classification:

• Definite IE: 2 major criteria OR 1 major + 3 minor OR 5 minor criteria
• Possible IE: 1 major + 1 minor OR 3 minor criteria
• Rejected: Alternative diagnosis OR resolution with antibiotic ≤4 days OR no pathological evidence at surgery/autopsy after ≤4 days antibiotics

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Clinical Features

1. General: Fever, sweats, cachexia, pallor (anaemia)
2. Hands: Splinter haemorrhages (proximal), Osler's nodes (painful), Janeway lesions (painless), clubbing, peripheral stigmata of immunosuppression
3. Eyes: Conjunctival petechiae, Roth spots (fundoscopy)
4. Mouth: Dental hygiene (source!), mucosal petechiae
5. JVP: Elevated (HF from valvular destruction)
6. Cardiac: New regurgitant murmur; change from previous murmur
7. Spleen: Splenomegaly (tender)
8. Urine dipstick: Haematuria (immune complex GN)
9. Neurological: Focal deficit (embolic stroke) Examiner make-or-break: Examine the hands thoroughly for ALL peripheral stigmata, then proceed to fundoscopy — state "I would arrange fundoscopy to look for Roth spots."

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Investigations

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Management

Antibiotic Regimens:

• All suspected IE in HK HA: Admit, blood cultures x3 within 1 hour, TTE same day, infectious disease/cardiology co-management
• TOE arranged within 24-48h if TTE non-diagnostic
• Benzylpenicillin: Standard HA formulation for Strep IE
• Vancomycin trough monitoring: Target 15-20 mg/L (conventional); AUC/MIC-guided dosing increasingly used at HA
• Gentamicin: Dose-once-daily regimen with renal monitoring; avoid prolonged use (nephrotoxicity + ototoxicity)
• Surgical referral: If ANY indication for surgery (see below)

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Indications for Emergency/Urgent Surgery

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IE Prophylaxis

• HK HA practice: Follow AHA/ESC high-risk categories for IE prophylaxis
• High-risk patients: Prosthetic valves, prior IE, unrepaired cyanotic CHD, cardiac transplant with valve disease, TAVI prostheses
• Drug: Amoxicillin 2g oral 30-60 min before dental procedure
• If penicillin allergy: Clindamycin 600 mg oral OR azithromycin/clarithromycin 500 mg oral
• NOT required for: GI/GU procedures, endoscopy, cardiac catheterisation, UNLESS active infection present
• HK Practitioner (2015): Confirmed HK practice diverges from NICE — prophylaxis maintained for high-risk cases

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Complications

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🚨 RED FLAGS BOX

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❓ COMMON EXAM QUESTION BOX

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⚠️ DRUG TRAPS TABLE

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📊 NOTABLE TRIALS TABLE

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🧠 MASTER MNEMONICS TABLE

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🔗 CROSS-MODULE LINKS

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• Valvular heart disease + driving (HK): Severe AS with syncope — must not drive; notify Transport Department under Cap. 374 Road Traffic Ordinance until treated
• ICD in structural heart disease: Patients with ICD — commercial driving prohibited; private driving after specialist clearance (no ICD shock for ≥6 months typically)
• HCM in competitive athletes (HK): Athletes with HCM should be restricted from competitive sport — Sports Medicine Federation HK guidelines; no specific HK legislation but medical standard of care applies
• IE and occupational exposure: Healthcare workers with bloodborne infection risk (IV catheter-related IE) — incident reporting required under HA policies
• Advanced Directive in severe valvular disease: Patients declining TAVI/surgery — respect autonomy; document in HA ACP framework; provide palliative symptom management
• TB pericarditis: TB is a statutory notifiable disease in HK — notify Department of Health within 24 hours under Infectious Disease Regulations (Cap. 559)

• Tuberculosis (including TB pericarditis, TB constrictive pericarditis): STATUTORY NOTIFIABLE — notify within 24 hours
• Group A Streptococcal infection causing scarlet fever (precipitant of rheumatic fever): STATUTORY NOTIFIABLE
• IE itself, valvular disease, cardiomyopathies: NOT notifiable
• Chagas disease (rare cause of DCM in imported cases): Consider public health notification if identified