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Arrhythmia & Heart Block — Full Coverage for HKMLE

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SECTION 1: BASICS OF CARDIAC CONDUCTION

Normal Conduction Pathway

Some Athletes Have Big Power

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SECTION 2: SINUS NODE DISORDERS

Sinus Bradycardia

• Rate < 60 bpm, normal P wave, normal PR interval
• Causes: Athletes (physiological), vasovagal, inferior MI, hypothyroidism, ↑ICP (Cushing reflex), drugs (β-blockers, digoxin, amiodarone, verapamil)
• Treatment: Atropine if symptomatic; permanent pacing if refractory

Sinus Tachycardia

• Rate > 100 bpm, normal P wave
• Always secondary (pain, fever, anaemia, thyrotoxicosis, CCF, PE, hypovolaemia)
• Treatment: treat underlying cause

Sick Sinus Syndrome (SSS)

• Alternating bradycardia + tachycardia ("tachy-brady syndrome")
• ECG: sinus pauses, SA block, junctional escape
• Treatment: Permanent pacemaker (PPM) ± anticoagulation if AF component

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SECTION 3: HEART BLOCK (AV BLOCK)

Classification Mnemonic: "1st = Delay, 2nd = Drop, 3rd = Divorce"

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First-Degree AV Block

• ECG: PR interval > 0.20 s (200 ms) in adults; every P conducted to ventricle
• All P waves conducted — just delayed
• Usually benign; can progress if vagal tone increases or rate speeds
• Causes: Increased vagal tone, inferior MI, digoxin, myocarditis, hyperkalaemia
• No treatment needed; stop causative drugs

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Second-Degree AV Block

Mobitz Type I (Wenckebach) — "Progressive PR, then DROP"

• PR interval progressively lengthens → QRS suddenly drops
• RR interval shortens progressively before the dropped beat
• Site: AV node (usually benign)
• Causes: Inferior MI, high vagal tone, inferior myocarditis, digoxin toxicity
• Treatment: Usually none; atropine if symptomatic; PPM rarely needed
• Key ECG feature: PR after the pause is the shortest in the cycle

Mobitz Type II — "Sudden DROP without warning"

• Fixed PR interval, then sudden non-conducted P wave (no preceding PR lengthening)
• Site: His-Purkinje system (bundle of His / bundle branches) — infranodal ⚠️
• Causes: Anterior MI, fibrosis of His-Purkinje (Lev's / Lenegre's disease), sarcoidosis, SLE
• Always pathological — high risk of progression to complete heart block
• Treatment: Permanent pacemaker (temporary pacing acutely)
• Atropine is INEFFECTIVE or may worsen (increases atrial rate, worsens ratio)

2:1 AV Block

• Every other P wave dropped; cannot always distinguish Wenckebach vs Type II
• Wide QRS → Type II likely (infranodal); Narrow QRS → Wenckebach likely (nodal)

High-Grade (Advanced) AV Block

• ≥2 consecutive P waves blocked
• Invariably requires pacing

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Third-Degree (Complete) AV Block

• ECG: Regular P waves + regular QRS, but NO relationship between them (AV dissociation)
• PR intervals vary randomly; PP interval regular; RR interval regular
• QRS: narrow (junctional escape, ~40–60 bpm) or wide (ventricular escape, ~20–40 bpm)

• Causes:
  • Congenital: maternal SLE (anti-Ro/La antibodies)
  • Acquired: Inferior MI (nodal — often reversible), Anterior MI (infranodal — often permanent), Lyme disease, sarcoidosis, surgical/catheter trauma, digoxin toxicity
• Symptoms: Stokes-Adams attacks (sudden syncope, pallor → flushing), heart failure, presyncope
• Treatment: Temporary pacing → Permanent pacemaker

• Lyme disease, Ischaemia (MI), Congenital (neonatal), Amiodarone/drugs, Myocarditis, Digoxin toxicity, Sarcoidosis/SLE

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Lev's Disease vs Lenegre's Disease

• Lev's: Calcification extending from aortic/mitral annulus → His bundle → bundle branches
• Lenegre's: Primary idiopathic sclerodegenerative fibrosis of bundle branches
• Both → bundle branch block → Mobitz II → complete heart block

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SECTION 4: BUNDLE BRANCH BLOCKS

• LBBB: W in V1, M in V6 (WiLLiaM)
• RBBB: M in V1, W in V6 (MaRRoW)

Left Bundle Branch Block (LBBB)

• QRS ≥ 0.12 s (120 ms), broad notched R in V5/V6 (M shape = "LBBB"), deep S in V1
• Axis: left axis deviation
• Always pathological — investigate for underlying structural disease
• Causes: IHD, hypertension, cardiomyopathy, aortic stenosis
• New LBBB in chest pain: treat as STEMI equivalent (Sgarbossa criteria)

Right Bundle Branch Block (RBBB)

• QRS ≥ 0.12 s, RSR' pattern in V1/V2 ("M" pattern), wide S in V5/V6
• May be normal variant (isolated RBBB without structural disease)
• Causes: RV strain (PE — classic), congenital heart disease (ASD), ischaemia, Brugada syndrome
• Incomplete RBBB: QRS 100–119 ms, same pattern — common in athletes

Bifascicular Block

• RBBB + left anterior fascicular block (LAD) — most common
• Risk of progression to complete heart block

Trifascicular Block

• RBBB + LAFB + long PR (1st-degree AV block) → implies all 3 fascicles impaired
• High risk → consider prophylactic PPM

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SECTION 5: SUPRAVENTRICULAR TACHYARRHYTHMIAS

Atrial Fibrillation (AF)

• Pulmonary (PE, pneumonia)
• Ischaemia/Infarction
• Rheumatic heart disease (mitral stenosis most common valvular cause)
• Alcohol ("holiday heart"), Anaemia, Atrial septal defect
• Thyrotoxicosis (most common reversible cause — check TFTs in new AF)
• Electrolytes (hypokalaemia, hypomagnesaemia)
• Sepsis / Surgery

AF Rate Classification:

Haemodynamic impact: Loss of atrial "kick" = ↓ CO by ~20%

STROKE RISK — CHA₂DS₂-VASc Score

• Score ≥ 2 in males, ≥ 3 in females → anticoagulate
• DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin (except valvular AF / severe renal impairment — use warfarin)
• Valvular AF (mechanical valve / moderate-severe mitral stenosis) → warfarin ONLY

BLEEDING RISK — HAS-BLED Score

AF Management:

• β-blockers (metoprolol, bisoprolol) — first-line
• Calcium channel blockers (diltiazem, verapamil) — avoid in HFrEF
• Digoxin — poor rate control with exercise; useful in sedentary/CCF

• Pharmacological: Flecainide ("pill-in-the-pocket" in structurally normal heart), amiodarone (AF with structural disease), ibutilide
• Electrical (DC cardioversion): synchronized shock
• 48-hour rule: AF > 48 hours → anticoagulate for ≥ 3 weeks before cardioversion OR perform TOE to exclude LA thrombus first; then anticoagulate for ≥ 4 weeks after
• AF < 48 hours: cardiovert without pre-anticoagulation (but still anticoagulate post)

• Pulmonary vein isolation (catheter ablation) — treatment of choice for symptomatic paroxysmal AF failing drugs
• Left atrial appendage occlusion (e.g., WATCHMAN device) — for patients unsuitable for anticoagulation

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Atrial Flutter

• Rate: Atrial 300 bpm → typically 2:1 block → ventricular rate ~150 bpm
• ECG: Sawtooth flutter waves in II, III, aVF; isoelectric baseline absent
• "Classic" atrial flutter: counter-clockwise re-entry around tricuspid annulus (typical)
• Management: Same as AF for anticoagulation; radiofrequency ablation very effective (>95%)
• Rate control: β-blockers, digoxin, CCBs; cardioversion if haemodynamically unstable

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AV Nodal Re-entrant Tachycardia (AVNRT)

• Mechanism: Re-entry circuit within AV node (fast + slow pathways)
• ECG: Regular narrow-complex tachycardia, HR 150–250 bpm, P waves buried in or just after QRS (RP interval very short, < 70 ms)
• Demographics: Usually young women, no structural heart disease
• Typical (slow-fast): Antegrade via slow pathway, retrograde via fast → retrograde P at end of QRS ("pseudo-R'" in V1, "pseudo-S" in inferior leads)

1. Vagal manoeuvres (Valsalva, carotid sinus massage) — first-line
2. Adenosine IV 6 mg → 12 mg if no response (DON'T use in asthma/Wolff-Parkinson-White with AF)
3. Verapamil or β-blockers if adenosine fails
4. DC cardioversion if haemodynamically unstable
5. Long-term prevention: Radiofrequency ablation (curative, >95% success), or AV nodal-blocking drugs

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AV Re-entrant Tachycardia (AVRT) / Wolff-Parkinson-White (WPW)

• Actually: Short PR (< 120 ms) + Delta wave (slurred QRS upstroke) + Wide QRS (> 120 ms)
• Pre-excitation: accessory pathway (Bundle of Kent) bypasses AV node → ventricle depolarises earlier

WPW Tachycardias:

• Treatment: Procainamide or DC cardioversion; long-term: radiofrequency ablation (curative)

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SECTION 6: VENTRICULAR ARRHYTHMIAS

Ventricular Premature Beats (VPBs / PVCs)

• Wide bizarre QRS without preceding P wave; followed by compensatory pause
• Usually benign if structurally normal heart; treat underlying cause (↓K⁺, ↑catecholamines)
• Concern if: frequent (>10,000/day), R-on-T phenomenon, multifocal, symptomatic

Ventricular Tachycardia (VT)

• ≥ 3 consecutive ventricular beats at rate ≥ 100 bpm
• ECG: Wide complex (≥ 0.12s), regular, AV dissociation (independent P waves), rate usually 100–280 bpm

• Broad QRS > 0.14 s
• Regular but with AV dissociation (cannon a waves clinically)
• Origin — concordance (all positive or all negative in V1-V6)
• Axis — extreme right axis (northwest axis, −150° to −180°)
• Delta: fusion/capture beats (pathognomonic for VT)

Types of VT:

Management:

• Pulseless VT: Defibrillation (unsynchronised shock) + CPR
• Pulsed, haemodynamically unstable: Synchronized DC cardioversion
• Pulsed, stable: Amiodarone IV (first-line); lidocaine; procainamide
• Torsades de Pointes: IV magnesium sulphate 2g; correct QT-prolonging factors; overdrive pacing
• Long-term: ICD (implantable cardioverter-defibrillator) — reduces sudden cardiac death

Long QT Syndrome

• Antiarrhythmics (amiodarone, sotalol, procainamide, quinidine)
• Brain injury / Bradycardia
• Congenital (Romano-Ward AD; Jervell-Lange-Nielsen AR + deafness)
• Drugs (macrolides, antipsychotics — haloperidol, tricyclics, methadone, chloroquine)
• Electrolytes (hypokalaemia, hypomagnesaemia, hypocalcaemia)

Ventricular Fibrillation (VF)

• Chaotic, irregular, no discernible QRS
• No effective cardiac output → cardiac arrest
• Treatment: Immediate unsynchronised defibrillation (200–360 J biphasic); follow ALS algorithm
• Adrenaline 1 mg IV every 3–5 min (after 3rd shock); amiodarone 300 mg IV (after 3rd shock)

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SECTION 7: ANTIARRHYTHMIC DRUGS (Vaughan-Williams Classification)

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SECTION 8: PACEMAKERS

Indications for Permanent Pacing

• Complete heart block (third-degree)
• High-grade (advanced second-degree)
• Asymptomatic SSS with significant pauses (> 3 s)
• Symptomatic second-degree Mobitz Type II
• Escape junctional rhythm with symptoms
• Type 2 (Mobitz II) always needs pacing

Pacemaker Code (NBG):

• VVI: Ventricular paced, ventricular sensed, inhibited — single-chamber, simple, common in AF with CHB
• DDD: Dual chamber, most physiological; maintains AV synchrony
• CRT (Cardiac Resynchronisation Therapy): Biventricular pacing for CCF with LBBB (QRS > 130 ms) + LVEF ≤ 35%

Pacemaker Complications: "TIDES"

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SECTION 9: SPECIFIC HIGH-YIELD SCENARIOS

Inferior MI + Heart Block

• AV node supplied by right coronary artery (RCA) in 90%
• Inferior MI → AV nodal block (1st degree, Wenckebach) — usually transient and reversible
• Treat with atropine; PPM rarely needed

Anterior MI + Heart Block

• His-Purkinje supplied by LAD (left anterior descending artery)
• Anterior MI + LBBB / bifascicular block / Mobitz II / CHB → poor prognosis
• Requires temporary pacing → consider PPM

Digoxin Toxicity Arrhythmias

• Any arrhythmia except rapid AF can occur with digoxin toxicity
• Classic: PAT with block (paroxysmal atrial tachycardia + AV block)
• Bidirectional VT = pathognomonic
• Treatment: stop digoxin, correct K⁺/Mg²⁺, digoxin-specific antibody fragments (Digibind) for severe toxicity

Hyperkalaemia ECG Changes (Mnemonic: "PAST")

• P wave flattening/disappearance
• All intervals (PR) prolonged
• Spiked (tall peaked) T waves — early sign
• Tentlike QRS widening → sine wave → VF/asystole

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SECTION 10: 10 HIGH-YIELD HKMLE MCQs

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This is complete (third-degree) heart block with a ventricular escape rhythm (wide QRS, rate ~35 bpm). Atropine is ineffective for infranodal block. Immediate pacing is required. - Braunwald's Heart Disease

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Short RP tachycardia (retrograde P buried in/just after QRS), narrow complex, regular — classic AVNRT using slow antegrade / fast retrograde pathways within the AV node.

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AF > 48 hours → risk of LA thrombus. Must anticoagulate ≥ 3 weeks before elective cardioversion OR perform TOE to exclude thrombus first, then anticoagulate ≥ 4 weeks post-cardioversion. - Braunwald's Heart Disease

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Mobitz Type I (Wenckebach) — progressive PR prolongation culminating in a dropped QRS. Wenckebach block occurs at the AV node level. Block at His-Purkinje level produces Mobitz Type II (sudden drop without prior PR prolongation).

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Fusion beats and AV dissociation are pathognomonic of VT. Fusion beats occur when a supraventricular impulse partially captures the ventricle simultaneously with a VT beat, producing an intermediate QRS morphology.

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AF with WPW — adenosine (also digoxin and verapamil) blocks the AV node, forcing all conduction through the fast accessory pathway → risk of VF. Treatment is DC cardioversion or procainamide/flecainide (which slow accessory pathway conduction).

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CHA₂DS₂-VASc ≥ 2 in males → anticoagulate. DOACs are preferred over warfarin for non-valvular AF (superior efficacy, less intracranial haemorrhage, no INR monitoring). Aspirin alone is inadequate.

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Anterior MI + Mobitz Type II = infranodal block due to LAD occlusion damaging His-Purkinje system. This is not reversible with atropine and carries high risk of complete heart block. Temporary (and often permanent) pacing is indicated. - Goldman-Cecil Medicine

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Torsades de Pointes = "twisting of the points" — polymorphic VT where QRS amplitude and axis rotate around the isoelectric line. It occurs in the setting of long QT (congenital or acquired). Treatment: IV magnesium sulphate 2g.

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Classic digoxin toxicity: GI symptoms (nausea/vomiting), visual disturbance (yellow-green xanthopsia), PAT with block, hypokalaemia (potentiates toxicity). Management: stop digoxin, correct electrolytes, and in severe toxicity (life-threatening arrhythmia) — digoxin-specific antibody fragments (Digibind/DigiFab).

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QUICK REFERENCE MNEMONICS SUMMARY

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Sources: Braunwald's Heart Disease (10th Ed.), Goldman-Cecil Medicine, Fuster & Hurst's The Heart (15th Ed.), Guyton & Hall Medical Physiology — all covering content identical to Davidson's Principles & Practice of Medicine chapters on cardiac arrhythmias.