This lecture by Dr. Jo Jo Hai (HKU Medicine) presents a unified framework for approaching two extremely common clinical presentations—palpitation and syncope—from a cardiovascular perspective. The central message is: palpitation and syncope are NOT diagnoses; they are symptoms. Your job is to find the underlying rhythm disturbance or structural cause, assess severity and haemodynamic impact, identify reversible contributors, and institute appropriate acute + long-term management. ^[1]

• Past papers have directly tested: features distinguishing syncope vs seizure (2016 SAQ Q1), exertional syncope causes (2021 MCQ Q8), and long QT syndrome management (2020 MCQ Q41). ^[6][7][8]
• In OSCE stations, you will be asked to take a focused history on palpitation/syncope, examine the cardiovascular system, interpret an ECG strip, and outline an acute management plan.
• In the written paper, expect MCQs on AV block classification, SVT management algorithm, AF rate vs rhythm control, CHA₂DS₂-VASc scoring, and the mechanisms of tachyarrhythmia (re-entry, triggered activity, abnormal automaticity).

1. Differentiate syncope from non-syncopal transient loss of consciousness (TLOC)
2. Classify causes of syncope (reflex, orthostatic, cardiac) and palpitation
3. Understand mechanisms of bradyarrhythmia and tachyarrhythmia
4. Describe AV block types and their ECG features
5. Classify tachycardias by QRS width (narrow vs wide complex)
6. Outline acute and long-term management of bradyarrhythmia, SVT, AF, VT/VF
7. Apply CHA₂DS₂-VASc score for anticoagulation in AF
8. Understand AED use, vagal manoeuvres, adenosine, DC cardioversion, defibrillation, and pacemaker indications

Palpitation = abnormal awareness of one's own heartbeat — it may be fast or slow, regular or irregular, transient or persistent, sudden or gradual in onset. ^[1]

• 16% of all visits to GPs
• 2nd leading cause of visits to cardiologists ^[1]

This is extremely common. Most palpitations are benign (ectopics, sinus tachycardia), but your job is to identify the minority with dangerous arrhythmias or structural heart disease.

The lecture organises differentials into four buckets ^[1]:

Arrhythmias are classified by rate (tachycardia vs bradycardia), site (atrial, junctional, ventricular), and mechanism. ^[1]

SVT = atrial tachycardia + junctional tachycardia + AVNRT + AVRT (i.e., any tachycardia originating at or above the bundle of His, excluding sinus tachycardia and AF/flutter in clinical usage). ^[1]

The lecture separates these into cardiac origin, systemic conditions, and de novo ^[1]:

Cardiac Origin:

1. Coronary artery disease / MI — scar tissue creates substrate for re-entry
2. Valvular heart disease — chamber dilation/hypertrophy → electrical remodelling
3. Cardiomyopathies — HCM, DCM, ARVC, laminopathy
4. Congenital heart disease
5. WPW syndrome — accessory pathway allows pre-excitation
6. Channelopathies — Long QT, Short QT, Brugada, CPVT

Systemic Conditions:

1. Metabolic: thyrotoxicosis, electrolyte imbalance (K⁺, Mg²⁺, Ca²⁺)
2. Medications:
   • Bradycardia: beta-blockers, CCBs, alpha-methyldopa, antiarrhythmics
   • Tachycardia: drugs prolonging QT (antihistamines, antipsychotics), sympathomimetics
3. Alcohol and illicit drugs

De Novo:

• Genetic, part of ageing, idiopathic ^[1]

This is a detailed framework directly from the lecture ^[1]:

1. Evaluate the arrhythmia (diagnosis + severity):

2. Functional status between attacks — consider underlying structural or systemic disease

3. Previous cardiac history — MI → consider ventricular tachyarrhythmias, especially with syncope/presyncope! ^[1]

4. Medications — prescribed AND over-the-counter

5. Family history — especially sudden death, arrhythmia, cardiomyopathy, premature CAD ^[1]

6. Social and occupational history — alcohol, driving, recreational activities

Syncope = Transient loss of consciousness (TLOC) due to global cerebral hypoperfusion, characterised by rapid onset, brevity, and spontaneous recovery. ^[1]

This definition is critical for exams. The mechanism is always global cerebral hypoperfusion — this distinguishes true syncope from epilepsy (electrical), psychogenic episodes, or metabolic causes of altered consciousness.

The clinical importance: syncope in the elderly is common, dangerous (falls → fractures → mortality), and often under-recognised.

The first key point is to differentiate syncope from non-syncopal TLOC. The second key point is to differentiate cardiovascular from non-cardiovascular syncope. ^[1]

TLOC
├── Traumatic (head trauma)
└── Non-traumatic
    ├── Syncope (cerebral hypoperfusion)
    │   ├── Neurally-mediated (Reflex) — 60%
    │   ├── Orthostatic hypotension — 15%
    │   ├── Cardiac arrhythmia — 10%
    │   ├── Cardiovascular structural — 5%
    │   └── Unexplained — ~10%
    ├── Epileptic seizures (generalised: tonic, clonic, tonic-clonic, atonic)
    ├── Psychogenic (PPS, PNES)
    └── Rare causes (vertebrobasilar TIA, SAH, cyanotic breath-holding spell)

Vasovagal syncope → LOW mortality risk (but recurrences frequent) Cardiac syncope → HIGH mortality risk (determined by severity of heart disease) ^[1]

This is why distinguishing cardiac from non-cardiac syncope is the most important clinical task. The Soteriades NEJM 2002 paper (referenced in the lecture) showed cardiac syncope has significantly worse survival.

True syncope: relatively sudden onset, temporary (usually < 1–2 min), self-limiting, rapid and complete recovery

Important nuances:

• Most often associated with a fall in systemic arterial pressure
• Prodrome possible but characteristics are autonomic activation (nausea, sweating, pallor, warmth)
• Seizure activities and urinary incontinence ARE possible in syncope — so their presence does NOT automatically mean epilepsy (convulsive syncope occurs from cerebral hypoperfusion triggering brief tonic-clonic activity)

This table is directly from the lecture and is extremely high yield:

• Patient AND witness interview — scenario, precipitants, prodrome/associated symptoms, duration, convulsion, incontinence, tongue biting, cyanosis, recovery pattern (post-ictal drowsiness?), post-syncopal symptoms, retrograde amnesia, previous events
• Injury assessment
• Past medical history
• Medications (especially vasodepressive agents, QT-prolonging drugs)
• Family history (sudden death, arrhythmia, cardiomyopathy)
• Social aspects: home environment, occupation, hobbies

• Detailed cardiovascular AND neurological examination + injury assessment
• Orthostatic vital signs — supine then standing BP/HR at 1 and 3 minutes
  • Orthostatic hypotension: ≥ 20 mmHg systolic drop or ≥ 10 mmHg diastolic drop within 2–5 minutes of standing ^[3]
• Examination for carotid/subclavian artery diseases
• Carotid sinus massage — always auscultate for bruit first; positive = asystole > 3s or SBP drop > 50 mmHg ^[3]

The diagnostic yield of initial evaluation (history + physical exam + ECG) is 60–70%, with history taking being the main factor.

This tells you: invest time in the history. Most syncope can be diagnosed at the bedside.

The key concept: an arrhythmia on monitoring is only diagnostic if it coincides with symptoms. Asymptomatic minor rhythm disturbances are common, especially in the elderly. ^[4]

1. Abnormal impulse formation — SA node fails to generate impulses at adequate rate
2. Abnormal impulse propagation — conduction block at AV node, His bundle, or infra-Hisian system

Sinus Node Disease:

• Sinus bradycardia
• Sinus arrest
• Sinoatrial (SA) block

AV Conduction Disease:

Bundle Branch & Fascicular Block:

• Right bundle branch block (RBBB)
• Left bundle branch block (LBBB)
• Left anterior fascicular block (LAFB)
• Left posterior fascicular block (LPFB)
• Bifascicular block (RBBB + LAFB or LPFB)
• Trifascicular block (bifascicular + 1° AV block)

This is the single most important classification for acute management:

Purpose: Increase vagal tone → slow AV nodal conduction → either (1) terminate SVT involving AV node as essential part of the circuit (AVNRT, AVRT); or (2) slow ventricular rate to reveal underlying atrial activities (atrial flutter, atrial tachycardia)

Methods:

• Carotid sinus massage
• Valsalva manoeuvre
• Gagging
• Drinking ice water
• Cold water immersion (face/arm)

Mechanism: Hyperpolarises ATP-sensitive K⁺-channel in AV node → transiently blocks AV nodal conduction

Key pharmacological facts:

• Short half-life < 10 seconds — must be given as rapid IV push followed by flush
• Contraindicated in asthma / bronchospasm (causes bronchospasm via A₁ receptor)
• Dose from lecture: ATP 20 mg IV

Diagnostic and therapeutic use:

This is why adenosine is both diagnostic AND therapeutic — it helps you figure out the mechanism while potentially curing the arrhythmia.

Acute:

1. Exclude reversible causes (hypothyroidism, drugs — BB, CCB, digoxin)
2. IV atropine (blocks muscarinic receptors → ↑HR)
3. IV dopamine (β₁ stimulation → ↑HR and contractility)
4. Temporary pacing (transcutaneous → bridge to transvenous)

Long-term:

• Permanent pacemaker implantation (indicated for symptomatic bradycardia, Mobitz II, complete heart block, tachycardia-bradycardia syndrome)

Acute:

1. Correct reversible causes (electrolytes, thyroid, drugs)
2. Haemodynamically stable → Vagal manoeuvres or pharmacological
3. Haemodynamically unstable → Electrical (DC cardioversion/defibrillation)

Long-term:

• Pharmacological and/or non-pharmacological (ablation)

Drugs are no longer first-line treatment for symptomatic and recurrent SVT, including atrial tachycardia / atrial flutter! ^[1]

This is an important paradigm shift: catheter ablation is now Class I recommendation for recurrent symptomatic SVT and typical atrial flutter.

This is one of the highest-yield topics in all of cardiology for exams.

Two pillars: Rate Control + Rhythm Control (+ Anticoagulation)

Anticoagulation may be required for prophylaxis of thromboembolism ^[1]

Anticoagulation recommended: score ≥ 2 for males / ≥ 3 for females ^[1]

The "Sc" (female sex) contributes 1 point but is a "risk modifier" — a woman with score 1 (only female sex) does not need anticoagulation; she needs score ≥ 3 total.

• The opening case is LQTS with QTc 590 ms
• 2020 MCQ Q41 tested LQTS management: 17-year-old with family history of sudden death (father died during soccer, brother died young), normal exam, ECG showed LQTS → answer was Beta-blocker (first-line for LQTS to reduce catecholamine-triggered events) ^[8]
• ICD is reserved for survivors of cardiac arrest or those who remain symptomatic despite beta-blockers
• Left cervicothoracic stellectomy (left cardiac sympathetic denervation) is second-line for refractory LQTS

The question asked which condition most likely presents with exertional syncope:

• Hypertrophic cardiomyopathy — correct answer (LVOT obstruction worsens with exercise → ↓CO → syncope)
• Aortic regurgitation — typically asymptomatic until severe; exertional syncope is uncommon
• Constrictive pericarditis — presents with right heart failure signs, not exertional syncope
• Postural hypotension — by definition positional, not exertional

From GC 069 and supporting notes:

• WPW syndrome: delta wave on ECG, short PR; risk of VF if AF conducts rapidly via accessory pathway (shortest pre-excited RR < 250 ms → ablation needed)
• Brugada syndrome: coved ST elevation in V1-V3; risk of VF; ICD in symptomatic patients
• CPVT: exercise-induced bidirectional VT; beta-blocker ± flecainide; ICD if refractory
• ARVC: epsilon waves, T-wave inversion V1-V3; exercise restriction; ICD in high risk

The lecture's homework explicitly asks students to review ACLS protocols. Key points:

• Cardiac arrest algorithm: shockable (VF/pulseless VT) → defibrillation; non-shockable (asystole/PEA) → CPR + adrenaline
• Tachycardia algorithm: stable → vagal/drugs; unstable → DC cardioversion
• Bradycardia algorithm: symptomatic → atropine → pacing; asymptomatic → observe

1. An 18-year-old collapses during exercise. Post-resuscitation ECG shows QTc 590 ms. What is the most likely underlying diagnosis?

   • Long QT syndrome (LQTS)

2. A 70-year-old with AF, hypertension, diabetes, and previous stroke. CHA₂DS₂-VASc score?

   • H(1) + D(1) + S₂(2) = 4 (minimum, plus age component); requires anticoagulation

3. Which of the following is contraindicated when giving adenosine?

   • Asthma / active bronchospasm

4. Wide complex tachycardia in a patient with previous MI — most likely diagnosis?

   • VT (until proven otherwise)

5. Which type of 2nd degree AV block most likely requires a pacemaker?

   • Mobitz Type II (infra-nodal block, risk of complete heart block)

1. List 5 features distinguishing syncope from seizure (2016 SAQ Q1) ^[6]

   • Markscheme: Brief LOC (< 1 min), rapid complete recovery without confusion, preceded by lightheadedness/autonomic activation, pallor during event, associated with standing/trigger, absence of sustained rhythmic convulsions, absence of post-ictal state, tongue biting rare (tip not lateral)

2. A patient with AF — outline your management approach (rate control, rhythm control, anticoagulation)

   • Markscheme: Acute — haemodynamic assessment → stable: rate control (IV BB/CCB or digoxin/amiodarone if HF); unstable: DC cardioversion. Long-term — rate control (oral BB/CCB/digoxin) vs rhythm control (AAD or catheter ablation). Anticoagulation based on CHA₂DS₂-VASc.

3. Describe the mechanism of re-entry and give two clinical examples

   • Markscheme: Requires two pathways with different conduction/refractory properties, unidirectional block in one, slow conduction in other, creating a self-sustaining circuit. Examples: AVNRT (dual AV nodal pathways), AVRT (accessory pathway), atrial flutter (macro-reentrant around tricuspid annulus).

• Take a focused history for palpitation (assess onset, regularity, precipitants, associated symptoms including polyuria, syncope; previous cardiac history; medications; FHx sudden death)
• Interpret an ECG showing complete heart block / AF / SVT
• Explain to a patient why they need anticoagulation for AF