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]

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. Interpret the slide-era CHA₂DS₂-VASc score and current CHA₂DS₂-VA approach to 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 age-stratified stacked bars add an important visual message: reflex syncope remains common at all ages, but orthostatic, arrhythmic, and structural causes occupy a progressively larger share in older adults. Do not assume an older person's collapse is “just a fall” ^[1].

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.

The survival plot should be read as a prognostic association, not proof that syncope itself causes death: the cardiac-cause curve separates sharply, whereas vasovagal/other syncope tracks close to the no-syncope curve. The underlying heart disease largely drives the excess risk ^[1].

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
  • Classical orthostatic hypotension: sustained systolic fall ≥20 mmHg or diastolic fall ≥10 mmHg within 3 minutes of standing; interpret symptoms and absolute BP as well ^[11]
• Examination for carotid/subclavian artery diseases
• Carotid sinus massage (CSM) appears in the slide, but it is a monitored diagnostic procedure, generally for selected patients older than 40 with compatible unexplained syncope—not a routine bedside or self-administered manoeuvre. It requires continuous ECG and beat-to-beat BP monitoring and exclusion of contraindications such as recent TIA/stroke or significant carotid disease. Carotid sinus syndrome requires reproduction of the patient's spontaneous symptoms, not an asymptomatic numerical response alone ^[11].

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 strongest evidence is symptom-rhythm correlation. However, some high-risk findings (for example, prolonged high-grade AV block or sustained VT) remain clinically actionable even if the patient did not press an event marker at that moment; conversely, incidental minor ectopy may not explain symptoms ^[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:

How to read the slide's rhythm-strip panel:

• Sinoatrial exit block: a pause interrupts sinus activity; assess whether the pause is a multiple of the baseline P-P interval.
• First-degree AV block: every P is followed by QRS, but the PR interval is prolonged.
• Mobitz I: the PR lengthens beat by beat before a non-conducted P wave.
• Mobitz II: PR intervals of conducted beats remain constant before an unexpected non-conducted P wave.
• Complete AV block: atria and ventricles march independently; identify the slower escape rhythm and QRS width ^[1].

The last column of the table needs nuance: permanent pacing is indicated for acquired Mobitz II, high-grade, or third-degree AV block when not caused by a reversible or physiological condition. Acute ischaemia, drugs/toxicity, metabolic disturbance, infection, and post-procedural causes must first be assessed; temporary pacing may be needed while an unstable patient is evaluated ^[13].

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” is an imprecise legacy label: bifascicular block plus first-degree AV block does not prove disease in the remaining fascicle, because PR prolongation is often AV-nodal. Describe the actual conduction findings and investigate unexplained syncope appropriately.

This is the single most important classification for acute management:

The WPW diagram links anatomy to the resting ECG: an accessory atrioventricular pathway bypasses normal AV-nodal delay, producing a short PR interval, slurred initial QRS upstroke (delta wave), and widened QRS. During pre-excited AF, do not give AV-nodal blocking drugs (adenosine, verapamil/diltiazem, beta-blockers, or digoxin), because preferential accessory-pathway conduction may precipitate VF ^[12].

For a regular wide-complex tachycardia, the slide's examples favour VT when there is AV dissociation, capture or fusion beats, precordial concordance, absence of an RS complex or a very prolonged RS interval, an extreme axis, or specific aVR/morphology features. These signs can confirm VT, but their absence does not exclude it; manage an undifferentiated wide-complex tachycardia as VT ^[10].

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)

For a stable regular narrow-complex SVT, use a modified Valsalva manoeuvre first; the post-strain supine repositioning with passive leg raise improves conversion compared with a standard Valsalva. The slide's list of gagging, drinking ice water, and cold-water immersion is not a modern adult treatment algorithm. Carotid sinus massage should be performed only by a trained clinician with monitoring and contraindication screening, not taught as a self-treatment ^[11][12].

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
• Avoid in active bronchospasm/severe asthma and check for relevant interactions or transplant-related dose sensitivity
• The slide's ATP 20 mg example is historical/local and is not interchangeable with adenosine dosing. The 2025 AHA adult tachycardia algorithm uses adenosine 6 mg rapid IV push with flush, then 12 mg if required, in a monitored resuscitation setting ^[10].

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.

Use it only when the rhythm and setting are appropriate: regular narrow-complex tachycardia, or selected regular monomorphic wide-complex tachycardia with expert/resuscitation support. Do not give adenosine to an irregular wide-complex rhythm or suspected pre-excited AF ^[10][12].

Acute:

1. Identify and treat reversible causes (hypoxia, ischaemia, hyperkalaemia and other electrolyte disturbance, beta-blocker/CCB/digoxin toxicity, hypothyroidism)
2. If persistent bradycardia is causing hypotension, altered mental status, shock, ischaemic chest discomfort, or acute heart failure: IV atropine
3. If atropine is ineffective: transcutaneous pacing and/or dopamine or adrenaline infusion while arranging expert review and possible temporary transvenous pacing ^[10]

Long-term:

• Permanent pacemaker implantation depends on documented symptom-rhythm correlation and conduction diagnosis. Acquired Mobitz II, high-grade, or third-degree AV block not due to a reversible/physiological cause is a major indication ^[13].

Acute:

1. Correct reversible causes (electrolytes, thyroid, drugs)
2. Tachyarrhythmia with a pulse and haemodynamic instability caused by the rhythm → synchronized cardioversion (sedate if feasible without delaying treatment)
3. Polymorphic VT, VF, or pulseless VT → unsynchronized defibrillation; cardiac arrest also requires immediate high-quality CPR ^[10]
4. Stable rhythm → identify QRS width and regularity before choosing vagal manoeuvres or a drug

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.

The following is the slide-era summary; it combines several rhythms whose acute treatment is not identical:

Current practical distinction: modified Valsalva and adenosine are aimed at regular AV node-dependent SVT (AVNRT/orthodromic AVRT). Adenosine may expose flutter waves but does not terminate the atrial-flutter circuit. An unstable SVT or flutter with a pulse needs synchronized cardioversion. Recurrent symptomatic AVNRT/AVRT and typical flutter are often treated definitively with catheter ablation. Never use AV-nodal blockers for pre-excited AF ^[10][12].

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]

Current AF-CARE framing: address comorbidities/risk factors; avoid stroke with appropriate anticoagulation; reduce symptoms using individualized rate and rhythm control; and reassess dynamically. Rhythm control is not reserved only for collapse or very low LVEF—it should be discussed with suitable symptomatic patients. If AF itself is causing haemodynamic instability, perform urgent synchronized cardioversion. If AF duration is over 24 hours, elective cardioversion generally requires at least 3 weeks of therapeutic anticoagulation or transoesophageal echocardiography to exclude thrombus, followed by post-cardioversion anticoagulation as indicated ^[15].

Historical slide threshold: CHA₂DS₂-VASc ≥2 for males / ≥3 for females ^[1]

The 2024 ESC guideline now uses CHA₂DS₂-VA, omitting sex category: oral anticoagulation is recommended at score ≥2 and should be considered at score 1 after patient-centred assessment. Use a locally adopted validated tool where different guidance applies. A DOAC is preferred over warfarin for eligible patients, except those with a mechanical heart valve or mitral stenosis; bleeding scores identify modifiable risks but should not be used alone to deny indicated anticoagulation ^[15].

The slide's broad list below must be interpreted by pulse, morphology, stability, substrate, and reversible cause; the options are not interchangeable:

• VF/pulseless VT: immediate defibrillation and CPR; amiodarone or lidocaine may be considered only for shock-refractory VF/pVT within the arrest algorithm.
• Unstable monomorphic VT with a pulse: synchronized cardioversion.
• Sustained polymorphic VT: immediate unsynchronized high-energy shock. For recurrent torsades with prolonged QT, stop QT-prolonging drugs, correct potassium/magnesium and bradycardia, and give IV magnesium; do not reflexively use a QT-prolonging antiarrhythmic such as amiodarone ^[10][14].
• Stable wide-complex tachycardia: monitor, obtain a 12-lead ECG, seek expert input, and use an appropriate antiarrhythmic infusion; adenosine is considered only if the rhythm is regular and monomorphic ^[10].
• Long-term antiarrhythmic medication, ablation, and ICD decisions require disease-specific risk assessment. “Class I AAD” is not a universal long-term treatment category for VT ^[14].