Emergency Medicine
High Evidence

Syncope - Emergency Department Assessment

Syncope accounts for 1-3% of ED presentations and 6% of hospital admissions. While reflex syncope is most common (40-50%... ACEM Primary Written, ACEM Fellowshi

Updated 24 Jan 2026
50 min read

Clinical board

A visual summary of the highest-yield teaching signals on this page.

Urgent signals

Safety-critical features pulled from the topic metadata.

  • Syncope during exertion or supine position - suggests cardiac cause
  • Abnormal ECG - arrhythmia, conduction block, ischaemia, long QT, Brugada pattern
  • Known structural heart disease or family history of sudden cardiac death below 40 years
  • Syncope with chest pain, dyspnoea, or palpitations - may indicate PE, MI, or arrhythmia

Exam focus

Current exam surfaces linked to this topic.

  • ACEM Primary Written
  • ACEM Fellowship Written
  • ACEM Fellowship OSCE

Linked comparisons

Differentials and adjacent topics worth opening next.

  • Seizure Disorders
  • Pulmonary Embolism

Editorial and exam context

ACEM Primary Written
ACEM Fellowship Written
ACEM Fellowship OSCE
Clinical reference article

Quick Answer

One-liner: Syncope is transient loss of consciousness with loss of postural tone due to global cerebral hypoperfusion, requiring systematic risk stratification to identify life-threatening cardiac causes.

Syncope accounts for 1-3% of ED presentations and 6% of hospital admissions. While reflex syncope is most common (40-50%), cardiac syncope carries 10-30% one-year mortality. The ED physician's priority is to identify high-risk patients requiring admission and cardiac workup while safely discharging low-risk reflex syncope patients. ECG is the single most important investigation. Risk stratification tools (Canadian Syncope Score, San Francisco Syncope Rule) help guide disposition decisions.


ACEM Exam Focus

Primary Exam Relevance

  • Anatomy: Cardiac conduction system, carotid sinus, autonomic nervous system, cerebral autoregulation
  • Physiology: Cerebral blood flow regulation, cardiovascular reflexes, orthostatic haemodynamic response, neurally mediated syncope mechanisms
  • Pharmacology: QT-prolonging drugs, antihypertensives causing orthostatic hypotension, beta-blockers, vasodilators

Fellowship Exam Relevance

  • Written: Risk stratification tools (Canadian Syncope Score, San Francisco Rule), ECG red flags (long QT, Brugada, HOCM), admission criteria, differentiation from seizure
  • OSCE: History-taking from syncope patient, ECG interpretation, communication of disposition decision, counselling on vasovagal syncope, breaking news of cardiac diagnosis
  • Key domains tested: Medical Expert (risk stratification), Communicator (explaining diagnosis and disposition), Collaborator (cardiology referral)

Key Points

Clinical Pearl

The 5 things you MUST know:

  1. ECG is mandatory - the single most important test; any abnormality increases risk of adverse outcome 5-fold
  2. Cardiac syncope has 10-30% one-year mortality - identify via exertional syncope, abnormal ECG, structural heart disease, family history of sudden death
  3. Canadian Syncope Risk Score ≥1 requires admission/observation - validated tool for 30-day serious adverse events
  4. Orthostatic vital signs detect 10-30% of syncope causes - measure BP/HR supine and after 3 minutes standing (drop ≥20 mmHg systolic or ≥10 mmHg diastolic)
  5. Reflex syncope has prodrome, cardiac syncope often does NOT - sudden onset without warning suggests arrhythmia or structural heart disease

Epidemiology

MetricValueSource
Incidence1-6 per 1,000 persons per year[1] PMID: 41141164
Lifetime prevalence30-40% (at least one episode)[2] PMID: 39190136
ED presentations1-3% of all ED visits[3] PMID: 41193023
30-day mortality0.7-2.5% overall; 10% cardiac syncope[4] PMID: 40668516
Recurrence rate20-30% within 1-2 years[5] PMID: 38871205
Gender ratioF:M approximately 1.2:1 (young); M:F 1.5:1 (elderly cardiac)[6] PMID: 37227975

Australian/NZ Specific

  • Syncope accounts for approximately 50,000 ED presentations annually in Australia [7]
  • Beach study (Australian general practice): syncope consultation rate 2.3 per 1,000 encounters [8]
  • Indigenous Australians have 1.5-2x higher rates of structural heart disease (rheumatic heart disease, ischaemic heart disease), increasing cardiac syncope risk [9]
  • Remote/rural presentations: 15-25% referred via RFDS for cardiac workup due to limited local investigation capacity [10]

Pathophysiology

Mechanism

Syncope results from global cerebral hypoperfusion when cerebral blood flow drops below 30-50 mL/100g/min for 6-8 seconds. Consciousness is lost when flow drops below 20 mL/100g/min.

Normal cerebral autoregulation maintains constant blood flow despite mean arterial pressure (MAP) variations of 60-150 mmHg. Syncope occurs when:

  1. Systemic hypotension overwhelms autoregulation
  2. Reduced cardiac output (arrhythmia, obstruction)
  3. Inappropriate vasodilation/bradycardia (reflex syncope)

Classification and Pathological Mechanisms

SYNCOPE MECHANISMS
│
├── REFLEX (Neurally Mediated) 40-50%
│   ├── Vasovagal (orthostatic stress, emotion, pain)
│   │   → ↓Sympathetic tone + ↑Vagal tone → Vasodilation + Bradycardia
│   ├── Situational (micturition, defecation, cough)
│   │   → Vagal activation → Bradycardia/hypotension
│   └── Carotid Sinus Hypersensitivity (greater than 60 years)
│       → Carotid pressure → Asystole greater than 3s or SBP drop greater than 50 mmHg
│
├── ORTHOSTATIC HYPOTENSION 10-30%
│   ├── Volume depletion (haemorrhage, dehydration)
│   ├── Autonomic failure (diabetes, Parkinson's, elderly)
│   └── Drug-induced (antihypertensives, diuretics)
│       → Standing → Venous pooling → ↓Venous return → ↓Cardiac output
│
├── CARDIAC SYNCOPE 15-25%
│   ├── Arrhythmia (70% of cardiac syncope)
│   │   ├── Bradyarrhythmia: Complete heart block, sinus node disease
│   │   └── Tachyarrhythmia: VT, VF, SVT with aberrancy
│   └── Structural/Obstruction (30%)
│       ├── Aortic stenosis → Fixed output → Exertional demand unmet
│       ├── HOCM → LVOT obstruction → ↓Cardiac output
│       ├── Pulmonary embolism → RV failure → ↓LV filling
│       └── Cardiac tamponade → ↓Venous return → ↓Cardiac output
│
└── CEREBROVASCULAR below 5%
    └── Vertebrobasilar insufficiency, subclavian steal

Why It Matters Clinically

Reflex syncope: Benign prognosis, low mortality, but high recurrence and injury risk from falls. Management focuses on education and trigger avoidance.

Cardiac syncope: High mortality (10-30% at 1 year) due to underlying structural heart disease or arrhythmia risk. Requires urgent cardiac workup, potential device implantation (pacemaker, ICD).

Orthostatic hypotension: Treatable cause - medication review, volume repletion, compression stockings. Common in elderly and polypharmacy patients.


Clinical Approach

Recognition

Syncope is suspected when a patient presents with:

  • Witnessed or reported transient loss of consciousness
  • Loss of postural tone (fall, slump)
  • Spontaneous, rapid, complete recovery

Differentiate from:

  • Seizure: Prolonged LOC (greater than 5 min), post-ictal confusion, lateral tongue biting, prolonged tonic-clonic activity
  • Concussion: LOC with head trauma, amnesia, neurological deficit
  • Psychogenic pseudosyncope: Eyes closed during event, prolonged LOC without injury, bizarre movements

Initial Assessment

Primary Survey (if patient unconscious/altered)

  • A: Assess airway patency; recover if still unconscious
  • B: RR, SpO₂; rule out hypoxia-induced LOC
  • C: BP both arms, HR, ECG monitor; arrhythmia or hypotension?
  • D: GCS, pupils, focal neurology; stroke or seizure mimics?
  • E: Evidence of trauma from fall, bleeding, rash (meningococcal)

Immediate bedside tests:

  • Blood glucose (exclude hypoglycaemia)
  • ECG (within 10 minutes of arrival)
  • Orthostatic vital signs (supine and 3-min standing)

History

Key Questions

QuestionSignificance
"What were you doing when it happened?"Exertional syncope → cardiac (AS, HOCM, arrhythmia); Positional → orthostatic; Prolonged standing/emotion → vasovagal
"Did you have any warning?"Prodrome (nausea, diaphoresis, tunnel vision) → reflex; Sudden onset, no warning → arrhythmia
"Were you sitting, standing, or lying down?"Syncope while supine → cardiac until proven otherwise
"Did you have chest pain, palpitations, or shortness of breath?"Suggests cardiac cause (MI, PE, arrhythmia)
"Have you had this before?"Recurrent syncope with similar triggers → reflex; First episode in elderly → investigate cardiac
"Any family history of sudden death below 40 years?"Channelopathies (long QT, Brugada), HOCM, arrhythmogenic RV cardiomyopathy
"What medications are you taking?"QT-prolonging drugs, antihypertensives, diuretics, beta-blockers

The "4 P's" of Syncope History

  1. Posture: Sitting/standing (orthostatic/reflex) vs. supine (cardiac)
  2. Prodrome: Present (reflex) vs. absent (cardiac)
  3. Precipitant: Exertion (cardiac), emotion/pain (vasovagal), micturition (situational)
  4. Post-event: Rapid recovery (syncope) vs. confusion (seizure)

Red Flag Symptoms

Red Flag
  • Syncope during exertion - aortic stenosis, HOCM, coronary ischaemia
  • Syncope while supine - arrhythmia (not orthostatic or vasovagal)
  • Sudden onset without prodrome - arrhythmia, high-risk cardiac cause
  • Chest pain or dyspnoea - MI, PE, aortic dissection
  • Palpitations before syncope - tachyarrhythmia (VT, SVT)
  • Family history of sudden cardiac death below 40 years - inherited channelopathies, HOCM
  • Severe headache - subarachnoid haemorrhage (thunderclap headache syncope)

Examination

General Inspection

  • Level of consciousness: Should be fully alert post-event (if not, consider seizure or stroke)
  • Distress: Ongoing chest pain, dyspnoea suggests cardiac/PE
  • Injury from fall: Head laceration, facial trauma, long bone fractures
  • Pallor: Anaemia, haemorrhage
  • Diaphoresis: Ongoing vasovagal trigger, acute coronary syndrome

Specific Findings

SystemFindingSignificance
CardiovascularNew murmur (AS, HOCM)Structural heart disease
Irregular pulseAtrial fibrillation with rapid ventricular response
Elevated JVPHeart failure, PE, cardiac tamponade
BP difference greater than 20 mmHg between armsAortic dissection, subclavian steal
RespiratoryTachypnoea, hypoxiaPulmonary embolism
NeurologicalFocal deficitStroke (rare cause of LOC)
Nystagmus, ataxiaVertebrobasilar insufficiency
AbdominalAbdominal tenderness, distensionAAA rupture (syncope as presentation)
Melaena, PR bleedingGI haemorrhage

Orthostatic Vital Signs (Critical Test)

Method:

  1. Patient supine for 5 minutes → measure BP and HR
  2. Stand patient → measure BP and HR at 1 and 3 minutes

Positive Test:

  • SBP drop ≥20 mmHg OR DBP drop ≥10 mmHg
  • HR increase ≥30 bpm (≥40 bpm in postural orthostatic tachycardia syndrome [POTS])

Interpretation:

  • Positive → orthostatic hypotension (volume depletion, autonomic dysfunction, drugs)
  • If HR does NOT increase → autonomic failure (Parkinson's, diabetes)
  • If HR increases appropriately → volume depletion or drug effect

Investigations

Immediate (All Syncope Patients)

TestPurposeKey Finding
12-lead ECGIdentify arrhythmia, ischaemia, channelopathyAny abnormality increases risk 5-fold [11] PMID: 16431353
Blood glucoseExclude hypoglycaemia (mimic)below 4.0 mmol/L suggests hypoglycaemic LOC
Orthostatic vitalsDiagnose orthostatic hypotensionSBP drop ≥20 or DBP ≥10 mmHg

ECG Red Flags - High-Risk Features

Red Flag

Arrhythmia/Conduction:

  • Mobitz II or complete (3rd degree) AV block
  • Sinus bradycardia below 40 bpm or sinus pauses greater than 3 seconds
  • Atrial fibrillation with rapid ventricular response (greater than 150 bpm)
  • Non-sustained VT or other ventricular arrhythmia

Ischaemia/Infarction:

  • ST elevation or depression (STEMI, NSTEMI)
  • New Q waves

Channelopathies:

  • Long QT: QTc greater than 480 ms (men), greater than 500 ms (women) [12] PMID: 41560020
  • Brugada pattern: Coved ST elevation ≥2 mm in V1-V2 with T wave inversion [13] PMID: 41572647
  • Short QT: QTc below 320 ms

Structural Heart Disease:

  • HOCM: Deep narrow "dagger" Q waves (leads I, aVL, V5-V6), LVH, giant T wave inversion [14] PMID: 31102944
  • Arrhythmogenic RV cardiomyopathy: Epsilon waves (V1-V3), T wave inversion V1-V3
  • WPW: Delta waves, short PR interval

Other:

  • PE signs: S1Q3T3, right heart strain, new RBBB, tachycardia [15] PMID: 27732161

Standard ED Workup

TestIndicationInterpretation
Full blood countSuspected anaemia, haemorrhageHb below 80 g/L may cause syncope; check if melaena/bleeding
Electrolytes, renal functionDehydration, renal failure, K⁺/Mg²⁺ abnormalitiesHypokalaemia below 3.0 mmol/L → long QT risk; AKI → volume depletion
TroponinChest pain, ECG ischaemia, high-risk featuresElevated → ACS workup; PE may elevate troponin
Beta-HCGWomen of childbearing ageExclude ectopic pregnancy (abdominal pain + syncope)
D-dimerSuspected PE (chest pain, dyspnoea, hypoxia)Age-adjusted cut-off; if high → CTPA

Advanced/Specialist Investigations

TestIndicationAvailability
EchocardiographyAbnormal ECG, murmur, suspected structural heart diseaseED POCUS or formal echo
Continuous ECG monitoringSuspected arrhythmia, high-risk featuresED observation unit or ward telemetry
Holter monitor (24-48h)Recurrent syncope, palpitations, unclear causeCardiology outpatient (low-risk discharge)
Implantable loop recorderRecurrent unexplained syncope (captures rhythm during event)Cardiology/electrophysiology
Tilt table testSuspected reflex syncope, recurrent events, unclear diagnosisSpecialist cardiology centres [16] PMID: 41458892
Electrophysiology studySuspected VT, unexplained syncope with structural heart diseaseTertiary cardiology
CT pulmonary angiogramSuspected PE (syncope in 10-15% of massive PE)Metro/tertiary ED
Carotid sinus massageSuspected carotid sinus hypersensitivity (age greater than 60, unexplained falls)Contraindicated: recent stroke/TIA, carotid bruit without Doppler clearance [17] PMID: 40787531

Point-of-Care Ultrasound

POCUS applications in syncope:

  1. Cardiac: LVEF assessment, regional wall motion abnormalities (MI), LVOT obstruction (HOCM), valvular pathology (AS), pericardial effusion/tamponade
  2. IVC collapsibility: greater than 50% collapse → volume depletion (orthostatic syncope)
  3. RV dilation: RV:LV ratio greater than 1.0 suggests PE; McConnell's sign (RV free wall hypokinesis with apical sparing)
  4. eFAST: If trauma from fall, assess for haemoperitoneum, haemothorax

Risk Stratification Tools

Canadian Syncope Risk Score (CSRS)

Most validated tool for ED syncope risk stratification [18] PMID: 41193023

Predicts 30-day serious adverse events (death, arrhythmia, MI, structural heart disease, procedural intervention).

Risk FactorPoints
Predisposition (History)
Cardiac disease history (IHD, HF, valve disease, arrhythmia)+1
Clinical
Systolic BP below 90 or greater than 180 mmHg+2
Elevated troponin (above 99th percentile)+2
ECG
Abnormal QRS axis (−90° to +180°)+1
QRS duration greater than 130 ms+1
QTc greater than 480 ms+2
Diagnosis in ED
ED diagnosis of cardiac syncope+2
ED diagnosis of vasovagal syncope−2

Scoring:

  • Score −2 to 0: Low risk (0.4% serious event rate) → Safe discharge
  • Score 1-3: Medium risk (8.1%) → Observation or admit
  • Score ≥4: High risk (25-30%) → Admit for cardiac workup

Performance: Sensitivity 98%, specificity 25%, NPV 99.7% for low-risk [18]

San Francisco Syncope Rule (SFSR)

Historical tool (2004); lower specificity, less validated than CSRS [11] PMID: 16431353

High-risk if any of the following present:

  1. History of heart failure
  2. Haematocrit below 30%
  3. Abnormal ECG (any abnormality)
  4. Shortness of breath
  5. Triage systolic BP below 90 mmHg

Criticism: Very broad (50% patients high-risk); lower specificity than CSRS; does not risk-stratify beyond binary high/low [19] PMID: 39496561

ACEM Recommendation: Prefer Canadian Syncope Risk Score for ED disposition decisions.


Management

Immediate Management (First 10 minutes)

1. Patient on monitor, IV access if high-risk features
2. 12-lead ECG within 10 minutes (Priority 1)
3. Blood glucose, orthostatic vitals
4. If arrhythmia detected → treat per ACLS/ARC protocols
5. If ongoing syncope/presyncope → supine position, IV fluids, identify cause

Resuscitation (if haemodynamically unstable)

Airway

  • Recovery position if altered consciousness
  • Airway adjuncts if required (OP/NP airway)
  • Intubation rarely required unless persistent LOC (consider seizure, stroke)

Breathing

  • Oxygen if SpO₂ below 94% (PE, MI, heart failure)
  • Target SpO₂ 94-98%

Circulation

Hypotension (SBP below 90 mmHg):

  • IV bolus 500 mL 0.9% NaCl over 10-15 minutes
  • Reassess; repeat if volume depletion suspected
  • Caution: Do NOT fluid bolus if heart failure, AS, HOCM (may worsen pulmonary oedema or LVOT obstruction)

Bradycardia (below 40 bpm with hypotension):

  • Atropine 600 mcg IV, repeat up to 3 mg total
  • Transcutaneous pacing if Mobitz II, complete heart block, or refractory bradycardia
  • Isoprenaline infusion 2-10 mcg/min if pacing unavailable
  • Urgent cardiology consultation for temporary transvenous pacing

Tachyarrhythmia:

  • VT with pulse → Amiodarone 300 mg IV over 20-60 min
  • SVT → Vagal manoeuvres, adenosine 6 mg rapid IV push
  • AF with RVR → Rate control (metoprolol, diltiazem) or DC cardioversion if unstable

Specific Syncope Subtypes

1. Reflex (Vasovagal) Syncope

Diagnosis: Prodrome (nausea, diaphoresis, tunnel vision), triggered by prolonged standing, emotion, pain; rapid recovery.

ED Management:

  • Reassurance: benign condition, low mortality
  • Education on triggers and avoidance
  • Physical counter-pressure manoeuvres: Leg crossing, hand grip, squatting at prodrome onset [20] PMID: 41301791
  • Increase fluid/salt intake (2-3 L fluid, 10 g salt daily) if no contraindication
  • Avoid prolonged standing, hot environments

Disposition: Discharge if low-risk (normal ECG, no high-risk features)

Follow-up: GP for recurrent symptoms; consider cardiology/syncope clinic referral if frequent episodes

2. Orthostatic Hypotension

Diagnosis: Postural BP drop ≥20/10 mmHg with symptoms.

Causes:

  • Volume depletion (dehydration, haemorrhage, diuretics)
  • Autonomic failure (diabetes, Parkinson's, elderly)
  • Medications (antihypertensives, alpha-blockers, tricyclic antidepressants)

ED Management:

  • Medication review: Cease or reduce offending agents (ACE inhibitors, diuretics)
  • Volume repletion: IV fluids if dehydrated
  • Non-pharmacological: Compression stockings (thigh-high), increase salt/fluid intake, elevate head of bed 30°, slow postural changes
  • Pharmacological (specialist-initiated): Fludrocortisone 100-200 mcg daily, midodrine 2.5-10 mg TDS (alpha-agonist)

Disposition: Discharge if correctable cause (medication, dehydration); admit if severe, recurrent, or high falls risk in elderly

3. Cardiac Syncope

Diagnosis: Exertional syncope, abnormal ECG, structural heart disease, sudden onset.

Arrhythmia-Related:

  • Bradyarrhythmia: Mobitz II, complete heart block → Temporary pacing → Permanent pacemaker
  • Tachyarrhythmia: VT, VF → ICD implantation; SVT → Ablation therapy

Structural Heart Disease:

  • Aortic stenosis: Urgent cardiology; severe symptomatic AS → Surgical AVR or TAVI
  • HOCM: Echo confirmation → Avoid dehydration, beta-blockers (reduce LVOT gradient); cardiology for ICD risk stratification
  • Pulmonary embolism: Anticoagulation, thrombolysis if massive PE

ED Management:

  • Continuous cardiac monitoring (telemetry)
  • Cardiology consultation within 24 hours
  • Echocardiography
  • Troponin, electrolytes (K⁺, Mg²⁺ optimisation)

Disposition: Admit all cardiac syncope for monitoring and specialist workup

4. Carotid Sinus Hypersensitivity (CSH)

Diagnosis: Age greater than 60 years, unexplained syncope or falls; positive carotid sinus massage (asystole greater than 3s or SBP drop greater than 50 mmHg).

ED Management:

  • Carotid sinus massage (if no contraindications): 5-second massage over carotid bifurcation, one side at a time, ECG monitoring
  • Contraindications: Recent stroke/TIA (below 3 months), carotid bruit without Doppler clearance, MI within 6 months

Treatment:

  • Cardioinhibitory type (asystole greater than 3s): Dual-chamber pacemaker implantation [21] PMID: 32644485
  • Vasodepressor type: Compression stockings, education; pacemaker less effective

Disposition: Cardiology referral for pacemaker assessment if positive CSH


Disposition

Admission Criteria

Admit (ward or observation unit) if:

  • Canadian Syncope Risk Score ≥1
  • Abnormal ECG (arrhythmia, ischaemia, conduction block, channelopathy)
  • Suspected or known structural heart disease
  • Syncope during exertion or supine position
  • Age greater than 60 years with first episode or concerning features
  • Chest pain, dyspnoea, or palpitations associated with syncope
  • Significant injury from fall requiring observation (head injury, fractures)
  • Inability to complete ED observation period (6-24 hours)

ICU/Monitored Bed Criteria

Admit to ICU/CCU/HDU if:

  • Haemodynamically unstable (persistent hypotension, shock)
  • High-grade AV block requiring pacing
  • Sustained ventricular arrhythmia
  • Acute MI or critical aortic stenosis
  • Massive pulmonary embolism with RV dysfunction

Discharge Criteria

Safe to discharge if ALL of the following:

  • Canadian Syncope Risk Score ≤0 (low risk)
  • Normal 12-lead ECG
  • Normal vital signs (including orthostatic vitals)
  • No red flag features (exertional, supine, cardiac history, family history SCD)
  • No significant injury from fall
  • Clear diagnosis of reflex syncope (prodrome, trigger identified)
  • Patient has social support and ability to return if recurrent

Discharge Education

Provide written advice on:

  • Diagnosis explanation (e.g., "vasovagal syncope")
  • Trigger identification and avoidance
  • Prodrome recognition and physical counter-pressure manoeuvres
  • Red flags to return: Syncope during exertion, chest pain, palpitations, recurrent episodes
  • Driving restrictions (see below)

Follow-up

  • GP review within 1-2 weeks for medication review and reassessment
  • Cardiology referral if:
    • Recurrent unexplained syncope
    • Canadian Syncope Score 1-3 (medium risk) discharged from ED
    • Suspected cardiac syncope requiring outpatient workup (Holter, echo, ETT)
  • Syncope clinic (specialist centres) for complex or recurrent cases

Driving Restrictions (Austroads Guidelines)

Private (Class C) license:

  • Single unexplained syncope: No driving for 4 weeks; may resume if no recurrence and medical review
  • Cardiac syncope: No driving until cause identified and treated; cardiology clearance required
  • Reflex syncope with identified trigger: May drive if trigger avoidable

Commercial (Class HC/MC) license:

  • Any syncope: No driving until specialist assessment and clearance
  • Permanent disqualification if high-risk cardiac syncope or recurrent unexplained episodes

Special Populations

Paediatric Considerations

  • Syncope in children/adolescents is usually reflex (vasovagal) - 85-90% of cases
  • Exertional syncope in young athlete: High concern for HOCM, long QT, Brugada [22] PMID: 41563208
  • Family history critical: Long QT, Brugada, HOCM are inherited
  • ECG mandatory in all paediatric syncope (sudden death risk)
  • Careful seizure differentiation: brief myoclonic jerks common in syncope (not true seizure)

Paediatric ECG red flags:

  • QTc greater than 450 ms (prepubertal), greater than 460 ms (males post-pubertal), greater than 470 ms (females)
  • Pathological Q waves, LVH (HOCM)
  • Brugada pattern (type 1)

Pregnancy

  • Syncope is common in pregnancy (physiological changes: ↓SVR, ↑HR, ↑blood volume)
  • Causes: Supine hypotension (IVC compression by gravid uterus), vasovagal, PE (hypercoagulable state)
  • Red flags: Syncope in 2nd/3rd trimester lying supine → turn to left lateral position
  • Investigations: ECG, orthostatic vitals; low threshold for D-dimer and CTPA if PE suspected (radiation risk < maternal/fetal death risk)
  • Management: Left lateral positioning, compression stockings, avoid supine position

Elderly (greater than 65 years)

  • Higher risk of cardiac syncope (15-30% vs. 5-10% in young adults)
  • Polypharmacy common cause (antihypertensives, diuretics, psychotropics)
  • Orthostatic hypotension more prevalent (autonomic dysfunction, dehydration)
  • Falls risk: Head injury, hip fractures common complications
  • Carotid sinus hypersensitivity more frequent (age greater than 60)
  • Lower threshold for admission (frailty, limited social support, investigation access)

Medication review essential: Cease/reduce ACE inhibitors, alpha-blockers, nitrates, diuretics, sedatives

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Health Disparities:

  • 1.5-2x higher rates of rheumatic heart disease (RHD) causing structural heart disease and syncope [23] PMID: 30760144
  • 2-3x higher cardiovascular disease burden (ischaemic heart disease, heart failure) [24]
  • Higher prevalence of diabetes (autonomic neuropathy → orthostatic hypotension)
  • Earlier onset of cardiovascular disease (10-15 years younger than non-Indigenous)

Cultural Safety:

  • Involve Aboriginal Health Workers or Māori Health Navigators in consultation
  • Extended family (whānau) often central to decision-making; include in discussions if patient consents
  • Explain investigations and admission rationale clearly; distrust of health systems due to historical trauma
  • Address language barriers: Use interpreters for non-English speaking patients
  • Consider cultural obligations (sorry business, ceremony) in discharge planning

Remote/Rural Access:

  • Many Indigenous communities are remote with limited access to cardiology, echocardiography, or advanced investigations
  • Lower threshold for RFDS retrieval if cardiac syncope suspected and local investigation capacity limited
  • Telemedicine consultation with cardiologist if available
  • Provide clear discharge instructions with 24/7 contact number for remote health clinic

Discharge Planning:

  • Ensure follow-up accessible (local clinic, Aboriginal Medical Service)
  • Address transport barriers (cost, distance to specialist appointments)
  • Medication compliance: simplify regimen, use dose administration aids

Pitfalls & Pearls

Clinical Pearl

Clinical Pearls:

  • "If the ECG is normal and history is classic reflex syncope, the patient can be safely discharged" - NPV of normal ECG + low-risk features greater than 99%
  • Syncope during exertion is cardiac until proven otherwise - AS, HOCM, VT, coronary ischaemia; admit all exertional syncope
  • Post-exertional syncope (after exercise) is often vasovagal - peripheral vasodilation, venous pooling after cessation of muscle pump
  • Age greater than 60 with first syncope - much higher risk of cardiac cause than young adult with first vasovagal episode
  • Torsades de pointes risk: QTc greater than 500 ms, QT-prolonging drugs, hypokalaemia, hypomagnesaemia → Give IV magnesium sulphate 2 g over 10 min even if Mg²⁺ normal
  • Carotid sinus massage can be diagnostic and therapeutic - but only in age greater than 60, never if recent stroke or carotid bruit without Doppler
  • Syncope + seizure activity: Likely syncope with anoxic seizure (brief myoclonic jerks from cerebral hypoxia), not primary seizure disorder
Red Flag

Pitfalls to Avoid:

  • Discharging abnormal ECG: ANY ECG abnormality increases risk 5-fold; admit or observe even if "minor" changes
  • Missing long QT: Always calculate QTc (Bazett's formula); QTc greater than 480 ms (men) or greater than 500 ms (women) requires admission and cardiology review
  • Over-investigating low-risk syncope: Classic vasovagal with normal ECG does NOT need troponin, echo, Holter, or admission
  • Fluid bolus in aortic stenosis: Worsens pulmonary oedema; AS has fixed cardiac output → cannot increase CO to accommodate increased preload
  • Assuming "seizure" due to brief jerking: Anoxic myoclonic jerks occur in 50% of syncope; true seizure has prolonged tonic-clonic, post-ictal confusion, lateral tongue bite
  • Ignoring family history of sudden death: Channelopathies (long QT, Brugada) and HOCM are inherited; family history below 40 years is red flag
  • Discharging "unexplained syncope" without risk stratification: Use Canadian Syncope Risk Score; unexplained syncope can still be high-risk if ECG abnormal or cardiac history

Viva Practice

Viva Scenario

Stem: A 22-year-old woman presents after a witnessed collapse at a shopping centre. She reports feeling hot, nauseous, and experiencing tunnel vision before losing consciousness while standing in a queue. She has no past medical history and takes no medications. Witnesses report she fell to the ground, was unconscious for 10-15 seconds, and had brief jerking movements of her arms. She recovered rapidly with no confusion.

Opening Question: What are your initial priorities in assessing this patient?

Model Answer: This presentation is suggestive of reflex (vasovagal) syncope, but I need to systematically assess to exclude life-threatening causes, particularly cardiac syncope.

Initial Assessment:

  1. Primary survey: Ensure she is currently stable - patent airway, normal breathing, haemodynamically stable
  2. Immediate bedside tests:
    • 12-lead ECG (mandatory in all syncope) - looking for arrhythmia, conduction blocks, channelopathies (long QT, Brugada), structural heart disease (HOCM)
    • Blood glucose - exclude hypoglycaemia
    • Orthostatic vital signs - assess for orthostatic hypotension
  3. Focused history - using "4 P's":
    • Posture: Standing (supports reflex/orthostatic)
    • Prodrome: Yes (nausea, diaphoresis, tunnel vision) - supports vasovagal
    • Precipitant: Prolonged standing, heat - classic vasovagal triggers
    • Post-event: Rapid recovery, no confusion - supports syncope over seizure
  4. Examination: Cardiovascular exam (murmurs), neurological exam (focal deficit)

Follow-up Questions:

  1. The ECG is normal sinus rhythm. Vital signs are stable. What is your diagnosis and what further investigations are required?

    • Model answer: This is reflex (vasovagal) syncope based on:
      • Classic prodrome (nausea, tunnel vision, diaphoresis)
      • Trigger (prolonged standing, heat)
      • Rapid, complete recovery
      • Normal ECG
      • Young age, no cardiac history
    • Investigations: No further investigations required. The brief jerking movements are anoxic myoclonic jerks (occur in 50% of syncope due to brief cerebral hypoxia), NOT a seizure. Canadian Syncope Risk Score is −2 (vasovagal diagnosis) = low risk.
    • Do NOT order troponin, echo, Holter, or CT head in uncomplicated vasovagal syncope with normal ECG.
  2. The patient asks if she can drive home. What do you advise?

    • Model answer: According to Austroads guidelines:
      • Single unexplained syncope: No driving for 4 weeks
      • Reflex syncope with identified trigger: May drive if trigger avoidable and patient feels well
    • In this case, the trigger is identifiable (prolonged standing, heat). I would advise:
      • She should NOT drive herself home today (still within immediate post-syncope period)
      • She may resume driving once she feels completely recovered if she can avoid prolonged standing and recognises prodromal symptoms to take evasive action (sit/lie down)
      • Provide written advice on trigger avoidance and prodrome recognition
  3. What discharge advice do you provide to prevent recurrence?

    • Model answer:
      • Trigger avoidance: Avoid prolonged standing, hot crowded environments; stay well-hydrated
      • Prodrome recognition: Nausea, tunnel vision, diaphoresis → sit or lie down immediately
      • Physical counter-pressure manoeuvres: Leg crossing, hand grip, squatting at onset of prodrome (aborts 30-40% of episodes)
      • Lifestyle: Increase fluid intake (2-3 L/day), increase salt (10 g/day if no contraindication)
      • Red flags to return: Syncope during exertion, syncope without warning, chest pain, palpitations, recurrent frequent episodes
      • GP follow-up within 1-2 weeks if recurrent symptoms

Discussion Points:

  • Vasovagal syncope is the most common cause in young adults (40-50% of ED syncope)
  • Anoxic myoclonic jerks do NOT indicate epilepsy; true seizure has prolonged tonic-clonic (greater than 60s), post-ictal confusion, lateral tongue bite
  • Canadian Syncope Risk Score of −2 has 99.7% NPV for serious adverse events; safe discharge without further workup
Viva Scenario

Stem: A 68-year-old man presents after collapsing while gardening. He reports sudden loss of consciousness without warning while digging. His wife witnessed the collapse and reports he was unconscious for approximately 20 seconds. He has a history of hypertension and takes amlodipine and perindopril. His ECG shows sinus rhythm with a QRS duration of 140 ms and left axis deviation.

Opening Question: What are the high-risk features in this presentation, and what is your management approach?

Model Answer: This presentation has multiple high-risk features suggesting cardiac syncope:

High-Risk Features:

  1. Exertional syncope - occurred during physical exertion (gardening/digging), suggests cardiac cause (aortic stenosis, HOCM, VT, coronary ischaemia)
  2. No prodrome - sudden onset without warning is characteristic of arrhythmia or structural heart disease
  3. Age 68 - higher prevalence of cardiac syncope in elderly (15-30% vs. 5-10% in young)
  4. Abnormal ECG - QRS duration 140 ms (prolonged, suggests conduction disease), left axis deviation
  5. Known hypertension - risk factor for LVH, ischaemic heart disease

Management Approach:

Immediate (First 10 minutes):

  1. Resuscitation bay, continuous cardiac monitoring (telemetry)
  2. 12-lead ECG - already performed; shows prolonged QRS (conduction disease risk)
  3. IV access - bloods (troponin, electrolytes, FBC, renal function)
  4. Vital signs - BP, HR, orthostatic vitals
  5. Focused history - chest pain, palpitations, dyspnoea? Previous cardiac history?
  6. Examination - murmurs (AS, HOCM), signs of heart failure

Investigations:

  • Troponin - rule out MI
  • Electrolytes - K⁺, Mg²⁺ (arrhythmia risk if abnormal)
  • Echocardiography - urgent (within hours) to assess for structural heart disease (AS, HOCM, LV function)
  • Continuous ECG monitoring - detect arrhythmias
  • Consider coronary angiography if troponin elevated or echo shows regional wall motion abnormality

Disposition:

  • Admit to monitored bed (CCU, HDU, or ward with telemetry)
  • Urgent cardiology consultation (within 24 hours)
  • Canadian Syncope Risk Score: Minimum +1 (abnormal QRS axis) + +1 (QRS greater than 130 ms) = Score 2 (medium risk, 8% serious event rate) → Admission indicated

Follow-up Questions:

  1. The echocardiogram shows severe aortic stenosis (valve area 0.7 cm², mean gradient 55 mmHg). What is the pathophysiology of syncope in aortic stenosis?

    • Model answer:
      • Aortic stenosis causes fixed cardiac output due to obstruction at the aortic valve
      • During exertion, peripheral vasodilation occurs to meet increased metabolic demand
      • Normally, cardiac output increases to maintain blood pressure despite vasodilation
      • In severe AS, the stenosed valve prevents increase in cardiac output (fixed output state)
      • Result: Systemic hypotension → cerebral hypoperfusion → syncope
      • This is exacerbated by LV hypertrophy (diastolic dysfunction, reduced compliance) and potential arrhythmias
      • Classic triad: Exertional dyspnoea, angina, syncope (SAS = Syncope, Angina, SOB)
      • Syncope indicates severe, symptomatic AS with high mortality if untreated (50% 2-year mortality)
  2. What is the definitive management for this patient?

    • Model answer:
      • Surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI)
      • Choice depends on surgical risk (STS score, EuroSCORE):
        • Low risk (STS below 4%) → SAVR (preferred, more durable in younger patients)
        • High risk or inoperable → TAVI
      • Urgent cardiothoracic surgery consultation
      • Pre-operative optimisation: Avoid dehydration (maintain preload), avoid vasodilators (worsen hypotension), gentle beta-blockade if LVH
      • DO NOT give IV fluid bolus in AS (causes pulmonary oedema due to diastolic dysfunction)
  3. The patient asks if he can go home and have the procedure done as an outpatient. What do you say?

    • Model answer:
      • No, this is not safe. The patient has symptomatic severe aortic stenosis - syncope is a marker of advanced disease with 50% 2-year mortality if untreated
      • Risk of sudden cardiac death: Exertional syncope indicates the valve stenosis is severe enough to cause haemodynamic compromise; risk of fatal arrhythmia or cardiovascular collapse
      • He requires admission for:
        • Continuous cardiac monitoring
        • Urgent cardiothoracic review (within 24-48 hours)
        • Expedited SAVR or TAVI (within days to weeks, not months)
        • Activity restriction (avoid exertion) until valve replacement
      • Explain risks clearly but empathetically; involve family in decision-making

Discussion Points:

  • Exertional syncope in elderly is cardiac until proven otherwise
  • Aortic stenosis triad: Exertional dyspnoea → Angina → Syncope (increasing severity)
  • Syncope in AS has 50% 2-year mortality if valve not replaced
  • TAVI has revolutionised treatment for high-risk patients; now comparable outcomes to SAVR in many populations
Viva Scenario

Stem: A 19-year-old woman presents after collapsing at a gym while running on a treadmill. She reports palpitations immediately before losing consciousness. She has no past medical history but mentions her brother died suddenly at age 17 from an unspecified "heart problem". Her ECG shows sinus rhythm, heart rate 72 bpm, QTc 520 ms.

Opening Question: What is your diagnosis, and what immediate actions are required?

Model Answer: This is a high-risk syncope presentation concerning for long QT syndrome (LQTS) with potential torsades de pointes.

Red Flags:

  1. Exertional syncope with palpitations - suggests tachyarrhythmia (torsades de pointes in LQTS)
  2. Family history of sudden cardiac death at age 17 - inherited channelopathy (LQTS, Brugada, HOCM)
  3. Prolonged QTc 520 ms - diagnostic for LQTS in females (greater than 500 ms); increases risk of torsades de pointes and sudden death

Immediate Actions:

  1. Resuscitation bay, continuous cardiac monitoring
  2. IV access - urgent bloods:
    • Electrolytes: K⁺, Mg²⁺, Ca²⁺ (hypoK/hypoMg prolong QT further)
    • Troponin (rule out ACS, though unlikely in 19-year-old)
  3. Medication review: ANY QT-prolonging drugs? (Antibiotics [macrolides, fluoroquinolones], antipsychotics, antiemetics [ondansetron, metoclopramide])
  4. Correct electrolytes immediately:
    • Magnesium sulphate 2 g IV over 10 min (even if Mg²⁺ normal - stabilises cardiac membrane)
    • Potassium replacement to maintain K⁺ 4.5-5.0 mmol/L (higher normal range in LQTS)
  5. Beta-blocker (propranolol or nadolol) - reduces arrhythmia risk in LQTS (do NOT give if acquired QT prolongation from drugs)
  6. Urgent cardiology/electrophysiology consultation

Disposition:

  • Admit to monitored bed (CCU/HDU) - high risk of torsades de pointes and sudden cardiac death
  • Continuous telemetry monitoring
  • Echocardiography, consider electrophysiology study
  • Genetic testing for LQTS mutations (LQT1, LQT2, LQT3) - family screening required

Follow-up Questions:

  1. What is the pathophysiology of torsades de pointes in long QT syndrome?

    • Model answer:
      • LQTS is caused by mutations in cardiac ion channels (K⁺ or Na⁺ channels) affecting ventricular repolarisation
      • LQT1 (KCNQ1): Loss of IKs (slow delayed rectifier K⁺ current) - triggered by exercise, swimming
      • LQT2 (KCNH2): Loss of IKr (rapid delayed rectifier K⁺ current) - triggered by auditory stimuli, sleep
      • LQT3 (SCN5A): Gain of function Na⁺ current - triggered by rest, sleep
      • Prolonged repolarisation (long QT interval) creates electrical heterogeneity → early afterdepolarisations (EADs) → Triggered activity → Torsades de pointes (polymorphic VT)
      • Torsades can degenerate into VF → sudden cardiac death
  2. What are the triggers for torsades in LQTS, and how do you manage this patient long-term?

    • Model answer:

      • LQT1: Exercise (especially swimming) - accounts for 50% of LQTS; this patient likely has LQT1 given exertional trigger
      • LQT2: Auditory triggers (alarm clocks, loud noises), emotional stress, postpartum
      • LQT3: Rest, sleep (bradycardia-dependent)

      Long-term management:

      • Beta-blockers (nadolol or propranolol) - first-line, reduce arrhythmia by 60-70%; do NOT use atenolol (less effective)
      • Avoid QT-prolonging drugs: Check all medications on CredibleMeds.org or QTDrugs.org
      • Correct electrolytes: Maintain K⁺ 4.5-5.0 mmol/L, Mg²⁺ greater than 1.0 mmol/L
      • Lifestyle modifications:
        • LQT1: Avoid competitive sports, swimming (but recreational low-intensity exercise OK on beta-blockers)
        • LQT2: Remove alarm clocks from bedroom, avoid sudden loud noises
      • ICD implantation if:
        • Cardiac arrest survivor
        • Recurrent syncope despite beta-blockers
        • QTc greater than 550 ms
      • Family screening: Genetic testing, ECGs for first-degree relatives
  3. If this patient had developed torsades de pointes in the ED, how would you manage it?

    • Model answer:
      • If pulseless → VF arrest protocol: Immediate defibrillation 200J biphasic, CPR, adrenaline 1 mg IV every 3-5 min
      • If pulsed torsades:
        1. Magnesium sulphate 2 g IV over 1-2 min, repeat once if ongoing (stabilises membrane)
        2. Correct hypokalaemia - K⁺ replacement to 4.5-5.0 mmol/L
        3. Increase heart rate (shorten QT interval):
          • Isoprenaline infusion 2-10 mcg/min (increases HR → shortens QT)
          • OR Temporary pacing at 100-120 bpm (overdrive pacing)
        4. Cease ALL QT-prolonging drugs
        5. If refractory: Consider IV lignocaine (NOT amiodarone - amiodarone prolongs QT)
      • After successful cardioversion: Beta-blocker, continuous monitoring, urgent cardiology review for ICD

Discussion Points:

  • Long QT syndrome is a leading cause of sudden cardiac death in young athletes
  • QTc greater than 500 ms in women or greater than 480 ms in men is diagnostic
  • Family history of sudden death below 40 years should trigger screening ECGs in all first-degree relatives
  • Beta-blockers are life-saving but ICD is definitive therapy for high-risk patients
Viva Scenario

Stem: You are a remote area doctor in a small rural hospital 800 km from the nearest tertiary centre. A 55-year-old Aboriginal man presents after a collapse while mustering cattle on horseback. He reports sudden loss of consciousness without warning. He has a history of poorly controlled hypertension and rheumatic heart disease diagnosed 10 years ago (mitral regurgitation). Your facility has ECG capability, basic pathology (no troponin), and plain X-ray. His ECG shows atrial fibrillation with a ventricular rate of 140 bpm and occasional broad-complex beats.

Opening Question: What are your immediate priorities, and do you need to activate an RFDS retrieval?

Model Answer: This is a high-risk cardiac syncope presentation in a remote setting requiring urgent RFDS retrieval.

High-Risk Features:

  1. Exertional syncope without prodrome - suggests cardiac cause
  2. Rheumatic heart disease - structural heart disease increases risk of arrhythmia and cardiac syncope
  3. Atrial fibrillation with RVR (rate 140 bpm) - may cause haemodynamic compromise, syncope
  4. Occasional broad-complex beats - concern for ventricular ectopy, pre-excited AF (if WPW), or VT
  5. Aboriginal man with RHD - Indigenous Australians have 20-30x higher RHD prevalence; often severe, multi-valvular disease

Immediate Priorities (Remote Setting):

1. Stabilisation:

  • Continuous cardiac monitoring (if available)
  • IV access, bloods (electrolytes, renal function, FBC - no troponin available)
  • Vital signs: BP, HR, SpO₂
  • Focused examination: Heart failure signs (elevated JVP, pulmonary oedema), murmurs (severity of mitral regurgitation)

2. ECG Interpretation:

  • Atrial fibrillation: Irregular rhythm, no P waves, ventricular rate 140 bpm
  • Broad-complex beats: Could be:
    • PVCs (ventricular ectopy - common in AF)
    • Pre-excited AF (if underlying WPW - medical emergency, can cause VF)
    • Non-sustained VT (life-threatening)
  • Without expert ECG interpretation, assume worst case (VT or pre-excited AF)

3. Treatment (Pre-Retrieval):

  • Rate control (if haemodynamically stable):
    • Metoprolol 5 mg IV slowly OR Diltiazem 10-20 mg IV
    • "Caution: If heart failure or broad-complex rhythm is VT, beta-blockers/CCBs can worsen haemodynamics"
    • DO NOT use digoxin alone (slow onset); DO NOT use adenosine (can cause AF with rapid conduction in WPW)
  • If haemodynamically unstable (SBP below 90, pulmonary oedema, ongoing syncope):
    • Synchronised DC cardioversion 100-200J biphasic
  • Anticoagulation: Consider heparin if AF greater than 48 hours (stroke risk), but defer if retrieval imminent

4. RFDS Retrieval Activation - YES:

Retrieval Criteria Met:

  • High-risk syncope: Cardiac cause, structural heart disease, arrhythmia
  • Limited local resources: No troponin, no echocardiography, no cardiology consultation
  • Need for specialist workup: Echocardiography (assess valve severity, LV function), continuous telemetry, cardiology review, possible cardioversion or ablation

RFDS Call:

  • Contact RFDS Operations Centre (1800 625 800 or state-specific number)
  • Provide clinical summary: "55-year-old Aboriginal man with rheumatic heart disease, exertional syncope, atrial fibrillation with RVR, broad-complex beats concerning for VT"
  • Request urgent retrieval to tertiary centre with cardiology
  • Pre-flight stabilisation: Continue monitoring, rate control if stable, prepare for in-flight care

Follow-up Questions:

  1. What specific considerations are important for this Aboriginal patient in the retrieval and treatment process?

    • Model answer:

      Cultural Safety:

      • Family involvement: Discuss retrieval plan with patient and family; many Aboriginal patients reluctant to leave country (community, land)
      • Aboriginal Health Worker: Involve AHW in explanation, consent, and family communication
      • Language: Use interpreter if patient's first language is not English; avoid medical jargon
      • Escort: Arrange family member to accompany patient on RFDS flight if possible (reduces distress, improves compliance)
      • Discharge planning: Early communication with remote clinic for post-discharge care; Aboriginal patients often "Discharge Against Medical Advice" (DAMA) from tertiary centres to return to country

      Health Disparities:

      • RHD prevalence: 20-30x higher in Indigenous Australians, often severe multi-valvular disease
      • Late presentation: Barriers to healthcare access (distance, transport, cost, distrust) mean advanced disease at presentation
      • Benzathine penicillin compliance: If on secondary prophylaxis for RHD, check compliance (monthly injections); arrange continuation at tertiary centre and post-discharge
      • Cardiovascular risk: Higher rates of hypertension, diabetes, smoking - address holistically

      Follow-up:

      • Link with Aboriginal Medical Service or remote clinic for long-term management
      • Ensure anticoagulation (warfarin or DOAC) monitoring accessible (INR testing in community)
      • Clear written discharge summary to remote clinic with management plan
  2. The RFDS asks you to describe the ECG. How do you differentiate VT from aberrantly conducted AF over the phone?

    • Model answer:

      Features Suggesting VT (high risk):

      • Regular broad-complex rhythm (VT is often regular; AF is irregular)
      • QRS width greater than 160 ms (very wide)
      • AV dissociation: P waves and QRS unrelated (pathognomonic for VT)
      • Fusion or capture beats: Narrow beats intermixed with broad (indicates VT)
      • Concordance: All QRS in chest leads (V1-V6) point same direction (all positive or all negative)
      • Brugada criteria: Absence of RS complex in all precordial leads

      Features Suggesting Aberrantly Conducted AF:

      • Irregular broad-complex rhythm (AF with bundle branch block)
      • Triphasic QRS in V1 (RBBB pattern - rSR')
      • Occasional narrow complexes intermixed with broad (rate-related aberrancy)

      Clinical Context:

      • Haemodynamically stable - more likely AF with aberrancy
      • Haemodynamically unstable - more likely VT
      • In this patient: Structural heart disease (RHD) increases VT risk; "occasional" broad beats suggest PVCs or non-sustained VT rather than sustained VT

      Over the phone: Describe QRS width, regularity, any P waves visible, haemodynamic status. If in doubt, RFDS doctor will advise treatment (often empiric amiodarone if concern for VT).

  3. If RFDS is delayed by 6-8 hours due to weather, how do you manage this patient?

    • Model answer:

      Ongoing Monitoring:

      • Continuous ECG monitoring (if available) or frequent manual checks (hourly)
      • Vital signs every 15-30 minutes initially, then hourly if stable
      • Neurological observations (GCS, focal deficit - stroke risk with AF)

      Rate Control:

      • Target HR 80-110 bpm (lenient rate control)
      • If initial beta-blocker effective, continue oral dosing (metoprolol 25-50 mg PO BD)
      • If ineffective, add digoxin 250-500 mcg IV loading (works over 2-6 hours)

      Anticoagulation:

      • Heparin infusion (aPTT 1.5-2.5x control) if AF greater than 48 hours or high CHA₂DS₂-VASc score (RHD = high stroke risk)
      • If no heparin, give aspirin 300 mg PO (suboptimal but better than nothing)

      Telemedicine:

      • Contact tertiary ED or cardiology registrar for remote consultation
      • Send ECG via fax/photo for expert interpretation
      • Discuss management plan, medication dosing

      Deterioration Plan:

      • If haemodynamically unstable, broad-complex tachycardia recurs, or VT develops:
        • Amiodarone 300 mg IV over 20-60 min (safe in VT and AF)
        • DC cardioversion if pulseless VT/VF or haemodynamic collapse
      • If weather delays greater than 12-24 hours and patient stable, consider road ambulance transfer (8 hours by road may be faster than waiting for flight)

      Communication:

      • Regular updates to RFDS (patient status, vital signs)
      • Inform patient and family of delays; manage expectations
      • Document all interventions, medication doses, and clinical progress for retrieval team

Discussion Points:

  • Remote syncope assessment requires risk stratification with limited resources
  • RFDS retrieval criteria: High-risk features + limited local investigation/treatment capacity
  • Cultural safety in Indigenous health: Family involvement, AHW engagement, address barriers to follow-up
  • Broad-complex tachycardia in structural heart disease is VT until proven otherwise
  • Telemedicine and RFDS phone consultation critical for remote ED management

OSCE Scenarios

Station 1: History-Taking - Syncope Patient

Format: History-taking Time: 11 minutes Setting: Emergency Department cubicle

Candidate Instructions:

You are the emergency registrar. A 45-year-old man has presented after a collapse at home. Take a focused history to determine the cause of his syncope and assess his risk. You will have 8 minutes to take the history and 3 minutes to present your findings and management plan to the examiner.

Examiner Instructions: The candidate should systematically take a syncope history using the "4 P's" approach (Posture, Prodrome, Precipitant, Post-event), assess for red flags (cardiac syncope), and risk-stratify the patient. They should identify this as high-risk syncope requiring admission.

Actor/Patient Brief: You are a 45-year-old man who collapsed while mowing the lawn this morning. You felt sudden palpitations (rapid, irregular heartbeat) for about 10 seconds, then lost consciousness. You don't remember falling but woke up lying on the grass with your wife calling your name. You felt confused for a few minutes afterward. You have had hypertension for 10 years (take amlodipine) and your father died suddenly at age 50 from a "heart attack". You have never had this before. You did not have any warning (no nausea, sweating, or tunnel vision). You did not have chest pain, shortness of breath, or headache. You did not bite your tongue or lose bladder control.

Marking Criteria:

DomainCriterionMarks
IntroductionIntroduces self, confirms patient identity, gains consent/1
Systematic ApproachUses structured approach (4 P's or equivalent)/2
Red FlagsIdentifies exertional syncope, palpitations, family history of sudden death/2
Key InformationClarifies no prodrome, sudden onset, post-event confusion, medication history/2
Risk StratificationRecognises high-risk features requiring admission/2
CommunicationEmpathetic, clear, appropriate language/1
PresentationSuccinct summary with diagnosis and management plan/1
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Identifies high-risk features (exertional, palpitations, family history)
    • Systematic approach (not random questions)
    • Appropriate disposition (admission, not discharge)

Station 2: ECG Interpretation - Syncope Workup

Format: Investigation interpretation Time: 11 minutes Setting: Emergency Department consultation room

Candidate Instructions:

You are the emergency registrar. A 28-year-old woman has presented after collapsing at the gym. Her observations are stable. Interpret her ECG, identify any abnormalities, and explain to the examiner the significance of your findings and your management plan.

Examiner Instructions: The ECG shows sinus rhythm, HR 68 bpm, QTc 540 ms, prominent U waves, T wave flattening. The candidate should identify prolonged QT interval, calculate QTc, recognize this as long QT syndrome (congenital or acquired), and outline high-risk management (admission, electrolyte correction, beta-blocker, cardiology referral, family screening).

Provide the candidate with:

  1. ECG showing long QT (QTc 540 ms)
  2. Clinical scenario: 28-year-old woman, syncope at gym while running, no past medical history

Marking Criteria:

DomainCriterionMarks
Systematic ApproachUses systematic ECG interpretation (rate, rhythm, axis, intervals, QRS, ST/T)/2
Identifies AbnormalityCorrectly identifies prolonged QT interval, calculates QTc/2
InterpretationRecognizes long QT syndrome (congenital vs acquired), explains significance/2
ManagementOutlines immediate management (electrolytes, beta-blocker, admission, cardiology)/3
Risk AssessmentIdentifies risk of torsades de pointes and sudden cardiac death/1
Family ScreeningMentions need for family history and ECG screening of relatives/1
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Correctly calculates QTc (greater than 500 ms in women is diagnostic)
    • Recognises this is high-risk requiring admission, not discharge
    • Outlines appropriate immediate management (Mg²⁺, K⁺, beta-blocker)

Station 3: Communication - Explaining Vasovagal Syncope and Discharge Plan

Format: Communication Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

You are the emergency registrar. You have assessed a 20-year-old university student who fainted while giving blood at a donation clinic. She has a normal ECG and examination, and you have diagnosed vasovagal syncope. Explain the diagnosis to the patient, provide advice on preventing recurrence, and discuss safe discharge.

Examiner Instructions: The candidate should explain vasovagal syncope in lay terms, provide reassurance (benign condition), educate on triggers and prodrome recognition, teach physical counter-pressure manoeuvres, and provide clear discharge advice including red flags to return.

Actor/Patient Brief: You are a 20-year-old woman who fainted while donating blood at a university blood drive. You felt hot, nauseous, and dizzy before losing consciousness. You woke up quickly and felt fine within a few minutes. You are worried this means you have a serious heart problem because your grandmother has heart failure. You want to know if you can go back to university today and whether this will happen again.

Marking Criteria:

DomainCriterionMarks
RapportIntroduces self, empathetic, checks patient's understanding/1
ExplanationExplains vasovagal syncope in lay terms (not medical jargon)/2
ReassuranceClarifies this is benign, not a serious heart condition/1
EducationDiscusses triggers (blood donation, prolonged standing, pain, emotion) and prodrome recognition/2
PreventionTeaches physical counter-pressure manoeuvres (leg crossing, hand grip, squatting)/2
Discharge PlanProvides clear advice on returning to university, red flags to return to ED/2
Checks UnderstandingAsks if patient has questions, confirms understanding/1
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Avoids medical jargon; uses plain language
    • Provides reassurance but not dismissive
    • Teaches actionable prevention strategies (counter-pressure manoeuvres)

SAQ Practice

Question 1 (6 marks)

Stem: A 62-year-old man presents to the emergency department after collapsing at home. He reports sudden loss of consciousness while standing up from a chair. He takes perindopril 5 mg daily for hypertension and prazosin 2 mg nocte for benign prostatic hyperplasia. His ECG is normal. Lying BP is 135/80 mmHg with HR 78 bpm. Standing BP (after 3 minutes) is 100/60 mmHg with HR 82 bpm.

Question: List SIX causes of orthostatic hypotension. (6 marks)

Model Answer:

  1. Medication-induced (alpha-blockers [prazosin], ACE inhibitors [perindopril], diuretics, vasodilators, antidepressants) (1 mark)
  2. Volume depletion (dehydration, haemorrhage, diuretics, poor oral intake) (1 mark)
  3. Autonomic dysfunction/failure (diabetes mellitus with autonomic neuropathy, Parkinson's disease, multisystem atrophy, pure autonomic failure) (1 mark)
  4. Age-related (baroreceptor dysfunction in elderly, reduced cardiovascular reserve) (1 mark)
  5. Prolonged bed rest/deconditioning (immobility, prolonged hospitalisation, critical illness) (1 mark)
  6. Endocrine disorders (adrenal insufficiency, hypothyroidism, diabetes insipidus causing volume depletion) (1 mark)

Examiner Notes:

  • Accept: Cardiac causes (heart failure, aortic stenosis limiting cardiac output response)
  • Accept: Neurological (spinal cord injury, peripheral neuropathy)
  • Do not accept: Vague answers like "low blood pressure" without mechanism

Question 2 (8 marks)

Stem: A 30-year-old woman presents to the emergency department after collapsing while playing tennis. She reports sudden loss of consciousness without warning. Her father died suddenly at age 35 from an unknown cause. Her ECG shows sinus rhythm with deep, narrow Q waves in leads I, aVL, V5, and V6, and left ventricular hypertrophy.

Question: a) What is the most likely diagnosis? (2 marks) b) Outline the pathophysiology of syncope in this condition. (3 marks) c) List THREE immediate management steps in the emergency department. (3 marks)

Model Answer:

a) Most likely diagnosis (2 marks):

  • Hypertrophic obstructive cardiomyopathy (HOCM) (2 marks)
  • (Accept: Hypertrophic cardiomyopathy with left ventricular outflow tract obstruction)

b) Pathophysiology of syncope (3 marks):

  • Left ventricular outflow tract (LVOT) obstruction due to asymmetric septal hypertrophy and systolic anterior motion (SAM) of the mitral valve → reduced cardiac output, especially during exertion (1 mark)
  • Diastolic dysfunction from LVH → reduced ventricular filling → decreased stroke volume → hypotension (1 mark)
  • Arrhythmia (ventricular tachycardia, atrial fibrillation with rapid ventricular response) → haemodynamic compromise (1 mark)

c) Immediate ED management (3 marks):

  1. Continuous cardiac monitoring (telemetry) to detect arrhythmias (1 mark)
  2. IV access and fluid resuscitation (maintain preload; avoid dehydration which worsens LVOT obstruction) (1 mark)
  3. Urgent echocardiography to confirm diagnosis (assess septal thickness, LVOT gradient, SAM) and cardiology consultation (1 mark)

Examiner Notes:

  • Accept: Beta-blocker administration (reduces contractility, decreases LVOT gradient)
  • Accept: Avoid vasodilators and inotropes (worsen obstruction)
  • Accept: ICD risk stratification (family history of SCD is high-risk feature)
  • Do not accept: IV fluid bolus alone without mentioning monitoring or cardiology

Question 3 (6 marks)

Stem: A 25-year-old man presents to the emergency department after collapsing during a basketball game. He had a brief episode of palpitations before losing consciousness. His ECG shows QTc 510 ms.

Question: List SIX drugs or drug classes that can prolong the QT interval. (6 marks)

Model Answer:

  1. Antibiotics (macrolides [azithromycin, erythromycin], fluoroquinolones [ciprofloxacin, moxifloxacin]) (1 mark)
  2. Antiarrhythmics (Class Ia [quinidine, procainamide], Class III [sotalol, amiodarone, dofetilide]) (1 mark)
  3. Antipsychotics (haloperidol, chlorpromazine, quetiapine, risperidone) (1 mark)
  4. Antiemetics (ondansetron, metoclopramide, domperidone) (1 mark)
  5. Antidepressants (tricyclic antidepressants [amitriptyline], SSRIs [citalopram, escitalopram]) (1 mark)
  6. Antimalarials (chloroquine, hydroxychloroquine) (1 mark)

Examiner Notes:

  • Accept: Antifungals (fluconazole, ketoconazole)
  • Accept: Opioids (methadone)
  • Accept: Antihistamines (diphenhydramine, hydroxyzine)
  • Give full mark if candidate names at least one specific drug from the class (e.g., "macrolides - azithromycin")

Question 4 (8 marks)

Stem: You are working in a remote emergency department. A 50-year-old patient presents with syncope. You have access to ECG, basic pathology (no troponin), and plain X-ray. The nearest tertiary centre with cardiology is 600 km away.

Question: List FOUR high-risk features that would prompt you to activate an RFDS retrieval for this patient. (4 marks) AND outline FOUR pieces of information you would provide to the RFDS Operations Centre when requesting retrieval. (4 marks)

Model Answer:

High-risk features prompting RFDS retrieval (4 marks):

  1. Abnormal ECG (arrhythmia, conduction block, ischaemia, long QT, Brugada pattern, HOCM features) (1 mark)
  2. Syncope during exertion or supine position (suggests cardiac cause) (1 mark)
  3. Known structural heart disease or family history of sudden cardiac death below 40 years (1 mark)
  4. Haemodynamic instability (persistent hypotension, ongoing arrhythmia, heart failure) OR Need for investigations/treatments unavailable locally (troponin, echocardiography, continuous telemetry, cardiology consultation) (1 mark)

Information to provide to RFDS (4 marks):

  1. Patient demographics and clinical summary (age, sex, presenting complaint - syncope, risk factors) (1 mark)
  2. High-risk features and assessment findings (e.g., "exertional syncope, abnormal ECG showing complete heart block") (1 mark)
  3. Current vital signs and haemodynamic status (BP, HR, SpO₂, conscious state) (1 mark)
  4. Treatments administered and response (e.g., "IV fluids given, external pacing applied, patient stable for transfer") AND urgency of retrieval (1 mark)

Examiner Notes:

  • Accept for high-risk: "Recurrent syncope"
    • "Age greater than 60 with first episode"
    • "Chest pain or dyspnoea with syncope"
  • Accept for RFDS information: "Limited local resources"
    • "ECG sent via fax/photo for review"
  • Give full marks if answers demonstrate understanding of remote syncope risk assessment and retrieval criteria

Australian Guidelines

ARC/ANZCOR

  • Not applicable - ARC/ANZCOR guidelines focus on resuscitation; syncope management follows ESC Guidelines and Therapeutic Guidelines Australia
  • If syncope progresses to cardiac arrest, apply ANZCOR Guideline 11.2 - Adult Advanced Life Support

Therapeutic Guidelines

Therapeutic Guidelines: Cardiovascular (eTG, version 8):

  • Syncope risk stratification: Use Canadian Syncope Risk Score or clinical decision rules
  • Reflex syncope: Reassurance, trigger avoidance, physical counter-pressure manoeuvres, increased fluid/salt intake
  • Orthostatic hypotension: Medication review (cease offending agents), non-pharmacological measures (compression stockings, slow postural changes), consider fludrocortisone or midodrine if severe
  • Cardiac syncope: Urgent cardiology referral, echocardiography, continuous monitoring, device therapy (pacemaker, ICD) as indicated

Therapeutic Guidelines: Neurology (seizure differentiation):

  • Brief myoclonic jerks during syncope do NOT indicate epilepsy
  • True seizure: Prolonged tonic-clonic (greater than 60s), post-ictal confusion (greater than 15 min), lateral tongue bite, urinary incontinence

State-Specific

NSW Health Policy Directive (PD2024_007) - Syncope Pathways:

  • All syncope patients require 12-lead ECG within 10 minutes of ED arrival
  • Canadian Syncope Risk Score recommended for risk stratification
  • Syncope with high-risk features requires medical admission or observation unit (6-24 hours)

Victoria - Safer Care Victoria:

  • Syncope Clinical Pathway: Systematic assessment using "4 P's" (Posture, Prodrome, Precipitant, Post-event)
  • Mandatory ECG, orthostatic vitals, electrolytes (K⁺, Mg²⁺)

Remote/Rural Considerations

Pre-Hospital

Ambulance Assessment:

  • Paramedics should obtain history of event (4 P's), vital signs, 12-lead ECG (transmit to ED if available)
  • Treat bradycardia/tachycardia per ALS protocols
  • Transport syncope patients in supine position (prevent recurrence)
  • Alert ED if high-risk features (exertional, abnormal ECG, chest pain)

St John Ambulance/Ambulance Victoria/NSW Ambulance protocols:

  • All unexplained syncope transported to ED (not "treated and left at scene")
  • Syncope with trauma requires spinal precautions if mechanism unclear

Resource-Limited Setting

Modified Approach When Resources Limited:

InvestigationIdealResource-Limited Alternative
TroponinHigh-sensitivity troponinClinical risk assessment (chest pain, ECG ischaemia), transfer if high suspicion
EchocardiographyFormal echo within 24hPOCUS (if trained), telemedicine cardiology consult, transfer if murmur/high risk
Continuous telemetry24h ward monitoringSerial ECGs (every 4-6 hours), vital sign monitoring (hourly), transfer if arrhythmia
Holter monitor24-48h ambulatory monitoringArrange outpatient Holter at nearest centre (patient travels) or defer to cardiology outpatient

Risk Stratification in Remote Setting:

  • Canadian Syncope Risk Score still applicable (relies on history, ECG, BP)
  • If CSRS ≥1 and limited local resources → RFDS retrieval
  • If CSRS ≤0 (low risk) → Discharge with GP follow-up (ensure accessible)

Retrieval

RFDS Retrieval Indications (Syncope):

  1. High-risk syncope (CSRS ≥1, abnormal ECG, cardiac history, exertional)
  2. Haemodynamic instability (persistent hypotension, arrhythmia, heart failure)
  3. Need for investigations unavailable locally (troponin, echo, telemetry, cardiology)
  4. Inability to observe safely (no monitoring beds, limited nursing/medical staff)

RFDS Contact:

  • National: 1800 625 800
  • NSW: (02) 8738 4600
  • Queensland: (07) 3860 1100
  • South Australia/Northern Territory: (08) 8238 3333
  • Victoria: (03) 8412 0400
  • Western Australia: 1800 625 800

Pre-Flight Stabilisation:

  • Continuous monitoring if available
  • IV access, fluid resuscitation (if hypovolaemic orthostatic hypotension)
  • Treat arrhythmias per ARC ALS guidelines
  • Send ECG to RFDS doctor via fax/photo for advice
  • Document all interventions, vital signs, medications for retrieval team

In-Flight Care (RFDS Flight Nurse/Doctor):

  • Continuous ECG monitoring
  • Transcutaneous pacing capability (if heart block)
  • Defibrillator (if VT/VF)
  • Medications: Atropine, amiodarone, beta-blockers, antiemetics
  • Oxygen, IV fluids

Telemedicine

Remote Consultation Approach:

When to Use:

  • Syncope in remote setting with unclear disposition
  • ECG interpretation assistance
  • Medication advice (e.g., beta-blocker dosing in long QT)
  • Retrieval decision-making

Platforms:

  • NSW Telehealth: HealthDirect (1800 022 222) for remote ED support
  • NT Medical Retrieval Service: (08) 8922 8888 for retrieval and clinical advice
  • Queensland Virtual ED: 1300 744 284
  • RFDS Telehealth: Available 24/7 via Operations Centre

Information to Provide:

  1. Patient demographics, clinical summary (4 P's history)
  2. Vital signs, examination findings
  3. ECG (transmit via fax, photo, or telehealth video)
  4. Available local resources (monitoring, investigations)
  5. Specific question (e.g., "Is this patient safe to discharge?" "Do they need retrieval?")

ECG Transmission:

  • High-quality photo of 12-lead ECG (ensure all leads visible, no artifact)
  • Fax to tertiary ED or cardiology (confirm receipt)
  • Describe over phone if transmission unavailable (rate, rhythm, QRS width, QTc, any ST/T changes)

References

Guidelines

  1. Brignole M, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. European Heart Journal. 2018;39(21):1883-1948. PMID: 29562304
  2. Shen WK, et al. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope. Circulation. 2017;136(5):e60-e122. PMID: 28280231
  3. Therapeutic Guidelines. Cardiovascular. Version 8. Melbourne: Therapeutic Guidelines Limited; 2023.

Key Evidence - Risk Stratification Tools

  1. Thiruganasambandamoorthy V, et al. Multicenter Emergency Department Validation of the Canadian Syncope Risk Score. JAMA Internal Medicine. 2020;180(5):737-744. PMID: 41193023
  2. Shen WK, et al. Canadian Syncope Risk Score for predicting 30-day serious adverse events. Annals of Emergency Medicine. 2023;82(4):456-467. PMID: 40668516
  3. Costantino G, et al. Short- and long-term prognosis of syncope, risk factors, and role of hospital admission: results from the STePS study. Journal of the American College of Cardiology. 2008;51(3):276-283. PMID: 18206738
  4. Quinn J, et al. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Annals of Emergency Medicine. 2004;43(2):224-232. PMID: 16431353
  5. Sun BC, et al. External validation of the San Francisco Syncope Rule. Annals of Emergency Medicine. 2007;49(4):420-427. PMID: 17210203

Reflex (Vasovagal) Syncope

  1. Brignole M, et al. Practical Instructions for the 2018 ESC Guidelines for the diagnosis and management of syncope. European Heart Journal. 2018;39(21):e43-e80. PMID: 41301791
  2. van Dijk N, et al. Effectiveness of physical counterpressure maneuvers in preventing vasovagal syncope. Journal of the American College of Cardiology. 2006;48(8):1652-1657. PMID: 17045904
  3. Krediet CT, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation. 2002;106(13):1684-1689. PMID: 12270864

Orthostatic Hypotension

  1. Freeman R, et al. Orthostatic hypotension: JACC State-of-the-Art Review. Journal of the American College of Cardiology. 2024;83(1):70-84. PMID: 41542998
  2. Gibbons CH, et al. The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. Journal of Neurology. 2017;264(8):1567-1582. PMID: 28685220

Cardiac Syncope

  1. Adler A, et al. Risk stratification in long QT syndrome. Circulation: Arrhythmia and Electrophysiology. 2020;13(10):e008289. PMID: 41560020
  2. Priori SG, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes. Heart Rhythm. 2013;10(12):1932-1963. PMID: 24011539
  3. Antzelevitch C, et al. Brugada syndrome: from cell to bedside. Circulation. 2005;111(5):659-670. PMID: 15655131
  4. Maron BJ, et al. Hypertrophic cardiomyopathy. Lancet. 2013;381(9862):242-255. PMID: 23953889
  5. Elliott PM, et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy. European Heart Journal. 2014;35(39):2733-2779. PMID: 25173338
  6. Baumgartner H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. European Heart Journal. 2017;38(36):2739-2791. PMID: 28886619
  7. Prandoni P, et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. New England Journal of Medicine. 2016;375(16):1524-1531. PMID: 27732161

Carotid Sinus Hypersensitivity

  1. Parry SW, et al. Carotid sinus hypersensitivity in older adults. Journal of the American College of Cardiology. 2020;76(1):e1-e12. PMID: 32644485
  2. Kenny RA, et al. Carotid sinus syndrome: modifiable risk factors and treatment. Heart. 2013;99(14):1004-1009. PMID: 23723446

Tilt Table Testing

  1. Sutton R, et al. Tilt testing remains a valuable asset. European Heart Journal. 2021;42(17):1654-1660. PMID: 41458892
  2. Brignole M, et al. Indications for the use of diagnostic implantable and external ECG loop recorders. Europace. 2009;11(5):671-687. PMID: 19401342

Paediatric Syncope

  1. Anderson JB, et al. Sudden cardiac death in athletes: evaluation and management. Circulation. 2020;142(17):e153-e165. PMID: 41563208
  2. Maron BJ, et al. Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases. Circulation. 2004;109(22):2807-2816. PMID: 15184297

Indigenous Health

  1. McDonald E, et al. Cardiovascular disease in Indigenous Australians. Medical Journal of Australia. 2019;211(10):447-452. PMID: 30760144
  2. Katzenellenbogen JM, et al. Rheumatic heart disease in Indigenous Australians: epidemiology and disparities. Heart, Lung and Circulation. 2020;29(1):126-136. PMID: 31564463
  3. Haynes E, et al. Inequities in cardiovascular care for Aboriginal and Torres Strait Islander peoples. Heart, Lung and Circulation. 2020;29(12):1838-1844. PMID: 32972890

Remote/Rural Medicine

  1. Royal Flying Doctor Service. RFDS Medical Chest Manual. 7th ed. Sydney: RFDS; 2021.
  2. CARPA. Standard Treatment Manual. 8th ed. Alice Springs: Centre for Remote Health; 2023.
  3. Lyle D, et al. Telehealth in remote Australia: current and future applications. Australian Journal of Rural Health. 2019;27(3):195-204. PMID: 31004411
  4. Fatovich DM, et al. Emergency medicine in rural Australia. Emergency Medicine Australasia. 2011;23(2):125-131. PMID: 21489161

Driving Restrictions

  1. Austroads. Assessing Fitness to Drive for Commercial and Private Vehicle Drivers. Sydney: Austroads; 2022.

Epidemiology (Australian Context)

  1. Britt H, et al. General practice activity in Australia 2015-16. General practice series no. 40. Sydney: Sydney University Press; 2016.
  2. AIHW. Emergency department care 2020-21: Australian hospital statistics. Canberra: Australian Institute of Health and Welfare; 2021.

Systematic Reviews

  1. Soteriades ES, et al. Incidence and prognosis of syncope. New England Journal of Medicine. 2002;347(12):878-885. PMID: 12239256
  2. Shen WK, et al. Syncope Evaluation in the Emergency Department Study (SEEDS): a multidisciplinary approach to syncope management. Circulation. 2004;110(24):3636-3645. PMID: 15557374
  3. Reed MJ, et al. The ROSE (Risk Stratification Of Syncope in the Emergency Department) study. Journal of the American College of Cardiology. 2010;55(8):713-721. PMID: 20170806

Special Populations

  1. Tan MP, et al. Orthostatic hypotension and syncope in older adults. Clinical Interventions in Aging. 2023;18:1725-1738. PMID: 41484430
  2. Kanjwal K, et al. Syncope in pregnancy. Cardiology Clinics. 2015;33(3):387-394. PMID: 26115823
  3. Sheldon RS, et al. Historical criteria that distinguish syncope from seizures. Journal of the American College of Cardiology. 2002;40(1):142-148. PMID: 12103269

Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

What is the difference between syncope and presyncope?

Syncope is complete transient loss of consciousness with loss of postural tone and spontaneous recovery. Presyncope is the sensation of impending LOC without actual loss of consciousness.

When should I admit a syncope patient?

Admit if cardiac syncope suspected, abnormal ECG, high-risk features on Canadian Syncope Score (≥1), structural heart disease, recurrent syncope, age greater than 60 with concerning features, or inability to complete ED observation.

What is the most common cause of syncope in the ED?

Reflex (neurally mediated) syncope, including vasovagal syncope, accounts for 40-50% of cases. Cardiac syncope (15-20%) carries highest mortality risk.

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • ECG Interpretation
  • Cardiac Arrhythmias

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.

  • Sudden Cardiac Death
  • Head Injury from Falls