What Syncope Is — and What It Is Not
"Syncope is a transient loss of consciousness due to global cerebral hypoperfusion, characterised by rapid onset, short duration and spontaneous complete recovery. The emergency task is not to explain every faint — most are benign and never fully explained — but to separate the reflex faint that needs reassurance from the cardiac syncope that is a warning shot before sudden death."
Tintinalli's Emergency Medicine, 9th Ed. Syncope. McGraw-Hill; 2020.Three mechanistic categories
- Reflex (neurally mediated) — commonest & benign: vasovagal (emotional/orthostatic triggers, prodrome of nausea/warmth/greying vision), situational (cough, micturition, defecation), carotid sinus.
- Orthostatic hypotension: drugs (antihypertensives, diuretics), volume depletion/bleeding, autonomic failure. Symptoms on standing.
- Cardiac — the dangerous group: arrhythmia (brady/tachy), structural (aortic stenosis, HCM), or cardiopulmonary (massive PE, tamponade, dissection, ACS). Carries the highest short-term mortality.
Brief myoclonic jerks and even a few seconds of incontinence can occur in convulsive syncope and do not prove epilepsy. Features favouring seizure: aura, lateral tongue-biting, prolonged post-ictal confusion, sustained rhythmic movements. And exclude the mimics that are not true syncope: hypoglycaemia, intoxication, head trauma, psychogenic pseudosyncope and vertebrobasilar TIA. True syncope has near-immediate return to full orientation.
Why Cardiac Syncope Is the One to Catch
"The prognosis of syncope is the prognosis of its cause. Reflex syncope has an excellent outcome; syncope from structural heart disease or arrhythmia may be the only warning before sudden cardiac death. Risk stratification, therefore, is really the search for cardiac syncope — and the single most useful test in that search is the 12-lead ECG."
Rosen's Emergency Medicine, 10th Ed. Syncope. Elsevier; 2023.- Syncope on exertion or when supine (as opposed to on standing)
- No prodrome ("sudden, like a switch") — especially with injury
- Palpitations immediately before, or chest pain / dyspnoea
- Structural heart disease or reduced LVEF; known CAD/heart failure
- Family history of sudden cardiac death or inherited channelopathy
- Age >60, abnormal vital signs, or an abnormal ECG
- Bradyarrhythmia: high-grade/complete AV block, sinus pauses, bifascicular block
- Pre-excitation (WPW): short PR + delta wave
- Long QT / short QT → torsades risk
- Brugada — coved ST elevation in V1–V2
- HCM — LVH with deep narrow Q waves; ARVC — epsilon wave, T-inversion V1–V3
- Ischaemia, or a dominant/rapid tachyarrhythmia
Work-up, Risk Scores & Disposition
Suspected bleed/PE/dissection: targeted imaging and bloods.
Reflex/orthostatic: usually clinical; carotid sinus massage or tilt testing in selected recurrent cases. Routine head CT and EEG are low-yield without focal signs or features of seizure.
High risk (any red flag, abnormal ECG, structural disease, exertional/supine syncope, persistent abnormal vitals): admit or arrange rapid, monitored evaluation.
Intermediate: ED observation unit / syncope pathway with monitoring and echo.
In younger patients, consider volume depletion from heat, dehydration and febrile illness (dengue, malaria, gastroenteritis) as common orthostatic/reflex triggers. Anaemia and postural hypotension are frequent contributors.
Do not overlook rheumatic aortic/mitral valve disease and peripartum or dilated cardiomyopathy as structural causes of exertional syncope. Prolonged rhythm monitoring (loop recorders) may be less accessible — use inpatient telemetry and repeated ECGs where indicated, and have a low threshold to admit high-risk patients.
Drug Reference — Syncope (cause-directed)
Most reflex syncope needs no drugs. Treatment is directed at the underlying cause.
| Drug / Measure | Indication | Dose | Notes |
|---|---|---|---|
| Atropine | Symptomatic bradycardia | 0.5 mg IV, repeat to 3 mg | Bridge to pacing; ineffective in infranodal block |
| Adrenaline / transcutaneous pacing | Bradycardia refractory to atropine | Adrenaline 2–10 µg/min; TCP as bridge | Arrange transvenous pacing / permanent pacemaker |
| Magnesium sulfate | Torsades de pointes (long QT) | 2 g IV over 1–2 min | Correct K⁺/Mg²⁺; stop QT-prolonging drugs |
| IV crystalloid | Orthostatic / hypovolaemic | Bolus titrated | Find and treat the source (bleeding, sepsis, dehydration) |
| Fludrocortisone / midodrine | Recurrent reflex/orthostatic (specialist) | Per specialist | Second-line for refractory reflex syncope after lifestyle measures |
| Stop/adjust culprit drugs | Drug-induced orthostasis / QT | — | Antihypertensives, diuretics, QT-prolonging agents |
Syncope Pathway
Confirm it was syncope — and is the patient safe now?
- True transient LOC with rapid full recovery? Exclude mimics (hypoglycaemia, seizure, intoxication, trauma, psychogenic)
- Assess vitals; treat any ongoing arrhythmia, bleeding or shock immediately
Core evaluation
- History (trigger, prodrome, position, exertion, palpitations, FHx SCD, drugs)
- Exam + lying/standing BP; 12-lead ECG; bedside glucose
Screen for red flags / dangerous ECG
- Exertional/supine syncope, no prodrome, palpitations, chest pain, structural disease, FHx SCD, age >60, abnormal vitals
- ECG: AV block, pauses, WPW, long/short QT, Brugada, HCM/ARVC, ischaemia, tachyarrhythmia
Risk-stratify & test
- Apply the Canadian Syncope Risk Score; if cardiac suspected → troponin, echo, monitoring
- Avoid routine head CT/EEG unless focal signs or seizure features
Disposition
- Low risk: reassure, discharge, safety-net + outpatient follow-up
- Intermediate: observation unit / syncope pathway with monitoring & echo
- High risk: admit with telemetry; treat the cause (pacemaker, ICD, valve, PE, bleed)
Common Mistakes in Syncope
Syncope during exertion or while supine is cardiac until proven otherwise (aortic stenosis, HCM, arrhythmia) — the opposite of the benign standing-triggered faint. Never discharge exertional syncope without cardiac evaluation.
The 12-lead ECG is the single highest-yield test. Long QT, Brugada, WPW, high-grade AV block and ischaemia are all missable and all lethal. Read it systematically every time.
Brief myoclonic jerks and even transient incontinence occur in syncope. Loading an anticonvulsant and missing the underlying arrhythmia or aortic stenosis is dangerous — use the features that truly distinguish seizure.
Both are low-yield in uncomplicated syncope without focal neurology or seizure features, and they distract from the cardiac work-up that actually changes outcome.
Orthostatic hypotension is common, easily confirmed at the bedside, and frequently drug-related — yet the postural BP is often not measured.
Syncope can be the presenting feature of massive PE, ruptured AAA/dissection, ectopic pregnancy or GI bleed. Reassess vitals and consider these where the story or exam hints at them.
A young patient with a clear vasovagal trigger, prodrome, normal ECG and exam does not need admission or a battery of tests. Validated risk scores help avoid both under- and over-triage.
Exam Pearls
Q: Define syncope.
Transient loss of consciousness due to global cerebral hypoperfusion, with rapid onset, short duration and spontaneous, complete recovery.
Q: What are the three mechanistic categories?
Reflex (neurally mediated — commonest, benign), orthostatic hypotension, and cardiac (arrhythmic/structural — highest mortality).
Q: Which single test is most useful, and what dangerous patterns must you spot?
The 12-lead ECG. Watch for high-grade AV block/pauses, WPW, long/short QT, Brugada, HCM, ARVC and ischaemia.
Q: List the red flags for cardiac syncope.
Exertional or supine syncope, absent prodrome, preceding palpitations, chest pain/dyspnoea, structural heart disease/low LVEF, family history of sudden cardiac death, age >60, abnormal vitals or ECG.
Q: How do you distinguish syncope from seizure?
Seizure favours aura, lateral tongue-biting, prolonged post-ictal confusion and sustained rhythmic activity; syncope has rapid full recovery and brief myoclonus. Also exclude non-syncope mimics (hypoglycaemia, intoxication, psychogenic).
Q: What is the Canadian Syncope Risk Score used for?
To predict 30-day serious adverse events after ED syncope and guide disposition — supplementing, not replacing, clinical judgement.
Q: Is routine head CT/EEG indicated?
No — low-yield in uncomplicated syncope without focal neurology or seizure features; prioritise the cardiac evaluation.
Q: How is torsades in long-QT syncope treated?
IV magnesium sulfate, correct electrolytes, stop QT-prolonging drugs, and treat the underlying cause (pacing/overdrive if recurrent).
References
- Brignole M, Moya A, de Lange FJ, et al. (ESC). 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39:1883–1948.
- Shen WK, Sheldon RS, Benditt DG, et al. (ACC/AHA/HRS). 2017 Guideline for the Evaluation and Management of Patients With Syncope. Circulation. 2017;136:e60–e122.
- Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score. CMAJ. 2016;188:E289–E298.
- Tintinalli JE, et al. Tintinalli's Emergency Medicine, 9th Edition. Syncope. McGraw-Hill; 2020.
- Walls RM, et al. Rosen's Emergency Medicine, 10th Edition. Syncope. Elsevier; 2023.
- Quinn J, McDermott D, Stiell I, et al. San Francisco Syncope Rule (CHESS). Ann Emerg Med. 2004/2006.