Syncope

• Syncope is a brief, self-limited loss of consciousness caused by a sudden fall in blood flow to the brain, with prompt and complete recovery.
• The three broad causes are reflex (neurally mediated) syncope, orthostatic hypotension, and cardiac syncope; cardiac causes carry the highest risk.
• A careful history, witnessed account and electrocardiogram (ECG) do more to reach the diagnosis than any test; risk stratification decides who can go home.
• High-risk features point to cardiac syncope and usually warrant admission and evaluation; low-risk, typical reflex syncope can usually be managed as an outpatient.
• Treatment follows the cause: education and counter-pressure measures for reflex syncope, stopping hypotensive drugs and compression for orthostatic syncope, and fixing the rhythm or structure (pacemaker, implantable cardioverter-defibrillator, valve or ablation) for cardiac syncope.

By the end of this page you should be able to:

1. Define syncope and tell it apart from seizures, hypoglycaemia, transient ischaemic attack (TIA) and psychogenic events.
2. Classify syncope as reflex (vasovagal, situational, carotid sinus), orthostatic hypotension or cardiac, and name the common causes in each group.
3. Recognise the high-risk features that suggest cardiac syncope, and use the San Francisco Syncope Rule (CHESS) and the Canadian Syncope Risk Score roughly.
4. Perform and interpret lying and standing blood pressure (BP) measurement, and list ECG findings that suggest an arrhythmic cause.
5. Choose and sequence investigations (echocardiography, ambulatory monitoring, implantable loop recorder, tilt-table testing, carotid sinus massage, exercise testing, electrophysiology study).
6. Manage syncope by cause, state when to admit, and outline special-group and low-resource considerations.

The wording matters. "Loss of consciousness" alone is not syncope: it also covers seizures, hypoglycaemia, drug or alcohol sedation and psychogenic events. What makes an episode syncope is the mechanism (global reduction in brain perfusion) and the course (sudden, lasts seconds to a minute, no confusion afterwards). ^[4]

The three mechanisms form the classification used in current guidelines. ^[1][2]

• Reflex (neurally mediated) syncope. The best-known form is vasovagal syncope, usually triggered by prolonged standing, emotion, fear, pain, blood or heat, and often preceded by a prodrome of nausea, sweating, warmth and dimming vision. Situational syncope is reflex syncope provoked by a specific action (micturition, defaecation, coughing, sneezing, laughing, swallowing or eating). Carotid sinus syncope is triggered by pressure on the carotid sinus, classically by a tight collar, shaving or head turning. ^[4]
• Syncope due to orthostatic hypotension (OH). Blood pressure (BP) falls on standing because autonomic or volume compensation fails. Causes include drugs (antihypertensives, diuretics, nitrates, vasodilators, alpha-blockers, dopaminergic agents, tricyclic antidepressants), hypovolaemia or dehydration, primary autonomic failure (Parkinson disease, multiple system atrophy, pure autonomic failure, diabetic autonomic neuropathy), secondary autonomic dysfunction and age-related stiffness. Volume depletion from bleeding, vomiting or diarrhoea also belongs here. ^[3][4]
• Cardiac syncope. Arrhythmic (bradyarrhythmia including sinus node dysfunction and atrioventricular block, or tachyarrhythmia such as ventricular tachycardia or supraventricular tachycardia) and structural (aortic stenosis, hypertrophic cardiomyopathy, cardiac tamponade, pulmonary embolism, acute myocardial infarction, prosthetic valve dysfunction, atrial myxoma). ^[4]

A practical first sorting question is whether the episode is cardiac (high risk of sudden death) or not. Reflex and orthostatic syncope are usually benign; cardiac syncope is the one you must not miss.

Seizure, hypoglycaemia, TIA and psychogenic events are the common traps.

• Seizure. Movements in syncope tend to start a few seconds after collapse, are brief and varied; seizure movements are generalised from the outset and last minutes. Tongue biting and confusion on waking favour seizure. Urinary incontinence can occur in syncope. ^[4]
• Hypoglycaemia. Low glucose can cause TLOC with sweating and confusion; it should be checked when suspected (for example in a person with diabetes on insulin or sulfonylureas), and treated as hypoglycaemia rather than syncope.
• TIA / stroke. TIAs produce focal neurological deficits rather than generalised loss of consciousness; brainstem ischaemia can cause "drop attacks" without loss of consciousness. Focal signs, aphasia or hemiparesis mean think TIA, not syncope. ^[4]
• Psychogenic pseudosyncope. Clues include eyes closed during the event, prolonged duration, unusual triggers, no prodrome and very frequent attacks. ^[4]
• Falls in older adults can be the presentation of syncope; repeated unexplained falls should be worked up as syncope. ^[4]

The ESC-style list above is the practical one to use at the bedside. ^[3] adds that older adults often have sinus or conduction disease, so their threshold for investigation should be low.

Neither score replaces clinical judgement; multiple scores have shown good sensitivity but poor specificity, and they perform no better than an experienced clinician. ^[4] They are useful as a checklist, not a verdict.

San Francisco Syncope Rule (CHESS). ^[5]

One or more positive items flags a patient for admission or close evaluation.

Canadian Syncope Risk Score (CSRS). ^[4] Points from nine items (predisposition to vasovagal syncope minus points; heart disease; any ED systolic BP < 90 or > 180 mmHg; troponin above the 99th percentile; abnormal QRS axis below -30 or above +100 degrees; QRS duration > 130 ms; QTc interval > 480 ms; ED diagnosis of cardiac syncope; ED diagnosis of vasovagal syncope) are summed. Scores of -3 to 0 are low risk, 0 to 3 high risk and 4 to 11 very high risk of serious events within 30 days. External validation in a large cohort achieved very good sensitivity (97.8 %) but poor specificity (44.3 %) at a threshold of -1 point. ^[4]

ESC 2018 and AHA/ACC/HRS 2017 differ in emphasis. ESC advises discharge when low-risk features are present, observation in the emergency department or a syncope unit when medium risk, and admission for high-risk features; AHA/ACC/HRS substrate risk mostly on the seriousness of the suspected underlying condition. ESC gives a stronger recommendation for early echocardiography and exercise testing; AHA/ACC/HRS give risk-stratification scores a class IIb recommendation. ^[3]

The history is the most important part of the assessment. ^[1][3]

• The episode itself. Circumstances (standing, exertion, supine, emotion, pain, urination, defaecation, cough), warning symptoms, duration of loss of consciousness, and recovery. A genuine syncopal attack usually lasts under a minute; recovery is rapid without confusion.
• Witnessed account. Ask about colour (pallor is typical of syncope, cyanosis of arrhythmia), abnormal movements, tongue biting, incontinence, breathing.
• Cardiovascular history. Palpitations before or during the event, chest pain, breathlessness, heart failure, prior myocardial infarction, known valve or congenital disease.
• Drugs. Antihypertensives, diuretics, nitrates, alpha-blockers, antidepressants, antiarrhythmics, QT-prolonging drugs.
• Family history. Sudden cardiac death in a relative under about 40, or inherited arrhythmia syndromes.
• Triggers and situational context. These point strongly to reflex or orthostatic mechanisms.

Physical examination usually adds little, but is essential. ^[3][4]

• General: pulse, BP in both arms, temperature, hydration, pallor.
• Cardiovascular: jugular venous pressure, signs of heart failure, murmurs (aortic stenosis, hypertrophic cardiomyopathy), rhythm.
• Neurological: focal signs are not expected in syncope; if present, reconsider TIA or seizure.

This is the single bedside test that converts a suspicion of OH into a diagnosis. Measure BP and heart rate (HR) after the patient has rested supine for at least 5 minutes, then repeat at 1 minute and 3 minutes of standing (or sooner if symptoms occur). A normal response shows a slight fall in systolic BP with a rise in heart rate. ^[6]

The test should be done in everyone with syncope, and especially before any ECG test is ordered; both guidelines emphasise orthostatic vital signs, which are frequently missed. ^[3]

An ECG is recommended for every patient presenting with syncope, even when the episode looks reflex. ^[4]

Findings that raise suspicion of an arrhythmic cause: ^[4]

• Bifascicular block (right bundle branch block with left anterior or posterior fascicular block, or left bundle branch block).
• Mobitz type II or third-degree atrioventricular block, prolonged PR interval.
• Pathological Q waves (prior myocardial infarction or scar).
• Long QT (a corrected QT interval of at least 480 ms, or at least 460 ms when syncope is cardiogenic). ^[4]
• Short QT interval (suggesting short QT syndrome).
• Pre-excitation (Wolff-Parkinson-White pattern).
• Brugada pattern.
• Epsilon wave (arrhythmogenic right ventricular cardiomyopathy).
• Signs of hypertrophic cardiomyopathy.
• Negative T waves, left ventricular hypertrophy.

Note that "abnormal ECG" is one component of the San Francisco Syncope Rule. ^[5] A normal ECG does not exclude syncope of later arrhythmic origin, and a bifascicular block plus unexplained syncope usually prompts an electrophysiology study. ^[4]

Choose tests in proportion to the pre-test probability; undirected "screening" batteries (head CT, EEG, Holter monitoring, carotid Doppler) are not useful unless there is focal neurological disease. ^[3]

• Transthoracic echocardiography. Recommended when structural heart disease is suspected: ESC gives a class I recommendation, AHA/ACC/HRS class IIa. ^[3] It screens for aortic stenosis, hypertrophic cardiomyopathy, arrhythmogenic or ischaemic left ventricular dysfunction, and tamponade.
• Ambulatory ECG monitoring. Continuous in-hospital monitoring when a cardiac cause is suspected (class I). ^[3] Holter monitoring is reasonable when syncope occurs more than once a week; an external monitor is class IIa when an arrhythmic cause is suspected. ^[3]
• Implantable loop recorder (ILR). ESC recommends early ILR in recurrent syncope of uncertain origin without high-risk features and when recurrence is likely within device life; AHA/ACC/HRS give class IIa for implanted monitoring if an arrhythmic cause is suspected. ^[3]
• Tilt-table testing. Reasonable (class IIa) when reflex syncope is suspected and the diagnosis remains unclear after initial evaluation; ESC also includes delayed hypotension and psychogenic pseudosyncope. ^[3]
• Carotid sinus massage (CSM). Performed in older patients with syncope of unknown cause. It is considered positive when asystole of 3 seconds or more and/or a fall in systolic BP of 50 mmHg or more reproduces the patient's symptoms. ^[4] Avoid it if there is a carotid bruit, recent stroke or TIA, or myocardial infarction within 3 months; keep resuscitation equipment available. ^[4]
• Exercise testing. Indicated (ESC class I) when syncope occurs during or shortly after exertion, or when second/third-degree AV block develops during exercise; AHA/ACC/HRS give class IIa. ^[3]
• Electrophysiology study. ESC gives a class I recommendation after a myocardial infarction or scar with unexplained syncope, and class IIa with bifascicular block. AHA/ACC/HRS give class IIa when an arrhythmic cause is suspected. ^[3]
• Blood testing. No routine panel; targeted tests (troponin if a cardiac cause is suspected, glucose if hypoglycaemia, blood count if bleeding) are reasonable. ^[3]

Most patients need explanation, reassurance and trigger avoidance; the condition is benign but frightening. ^[8]

• Education and lifestyle. Explain the mechanism, reassure, liberal salt and fluid intake, recognise and avoid triggers (prolonged standing, hot environments, dehydration). ^[8]
• Counter-pressure manoeuvres (leg crossing, handgrip, tensing) abort or delay the faint and reduced recurrence in a randomised trial. ^[8]
• Tilt (orthostatic) training can reduce recurrence; evidence varies with protocol and adherence. ^[8]
• Pharmacological. Midodrine, an alpha-agonist that supports vascular tone, reduced recurrence in selected patients; fludrocortisone gave a borderline reduction; beta-blockers are not effective overall (AHA/ACC/HRS allow beta-blockers in patients older than 42 years as class IIb). ^[3][8]
• Pacing. Dual-chamber pacing is reasonable in selected, recurrent, unpredictable cardioinhibitory (asystolic) cases after documented spontaneous pauses (>3 s if symptomatic, >6 s if asymptomatic), or asystole on tilt-table testing in patients 40 years or older; pacing is not indicated in pure vasodepressor syncope. ^[3]
• Cardioneuroablation (endocardial ablation of vagal inputs to the sinus and atrioventricular nodes) is an emerging alternative to pacing in selected patients with documented vagally induced bradycardia or asystole; it is best regarded as a concept and investigational therapy rather than routine care. ^[9]
• For carotid sinus syncope: pacing is reasonable with a cardioinhibitory or mixed response; avoid massage-triggered advice and tighten-collar triggers. ^[3]

1. Review and reduce or stop drugs that lower BP. ^[3]
2. Education, lifestyle measures: rise slowly, avoid prolonged standing, head-up sleeping, compression garments (class IIa in both guidelines). ^[3]
3. Acute relief: drinking at least 240 mL, preferably more than 480 mL, of water gives a transient pressor response (salty water may help in dehydration but can blunt the effect in neurogenic OH). ^[3]
4. Pharmacological: fludrocortisone (mineralocorticoid, volume expansion) and midodrine are used; AHA/ACC/HRS also recommends droxidopa (the only FDA-approved drug for symptomatic neurogenic OH) and consider pyridostigmine or octreotide; ESC does not mention droxidopa (not available in Europe). ^[3][7]
   • Midodrine is given as 2.5 to 10 mg three times daily in trials, titrated to symptom and supine BP; fludrocortisone is usually 0.1 to 0.2 mg daily. ^[7]
5. Treat the underlying cause (diabetic autonomic neuropathy, Parkinson disease, amyloidosis, bleeding, volume depletion).

Treat the underlying arrhythmia or structural problem; the syncope is the symptom, not the disease.

• Bradyarrhythmia: pacemaker for sick sinus syndrome or symptomatic AV block (class I), and in selected cases of bifascicular block with documented pauses. ^[3]
• Tachyarrhythmia: manage as per the arrhythmia (catheter ablation for supraventricular tachycardia, antiarrhythmic drugs or ablation, ICD for life-threatening ventricular arrhythmia). ^[3]Atrial fibrillation and flutter, ventricular arrhythmias, bradyarrhythmias and AV block, supraventricular tachycardias and approach to tachyarrhythmias are related topics.
• Structural heart disease: aortic valve replacement for severe aortic stenosis, myectomy or alcohol septal ablation for hypertrophic cardiomyopathy, ICD when indicated, anticoagulation or reperfusion for ischaemia, surgery for cardiac tumours. ^[3]
• If no cause is found after thorough evaluation and an arrhythmic origin remains likely, an ICD or ILR strategy is chosen according to risk (for example in ischaemic left ventricular dysfunction or inherited arrhythmia syndromes). ^[3]

Use ESC's risk-based approach: discharge low-risk (typical reflex or orthostatic) patients with advice; observe medium-risk patients in the emergency department or a syncope unit rather than admitting unselectively; admit high-risk or cardiac-suspicion patients for evaluation. ^[3]

Very high-risk features that usually warrant admission or same-day specialist assessment: syncope with known heart failure, markedly abnormal ECG, suspected arrhythmic or structural cause, or recovery that is incomplete. ^[3][4]

Driving after syncope is a safety issue for the patient and others. Rules vary between countries and sometimes between private and commercial licences: some authorities require a symptom-free interval and a documented cause or treatment before driving is resumed, and commercial drivers face stricter criteria. Advise the patient to check and follow the local driver-licensing authority's current rules, and document the advice given. ^[3]

• Older adults. Falls may be syncope. Autonomic impairment, stiff ventricles and polypharmacy make orthostatic and cardiac causes more common; ESC gives no specific recommendations, while AHA/ACC/HRS recommend a comprehensive geriatric assessment for syncope. ^[3]
• Athletes. AHA/ACC/HRS give class I for cardiovascular assessment before returning to competitive sport after syncope, and do not recommend return in high-risk inherited syndromes (phenotype-positive hypertrophic cardiomyopathy, catecholaminergic polymorphic ventricular tachycardia, long QT type 1, arrhythmogenic cardiomyopathy) until assessed. ESC gives no specific recommendations. ^[3]
• Children. AHA/ACC/HRS suggest midodrine if lifestyle measures fail for reflex syncope, and tilt-table testing if vasovagal syncope is suspected; beta-blockers are not recommended in paediatric syncope. ESC mentions infantile reflex anoxic seizures and breath-holding spells as paediatric causes, with workup as for adults. ^[3]
• Pregnancy. Vasovagal and orthostatic syncope are common; avoid unnecessary radiation, keep BP assessment supine with left tilt, and involve cardiology or obstetrics for suspected cardiac causes. ^[4]

• The diagnosis is usually clinical: history, witnessed account, ECG and lying-standing BP catch most cases without cost. ^[3][6]
• A single 12-lead ECG is the most informative cheap test; when it is unavailable, suspicion-based referral is safer.
• Avoid CT head, EEG and carotid duplex in patients without focal neurological findings; they add cost without value. ^[3]
• If echo is unavailable, refer red-flag patients to a centre with echocardiography and cardiology.
• Midodrine, fludrocortisone, compression and salt/fluid advice are inexpensive and usable where advanced electrophysiology is absent; pacemakers and ICDs need referral centres.
• After a stroke-like episode or suspected cardiac syncope in a young patient, refer early.

• Syncope is cerebral hypoperfusion; not every TLOC is syncope. Seizure, hypoglycaemia, TIA and psychogenic events must be excluded.
• Mechanisms: reflex (vasovagal, situational, carotid sinus), orthostatic hypotension, cardiac (arrhythmic or structural). Cardiac causes are dangerous.
• History plus witnessed account and ECG outrank most tests; orthostatic BP is a bedside must.
• Red flags for cardiac syncope: exertional or supine syncope, chest pain or palpitation, prior heart disease or myocardial infarction, heart failure signs, abnormal ECG.
• ECG clues to an arrhythmic cause: bifascicular block, AV block, pathological Q waves, long or short QT, pre-excitation, Brugada pattern, epsilon wave.
• ESC-style risk stratification: discharge low risk, observe medium risk, admit high risk.
• Investigations are selective: echo if structural disease suspected; continuous or ambulatory monitoring; ILR for recurrent unexplained syncope; tilt test for reflex syncope; carotid sinus massage in selected older adults; exercise testing after exertional syncope; EPS after scar or bifascicular block.
• Reflex syncope treatment: education, trigger avoidance, salt and fluids, counter-pressure manoeuvres, tilt training; selected drug therapy (midodrine, possibly fludrocortisone); pacing or assessment for cardioneuroablation only with documented cardioinhibitory asystole.
• Orthostatic hypotension: stop offending drugs, compression, fluids, midodrine or fludrocortisone, and treat the underlying cause.
• Cardiac syncope: fix the rhythm or structure (pacemaker, ICD, valve, ablation).
• Special groups (older adults, athletes, children, pregnancy) and low-resource practice need modified approaches; driving rules differ by country.

• Heart failure
• ECG interpretation
• Cardiac physical examination
• Atrial fibrillation and flutter
• Ventricular arrhythmias
• Bradyarrhythmias and AV block
• Supraventricular tachycardias
• Approach to tachyarrhythmias

All references, with full details, authors and access dates, are listed in the front matter and are cited in the text as numbered superscripts.