Syncope

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Syncope is a mechanism, not a final aetiology. The differential includes reflex/situational syncope, postural hypotension, arrhythmia, structural cardiopulmonary disease, seizure, metabolic disturbance and psychogenic events.

NICE CG109 (updated November 2023) gives the TLoC pathway; NICE NG136 was updated in February 2026 and supplies the current postural-BP technique/threshold.

There is no routine 'syncope drug'. Management follows the cause. Midodrine below is a licensed, specialist conditional option for severe autonomic postural hypotension only, not a treatment for unexplained blackout.

Key points

Syncope is transient loss of consciousness from cerebral hypoperfusion, with rapid onset, short duration and spontaneous complete recovery; confirm that true TLoC occurred before naming the cause.
Get the witness story: posture, trigger/prodrome, colour, eyes, movements and their duration, tongue-bite site, injury, event duration, recovery confusion and focal weakness.
Every suspected TLoC needs vital signs, cardiovascular/neurological examination, medication review and a 12-lead ECG unless an immediately life-threatening cause dictates treatment first.
NICE cardiac red flags: abnormal ECG, heart failure, TLoC during exertion, family sudden cardiac death under 40/inherited disease, new unexplained breathlessness or murmur; consider the same 24-hour route if over 65 with no prodrome.
The three Ps support uncomplicated vasovagal faint: posture (prolonged standing), provoking factor (pain/procedure) and prodrome (warmth/sweating). Brief jerks can occur in syncope.
Seizure markers include lateral tongue bite, head turning, witnessed abnormal behaviour with amnesia, unusual posturing, prolonged jerking, post-event confusion or déjà/jamais vu; do not routinely order EEG for undifferentiated TLoC.
Measure postural BP supine then after standing at least 1 minute; a fall of at least 20 mmHg systolic or 10 mmHg diastolic is significant under current NICE guidance.
For suspected arrhythmic syncope, NICE chooses ambulatory ECG by event frequency and says not to use tilt testing first.
Syncope during exercise needs exercise testing within 7 days unless contraindicated, and no exercise until assessed; post-exercise syncope is more often reflex.
NICE says all people with TLoC must not drive while waiting for specialist assessment; apply current DVLA rules after diagnosis.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Reflex and situational syncope

Pain, emotion, prolonged standing, coughing, swallowing or micturition can trigger reflex vasodilation and sometimes bradycardia. The resulting pressure fall is often preceded by warmth, nausea, sweating or visual dimming.

Postural hypotension

Volume loss, autonomic failure or vasodilating and diuretic medicines can prevent compensation after standing. Symptoms relate to posture and improve with sitting or lying as venous return recovers.

Cardiac arrhythmia

Ventricular tachycardia, rapid supraventricular rhythms, sinus-node disease or atrioventricular block can abruptly reduce output. Structural disease, an abnormal ECG, palpitations or absent prodrome increase concern.

Structural or cardiopulmonary obstruction

Aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism or severe pulmonary hypertension can limit or abruptly reduce cardiac output. Syncope during exertion, breathlessness or a murmur is particularly concerning.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
A circulatory disturbance begins
A reflex, postural pressure fall, rhythm disturbance or fixed obstruction reduces systemic arterial pressure or cardiac output sufficiently to limit the blood available to the brain.
2
Cerebral autoregulation is exceeded
When compensation cannot maintain flow, global cerebral hypoperfusion affects cortical and reticular activating networks. Awareness and postural tone are lost rapidly, typically without a persistent focal neurological deficit.
3
Brief motor activity may occur
Continued cerebral hypoperfusion can produce stiffening or brief myoclonic jerks. Their presence alone does not establish epilepsy; movement duration, tongue-bite site, colour, prodrome and recovery pattern remain discriminating.
4
Recumbency and recovery restore perfusion
Recumbency may improve venous return while the transient reflex or rhythm disturbance resolves. Spontaneous, rapid and complete recovery supports syncope; prolonged confusion or persistent neurological abnormality suggests another diagnosis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Uncomplicated vasovagal faint

No alternative-diagnosis features plus the three Ps: prolonged standing/posture, provoking pain or procedure, and warmth/sweating prodrome. Pallor and rapid clear recovery support syncope; brief jerking does not automatically mean epilepsy.

Cardiac red flagsRed flag

Abnormal ECG, heart failure, TLoC during exertion, family sudden cardiac death under 40 or inherited cardiac condition, new unexplained breathlessness, or murmur; also consider urgent referral when older than 65 with no prodrome.

High-risk event contextRed flag

Syncope while supine/sitting, during exercise, with sudden palpitations or chest pain, major injury, known structural disease, persistent hypotension or abnormal examination raises arrhythmic/structural concern even if recovery is complete.

Seizure markers

Tongue bite, head turning, amnesia for witnessed abnormal behaviour, unusual posturing, prolonged limb jerking, post-event confusion or déjà/jamais vu support epilepsy referral within two weeks. Sweating, pallor, prolonged standing and symptoms prevented by lying down argue away from epilepsy.

Postural hypotension

Typical postural symptoms with a fall after at least 1 minute standing of 20 mmHg or more systolic or 10 mmHg or more diastolic from supine (seated only if supine is inconvenient).

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Patient and witness historyFirst step
Why
Reconstruct before, during and after the event and confirm genuine TLoC.
Interpretation and limitations
If uncertain whether TLoC occurred, NICE says assume it did until proved otherwise; distinguish brief syncopal jerks from prolonged seizure activity.
02
Vital signs, cardiovascular and neurological examination, medication/family history
Why
Find shock, heart failure, murmur, focal deficit, bleeding, drug-induced hypotension and inherited risk.
Interpretation and limitations
Persistent abnormality or incomplete recovery is not uncomplicated syncope and requires immediate cause-directed care.
03
12-lead ECG with competent review
Why
Detect conduction disease, ventricular/atrial arrhythmia, long/short QT, Brugada, pre-excitation, hypertrophy, pathological Q waves and ST-T abnormalities.
Interpretation and limitations
NICE treats any degree of heart block, complete bundle-branch block, long/short QT or ST-T abnormality as a red flag; it uses QTc over 450 ms or under 350 ms in its manual-review list.
04
Supine and standing BP
Why
Diagnose postural hypotension with the current NICE technique.
Interpretation and limitations
Measure supine (seated only if needed), then after standing at least 1 minute. A fall at least 20 systolic or 10 diastolic is significant; if suggestive symptoms persist without confirmation, repeat from supine/refer for specialist assessment.
05
Targeted blood tests
Why
Check glucose if hypoglycaemia suspected, haemoglobin if anaemia/bleeding suspected, and electrolytes/renal function/troponin or other tests only from the clinical differential.
Interpretation and limitations
Routine scattergun testing does not replace event history and ECG; an abnormal result must plausibly explain TLoC.
06
Ambulatory ECG selected by frequency
Why
Obtain symptom-rhythm correlation in suspected arrhythmic or unexplained syncope.
Interpretation and limitations
Several times/week: Holter up to 48 h, then external recorder if no event. Every 1-2 weeks: external event recorder, then implantable if missed. Less often than every 2 weeks: implantable recorder; Holter usually not unless baseline conduction abnormality.
07
Exercise test
Why
Assess syncope occurring during exertion.
Interpretation and limitations
Offer within 7 days unless a contraindication such as suspected aortic stenosis/HCM first requires imaging; refrain from exercise meanwhile.
08
Echocardiography/structural imaging
Why
Investigate murmur, heart failure, abnormal ECG or suspected structural disease.
Interpretation and limitations
Structural disease does not exclude a coexisting arrhythmia; NICE says consider both structural and ambulatory rhythm assessment.
09
Tilt test or carotid sinus massage in selected specialist pathways
Why
Tilt: assess severe cardioinhibitory response in recurrent injurious/QoL-limiting suspected vasovagal syncope. Carotid sinus massage: suspected carotid sinus or unexplained syncope age 60 or over.
Interpretation and limitations
Do not tilt-test an uncomplicated faint or before ambulatory ECG in unexplained/arrhythmic syncope. Carotid massage must be controlled with ECG and resuscitation equipment and diagnosis requires reproduction of syncope, not an asymptomatic pause/drop.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Generalised epileptic seizure

Lateral tongue biting, prolonged rhythmic jerking, head turning, unusual posturing and prolonged post-event confusion favour epilepsy. Pallor, sweating, a standing trigger and rapid clear recovery favour syncope.

Hypoglycaemia

Sweating, hunger, behavioural change and progressive impaired consciousness suggest low glucose, particularly with diabetes treatment. Documented hypoglycaemia and recovery after correction distinguish it from brief spontaneous syncope.

Psychogenic pseudosyncope

Frequent prolonged apparent unresponsiveness, eye closure and inconsistent triggers may suggest a functional event. Diagnosis requires careful specialist assessment and preferably normal haemodynamics during a captured typical episode.

Neurological or mechanical event

Persistent focal weakness, speech disturbance or ataxia suggests a neurological cause, while a witnessed trip without loss of awareness suggests a mechanical fall. Either pattern points away from transient global cerebral hypoperfusion.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ImmediateUnrecovered, injured or unstable patientFirst stepIncomplete recovery, serious injury, persistent ABC/neurological abnormality or an active arrhythmia.

1Manage ABCDE and the immediate cause; check glucose when relevant and treat cardiac arrest/arrhythmia using the RCUK pathway.
2Do not label as a simple faint until recovery, examination and ECG support it.
3EscalationEscalate suspected ACS, PE, aortic stenosis/HCM, haemorrhage, stroke or toxic/metabolic cause through its emergency pathway.

02Red flagsUrgent cardiovascular assessmentAny NICE cardiac red flag or age over 65 without prodrome.

1Arrange urgent specialist cardiovascular assessment, reviewed and prioritised within 24 hours; use clinical judgement for admission/monitoring rather than treating 24 hours as a discharge target.
2For syncope during exercise, arrange exercise testing within 7 days unless contraindicated and advise no exercise until assessed.
3If arrhythmia is suspected, select ambulatory ECG by frequency; do not use tilt as the first test.
4Advise no driving while awaiting specialist assessment and give event recurrence/safety advice.

03Clear benign patternUncomplicated or situational syncopeThree-P vasovagal pattern or consistent micturition/cough/swallow trigger, normal initial assessment and no clinical/social concern.

1Explain the mechanism, prognosis, trigger avoidance and early actions such as sitting/lying at prodrome; provide injury and recurrence safety-netting.
2No further immediate management is required under NICE. If ECG was not recorded outside GP care, arrange one and competent interpretation within 3 days.
3Reassess if events recur, change character, happen during exertion/supine, or acquire cardiac/neurological red flags.

04PosturalPostural hypotensionTypical postural history and diagnostic BP drop.

1Review causes, especially antihypertensives/diuretics and dehydration; manage the contributor and use standing BP for subsequent treatment decisions.
2Educate on slow position change, trigger avoidance and fall prevention; individualise fluid/salt advice because heart/renal disease may make generic loading unsafe.
3If symptoms persist despite correcting causes, refer for specialist assessment.
4Only for severe orthostatic hypotension from autonomic dysfunction when corrective factors are excluded and other treatment is inadequate, consider specialist midodrine using the licensed regimen below.

05Possible seizure/uncertainNeurology and diagnostic uncertaintyStrong seizure markers, psychogenic features or persistent unexplained events.

1Strong seizure markers: refer to an epilepsy specialist to be seen within 2 weeks; do not routinely use EEG for undifferentiated TLoC.
2If PNES/psychogenic pseudosyncope is suspected, refer for neurological assessment; avoid suggesting that the events are fabricated.
3Ask the person/witness to record future events safely by detailed account or video when feasible.
4Consider coexistence of more than one mechanism when evaluation or treatment does not explain recurrence.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Severe orthostatic hypotension due to autonomic dysfunction after corrective factors are excluded and other treatment is inadequate—not unexplained syncope or routine vasovagal faint.

Midodrine (licensed specialist option)

2.5 mg PO three times daily initially; increase at weekly intervals according to supine/standing BP up to 10 mg three times daily. Give during daytime; last dose at least 4 hours before bed.

Check supine/standing BP and renal/hepatic function; stop if supine hypertension persists despite dose reduction. Contraindicated in acute/severe renal impairment (CrCl under 30 in cited SmPC), hypertension, serious vascular disease, urinary retention/serious prostate disorder, phaeochromocytoma, hyperthyroidism and narrow-angle glaucoma.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Traumatic injury

Sudden loss of postural tone can cause head injury, fractures, soft-tissue trauma or drowning. Events without warning, during exertion or in hazardous surroundings carry greater immediate risk.

Recurrent falls and functional decline

Repeated episodes can reduce confidence, mobility and independence, particularly in older people. Avoidance and deconditioning may then worsen postural tolerance and increase future fall risk.

Road and occupational harm

Recurrence while driving, working at height or operating machinery can injure the patient and others. Temporary restriction and current diagnosis-specific DVLA guidance are therefore part of management.

Cardiac arrest or sudden death

When syncope reflects ventricular arrhythmia or severe structural disease, recurrence may be fatal. Exertional or supine events, abnormal ECG findings and inherited-disease clues require urgent cardiovascular assessment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat observations and neurological/perfusion assessment until full recovery; reassess the diagnosis if recovery is prolonged.
Use continuous ECG in high-risk/arrhythmic presentations; choose outpatient ambulatory modality by event frequency rather than convenience.
For postural hypotension, use standing BP for subsequent monitoring and review medicines after any fall/syncope or dose change.
Midodrine: regular supine and standing BP, symptoms of supine hypertension, renal/hepatic function and urinary retention; ensure last dose is at least four hours before bed.
Document driving advice at first presentation and update after specialist diagnosis using current DVLA guidance.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Jerking does not equal epilepsy

Brief seizure-like movements can accompany cerebral hypoperfusion. Duration, tongue-bite site, colour, prodrome and recovery pattern are discriminating details.

Event frequency chooses the monitor

A normal 24-hour Holter is unsurprising when blackouts occur every two months. NICE moves infrequent events directly to an implantable recorder.

During versus after exercise matters

Syncope during exercise is more suggestive of arrhythmia/structural disease; immediately after stopping is more often reflex, though the whole clinical picture still governs.

Tilt is not a generic blackout test

NICE reserves it mainly to document a severe cardioinhibitory response in recurrent injurious/QoL-limiting suspected vasovagal syncope after more appropriate testing.

Driving advice is part of treatment

NICE says no driving while awaiting specialist assessment. Exact restriction/notification then follows current DVLA diagnosis-specific rules.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing epilepsy from brief jerking without a witness-led TLoC history.
02
Ordering a routine EEG for unexplained TLoC despite NICE advice.
03
Reassuring a patient with exertional/supine syncope or an abnormal ECG because they recovered quickly.
04
Using a 24-hour Holter for events occurring every few months instead of a frequency-matched recorder.
05
Measuring postural BP only seated-to-standing when supine measurement is feasible, or failing to wait at least 1 minute standing.
06
Starting midodrine for unexplained syncope without documenting severe autonomic orthostatic hypotension and supine BP.