Syncope

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Syncope is a transient loss of consciousness caused by transient global cerebral hypoperfusion characterised by rapid onset, short duration, and spontaneous complete recovery.[1] The term syncope excludes seizures, coma, shock or other states of altered consciousness.[2]

Patients presenting with a history of blackouts, faints or collapse need careful evaluation to assess the precise nature of the problem. A thorough history and examination are essential to assess the risk of a serious underlying disorder and to guide further investigations and management.

  • Neurally mediated syncope (NMS) - also called reflex syncope:
    • Vasovagal syncope (common faint).
    • Situational syncope - eg, cough, sneeze, gastrointestinal stimulation (swallowing, defecation, visceral pain), micturition.
    • Carotid sinus hypersensitivity.
    • Glossopharyngeal neuralgia.
  • Orthostatic hypotension (postural hypotension).

  • Autonomic failure - eg, multiple system atrophy, Parkinson's disease, diabetes, amyloidosis.
    • Medications - eg, antihypertensives.
    • Hypovolaemia - eg, haemorrhage, vomiting, diarrhoea, Addison's disease.
    • Post-exercise.
    • Postprandial.
  • Cardiac arrhythmias:
    • Sick sinus syndrome, atrioventricular (AV) conduction system disease.
    • Paroxysmal supraventricular tachycardia, ventricular tachycardia.
    • Inherited syndromes - eg, long QT syndrome, Brugada's syndrome.
    • Malfunction of pacemaker or implantable cardioverter defibrillator (ICD).
    • Drug-induced arrhythmias.
  • Structural cardiac or cardiopulmonary disease:
    • Obstructive cardiac valvular disease.
    • Acute coronary syndrome.
    • Hypertrophic obstructive cardiomyopathy.
    • Atrial myxoma.
    • Acute aortic dissection.
    • Pericardial disease or tamponade.
    • Pulmonary embolus or pulmonary hypertension.
  • Cerebrovascular:
    • Vascular steal syndromes - eg, subclavian steal syndrome.
  • Substance abuse, alcohol intoxication.

  • Psychogenic: factitious, anxiety, panic attacks, hyperventilation.

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  • Syncope is common in all age groups and affects 40% of people during their lifetime, but only a minority of people with syncope will seek medical attention.[4]
  • Only 5% of adults in the community have a first syncope over the age of 40 years.
  • NMS is by far the most common cause. The majority have experienced reflex-mediated episodes as teenagers and adolescents.[1]
  • The lifetime risk for NMS is 50% for females and 25% for males.[5]
  • Cardiac causes, orthostatic and postprandial hypotension, and the effects of medications are common causes in the elderly.[5]
  • One study reported a definite diagnosis of the cause of syncope in 98% of patients, of which NMS accounted for the majority (60%), orthostatic hypotension occurred in 10% and there were cardiac causes in 17%.[6]

A thorough history and examination are essential. See also separate articles Cardiovascular History and Examination and Neurological History and Examination.

A careful history, physical examination (full cardiovascular examination including standing and supine blood pressure and pulse) combined with an electrocardiogram (ECG) will yield a diagnosis in 50% of cases. Initial evaluation may lead to a certain diagnosis based on symptoms, physical signs or ECG findings. However, syncope is often multifactorial, especially in older individuals.

  • In some forms of syncope there may be a prodromal period with light-headedness, nausea, sweating, weakness or visual disturbances, but loss of consciousness often occurs without warning.[1]
  • Syncope is usually brief, with complete loss of consciousness in reflex syncope not lasting more than 20 seconds (but may occasionally be up to several minutes).[1]
  • Recovery from syncope is usually associated with almost immediate restoration of appropriate behaviour and orientation, but there may be marked fatigue. Retrograde amnesia may occur, especially in older individuals.[1]

In the absence of an obvious diagnosis, the following may indicate a likely underlying cause:

  • NMS: syncope may occur in various situations, including:
    • After fear, severe pain, emotional distress or sudden unexpected unpleasant sight, sound or smell.
    • With prolonged standing or when in crowded, hot places.
    • Associated with nausea and/or vomiting.
    • During or shortly after coughing, sneezing, gastrointestinal stimulation or micturition.
    • With head rotation, pressure on the carotid sinus (as in tumours, shaving, tight collars).
    • Following exertion.
  • Syncope caused by orthostatic hypotension:
    • Syncope occurs after standing up.
    • Following the start of medication, leading to hypotension or changes of dosage.
    • With prolonged standing, especially in crowded, hot places.
    • The presence of autonomic neuropathy or Parkinsonism.
    • Following exertion or shortly after a meal.
    • There may be examination evidence of a drop in blood pressure (usually >20/10 mm Hg) within three minutes of standing, associated with syncope or presyncope.[7]
  • Cardiac syncope:
    • Presence of severe structural heart disease.
    • During exertion or when supine.
    • Preceded by palpitation or accompanied by chest pain.
    • Family history of sudden death.
    • There may be ECG evidence of ischaemia or arrhythmias.
  • Cerebrovascular syncope:
    • With arm exercise.
    • Differences in blood pressure or pulse in the two arms.

 Transient loss of consciousness is usually due to syncope. Other possible causes are:[1] 

See also separate article Dizziness, Giddiness and Feeling Faint.

NB: prolonged unconsciousness, confusion after the event, or neurological signs and lateral tongue biting suggest a non-syncopal event, and this should prompt neurological evaluation.[4]

Psychogenic pseudosyncope[1] 

  • May be factitious.
  • Most often occurs in younger adults or teenagers.
  • There is often underlying anxiety - eg, poor performance at school.
  • There is often a high frequency of attacks with many attacks occurring in a day, and there is usually a lack of a recognisable trigger.
  • Pseudosyncope usually lasts longer than syncope; patients may lie on the floor for many minutes.
  • Symptoms are often vague, and typical features of NMS, such as pallor and sweatiness, are absent.
  • The eyes are usually open in epileptic seizures and syncope but are usually closed in functional transient loss of consciousness.
  • Attacks may be induced on a tilt table, but there is no change in heart rate or blood pressure and the ECG is unchanged during the syncope.

The initial evaluation of a patient presenting with transient loss of consciousness consists of careful history, physical examination, including orthostatic blood pressure measurements, and an ECG.[1] Further investigations are guided by the history and examination. Initial tests in primary care include:[8] 

  • FBC: acute anaemia will cause syncope, but patients adapt in cases of chronic anaemia.
  • Fasting blood glucose (hypoglycaemia).
  • 12-lead ECG.

In most cases, the initial assessment will lead to a definite, or at least a likely, diagnosis, which will clarify the selection of further investigations and management.[4]

Risk stratification

It is essential to assess the risk of major cardiovascular events or sudden cardiac death. The indications for urgent hospital assessment include:[1]

  • Severe structural or coronary artery disease - eg, heart failure, low left ventricular ejection fraction, previous myocardial infarction.
  • Clinical or ECG features suggesting arrhythmic syncope:
    • Syncope during exercise or whilst supine.
    • Palpitations at the time of syncope.
    • Family history of sudden cardiac death.
    • Non-sustained ventricular tachycardia.
    • Bifascicular block (right bundle branch block and either left anterior or left posterior fascicular block).
    • Bradycardia with pulse heart rate below 50 or sinoatrial block in the absence of negative chronotropic drugs (eg, beta-blockers) or physical training.
    • QRS complex longer than 120 milliseconds.
    • Prolonged or short QT interval.
    • Right bundle branch block pattern with ST elevation in leads V1-V3 (Brugada pattern).
    • Features suggestive of arrhythmogenic right ventricular cardiomyopathy.
  • Important comorbidities - eg, severe anaemia, electrolyte disturbance.

People with frequent syncope, syncope causing injuries, or implications for driving also warrant specialist assessment.[4]

There are several risk scores to help identify those patients with syncope who are at high risk of adverse events but none of the scores are widely accepted:[4]

  • Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score.[9]
  • San Francisco Syncope Rule (SFSR); this is the simplest, and uses an abnormal ECG, heart failure, anaemia and systolic hypotension (below 90 mm Hg) to identify patients who require urgent action. [10]
  • European Guidelines in Syncope Study (EGSYS) score.[11]

Investigations in secondary care[3]

  • NMS:
    • Carotid sinus massage, tilt testing (see below),[12] implantable loop recorder.
    • Carotid sinus massage should be avoided in patients with previous transient ischaemic attack, stroke within the preceding three months, or with a carotid bruit, except if carotid Doppler studies excluded significant stenosis.[1]
  • Cardiac syncope:
    • ECG ambulatory monitoring - eg, conventional ambulatory Holter monitoring, in-hospital monitoring, event recorders, external or implantable loop recorders, or remote (at home) telemetry. The gold standard for the diagnosis of syncope is when a correlation between the symptoms and a documented arrhythmia is recorded.[1]
    • Adenosine triphosphate (ATP) test: rapid injection of a bolus of ATP (or adenosine) during ECG monitoring; the induction of AV block with ventricular asystole lasting over six seconds, or the induction of AV block lasting over ten seconds are considered abnormal.[1]
    • Echocardiogram: to identify structural cardiac abnormalities and assess left ventricular function.
    • Transoesophageal echocardiography, CT and MRI may be performed in selected cases (eg, aortic dissection and haematoma, pulmonary embolism, cardiac masses, pericardial and myocardial diseases, congenital anomalies of coronary arteries).[1]
    • Cardiac catheterisation and coronary angiography may be indicated for suspected cardiac ischaemia.
  • Exercise testing:[1][13]
    • For patients who have experienced episodes of syncope during or shortly after exertion.
    • Careful ECG and blood pressure monitoring should be performed during both the test and the recovery phase.
    • Syncope occurring during exercise may be due to cardiac causes; syncope occurring after exercise is almost invariably due to a reflex mechanism.
  • Tests that are less useful but may be indicated include electroencephalography (EEG), brain CT/MRI, carotid Doppler ultrasound, pulmonary CT/scintigraphy.
  • Tilt testing: the patient lies flat on the table and is attached to an ECG and a blood pressure monitor. After a short time the table is tilted head up to 60° or 70° and the position maintained for 40 minutes, or until typical symptoms occur. 50%-60% of patients with unexplained syncope develop symptoms after about 20 minutes.

If the cause still remains unclear then repeat evaluation with repeat investigations may be required.[3] Patients may require psychiatric evaluation or may need admission to hospital for further management.

  • Most patients with syncope require only reassurance and education regarding the nature of the problem and avoidance of triggering events.
  • The essential aspect of management is to establish the precise cause of the patient's episodes of syncope in order to provide appropriate treatment and advice.[8] 
  • Referral is indicated if there is any suggestion of a serious underlying cause requiring investigation and management (especially any suggestion of a cardiovascular cause), or if the episodes of syncope cannot be controlled by simple avoidance of precipitating factors and general advice.[8] 
  • Reassess medications which may need either reduction in dosage or withdrawal.
  • Management of any underlying cause - eg, pacemakers.

NMS

  • Reassurance and education are usually all that is required.
  • Avoid potential triggers likely to induce syncope - eg, prolonged standing in a hot environment or having a long hot bath.
  • Take action at the first warning sign of collapse:
    • If it is imminent, lie down flat with the legs up on a chair or against a wall or sit down with the head between the knees.
    • Squatting down on the heels can be very effective and is less noticeable in public.
    • These techniques help move venous blood that has pooled in the limbs, aiding circulation to the brain.
    • When feeling better, get up carefully. If symptoms return, resume the position.
  • Treatment may be required if syncope is very frequent, the patient is at risk of injury as attacks are unpredictable, or if syncope occurs during high-risk activities such as driving. However, treatment options are limited and include:
    • Tilt training: prolonged periods of upright posture; requires good compliance, as several sessions are needed and deconditioning occurs quickly on stopping.[3]
    • Isometric counterpressure manoeuvres - eg, leg crossing or arm tensing, which can increase blood pressure enough to prevent syncope.
    • Medications: various medications have been used - eg, beta-blockers, clonidine, fludrocortisone; however, large randomised controlled trials have failed to show any conclusive benefits of these measures.[3]
    • Cardiac pacing (dual-chamber preferred) does not also appear to have any general benefit for syncope but it may be useful in carotid sinus syncope.

Orthostatic hypotension

  • Stop any offending drugs.
  • Avoid alcohol.
  • Encourage a plentiful oral fluid intake.
  • Raise the head of the bed.
  • Wear support stockings to reduce pooling of vascular volume.
  • Leg crossing and arm tensing.
  • In some patients the above may not be enough and the following may be useful:
    • Low dose of fludrocortisone.
    • Drugs that increase total peripheral resistance - eg, midodrine, an alpha-1 adrenergic agonist (available in UK on a named patient basis only).

Cardiac cause of syncope

  • Treatment is aimed at the underlying cause - eg, antiarrhythmic drugs, pacing, implantable cardiac defibrillators, correction or amelioration of structural disorders.
  • Electrophysiological studies and ablation may also be required for arrhythmias.

Driving and syncope

  • Driving is not a problem for a simple faint but greater restrictions apply if the situation is more complicated or if diagnosis is less clear.
  • If in doubt, contact the Driver and Vehicle Licensing Agency (DVLA).
  • The DVLA does not have to be informed of a simple faint but failure to notify other conditions can lead to a fine.
  • Recurrent syncope has serious effects on quality of life. The physical impairment due to syncope is comparable with chronic illnesses such as chronic arthritis, recurrent moderate depressive disorders, and end-stage renal disease.
  • Syncope reduces mobility, usual abilities, and self-caring, and increases depression, pain, and discomfort.
  • Female gender, a high level of comorbidity, the number of episodes of syncope, and the presence of presyncope seem to be associated with poorer quality of life.
  • Physical injury; soft tissue and bone injuries may occur. Syncope was found to be the cause of 21% (second highest behind epilepsy) of road accidents involving loss of consciousness at the wheel.[13].
  • Morbidity is particularly high in the elderly and includes loss of confidence, depressive illness, fear of falling, fractures and subsequent institutionalisation.
  • Prognosis varies according to the underlying cause. The all-cause mortality in subjects with reflex syncope is not higher than in the general population.[5]
  • Approximately 35% of patients have recurrences of syncope at three years of follow-up.[13]
  • In young patients, syncope is a benign event. Isolated syncope (transient loss of consciousness in the absence of prior or concurrent neurological, coronary, or other cardiovascular disease) is not associated with any increased risk of transient ischaemic attack, stroke or myocardial infarction and is not associated with any excess of all-cause or cardiovascular mortality (including sudden death).
  • Most of the deaths and many poor outcomes seem to be related to the severity of the underlying disease rather than to syncope. Structural heart disease and primary cardiac electrical disease are major risk factors for sudden cardiac death and overall mortality in patients with syncope. Orthostatic hypotension is associated with a two-fold higher risk of death, owing to the severity of comorbidities compared with the general population.[1]
  • For non-cardiac causes of syncope, excluding children and adolescents, five-year mortality is 30%. The presence of the following risk factors is associated with increased mortality at one year (presence of two or more factors is associated with over 16% mortality):[14]
    • Abnormal ECG (not sinus bradycardia or sinus tachycardia, or nonspecific ST/T-wave changes).
    • Older than 45 years.
    • History of ventricular arrhythmias or congestive cardiac failure.

Further reading & references

  1. Guidelines on Diagnosis and Management of Syncope; European Society of Cardiology (2009)
  2. Morag R et al; Syncope, Medscape, Jun 2012
  3. Brignole M; Diagnosis and treatment of syncope. Heart. 2007 Jan;93(1):130-6.
  4. Parry SW, Tan MP; An approach to the evaluation and management of syncope in adults. BMJ. 2010 Feb 19;340:c880. doi: 10.1136/bmj.c880.
  5. Colman N, Nahm K, Ganzeboom KS, et al; Epidemiology of reflex syncope. Clin Auton Res. 2004 Oct;14 Suppl 1:9-17.
  6. Brignole M, Alboni P, Benditt DG, et al; Guidelines on management (diagnosis and treatment) of syncope-update 2004. Executive Summary. Eur Heart J. 2004 Nov;25(22):2054-72.
  7. Lahrmann H, Cortelli P, Hilz M, et al; EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur J Neurol. 2006 Sep;13(9):930-6.
  8. Transient loss of consciousness in adults and young people, NICE Clinical Guideline (August 2010)
  9. Reed MJ, Newby DE, Coull AJ, et al; The Risk stratification Of Syncope in the Emergency department (ROSE) pilot Emerg Med J. 2007 Apr;24(4):270-5.
  10. Quinn JV, Stiell IG, McDermott DA, et al; Derivation of the San Francisco Syncope Rule to predict patients with short-term Ann Emerg Med. 2004 Feb;43(2):224-32.
  11. Del Rosso A, Ungar A, Maggi R, et al; Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart. 2008 Dec;94(12):1620-6. Epub 2008 Jun 2.
  12. Kenny RA, O'Shea D, Parry SW; The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000 May;83(5):564-9.
  13. Brignole M, Alboni P, Benditt DG, et al; Guidelines on management (diagnosis and treatment) of syncope--update 2004. Europace. 2004 Nov;6(6):467-537.
  14. Ebell MH; Syncope: initial evaluation and prognosis. Am Fam Physician. 2006 Oct 15;74(8):1367-70.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr Hayley Willacy
Last Checked:
20/11/2012
Document ID:
2828 (v24)
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