• Syncope is transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery
  • Such an event without loss of consciousness is often termed “presyncope”
  • Underlying cause is often not found in the emergency department (~50%)
  • In most cases for which an underlying cause is diagnosed, this comes  from the history and examination rather than investigations
  • Syncopal events can be a benign physiological response, but may also be due to potentially life-threatening underlying condition


  • common; about 3–5% of ED visits and 1–6% of hospital admission
  • underlying cause: unknown (34-36%), vasovagal (18-21%), and cardiac (9.5-18%)
  • cardiac causes are much more common in the elderly and those with a history of cardiac disease, and these patients have the highest mortality


Neurally-mediated reflex syncopal syndromes

  •  Vasovagal faint (common faint)
  •  Carotid sinus syncope
  •  Situational faint
    • acute haemorrhage
    • cough, sneeze
    • gastrointestinal stimulation (swallow, defaecation, visceral pain)
    • micturition (post-micturition)
    • post-exercise
    • others (e.g. brass instrument playing, weightlifting, post-prandial)
  • Glossopharyngeal and trigeminal neuralgia


  •  Autonomic failure
    • Primary autonomic failure syndromes (e.g. pure autonomic failure, multiple system atrophy, Parkinson’s disease with autonomic failure)
    • Secondary autonomic failure syndromes (e.g. diabetic neuropathy, amyloid neuropathy)
    • Drugs and alcohol
  •  Volume depletion
    • Haemorrhage, diarrhoea, Addison’s disease

Cardiac arrhythmias as primary cause

  •  Sinus node dysfunction (including bradycardia/tachycardia syndrome)
  •  Atrioventricular conduction system disease
  •  Paroxysmal supraventricular and ventricular tachycardias
  •  Inherited syndromes (e.g. long/ short QT syndrome, Brugada syndrome, WPW, Arrhythmogenic RV cardiomyopathy)
  •  Implanted device (pacemaker, ICD) malfunction
  •  Drug-induced proarrhythmias

Structural cardiac or cardiopulmonary disease

  •  Cardiac valvular disease (e.g. aortic stenosis)
  •  Acute myocardial infarction/ischaemia (e.g. RV infarction)
  •  Obstructive cardiomyopathy
  •  Atrial myxoma
  •  Acute aortic dissection
  •  Pericardial disease/tamponade
  •  Pulmonary embolus/pulmonary hypertension


  •  Vascular steal syndromes


Disorders with impairment or loss of consciousness

  •  Metabolic disorders, including hypoglycaemia (not true syncope as not spontaneously reversible), hypoxia, hyperventilation with hypocapnia
  •  Epilepsy
  •  Intoxications
  •  Vertebro-basilar transient ischaemic attack

Disorders resembling syncope without loss of consciousness

  •  Cataplexy
  •  Drop attacks
  •  Psychogenic ‘syncope’ (somatization disorders)
  •  Transient ischaemic attacks (TIA) of carotid origin


“HEAD, HEART, VESSELS” (mnemonic created by William Young MD and described in the book Emergency Medicine Secrets)

CNS causes include HEAD:

  • Hypoxia (hypoglycemia does not cause syncope)
  • Epilepsy (not a true cause of syncope)
  • Anxiety and hyperventilation
  • Dysfunctional brain stem (basivertebral TIA)

Cardiac causes are HEART:

  • Heart attack (ACS)
  • Embolism (PE)
  • Aortic obstruction (IHSS, AS or myxoma)
  • Rhythm disturbance, ventricular
  • Tachycardia

Vascular causes are VESSELS:

  • Vasovagal (emotional reactions) or Valsalva (micturition, cough, straining etc)
  • Ectopic (and other causes of hypovolemia)
  • S ituational
  • S ubclavian steal
  • ENT (glossopharyngeal neuralgia)
  • Low systemic vascular resistance
    • autononic dysfunction: Addison’s, diabetic vascular neuropathy
    • Drugs such as CCBs, beta-blockers, anti-hypertensives
  • Sensitive carotid sinus


Circumstances just prior to attack

  • Position (supine, sitting or standing)
  • Activity (rest, change in posture, during or after exercise, during or immediately after urination, defaecation, cough or swallowing)
  • Predisposing factors (e.g. crowded or warm places, prolonged standing, post-prandial period)
  • Precipitating events (e.g. fear, intense pain, neck movements)

Onset of attack

  •  Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision

Nature of the attack (eyewitness)

  • Type of collapse (slumping or keeling over)
  • skin colour (pallor, cyanosis)
  • duration of loss of consciousness
  • breathing pattern (snoring)
  • movements (tonic, clonic, tonic-clonic or minimal myoclonus, automatism) and their duration, onset of movement in relation to fall, tongue biting

End of attack

  •  Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin colour, injury, chest pain, palpitations
  • urinary or faecal incontinence


  •  Family history of sudden death, congenital arrhythmogenic heart disease or fainting
  •  Previous cardiac disease: check for scars, pulses, murmurs, pacemakers and other devices?
  •  Neurological history (Parkinsonism, epilepsy, narcolepsy)
  •  Metabolic disorders (diabetes, etc.)
  •  Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic, diuretics and QT prolonging agents)
  •  (In case of recurrent syncope.)
  • Information on recurrences such as the time from the first syncopal episode and on the number of spells


  • hydration status
  • pallor
  • evidence of blood loss
  • check for injuries due to the collapse
  • postural drop (aka ‘orthostatics’)
    • on standing, look for SBP <90 mmHg or a fall >25 mmHg
    • reflex tachycardia: present suggests hypovolemia; absent suggests autonomic dysfunction
    • reproduction of symptoms is more important than actual numbers
    • measurements are poor predictors of volume status
  • rectal examination (melaena?)


  • Guided by history and examination

Laboratory tests

  • FBC (anaemia?)
  • UEC
  • glucose
  • blood gas (venous often sufficient)
  • Consider D-dimers if pulmonary embolism is suspected
  • Blood alcohol, as clinically indicated.

ECG for causes of sudden collapse:

  • Can Quick BRAD Walk Home?: Conduction blocks, Long/ short QT, Brugada, RV infarction, ARVD, DCM, WPW, Hypertrophy (HCM or LVH due to AS)

CT brain:

  • if suspected first seizure
  •  if secondary trauma sustained during the syncopal episode (“trauma above the clavicle”)
  • if suspected TIA or stroke
  • if neurological deficit or ongoing altered conscious state / confusion
  • if Age >65
  • if sudden onset headache
  • if patients on warfarin (coumadin)


Seek and treat underlying cause and complications

  • If no obvious cause  found, the main management issue in ED is to determine appropriate disposition

Lower threshold for admission if:

  • Syncope unwitnessed
  • Significant risk factors, including:
    • Cardiovascular disease
    • Documented or suspected arrhythmias
    • Known epileptic with greater than one seizure or without home supervision
    • Cardiac pacemaker or other devices
  • Elderly
  • Suspected cardiac cause:
    • admit for monitoring and cardiology review (do not sent home for a Holter monitor)
    • need to rule out an ischemic event and / or arrhythmias

High risk factors for a cardiac cause include:

  • Age
  • Known electrophysiological abnormalities, or previously documented malignant arrhythmias
  • Diabetes
  • newly abnormal ECG
  • Elevated troponin level
  • Significant depression of ventricular function, documented on echocardiogram
  • Documented IHD including past STEMI, non-STEMI, abnormal cardiac functional study or abnormal angiogram
  • Patients with pacemakers or other cardiac devices:
    • have a high index of suspicion in these patients for arrhythmia and / or cardiac device malfunction
    • All patients with pacemakers with unexplained collapse must be admitted until such time as their pacemaker can be checked
    • Most devices can be interrogated for a record of significant arrhythmia over an extended period of weeks

Suspected drug related cause

  • These patient should be admitted for drug medication review and observation


  • Even if the cause is “benign”, consider admission should still be considered in elderly patients or those with significant co-morbidities
  • This is particularly important when:
    • Episodes have been recurrent
    • Significant injuries have occurred
    • Lack of supervision at home

A short stay admission may be appropriate for:

  • observation
  • care coordination
  • Aged Care Assessment Team (ACAT) assessment
  • physiotherapy assessment


Patients can usually be discharged if:

  • They do not have significant clinical risk factors, including:
    • abnormal ECG
    • CVS risk factors
    • Initial hypotension
    • Initial history of shortness of breath
  • Witnessed seizure activity or a history of seizures, especially when the event is unwitnessed
  • Observations and clinical findings are normal
  • Medications reviewed
  • Safe home environment (especially the elderly)

If uncertain then observe for 24 hours


Seizure is more likely if:

  • Tonic-clonic movements are usually prolonged and their onset coincides with loss of consciousness
  • Hemilateral clonic movement
  • Clear automatisms such as chewing or lip smacking or frothing at the mouth (partial seizure)
  • Tongue biting (especially laterally)
  • Blue face
  • Prior to the event: aura (such as unusual smell) 
  • Post-ictal confusion
  • urinary incontinence

Syncope is more likely if:

  • Tonic-clonic movements are always of short duration (<15 sec) and they start after the loss of consciousness
  • Prior to the event: Nausea, vomiting, feeling of cold, sweating (neurally-mediated)
  • short duration


  • no clinical predication rules are sufficiently accurate to replace clinical judgement
  • the studies they are based on tend to under-represent the elderly
  • attempts at validation in the clinical setting have not outperformed clinical judgement
  • examples include: Boston Syncope Rule, EGSYS, OESIL risk score, ROSE risk score and the San Francisco Syncope Rule (summarised in a table on ALIEM)


References and links

Journal articles

  • Al-Nsoor NM. Brain Computed Tomography in Patients with Syncope. Neurosciences 2010 Apr; 15(2): 05–9. PMID: 20672498
  • Huff JS, Decker WW, Quinn JV, Perron AD, Napoli AM, Peeters S, Jagoda AS; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007 Apr;49(4):431-44. PMID: 17371707. [pdf]
  • Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med. 2009 Jul 27;169(14):1299-305. PMC3752785.
  • Dovgalyuk J, Holstege C, Mattu A, Brady WJ. The electrocardiogram in the patient with syncope. Am J Emerg Med. 2007 Jul;25(6):688-701. PMID: 17606095.
  • McKeon A, Vaughan C, Delanty N. Seizure versus syncope. Lancet Neurol. 2006 Feb;5(2):171-80. Review. Erratum in: Lancet Neurol. 2006 Apr;5(4):293. PubMed PMID: 16426993. [Free Full Text]
  • Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS), Moya A, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009 Nov;30(21):2631-71. PMC3295536.
  • National Institute for Health and Clinical Excellence (NICE) guideline 109, Transient loss of consciousness (‘blackouts’) management in adults and young people, August 2010 [Accessed August 29 2015 at URL: www.nice.org.uk/guidance/CG109]
  • Snead GR, Wilbur LG. Can the San Francisco Syncope Rule predict short-term serious outcomes in patients presenting with syncope? Ann Emerg Med. 2013 Sep;62(3):267-8. PMID: 23332611
  • Soteriades ES et al. Incidence and Prognosis of Syncope. NEJM 2002; 347:878–85. PubMed PMID: 12239256.
  • Sun BC et al. Predictors of 30-day Serious Events in Older Patients with Syncope. Ann Emerg Med 2009 Dec; 54(6): 769–778. PMID: 19766355

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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