Author: Matthew J Dunn / Editor: Jason Kendall / Reviewer: Suzy Connor, Amanda King / Codes: CC10, CC12, CC3, CP4, ELP10, SLO1Published: 15/11/2021

Context and Definition

It is a common presentation which accounts for 3-5% of ED attendances [1]. The incidence is not constant throughout life, but rises sharply over the age of 70 years with further rises over the age of 80 in women. In elderly patients in long term care, the incidence can be as high as 6%.

The Framingham Study found that around 30% of patients with syncope had more than one episode. For a single episode of syncope, prognosis varies greatly and is related to the underlying cause.

Identification of the underlying cause following a single episode of syncope can be challenging. The role of the Emergency Physician is pivotal in risk stratifying serious from non-serious causes of syncope and ensuring appropriate intervention when required while at the same time avoiding unnecessary investigations.

Pathophysiology and causes of syncope

Syncope results from a temporary reduction in cerebral perfusion. Although in a significant proportion of cases (up to 50%) no underlying pathology is identified, there are a number of recognised causes of syncope:

Classification of Syncope  
Neurally mediated syncope vasovagal (common faint), carotid sinus syncope, Situational – e.g. cough, sneeze, GI   stimulation, micturition, post prandial
Orthostatic Drug effects
Volume depletion
Autonomic failure – e.g. Parkinson’s disease, diabetic neuropathy
Cardiac arrythmias  e.g. SVT, VT, Inhereted syndromes (long / short QT, Brugada, WPW)
Structural cardiac disease Ventricular failure
Aortic stenosis
Cerebrovascular Vascular steal

Neurocardiogenic syncope or vasovagal syncope (35-50% of cases) arises from an initial increase in sympathetic outflow followed by a rebound reduction in sympathetic activity leaving unopposed parasympathetic activity causing vasodilatation, bradycardia and hypotension (Fig 1, opposite).

Cardiac (10-30% of cases): arrhythmias, cardiac failure, ventricular dysfunction (e.g. hypertrophic obstructive cardiomyopathy HOCM) and valvular heart disease can all cause syncope.

Orthostatic syncope (10% of cases) is defined as an orthostatic drop of >20 mm systolic blood pressure or >10 mm diastolic blood pressure. This may be due to absolute volume depletion from dehydration or haemorrhage or to venodilatation caused by medications or autonomic insufficiency (eg as occurs in Parkinsons disease).

Neurological/psychiatric syncope (5% of cases) include basilar artery migraine, vestibular dysfunction and vertebrobasilar ischaemia. Psychiatric syncope is a recognised syndrome consisting of syncopal episodes found in anxiety, depression and conversion disorder that resolve with treatment of the psychiatric disorder.

No cause found (35-50%of cases)

Learning Bite

There are a wide variety of important causes for a patient presenting with syncope and upto 50% may not reach a diagnosis in the Emergency Department.

Syncope presents the emergency physician (EP) with a unique challenge: by definition, there will have been full recovery from the index event, approximately half of these patients will never have a cause identified and the majority of the remainder will have a benign underlying problem (eg. vasovagal syncope). The key for the EP is to risk stratify patients into low risk (the majority) and high risk by taking a careful history, performing a focussed clinical examination and, where necessary, ordering a limited number of basic investigations.

In particular, in addition to recognising orthostatic aetiologies (hypovolaemia or drug-related) it is critical to identify those patients who may have an underlying cardiac pathology for their syncope; the history and examination will be largely directed towards identifying cardiovascular abnormalities (cardiac failure, valvular problems, arrhythmias, etc.) that may require further investigation. A systematic approach to syncope can allow for the safe discharge of the majority of patients without the use of expensive and inappropriate investigations.

i) History

A careful history will give key information indicating the potential cause of syncope. The first key point in the history is to confirm that the presentation was actually syncope; it must be differentiated from conditions such as seizures, collapse without loss of consciousness (drop attacks), and vertigo.

Key features to be established in the history are shown below:

  1. Circumstances: what lead up to the episode?
  2. Duration: how long was the period of loss of consciousness?
  3. Associated symptoms: was there chest pain, breathlessness or palpitations? Was there a prodrome?
  4. Position: was the patient supine, sitting or standing?
  5. Activity: did the episode occur at rest; after a change in posture; during or after exercise; during or after urination, defecation, cough or swallowing?
  6. Predisposing factors: was this in a crowded or warm place; after prolonged standing; or after a meal. Were there precipitating events?
  7. Post recovery symptoms: was there nausea or vomiting? Was there incontinence or tongue biting? Was there a confusional state?

Other factors which are important to establish in the history:

  • A witness account is often critical in helping to determine a cause: was there cyanosis or pallor? Were there movements suggestive of a fit? If so did it occur before or after the collapase?
  • Relevant comorbid diseases: particularly previous cardiac disease, diabetes, Parkinsons disease, etc.
  • Relevant family history: is there a family history of sudden death (could indicate underlying arrhythmic disorder eg. Brugada syndrome)?
  • Relevant drug History: specifically ask about cardiovascular drugs (eg. beta blockers, ACE inhibitors, nitrates, calcium antagonists, digoxin, diuretics, antiarrythmics) and other drugs (eg. phenothiazines, insulin).

ii) Physical examination

The majority of patients with syncope will have a normal physical examination. However, it is important to exclude serious underlying pathology in the minority. Although syncope is often seen as a neurological presentation, cardiac causes of syncope are more common than neurological (and often carry a poorer prognosis), and so a thorough cardiovascular examination is required. It is crucial to identify evidence of cardiac failure or valve lesions.

Learning Bite

Cardiac causes of syncope are more common than neurological causes and often carry a poorer prognosis

Cardiovascular examination

Tachycardia and hypotension could indicate volume depletion and a cause should be sought. Orthostatic hypotension (a drop of systolic BP of at least 20 mm Hg on standing) is common particularly in the older patient. Its presence does not exclude the possibility of a more serious cause of syncope.

Specific issues to consider in cardiovascular examination are (see Table 1):

  • Jugular venous pulse (JVP)
  • Third heart sound
  • Fourth heart sound
  • Heart Murmurs
Table 1 Relevant specific features to be sought in the cardiovascular examination
Examination finding Features Significance
Elevated JVP JVP elevated more than 5 cm above sternal angle with patient at 45 degrees May indicate underlying cardiac failure implicated in aetiology of syncope
Hepatojugular reflex A sustained rise of at least 3 cm in JVP with upper abdominal pressure. This is more easily seen as the drop in JVP when the pressure is removed. Diagnostic of biventricular cardiac failure even in the absence of absolute elevation
Third heart sound A quiet low pitched sound heard near the apex with the patient in the left lateral decubitus position. Is a normal variant up to the age of 40 and is common in pregnant women. Otherwise suggests dilated cardiomyopathyor cardiac failure
Fourth heart sound A low pitched sound best heard at the apex. More easily heard than the third sound. Very sensitive to small changes in venous filling. Common in older patients. A loud fourth sound, a sound that does not disappear on standing, or one in a younger patient, suggests reduced ventricular compliance. It is associated with ventricular hypertrophy (eg. secondary to aortic stenosis) or cardiac failure
Ejection systolic murmur Crescendo-decrescendo murmur; usually harsh and low pitched. In the presence of features of ventricular hypertrophy is suggestive of aortic stenosis or outflow obstruction. The murmur of hypertrophic obstructive cardiomyopathy (HOCM) is unusual in that it is one of the few murmurs that increases in intensity when the patient stands up.

Neurological examination

It is extremely important to complete a full peripheral and central neurological examination on all patients who present with syncope as part of a full assessment. However a normal neurological examination does not exclude a neurological cause of loss of consciousness. For example, looking specifically for evidence of tongue injury from biting during a seizure is a clue towards possible seizure but it is an insensitive sign and its absence does not exclude seizure.

Other important points to consider on clinical assessment:

  1. Associated injuries caused by the collapse (think of hips in elderly patients).
  2. There may be more than one cause of the collapse, particularly in elderly patients.
  3. Increasing frequency of collapse is suggestive of a cardiac cause and in the presence of cardiac pathology, is an ominous sign.
  4. Simple syncope during exercise is rare. The presence of exertional syncope is strongly suggestive of either an arrhythmia or a structural cardiac abnormality (eg HOCM) which warrants further urgent investigation.

Learning Bite

Patients with a vasovagal syncope may have had urine incontinence and / or some convulsive type of movements

iii) Differential diagnosis

As previously noted, clinical examination is often normal in syncope, so differentiation from other causes of collapse is usually based on the history.

Epileptic seizure

May be preceded by aura. Post ictal state common. Unlikely if recovery is rapid.

Cardiac arrythmia

Abrupt onset of LOC, usually with no warning, rapid recovery. CV risk factors common. Unlikely in younger patients in the absence of cardiac history. Exercise induced syncope always warrants further investigation.

Cardiac outflow obstruction

Symptoms on exercise; rapid recovery usual. Absence of murmur at rest does not exclude cardiac outflow obstruction. Unlikely in the absence of mechanical valves, exertional murmur, or evidence of ventricular hypertrophy.


Usually gradual onset with prodromal symptoms. Unless given glucose recovery may be slow and incomplete.

Pulmonary embolus

Abrupt loss of consciousness. Tachypnoea usual after recovery. Unlikely in low risk patients.

Basilar artery migraine

Although a rare diagnosis, it is more common in young women, who may be aware of specific triggers.

Vertebrobasilar insufficiency

Vertigo, nausea, dysphagia and dysarthria common. Transient loss of consciousness is rarely the sole presenting symptom.

This list of differential diagnoses is not exhaustive, and a clinician must be open-minded when considering any possible diagnosis.

The two most frequently used risk stratification systems in the UK are the OESIL Score and the San Fransisco Syncope Rule. Both have been well validated for use in the ED and have been designed to identify patients who are at low short-term risk of serious adverse events following syncope and who can safely be investigated as outpatients.

The EGSYS score has been developed and validated in a smaller patient group to identify patients at high risk of cardiac syncope. There is considerable scope for further research to develop simple scoring systems that will have the high sensitivity of the current systems but improved specificity.

The American College of Emergency Physicians Guideline on syncope recommends (based on class B evidence) that patients with syncope and evidence of heart failure or structural heart disease or patients with syncope and other high risk factors (older age, haematocrit < 30%, abnormal ECG or history or presence of structural heart disease, coronary artery disease or cardiac failure) should be admitted. “Older age” is not defined.

Risk stratification tools

The San Francisco Rule

The San Francisco Rule [3] identifies high-risk patients based on the presence of the following factors:

  • History of congestive cardiac failure
  • Haematocrit <30%
  • Abnormal ECG
  • Complaint of shortness of breath
  • Systolic Blood Pressure <90 mm Hg

The presence of any factor is considered sufficient for the patient to be high risk.

If a patient score zero in the risk stratification tool, they are then said to be in the low risk group for serious outcome.

In the original validation study, the incidence of serious adverse events was 6.7% with the rule being 98% sensitive and 56% specific to predict adverse events.

NICE guidelines (5) also recommend that for patients presenting with transient loss of consciousness, refer anyone with the following for further assessment :

  • An abnormal ECG
  • TLOC during exercise
  • Family history of sudden death (in a person <40 years old or an inherited cardiac condition)
  • New or unexplained breathlessness
  • Heart murmur

Specific investigations should be carried out directed by the history and examination and in order to complete appropriate risk stratification rather than following a blunderbuss approach which will produce a low yield of true positives. There are, however, some routine ED based investigations that are appropriate in all patients with syncope.

The following investigations should be ordered for all patients:

Bedside glucose level (BGL)

A bedside glucose test helps rule out hypoglycaemia, although it is unlikely that you would make a quick recovery from hypoglycaemia induced LOC unless intervention was given.


ECG is an essential investigation into cardiac causes. Look for (amongst other things);Long / short QT, conduction blocks, pacemaker function, bradycardia, Brugada, WPW, LV hypertrophy (think about HOCM).


Measurement of haematocrit < 30% is required to complete the San Francisco Rule to identify which patients can be safely discharged.

Learning Bite

ECG is essential for picking up cardiac causes of collapse and should be done on all patients presenting with Syncope.

By this stage a history, examination and limited ED-based investigations will have allowed appropriate risk stratification. High-risk patients will require admission for further urgent investigation and appropriate intervention. Low-risk patients can be discharged, a proportion of whom may require further investigation which can appropriately be performed as an outpatient. The following investigations should be ordered where necessary:

Transthoracic echocardiogram

Echocardiography should be performed in any patient with a cardiac murmur and should be used to diagnose and quantify heart failure when this is suspected. If aortic stenosis is suspected, echocardiography should be performed urgently. This will commonly be done as an inpatient.

For people with a suspected cardiac arrhythmia cause of syncope, ambulatory ECG monitoring can be requested as an out patient. The type of monitor would depend on the frequency of symptoms.

Management in the ED for patients who have presented with syncope is naturally limited by the fact that, by definition, they have made a full recovery from their index event. Intervention in the ED is essentially geared towards achieving robust risk stratification (as described previously) and confidently discharging patients at low risk with no follow-up (ie. normal examination, no risk factors), whilst identifying those who require either admission for urgent investigation or further outpatient investigation.

Clear guidance should also be provided for patients about their driving status and obligation to inform the DVLA dependent on their suspected underlying pathology and/or diagnosis.

  1. Failure to consider more than one cause of the transient loss of conciousness
  2. Failure to assess associated injuries
  3. Failure to recognise the importance of increasing frequency of syncope: cardiac causes of syncope are more common in patients with recurrent syncope. Increasing frequency of syncopal episodes can therefore be a marker of deterioration in a cardiac disorder
  4. Failure to recognise the significance of exercise associated syncope, in a significant minority the cause is a serious cardiac cause that can lead to sudden death


The ‘ejection systolic murmur’

Differentiation between a benign flow murmur, aortic stenosis and subvalvular obstruction (ie. HOCM) can be difficult. As a rule a shorter (rather than a quieter) ejection systolic murmur is more likely to be benign. The murmur of HOCM is unusual in that it becomes louder on standing up (due to decreased venous return reducing the size of the heart). Echocardiography is a cheap, safe and readily available investigation and any patient with a murmur in the context of collapse warrants echocardiography.

Learning Bite

Any patient with a murmur in the context of collapse warrants echocardiography.

Exercise associated syncope

Exercise associated syncope is defined as syncope occurring during or immediately after exercise and accounts for 3 to 20% of cases of syncope. Patients with exercise associated syncope include groups of patients at high risk of sudden death. Serious causes to be considered include arrythmogenic right ventricular dysplasia, Brugada syndrome and HOCM. Although there can be pointers to these at presentation, there may not be: in all of these conditions the ECG may be normal or may show non-specific changes; and the murmur of HOCM may not always be heard.

The elderly patient with syncope

Syncope is increasingly common with increasing age and the great majority of patients presenting to the ED with syncope will be aged over 65. Older patients have a wide range of problems likely to cause syncope: there may be a poor baroreceptor response, there may be a degree of cardiac failure, and drugs that can cause syncope are commonly taken by the elderly. In addition, although neurocardiogenic syncope is more common in older patients, 10% of elderly patients without neurocardiogenic syncope have a positive tilt table test.


If a patient has had a typical, solitary vasovagal syncope while standing, with reliable prodrome, with a normal ECG and no clinical evidence of structural heart disease, they can keep driving and do not need to inform the DVLA.

For a further information see the full DVLA guidance.

  1. Soteriades ES, Evans JC, Larson MG, et al.Incidence and prognosis of syncope. N Engl J Med. 2002 Sep 19;347(12):878-85.
  2. Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M; OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003 May;24(9):811-9.
  3. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006 May;47(5):448-54.
  4. 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.
  5. National Institute for Health and Care. Transient loss of consciousness (‘blackouts’) in over 16s; [NICE guideline CG109]. Published: 2010, Updated: 2014.