IntroductionMan with syncope
Risk factors
Orthostatic syndromes
Initial assessment
Duration of symptoms
Risk stratification

This is part 1 of a two-part article.

Part 2 can be found here.




Syncope is defined as a sudden, but brief loss of consciousness caused by inadequate perfusion to the brain. It is usually benign, but it could also be suggestive of other underlying pathology hence proper investigation of a presentation of syncope is important.

Various conditions can present with syncope-like episodes and it is important to make a distinction between actual syncope and other presentations such as seizures, or cardiac arrest (Table 1).

Some key questions can help determine whether an episode is true syncope or a non-syncopal event.

  • Was there complete loss of consciousness?
  • Was the loss of consciousness transient with a rapid onset and short duration?
  • Was recovery spontaneous, complete and without consequences?
  • Was there a loss of postural tone?

If the answer to all the above is yes, the episode is most likely to be true syncope, if the answer to one or more is no then other causes of the presentation should be excluded.


Disorders with partial or complete LOC but with global cerebral hypoperfusion Disorders without impairment of consciousness
Epilepsy Cataplexy
Metabolic disorders including hypoglycaemia, hypoxia, hyperventilation with hypocapnia Drop attacks
Intoxication Falls
Vertebrobasilar TIA Functional (psychogenic pseudosyncope)
  TIA or carotid origin


Risk factors 

Although syncope is commonly benign, some predisposing risk factors include: cardiovascular disease, hypertension, increasing age, autonomic neuropathy, fibromyalgia, lower body mass, diabetes and increased alcohol intake.



Figure 1: Causes of syncope by ageAbout 40% of individuals will be affected by syncope in their lifetime, and this is usually across all age groups; the most common cause being neurally mediated syncope (NMS). There are distinct age categories at which a first faint (usually vasovagal syncope) is common. As can be seen from figure 1, NMS is more prevalent in the younger population, whilst cardiac and orthostatic causes are prevalent in the elderly (however NMS is still common in the elderly).



In busy acute settings, the first thing to rule out is an acute cause for syncope such as: pulmonary embolism, acute coronary syndrome, heart failure, sepsis, diarrhoea etc. The other underlying cause of syncope can be divided into various types as follows: orthostatic syndromes, cardiac, cerebrovascular, psychogenic, substance abuse or alcohol intoxication or unknown. For the purpose of this article only the first few categories will be described further. The basic pathophysiology of syncope involves a drop in blood pressure resulting in global hypoperfusion. (Table 2)



(Reflex) Neurally mediated Vasovagal, carotid sinus,

Situational (cough/post-exercise/prandial/micturition
Orthostaticn Drug induced, Volume depletion,

ANS failure(primary/secondary)
Cardiac arrhythmia Brady (sick sinus/AV Block), Tachy(VT/SVT)

Long QT syndrome
Structural cardio-pulmonary Aortic stenosis, HOCM, PHT, tamponade, myxoma, AMI 5%
Non-cardio-vascular Psychogenic, metabolic eg. hyperventilation, epilepsy

TIA or carotid origin


Orthostatic syndromes

The 2009 ESC guidelines identify six orthostatic syndromes, five of which are found to be causes of syncope:


Classic orthostatic hypotension (OH)

This is defined as a decrease in systolic blood pressure of ≥20mmHg and in diastolic blood pressure ≥10mmHg within three minutes of standing. It is diagnosed by active standing or tilt testing.


Initial OH

This is defined by a blood pressure decrease immediately upon standing, of >40mmHg with blood pressure spontaneously and rapidly returning to normal, making the period of hypotension and symptoms under 30 seconds. This is also diagnosed by active standing.


Reflex syncope (vasovagal syncope)

This is triggered by standing and is characterised by an initial normal adaption reflex followed by rapid fall in venous return and vasovagal reaction (reflex bradycardia and vasodilatation). This is diagnosed by tilt table.


Delayed (progressive) OH

This is defined by a slow progressive decrease in systolic blood pressure on standing without a bradycardic reflex (in contrast to reflex syncope). This is also diagnosed by tilt table.

Delayed (progressive) OH plus reflex syncope occurs when a vasovagal reaction (reflex bradycardia and vasodilation) follows delayed OH. This is diagnosed by tilt table.

Postural orthostatic tachycardia syndrome (POTS) presents with severe orthostatic intolerance (not syncope) with significant increase in heart rate (by >30 beats per minute or to >120 beats per minute) and blood pressure instability. This is also diagnosed by tilt table.


Cardiac causes

These could be due to arrhythmias (eg. paroxysmal supraventricular tachycardia, atrioventricular conduction system disease, ventricular tachycardia, inherited syndromes, and drug induced or secondary to pacemaker malfunction). Structural cardiac causes, some of which are: acute coronary syndromes, obstructive cardiac valvular disease, hypertrophic obstructive cardiomyopathy can also lead to syncope.


Non-cardiac causes

Some non-cardiac causes of syncope include: metabolic disorders (such as hypoglycaemia, hypoxia, hyperventilation etc.); psychogenic, intoxication and epilepsy.


Initial assessment

Syncope is a common cause for presentation to the emergency department and a thorough assessment of these individuals is essential to help distinguish between syncope and other underlying sinister cause of the presentation. The following are important in the assessment of syncope:



The first and most important aspect of history taking in a patient presenting with syncope is to rule out an acute presentation of a more sinister underlying cause, or systemic cause such as: syncope secondary to pulmonary embolism, acute coronary syndrome, gastrointestinal bleed, sepsis, diarrhoea and vomiting etc. When sinister causes have been excluded, the syncopal presentation can be explored further as follows: any preceding or pre-syncopal symptoms; associated symptoms (eg. chest pain or palpitations); triggers eg. coughing, defecation etc.; duration of symptoms; previous episodes, associated injuries, medications, family history, any seizure-like symptoms. A collateral history from a witness may also be useful. A more detailed assessment of the history is as follows:


Number of episodes

Benign causes of syncope are associated with a single syncopal episode in most patients, but some have multiple episodes over many years. By comparison, the patient with multiple episodes occurring over a short period of time is more likely to suffer from a serious underlying disorder.


Associated symptoms

Symptoms occurring in association with syncope can point towards a specific cause. For example: dyspnoea may suggest an acute pulmonary embolism; angina frequently indicates an underlying cardiac cause; a history of focal neurologic abnormalities favours a neurologic origin; and urinary and/or faecal incontinence suggest, but do not prove, a seizure.



Auras” are associated with seizures. In comparison, vasovagal (neurocardiogenic) syncope is usually, but not always, associated with a prodrome of nausea, warmth, pallor, light-headedness, and/or diaphoresis. Such symptoms may also occur without an episode of syncope. Older individuals with vasovagal syncope are less likely to experience a prodrome.


Sudden onset

Sudden onset of syncope without a prodrome is more typical of patients with cardiac syncope than those with non-cardiac syncope. However, since non-cardiac syncope is far more common than cardiac syncope, the majority of patients with sudden onset of syncope have a non-cardiac cause.



Neurocardiogenic syncope commonly occurs when the patient is erect, not usually when supine. Syncope resulting from orthostatic hypotension is frequently associated with the change from a supine to erect posture. In comparison, syncope that occurs when the patient is supine suggests an arrhythmia.


Provocative factors

Situational syncope is a type of reflex (neurally-mediated) syncope that occurs during or immediately after provocative stimuli such as coughing, swallowing (particularly cold liquid), crowded or warm places, prolonged standing, post-prandial state, fear, intense pain, urinating, or defecating.

Neck movements can precipitate carotid sinus syncope, a type of reflex syncope caused by hypersensitivity of the carotid sinus.


Exertional syncope

An evaluation to rule out potentially life-threatening causes for syncope is required if syncope occurs during exertion. Among the pathologic causes of exertional syncope are ventricular tachycardia and obstruction resulting from aortic stenosis or hypertrophic cardiomyopathy, and hypotension due to vagally-mediated vasodepression in patients with hypertrophic cardiomyopathy.

Syncope associated with exercise also occurs in patients, usually young, who do not have underlying heart disease. If exertional syncope has occurred, neurocardiogenic syncope is diagnosed after exclusion of other causes.


Duration of symptoms

A prolonged loss of consciousness may indicate a seizure. By comparison, arrhythmias and neurocardiogenic syncope are often associated with a brief period of syncope, since the supine position re-establishes some blood flow to the brain and can therefore result in the restoration of consciousness.

Persistence of nausea, pallor, and diaphoresis in addition to a prolonged recovery from the episode suggest a vagal event. These findings are helpful in distinguishing neurocardiogenic syncope from syncope due to an arrhythmia. Significant neurologic changes or confusion during the recovery period may be due to a seizure.


Family history

Important elements of the family history include history of sudden death, cardiomyopathy, or fainting. It is also very important to distinguish syncope from epilepsy. Table 3 provides some key aspects of this differentiation.



Observations (vital sings—including orthostatic blood pressure), cardiovascular and respiratory exam to exclude, arrhythmia or murmur or crackles suggestive of heart failure. Neurologic examination (true syncope should not be associated with any neurological deficit); Neck exam (for carotid bruits or murmur radiation); rectal examination to rule out haemorrhage as a cause for syncope; general examination to asses for evidence of trauma or injuries.


  Seizure Syncope
Triggers Sleep deprivation
Flickering movements
Prolonged standing
Head movement
Postural change
Cough, micturition etc
Warning Symptoms None
‘Aura’ (funny smell, epigastric aura, Déjà vu)
Light-headedness, dizziness, blurred vision, Nausea, sweating
Unconscious Period Jerky movements (prolonged & coincides with LOC)
Tongue bites (Lateral)
Clear automatism—chewing, lip smacking, frothing
Urine incontinence
Jerky movements (<15 sec & start after LOC)
Tongue bites (Tip)
No automatism
Urine incontinence
Recovery Prolonged (>1 hr)
Confusion and drowsy
Headache, myalgia
Focal neurology
Quick recovery—few minutes
Nausea, light-headedness


Risk stratification

  • Syncope during exertion or supine
  • Palpitation at the time of syncope
  • Family history of SCD
  • Syncope during driving
  • ECG abnormalities
    • Cardiac ischaemia
    • Non-sustained VT
    • New onset Bifascicular/Tri fascicular block, CHB
    • Sinus bradycardia (<50bpm) /sinoatrial block, Mobitz type 2
    • Prolong QT interval
    • RBBB with ST elevation in V1-V3 (Brugarda Pattern)
  • Persistently abnormal vital signs eg. hypotension, hypoxia
  • Acute bleeding or low haemoglobin
  • Evidence of dehydration, sepsis, heart failure

If after initial assessment of a patient the diagnosis remains uncertain, then further evaluation and management is guided by risk stratification as follows:

  • Single or rare syncopal episodes with low risk clinical features: no further investigation required
  • Recurrent episodes with low risk features: additional testing required.
  • Presence of high risk clinical features (evidence of significant heart disease, clinical or ECG features suggesting arrhythmic syncope, comorbidities such as severe anaemia or electrolyte disturbance): intensive evaluation or prompt hospitalisation required.
  • In the presence of an ECG abnormality, heart failure, transient loss of consciousness on exertion, new or unexplained breathlessness, family history of sudden cardiac death in individuals below age 40 and/or inherited cardiac condition or a new heart murmur, referral for specialist cardiovascular assessment must be done within 24 hours.

There are some risk scores to help identify those high risk syncope patients, however none of them have currently been set as a standard assessment; these include: San Francisco syncope rule (SFSR), Oservatorio Epidemiologico Sulla Sincope nel Lazio (OESIL) score and European Guidelines in Syncope Study (EGSYS). Figure 2 provides a summary of criteria for admission.


Syncope is mostly benign, but even the most benign forms of syncope can have significant consequences for the individual. Thorough assessment of patients with syncope is essential both in primary and secondary care, not only to aid in its management but also assess those at higher risk and those who may benefit from specialist investigation or assessment. Various risk scores can be applied to help make clinical decisions. If the syncopal episode does not fit all of the following: complete, transient loss of consciousness with short duration and rapid onset, spontaneous recovery, absence of sequelae and loss of postural tone, then other causes of the presentation must be considered.


Dr A Ntrakwah, Foundation Year 2 in Elderly care, Walsall Manor Hospital 
Dr U Fernando, Consultant Physician in Elderly care, Walsall Manor Hospital

Conflict of interest: none declared