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Syncope, commonly known as ‘fainting’ or ‘passing out’, is a symptom which presents frequently in the emergency department. While seemingly straightforward, the fact that it is often a heavily history-focused diagnosis means that it is an important topic to know about.
There are a number of disorders which present similarly and a variety of different underlying causes, ranging from completely benign to serious and life-threatening. This article will get you up to speed on how to distinguish syncope from other causes of a transient loss of consciousness and the key questions to ask in your history when you think your patient may have had a faint. Management of specific causes is not discussed.
It’s important to be clear on what the term syncope actually means.
There are three major criteria within the definition of syncope:
There must be a loss of consciousness. An initial loss of postural tone (going floppy) is a good indication of this – if the patient did not lose postural tone, other possible causes should be considered first.
The loss of consciousness must be transient. This means it is self-limiting (i.e. no intervention is needed for the patient to fully recover). This, therefore, excludes events such as cardiac arrest and hypoglycaemic coma which do not normally involve spontaneous recovery.
It is caused by global cerebral hypoperfusion, which almost always means a reduction in systemic blood pressure. Focal cerebral hypoperfusion (e.g. a transient ischaemic attack from carotid artery thrombo-embolism) does not cause or constitute syncope.
The transient loss of consciousness is often easy enough to confirm by asking. But how do we know that it was caused by low blood pressure? To help with this, the European Society of Cardiology (ESC) definition states that syncope is characterised by:¹
Short duration (typically no longer than 20 seconds, but can be several minutes)
Spontaneous and complete recovery (although some disorientation is common with increasing age)
The presence of these three characteristics is strongly suggestive of a syncopal episode (i.e. a transient loss of consciousness caused by transient global cerebral hypoperfusion).
Syncope vs Seizure
Every year, many patients experiencing syncope are wrongly diagnosed with epilepsy and vice versa, with long term consequences. It is very important to distinguish these two classically similar events. In addition to the three characteristics above, it is helpful to think in terms of what happened before, during and after the event.
Was there a trigger?
This is an extremely useful piece of information for any presenting complaint but particularly so in the context of loss of consciousness.
Syncope often includes an immediate preceding trigger such as emotion, pain or exercise.
Was there a prodrome?
Syncope often involves an immediate warning (called ‘pre-syncope’), consisting of symptoms such as feeling faint, dizzy, sick, visual disturbances and ringing in the ears (tinnitus).
The presence of palpitations or other cardiac symptoms suggests a cardiac cause of syncope.
Did the patient change colour?
Pallor occurs from systemic hypotension, thus indicating syncope.
A blue colour (cyanosis) occurs from transient loss of respiratory muscle action in any seizure beginning with a tonic phase (e.g. generalised tonic-clonic seizure).
How long did the unconsciousness last?
Typically seconds in syncope (often longer in seizures).
Was there a convulsion?
Convulsions may occur in both epilepsy and syncope and thus do NOT distinguish between the two.
However specific patterns (e.g. tonic-clonic) may be recognisable if the eye witness provides a detailed, reliable account.
Was there tongue biting?
Although this can rarely happen in syncope, this is more strongly associated with seizures.
Was there urinary incontinence?
Urinary and faecal incontinence are more strongly associated with seizures and not a typical feature of syncope (although not impossible).
How long did it take for full recovery?
Seizures are followed by a post-ictal fatigue lasting hours, in contrast, syncope is usually followed by near-immediate complete recovery with no lasting effects.
Causes of Syncope
Once you have decided that the patient’s history does indeed constitute syncope, there are two important aims for further assessment:
Determine the underlying cause, in the hope of providing treatment and preventing further events.
Ascertain their risk of further events.
There are 4 classifications of syncope:
Structural and arrhythmic syncope are potentially life-threatening.
Neurally mediated and postural syncope are both typically benign (although they can have more serious underlying causes).
You can remember them with acronym SNAP if needed.
Neurally mediated syncope is due to an inappropriate autonomic reflex in response to a trigger and hence this is also known as reflex syncope.
Also known as a ‘simple faint’, this is by far the most common type of syncope overall.
It is common in young people right after an emotional response, such as fear, anxiety or disgust, but may also happen due to prolonged standing.
This is a curious set of conditions where syncope occurs consistently after a specific trigger:
Post-micturition (the most common)
*Post-exercise syncope MUST be investigated further to rule out a structural cardiac cause (see below).
Carotid sinus hypersensitivity
This involves syncope after mechanical manipulation of the carotid sinus, which can happen accidentally whilst shaving, wearing a tight shirt collar or even head movement (e.g. looking over shoulder).
Key points in the history relevant to neurally mediated syncope
Precipitant/trigger – if situational, ask if the trigger consistently causes syncope
Position – vasovagal syncope usually happens when standing
If there is no underlying cardiac disease, a typical history is enough to diagnose reflex syncope.
Investigations for neurally mediated syncope
Lying and standing blood pressure
Tilt table testing – recreates trigger/situation while measuring BP and other signs to confirm the diagnosis
Carotid sinus massage – not as simple as it sounds – this is a diagnostic test with a specific protocol which is only carried out after the patient has been assessed for contraindications and where full resuscitation services are available
Postural (Orthostatic) Syncope
Although it may be straightforward, this is not simply syncope upon standing. It involves a variety of syndromes (called initial, classical and delayed orthostatic hypotension) in which syncope is dependent on standing up, however, the length of time from standing to syncope can be up to 45 minutes. What distinguishes this from vasovagal syncope is that autonomic function is chronically impaired and it is the insufficiency of the baroreceptor response which causes syncope – not a reflex.
Causes of orthostatic hypotension
Autonomic nervous failure secondary to drugs:
This is the commonest cause of orthostatic hypotension.
Culprits include antihypertensives, diuretics, tricyclic antidepressants, antipsychotics and alcohol.
Hypovolaemia may be a key contributing factor in syncope.
There may be a sinister underlying cause such as a gastrointestinal bleed.
Primary autonomic nervous failure:
This is usually present to some degree in the spectrum of disorders which includes Parkinson’s disease, Lewy body dementia and multi-system atrophy.
Secondary autonomic nervous failure:
Occurs secondary to other conditions such as diabetes, uraemia and spinal cord lesions
Key points in the history relevant to orthostatic syncope
Position – clear association with standing
Prodrome – may be prolonged in delayed postural syncope
Drug history is crucial
Any cause for hypovolaemia – haemorrhage, diarrhoea, vomiting, burns etc
Past medical history – anything that could result in failure of the autonomic nervous system (e.g. diabetes)
Investigations for orthostatic syncope
Lying and standing blood pressure
Tilt table testing – this will distinguish between postural and vasovagal syncope
Arrhythmias can cause a variety of cardiac symptoms:
Bradyarrhythmias are more likely to cause syncope than tachyarrhythmias. One of the most important things to ask in any syncope history is a family history of sudden death. Omitting this may miss a potentially fatal disease such as a familial channelopathy (e.g. long QT syndrome, Brugada syndrome) or cardiomyopathy (e.g. hypertrophic cardiomyopathy).
Bradyarrhythmias which can cause syncope include:
Sick sinus syndrome
Second-degree atrioventricular block
Third-degree (complete) atrioventricular block
In each case, there is either failure of impulse initiation by the sinus node (sick sinus syndrome) or impulse conduction to the ventricles. When this occurs sporadically, there is usually an ectopic site further down the pathway which will take over and continue to beat at its own slower rate. The reduction in blood pressure responsible for the syncope occurs when there is a long pause (usually >3 secs) between the impulse conduction failure and the ectopic escape mechanism.
If the patient already has a pacemaker, an important cause of syncope to consider is pacemaker dysfunction. This would then unmask whatever bradyarrhythmia the pacemaker was originally implanted for.
Ventricular tachycardia (VT) is much more likely to cause syncope than supraventricular tachyarrhythmias. VT is most commonly occurs in individuals with pre-existing structural cardiac disease and so this must be ruled out when anyone presents with ventricular tachycardia. A specific type of VT (torsades de pointes) can also occur due to long QT syndrome, which can be caused by genetic mutations or medications (e.g. antipsychotics, macrolide antibiotics).
Structural causes of syncope are usually due to mechanical obstruction in the left ventricular inflow or outflow tract. Normally during exertion, systemic vasodilatation occurs in order to increase perfusion to skeletal muscle and the reduction in blood pressure is compensated for by an increased stroke volume and heart rate. However, when there is an obstruction to outflow, this compensation does not happen and exertional syncope can occur due to a reduction in blood pressure during exercise. Post-exertional syncope as a neurally mediated reflex normally occurs after exercise, whereas syncope from outflow tract obstruction occurs during exercise. Younger patients are more likely to have inherited causes (e.g. hypertrophic cardiomyopathy) whereas older patients are more likely to have acquired causes (e.g. aortic stenosis) and present readily with other symptoms such as breathlessness, fatigue, low exercise tolerance and/or peripheral oedema.
ECG monitoring is used to confirm an association between syncope and the arrhythmia (this is the only way to definitively diagnose arrhythmic syncope)
Ambulatory ECG monitoring
External and implantable loop recorders
Non-cardiac disease (e.g. pulmonary hypertension)
General History Tips
While some of the important topics to cover when taking a history are specific to a loss of consciousness history (e.g. family history of sudden death), most are part of the regular history framework (e.g. possible trigger, drug history, past medical history etc).
Some mnemonics to help you remember the specific questions are:
5 Cs –Colour / Convulsions / Continence / Cardiac problems / Cardiac death family history
Always remember that different types of syncope may co-exist, meaning that a patient with extensive cardiac disease may still experience a simple vasovagal syncope and vice versa.
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):2631-2671.
Anderson J, O’Callaghan P. Cardiac syncope. Epilepsia 2012;53(s7):34-41.
Douglas G, Nicol F, Robertson C, editors. Macleod’s clinical examination. Elsevier Health Sciences; 2013 Jun 21.
Gauer RL. Evaluation of syncope. American family physician. 2011 Sep 15;84(6):640.