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Syncope

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Key points ⚡
Succinct notes to superpower your revision
Syncope\: transient loss of consciousness due to global cerebral hypoperfusion; rapid onset, short duration, spontaneous
recovery.
De
Key features\: rapid onset, short duration (typically ≤20 seconds), complete recovery.
Distinguish from seizure\: syncope often has triggers (emotion, pain), prodrome (dizziness, nausea), brief unconsciousness,
no post-ictal state.
Neurally mediated syncope\: common, due to inappropriate autonomic re
sinus hypersensitivity).
Postural syncope\: caused by orthostatic hypotension; common causes include drugs (antihypertensives, diuretics),
hypovolaemia, autonomic failure.
Arrhythmic syncope\: caused by bradyarrhythmias (sick sinus syndrome, AV block) or tachyarrhythmias (VT, long QT
syndrome); check for family history.
Structural syncope\: mechanical obstruction in the heart (e.g. aortic stenosis, hypertrophic cardiomyopathy), usually during
exertion.
Investigations\: ECG, ambulatory ECG, echocardiography, tilt table testing, lying and standing BP, carotid sinus massage.
History tips\: ask about precipitants, prodrome, position, palpitations, post-event phenomena, colour, convulsions,
continence, cardiac problems, family history of sudden cardiac death.
Article 🔍
A comprehensive topic overview

Introduction

Syncope, commonly known as ‘fainting’ or ‘passing out’
, is a common presenting complaint.
There are several disorders which present similarly and a variety of di
serious and life-threatening.
This article will cover how to distinguish syncope from other causes of a transient loss of consciousness and the key areas
to cover in the history.

De

There are three major criteria within the de
1. There must be a loss of consciousness\: an initial loss of postural tone (going
patient did not lose postural tone, other causes should be considered
2. 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.
3. It is caused by global cerebral hypoperfusion, which almost always means a reduction in blood pressure. Focal cerebral
hypoperfusion (e.g. a transient ischaemic attack from carotid artery thrombo-embolism) does not cause or constitute
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syncope.
An episode of transient loss of consciousness can often be established from the history. But how do we know that it was
caused by low blood pressure?
To help with this, the European Society of Cardiology (ESC) de
Rapid onset
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 misdiagnosed with epilepsy and vice versa, with long term
consequences (e.g. restrictions on driving).
It is important to distinguish these two 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.
Before the event
Was there a trigger?
Establish whether there was a trigger to the event. Syncope often includes an immediately 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).
During the event
How long did the unconsciousness last?
Typically, patients are unconscious for seconds in syncope. The duration of unconsciousness is 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 speci
patterns (e.g. tonic-clonic) may be recognisable if the eyewitness provides a detailed, reliable account.
Was there tongue biting?
Although tongue biting 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).
After the event
How long did it take for full recovery?
Seizures are followed by a post-ictal fatigue lasting several hours. In contrast, syncope is usually followed by near-
immediate complete recovery with no lasting e

Causes of syncope

Once it has been established syncope has occurred, there are two important aims for further assessment\:
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Determine the underlying cause, in the hope of providing treatment and preventing further events
Ascertain their risk of further events
There are four classi
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).
The mnemonic SNAP can be used to remember this classi
Neurally mediated
Neurally mediated syncope is due to an inappropriate autonomic re
known as re
Vasovagal syncope
Vasovagal syncope. also known as a ‘simple faint’
, is by far the most common type of syncope overall.
It is common in young people following emotional response, such as fear, anxiety or disgust, but may also happen due to
prolonged standing.
Situational syncope
Situational syncope occurs when syncope occurs consistently after a speci
Post-micturition (the most common)
Post-cough
Post-swallow
Post-defecation
Post-prandial
Post-exercise*
*Post-exercise syncope is a red
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).
Neurally mediated syncope\: key history areas
Important areas to cover in the history include\:
Precipitant/trigger\: if situational, ask if the trigger consistently causes syncope
Warning symptoms\: classic pre-syncopal symptoms of nausea, sweating, feeling faint
Position\: vasovagal syncope usually happens when standing
If there is no underlying cardiac disease, a typical history is enough to diagnose re
Investigations
Relevant investigations for neurally mediated syncope include\:
Lying and standing blood pressure
Tilt table testing\: recreates trigger/situation while measuring BP and other signs to con
Carotid sinus massage\: this is a diagnostic test with a speci
been assessed for contraindications and where full resuscitation services are available
Postural (orthostatic) syncope
Postural (orthostatic) syncope involves a variety of syndromes (called initial, classical and delayed orthostatic hypotension)
in which syncope is dependent on standing up. The length of time from standing to syncope can be up to 45 minutes.
Postural (orthostatic) syncope results from insubaroreceptor response, resulting in syncope.
Causes of orthostatic hypotension
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Causes of orthostatic hypotension include\:
Autonomic nervous failure secondary to drugs\: this is the commonest cause of orthostatic hypotension. Common
drugs include antihypertensives, diuretics, tricyclic antidepressants, antipsychotics and alcohol.
Hypovolaemia\: 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
Postural (orthostatic) syncope\: key history areas
Important areas to cover in the history include\:
Position\: clear association with standing
Prodrome\: may be prolonged in delayed postural syncope
Drug history
Any cause for hypovolaemia\: haemorrhage, diarrhoea, vomiting, burns
Past medical history\: anything that could result in failure of the autonomic nervous system (e.g. diabetes)
Investigations
Relevant investigations for postural (orthostatic) syncope include\:
Lying and standing blood pressure
Tilt table testing\: this will distinguish between postural and vasovagal syncope
Arrhythmic syncope
Arrhythmias can cause a variety of cardiac symptoms including palpitations, syncope, chest pain and breathlessness.
Bradyarrhythmias
Bradyarrhythmias are more likely to cause syncope than tachyarrhythmias.
It is important to ask about a family history of sudden death. Omitting family history 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.
Tachyarrhythmias
ventricular.
Tachyarrhythmias can be supraventricular (e.g. atrial , atrial
Ventricular tachycardia (VT) is much more likely to cause syncope than supraventricular tachyarrhythmias.
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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 speci
mutations or medications (e.g. antipsychotics, macrolide antibiotics).
Structural syncope
Structural causes of syncope are usually due to mechanical obstruction in the left ventricular in
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 out
due to a reduction in blood pressure during exercise.
Post-exertional syncope as a neurally mediated re
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.
Causes of structural syncope
Causes of structural syncope include\:
Valvular disease (e.g. aortic stenosis)
Cardiac masses (e.g. atrial myxoma)
Cardiomyopathy (e.g. hypertrophic cardiomyopathy)
Pericardial disease (e.g. constrictive pericarditis)
Non-cardiac causes (e.g. pulmonary embolism, aortic dissection)
Arrhythmic and structural syncope\: key history areas
Important areas to cover in the history include\:
Palpitations
Other cardiac symptoms (e.g. chest pain, breathlessness, oedema)
No prodromal warning (unlike in re
Onset when sitting or lying down
Onset with exercise (clarify if it is after or during exercise)
Presence of any previous heart disease including myocardial infarctions, surgeries, and any cardiac device details
(pacemakers and ICDs)
Drug history
Family history of sudden cardiac death
Investigations
Relevant investigations for arrhythmic and structural syncope include\:
Resting 12-lead ECG\: may show evidence of ischaemic heart disease (e.g. pathological Q waves), long QT interval
or Wol
ECG monitoring\: ECG monitoring is used to con
way to de
loop recorders.
Echocardiography\: may show heart failure, cardiomyopathies, valvular disease or non-cardiac disease (e.g. pulmonary
hypertension)
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General history tips

While some of the important topics to cover when taking a history are speci
history of sudden death), most are part of the regular history framework (e.g. possible trigger, drug history, past medical
history etc).
For more information, see the Geeky Medics guide to taking a loss of consciousness history.
Remember di
experience a simple vasovagal syncope and vice versa.
Mnemonics
The
Precipitant
Prodrome
Position
Palpitations
Post-event phenomena
The
Colour
Convulsions
Continence
Cardiac problems
Cardiac death family history

References

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). E u r H e a r t J 2009 Nov;30(21)\:2631-2671.
Anderson J, O’Callaghan P. Cardiac syncope. E p i l e p s i a 2012;53(s7)\:34-41.
Douglas G, Nicol F, Robertson C, editors. M a c l e o d' s c l i n i c a l e x a m i n a t i o n . Elsevier Health Sciences; 2013 Jun 21.
Gauer RL. Evaluation of syncope. A m e r i c a n f a m i l y p h y s i c i a n . 2011 Sep 15;84(6)\:640.

Related notes

Aphasia
Benign Paroxysmal Positional Vertigo (BPPV)
Cervical Radiculopathy
Chiari Malformations
Down's Syndrome

Test yourself

Contents

Introduction
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De
Syncope vs seizure
Causes of syncope
General history tips
Source\: geekymedics.com
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