Syncope

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 different underlying causes, ranging from benign to 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. 

Definition of syncope

There are three major criteria within the definition of syncope:

1. 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 causes should be considered first.
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 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) definition states that syncope is characterised by:¹

• 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 specific 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 effects.

Causes of syncope

Once it has been established syncope has occurred, 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 four 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).

The mnemonic SNAP can be used to remember this classification of syncope.

Neurally mediated

Neurally mediated syncope is due to an inappropriate autonomic reflex in response to a trigger and hence this is also known as reflex syncope.

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 specific trigger:

• Post-micturition (the most common)
• Post-cough
• Post-swallow
• Post-defecation
• Post-prandial
• Post-exercise*

*Post-exercise syncope is a red flag and 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).

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 confirm the diagnosis
• Carotid sinus massage: 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

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 insufficiency of the baroreceptor response, resulting in syncope.

Causes of orthostatic hypotension

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

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

Tachyarrhythmias can be supraventricular (e.g. atrial fibrillation, atrial flutter, atrioventricular nodal re-entry tachycardia) or ventricular.

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 syncope

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.

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)

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 Wolff-Parkinson-White syndrome
• ECG monitoring: ECG monitoring is used to confirm an association between syncope and the arrhythmia (this is the only way to definitively diagnose arrhythmic syncope). Options include ambulatory ECG monitoring or external/implantable loop recorders.
• Echocardiography: may show heart failure, cardiomyopathies, valvular disease or 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).

For more information, see the Geeky Medics guide to taking a loss of consciousness history.

Remember different types of syncope can co-exist, meaning that a patient with extensive cardiac disease may still experience a simple vasovagal syncope and vice versa.

Mnemonics

The five Ps:

• Precipitant
• Prodrome
• Position
• Palpitations
• Post-event phenomena

The five Cs:

• Colour
• Convulsions
• Continence
• Cardiac problems
• Cardiac death family history

References

1. 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.
2. Anderson J, O’Callaghan P. Cardiac syncope. Epilepsia 2012;53(s7):34-41.
3. Douglas G, Nicol F, Robertson C, editors. Macleod’s clinical examination. Elsevier Health Sciences; 2013 Jun 21.
4. Gauer RL. Evaluation of syncope. American family physician. 2011 Sep 15;84(6):640.