Vasovagal syncope



Vasovagal syncope is a form of ‘reflex syncope’ more colloquially known as a ‘common faint’.

Syncope is a broad term for transient loss of consciousness. The loss of consciousness is usually due to a brief reduction in cerebral perfusion due to an abrupt fall in blood pressure. The loss of consciousness inevitably leads to a collapse with subsequent recovery as perfusion is restored (average 12 seconds).

There are many different causes of syncope of which the most common is vasovagal syncope. Vasovagal syncope is also known as a ‘common faint’ and typically occurs in the setting of a stressful event (e.g. phlebotomy). It is characterised by prodromal symptoms (e.g. lightheadedness, sweating, palpitations) and then loss of consciousness due to alteration in activation of the autonomic nervous system.


Vasovagal syncope is extremely common.

Vasovagal syncope accounts for more than one-third of cases of syncope. It is the most cause of syncope in young patients. It is common in older adults, but usually, a deeper search to exclude other causes of syncope is required.

Aetiology & pathophysiology

Vasovagal syncope is due to altered activation of the autonomic nervous system.

Vasovagal syncope is a type of ‘reflex syncope’ that causes loss of consciousness due to a reflex response in the autonomic nervous system. Other types of reflex syncope include:

  • Situational syncope (faint in response to a specific trigger): coughing, swallowing, sneezing, micturition
  • Carotid sinus syndrome: exaggerated response to carotid sinus baroreceptor stimulation. Baroreceptors are mechanoreceptors that sense arterial stretch and alter blood pressure through the autonomic nervous system.


Vasovagal syncope, particularly in young patients, may be associated with specific triggers that lead to reflex autonomic nervous system changes. Classic triggers include:

  • Emotional events
  • Painful or noxious stimuli
  • Prolonged standing
  • Heat exposure
  • Physical exertion

Some patients may have no specific trigger, particularly in the elderly. Instead, there may be a history of recurrent syncope without apparent cause. When there is a very specific trigger (e.g. micturition) this is known as a ‘situational syncope’ as discussed above.

Altered autonomic nervous system

Vasovagal syncope is a neurally-mediated condition that results in reflex changes in the autonomic nervous system. Broadly speaking, these reflex responses result in:

  • Vasodilatation, AND/OR
  • Bradycardia

The result of these two mechanisms is a fall in blood pressure (hypotension) and subsequent reduction in cerebral perfusion (hypoperfusion). The cerebral hypoperfusion results in the temporary loss of consciousness.

Looking at these mechanisms in more detail, there are two major responses in vasovagal syncope:

  • Cardioinhibitory response: increased parasympathetic activity that causes altered electrical activity in the heart manifesting as bradycardia (or higher degree of heart block).
  • Vasodepressor response: decreased sympathetic activity that leads to systemic vasodilatation and subsequent hypotension.

In vasovagal syncope, there is usually a combination of both cardioinhibitory and vasodepressors mechanisms, which is known as a ‘mixed response’. Other autonomic pathways may be involved including the baroreceptor reflex and carotid sinus reflex.

Clinical features

Vasovagal syncope is classically associated with a series of prodromal symptoms including nausea, pallor and sweating.

Vasovagal syncope typically occurs in the standing or sitting position. This is because the supine position (i.e. lying down) helps maintain adequate cerebral perfusion. This is why lying patients down is recommended following a collapse.

Prior to the onset of loss of consciousness, typical features can occur that are related to changes in the autonomic nervous system. These include:

  • Lightheadedness
  • Pallor
  • Sweating
  • Feeling of warmth/cold
  • Palpitations
  • Nausea
  • Visual alteration: usually described as blurring, then temporary darkening of vision
  • Reduction in hearing

Although the loss of consciousness is brief (~8-12 seconds), there may be some fatigue after the event with full recovery slightly delayed. This helps differentiate vasovagal syncope from cardiac syncope due to an arrhythmia for example, when there is sudden-onset syncope without autonomic prodromal changes or post-syncope fatigue.


The diagnosis of vasovagal syncope is usually based on the clinical assessment and exclusion of other causes.

The diagnosis of vasovagal syncope requires a thorough history and clinical examination. The history of prodromal symptoms following a typical trigger in a patient with no significant medical history is usually classic for vasovagal syncope. During the actual event, hypotension and bradycardia are commonly observed that quickly improve. The physical examination is otherwise typically normal.

It is more difficult to make the diagnosis in the absence of a typical trigger, in elderly patients, or those with co-morbidities when a number of other causes could have potentially led to syncope. This typically leads to a more thorough workup or period of observation.

NOTE: A witness account of the syncope can be really important, especially to exclude other potential causes of loss of consciousness including seizures.

Differential diagnosis

The other major causes of syncope include orthostatic hypotension, arrhythmias, and structural cardiac or cardiopulmonary disease.

Syncope is a very common clinical problem. It is important to recognise the other causes of syncope that are potentially life-threatening. These can be broadly organised into four main groups:

  • Orthostatic hypotension: fall in systolic blood press > 20 mmHg on standing, which leads to syncope
  • Arrhythmias: both tachyarrhythmias (e.g. ventricular tachycardia) and bradyarrhythmias (e.g. complete heart block)
  • Structural cardiac disease: aortic stenosis, hypertrophic cardiomyopathy
  • Cardiopulmonary disease: massive pulmonary embolism

NOTE: rare causes of syncope may exist including vascular steal syndrome (shunting of blood due to an obstructed upper limb arterial vessel) and vertebrobasilar insufficiency (poor blood flow through the posterior circulation of the brain, but usually occurs with other preceding symptoms).

Non-syncopal attacks

It is important to differentiate true syncope from other causes of collapse/loss of consciousness that do not occur from cerebral hypoperfusion. Some of these causes may cause a partial or complete loss of consciousness due to other mechanisms, which include:

  • Seizures
  • Non-epileptiform seizures
  • Intoxication
  • Metabolic disturbances (e.g. hypoglycaemia, hypoxia)

Other causes may lead to collapse without impaired consciousness, but without proper history and examination, may be confused with syncope, which includes:

  • Cataplexy: sudden loss of muscle tone
  • Drop attacks: sudden spontaneous fall without external physical trigger
  • Falls


A brief series of investigations may be completed, depending on the setting, to exclude other causes.

Investigations may be completed by an ambulance crew or healthcare staff if seen within a hospital/primary care setting. These include:

  • Capillary blood glucose
  • Electrocardiogram (ECG)
  • Venous blood gas
  • Basic bloods (e.g. full blood count, urea & electrolytes)

Further investigations may be requested if an alternative cause is suspected (e.g. echocardiography for aortic stenosis).

Confirmatory testing

When the diagnosis is unclear or atypical, some confirmatory tests may be requested including the tilt-table test.

Tilt-table test

This test may be performed in patients with suspected vasovagal syncope or orthostatic syncope (fall in systolic BP on standing with resultant syncope) when the diagnosis is not clear.

The test first involves putting the patient on a motorised table with ECG monitoring. Continuous assessments are then made including beat-to-beat blood pressure, heart rate, symptoms, and ECG changes as the patient is moved from a supine position to a head-up position at 60-80º. The idea is to induce syncope and assess the changes on non-invasive monitoring. Provocation drugs may be used if syncope does not occur during passive monitoring.

A positive test for vasovagal syncope is suggested by the development of syncope during the test with evidence of a cardioinhibitory and/or vasodepressor response that leads to hypotension.

ECG monitoring

Monitoring of the heart's electrical activity with an ambulatory ECG monitor is important in patients with suspected cardiac arrhythmias. It may be difficult to differentiate between arrhythmias and vasovagal syncope and this is useful to assess the heart rhythm during syncopal events.

Devices include:

  • 24-hour tape recorder
  • 7-day tape recorder
  • Implantable loop recorders


Long-term management for vasovagal syncope is only required in recurrent cases.

Patients presenting with syncope may need supportive management during the event, but the majority make a quick recovery. In patients presenting with recurrent vasovagal syncope, a number of measures may be recommended but none have consistently proven to be effective.

Conservative measures

Several simple measures may be advised to prevent vasovagal syncope including:

  • Trigger avoidance
  • Patient education: help recognise prodromal symptoms and take action to avoid syncope (e.g. move to seated or supine position).
  • Increase fluid intake: aim 1.5 - 3 L per day
  • Increase salt intake (unless contraindication)
  • Compression stockings
  • DVLA consideration: check local government advice on driving

Medical therapy

Medications may be used to prevent vasovagal syncope by improving blood pressure. Two commonly used drugs include:

  • Fludrocortisone: potent mineralocorticoid that enhances fluid retention.
  • Midodrine: alpha-adrenergic receptor agonist. Increases vascular tone. Limited evidence and side-effects often lead to cessation (e.g. supine hypertension, frequent urination).

Other therapy

Older patients with a significant cardioinhibitory response (i.e. bradycardia or brief asystolic episodes) may be considered for permanent pacing. If there is any significant vasodepressor response (i.e. vasodilatation), pacing is unlikely to be offered.

Last updated: June 2022
Author The Pulsenotes Team A dedicated team of UK doctors who want to make learning medicine beautifully simple.

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