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Fainting or syncope (IPA: /ˈsɪnkəpi/ or /ˈsɪŋkəpi/) is a sudden (and generally momentary) loss of consciousness, or blacking out due to the Central Ischaemic Response, because of a lack of sufficient blood and oxygen reaching the brain. The first symptoms a person feels before fainting are dizziness, a dimming of vision, or brownout, tinnitus, and feeling hot. Moments later, the person's vision turns black and he or she drops to the floor (or slumps if seated in a chair). If the person is unable to slump from the position to a near horizontal position they risk dying due to the Suspension Trauma effect.

Factors that influence fainting are taking in too little food and fluids, low blood pressure, hypoglycemia, growth spurts, physical exercise in excess of the energy reserve of the body, and lack of sleep. Even standing up too quickly or being in too hot a room can cause fainting. Recommended treatment is to allow the person to lie on the ground with his or her legs a little elevated. As the dizziness and the momentary blindness passes, the person may experience visual disturbances in the form of small bright dots (phosphene). These will also pass within a few minutes. If fainting happens frequently, or if there is no obvious explanation, it is important to see a doctor about it.

More serious causes of fainting include cardiac (heart-related) causes such as an abnormal heart rhythm (an arrhythmia), where the heart beats too slowly, too rapidly or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Other important cardio-vascular conditions that can be manifested by syncope include subclavian steal syndrome and aortic stenosis.


It is convenient to think of three types of fainting, or syncope. The usual type is benign and is vaso-vagal. Less common is a pure cardiac syncope. Finally there is syncope from vertebro-basilar arterial disease. Epilepsy appearing as syncope is not considered.

Vasovagal syncope

Main article: Vasovagal syncope

The vasovagal type can be considered in two forms:

  • Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining or circumstances promoting vaso-dilatation (eg heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
  • Recurrent syncope with complex associated symptoms. This is so-called Neurally Mediated Syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes), sweating, light-headedness. The subject is usually but not always upright.

A pattern of background factors contributes to the attacks. There is typically an unsuspected relatively low blood volume, for instance, from taking a low salt diet in the absence of any salt-retaining tendency. Heat causes vaso-dilatation and worsens the effect of the relatively insufficient blood volume. That sets the scene, but the next stage is the adrenergic response. If there is underlying fear or anxiety (e.g. social circumstances), or acute fear (e.g. acute threat, needle phobia), the vaso-motor Centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain but the heart is unable to meet requirement because of the low blood volume, or decreased return of blood to the heart (abdominal straining). However, the heart's increased left ventricular muscle activity is recognised by the Vaso-Motor Centre via activity in Vagal nerve fibres traveling from the heart to the brain. Normally, the Vagal response would modulate this activity. However, in NMS, the abnormal response that follows is in the exaggerated strength of the return vagal flow, actually causing minor further peripheral vaso-dilatation and slowing the heart decisively - to a point where fainting occurs. In other words, an adrenalin effect causes an over-compensation by the Vagus. Interestingly, some people faint lying in a dentist's chair after receiving adrenalin in a local anaesthetic, endorsing the explanation.

The tilt-table test typically evokes the attack.

Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defense mechanism when confronted by danger ("playing possum"). This reflex only occurs in some people and may be similar to the animal's reflex.

The mechanism described here suggests that a practical way to prevent attacks would be, counter-intuitively, to block the adrenergic signal with a Beta Blocker. But simpler plan is to explain the mechanism, discuss causes of fear, and optimise salt as well as water intake.

Pure cardiac syncope

Fainting can also occur if pressure on the carotid artery in the neck triggers a vagal signal to the Vaso-Motor Centre, reflexly causing a vagal response to slow the heart. A pure cardiac arrhythmia is a serious matter that can appear as syncope but this is unusual. Severe narrowing of the Aortic Valve leading to syncope is included for completeness.

Syncope from vertebro-basilar arterial disease

Arterial disease in the upper spinal cord, or lower brain, causes syncope if there is a reduction in blood supply, which may occur with extending the neck or after drugs to lower blood pressure.

Particular causes

Clinical symptoms

If the patient states, "I felt dizzy with blurry vision, muscle weakness, during the fall I bumped my knee, hit my head and passed out," then it is not syncope, it is termed pre or near-syncope.

If the patient states, "I felt dizzy, shadows came over my eyes, and when I woke up I was lying on the floor," then it is diagnosed as syncope.

Patients who experience a syncoptic episode do not remember falling.

Syncope in children

Syncope in older adults

Syncope in mental health settings

Syncope in occupational settings

See also



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