fainting is a transient, reversible loss of
consciousness due to an acute reduction in blood supply to the brain. Lack of cerebral perfusion for 2–3 sec can cause premonitory symptoms (such as light-headedness,
dizziness); after 10 sec fainting results. Fainting is synonymous with
syncope (from the Greek ‘to strike’ or ‘cut off’). Slumping in a chair or falling to the ground characteristically occurs because of loss of postural
muscle tone, although occasionally there may be jerky movements, muscle spasms, or urinary incontinence as a result of transient ‘decerebration’. Fainting usually occurs when the subject is upright, and falling results in recovery of cerebral blood flow and spontaneous recovery.
Fainting does not cause damage to the nervous system, unless there is injury from the fall, but it can cause concern, embarrassment, and loss of confidence. However some of the conditions associated with fainting are potentially serious or even potentially fatal. It has been said that ‘the only difference between fainting and sudden death is that in one you wake up’ (Engel, 1978).
Maintenance of blood flow to the brain is dependent on an adequate
blood pressure and on patent and responsive cerebral blood vessels. These vessels dilate to maintain flow when blood pressure falls within its normal range of variation, but a major or rapid fall can defeat this compensation. Thus, there are numerous causes of fainting.
Low blood pressure (
hypotension) may occur with postural (
orthostatic) change, on moving from the horizontal to the upright position such as when rising after sleep. The sympathetic nervous system normally responds to gravitational change and prevents pooling of blood in the lower limbs by an increase in its activity, which causes constriction of blood vessels. The majority of the population do not faint, as adaptive mechanisms to standing erect are well developed. However, in certain situations even the fittest can faint (such as guardsmen standing still at attention on a hot day), and there are some disease conditions, and some drugs, which impair the reflex response. Fainting caused by postural hypotension classically occurs on assumption of the head-up posture, with relief by lying flat.
Intermittent abnormal activity of the
autonomic nervous system (
neurally-mediated syncope) also may occur. During these episodes increased parasympathetic activity slows the heart rate whilst diminished sympathetic activity allows blood vessels to dilate, lowering blood pressure. The most common form is known as
vasovagal syncope — the ‘emotional’ or ‘common’ fainting. This is often of teenage onset, in females, and with a family history.
A variety of factors, such as fear of needles, sight of blood, or pain, can precipitate this type of fainting. There is often prompt recovery on attaining the horizontal position. In the elderly, similar autonomic effects on the heart and circulation may occur, when there is hypersensitivity of the
baroreceptors in the carotid sinus in the neck; tightening the collar, or moving the head whilst shaving, stimulates nerves that normally signal a rise in blood pressure. The result is a ‘correction’ of this false signal — a fall in heart rate and blood pressure. This can be a potentially serious condition, with severe injury from falls, and may require treatment with a cardiac
pacemaker and drugs that maintain blood pressure.
There are other, rarer, causes of fainting mediated by the nervous system, precipitated by a range of factors such as urination, coughing, or swallowing.
Another cause of fainting is a change in cardiac rhythm, when the heart beats too fast or too slowly, resulting in a poor cardiac output and inadequate blood flow to the brain. The best known is the
Stokes–Adams attack, when the ventricles of the heart fail to beat because of
heart block.
There are also more direct — mechanical or hydraulic — causes of low blood pressure; these include depletion of the circulating blood volume due to
haemorrhage or plasma loss, and inadequate fluid intake or excessive fluid loss due to
vomiting or
diarrhoea, or from the kidneys in some abnormal conditions. Excessive dilatation of blood vessels, due to drugs (such as glyceryl trinitrate used in angina, or from excessive alcohol ingestion), circulating vasodilator substances, or venous disorders (extensive varicose veins), may be contributory.
Finally, constriction of the cerebral blood vessels may contribute to fainting. For example, during
hyperventilation, even in healthy people, low carbon dioxide in the blood causes constriction of the blood vessels. Or when a major vessel supplying the brain is partly or severely occluded in
carotid artery stenosis, even small decreases in blood pressure or changes in cardiac rhythm threaten the blood supply.
In summary, fainting may occur in any individual, from the young (
vasovagal syncope), to the elderly (
carotid sinus hypersensitivity). It is estimated to occur at some time in 3% of the adult population, and sometimes in extremely healthy and fit people (oarsmen, athletes, and in particular weightlifters). There may be an occupational hazard — as in trumpet players. Fainting is usually involuntary, but it may be deliberately induced, as in the so-called ‘fainting lark’: a combination of squatting, overbreathing, forceful expiration, and standing up suddenly. The ‘Mess trick’ is a variation of this.
Fainting can sometimes be ominous, especially in those with an untreated cardiac rhythm disorder, consistent with ancient observations that ‘those who suffer from frequent and severe fainting without cause often die suddenly’ ( Hippocrates,
Aphorisms 2.41). But in many other conditions, such as vasovagal syncope, the prognosis is excellent.
C. J. Mathias
See also
autonomic nervous system;
blood pressure.
