Faintness and syncope are among the most common of all medical problems. Practically every adult has experienced some presyncopal symptoms, if not a fully developed syncopal attack, or has observed such attacks in others. Description of these symptoms, as with other predominantly subjective states, is often ambiguous. The patient may refer to the experience as light-headedness, dizziness, a “drunk feeling,” a weak spell, or, if consciousness was lost, a “blackout.” Careful questioning may be necessary to ascertain the exact meaning the patient has given to these words. In many instances the nature of the symptoms is clarified by the fact that they include a sensation of faintness and then a momentary loss of consciousness, which is easily recognized as a faint, or syncope. This sequence also informs us that under certain conditions any difference between faintness and syncope is only one of degree. These symptoms must be clearly set apart from certain types of epilepsy, the other major cause of episodic unconsciousness, and from disorders such as cataplexy, transient ischemic attacks (TIAs), “drop attacks,” and vertigo, which are also characterized by episodic attacks of generalized weakness or inability to stand upright, but not by a loss of consciousness.
From a clinical perspective, syncope is essentially of three main types, all ultimately causing hypotension and each of which may lead to a temporary reduction in the flow of blood to the brain. The first, reflex withdrawal of vascular sympathetic tone (vasodepressor effect), triggered by centrally mediated inhibition of the normal tonic sympathetic influences, is often associated with excessive vagal effect and bradycardia (vagal effect). The type associated with bradycardia is called vasovagal syncope, a special form of neurogenic, or neurocardiogenic syncope, by which is meant the withdrawal of sympathetic tone through a reflex neural mechanism. Neurocardiogenic syncope usually signifies that the inciting stimulus originates in neural receptors within the heart.
The second is a failure of sympathetic innervation of blood vessels and of autonomically activated compensatory responses (reflex tachycardia and vasoconstriction), which occurs with assumption of the upright body position and leads to pooling of blood in the lower parts of the body—causing orthostatic hypotension and syncope. Typically, in individuals with these first two forms of syncope, there is no evidence of underlying cardiac disease.
Syncope of a third type is caused by a primary diminished cardiac output because of disease of the heart itself as in the Stokes-Adams bradyarrhythmia attack, severe aortic or subaortic stenosis, or ischemic heart disease. Greatly reduced blood volume from dehydration or blood loss usually causes only near syncope, but complete loss of consciousness may certainly occur in severe circumstances.
As a rough guide to the relative frequency of the various causes of syncope, the large amount of information from the Framingham Heart Study accumulated by Soteriades and colleagues can be taken as representative: the leading cause was vasovagal, a cardiac cause was established in about 10 percent; and orthostatic hypotension in another 10 percent. Also, 7 percent of cases were attributed to medications, mainly those that interfered with sympathetic tone, and remaining 40 percent could not be categorized.
The three main types of syncope as well as several others that cannot readily be classified within these categories can be further subdivided by their pathophysiologic mechanism, as follows:
I. Neurogenic vasodepressor reactions
A. Elicited by extrinsic signals to the medulla from baroreceptors 1. Vasodepressor (vasovagal) 2. Neurocardiogenic 3. Carotid sinus hypersensitivity 4. Vagoglossopharyngeal 5. Severe pain, especially if arising in a viscera (bowel, ovary, testicle, etc.)
B. Coupled with diminished venous return to the heart 1. Micturitional 2. Tussive 3. Valsalva, straining, breathholding, weight lifting 4. Postprandial