This is the common faint, seen mainly in young individuals. A familial predisposition is well known (Mathias et al). The evocative factors are usually strong emotion, physical injury—particularly to viscera (testicles, gut)—or other factors (see in the following text). As described earlier, the vasodilatation of adrenergically innervated “resistance vessels” is postulated to lead to a reduction in peripheral vascular resistance, but cardiac output fails to exhibit the compensatory rise that normally occurs in hypotension. Some physiologic studies suggest that the dilatation of intramuscular vessels, innervated by β-adrenergic fibers, may be more important than dilatation of the splanchnic ones.
Skin vessels, in contrast, are constricted. Vagal activation may be superimposed either as a primary or a reactive phenomenon (hence the term vasovagal) causing bradycardia and leading possibly to a slight further drop in blood pressure. Other vagal effects are perspiration, increased peristaltic activity, nausea, and salivation. However, bradycardia probably contributes little to the hypotension and syncope. The term vasovagal was used originally by Thomas Lewis. As Lewis himself pointed out, atropine, “while raising the pulse rate up to and beyond normal levels during the attack, leaves the blood pressure below normal and the patient still pale and not fully conscious.”
The vasodepressor faint occurs (1) in normal health under the influence of strong emotion, particularly in some susceptible individuals (sight of blood or an accident) or in conditions that favor peripheral vasodilatation, for example, hot, crowded rooms (“heat syncope”), especially if the person is hungry or tired or has had alcoholic drinks; (2) during a painful illness or after bodily injury (especially of the abdomen or genitalia), as a consequence of fright, pain, and other factors (where pain is involved, the vagal element tends to be more prominent in the genesis of the faint); and (3) after standing immobile for prolonged periods, particularly in warm environments (military at attention, marching bands) (4) during exercise in some sensitive persons (see further on).
The clinical manifestations of fainting attacks vary to some extent, depending on their mechanisms and the settings in which they occur. The most common types of faint—namely, vasodepressor and vasovagal syncope, conform more or less to the following pattern. In these types, which are taken in this section as one characteristic manifestation, the patient is usually in the upright position at the beginning of the attack, either sitting or standing. Certain subjective symptoms, the prodrome, mark the onset of the faint. The person feels queasy, is assailed by a sense of giddiness and apprehension, may sway, and sometimes develops a headache. What is most noticeable at the beginning of the attack is pallor or an ashen-gray color of the face; often the face and body become bathed in cool perspiration. Salivation, epigastric distress, nausea, and sometimes vomiting may accompany these symptoms, and the patient tries to suppress them by yawning, sighing, or breathing deeply. Vision may dim or close in concentrically, the ears may ring, and it may be impossible to think clearly (“grayout”). This serves to introduce the common faint that is known to all physicians and most laypersons.
The duration of the prodromal symptoms is variable from a few minutes to only a few seconds. If, during the prodromal period, the person is able to lie down promptly, the attack may be averted before complete loss of consciousness occurs; otherwise, consciousness is lost and the patient falls to the ground. The more or less deliberate onset of this type of syncope enables patients to lie down or at least to protect themselves as they slump. A hurtful fall is exceptional in the young, although an elderly person may be injured.