There are two types of abnormal response to upright tilting: (1) early hypotension (occurring within moments of tilting) that slowly progresses with continued upright posture; this signifies inadequate sympathetic tone and baroreceptor function; and (2) a delayed (up to several minutes) hypotension that appears abruptly at the end of that period and indicates a neurocardiogenic mechanism.
The normal response to a 60to 80-degree head-up tilt after approximately 10 min is a transient drop in systolic blood pressure (5 to 15 mm Hg), a rise in diastolic pressure (5 to 10 mm Hg), and a rise in heart rate (10 to 15 beats per minute). Hypotension and fainting after tilting for this duration, a positive test, as already emphasized, is taken as a proclivity to neurocardiogenic fainting and at least an ostensible explanation for the problem. However, because it occurs in a proportion of individuals who have never fainted; it is not to be taken as incontrovertible evidence that a recent spell is explained by this mechanism. Although controversial, in some circumstances the infusion of the catecholamine isoproterenol (1 to 5 mcg/min for 30 min during head-up tilt) may be a more effective means of producing hypotension (and syncope) than the standard tilt test alone (Almquist et al; Waxman et al). While it brings out more cases of neurocardiogenic syncope, some of these are false positives.
Patients seen during the preliminary stages of fainting or after they have lost consciousness should be placed in a position that permits maximal cerebral blood flow, that is, with head lowered between the knees if sitting, or, far preferably, in the supine position with legs elevated. All tight clothing and other constrictions should be loosened and the head and body positioned so that the tongue does not fall back into the throat and the possible aspiration of vomitus is avoided. Nothing should be given by mouth until the patient has regained consciousness. The patient should not be permitted to rise until the sense of physical weakness and the appearance of pallor have passed and he should be watched carefully for a few minutes after arising.
As a rule, the physician sees the patient after recovery from the faint and is asked to explain why it happened and how it can be prevented in the future. One should think first of those causes of fainting that constitute a therapeutic emergency. Among them are massive internal hemorrhage and myocardial infarction, and cardiac arrhythmias. In an elderly person, a sudden faint without obvious cause must always arouse the suspicion of a complete heart block or other cardiac arrhythmia.
The prevention of fainting depends on the mechanisms involved. In the usual vasodepressor faint of adolescents—which tends to occur in circumstances favoring vasodilatation (warm environment, hunger, fatigue, alcohol intoxication) and periods of emotional excitement—it is enough to advise the patient to avoid such circumstances and to maintain adequate hydration. In postural hypotension, patients should be cautioned against arising suddenly from bed. Instead, they should first exercise the legs for a few seconds, then sit on the edge of the bed and make sure they are not light-headed or dizzy before starting to walk. Standing for prolonged periods can sometimes be tolerated without fainting by crossing the legs forcefully. The same regimen suffices for cases of syncope from deconditioning. Alternatives should be found for medications that are conceivable causes of orthostasis. β-Adrenergic blocking agents, diuretics, antidepressants, and sympatholytic antihypertensive drugs are the common culprits.