Syncope as a result of a severe paroxysm of coughing was first described by Charcot in 1876. Affected patients are usually heavyset males who smoke and have chronic bronchitis. Occasionally, the problem occurs in children, particularly following paroxysmal coughing spells of pertussis and laryngitis. After sustained hard coughing, the patient suddenly becomes weak and may lose consciousness momentarily. This is mainly attributable to the greatly elevated intrathoracic pressure, which interferes with venous return to the heart. Increased cerebrospinal fluid pressure and diminished PCO2, with resultant cerebral vasoconstriction, are possibly contributing factors.
Powerful efforts to exhale against a closed glottis (as occurs in tussive syncope) are referred to as the
Valsalva maneuver. The unconsciousness that results from breathholding spells in infants is probably based on this mechanism as well; the so-called pallid attacks in infants probably represent reflex vasodepression. Also, the loss of consciousness that occurs during competitive weight lifting (“weight lifters’ blackout”) is mainly the effect of a Valsalva maneuver, added to which are the effects of vascular dilatation produced by squatting and hyperventilation. Lesser degrees of this phenomenon (faintness and light-headedness) often follow other kinds of strenuous activity, such as unrestrained laughing, straining at stool, heavy lifting, underwater diving, or effortful playing of a wind instrument (e.g., trumpet). Rarely, a brief faint may occur in each of these circumstances.
Syncope may occur occasionally in the course of prostatic or rectal examination, but there is only pallor and bradycardia unless the patient stands immediately (prostatic syncope). A Valsalva effect and reflex vagal stimulation appear to be contributing factors. Postprandial hypotension may occasionally lead to syncope in elderly persons, in whom impaired baroreflex function cannot compensate for pooling of blood in splanchnic vessels.
This type of syncope is the result of an orthostatic drop in of blood pressure. It affects persons whose adrenergic innervation to the blood vessels is defective or, of course, those who are hypovolemic. The patient with autonomic failure, on assuming an upright position, shows a steady decline in blood pressure that begins almost immediately and, if not checked, declines to a level at which the cerebral circulation cannot be supported. This rapid effect and the slow decline in pressure are quite different from the situation in neurocardiogenic syncope, in which there is a delayed but then rapid onset of hypotension.
These conditions are easily understood if one keeps in mind that, on assuming the erect posture, the pooling of blood in the lower parts of the body is normally prevented by (1) reflex arteriolar and arterial constriction, through αand β-adrenergic effector mechanisms; (2) reflex acceleration of the heart by means of aortic and carotid reflexes, as described earlier; and (3) muscular activity, which improves venous return. Lipsitz has pointed out that aging is associated with a progressive impairment of these compensatory mechanisms, thus rendering the older person especially vulnerable to syncope. However, even in some younger persons, after the blood pressure has fallen slightly and stabilized at a lower level, the compensatory reflexes may also fail suddenly, with a precipitant drop in blood pressure.
With few exceptions (see Chap. 25), peripheral autonomic failure includes an element of vagal dysfunction that precludes the development of a compensatory tachycardia because vagal tone has already been maximally reduced, and also contrary to what happens in vasodepressor syncope, there tend to be no autonomic responses such as pallor, sweating, nausea, or release of norepinephrine.