Aerobic exercise, particularly running, is known to induce fainting in some persons, a trait that may become apparent in late childhood or later and may be familial. There is nausea as well as other presyncopal symptoms; the faint can be avoided by discontinuing exercise or not exceeding a threshold of effort set by the patient himself. Such persons do not seem unduly sensitive to nonaerobic exercise and have no recognizable electrocardiographic or structural heart problems. They have a predilection to faint with prolonged tilt-table testing and with isoproterenol infusion, suggesting that this represents a form of neurocardiogenic syncope. For this reason, these patients may benefit from β-adrenergic-blocking drugs if given under careful supervision. As discussed further on, exercise can also precipitate syncope in patients with a number of underlying cardiac conditions (myocardial ischemia, long QT syndrome, aortic outflow obstruction, cardiomyopathy, structural chamber anomalies, exercise-induced ventricular tachycardia, and, less often, supraventricular tachycardias).
Athletes who faint unpredictably during exercise pose a particularly difficult problem. Obviously those found to have serious heart disease should give up competitive sports, but the majority has no demonstrable cardiac abnormality. Subjecting these patients to intense exercise and other testing sometimes fails to elicit the faints, but many have varying degrees of hypotension when subjected to prolonged head-up tilt, again suggesting that the cause of fainting is essentially neurocardiogenic (see above). Implanted cardiac pacemakers are not curative in these vasodepressor faints, as the main deficiency is in vascular resistance. Unless the results of tilt-table testing are unequivocal and reproducible, it is best to consider the more serious causes of exercise-induced syncope due, for example, to ischemic heart disease or aortic valve disease, and to treat the patient appropriately.
The carotid sinus is normally sensitive to stretch and gives rise to sensory impulses carried via the nerve of Hering, a tributary of the glossopharyngeal nerve, to the medulla. Massage of one of the carotid sinuses or of both alternately, particularly in elderly persons, causes (1) a reflex cardiac slowing (sinus bradycardia, sinus arrest, or even atrioventricular block)—the vagal type of response, or (2) a fall of arterial pressure without cardiac slowing—the vasodepressor type of response. Another (“central”) type of carotid sinus syncope was in the past ascribed to cerebral arteriolar constriction, but such an entity has never been validated.
Faintness or syncope because of carotid sinus sensitivity reportedly has been initiated by turning of the head to one side while wearing a tight collar or even by shaving over the region of the sinus. However, the absence of a history of such an association does not exclude the diagnosis. The attack nearly always occurs when the patient is upright, usually standing. The onset is sudden, often with falling. Small convulsive movements occur quite frequently in both the vagal and vasodepressor types of carotid sinus syncope. The period of unconsciousness in carotid sinus syncope seldom lasts longer than 30 s, and the sensorium is immediately clear when consciousness is regained. The majority of the reported cases have been in men.
In some circumstances, it is important to avoid compression of the carotid artery as an evocative test, particularly if a carotid bruit is heard over either carotid vessel. Moreover, carotid sinus compression for syncope testing should be conducted in controlled circumstances.
A number of other types of purely reflexive cardiac slowing can be traced to direct irritation of the vagus nerves (from esophageal diverticula, mediastinal tumors, gallbladder stones, carotid sinus disease, bronchoscopy, and needling of body cavities). Here, the reflex bradycardia is more often of sinoatrial than atrioventricular type. Weiss and Ferris called such faints vagovagal.