Aortic stenosis or subaortic stenosis from cardiomyopathy often sets the stage for exertional syncope, because cardiac output cannot keep pace with the demands of exercise. Primary pulmonary hypertension and obstruction of right ventricular outflow (pulmonic valvular or infundibular stenosis) or intracardiac tumors may also be associated with exertional syncope. Syncope may also be a manifestation of large pulmonary embolism. Vagal overactivity may be a factor contributing to the syncope in these conditions as well as in the syncope that may accompany acute aortic outflow obstruction. Tetralogy of Fallot is the congenital cardiac malformation that most often leads to syncope. Other cardiac causes are listed in the classification given at the opening of this chapter.
It is now widely appreciated that syncope is not a manifestation of conventional cerebrovascular disease (see further on for discussion and the problem of “drop attacks” that do not have loss of consciousness as a feature). Specifically, syncope does not occur as a manifestation of TIAs that are confined to the territory of the internal carotid arteries and it is rare, if ever, that pure syncopal attacks occur with vertebrobasilar ischemia (see further on). Cases of syncope that do occur are usually associated with multiple occlusions of the large arteries in the thorax or neck. The main examples are found in patients with the aortic-arch syndrome (Takayasu disease) in which the brachiocephalic, common carotid, and vertebral arteries have become narrowed. Physical activity may then critically reduce blood flow to the upper part of the brainstem, causing abrupt loss of consciousness. Stenosis or occlusion of vertebral arteries and the “subclavian steal syndrome” are other examples of cerebrovascular diseases that may cause syncope under the special circumstance of overuse of an arm (see Chap. 33). Fainting also occurs occasionally in patients with congenital anomalies of the upper cervical spine (Klippel-Feil syndrome) or cervical spondylosis, in which the vertebral circulation is compromised. Head turning may then cause vertigo, nausea and vomiting, visual scotomas and, finally, unconsciousness.
The onset of a subarachnoid hemorrhage may be signaled by a syncopal episode, often with transient apnea. Because the bleeding is arterial, there is a momentary cessation of cerebral circulation as the levels of intracranial pressure and blood pressure approach one another. Unless there has been vomiting, a complaint of headache immediately preceding the syncope, or the discovery of severe hypertension or stiff neck when the patient awakens, the diagnosis may not be suspected until a CT scan or lumbar puncture is performed.
An associated problem, with which we have had numerous unsatisfactory encounters, is posed by the patient who falls suddenly forward, striking the head without apparent cause, has headache, and is found to have bifrontal hematomas and subarachnoid blood on CT. These cases highlight the difficulty of distinguishing a primary aneurysmal subarachnoid hemorrhage from an accidental fall or syncope with secondary frontal brain contusions; in almost every case, we have felt obliged to perform some form of cerebral angiography to exclude an anterior communicating artery aneurysm, but we have rarely found one.
Hysterical fainting is rather frequent and usually occurs under dramatic circumstances (see Chap. 47). The evident lack of change in pulse, blood pressure, or color of the skin or any outward display of anxiety distinguishes it from the vasodepressor faint. Irregular jerking movements and generalized spasms without loss of consciousness or change in the EEG are typical features (Linzer et al, 1992). The diagnosis is based on these negative findings in a person who exhibits the general personality and behavioral characteristics of hysteria. Several interesting instances of mass faintness and syncope of hysterical type have been described—for example, in school marching bands (R.J. Levine).
Syncope of Unknown Cause