Vasovagal syncope is characterized by transient failure of usually reliable physiologic mechanisms responsible for maintaining both systemic arterial pressure and cerebral blood flow. Two circulatory phenomena are almost universally present : systemic arterial vasodilation and bradycardia. A third phenomenon, cerebrovascular constriction, has also been described but its contribution to the faint is less well established. The neural reflex pathways responsible for triggering the circulatory changes in the vasovagal faint are incompletely understood, but have recently been the subject of renewed interest. In part, this interest probably stems from the frequency with which vasovagal symptoms are now recognized to be the cause of fainting spells. Additionally, however, there is an increasingly recognized need to develop treatment strategies for those affected patients in whom recurrent vasovagal symptoms are particularly troublesome. It is the goal of this discussion to focus on those aspects of circulatory control, and in particular on potential interactions among certain neural and humoral systems, which may contribute to the inappropriate physiologic responses associated with the vasovagal faint.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Interventional Cardiac Electrophysiology|
|State||Published - Jan 1 1997|