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 univ
ersally present : systemic arterial vasodilation and bradycardia. A third p
henomenon, cerebrovascular constriction, has also been described but its co
ntribution to the faint is less well established.
The neural reflex pathways responsible for triggering the circulatory chang
es in the vasovagal faint are incompletely understood, but have recently be
en the subject of renewed interest, In part, this interest probably stems f
rom the frequency with which vasovagal symptoms are now recognized to be th
e cause of fainting spells. Additionally, however, there is an increasingly
recognized need to develop treatment strategies for those affected patient
s in whom recurrent vasovagal symptoms are particularly troublesome. It is
the goal of this discussion to focus on those aspects of circulatory contro
l, and in particular on potential interactions among certain neural and hum
oral systems, which may contribute to the inappropriate physiologic respons
es associated with the vasovagal faint.