Pathophysiology of Reflex Syncope: A Review

Wayne O. Adkisson MD; David G. Benditt MD


J Cardiovasc Electrophysiol. 2017;28(9):1088-1097. 

In This Article

Abstract and Introduction


In this correspondence, the pathophysiology of reflex syncope (vasovagal syncope, carotid sinus syndrome, and situational syncope) is reviewed, including clarification of the nomenclature.


  • Clarify the nomenclature of reflex syncope.

  • Understand how reflex syncope fits into the umbrella category of transient loss of consciousness (TLOC), as well as in the more specific category of syncope in general.

  • Review the pathophysiology of syncope in general and, more specifically, in the various forms of reflex syncope.

  • Finally, provide a brief review of the management of specific types of reflex syncope.


Syncope is one of several conditions that result in TLOC. Other causes of TLOC include: seizures disorders, trauma (concussions), some metabolic disturbances, and certain intoxications. However, complicating matters for clinicians, there are also so-called TLOC-mimics, such as psychogenic pseudo-syncope, psychogenic pseudo-seizures, and cataplexy. These latter conditions do not cause true loss of consciousness, but appear to do so, and may be the source of substantial diagnostic uncertainty.

Excluding TLOC-mimics, all "true" TLOC conditions share certain features; namely, they are:

  1. Associated with obligatory loss of postural tone, and occasionally disturbances of smooth muscle control.

  2. Transient, usually lasting less than a minute or only a few minutes at most.

  3. Spontaneously reversible (i.e., no intervention is needed for restoration of consciousness).

Syncope is distinguished from the other TLOC entities by its pathophysiology; specifically, syncope results from a temporary global inadequacy of cerebral oxygenation (almost always due to cerebral hypoperfusion, but on rare occasions the result of acute hypoxemia). This latter component of the definition of syncope distinguishes syncope from seizures in which cerebral dysfunction is the result of a primary electrophysiological disturbance in the brain. The clinical distinction between TLOC due to syncope and that due to seizure can be difficult, and is particularly complicated by the fact that syncope may be associated with jerky muscular movements that are readily mistaken for seizure activity by nonexpert witnesses, including many physicians.[1]

Apart from distinguishing TLOC due to syncope from other causes of TLOC, the clinician must also consider the multiple potential causes for true faints. In this regard, the etiology of syncope can be divided into three categories[2] (Table 1):

  1. Reflex syncope

  2. Orthostatic syncope

  3. Cardiac syncope

In this review, we focus primarily on "reflex syncope"; specifically, those conditions in which neural reflex activity causes hypotension and/or bradycardia with consequent symptomatic cerebral hypoperfusion. In this regard, we assume that the practitioner has already established that the patient's TLOC event was due to syncope and that other causes of TLOC and TLOC-mimics have been reasonably excluded. For a more general discussion of the approach to the evaluation of the patient with TLOC, readers are referred to a recent review.[1]