Reflex syncope (neurally-mediated syncope)

Douglas J Lanska MD FAAN MS MSPH (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released October 21, 1993; last updated May 2, 2020; expires May 2, 2023

This article includes discussion of reflex syncope, neurocardiogenic syncope, neurally mediated hypotension, simple faint, and vasovagal syncope. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Reflex syncope is one of the main causes of fainting. Cardiac and cerebrovascular regulatory mechanisms are both involved in its pathogenesis. Patients often describe specific triggers such as sudden postural changes, upright position, extreme emotional stress, pain, or trauma. Most cases of reflex syncope, particularly in the dominant subgroup of vasovagal syncope, do not require pharmacotherapy or extensive evaluation. Prevention remains the best management. Reflex syncope is associated with psychological distress, which may be more salient to the patient than the number of syncopal episodes experienced.

Key points


• Syncope denotes loss of consciousness secondary to inadequate blood supply to the brain.


• Reflex syncope is a neurally-mediated transient loss of consciousness that occurs when the body inappropriately reacts to certain triggers, such as intense emotion, the sight of blood, extreme heat, dehydration, a long period of standing, or intense pain.


• Usually, no focal neurologic symptoms are observed during and after these attacks unless the patient has a preexisting neurologic deficit.


• Almost all cases of reflex syncope occur in the standing position.


• Pharmacological agents can cause or exacerbate reflex syncope.


• Most cases of reflex syncope, particularly in the dominant subgroup of vasovagal syncope, do not require pharmacotherapy or extensive evaluation.

Historical note and terminology

The term “syncope” (derived from synkope, the Greek word that means “cutting short”) is now used for describing the symptom of loss of consciousness resulting from insufficient blood flow to the brain (Adams 2001).

Neuroanatomical connections between the brain and heart have been known since the time of Galen of Pergamon (129 AD-c. 200) (Nahm and Freeman 2003).

Image: Galen
Persian physician Ibn Sīnā (ca. 980-1037), known in the West as Avicenna, was the first to note carotid sinus hypersensitivity, which presents with vasovagal syncope following compression of the carotid artery (Shoja et al 2009).
Image: Ibn Sīnā (Avicenna)

In the late 18th and 19th centuries, various authors—eg, Denis Diderot, Jane Austen, Charles Dickens, Gustave Flaubert, George Eliot, Fedor Dostoyevsky—wrote fictional accounts of vasovagal syncope, establishing that this phenomenon was already well-recognized, even outside of medical circles (Perkin 1994). Review of these early accounts shows that the phenomenon was recognized as occurring in both sexes but much more frequently in women, and further that venesection was a potent trigger of the phenomenon (Perkin 1994).

One early fictional account was given by French philosopher, art critic, and writer Denis Diderot (1713-1784) in The Nun (1796):

Image: Denis Diderot


I moved towards the superior with my arms held out in supplication and my body leaning backwards, swooning. I fell, but it was not a heavy fall. In such fainting fits when one's strength abandons one, the limbs seem to give way and as it were fold up unawares; nature, unable to hold up, seems to try to collapse gently. I lost consciousness and the sense of feeling, and merely heard confused and distant voices buzzing round me; whether it was real speech or a singing in my ears, I could make out nothing but this continual buzzing.

Another fictional account of reflex syncope, in this case triggered by venesection, was given by French novelist Gustave Flaubert (1713-1784) in Madame Bovary (1856-1857):

Image: Gustave Flaubert


So Bovary ordered a bandage and a basin, and asked Justin to hold it. Then addressing the peasant, who was already pale—

"Don't be afraid, my lad."

"No, no, sir," said the other; "get on."

And with an air of bravado he held out his great arm. At the prick of the lancet the blood spurted out, splashing against the looking-glass.

"Hold the basin nearer," exclaimed Charles.

"Lor!" said the peasant, "one would swear it was a little fountain flowing. How red my blood is! That's a good sign, isn't it?"

"Sometimes," answered the doctor, "one feels nothing at first, and then syncope sets in, and more especially with people of strong constitution like this man."

At these words the rustic let go the lancet-case he was twisting between his fingers. A shudder of his shoulders made the chair-back creak. His hat fell off.

"I thought as much," said Bovary, pressing his finger on the vein.

The basin was beginning to tremble in Justin's hands; his knees shook, he turned pale.

"Emma! Emma!" called Charles.

With one bound she came down the staircase.

"Some vinegar," he cried. "O dear! two at once!"

In 1907, British neurologist Sir William R Gowers MD FRS (1845-1915) described a hodge-podge of disorders under the umbrella of “vagal and vaso-vagal attacks,” while trying to relate these to epileptic seizures (Gowers 1907a; Gowers 1907b; Nahm and Freeman 2001).

Image: Sir William R Gowers
These events, as Gowers understood them, were prolonged (typically more than 10 minutes in duration, and often more than 30 minutes) and not associated with loss of consciousness. For Gowers, the descriptor vagal was “a purely descriptive term to characterize the gastric, respiratory, and cardiac symptoms, which included the sense of epigastric oppression or fullness, respiratory distress, difficulty breathing, cardiac discomfort and pain, and the sense of impending death” (Nahm and Freeman 2001). Gowers suggested further that the term vaso-vagal be used for attacks characterized by the vasomotor symptoms of coldness and pallor.

During World War I, Canadian cardiologist Thomas Forrest Cotton (1884-1965) was selected to be part of the group that Welsh-born British cardiologist Sir Thomas Lewis CBE FRS (1881-1945) was assembling to study “soldier's heart syndrome” at the Military Heart Hospital at Hampstead, England (Anonymous 1965; Bedford 1966; Roland and Fye 2007).

Image: Sir Thomas Lewis
In 1918, Cotton and Lewis published their observations on “fainting attacks due to inhibitory cardiac impulses” based on observations of soldiers with vasovagal syncope during World War I (Cotton and Lewis 1918). In 1932, Lewis took issue with Gowers' vague descriptive characterization of “vasovagal attacks” and instead advocated calling Gowers' constellation of symptoms “Gowers' syndrome” to avoid confusion with how Lewis wished to redefine use of the term “vasovagal” (Lewis 1932). Lewis coined the label “vasovagal syncope” to encompass brief loss of consciousness with hypotension and bradycardia. Lewis recognized common precipitants of such attacks:

In healthy people, completely at ease, the provocation may be adequate without arousing feelings either of disgust or dread. In these instances there is usually an element of surprise, as when a subject sees blood flow into a syringe from his own arm, the arm redden in reactive hyperemia, or a sphygmograph lever begin to move on his own wrist.

Lewis also recognized key clinical features and used these to propose pathophysiological mechanisms underpinning the syncopal episodes. In particular, Lewis recognized the bradycardia, correctly determined that it was vagally mediated, and he also correctly inferred that it alone could not readily account for syncope.

The slow pulse in the attack is due, as has been shown polygraphically, to a slowing of the whole heart; irregularity, a common feature of vagal slowing, is often displayed. The proof that slowing is vagal is given by atropine, which promptly drives the rate to usual levels under atropine.

The slowing of the heart to 50 or 40, exceptionally to 30 beats per minute, is insufficient to induce unconsciousness; such rates are frequently seen in cases of heart-block that are without symptoms. The idea that, because the vagus is responsible for the slowing, the force of ventricular contractions will be weakened, is open to serious doubt. Appreciable weakening of the beats from this cause has not been demonstrated in mammals; in dogs, the heart rate may be reduced to one half by vagal stimulation without altering the mean blood pressure materially.

Instead, Lewis concluded that the vasodepressor component was more fundamental than the cardioinhibitory component. Undoubtedly the main cause of the fall in blood pressure in these attacks and the enfeeblement loss of pulse is independent of the vagus and lies in the blood vessels. Although atropine raises the pulse rate to and beyond normal levels during the attack, it leaves the blood pressure below normal and the patient still pale and not fully conscious. Attacks in which the blood pressure sinks without a lowering of the pulse rate and the patient verges on unconsciousness whenever the pressure reaches certain low levels have been encountered. Thus, the cause of the syncope is mainly vasomotor and not vagal; however, the vagus adds impressively to the clinical picture by inducing conspicuous slowing of the heart and gastric manifestations.

In 2011, Dutch internist Wouter Wieling and colleagues coined the term “prolonged post-faint hypotension” for a severe variant of vasovagal syncope that had been described as early as 1918 by Cotton and Lewis and subsequently was observed most often during blood donation and tilt tests (Cotton and Lewis 1918; Wieling et al 2011). Patients with “prolonged post-faint hypotension” characteristically experience bradycardia and marked hypotension, along with weakness, malaise, and nausea. Wieling and colleagues proposed that sustained high vagal outflow results in pronounced bradycardia and decreased cardiac contractility, resulting in loss of cardiac output and a marked drop in systemic blood pressure (Wieling et al 2011).

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