Neurocardiogenic syncope

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Kashish Goel, M.D.

Syncope or loss of consciousness is one of the most common presenting symptoms to the ER (about 3%) and accounts for 1% of the hospital admissions. The most common type of syncope is neurocardiogenic syncope, especially in young adults and pediatric patients. It is also called “vasovagal syncope” and accounts for 50-60% of the unexplained syncope cases^[1]. Neurocardiogenic syncope involves loss of the autonomic nervous system, and inability of the body to maintain blood pressure and heart rate. It can be provoked by fear, emotional stress, excruciating pain, prolonged standing or vigorous exercise. Some of the cases are associated with particular situations like urination, defecation, or coughing^[2].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]

Neurocardiogenic syncope is defined as a syndrome in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral vasodilation.^[1][2]

It is caused by an abnormal or exaggerated autonomic response to various stimuli, commonly standing and emotion.^[3][4] The underlying mechanism for this exaggerate autonomic response remains unclear; however, the activation of cardiac C fibres has shown to play role which subsequently causes reflex-mediated changes in the vascular tone and heart rate.^[5] On the contrary, failure of autonomic reflex response results in orthostatic hypotension.

The pathogenesis for syncope in patients with hypersensitive carotid sinus and neurocardiogenic syncope remain the same with the only difference being the receptor involved to stimulate the brainstem nucleus.

The underlying mechanism of exaggerated autonomic response to various stimuli in patients with neurocardiogenic stimuli remains unclear. However, the activation of cardiac C-fibres has been implicated in the pathogenesis of neurocardiogenic syncope.^[6]

Regardless of the triggers, the mechanism of syncope is similar among various vasovagal syncope syndromes.

Multiple triggering stimuli activate the nucleus tractus solitarius of the brainstem via the cardiac C fibres, which then results in the simultaneous enhancement of the parasympathetic nervous system (vagal) tone and withdrawal of the sympathetic nervous system tone.^[7][5][8]

This results in a spectrum of hemodynamic responses:

• On one end of the spectrum is the cardioinhibitory response caused by an increased vagal tone that is characterized by bradycardia and consequent hypotension that is significant enough to result in loss of consciousness.

• On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure without much change in heart rate. This phenomenon occurs due to vasodilation secondary to the withdrawal of sympathetic nervous system tone.

As a result of increased vagal tone and vasodilation, subsequent decrease in venous return and cardiac output is observed which is significant enough to cause syncope or loss of consciousness.^[9][10]

Triggers such as pain, post-exercise stimulate the sympathetic nervous system causing an increase in the sympathetic tone (tachycardia and increased cardiac contractility) which then causes reflex-mediated activation of the cardiac C fibres and brainstem nucleus to counterbalance these effects and results in an increased vagal tone and bradycardia.

Triggers such as carotid massage, rapid head turning cause stimulation of the carotid sinus and cardiopulmonary receptors which subsequently activate the brainstem nucleus to follow the common pathway of increased vagal tone and bradycardia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Neurocardiogenic syncope is the most common cause of syncope in children and adults and accounts for approximately 10-40% of all syncopal episodes.

The prevalence is 22% in the general population. Approximately 50%-66% of syncope cases are classified as due to vasovagal syncope.

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Young adults and children are at the highest risk for experiencing Neurocardiogenic syncope but, they commonly grow out of this condition as they reach adulthood. It also tends to occur in persons who have a family history of fainting spells. It is thought to affect persons who have a genetic predisposition towards poor resistance in the blood vessels of the lower extremities, causing blood to pool away from the brain in response to certain situations.

Neurocardiogenic syncope occurs when the part of the nervous system that regulates heart rate and blood pressure temporarily malfunctions. Usually in response to some sort of trigger such as fear or the sight of blood, the heart rate slows down, and the blood vessels in the legs dilate. This causes blood to pool in the lower region of the body, and therefore a lack of blood and oxygen to the brain which causes fainting. This is similar to what happens when one feels faint after suddenly standing up. When a person faints, gravity causes blood flow to to the brain to be restored and the person gains consciousness. Neurocardiogenic syncope is a symptom of the body, rather than a disease. Possible triggers causing neurocardiogenic syncope are as follows;

• Seeing blood or losing blood
• Pain
• Emotional stress or anxiety
• Prolonged standing
• Heat
• Physical exertion
• Defecation or urination
• Standing up suddenly
• Coughing spells
• Certain “sensitive periods” such as during a viral illness or menstruation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Vasovagal syncope usually has an easily identified triggering event such as emotional stress, trauma, pain, the sight of blood, or prolonged standing. Syncope recurs in few patients, while others just experience a single episode. The prognosis is usually good, although prolonged hypotension may cause severe damage. Mortality associated with syncope is largely due to severity of the underlying disease rather than syncope per se.

The natural history of neurocardiogenic syncope is extremely variable; some patients experience single episode while others have recurrent episodes. ^[1]

In an european study, 465 patients were evaluated for an early (1 month) and late (2 years) death rate and syncopal relapses of patients referred for syncope to 11 general hospitals emergency departments. The following results were found:^[2]

• The death rate was higher (17% of all deaths) in the first month of observation
• Reoccurrence of the syncopal episode was low overall in both the short and the long term (0.3% and 0.8% in the first month and in the second year, respectively).
• Mortality was higher in patients having previous cardiovascular disease or in those displaying ECG abnormalities. Both of these two factors represent the main predictors of short or long-term mortality on multivariate analysis

Vasovagal syncope appears to have a benign prognosis.^[3] Patients recover completely within minutes to hours and have excellent prognosis as far as survival is concerned.^[4] If syncope is symptomatic of an underlying condition, then the prognosis will reflect the course of the disorder and not the syncope itself.^[5][6] Such patient’s should be stratified with respect to the risk of a cardiovascular event and/or sudden cardiac death and further evaluation should be made. ^[7]

• A study of 334 patients with a mean follow up of 30.4 ± 21 months, showed good survival of patients with neurocardiogenic syncope, presenting after an abnormal head-up tilt (HUT) test. ^[8] The study showed that there were no cardiac deaths in during 30.4 ± 21 months. However, 101 patients (30.2%) had recurrences (1 recurrence, n = 64; > or =2, n = 37), which were not influenced by the type of response during HUT or by age.

• The duration of loss of consciousness during the syncope.^[9]
• Co-morbid disease or Underlying cardiac illness (Hemodynaically important aortic stenosis) ^[10]
• Increased age.

The presence of following conditions increase the risk of vasovagal syncope: ^[11]

• The number of previous syncope and presyncope.
• Female gender.
• History of bronchial asthma.

A group of authors have designed a simple clinical risk score to predict the risk of recurrence of vasovagal syncope.^[11]

The main danger of fainting fits or vasovagal syncope is the risk of injury by falling while unconscious. American Heart Association (AHA), North American Society of Pacing and Electrophysiology (NASPE, now Heart Rhythm Society, HRS) and European Society of Cardiology have published recommendations for driving in patients with syncope.^[12][13][14]

The quality of life (QoL) of patients suffering from neurocardiogenic shock is similar to those with NYHA class II-III heart failure.^[15]

Major risk factors for sudden cardiac death and overall mortality in patients are structural heart diseases^[16][17] and primary electrical disturbances.^[18]

• Morbidity is particulary high in the elderly due to the following contributing factors:^[19][20]
  • Loss of confidence.
  • Depressive illness.
  • Fear of falling, to fractures and subsequent institutionalization.

• Mortality in syncope patients depends on the underlying cause:^[21]
  • Cardiac causes (arrhythmias or cardiovascular disease) have a 20-30% mortality.
  • Non-cardiac causes have 5-10% mortality.

However, a major drawback in determining the true mortality rate is that most individuals with transient loss of consciousness do not seek medical advice.

• Vasovagal syncope
• Postural orthostatic tachycardia syndrome
• Dysautonomia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Neurocardiogenic syncope must be distinguished from situational syncope (cough syncope, defecation syncope, micturation syncope, neurally mediated syncope and carotid sinus hypersensitivity). Some patients will have what is called an “atypical” syncope, which is non-neurocardiogenic and without any identifiable triggers.

The syncope comes on after cough, defecation, or micturation

This form of syncope occurs in the context of severe throat or facial pain as occurs in glossopharyngeal neuralgia or trigeminal neuralgia.

Syncope following exposure to a noxious stiumulus, fear, or pain is consistent with neurocardiogenic syncope.

Carotid sinus syncope may occur with rotation or turning of the head or pressure on the carotid sinus (for example, carotid massage, shaving, tight collars or neck wear, or tumor compression).

Occurs due to an arrythmia, and is of abrupt onset and short duration, without any recovery phase.

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