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Vasovagal syncope

Vasovagal syncope (also vasodepressor syncope, neurally mediated syncope or neurocardiogenic syncope), a form of dysautonomia, is the most common cause of fainting ("syncope" in medical terminology). Although it is particularly common (both historically and stereotypically) among young women, it is seen across all ages and genders and in otherwise completely healthy people. It is triggered by a number of factors, including prolonged standing, alcohol, fatigue, hunger, and anxiety. more...

VACTERL association
Van der Woude syndrome
Van Goethem syndrome
Varicella Zoster
Variegate porphyria
Vasovagal syncope
VATER association
Velocardiofacial syndrome
Ventricular septal defect
Viral hemorrhagic fever
Vitamin B12 Deficiency
VLCAD deficiency
Von Gierke disease
Von Hippel-Lindau disease
Von Recklinghausen disease
Von Willebrand disease

Vasovagal syncope is caused by low heart rate and blood pressure, leading to inadequate circulation. The reduced oxygen supply to the brain results in syncope, or temporary loss of consciousness. Individuals usually regain consciousness within a few minutes and their prognosis is good, although the syncope has a tendency to recur.


Prior to losing consciousness, the individual usually experiences symptoms such as nausea, inability to hear properly, difficulty speaking, exhaustion, tightness in the throat and blurry vision. Sweatiness and dizziness are also very common. These symptoms may last anywhere from seconds to minutes. This is followed by an episode of fainting; the individual regains consciousness within seconds to minutes. It is uncommon for vasovagal syncope to occur while the individual is lying down (supine); it normally occurs while standing or sitting.

During the episode, the individual will be unresponsive, and the pulse and blood pressure will be low. In some cases the individual may react violently while unconscious, this may be due to a fear response and increased adrenaline. The reaction may have the appearance of a seizure. Upon regaining consciousness, the individual may appear flushed and feel generally lethargic. The heart rate may still be slow, although it soon returns to normal.


In addition to vasovagal syncope, a number of other medical conditions may cause fainting. It is essential to perform a thorough history (interview of the patient) and physical examination. If there is no sign of other medical problems or causes of fainting, and the patient's description is consistent with or suggestive of vasovagal syncope, no diagnostic testing may be necessary. However, if the fainting is recurrent, a tilt table test is usually performed. In this test, the patient lies flat on a table and is then tilted upright so that blood pressure and heart rate may be observed and measured to identify any severe changes. This test is particularly effective in identifying patients suffering from sensitive nervous systems. Depending on the physician's level of suspicion, other tests, including an electrocardiogram, may be performed.


Vasovagal syncope is due to a disorder of autonomic control of the cardiovascular system. It commonly occurs in normal people of all ages. Precipitating factors include alcohol consumption, fatigue, pain, hunger, and prolonged standing. It can also be triggered by situations causing anxiety, such as having blood drawn, as well as by hot or crowded situations.

The initial responses appear to be venous pooling and increased activity of the sympathetic nervous system. This causes the heart to contract forcefully while relatively empty, triggering ventricular mechanoreceptors and vagal nerve fibers. This has the effect of reducing sympathetic activity while stimulating parasympathetic activity, resulting in bradycardia and vasodilation, followed by syncope.


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Vasovagal syncope: A new treatment for an old problem
From Military Medicine, 7/1/01 by Fisher, Nick G

Vasovagal syncope is an extremely common condition that is most often benign. However, in some individuals it can be far more severe, with frequent, sudden, and prolonged episodes of loss of consciousness. The effects can be traumatic, not only from the acute event but from the lifestyle changes that are necessitated by these attacks. We report on the presentation and diagnosis of once such individual and discuss the various treatment options. In addition, supported by recently published evidence, we demonstrate how a pacemaker with rate-- drop response is an effective form of treatment.

Case Report

A 30-year-old female rating was serving on a frigate in the southern hemisphere when she experienced a sudden loss of consciousness. Fearing a seizure, she was repatriated to another hospital. Investigations included electroencephalography, computed tomography, and magnetic resonance imaging of the head, all of which were normal. However, the patient was noted to have labile blood pressure with systolic readings as low as 80 mm Hg. To investigate a cardiologic cause, she was referred to the cardiothoracic unit at this center.

A careful history revealed that she had experienced several episodes of loss of consciousness and many more events during which she averted feelings of presyncope by lying down. A feeling of nausea and light-headedness would always precede a classic attack. If she was unable to prevent it, she would then lose consciousness for approximately 5 minutes. These events had been witnessed, and she had never been observed to have a typical seizure. However, she had injured herself and been incontinent of urine with the attacks. On recovery, she would feel systemically unwell, light-headed, and nauseated for several hours. Review of the notes revealed that hypotension and bradycardia usually occurred in association with these attacks. Some attacks were precipitated by exertion. The patient was physically fit and was a keen rugby player. Such were the severity, unpredictability, and debilitating nature of the attacks that she was unable to drive, was medically down-graded, and her friends had set up a rota to remain with her during the evenings.

A subsequent tilt-table test was strongly positive, showing profound bradycardia after 20 minutes of tilt with associated hypotension, which caused her to lose consciousness (Fig. 1). The outcome of this investigation strongly suggested that her symptoms were attributable to severe vasovagal syncope.

The patient was desperate to be free of these debilitating symptoms, and initially a pharmacological approach was attempted. However, a trial with /-blockers and then fluoxetine produced intolerable symptoms of continuous lethargy and nausea, respectively.

Thus, in view of the severity and frequency of the patient's attacks, it was necessary to consider other options. Encouraged by the recent publication of the North American Vasovagal Pacemaker Study,1 we counseled her about the potential benefits and disadvantages of pacemaker insertion. Accordingly, she decided to undergo implantation of a permanent system. On the day of this procedure, the necessity of treatment was supported by the occurrence of her typical symptoms, which were provoked while lying flat, during the insertion of an intravenous cannula. This required treatment with plasma expanders and atropine as well as a small dose of diazepam. Subsequently, a dual-chamber rate-drop response and rate-variable pacemaker was inserted under local anesthetic and sedation. This has successfully prevented further syncopal attacks; however, in keeping with the published data, the patient does continue to experience some, albeit fewer, presyncopal symptoms.

Because our patient was dependent on the normal function of her pacemaker and would require regular and specialized follow-up,2 it was deemed appropriate to make her unfit for sea duty permanently, a decision that will inevitably lead to a medical board of survey and a medical discharge. Although this is not entirely satisfactory, the patient is aware that this would have been necessary without a pacemaker in view of the fact that her symptoms would have ensured that she would have been permanently unfit for full duty. Now at least she is in a better position to continue her personal and professional life outside the service.


Vasovagal syncope is also known as vasodepressor syncope, neurocardiogenic syncope, and neurally mediated syncope. Quite literally, it is the common faint and has been described since the 1800s, is commonly associated with sudden stress, and is experienced by two-thirds of the population at some stage of their lives. During a classic attack, there is abrupt loss of sympathetic vascular tone, increased vagal activity, and associated bradycardia. The resultant hypotension causes cerebral hypoperfusion and loss of consciousness.

Some people, however, suffer repeated attacks with little provocation. This can lead to serious injury and have a profoundly detrimental effect on the person's lifestyle and career.

The tilt-table test is now the gold standard for the diagnosis of this condition. A tilt of 60 deg for 45 minutes is a reliable and reproducible method of diagnosis.3 The British Cardiac Society has indicated that the sensitivity of the test is 85%, with the number of false positives being less than 15%. The act of tilting a patient to 60 deg decreases ventricular filling due to pooling of blood in the legs. This results in a compensatory increase in ventricular contraction, which, although in itself is beneficial, causes stimulation of mechanical stretch receptors with the left ventricular wall. These stretch receptors are thought to be the underlying fault, because a surge in vagal afferent activity is sent to the medullary cardioinhibitory center, which in turn tries to respond by increasing overall vagal tone and decreasing sympathetic activity. The resultant effect on the arterials and sinus node is hypotension with inappropriate bradycardia. Crucially, patients can vary with regard to the relative degrees of hypotension and bradycardia.


Pharmacological therapy for vasovagal syncope is varied, based mainly on uncontrolled studies, which invariably found in favor of the drug concerned; paradoxically, many of these treatments have opposing actions. In patients who suffer excessive tachycardia before experiencing syncope, Beta-blockers (metoprolol or propranolol) can be effective. Some of their success may result from reducing cardiac contractility and therefore mechanoreceptor stimulation within the left ventricle.4 In patients in whom the hypotension occurs before the bradycardia, fludrocortisone has been shown to be effective by helping to increase plasma volumes More recently, the serotonin reuptake inhibitor fluoxetine has gained favorable attention,6 but again, a randomized, controlled study has yet to be published. Although its cardiac effects have been investigated showing it to have class I and IV antiarrhythmic properties and an ability to impair intraventricular conduction and shorten repolarization,7 the mechanism of action of the drug in this setting is not known and is likely to be multifactorial.

Because most cases of vasovagal syncope involve some degree of bradycardia, pacemakers may offer a possible solution. At present, this is a class II indication for pacemaker insertion according to the guidelines of the British Pacing and Electrophysiological Working Group.8 This implies that although they may be frequently used, there is a divergence of opinion on when they are needed. Some doubts regarding the use of pacemakers have been addressed by the development of rate-drop response units. In contrast to standard pacemakers, which maintain a basic physiological rate when the intrinsic rate falls below a predetermined level, these specialized units sense the small but rapid drops in heart rate frequently associated with vasovagal syncope and respond by pacing the ventricle at much faster rates than occurred before the rate drop was detected. This exaggerated response is designed to increase cardiac output to a degree that will compensate for the presumed vasodilation that is occurring simultaneously. The recently published North American Vasovagal Pacemaker Study used these devices in the first randomized, controlled trial of pacemakers for this indication. There was a 48% reduction in syncopal events in patients fitted with the devices.' Such was the significance of the data that the trial was stopped prematurely because of the benefit being derived from pacemaker insertion.

Although this trial gave very convincing results, insertion of a pacemaker into a young person should not be undertaken lightly, because the patient will require numerous box changes during his or her lifetime and there is a significant risk of lead fracture. Repeated device changes increase the risk of infection and other complications. However, in cases such as ours, in which an individual is severely impaired by his or her condition, the improvement in lifestyle is believed to outweigh these disadvantages.


Syncopal attacks are a frequent presentation in the military, and most medical officers will be faced with such a case during their service. We have highlighted the typical presentation of vasovagal syncope, its diagnosis, and the treatment required for some patients. It must be emphasized that most people can be diagnosed on the history alone, and in the majority of mild cases, reassurance is often all that is required. However, one must be aware that there are people who will be incapacitated by the condition and will need specialist intervention.

Ministry of Defence Hospital Unit, Derriford Cardiothoracic Centre, Plymouth PL6 8DH, United Kingdom.

This manuscript was received for review in June 2000. The revised manuscript was accepted for publication in December 2000.

Reprint & Copyright by Association of Military Surgeons of U.S., 2001.


1. Conolly SC, Sheldon R, Roberts R, Gent M: The North American Pacemaker Study. J Am Coll Cardiol 1999; 33: 16-20.

2. Turner M, Nash A. George M, Marshall AJ: Proper pacemaker programming prevents palpitations. Br J Cardiol 1999; 6: 563-5.

3. Fitzpatrick A, Sutton R: Tilting towards a diagnosis in recurrent unexplained syncope. Lancet 1989; 1: 658-60.

4. Kapoor WN, Smith M, Miller NL: Upright tilt testing in evaluating syncope: a comprehensive literature review. Am J Med 1984: 97: 78.

5. Grubb BP, Temesy-Armos P, Moore J, et al: Head upright tilt testing in the evaluation and management of the malignant vasovagal syndrome. Am J Cardiol 1992;69: 904.

6. Grubb BP, Wolfe DA, Samoil D, Temesy-Armos P, Hahn H, Elliott L: Usefulness of fluoxetine hydrochloride for prevention of resistant upright tilt induced syncope. Pacing Clin Electrophysiol 1993; 16: 458-64.

7. Pacher P, Ungvari Z, Nanasi PP, Furst S, Kecskemeti V: Speculations on difference between tricyclic and selective reuptake inhibitor antidepressants on their cardiac effects. Is there any? Curr Med Chem 1999: 6: 469-80.

8. Recommendations for pacemaker prescription for symptomatic bradycardia: report of a working party of the British Pacing and Electrophysiology Group. Br Heart J 1991; 66: 185-91.

Guarantor: Surgeon Lieutenant Commander Nick G. Fisher, Royal Navy

Contributors: Surgeon Lieutenant Commander Nick G. Fisher, Royal Navy; Wing Commander Tim Gilbert, Royal Air Force

Copyright Association of Military Surgeons of the United States Jul 2001
Provided by ProQuest Information and Learning Company. All rights Reserved

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