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.
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.
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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
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