Approach

The foundation for treatment of most NMRS syndromes is patient education.[1] Provide patients with advice on physical techniques to abort imminent NMRS or prevent recurrence.

There is insufficient evidence to support the use of most pharmacologic treatments for NMRS. Several drugs have been proposed, but there are few randomized clinical trials to rely on.[58] Consequently no agent, except perhaps midodrine, can be strongly recommended in the treatment of neurally mediated faints.[59]

Patient education

Patient education is an important factor in treatment for all types of NMRS.[1] Inform patients that although NMRS is rarely life-threatening, these types of faints tend to recur and injury can result if preventive measures are not taken.[2] Patients need to recognize and respond to warning symptoms, and may benefit from knowledge of basic pathophysiology; such understanding reduces injury risk and may ultimately enhance treatment compliance. Educate patients on the avoidance of triggers such as prolonged standing, warm environments, and coping with dental and medical settings.[1]

Medications that cause hypotension may be reduced or withdrawn where appropriate and safe.[1]

Patients susceptible to recurrent vasovagal faints should learn techniques for both aborting attacks and reducing susceptibility to future episodes (e.g., physical maneuvers, hydration with electrolyte-rich fluids). These patients should also be taught the value and possible risks of increased salt intake. In situational faints, inform patients of the potential for ameliorating or entirely avoiding triggers. For instance, suppression by smoking cessation in cough syncope, and sitting to void in micturition syncope. In some cases, desensitization techniques (e.g., syncope associated with fear of air flight) may help. Those with carotid sinus syndrome (CSS) should avoid wearing tight collars or neckties, although cardiac pacing is also usually recommended.

Physical techniques

1. Physical counter-pressure maneuvers (PCM)

  • PCM are advocated to abort imminent NMRS or orthostatic faints when warning symptoms are first recognized. Useful techniques include squatting, arm tensing, leg crossing, and leg crossing with tensing of the lower body muscles.[60][61] In the Physical Counterpressure Manoeuvres Trial, physical maneuvers reduced total burden and recurrence rate of syncopal events.[62] Consequently, PCM should be an essential part of the treatment strategy for vasovagal faints. Data are lacking for the role of PCM in patients with situational faints or carotid sinus syncope, but may have been used in selected cases.

2. Tilt training (standing training)

  • The principal goal of tilt training (more accurately termed standing training) is to enhance the neurovascular response to orthostatic stress.[63] The favored method entails standing training (usually at home) for progressively longer periods of time over 10-12 weeks. The recommended starting duration is 3-5 minutes twice daily; standing duration is then gradually lengthened every 3 or 4 days to 30-40 minutes twice daily.

  • The American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS) advise that the usefulness of orthostatic training is uncertain in patients with frequent vasovagal syncope.[1] Nonrandomized studies suggest that standing training reduces susceptibility to reflex syncope if undertaken consistently.[64][65][66] However, compliance is often a problem because the process is time consuming and boring.[13] Randomized controlled trials have been less encouraging, suggesting that the method may not be as effective as originally thought; further study is needed.[67][68]

Pharmacotherapy

Volume expansion is an essential recommendation for most patients who require medical therapy for vasovagal faints, but evidence is limited.[1][27] Conventional approaches include increased dietary salt and electrolyte-rich sports drinks. The primary safety concern is initiation of hypertension. Fortunately, this is rare in younger patients, but it is a concern in older patients. Contraindications to increased salt and fluid intake include history of hypertension, renal disease, heart failure, or cardiac dysfunction.

If a prescription drug is needed for volume expansion, fludrocortisone can be used.[1] Adverse effects include hypertension and hypokalemia. However, clinical evidence for the efficacy of fludrocortisone is weak.[69][70] The Second Prevention of Syncope Trial (POST II) reported a nonsignificant decrease in episodes of vasovagal syncope in the fludrocortisone group compared with placebo.[71]

Among other drugs suggested for preventing vasovagal faints, beta-blockers remain widely used despite absence of strong supporting evidence. Beta-blockers were initially advocated to prevent reflex syncope by diminishing the impact of the adrenergic surge that commonly precedes and may be part of the vasovagal trigger. The positive supportive evidence is derived largely from small observational studies and one single small randomized controlled trial.[72] One large randomized controlled trial (POST I) showed no statistically significant benefit with beta-blockers in patients of all age ranges.[73]

Vaso- and venoconstrictors have also been of interest for preventing faints associated with orthostatic intolerance. Midodrine is the principal drug in this class used for this indication. While midodrine has been studied most extensively in patients with orthostatic hypotension, research suggests it is also effective in vasovagal syncope.[74][75][76] In one multicenter randomized controlled trial (POST IV), midodrine reduced the recurrence of syncope compared with placebo in healthy, younger patients.[77] Methylphenidate has also been proposed for midodrine-intolerant patients, although its value has not been established.[78] Etilephrine, which is a modest alpha- and beta-agonist, was found to be ineffective at preventing vasovagal faints in the Vasovagal International Study.[79]

Several other drug classes have been advocated but remain of uncertain value at best. The most important among these are the selective serotonin-reuptake inhibitors (SSRIs).[80] SSRI pretreatment is thought to blunt a hypothesized hypersensitive serotonin response in the central nervous system that may contribute to triggering NMRS. However, clinical trial results have been mixed.

Disopyramide, pure anticholinergics (e.g., scopolamine), and theophylline were also advocated in the past, but the evidence is unconvincing.

Data are lacking for the role of volume expansion, fludrocortisone, and midodrine in patients with situational faints or carotid sinus syncope, but may have been used in selected cases.

Cardiac pacing

Cardiac pacing may play a role in the treatment of carotid sinus syndrome with documented bradycardia to prevent bradycardia-induced faint. However, patients may remain symptomatic because of persistent vasodepressor response.

The usefulness of pacing in patients with refractory vasovagal syncope is less certain. Intuitively, it was thought that preventing severe bradycardia (cardioinhibitory syncope) by pacing would be desirable. Three unblinded trials showed efficacy for pacing, whereas two subsequent trials that used pacemakers in both treatment arms did not show benefit.[42][79][81][82][83] In a randomized crossover study of otherwise healthy patients with refractory vasovagal syncope, dual-chamber closed-loop stimulation (CLS on) reduced syncope recurrence compared with regular pacing (CLS off).[84] However, a systematic review found insufficient evidence to support the use of pacemaker treatments.[58] The ACC/AHA/HRS guidelines recommend consideration of dual-chamber pacing in a narrow group of patients who are "40 years of age or older with recurrent vasovagal syncope and prolonged spontaneous pauses".[1]

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