Elsevier

Autonomic Neuroscience

Volume 184, September 2014, Pages 27-32
Autonomic Neuroscience

Non-invasive management of vasovagal syncope,☆☆

https://doi.org/10.1016/j.autneu.2014.06.004Get rights and content

Highlights

  • Non-pharmacological therapy is often effective in preventing vasovagal syncope.

  • Drugs may be needed in select patients only.

  • Education, hydration, and physical counter-measures are quite effective.

  • Midodrine and fludrocortisone are the primary drugs used for VVS.

Abstract

Vasovagal syncope (VVS) is a common disorder of the autonomic nervous system. While recurrent syncope can cause very impaired quality of life, the spells are not generally life-threatening. Both non-pharmacological and pharmacological approaches can be used to treat patients. Conservative management with education, exercise and physical maneuvers, and aggressive volume repletion is adequate for controlling symptoms in most patients. Unfortunately, a minority of patients will continue to have recurrent syncope despite conservative therapy, and they may require medications. These could include vasopressor agents, beta-blockers, or neurohormonal agents. Some patients may require more aggressive device based therapy with pacemakers or radiofrequency ablation, which are emerging therapies for VVS. This paper will review non-procedure based treatments for VVS.

Introduction

VVS is an illness that is debilitating but treatable. It is a common cause of fainting. While most patients faint only infrequently, some patients faint frequently. Recurrent VVS is associated with a poor quality of life (Rose et al., 2000) that can be improved with treatments that decrease the burden of syncope (Sheldon et al., 1998).

The most commonly used pathophysiological model for VVS was first described by Edward P Sharpey-Shafer of St. Thomas' Hospital in London, UK (Sharpey-Schafer, 1956). In gravity-dependent vasovagal syncope, the blood pooling that results from upright posture leads to relative central volume depletion and reduced cardiac preload. In order to maintain blood pressure, there is a baroreceptor-mediated increase in sympathetic nervous system tone, with a resultant increase in cardiac contractility. The high contractility, combined with under-filled ventricles, can be sensed as excessive by cardiac mechanoreceptors. This then leads to a baroreceptor-mediated sudden increase in parasympathetic tone and withdrawal of sympathetic tone. VVS patients can then experience bradycardia or periods of asystole, and/or vasodilation or venodilation.

The common triggers include prolonged sitting or standing (upright posture) or the activation of large muscles via a reduction in cardiac preload. Cortical triggers such as anxiety (such as with blood exposure), severe emotion or pain can also trigger a VVS response, likely by direct actions on the medulla. These triggers are common, “everyday” experiences that can be difficult to avoid, and this can lead to recurrent VVS spells. These spells can also cause significant injury in 5% of cases and can lead to significantly impaired quality of life (van Dijk et al., 2007, Bartoletti et al., 2008).

Fortunately, there are a variety of simple treatments available to decrease the frequency of these episodes. The treatment of VVS generally involves layered, synergistic therapies including lifestyle change, physical maneuvers, medical therapy, and when needed, implantable devices (Fig. 1). Non-pharmacologic therapy is generally cheap, easily accomplished, and effective in VVS patients. The vast majority of patients are responsive to conservative therapies including educating patients about VVS, reviewing common VVS triggers, physical maneuvers to perform when they are feeling unwell, and increased oral fluid intake (Table 1). In the few patients that do not respond adequately to these therapies, pharmacologic options are available (Table 2). Patient categories such as age and comorbidities (especially hypertension) become important when choosing potential medications for VVS. When considering treatment, communication with the patient is extremely important, as therapies often must be tailored to individual response. There is trial data to support the use of many of these therapies, although these trials vary in both design strength (randomized controlled trial vs. observational study) and study size. The recommendations that follow are based on both these trial data and on clinical experience.

Device therapies are also important for treatment-refractory VVS. These treatment options will be discussed elsewhere in another article in this Special Issue on Syncope (Solbiati and Sheldon, 2014-in this issue).

Section snippets

Education

A wide range of non-pharmacologic approaches are beneficial for the treatment of VVS (Table 1). Education, in particular, is a quite helpful and necessary initial strategy (White et al., 2003). It is common for patients to fear that they are at an increased risk of having a myocardial infarction of even dying when suffering from VVS. An initial priority is to make sure the patient is aware that VVS is not a fatal illness (Soteriades et al., 2002). Especially in younger patients, VVS almost

Pharmacological treatment of VVS

Pharmacological therapy for VVS should be considered in patients in whom non-pharmacologic measures, including education, fluid intake, and physical countermeasures, have failed. Many pharmacological treatments exist for VVS, but none has shown significant effectiveness in large, randomized, controlled trials. In spite of this, clinical management of refractory and recurrent VVS in well-chosen patients can result in decreased symptom burden (Table 2).

Alpha-1 agonists

Midodrine has been used to affect peripheral alpha-1 adrenergic activity via its active metabolite, which is an agonist at alpha-1 receptors. It is known to cause arteriolar constriction as well as venoconstriction, which increases peripheral vascular resistance and cardiac output. Trial data has shown that in the majority of patients with VVS, a moderate fall in cardiac output with coincident vasodilatation occurs during a syncopal event (Fu et al., 2012). A number of clinical studies have

4. Summary

VVS is a syndrome that is challenging to treat, and a multi-pronged strategy is usually required for effective symptom control. We present an algorithm that we have found to be clinically useful which is based on both clinical experience and objective study data. First line therapy for VVS is education about physiology and the benign course of the disease and a discussion of potential triggering situations or contributing medications. Early interventions should include encouragement of

References (53)

  • M.A. Salim et al.

    Effectiveness of fludrocortisone and salt in preventing syncope recurrence in children: a double-blind, placebo-controlled, randomized trial

    J. Am. Coll. Cardiol.

    (2005)
  • W.A. Scott et al.

    Randomized comparison of atenolol and fludrocortisone acetate in the treatment of pediatric neurally mediated syncope

    Am. J. Cardiol.

    (1995)
  • R. Sheldon et al.

    Methodology of isoproterenol-tilt table testing in patients with syncope

    J. Am. Coll. Cardiol.

    (1992)
  • R. Sheldon et al.

    Effect of dual-chamber pacing with automatic rate-drop sensing on recurrent neurally mediated syncope

    Am. J. Cardiol.

    (1998)
  • R. Sheldon et al.

    A randomized clinical trial of fludrocortisone for the prevention of vasovagal syncope (POST2)

    Can. J. Cardiol.

    (2011)
  • J.S. Sra et al.

    Use of intravenous esmolol to predict efficacy of oral beta-adrenergic blocker therapy in patients with neurocardiogenic syncope

    J. Am. Coll. Cardiol.

    (1992)
  • N. van Dijk et al.

    Effectiveness of physical counterpressure maneuvers in preventing vasovagal syncope: the Physical Counterpressure Manoeuvres Trial (PC-Trial)

    J. Am. Coll. Cardiol.

    (2006)
  • N. van Dijk et al.

    Quality of life within one year following presentation after transient loss of consciousness

    Am. J. Cardiol.

    (2007)
  • M.B. Waxman et al.

    Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons

    Am. J. Cardiol.

    (1989)
  • M.A. Aydin et al.

    A standardized education protocol significantly reduces traumatic injuries and syncope recurrence: an observational study in 316 patients with vasovagal syncope

    Europace

    (2012)
  • A. Bartoletti et al.

    Physical injuries caused by a transient loss of consciousness: main clinical characteristics of patients and diagnostic contribution of carotid sinus massage

    Eur. Heart J.

    (2008)
  • E. Bellard et al.

    Increased hydration alone does not improve orthostatic tolerance in patients with neurocardiogenic syncope

    Clin. Auton. Res.

    (2007)
  • H. Ector et al.

    Repeated tilt testing in patients with tilt-positive neurally mediated syncope

    Europace

    (2005)
  • B.A. Eldadah et al.

    Failure of propranolol to prevent tilt-evoked systemic vasodilatation, adrenaline release and neurocardiogenic syncope

    Clin. Sci. (Lond.)

    (2006)
  • H. El-Sayed et al.

    Salt supplement increases plasma volume and orthostatic tolerance in patients with unexplained syncope

    Heart

    (1996)
  • B. Flint et al.

    Level of psychosocial impairment predicts early response to treatment in vasovagal syncope

    Europace

    (2009)
  • Cited by (11)

    • Autonomic Dysfunction in Cardiology: Pathophysiology, Investigation, and Management

      2017, Canadian Journal of Cardiology
      Citation Excerpt :

      Approaches to increase venous return such as physical counter-pressure manoeuvres (eg, leg crossing, clenching the buttocks, inspiratory resistance) and devices (eg, compression stockings or abdominal binders) may be useful.3 Orthostatic training may reduce syncopal episodes in VVS (eg, repeated HUT testing or standing against a wall); however, there is limited efficacy data and poor patient compliance.3,20 Patients managed by a syncope expert may report improvement in the absence of therapy (“expectancy effect”).14

    • Orthostatic Hypotension and Vasovagal Syncope

      2017, Encyclopedia of Cardiovascular Research and Medicine
    View all citing articles on Scopus

    Research funding: Supported in part by NIH grants R01 HL102387, P01 HL56693, and UL1 RR024975 (Clinical and Translational Science Award).

    ☆☆

    Conflicts of interest: None

    View full text