Non-invasive management of vasovagal syncope☆,☆☆
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
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2017, Canadian Journal of CardiologyCitation 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
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Research funding: Supported in part by NIH grants R01 HL102387, P01 HL56693, and UL1 RR024975 (Clinical and Translational Science Award).
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Conflicts of interest: None