Elsevier

Cardiology Clinics

Volume 31, Issue 1, February 2013, Pages 89-100
Cardiology Clinics

Confounders of Vasovagal Syncope: Orthostatic Hypotension

https://doi.org/10.1016/j.ccl.2012.09.003Get rights and content

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Key points

  • Most patients who present with syncope have vasovagal (reflex) syncope, but neurogenic orthostatic hypotension can also cause syncope, especially in older patients.

  • Patients with neurogenic orthostatic hypotension have a fall in blood pressure greater than or equal to 20/10 mm Hg within 3 minutes of assumption of an upright posture.

  • Neurogenic orthostatic hypotension can often be differentiated from vasovagal syncope by its differing hemodynamic patterns during tilt table test and differing

Not all syncope is vasovagal syncope, even with a normal heart

Cardiologists are trained to assess syncope patients for life-threatening causes. This usually involves a detailed evaluation to exclude valvular heart diseases, myocardial diseases, and cardiac arrhythmia. After these potentially lethal causes of syncope have been excluded, most cases are ascribed to vasovagal syncope (VVS). Cardiologists working in a syncope clinic or in a tilt table laboratory quickly realize that there are other causes for syncope and presyncope, including neurogenic

Hemodynamic physiology of standing: healthy and orthostatic hypotension

With the assumption of an upright posture, there is a downward shift of approximately 500 mL of blood to the dependent areas (mainly abdomen and legs). This gravitational shift in blood results in decreased venous return, decreased cardiac output, and eventually decreased BP (Fig. 2A).1 This “unloads” the baroreceptors, and triggers a reflex sympathetic activation with a resultant increase in heart rate (HR) and systemic vasoconstriction (countering the initial decline in BP). In a healthy

Neurogenic orthostatic hypotension

nOH is defined as a sustained decrease in systolic BP greater than or equal to 20 mm Hg or diastolic BP greater than or equal to 10 mm Hg within 3 minutes of the assumption of an upright posture,2 although in almost all cases these diagnostic thresholds are met within 2 minutes.3, 4 More recent guidelines for patients with severe supine hypertension raise the threshold to a reduction in systolic BP greater than or equal to 30 mm Hg.2 “Delayed orthostatic hypotension” has also been described

Summary

Orthostatic hypotension is an important cause of syncope, especially in the older patients. Although there are multiple causes, the treatments are focused on improving symptoms. The mainstays of therapy are careful attention to hydration; bolus ingestion of water (osmopressor response); and the judicious use of short-acting pressor agents for the orthostatic hypotension. A significant proportion of patients can also have supine hypertension, which may necessitate the use of short-acting pressor

Acknowledgments

The authors thank Dr David Robertson for his leadership in the field of autonomic disorders, and his training of numerous investigators in the field of autonomic physiology. They also thank Dr Emily M. Garland for her thoughtful review of this manuscript.

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      The normal compensatory increase in norepinephrine on standing, however, is blunted in MSA and other forms of autonomic failure. Detailed information on diagnostic tools for primary autonomic failure is provided in recent reviews.39,40 Treatment approaches for nOH are similar to those for idiopathic OH and are described in detail in this issue of the Canadian Journal of Cardiology in the article “Orthostatic Hypotension: A Practical Approach to Investigation and Management.”7

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      These nonpharmacological approaches are cost-effective and can be safely combined with pharmacological interventions; however, there is often poor compliance. The use of additional pharmacological interventions might be necessitated in patients with severe OH, when nonpharmacological approaches are insufficient to prevent presyncopal symptoms (Table 1).2,5 Pharmacological treatment is unlikely to improve outcomes in asymptomatic patients.

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    Research Funding: Supported in part by NIH grants R01 HL102387, P01 HL56693, and UL1 TR000445 (Clinical and Translational Science Award).

    Conflicts of Interest: None.

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