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J Cardiovasc Electrophysiol. 2009 Mar;20(3):352-8. doi: 10.1111/j.1540-8167.2008.01407.x. Epub 2009 Jan 16.

Postural tachycardia syndrome (POTS).

Author information

1
Department of Neurology, Mayo Clinic, Rochester, Minnesota 55905, USA.

Abstract

INTRODUCTION:

POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment >or=30, usually to >or=120 bpm without orthostatic hypotension. Symptoms of orthostatic intolerance are those due to brain hypoperfusion and those due to sympathetic overaction.

METHODS:

We provide a review of POTS based primarily on work from the Mayo Clinic.

RESULTS:

Females predominate over males by 5:1. Mean age of onset in adults is about 30 years and most patients are between the ages of 20-40 years. Pathophysiologic mechanisms (not mutually exclusive) include peripheral denervation, hypovolemia, venous pooling, beta-receptor supersensitivity, psychologic mechanisms, and presumed impairment of brain stem regulation. Prolonged deconditioning may also interact with these mechanisms to exacerbate symptoms. The evaluation of POTS requires a focused history and examination, followed by tests that should include HUT, some estimation of volume status and preferably some evaluation of peripheral denervation and hyperadrenergic state. All patients with POTS require a high salt diet, copious fluids, and postural training. Many require beta-receptor antagonists in small doses and low-dose vasoconstrictors. Somatic hypervigilance and psychologic factors are involved in a significant proportion of patients.

CONCLUSIONS:

POTS is heterogeneous in presentation and mechanisms. Major mechanisms are denervation, hypovolemia, deconditioning, and hyperadrenergic state. Most patients can benefit from a pathophysiologically based regimen of management.

PMID:
19207771
PMCID:
PMC3904426
DOI:
10.1111/j.1540-8167.2008.01407.x
[Indexed for MEDLINE]
Free PMC Article
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