Postural tachycardia syndrome (POTS): Clinical review

Phillip Anson Low, Paola Sandroni, Michael Joseph Joyner, Win Kuang Shen

Research output: Contribution to journalArticle

160 Citations (Scopus)

Abstract

Postural Tachycardia Syndrome. Introduction: POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥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, β-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 β-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.

Original languageEnglish (US)
Pages (from-to)352-358
Number of pages7
JournalJournal of Cardiovascular Electrophysiology
Volume20
Issue number3
DOIs
StatePublished - Mar 2009

Fingerprint

Postural Orthostatic Tachycardia Syndrome
Denervation
Hypovolemia
Orthostatic Intolerance
Orthostatic Hypotension
Vasoconstrictor Agents
Age of Onset
Brain Stem
Anxiety
Salts
Heart Rate
Diet
Brain

Keywords

  • Deconditioning
  • Denervation
  • Hyperadrenergic state
  • Hypovolemia
  • Orthostatic
  • POTS

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Postural tachycardia syndrome (POTS) : Clinical review. / Low, Phillip Anson; Sandroni, Paola; Joyner, Michael Joseph; Shen, Win Kuang.

In: Journal of Cardiovascular Electrophysiology, Vol. 20, No. 3, 03.2009, p. 352-358.

Research output: Contribution to journalArticle

@article{ffdf10c45271469b91acca416c312562,
title = "Postural tachycardia syndrome (POTS): Clinical review",
abstract = "Postural Tachycardia Syndrome. Introduction: POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥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, β-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 β-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.",
keywords = "Deconditioning, Denervation, Hyperadrenergic state, Hypovolemia, Orthostatic, POTS",
author = "Low, {Phillip Anson} and Paola Sandroni and Joyner, {Michael Joseph} and Shen, {Win Kuang}",
year = "2009",
month = "3",
doi = "10.1111/j.1540-8167.2008.01407.x",
language = "English (US)",
volume = "20",
pages = "352--358",
journal = "Journal of Cardiovascular Electrophysiology",
issn = "1045-3873",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - Postural tachycardia syndrome (POTS)

T2 - Clinical review

AU - Low, Phillip Anson

AU - Sandroni, Paola

AU - Joyner, Michael Joseph

AU - Shen, Win Kuang

PY - 2009/3

Y1 - 2009/3

N2 - Postural Tachycardia Syndrome. Introduction: POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥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, β-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 β-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.

AB - Postural Tachycardia Syndrome. Introduction: POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥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, β-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 β-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.

KW - Deconditioning

KW - Denervation

KW - Hyperadrenergic state

KW - Hypovolemia

KW - Orthostatic

KW - POTS

UR - http://www.scopus.com/inward/record.url?scp=60949083464&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=60949083464&partnerID=8YFLogxK

U2 - 10.1111/j.1540-8167.2008.01407.x

DO - 10.1111/j.1540-8167.2008.01407.x

M3 - Article

C2 - 19207771

AN - SCOPUS:60949083464

VL - 20

SP - 352

EP - 358

JO - Journal of Cardiovascular Electrophysiology

JF - Journal of Cardiovascular Electrophysiology

SN - 1045-3873

IS - 3

ER -