Postural hyperventilation as a cause of postural tachycardia syndrome: Increased systemic vascular resistance and decreased cardiac output when upright in all postural tachycardia syndrome variants

Julian M. Stewart, Paul Pianosi, Mohamed A. Shaban, Courtney Terilli, Maria Svistunova, Paul Visintainer, Marvin S. Medow

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Background—Postural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation-associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO2. Methods and Results—Fifty-eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO2 <30 Torr during head-up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat-to-beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head-up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO2 in hyperventilation by addition of exogenous CO2 into a rebreathing apparatus. With added CO2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control. Conclusions—We conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

Original languageEnglish (US)
Article numbere008854
JournalJournal of the American Heart Association
Volume7
Issue number13
DOIs
StatePublished - Jul 1 2018
Externally publishedYes

Bibliographical note

Funding Information:
Funding for this project was provided by the following National Institutes of Health sources: RO1 HL 134674 and RO1 HL 112736 from the National Heart, Lung, and Blood Institute; and R21 NS 094644 from the National Institute of Neurological Disorders and Stroke.

Publisher Copyright:
© 2018 The Authors.

Keywords

  • Blood flow regulation
  • Blood volume
  • Hyperventilation
  • Orthostatic intolerance
  • Tachycardia
  • Vasoconstriction
  • Ventilation

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