Postural orthostatic tachycardia syndrome

Postural orthostatic tachycardia syndrome (also postural tachycardia syndrome) is recognised as an abnormal response by the autonomic (involuntary) nervous system characterised by orthostatic intolerance (the development of symptoms when upright that are relieved by lying down).


When a healthy person stands up, approximately 750 mL of thoracic blood is abruptly translocated downward. If automatic adjustment to standing does not work correctly, it can result in an excessive rise in heart rate (tachycardia), increased epinephrine in the blood and altered blood flow to the brain. In PoTS, orthostatic intolerance (OI) occurs because standing upright requires rapid and effective circulatory and neurologic compensations to maintain blood pressure, cerebral blood flow, and consciousness. People who suffer from OI lack the basic mechanisms to compensate for this deficit.


It is commonly said that to be diagnosed with PoTS, a person must experience the following:
1. A group of symptoms in an upright position (usually standing) that are relieved by lying down.
2. These symptoms should be associated with an abnormally high and persistent increase in heart rate of 30 beats per minute (40 bpm if under 19 years of age) within ten minutes of standing.


In review of the research, Abed et al (2012) states that most authors agree POTS is characterised by an excessive increase in heart rate (tachycardia), either by 30 beats per minute or to a rate of more than 120 beats per minutes, after standing (5∼30 min). However, opinions diverge on the inclusion, or exclusion, of blood pressure changes (orthostatic hypo- or hyper-tension) as a defining feature of PoTS.


The development of PoTS can be linked to a number of different diseases or situations but in some cases a cause is never identified. The reason for this is not properly understood but it is possible that there is a malfunction of the nervous system that controls autonomic functions in the body.


National Institute of Neurological Disorders and Stroke (NINDS) reports that current thinking is that there are a number of mechanisms. Some patients have peripheral denervation (neuropathic POTS); some have symptoms that are due to sustained or parosyxmal overactivity of the sympathetic nervous system (hyperadrenergic POTS); and some individuals have PTOS dominated by features of deconditioning.


PoTS UK indicate that PoTS can follow a viral illness such as glandular fever, or be linked to pregnancy or a traumatic event. Sometimes teenagers are affected after a rapid growth spurt and most will improve within a few years. Some patients develop PoTS-like symptoms due to lack of fitness and the heart pumping inefficiently after being confined to bed for some time.

PoTS is complex and likely has numerous, concurrent pathophysiologic etiologies, presenting along a wide spectrum of potential symptoms. Symptoms can be debilitating, ranging from mild to severe and can vary from day to day.


Nonpharmacologic treatment includes (1) increasing aerobic exercise, (2) lower-extremity strengthening, (3) increasing fluid/salt intake, (4) psychophysiologic training for management of pain/anxiety, and (5) family education.


Fu et al (2010) found in a number of studies, exercise has been reported to be beneficial both in alleviating POTS symptoms, as well as playing a role in curing the condition. In one study, POTS patients without blood pressure fluctuations, were trained gradually to move from lying to sitting to a standing position during different activities, such as swimming, rowing, and cycling. Grubb (2006) reported aerobic exercise three times a week for 20 min is enough to be beneficial for patients who can tolerate it.


Abed et al (2012) compiled the literature on symptoms, diagnosis, treatment and management of POTS to demonstrate further research is required to fully characterise this syndrome and guide optimal management.



Howraa Abed, Patrick A Ball, and Le-Xin Wang Diagnosis and management of postural orthostatic tachycardia syndrome: A brief review J Geriatr Cardiol. 2012 Mar; 9(1): 61–67.
Jonathan N. Johnson, MD, Kenneth J. Mack, MD, PhD, Nancy L. Kuntz, MD, Chad K. Brands, MD, Coburn J. Porter, MD, Philip R. Fischer, MD. Postural Orthostatic Tachycardia Syndrome: A Clinical Review. Pediatric Neurology Volume 42, Issue 2, February 2010, Pages 77–85
Fu Q, Vangundy TB, Galbreath MM, Shibata S, Jain M, Hastings JL, Bhella PS, Levine BD. Cardiac origins of the postural orthostatic tachycardia syndrome. J Am Coll Cardiol. 2010;55:2858–2868.
Grubb BP, Kanjwal Y, Kosinski DJ. The postural tachycardia syndrome: A concise guide to diagnosis and management. J Cardiovasc Electrophysiol. 2006;17:108–112.


The comments above are the implicit advice of Workplace Physiotherapy. The views expressed are based on current evidence-based research and accepted best practice approaches. Unless otherwise stated, these comments are not the view of WorkCover NSW or any other professional body. No reproduction or forwarding of this advice is permitted without the consent of the author.


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