Experiences of living with postural tachycardia syndrome

Objective Postural tachycardia syndrome (PoTS) is a disorder of the autonomic nervous system which involves a range of symptoms, worsened when adopting an orthostatic (upright) position. Symptoms can include tachycardia, dizziness, fainting, nausea as well as many others which, as is typical of a syndrome, vary from person to person. Although research is increasing into this condition, the unifying experiences of managing it on a daily basis have not been extensively investigated. This study aimed to capture participants’ experiences of living with PoTS. Method A longitudinal digital ethnographic approach was employed. Eight participants recorded daily video diaries discussing their experiences of PoTS and its impact for 17 days. Interpretative phenomenological analysis was utilised to analyse the data and identify connections across participants’ accounts. Results Four superordinate themes emerged: ‘loss of control and lack of agency over body’, ‘identity changes’, ‘lack of understanding from others’ and ‘adapting to cope with PoTS’. Discussion The findings demonstrated the complex and widespread impact these participants experience from their PoTS symptoms, including the consequent emotional difficulties that result from managing this condition. An overall lack of understanding about PoTS by others was emphasised, suggesting the requirement for better education and support services for this condition.

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Recent advances in the understanding of the mechanisms underlying postural tachycardia syndrome in children: practical implications for treatment

Cardiology in the Young ◽

10.1017/s1047951116002559 ◽

2016 ◽

Vol 27 (3) ◽

pp. 413-417 ◽

Cited By ~ 6

Author(s):

Xiaochun Zheng ◽

Yonghong Chen ◽

Junbao Du

Keyword(s):

Heart Rate ◽

Upright Position ◽

Postural Tachycardia Syndrome ◽

Postural Orthostatic Tachycardia Syndrome ◽

Vascular Endothelial ◽

Vascular Endothelial Function ◽

Pathophysiological Mechanisms ◽

Postural Tachycardia ◽

Β Receptor ◽

Practical Implications

AbstractPostural tachycardia syndrome is defined by a heart rate increment of 40 beats/minute (bpm) (or a heart rate that exceeds 125 bpm) within 10 minutes of change from the supine position to an upright position in the absence of obvious orthostatic hypotension. There are multiple pathophysiological mechanisms that underlie postural tachycardia syndrome, including peripheral denervation, β-receptor supersensitivity, hypovolaemia, and impaired muscle pump. Some children afflicted with postural orthostatic tachycardia syndrome and hypovolaemic dysregulation have been found to have perturbed renin–angiotensin–aldosterone profile, disturbed vascular endothelial function, and abnormal vasodilation. The hyperadrenergic state in some postural tachycardia syndrome patients is likely a driver for orthostatic tachycardia. Other mechanisms include the presence of treatable autonomic neuropathies. An understanding of these pathophysiological mechanisms might be helpful for the effective treatment of postural tachycardia syndrome.

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Arterial baroreflex control of heart rate during exercise in postural tachycardia syndrome

Journal of Applied Physiology ◽

10.1152/japplphysiol.00176.2007 ◽

2007 ◽

Vol 103 (4) ◽

pp. 1136-1142 ◽

Cited By ~ 21

Author(s):

Shizue Masuki ◽

John H. Eisenach ◽

William G. Schrage ◽

Niki M. Dietz ◽

Christopher P. Johnson ◽

...

Keyword(s):

Heart Rate ◽

Baroreflex Sensitivity ◽

Systolic Pressure ◽

Upright Position ◽

Postural Tachycardia Syndrome ◽

Healthy Controls ◽

Arterial Baroreflex ◽

Cycle Exercise ◽

Baroreflex Control ◽

Postural Tachycardia

Patients with postural tachycardia syndrome (POTS) have excessive tachycardia without hypotension during orthostasis as well as exercise. We tested the hypothesis that excessive tachycardia during exercise in POTS is not related to abnormal baroreflex control of heart rate (HR). Patients ( n = 13) and healthy controls ( n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter) and HR (ECG) were measured. Baroreflex sensitivity of HR was assessed by bolus intravenous infusion of phenylephrine at each workload. In both positions, HR was higher in the patients than the controls during exercise. Supine baroreflex sensitivity (HR/systolic pressure) in POTS patients was −1.3 ± 0.1 beats·min−1·mmHg−1 at rest and decreased to −0.6 ± 0.1 beats·min−1·mmHg−1 during 75-W exercise, neither significantly different from the controls ( P > 0.6). In the upright position, baroreflex sensitivity in POTS patients at rest (−1.4 ± 0.1 beats·min−1·mmHg−1) was higher than the controls (−1.0 ± 0.1 beats·min−1·mmHg−1) ( P < 0.05), and it decreased to −0.1 ± 0.04 beats·min−1·mmHg−1 during 75-W exercise, lower than the controls (−0.3 ± 0.09 beats·min−1·mmHg−1) ( P < 0.05). The reduced arterial baroreflex sensitivity of HR during upright exercise was accompanied by greater fluctuations in systolic and pulse pressure in the patients than in the controls with 56 and 90% higher coefficient of variations, respectively ( P < 0.01). However, when baroreflex control of HR was corrected for differences in HR, it was similar between the patients and controls during upright exercise. These results suggest that the tachycardia during exercise in POTS was not due to abnormal baroreflex control of HR.

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