Potts Chicken Stock in 100% Recyclable Can 500ml | Pack of 2

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The causes of POTS are varied. [13] POTS may develop after a viral infection, surgery, trauma, or pregnancy. [7] It has been shown to emerge in previously healthy patients after COVID-19, [14] [15] or in rare cases after COVID-19 vaccination. [16] Risk factors include a family history of the condition. [1] A POTS diagnosis in adults is characterized by an increased heart rate of 30 beats per minute within ten minutes of standing up, while accompanied by symptoms. [1] This increased heart rate should occur in the absence of orthostatic hypotension (>20mm Hg drop in systolic blood pressure) [17] to be considered POTS. A spinal fluid leak (called spontaneous intracranial hypotension) may have the same signs and symptoms as POTS and should be excluded. [18] Prolonged bedrest may lead to multiple symptoms, including blood volume loss and postural tachycardia. [19] Other conditions which can cause similar symptoms, such as dehydration, orthostatic hypotension, heart problems, adrenal insufficiency, epilepsy, and Parkinson's disease, must not be present. [6] a b c Raj SR (April 2006). "The Postural Tachycardia Syndrome (POTS): pathophysiology, diagnosis & management". Indian Pacing and Electrophysiology Journal. 6 (2): 84–99. PMC 1501099. PMID 16943900. Sivan M, Corrado J, Mathias C (2022-08-08). "The adapted Autonomic Profile (aAP) home-based test for the evaluation of neuro-cardiovascular autonomic dysfunction". ACNR, Advances in Clinical Neuroscience and Rehabilitation. doi: 10.47795/qkbu6715. Archived from the original on 2023-05-16 . Retrieved 2023-05-16.

a b Blitshteyn S, Fedorowski A (12 December 2022). "The risks of POTS after COVID-19 vaccination and SARS-CoV-2 infection: it's worth a shot". Nature Cardiovascular Research. 1 (12): 1119–1120. doi: 10.1038/s44161-022-00180-z. ISSN 2731-0590. S2CID 254617706. a b c d e Shaw BH, Stiles LE, Bourne K, Green EA, Shibao CA, Okamoto LE, etal. (October 2019). "The face of postural tachycardia syndrome - insights from a large cross-sectional online community-based survey". Journal of Internal Medicine. 286 (4): 438–448. doi: 10.1111/joim.12895. PMC 6790699. PMID 30861229. Lambert E, Lambert GW (2014). "Sympathetic dysfunction in vasovagal syncope and the postural orthostatic tachycardia syndrome". Frontiers in Physiology. 5: 280. doi: 10.3389/fphys.2014.00280. PMC 4112787. PMID 25120493.Ferri FF (2016). Ferri's Clinical Advisor 2017 E-Book: 5 Books in 1. Elsevier Health Sciences. p.1019.e2. ISBN 9780323448383. Archived from the original on 2023-09-06 . Retrieved 2020-08-27. Thieben MJ, Sandroni P, Sletten DM, Benrud-Larson LM, Fealey RD, Vernino S, etal. (March 2007). "Postural orthostatic tachycardia syndrome: the Mayo clinic experience". Mayo Clinic Proceedings. 82 (3): 308–313. doi: 10.4065/82.3.308. PMID 17352367. While people with POTS typically have normal or even elevated arterial blood pressure, the neuropathic form of POTS is presumed to constitute a selective sympathetic venous denervation. [87] In these patients the selective Alpha-1 adrenergic receptor agonist midodrine may increase venous return, enhance stroke volume, and improve symptoms. [87] Midodrine should only be taken during the daylight hours as it may promote supine hypertension. [87] Raj V, Opie M, Arnold AC (December 2018). "Cognitive and psychological issues in postural tachycardia syndrome". Autonomic Neuroscience. 215: 46–55. doi: 10.1016/j.autneu.2018.03.004. PMC 6160364. PMID 29628432. Fu Q, Vangundy TB, Shibata S, Auchus RJ, Williams GH, Levine BD (August 2011). "Exercise training versus propranolol in the treatment of the postural orthostatic tachycardia syndrome". Hypertension. 58 (2): 167–175. doi: 10.1161/HYPERTENSIONAHA.111.172262. PMC 3142863. PMID 21690484.

a b c d Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I, etal. (April 2011). "Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome". Clinical Autonomic Research. 21 (2): 69–72. doi: 10.1007/s10286-011-0119-5. PMID 21431947. S2CID 11628648. Chen L, Du JB, Jin HF, Zhang QY, Li WZ, Wang L, Wang YL (September 2008). "[Effect of selective alpha1 receptor agonist in the treatment of children with postural orthostatic tachycardia syndrome]". Zhonghua Er Ke Za Zhi = Chinese Journal of Pediatrics. 46 (9): 688–691. PMID 19099860.In the 30% to 60% of cases classified as hyperadrenergic POTS, norepinephrine levels are elevated on standing, [1] often due to hypovolemia or partial autonomic neuropathy. [29] A smaller minority of people with POTS have (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as central hyperadrenergic POTS. [29] [35] The high norepinephrine levels contribute to symptoms of tachycardia. [29] Another subtype, neuropathic POTS, is associated with denervation of sympathetic nerves in the lower limbs. [29] In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs. [1] Heart rate increases to compensate for this blood pooling. [49] Rahman, Masum; Anjum, Fatima (April 27, 2023). "Fludrocortisone". PMID 33232001 . Retrieved 20 October 2023. {{ cite journal}}: Cite journal requires |journal= ( help) a b c d e "2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope". Archived from the original on 2017-03-03 . Retrieved 2017-03-03. Haensch CA, Mallien J, Isenmann S (2012-04-25). "Sleep Disturbances in Postural Orthostatic Tachycardia Syndrome (POTS): A Polysomnographic and Questionnaires Based Study (P05.206)". Neurology. 78 (1 Supplement): P05.206. doi: 10.1212/WNL.78.1_MeetingAbstracts.P05.206. Crnošija L, Krbot Skorić M, Adamec I, Lovrić M, Junaković A, Mišmaš A, etal. (February 2016). "Hemodynamic profile and heart rate variability in hyperadrenergic versus non-hyperadrenergic postural orthostatic tachycardia syndrome". Clinical Neurophysiology. 127 (2): 1639–1644. doi: 10.1016/j.clinph.2015.08.015. PMID 26386646. S2CID 6008891.