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Journal articles on the topic 'Postural orthostatic tachicardia syndrome'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

Cline, Holly M., and Adam Einhardt. "Postural orthostatic tachycardia syndrome." Nurse Practitioner 47, no. 1 (January 2022): 12–19. http://dx.doi.org/10.1097/01.npr.0000802968.90212.70.

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2

Agarwal, A. K., R. Garg, A. Ritch, and P. Sarkar. "Postural orthostatic tachycardia syndrome." Postgraduate Medical Journal 83, no. 981 (July 1, 2007): 478–80. http://dx.doi.org/10.1136/pgmj.2006.055046.

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3

Brooks, John K., and Laurie A. P. Francis. "Postural orthostatic tachycardia syndrome." Journal of the American Dental Association 137, no. 4 (April 2006): 488–93. http://dx.doi.org/10.14219/jada.archive.2006.0221.

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4

Grossman, Valerie G. A., and Becky A. McGowan. "Postural Orthostatic Tachycardia Syndrome." AJN, American Journal of Nursing 108, no. 8 (August 2008): 58–60. http://dx.doi.org/10.1097/01.naj.0000330266.83852.96.

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5

Bryarly, Meredith, Lauren T. Phillips, Qi Fu, Steven Vernino, and Benjamin D. Levine. "Postural Orthostatic Tachycardia Syndrome." Journal of the American College of Cardiology 73, no. 10 (March 2019): 1207–28. http://dx.doi.org/10.1016/j.jacc.2018.11.059.

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6

Busmer, Lorna. "Postural orthostatic tachycardia syndrome." Primary Health Care 21, no. 9 (November 2011): 16–20. http://dx.doi.org/10.7748/phc2011.11.21.9.16.c8794.

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7

Safavi-Naeini, Payam, and Mehdi Razavi. "Postural Orthostatic Tachycardia Syndrome." Texas Heart Institute Journal 47, no. 1 (February 1, 2020): 57–59. http://dx.doi.org/10.14503/thij-19-7060.

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8

Graham, U., and K. M. Ritchie. "Postural orthostatic tachycardia syndrome." Case Reports 2009, apr19 1 (April 19, 2009): bcr1020081132. http://dx.doi.org/10.1136/bcr.10.2008.1132.

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9

Czosek, Lauren. "Postural orthostatic tachycardia syndrome." Nursing 53, no. 2 (February 2023): 18–22. http://dx.doi.org/10.1097/01.nurse.0000905696.14880.53.

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10

Schondorf, Ronald, and Phillip A. Low. "Idiopathic postural orthostatic tachycardia syndrome." Neurology 43, no. 1 Part 1 (January 1993): 132. http://dx.doi.org/10.1212/wnl.43.1_part_1.132.

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11

Abdulla, Aza, and Thirumagal Rajeevan. "Reversible postural orthostatic tachycardia syndrome." World Journal of Clinical Cases 3, no. 7 (2015): 655. http://dx.doi.org/10.12998/wjcc.v3.i7.655.

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12

Sidhu, B., N. Obiechina, N. Rattu, and S. Mitra. "Postural orthostatic tachycardia syndrome (POTS)." Case Reports 2013, sep16 1 (September 16, 2013): bcr2013201244. http://dx.doi.org/10.1136/bcr-2013-201244.

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13

Dwivedi, Rajesh Kumar. "P0173 POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME." European Journal of Internal Medicine 20 (May 2009): S63. http://dx.doi.org/10.1016/s0953-6205(09)60193-x.

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14

Pavlik, Daniel, Donna Agnew, Lauren Stiles, and Rachel Ditoro. "Recognizing postural orthostatic tachycardia syndrome." Journal of the American Academy of Physician Assistants 29, no. 4 (April 2016): 17–23. http://dx.doi.org/10.1097/01.jaa.0000481398.76099.09.

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15

Mizumaki, Koichi. "Postural Orthostatic Tachycardia Syndrome (POTS)." Journal of Arrhythmia 27, no. 4 (2011): 289–306. http://dx.doi.org/10.1016/s1880-4276(11)80031-1.

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16

Watari, Mari, Shunya Nakane, Akihiro Mukaino, Makoto Nakajima, Yukiko Mori, Yasuhiro Maeda, Teruaki Masuda, et al. "Autoimmune postural orthostatic tachycardia syndrome." Annals of Clinical and Translational Neurology 5, no. 4 (February 28, 2018): 486–92. http://dx.doi.org/10.1002/acn3.524.

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17

Shahi, Niti, Gabrielle Shirek, Kaci Pickett, Alexandra Schwartz, Jamie Shoop, Ryan Phillips, Rachel Workman, David Kaplan, Clio Pitula, and Steven Moulton. "A Pilot Study using the Compensatory Reserve Index to evaluate individuals with Postural Orthostatic Tachycardia syndrome." Cardiology in the Young 30, no. 12 (September 30, 2020): 1833–39. http://dx.doi.org/10.1017/s1047951120002905.

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AbstractPurpose:The diagnosis of Postural Orthostatic Tachycardia syndrome traditionally involves orthostatic vitals evaluation. The Compensatory Reserve Index is a non-invasive, FDA-cleared algorithm that analyses photoplethysmogram waveforms in real time to trend subtle waveform features associated with varying degrees of central volume loss, from normovolemia to decompensation. We hypothesised that patients who met physiologic criteria for Postural Orthostatic Tachycardia syndrome would have greater changes in Compensatory Reserve Index with orthostatic vitals.Methods:Orthostatic vitals and Compensatory Reserve Index values were assessed in individuals previously diagnosed with Postural Orthostatic Tachycardia syndrome and healthy controls aged 12–21 years. Adolescents were grouped for comparison based on whether they met heart rate criteria for Postural Orthostatic Tachycardia syndrome (physiologic Postural Orthostatic Tachycardia syndrome).Results:Sixty-one patients were included. Eighteen percent of patients with an existing Postural Orthostatic Tachycardia syndrome diagnosis met heart rate criteria, and these patients had significantly greater supine to standing change in Compensatory Reserve Index (0.67 vs. 0.51; p<0.001). The optimal change in Compensatory Reserve Index for physiologic Postural Orthostatic Tachycardia syndrome was 0.60. Patients with physiologic Postural Orthostatic Tachycardia syndrome were more likely to report previous diagnoses of anxiety or depression (p = 0.054, 0.042).Conclusion:An accurate diagnosis of Postural Orthostatic Tachycardia syndrome may be confounded by related comorbidities. Only 18% (8/44) of previously diagnosed Postural Orthostatic Tachycardia syndrome patients met heart rate criteria. Findings support the utility of objective physiologic measures, such as the Compensatory Reserve Index, to more accurately identify patients with true autonomic dysfunction.
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18

Khurana, Ramesh K., and Lindsay Eisenberg. "Orthostatic and non-orthostatic headache in postural tachycardia syndrome." Cephalalgia 31, no. 4 (September 6, 2010): 409–15. http://dx.doi.org/10.1177/0333102410382792.

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Objective Orthostatic and non-orthostatic headache spectrum was prospectively studied in 24 consecutive patients with postural orthostatic tachycardia syndrome (POTS). Methods Patients were interviewed about clinical aspects of headache and its precipitation during head-up tilt (HUT). Autonomic functions were assessed using a standard battery of tests. The relationship of orthostatic headache to cardiovascular variables was examined using unpaired two-tailed t-test. Results Orthostatic headache occurred during daily activity in 14 patients (58.3%) and during HUT in 15 patients (62.5%). Age under 30 years and increasing duration of tilt were predictive for orthostatic headache. Of the 24 patients, 23 (95.8%) had non-orthostatic headache fitting the criteria of migraine or probable migraine. Conclusions Orthostatic headache affected two-thirds of POTS patients, especially those under age 30. Patients with orthostatic headache should be clinically assessed for POTS and informed of this association to reduce short-term morbidity. Migraine afflicted almost all POTS patients. This co-morbidity should be considered in management of POTS.
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19

GLATTER, KATHRYN A., DIPIKA TUTEJA, NIPAVAN CHIAMVIMONVAT, MOHAMED HAMDAN, and JEANNY K. PARK. "Pregnancy in Postural Orthostatic Tachycardia Syndrome." Pacing and Clinical Electrophysiology 28, no. 6 (June 2005): 591–93. http://dx.doi.org/10.1111/j.1540-8159.2005.50026.x.

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20

Busmer, Lornar. "Living with postural orthostatic tachycardia syndrome." British Journal of Cardiac Nursing 6, no. 7 (July 2011): 358–59. http://dx.doi.org/10.12968/bjca.2011.6.7.358.

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21

Benditt, David G., and Lin Y. Chen. "Peptides in Postural Orthostatic Tachycardia Syndrome." Journal of the American College of Cardiology 60, no. 4 (July 2012): 321–23. http://dx.doi.org/10.1016/j.jacc.2012.04.021.

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22

Cutsforth-Gregory, Jeremy K., Eduardo E. Benarroch, and Guillaume Lamotte. "Platypnea-orthodeoxia syndrome mimicking postural orthostatic tachycardia syndrome." Clinical Autonomic Research 31, no. 4 (April 22, 2021): 573–76. http://dx.doi.org/10.1007/s10286-021-00805-6.

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23

Kanjwal, Khalil, Sameer Jamal, Asim Kichloo, and Blair Grubb. "New-onset Postural Orthostatic Tachycardia Syndrome Following Coronavirus Disease 2019 Infection." Journal of Innovations in Cardiac Rhythm Management 11, no. 11 (November 1, 2020): 4302–4. http://dx.doi.org/10.19102/icrm.2020.111102.

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Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2. We report a case of new-onset postural orthostatic tachycardia syndrome in an otherwise healthy female patient following COVID-19 infection. The patient presented with fatigue, orthostatic palpitations, dizziness, and presyncope. She underwent head-up tilt-table testing and the findings were suggestive of postural orthostatic tachycardia syndrome.
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24

Yang, Jinyan, Lulu Zhu, Stella Chen, Xueying Li, Qingyou Zhang, Fengwen Zhang, Li Chen, Chaoshu Tang, Junbao Du, and Hongfang Jin. "Modified Calgary score in differential diagnosis between cardiac syncope and postural orthostatic tachycardia syndrome-associated syncope in children." Cardiology in the Young 23, no. 3 (October 9, 2012): 400–404. http://dx.doi.org/10.1017/s1047951112001266.

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AbstractThe present study was designed to analyse the usefulness of a modified Calgary score system during differential diagnosis between cardiac syncope and postural orthostatic tachycardia syndrome-associated syncope through a large sample sized clinical investigation. The study included 213 children, including 101 boys and 112 girls, with cardiac syncope or postural orthostatic tachycardia syndrome-associated syncope in the age group of 2–19 years (mean 11.8 ± 2.9 years). A modified Calgary score was created, which was analysed to predict differential diagnoses between cardiac syncope and postural orthostatic tachycardia syndrome-associated syncope using a receiver operating characteristic curve. The median of modified Calgary scores for cardiac syncope was −5.0, which significantly differed from that of postural orthostatic tachycardia syndrome (0.0; p < 0.01). The sensitivity and specificity of a differentiation score of less than −2.5 was 96.3% and 72.7%, respectively. Owing to the fact that the modified Calgary score was an integer, when less than −3.0 the diagnosis could be considered as cardiac syncope. The modified Calgary score could be used to make an initial differential diagnosis between cardiac syncope and postural orthostatic tachycardia syndrome-associated syncope in the clinic.
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25

Mar, Philip L., and Satish R. Raj. "Postural Orthostatic Tachycardia Syndrome: Mechanisms and New Therapies." Annual Review of Medicine 71, no. 1 (January 27, 2020): 235–48. http://dx.doi.org/10.1146/annurev-med-041818-011630.

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Postural orthostatic tachycardia syndrome (POTS) is a clinically heterogeneous disorder with multiple contributing pathophysiologic mechanisms manifesting as symptoms of orthostatic intolerance in the setting of orthostatic tachycardia (increase in heart rate by at least 30 beats per minute upon assuming an upright position) without orthostatic hypotension. The three major pathophysiologic mechanisms include partial autonomic neuropathy, hypovolemia, and hyperadrenergic state. Patients often will exhibit overlapping characteristics from more than one of these mechanisms. The approach to the treatment of POTS centers on treating the underlying pathophysiologic mechanism. Stockings, abdominal binders, and vasoconstrictors are used to enhance venous return in partial neuropathic POTS. Exercise and volume expansion are the main treatment strategies for hypo-volemic POTS. For hyperadrenergic POTS, beta-blockers and avoidance of norepinephrine reuptake inhibitors is important. Attempts should be made to discern which pathophysiologic mechanism(s) may be afflicting patients so that treatment regimens can be individualized.
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26

Stewart, Julian M., and Paolo T. Pianosi. "Postural orthostatic tachycardia syndrome: A respiratory disorder?" Current Research in Physiology 4 (2021): 1–6. http://dx.doi.org/10.1016/j.crphys.2021.01.002.

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27

KHAN, ARSHAN. "COVID-19-INDUCED POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME." Chest 162, no. 4 (October 2022): A502. http://dx.doi.org/10.1016/j.chest.2022.08.388.

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28

Ishibashi, Yuki, Kihei Yoneyama, Tomoya Tsuchida, and Yoshihiro J. Akashi. "Post-COVID-19 Postural Orthostatic Tachycardia Syndrome." Internal Medicine 60, no. 14 (July 15, 2021): 2345. http://dx.doi.org/10.2169/internalmedicine.7626-21.

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29

Seslar, S. "Cardiac Origins of Postural Orthostatic Tachycardia Syndrome." AAP Grand Rounds 24, no. 6 (December 1, 2010): 73. http://dx.doi.org/10.1542/gr.24-6-73.

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30

Carew, S., M. O. Connor, J. Cooke, R. Conway, C. Sheehy, A. Costelloe, and D. Lyons. "A review of postural orthostatic tachycardia syndrome." Europace 11, no. 1 (November 12, 2008): 18–25. http://dx.doi.org/10.1093/europace/eun324.

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31

Abou-Diab, Jane, Dina Moubayed, Danielle Taddeo, Olivier Jamoulle, and Chantal Stheneur. "Acrocyanosis Presentation in Postural Orthostatic Tachycardia Syndrome." International Journal of Clinical Pediatrics 7, no. 1-2 (2018): 13–16. http://dx.doi.org/10.14740/ijcp293w.

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32

Collins, Thomas R. "In the Pipeline-Postural Orthostatic Tachycardia Syndrome." Neurology Today 18, no. 7 (April 2018): 1. http://dx.doi.org/10.1097/01.nt.0000532343.13867.d1.

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33

Johnson, Jonathan N., Kenneth J. Mack, Nancy L. Kuntz, Chad K. Brands, Coburn J. Porter, and Philip R. Fischer. "Postural Orthostatic Tachycardia Syndrome: A Clinical Review." Pediatric Neurology 42, no. 2 (February 2010): 77–85. http://dx.doi.org/10.1016/j.pediatrneurol.2009.07.002.

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34

Watari, M., S. Nakane, A. Mukaino, M. Nakajima, T. Masuda, K. Takamatsu, Y. Mori, et al. "Autoimmune basis in postural Orthostatic Tachycardia syndrome." Journal of the Neurological Sciences 381 (October 2017): 912. http://dx.doi.org/10.1016/j.jns.2017.08.2564.

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35

Fu, Qi, and Benjamin D. Levine. "Exercise in the postural orthostatic tachycardia syndrome." Autonomic Neuroscience 188 (March 2015): 86–89. http://dx.doi.org/10.1016/j.autneu.2014.11.008.

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36

Thanavaro, Joanne L., and Kristin L. Thanavaro. "Postural orthostatic tachycardia syndrome: Diagnosis and treatment." Heart & Lung 40, no. 6 (November 2011): 554–60. http://dx.doi.org/10.1016/j.hrtlng.2009.12.014.

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37

Joyner, Michael J. "Exercise Training in Postural Orthostatic Tachycardia Syndrome." Hypertension 58, no. 2 (August 2011): 136–37. http://dx.doi.org/10.1161/hypertensionaha.111.173872.

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38

Pandian, J. D., K. Dalton, R. D. Henderson, and P. A. McCombe. "Postural orthostatic tachycardia syndrome: an underrecognized disorder." Internal Medicine Journal 37, no. 8 (April 16, 2007): 529–35. http://dx.doi.org/10.1111/j.1445-5994.2007.01356.x.

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39

Bogle, Jamie M., Brent P. Goodman, and David M. Barrs. "Postural orthostatic tachycardia syndrome for the otolaryngologist." Laryngoscope 127, no. 5 (August 31, 2016): 1195–98. http://dx.doi.org/10.1002/lary.26269.

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40

Tripathi, Richa, and Evanthia Bernitsas. "From Postural Orthostatic Tachycardia Syndrome to Radiologically Isolated Syndrome." Case Reports in Neurological Medicine 2018 (2018): 1–3. http://dx.doi.org/10.1155/2018/2956387.

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Background. Autonomic dysfunction is common in Multiple Sclerosis (MS) patients. Most spinal cord lesions entail some degree of autonomic nervous system dysfunction. MS patients may develop autonomic dysfunction later in their disease course. Methods. We report a patient with no prior history of MS presenting with orthostatic symptoms and diagnosed initially with postural orthostatic tachycardia syndrome (POTS). Four months later, she was diagnosed with radiologically isolated syndrome (RIS). The diagnosis was supported by imaging and CSF analysis. Conclusion. Our case sheds light on the need to consider autonomic dysfunction as an initial presentation of demyelinating pathology. Larger trials are needed to outline the possible association between POTS and RIS.
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41

Velasco-Benitez, Carlos Alberto, Cara Axelrod, Ana C. Falcon, Lilibet Fernadez Valdes, and Miguel Saps. "Prevalence of joint hypermobility, postural orthostatic tachycardia syndrome (POTS), and orthostatic hypotension in school-children." Andes Pediatrica 93, no. 1 (February 14, 2022): 53. http://dx.doi.org/10.32641/andespediatr.v93i1.3755.

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Los niños con hipermovilidad articular, síndrome de taquicardia ortostática postural e hipotensión ortostática presentan síntomas autonómicos como mareos, náuseas, dolores de cabeza y palpitaciones. Se desconoce si existe una relación fisiopatológica entre los trastornos del tejido conectivo y los síntomas autonómicos. No hay datos publicados sobre la prevalencia de los trastornos a nivel comunitario. Objetivo primario: Evaluar la prevalencia de la hipermovilidad articular, la hipotensión ortostática y el síndrome de taquicardia ortostática postural en niños. Objetivo secundario: Determinar la relación entre la hipermovilidad articular, la hipotensión ortostática y el síndrome de taquicardia ortostática postural. Pacientes y Método: Se seleccionaron participantes de 10 a 18 años de colegios públicos de tres ciudades colombianas. Las encuestas incluían preguntas sobre la incidencia de mareos, náuseas, cefaleas, temblores, visión borrosa, vértigo, ansiedad, presíncope y síncope, sudoración y palpitaciones desencadenadas por estar de pie en los dos meses anteriores a la investigación. Cada uno de estos signos y síntomas también se evaluaron durante las fases de decúbito (10 minutos) y de pie (2, 5 y 10 minutos) de la investigación. Se midió la FC y la PA durante los mismos intervalos. La movilidad articular se midió con un goniómetro mecánico y se evaluó con la puntuación de Beighton. Resultados: En cuanto a la prevalencia, de 306 niños, 87 (28,4%) presentaron hiperlaxitud articular, 5 (1,6%) hipotensión ortostática y 6 (2,0%) síndrome de taquicardia ortostática postural. De los 87 niños con hiperlaxitud articular, dos niños presentaron hiperlaxitud articular y al mismo tiempo hipotensión postural (1,2%) (p = 0,6735) y síndrome de taquicardia ortostática postural (1,2%) (p = 0,5188), respectivamente. Conclusiones: Los niños con hiperlaxitud articular no tuvieron una mayor prevalencia de síndrome de taquicardia ortostática postural ni de hipotensión ortostática. Parece poco probable que los trastornos del tejido conectivo sean los responsables de la mayoría de los casos de síndrome de taquicardia postural e hipotensión ortostática en la comunidad. Cabe destacar que la fisiopatología del síndrome de taquicardia ortostática postural y de la hipotensión ortostática requiere una mayor investigación.
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42

Wong, Sammi, Sara Hasan, Christina Parducci, and Bernadette Ann Riley. "The gastrointestinal effects amongst Ehlers-Danlos syndrome, mast cell activation syndrome and postural orthostatic tachycardia syndrome." AIMS Allergy and Immunology 6, no. 2 (2022): 19–24. http://dx.doi.org/10.3934/allergy.2022004.

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<abstract> <p>Ehlers-Danlos syndrome (EDS), mast cell activation syndrome, and postural orthostatic tachycardia syndrome are a triad of comorbid conditions that can occur simultaneously in many patients. Specifically, Ehlers-Danlos syndrome is a group of inherited connective tissue disorders that weakens the connective tissue and causes easy bruising. Mast cell activation syndrome (MCAS) is a condition in the connective tissue of vascularized organs that causes recurrent episodes of anaphylactic symptoms. The irregular activation of mast cells may contribute to immunological manifestations in EDS patients. Postural orthostatic tachycardia syndrome (POTS) is an autonomic nervous system disorder characterized by orthostatic intolerance. Review of the literature suggests an overlap of gastrointestinal (GI) symptoms such as nausea and abdominal pain, hernias, perforations, and more. Thus, this paper will delineate each condition's distinct gastrointestinal symptoms and explore similar gastrointestinal relationships among these conditions.</p> </abstract>
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43

Boris, Jeffrey R. "The role of the cardiologist in the evaluation of dysautonomia." Cardiology in the Young 20, S3 (December 2010): 135–39. http://dx.doi.org/10.1017/s1047951110001198.

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AbstractDysfunction of the autonomic nervous system, or dysautonomia, is an uncommon disease. Postural orthostatic tachycardia syndrome is one of the several types of dysautonomia. Postural orthostatic tachycardia syndrome, also known as chronic orthostatic intolerance, is the most common but least severe of the dysautonomic disorders; it will serve as the model for evaluation and management of the other dysautonomias. Overall, these patients can have variable dysfunction of the autonomic nervous system that is more severe than that observed in typical neurocardiogenic syncope. Frequently, providers are not familiar with either the evaluation or the management of this syndrome, or are just not interested in doing so. This article attempts to describe strategies for evaluation and management of postural orthostatic tachycardia syndrome. The diagnosis of postural orthostatic tachycardia syndrome is made by the finding of orthostatic intolerance associated with a pulse greater than 120 beats per minute in the first 10 minutes of upright position or an elevation in pulse greater than 30 beats per minute in the first 10 minutes of upright position. Overall, these patients can have variable dysfunction of the autonomic nervous system that is more severe than that seen in typical neurocardiogenic syncope. A wide variety of associated symptoms may exist and these symptoms can have tremendous impact on the lives of the patients and their families. Management of these patients can be difficult as well as rewarding. It is helpful to perform an extensive education up front with these patients and their families. Interventions for patients with postural orthostatic tachycardia syndrome typically fall into two broad categories: non-pharmacological and pharmacological. Non-pharmacological therapies are varied, but are based primarily on ensuring adequate status of intravascular fluid. Polypharmacy may be required to control symptoms associated with postural orthostatic tachycardia syndrome. On account of the severity of their symptoms, these patients frequently have difficulty in completing their school assignments. The physician may need to help support the attempts of the family to work with the school to help the patient stay in school. As postural orthostatic tachycardia syndrome is underdiagnosed and poorly understood, it is a disease that provides an excellent opportunity to perform research. The most important studies would be those that aim to elucidate an aetiology and a pathophysiology of postural orthostatic tachycardia syndrome. In the final analysis, the role of the cardiologist in the evaluation and management of a patient with dysautonomia is to help a patient with severe disability to feel as if they are normal, or much closer to it.
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44

Zheng, Xiaochun, Yonghong Chen, and Junbao Du. "Recent advances in the understanding of the mechanisms underlying postural tachycardia syndrome in children: practical implications for treatment." Cardiology in the Young 27, no. 3 (December 12, 2016): 413–17. http://dx.doi.org/10.1017/s1047951116002559.

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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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45

Freeman, Roy, and Horacio Kaufmann. "DISORDERS OF ORTHOSTATIC TOLERANCE-ORTHOSTATIC HYPOTENSION, POSTURAL TACHYCARDIA SYNDROME, AND SYNCOPE." CONTINUUM: Lifelong Learning in Neurology 13 (December 2007): 50–88. http://dx.doi.org/10.1212/01.con.0000299966.05395.6c.

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46

Eftekhari, Helen, and Sajad Hayat. "Review of postural orthostatic tachycardia syndrome: a predominantly female condition." British Journal of Cardiac Nursing 14, no. 12 (December 2, 2019): 1–10. http://dx.doi.org/10.12968/bjca.2019.0090.

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Postural orthostatic tachycardia syndrome is a debilitating and underdiagnosed condition, affecting five times as many women of childbearing age as it does men. The true prevalence is difficult to estimate, with charities reporting up to potentially 3 million people with the condition in the United States. There is a lack of awareness and knowledge regarding how to manage people with postural orthostatic tachycardia syndrome. This results in a difficult journey to diagnosis. The average length of time to diagnosis from symptom onset is 4 years in the UK with dismissals of symptoms and misdiagnosis being common experiences. The largest online survey by an American charity found that 75% of women were misdiagnosed with anxiety compared with 25% of men. This article aims to raise awareness of postural orthostatic tachycardia syndrome, its underlying pathophysiology, diagnosis and the impact on quality of life, as well as the management and socioeconomic impact of the condition. Cardiac nurses who meet people with postural orthostatic tachycardia syndrome can improve the patient experience. Being aware of the condition, validating the experiences of these young, predominantly female, patients to rebuild trust, and providing support can make a huge difference.
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47

Bessis, D., V. Pallure, and É. Jeziorski. "BASCULE syndrome, orthostatic cyanosis and postural orthostatic tachycardia syndrome: time for decanting old wine?" British Journal of Dermatology 175, no. 5 (September 12, 2016): 1110–11. http://dx.doi.org/10.1111/bjd.14918.

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48

Park, Jung A., and Jae Han Park. "Clinical Significance and Update of Postural Orthostatic Tachycardia Syndrome." Research in Vestibular Science 21, no. 1 (March 15, 2022): 1–5. http://dx.doi.org/10.21790/rvs.2022.21.1.1.

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Postural orthostatic tachycardia syndrome (POTS) is a cerebrovascular autonomic dysfunction that is common in young women. POTS can cause dizziness due to orthostatic intolerance. In patients with orthostatic intolerance, it can be diagnosed when the heart rate increases by more than 30 beats per minute within 10 minutes of standing up through the head-up tilt test. However, even a neuro-otologist has difficulty in diagnosing POTS due to the high possibility of misdiagnosis if not paying attention. In this paper, the clinical symptoms, pathophysiology, diagnosis, and treatment of POTS are investigated. In addition, the latest knowledge of POTS is searched to help diagnose and treat POTS.
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49

Lee, Jeongho. "Postural orthostatic tachycardia syndrome in children and adolescents." Journal of the Korean Medical Association 65, no. 2 (February 10, 2022): 101–7. http://dx.doi.org/10.5124/jkma.2022.65.2.101.

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Background: Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous disorder in children and adolescents. Recently, there have been some data concerning the prevalence of POTS in adults. However, current studies on POTS in children and adolescents are rare. Thus, many young patients with POTS are misdiagnosed with migraine or other diseases.Current Concepts: The diagnosis and treatment of POTS differ between pediatric and adult patients. POTS in children and adolescents is diagnosed with chronic symptoms of orthostatic intolerance, such as a heart rate rise of 40 beat per minute (bpm) or a heart rate exceeding 130 bpm without orthostatic hypotension. There are three major POTS categories: hypovolemic POTS, neuropathic POTS, and hyperadrenergic POTS. These categories are distinguished by their major mechanisms. The different subtypes of POTS in children and adolescents have their own clinical characteristics and laboratory findings.Discussion and Conclusion: Treatment of POTS in children and adolescents should always include lifestyle changes, nutritional adjustments, exercise, and drugs depending on the different subtypes of POTS.
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50

Baker, J., IS Palamarchuk, and K. Kimpinski. "A prospective 1-year study of postural tachycardia and the relationship to non-postural versus orthostatic symptoms." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (May 2015): S28. http://dx.doi.org/10.1017/cjn.2015.137.

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Background: Postural tachycardia syndrome (POTS) is defined as heart rate (HR) increments ≥30 bpm on head-up tilt (HUT) associate with orthostatic symptoms (lightheadedness, dizziness, palpitations, etc.). A large proportion of asymptomatic young adults naturally express excessive HR increments on HUT, which has raised questions regarding whether revision to the diagnostic criteria for POTS in younger patient populations is needed. In addition, poor adaptation to environmental stressors may contribute to the disability experienced by POTS patients. Objectives: 1) determine whether asymptomatic patients were predisposed to developing constitutional symptoms that could result in the full syndrome of POTS, and 2) determine whether these symptoms correlated to postural HR or orthostatic symptoms. Methods: HR response to HUT and orthostatic and constitutional symptoms in 30 asymptomatic POTS patients were evaluated after 1 year. Results: HR increment at follow-up demonstrated no correlation with general fatigue (r = 0.006), body vigilance (r = 0.195), physical (r = -0.087) and mental (r = -0.137) health, or orthostatic scores (r = 0.04). Orthostatic scores significantly correlated with general fatigue (r = 0.374) and body vigilance (r = 0.392) (p<0.05). Conclusion: These data support that the majority of young individuals express benign orthostatic tachycardia and further argue for re-evaluation of the HR criteria for diagnosing POTS in younger populations.
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