Review Article | Open Access2023|Volume 4|Issue 3| https://doi.org/10.37191/Mapsci-JCCR-4(3)-087

Postural Orthostatic Tachycardia Syndrome (POTS): Diagnostic Insights and Multifaceted Treatment Including Clinical Presentation of Post Covid POTS

Howard B Reinfeld*

Cardiology Graduate of Mount Sinai Hospital Miami Beach Florida and Cardiologist at Private Practice, Associates MD, PA, and BS Pharmacy, St. John’s University, Jamaica, New York, USA

*Corresponding Author: Howard B Reinfeld, Cardiology Graduate of Mount Sinai Hospital Miami Beach Florida and Cardiologist at Private Practice, Associates MD, PA, and BS Pharmacy, St. John’s University, Jamaica, New York, USA.

ReceivedNov 16, 2023RevisedNov 30, 2023AcceptedDec 15, 2023PublishedDec 30, 2023

Postural Orthostatic Tachycardia Syndrome (POTS) poses an intricate challenge within the domain of autonomic dysfunction, affecting individuals across diverse age groups. This comprehensive article delves into the multifaceted landscape of POTS, exploring its etiology, manifestations, diagnosis, and treatment modalities. The investigation particularly focuses on the indispensable role of Tilt Table Testing (TTT) in the diagnostic process.

The introduction lays the groundwork by elucidating the fundamental characteristics of POTS, emphasizing the intricate interplay between the autonomic nervous system and cardiovascular dynamics. A nuanced discussion of the epidemiology and potential risk factors provides a contextual understanding of the syndrome. The subsequent section explores the intricate diagnostic landscape, with Tilt Table Testing emerging as a pivotal tool in unraveling the physiological intricacies associated with POTS.

The diagnosis section meticulously outlines the criteria for diagnosing POTS, with a special emphasis on the significance of Tilt Table Testing in capturing the dynamic cardiovascular responses that define this syndrome. The procedural intricacies of TTT are dissected, offering a detailed insight into its methodology and interpretative nuances. Moving forward, the article navigates through the diverse treatment modalities employed to manage POTS, ranging from lifestyle modifications to pharmacological interventions. The complexities of patient management are explored, recognizing the heterogeneity in symptomatology and the need for personalized therapeutic approaches.

The conclusion synthesizes the intricate threads of the article, underscoring the evolving landscape of POTS research and the imperative for continued exploration in both diagnostic methodologies, with Tilt Table Testing at the forefront and treatment strategies.

The article serves as a comprehensive guide for healthcare professionals, researchers, and students seeking a profound understanding of POTS, offering a platform for future advancements in the field.


Postural orthostatic tachycardia syndrome; Dynamic cardiovascular; COVID


Postural Orthostatic Tachycardia Syndrome (POTS) demonstrates the complex relationship between the autonomic nervous system and cardiovascular dynamics. However, this mysterious illness, which is defined by an aberrant increase in heart rate upon acquiring an upright posture, presents a much more complex diagnostic and therapeutic challenge than its seemingly easy symptomatology would suggest. POTS, a syndrome that frequently affects people in the prime, has a severe influence on everyday functioning, significantly decreasing quality of life.

The origin of POTS is rooted in the disruption of autonomic controlling mechanisms, resulting in a variety of symptoms including irregular heartbeats, dizziness, and decreased cognitive function, especially when taking an upright position. In order to contextualize the significance of POTS, it is essential to have a solid understanding of the epidemiological landscape. Although POTS can impact people of all age groups, it tends to occur more frequently throughout adolescence and early adulthood. As the researcher study the intricate details of the spread and impact of the disease, the author discovers that some factors, such as genetic predispositions and existing medical disorders, have a significant role in increasing the risk, adding more complexity to understanding the causes of the syndrome. To fully understand POTS, it is important to have a deep understanding of the underlying pathophysiology. The core of POTS pathophysiology is in the disruption of blood flow and heart rate when standing, necessitating the use of advanced diagnostic methods to understand its complexities. In the following sections, the author will conduct a thorough analysis of the diagnostic environment, specifically highlighting the crucial significance of Tilt Table Testing (TTT). This diagnostic technique is essential for diagnosing POTS and provides valuable insights into the fluctuating circulatory alterations that characterize the condition. As the author explore the intricate procedures of TTT, and gain a better understanding, which allows us to analyze the many therapeutic methods used to manage this disease.


The diagnosis of Postural Orthostatic Tachycardia Syndrome (POTS) requires a thorough examination of clinical symptoms and, importantly, the use of specialized diagnostic techniques. POTS is commonly identified by a combination of symptoms, such as heart palpitations, feeling lightheaded, and difficulties with thinking, which worsen when standing upright. In order to establish a conclusive diagnosis, medical practitioners use a certain set of criteria which usually involve a consistent rise in heart rate of at least 30 beats per minute (bpm) within 10 minutes after assuming an upright position, without experiencing a drop in blood pressure. One important diagnostic method that reveals the dynamic cardiovascular reactions involved in POTS is Tilt Table Testing (TTT).

Picture 1.png

Figure 1: Tilt table test (Passive head-up tilt test).

In the toolbox of diagnostic options for POTS, the Tilt Table Test is regarded as a crucial component. During tilt table testing (TTT), the patient is firmly fastened to a customized table that can be inclined to replicate the shift in body position from lying down to standing up. Within this regulated setting, healthcare professionals can closely monitor alterations in heart rate, blood pressure, and symptoms that occur as a result of changes in body position at different angles, maintaining the patient's head in an elevated position. POTS is characterized by an excessive rise in heart rate without a corresponding decrease in blood pressure, indicating a disruption in the regulation of autonomic regulatory mechanisms. TTT serves the purpose of not only verifying the diagnosis but also offering significant insights into the severity and characteristics of the disease.

In addition to Tilt Table Testing, additional examinations may be used to eliminate other possible causes of symptoms and to further understand the autonomic dysfunction linked to POTS. The diagnostic algorithm can be improved by incorporating ambulatory monitoring, blood volume evaluation, and autonomic reflex testing, which will enhance the accuracy of the diagnostic procedure.


The treatment of Postural Orthostatic Tachycardia Syndrome (POTS) requires a comprehensive approach that is customized to the individual's symptoms and general health. The foundation of POTS management lies in making changes to one's lifestyle, with a focus on ensuring sufficient fluid intake and supplementing with salt to address the commonly observed condition of low blood volume in these individuals. In addition, a structured exercise regimen is developed, which includes both aerobic and strength training, with the goal of improving orthostatic tolerance and enhancing general physical well-being. The management of symptoms is based on pharmacological therapies that are targeted to treat the various signs and symptoms of POTS. To lessen the high heart rate response, doctors may prescribe beta-blockers like propranolol or Atenolol. In order to increase blood volume and lessen the severity of the symptoms, a mineralocorticoid known as fludrocortisone is frequently used. Further, the vasoconstrictor midodrine can be used to prevent blood pooling in the extremities, which will reduce dizziness and enhance orthostatic tolerance. In parallel, the psychological impact of POTS is acknowledged, with many individuals experiencing anxiety and depression as a consequence of chronic symptoms. Integrating psychological support, such as cognitive-behavioral therapy, into the comprehensive management plan is essential to address the holistic well-being of individuals grappling with POTS.

As the understanding of POTS continues to evolve, new treatment options are being investigated, including the use of new drugs and creative procedures. The personalized character of POTS management highlights the importance of a cooperative, patient-focused approach, in which healthcare professionals and individuals work together to improve treatment options and promote overall well-being.

Clinical presentation of post-COVID-POTS

Research has shown that long COVID and POTS are multisystem disorders. Within 6-8 months of infection, it was observed that 2%–14% of patients who have survived COVID-19 might develop POTS, while 9%–61% will suffer symptoms similar to POTS, such as palpitations and tachycardia. In addition, gastrointestinal dysfunction and orthostatic intolerance, the symptoms of MCAS, and a hyperadrenergic state have been noted as an indication of autonomic dysfunction. However, it was also researched that the most common form of autonomic dysfunction is POTS in long COVID patients [1].

Orthostatic intolerance was the most frequent abnormality found in individuals with autonomic dysfunction symptoms that appeared during the par infectious or postinfectious phases of COVID-19. The majority of individuals who reported orthostatic symptoms, however, received normal results from autonomic testing. Eventually, more investigations are required to fully understand the etiology, range, and therapy of COVID-19-related autonomic dysfunction [1].

Possible Mechanisms

Research on the mechanisms behind POTS associated with COVID is evolving. Possible pathophysiological pathways can also occur simultaneously and are more likely to overlap as well. One potential mechanism is that SARS-CoV-2 causes the production of autoantibodies [2]. These antibodies lead to the dysfunction of the autonomic nervous system by reacting with autonomic ganglia, G protein-coupled receptors, autonomic nerve fibers, or other neuronal or cardiovascular receptors. Autoantibodies may lead to venous pooling, autonomic dysregulation, tachycardia, and peripheral nervous system dysfunction by activating muscarinic and adrenergic receptors. It eventually manifests as POTS. For example, it was discovered that autoimmunity markers and inflammatory cytokines increase in patients indicating POTS. In a different case report, a patient with post-COVID-19 POTS had high ganglionic acetylcholine receptor antibody levels. The physical deconditioning of many individuals following SARS-CoV-2 infection may further contribute to the development of POTS [3].

In contrast, POTS associated with COVID-19 may develop as a result of tissue damage caused by SARS-direct CoV-2's toxic effect on its target cells. Angiotensin-converting enzyme 2 receptors are expressed in many organs, and SARS-CoV-2 binds its spike protein to these receptors to penetrate cells and cause multisystem damage that is shown as extrapulmonary and pulmonary COVID-19 [4]. Dysregulation of the renin-angiotensin-aldosterone system, hypercoagulability with thrombosis, and hyperinflammation can all lead to damage to the cardiovascular system. Even in low-risk individuals who are not hospitalized or who have only minor symptoms, SARS-CoV-2 can result in structural damage to the kidneys, lungs, heart, liver, and pancreas. Many of these COVID-19 manifestations have been suggested as potential contributors to post-COVID-19 POTS and post-COVID-19 tachycardia through a variety of different mechanisms. For instance, patients with COVID-19 may experience oxygen desaturation and reflex tachycardia as a result of pulmonary damage caused by COVID-19 [5].

In addition, research has shown that SARS-CoV-2 spike proteins can have neurotoxic effects such as autoimmunity mechanisms, endothelial damage, or neuroinflammation. It might be the cause of POTS symptoms like brain fog and chronic fatigue after infection [5].

Moreover, research has shown that night sweats, nausea, fever, and excess bed rest are associated with infection of SARS-CoV-2 and interact to produce baroreflex dysfunction, hypovolemia, cardiac SNS activation, and diminished cardiac output [6]. Physical deconditioning is caused by all these symptoms and leads to POTS. It may cause a patient to have low stroke volume, chronic fatigue, exercise intolerance, and increased SNS activation [4].

Additionally, stress caused by an illness can engage the SNS. It might initiate a cytokine storm and overstimulate the sympathetic nervous system, resulting in tremors, tachycardia, and sweating. For instance, individuals with long COVID who report orthostatic intolerance, chronic tiredness, presyncope, and brain fog may have COVID-19-related cytokine hyperactivation, which is associated with SNS stimulation [3].

Management of POTS associated with COVID

Treating POTS associated with COVID is a bit different than treating POTS without COVID. Research has analyzed non-pharmacotherapy options such as wearing compression socks, intake of salt (10–12 g/d), fluid increase (2–3 L/d), avoiding dehydration and excessive standing, and doing physical measures. Heart Rhythm Society has suggested using these therapies first in order to treat POTS-associated COVID. However, pharmacological intervention should only be preferred when it's highly needed [7].

However, there are still no particular pharmacological therapies approved to treat POTS patients. Still, a few medications and the pathophysiological pathways may work, including β-blockers, antihistamines, desmopressin acetate, clonidine, and α-methyldopa, droxidopa, fludrocortisone. Moreover, midodrine, ivabradine, nondihydropyridine calcium channel blockers, modafinil, saline intravenously, and pyridostigmine are also included. Only low dosages are suggested to improve symptoms [8].

It is highly recommended to use all these medications when it is quite necessary; otherwise, it is better to change lifestyle and adopt nonpharmacological therapies in order to treat POTS associated with COVID [7].

Medications that are more likely to lower blood pressure, increase heart rate or lead to orthostatic intolerance should be avoided. These may include angiotensin-converting enzyme inhibitors, α-receptor blockers, diuretics, sildenafil citrate, norepinephrine transporter inhibitors, tricyclic antidepressants, hydralazine, nitrates, phenothiazines, opiates, monoamine oxidase inhibitors, ganglionic blocking agents, and oral contraceptives containing drospirenone [9].


In conclusion, the intricate landscape of Postural Orthostatic Tachycardia Syndrome (POTS) unfolds as a multifaceted challenge that intertwines the realms of autonomic dysfunction, cardiovascular dynamics, and the lived experiences of those affected. As the author navigate through the various facets of this syndrome, it becomes evident that POTS is not merely a disorder of the cardiovascular system but a complex interplay of physiological processes that necessitate a comprehensive diagnostic and therapeutic approach.

The diagnostic journey emphasizes the pivotal role of Tilt Table Testing (TTT) as a linchpin in unraveling the mysteries of POTS. The controlled environment of TTT allows for a dynamic exploration of cardiovascular responses, offering not only a confirmatory diagnosis but also a nuanced understanding of the severity and nature of the syndrome. Beyond TTT, a collaborative integration of supplementary diagnostic modalities refines the diagnostic precision, recognizing the heterogeneity inherent in POTS presentation.

The therapeutic landscape of POTS is similarly intricate, reflecting the individualized nature of symptomatology and treatment response. The multifaceted approach to improving the quality of life for patients with POTS includes lifestyle changes, medication, and psychological support. The evolving nature of POTS research underscores the imperative for ongoing exploration, with novel treatment avenues and diagnostic refinements on the horizon.

Since the COVID-19 pandemic arose, there has been a significant increase in the prevalence of POTS as SARS-CoV-2 is a viral trigger. Several potential pathophysiological explanations for post-COVID-19 POTS were observed. Similar to non-COVID-19-related POTS, dysautonomia symptoms and orthostatic tachycardia can be managed with dietary changes and HR-lowering medications. Since patients with POTS associated with COVID are more likely to have depression and anxiety, practitioners should routinely screen for mental health symptoms. In the end, a patient's treatment strategy should be given according to the symptoms. Both therapies involve medication and lifestyle changes together. Finally, more investigation into this public health issue is required in order to properly comprehend and treat people with POTS-COVID.


1. Low PA, Sandroni P. Postural Tachycardia Syndrome (POTS). Neurology. 2012;517-9. PubMed | CrossRef

2. Abed H, Ball PA, Wang LX. Diagnosis and Management of Postural Orthostatic Tachycardia Syndrome: A Brief Review. J Geriatr Cardiol. 2012;9(1):61. PubMed | CrossRef

3. Postural Orthostatic Tachycardia Syndrome (POTS). Johns Hopkins Medicine. 2022.

4. Plash WB, Diedrich A, Biaggioni I, Garland EM, Paranjape SY, Black BK, et al. Diagnosing Postural Tachycardia Syndrome: Comparison of Tilt Testing Compared with Standing Haemodynamics. Clin Sci. 2013;124(2):109-14. PubMed | CrossRef

5. Bagai K, Song Y, Ling JF, Malow B, Black BK, Biaggioni I, et al. Sleep Disturbances and Diminished Quality of Life in Postural Tachycardia Syndrome. J Clin Sleep Med. 2011;7(2):204-10. PubMed | CrossRef

6. OH G. Postural Changes in the Circulation. Circulation. 1965:2409-39.

7. Ormiston CK, Świątkiewicz I, Taub PR. Postural Orthostatic Tachycardia Syndrome as a Sequela of COVID-19. Heart Rhythm. 2022;19(11):1880-9. PubMed | CrossRef

8. Shouman K, Vanichkachorn G, Cheshire WP, Suarez MD, Shelly S, Lamotte GJ, et al. Autonomic Dysfunction Following COVID-19 Infection: An Early Experience. Clin Auton Res. 2021;31:385-94. PubMed | CrossRef

9. Blitshteyn S, Fedorowski A. The risks of POTS after COVID-19 Vaccination and SARS-CoV-2 Infection: It’s Worth a Shot. Nat Cardiovasc Res. 2022;1(12):1119-20. CrossRef

10. Goodman BP, Khoury JA, Blair JE, Grill MF. COVID-19 Dysautonomia. Front Neurol. 2021;12:624968. PubMed | CrossRef

11. Kokorelis C, Malone L, Byrne K, Morrow A, Rowe PC. Onset of Postural Orthostatic Tachycardia Syndrome (POTS) Following COVID-19 Infection: A Pediatric Case Report. Clin Pediatr. 2023;62(2):92-5. PubMed | CrossRef

12. Aladham A, Ramesh N. POTS and COVID-What’s the Connection? A47 COVID-19 and its Complications. Am Thorac Soc. 2022;A1664-A1664. CrossRef

13. Varanasi S, Sathyamoorthy M, Chamakura S, Shah SA. Management of Long-COVID Postural Orthostatic Tachycardia Syndrome with Enhanced External Counterpulsation. Cureus. 2021;13(9). PubMed | CrossRef

14. Dani M, Dirksen A, Taraborrelli P, Torocastro M, Panagopoulos D, Sutton R, et al. Autonomic Dysfunction in ‘Long COVID’: Rationale, Physiology and Management Strategies. Clin Med. 2021;21(1):e63. PubMed | CrossRef

Download PDF