Time’s Up for POTS

Postural Orthostatic Tachycardia Syndrome (POTS) is estimated to affect approximately 500,000 people in the United States (Bryarly et al 2019) and has been identified as the leading cause of disability in women* of child-bearing age (Novak, 2018), but I didn’t learn about POTS while earning a doctorate in physical therapy. And I certainly didn’t know that I had it. 

 

In PT school we learned how to take orthostatic vital signs. We practiced on each other, taking blood pressure and heart rate in lying, sitting, and standing to observe the body’s response to gravity. When it was my turn to be a “patient,” my classmates observed that my heart rate was normal while lying and was abnormally fast (tachycardic) in upright positions.

 

Remarkable physiological shifts occur in order to get oxygenated blood to the brain even when gravity is pulling it toward the feet. Autonomic control of those physiological mechanisms can become dysregulated for a variety of reasons. Dysautonomia is an umbrella term for dysfunction of the autonomic nervous system that includes POTS and other forms of orthostatic intolerance in which the following mechanisms are disrupted:

  • With a shift to upright position, (assuming Earth’s gravity is in effect) baroreceptors and chemoreceptors in vessels near the brain and heart detect low blood volume/pressure and oxygen levels are low. 
  • Since the brain and heart have a critical need for oxygen, these sensors exist near the heart and brain only. After all, if the brain and heart are getting enough oxygen, they should be able to direct it anywhere else it needs to go, via adjustments to heart rate and through vasodilation/ vasoconstriction of blood vessels throughout the body that act as an adjustable shunt that gets blood where it is most needed. 
  • As blood moves downward with gravity, the ANS coordinates vasoconstriction in the lower body to shunt blood upward, effectively getting oxygenated blood up to the brain and heart.
  • If this process doesn’t coordinate precisely, blood may pool in the lower body resulting in a temporary lack of oxygenated blood to the brain. This may be asymptomatic or creates transient dizziness, weakness, fuzzy thinking, vision changes, feeling faint or actually fainting. If it is detected as a drop in blood pressure, it may be called orthostatic hypotension.
  • Collectively, these symptoms are known as pre-syncope if it occurs without fainting/loss of consciousness or syncope in the case that it leads to loss of consciousness. In the case of the latter, the individual falls and assumes a less upright position while the brain goes into a mode that requires less oxygen to maintain. Essentially, the system figures out how to solve the problem, albeit in a rather inconvenient way.
  • Estrogen is a vasodilator and predisposes women to these issues.
  • Over time, the autonomic nervous system may adapt by increasing heart rate in upright positions in an attempt to pump blood faster so that the brain gets oxygen sooner. 

 

Most of these points were covered in PT school, which helped me to understand my own history of vision loss upon standing (presyncope) as often as 10+ times a day. Luckily I had good balance and I could wait out the 10-20 seconds of vision loss without falling.

 

My medical doctors dismissed my experience with a casual “you are fine, you just have low blood pressure,” and sent me on my way. Did they not learn how to take orthostatic vitals in medical school? Unlikely. Did they not have time or enough nursing support to delegate this task? Perhaps. Did they disregard me as an anxious young woman? Quite likely. 

 

At the time I assumed they knew better than I did, but I’ve come to understand the dismissal of women’s complaints is a well-established form of misogyny in the medical system. Consider if POTS were the leading cause of disability in men of a similar age group–it would likely not be so easily ignored. A recent webinar for physicians that I attended emphasized that POTS is a problem that occurs in young, anxious women. The presenting MD failed to highlight study findings that indicate that anxiety does not cause POTS (Masuki et al 2007) or that anxiety is not higher in POTS patients than in the general population (Raj et al 2009.) He referred to it to as a “first-world problem” experienced by stressed-out young women, and proceeded to provide mis-information that, in my professional opinion, serves to foster stigma, misunderstanding and medical gaslighting.

 

When orthostatic tachycardia becomes a chronic response, the sympathetic (fight or flight) overdrive that increases heart rate to prevent syncope may present in a number of other ways. A person with chronic sympathetic upregulation may experience other symptoms associated with dysfunction of the ANS, which innervates every organ system of the body:

  • Discolored skin, flushing and rashes/hives
  • Nausea, diarrhea, constipation, painful bloating
  • Shortness of breath as the body attempts to get more oxygen (even though it has enough oxygen that simply isn’t getting to the upright brain)
  • Pain, particularly headaches, neck and upper back pain as these areas are subjected to intermittent hypoxia, which sensitizes tissues so that they are more prone to pain
  • Migraine-like symptoms including light and sound sensitivity
  • Flare-ups of symptoms with the menstrual cycle (due to the effects of fluctuating estrogen levels)
  • Acute episodes of dizziness and presyncope or syncope upon upright positioning
  • Chronic malaise and fatigue even when sitting or lying down
  • Poor or unrefreshing sleep
  • Exacerbation of all of the above with known triggers like heat, exertion, eating a large meal, dehydration, stress, immune challenge, etc.

 

By the time I was experiencing all of the above, I did experience anxiety– especially when my healthcare team failed to provide a useful diagnosis or treatment plan. I am a cis-gender white woman, living in the wealthiest nation in the world, and my father is a medical doctor (a general practitioner who had no idea what POTS was until I told him about it.) It took more than two decades from the onset of symptoms for me to find a medical doctor who knew what POTS was and could diagnose/treat it. This is not uncommon– a recent study found that it took POTS patients an average of 8-10 years to get diagnosed (Jiménez-Cohl et al 2019.) If it takes one or two decades to get diagnosed as a highly educated white person with good health insurance in an industrialized nation, how many of these cases go undiagnosed for those who are less privileged? We don’t know because those studies haven’t been done, but I’m guessing they may encounter more barriers than what I endured. This case study describes a male African American medical student who was diagnosed with POTS relatively quickly, but even his diagnosis was delayed by the belief that POTS affects young, Caucasian women. 

 

Some people are genetically prone to developing dysautonomia, but many cases have a viral or traumatic trigger. COVID-19 is rapidly increasing the prevalence of dysautonomia/POTS, with some experts anticipating that Long-COVID POTS will likely overwhelm a healthcare system that is not adequately trained to identify and manage POTS (Raj et al 2021.) 

 

Long-COVID and Long-COVID POTS are, not surprisingly, reported more frequently in females.  Testosterone is a mild immune suppressant, while estrogen is a known immune booster. This may contribute to increased COVID fatalities in males, while more females survive to report persistent symptoms that are likely a result of immune-mediated autonomic dysfunction (Strope et al 2020.) It is not because we are hysterical, anxious, weak, or complain too much. If anything, this situation may require more “complaining” (aka assertive and direct self-advocacy.) Women like me who were socialized to believe “nice girls” don’t speak up may need to heal that wound before they can advocate for themselves and get the support they need to heal from chronic illness. 

 

Early reports of Long COVID were dismissed by medical professionals as anxiety– something familiar to those of us living with POTS. Although anxiety is not the cause of underlying pathophysiology in the case of POTS, Long-COVID, or Long-COVID POTS, the effects of anxiety and medical trauma (emotional and/or physical trauma from being dismissed, ignored and mistreated by healthcare providers) may further aggravate an underlying dysfunction. Fortunately, enough people spoke up about their persistent COVID symptoms such that the medical system could no longer deny the phenomenon of Long-COVID.

 

We are long overdue for a change in how chronic illness is managed, and I’m cautiously optimistic that the rising numbers of people living with POTS/Long-COVID will challenge the system to adapt in ways that better serve people with chronic health issues.

 

As a practitioner, I’ve tried to do my part by using my experience as a platform for learning. I’ve become proficient in screening for dysautonomia and I train others how to identify signs and symptoms in the hopes that people won’t have to wait a decade or two to get answers. 

 

As a patient, I’m still learning to speak up for myself. I’ve discovered that the roots of explicit and implicit misogyny run deep and that re-programming these messages requires patience and persistence. 

 

Anxiety (and its corresponding sympathetic shift into fight-flight) isn’t always a sign of pathology. The sympathetic system mobilizes us to take action, and when that action brings resolution, we can return to a resting parasympathetic state, maintaining overall balance and homeostasis. If you are experiencing symptoms and don’t feel adequately heard, necessary action may include finding healthcare professionals who will hear you out and validate your experience. If they can’t help you find answers or solutions, speak up and ask for a referral to someone who can. Let your anxiety, anger or outrage fuel  actions that move you closer to health and well-being.

 

Feel free to practice speaking up in the comments below, or schedule a health consult with Dr. Lewan.

 

*Please note the use of women/men/male/female used to refer to predominant sex hormones at play and their influence on the physiology of POTS and Long COVID. The author also refers to socialization as a female (social construct of gender) which also influences her experience of chronic illness. Gender identity may or may not align with a person’s sex hormones or sex organs and this blog is not intended to exclude or disrespect anyone who is gender-nonconforming. 

 

Dani M, Dirksen A, Taraborrelli P, Torocastro M, Panagopoulos D, Sutton R, Lim PB. Autonomic dysfunction in ‘long COVID’: rationale, physiology and management strategies. Clin Med (Lond). 2021 Jan;21(1):e63-e67. doi: 10.7861/clinmed.2020-0896. Epub 2020 Nov 26. PMID: 33243837; PMCID: PMC7850225.

 

Strope JD, Chau CH, Figg WD. Are sex discordant outcomes in COVID-19 related to sex hormones?. Semin Oncol. 2020;47(5):335-340. doi:10.1053/j.seminoncol.2020.06.002

 

Jiménez-Cohl P, Earle NM, González BR, Thieck EJ. Taquicardia postural ortostática en 15 pacientes: disautonomía compleja [Postural orthostatic tachycardia syndrome (POTS): report of 15 cases]. Rev Med Chil. 2012 Feb;140(2):145-52. Spanish. doi: 10.4067/S0034-98872012000200001.

 

Low PA, Sandroni P, Joyner M, Shen WK. Postural tachycardia syndrome (POTS). J Cardiovasc Electrophysiol. 2009;20(3):352-358. doi:10.1111/j.1540-8167.2008.01407.x

 

Bryarly M, Phillips LT, Fu Q, Vernino S, Levine BD. Postural Orthostatic Tachycardia Syndrome: JACC Focus Seminar. J Am Coll Cardiol. 2019 Mar 19;73(10):1207-1228. doi: 10.1016/j.jacc.2018.11.059. PMID: 30871704.

 

Masuki S, Eisenach JH, Johnson CP, Dietz NM, Benrud-Larson LM, Schrage WG, Curry TB, Sandroni P, Low PA, Joyner MJ. Excessive heart rate response to orthostatic stress in postural tachycardia syndrome is not caused by anxiety. J Appl Physiol (1985). 2007 Mar;102(3):896-903.

Figueroa JJ, Basford JR, Low PA. Preventing and treating orthostatic hypotension: As easy as A, B, C. Cleve Clin J Med. 2010;77(5):298-306. doi:10.3949/ccjm.77a.09118

 

Low PA, Sandroni P, Joyner M, Shen WK. Postural tachycardia syndrome (POTS). J Cardiovasc Electrophysiol. 2009 Mar;20(3):352-8. doi: 10.1111/j.1540-8167.2008.01407.x. Epub 2009 Jan 16. PMID: 19207771; PMCID: PMC3904426.

 

White RE. Estrogen and vascular function. Vascul Pharmacol. 2002 Feb;38(2):73-80. doi: 10.1016/s0306-3623(02)00129-5. PMID: 12379953.

 

Novak P. Hypocapnic cerebral hypoperfusion: A biomarker of orthostatic intolerance. PLoS One. 2018;13(9):e0204419. Published 2018 Sep 26. doi:10.1371/journal.pone.0204419

 

Raj V, Haman KL, Raj SR, Byrne D, Blakely RD, Biaggioni I, Robertson D, Shelton RC. Psychiatric profile and attention deficits in postural tachycardia syndrome. J Neurol Neurosurg Psychiatry. 2009 Mar;80(3):339-44. doi: 10.1136/jnnp.2008.144360. Epub 2008 Oct 31. PMID: 18977825; PMCID: PMC2758320.