POTS Specialist and Treatment
Your heart pounds the moment you stand. The room tilts, you put a hand on the counter, and it passes, mostly, until the next time. Your cardiac workup came back normal and someone suggested anxiety. What you are describing has a name, a measurable definition, and a body of research behind it. A POTS specialist will test for it, and that testing is usually the missing step.
POTS Defined
Postural orthostatic tachycardia syndrome, or POTS, is a disorder of the autonomic nervous system, the part of your nervous system running everything you never think about. Heart rate. Blood pressure. Digestion. Temperature. Where blood goes when you change position.
Picture a watering can. Tip it, and the water runs to the low end and stays there. Your circulation faces that problem every time you stand up. Gravity pulls blood toward your legs and abdomen, and a healthy autonomic system tightens those vessels within seconds to push it back toward your head.
In POTS, the squeeze does not arrive the way it should. Blood pools in your lower body, less of it reaches your brain, and the heart speeds up trying to close the gap.
The racing heart is the compensation, not the disease. Because a treatment aimed only at slowing the pulse leaves the reason for the pulse untouched, that distinction decides what your care actually does.
Two sides of the problem
Two overlapping problems drive POTS: a hyperadrenergic state, meaning excess sympathetic nervous system activity, and hypovolemia, meaning too little blood volume to hold circulation against gravity. Most people have some of both, so subtyping comes before prescribing; the detail lives on types of POTS.
Why your symptoms cannot define if you have POTS
In 2025, researchers prospectively evaluated 467 non-hospitalized patients with highly symptomatic Long COVID, all on sick leave of 50% or more, at a median of 12 months after infection. Everyone with clinically suspected POTS went on to a cardiologist evaluation with 48-hour ECG, head-up tilt testing and an Active Stand Test.1
143 of them, or 31%, met diagnostic criteria. They were younger than the rest of the cohort, mean age 40 against 44 and 47, and 91% were women.1
Then the researchers compared symptoms across three groups, patients who met POTS criteria, patients who were tested and did not meet them, and patients with no clinical signs of POTS at all.
The distribution of symptoms showed no significant differences between the three groups.1
What this means, is two people can describe the same fatigue, the same brain fog, the same palpitations and the same crash after activity. One has POTS and one does not. You cannot sort them by asking. The only thing separating them is objective measurement of what the heart and blood pressure do when the body changes position.
If a symptom questionnaire cannot rule POTS in, and cannot rule it out either, then the questionnaire was never the right tool for this job. It cuts both ways, and both are worth being honest about. People get missed. People also get told they must have POTS when they might not. Neither error is harmless, because the treatments differ.
The same study measured function rather than relying on self-report. On a six-minute walk test, the POTS group covered 448 meters against 472 and 509 for the two comparison groups, with higher heart rates both during the walk and at rest afterward, and significantly lower physical activity than either group.1
The exhaustion is not a perception problem.
Finding a POTS specialist
POTS is not listed under a single specialty.
What separates a useful appointment from another dead end is whether three things happen. Your heart rate and blood pressure get measured across a change in position rather than only while you sit. Someone hunts for a secondary cause instead of stopping at the tachycardia. And whoever you see is clear with you about which of the two they are treating, the pulse or the autonomic dysfunction driving it.
Ask directly. A practice with real POTS experience will answer those questions without hesitation, and one without it often changes the subject back to the heart rate. If you are still deciding which kind of clinician to start with, that question has its own page: what type of doctor treats POTS.
Why it takes so long to get an answer
It takes so long, because the pattern is invisible to the tests most patients get first, the delay is not really a mystery. An echocardiogram, a resting ECG, a standard blood panel, all of them can be entirely normal in someone with textbook POTS, because the abnormality only appears when the body is upright and nobody measured it upright.
The scale of the delay has been measured. A survey of 4,835 POTS patients found a median of 24 months between first raising the symptoms with a physician and receiving the diagnosis, with the slowest quarter waiting six years or more. 94% of respondents were women and roughly half first developed symptoms in adolescence.3
Lightheadedness in 99%, tachycardia in 97%, presyncope in 94%, headache in 94%, difficulty concentrating in 94%.3 These were not vague or scattered complaints. Thousands of people described the same thing as each other, for two years, before anyone measured what happened when they stood up.
If you have been told your tests are normal, the tests were probably normal. Results can be a statement about what was measured, not about whether something is wrong with you. The autonomic nervous system is not directly readable on a standard blood panel or on routine imaging, and many tests are answering a different question than the one you came in with.
What diagnosis requires
The Canadian Cardiovascular Society position statement sets the central threshold at a heart-rate rise of at least 30 beats per minute that is still present after 10 minutes (or longer) of standing, without the blood pressure drop of orthostatic hypotension. The timing is not a technicality. The rise has to be sustained, so the diagnosis is not made before the 10 minute mark, and a spike two minutes in that settles on its own is not POTS.2 There are further conditions covering age, how long symptoms have lasted and what else has been ruled out, and all of them are set out on how POTS is diagnosed.
That last condition is what turns a number into a diagnosis. A pulse climbing 35 beats on standing is a finding. Whether it is POTS depends on what else has been ruled out. That is why formal evaluation exists, and why nothing you measure at home can substitute for it.
Not meeting the definition of POTS, is not the same as nothing being wrong. You could miss the POTS threshold and still be genuinely orthostatic, lightheaded and tachycardic whenever you are upright. The criteria are a threshold for one named syndrome, not a verdict on whether your body is handling standing properly. This matters for treatment rather than for paperwork, because orthostatic intolerance is worth treating whether or not it earns the label.
Beyond confirming POTS, what changes treatment is the cause underneath. Dysautonomia has primary causes (genetic) and secondary causes (acquired). Secondary causes are the ones worth hunting, because acquired is not the same as permanent. The list is long and routinely skipped. Autoimmune disease, prior infection, diabetes, post-viral syndromes including Long COVID, trauma, thyroid disorders and nutritional deficiency all belong on it. Vitamin B12 and thiamine deficiency can each produce autonomic dysfunction, and both are correctable.
Medications belong on that list too. Some antidepressants, particularly TCAs and SNRIs, increase sympathetic activity and reduce vagal tone. If your symptoms worsened after a medication change, that sequence is worth reviewing with whoever prescribed it.
Treatment for POTS
Treatment splits in two sections. Manage the circulatory failure so you can function, and address the autonomic dysfunction underneath so the failure has a reason to improve. There is no single drug for POTS and no protocol fitting everyone. What follows is education rather than a prescription, and none of it should be started without a clinician who knows your case.
The question deciding treatment, is the tachycardia compensatory?
This is the most important thing to establish before anything is prescribed. A fast heart rate is often doing a job. If the underlying problem is low effective plasma volume, the tachycardia is what is keeping blood moving to your brain, and slowing it without replacing the volume takes away the compensation and leaves the problem. Patients treated that way feel worse, not better.
A racing pulse that is compensating and a racing pulse driven by sympathetic overactivity look identical from the outside and need opposite treatment options. Which one you have is the question worth answering first.
Volume and mechanics
Increasing fluid and salt intake expands blood volume, which is the most direct answer to the hypovolemic half of the problem.
(Note: Sea salt and Himalayan salt do nothing for blood volume that ordinary table salt does not.)
Salt is not for everyone.
Sodium loading is not appropriate with high blood pressure or kidney disease, and it can make both worse. No amount is given here on purpose. Talk with your care provider rather than starting salt intake on your own.
Compression garments reduce pooling in the legs and are simple enough to make them worth trying early.
Structured, graded reconditioning has been studied directly in POTS, and its effects reach further than the pulse. Three months of exercise training in POTS increases cardiac size and mass, blood volume and peak oxygen uptake, and after training the heart moves more blood per beat at a lower rate for the same workload.4
The order matters enormously, and it is where most attempts fail. Programs for POTS begin lying down or seated because upright exercise is what the body cannot yet tolerate. If you begin a reconditioning program upright, in the position your body cannot yet handle, the crash that follows will teach you the wrong lesson about exercise. The staged approach is on our Levine protocol page.
If you also have post-exertional malaiseIf activity reliably makes you worse for days afterward, standard exercise progression can harm you, and pacing has to come first. Tell your clinician about that pattern before beginning any reconditioning program. See PEM and pacing.
Medications
If you have already tried a medication for POTS and found it did little, the drug was not necessarily the wrong idea. Matching a drug to the wrong half of the problem is a common reason a trial disappoints; the subtype question comes first for that reason.
Several classes are used. Beta-blockers such as propranolol, metoprolol and atenolol are used at low dose to control the tachycardia. Fludrocortisone expands blood volume. Midodrine constricts blood vessels to support blood pressure.
These help people function, and for some people that is enough to change a daily life. They are also, by design, aimed at the output rather than the cause.
(Discuss any new medication with your doctor before starting.)
Treating the autonomic dysfunction
In post-viral dysautonomia, the sympathetic side tends to stay elevated while the parasympathetic side stays suppressed, and a body held in that state cannot reach deep sleep, cannot repair efficiently, and keeps generating inflammation. Two interventions aim at that directly. Vagus nerve stimulation activates the parasympathetic side. A stellate ganglion block quiets the overactive sympathetic side.
Stellate ganglion block places local anesthetic around the stellate ganglion, a cluster of sympathetic nerves in the neck. For Long COVID and post-viral autonomic dysfunction I modified the standard approach. I inject at two levels, C6 and C4, use live ultrasound guidance throughout, use an echogenic short-bevel needle, and add no steroid, which earns its place in certain pain procedures and is unnecessary here. It is done one side at a time, never both at once.
Expected temporary effects on the injected side resolve within hours, such as a drooping eyelid and smaller pupil with no sweating on that side, hoarseness, facial flushing and nasal congestion.
A 2023 retrospective study of 41 patients reported symptom relief in 86% of those treated with SGB for Long COVID.5 That study was small, retrospective, and was not conducted at this clinic. A 2025 correction to it also disclosed that all of its authors were employed by the pain clinic where the procedures were performed,6 so it is offered here as supporting evidence, not a prediction of your result. Response can be durable, or it may not hold, depending on how stuck the sympathetic system has become, and stress or another illness can bring symptoms back. I would rather say that plainly than promise otherwise.
SGB is aimed mostly at hyperadrenergic POTS, where the driver is sympathetic overactivity. It is not the right first move for someone whose dominant problem is blood volume, which is the same point as above in a different form.
If you are considering SGB, ask whether live ultrasound guidance is used throughout. The stellate ganglion sits near the carotid artery, the vertebral artery and the spine. Operator experience and imaging are not optional extras here.
For how SGB applies specifically to POTS, including candidacy, see stellate ganglion block for POTS.
The surges patients call adrenaline dumps come out of that same overactive sympathetic state.
Is POTS reversible?
When POTS is secondary, meaning acquired rather than inherited, the honest answer is that it is potentially reversible, and that is a genuinely different situation from a permanent diagnosis.
I will not tell you it resolves for everyone, because it does not. What I will say is that treating the dysautonomia underneath tends to move several symptoms at once, in a way that treating each symptom separately rarely does. When autonomic balance shifts, the racing pulse, the sleep, the brain fog and the temperature swings tend to move together, because they were never separate problems.
I had Long COVID myself so I understand the recovery proces.
Where POTS sits in the wider picture
Dysautonomia is the first of six biological mechanisms I work through in Long COVID, and in my experience it almost never appears alone. Mitochondrial dysfunction limits the energy available to the muscles supporting circulation. Endothelial damage affects the vessels that have to constrict when you stand. Mast cell activation can drive flushing, tachycardia and blood pressure swings that resemble POTS and sometimes accompany it.
POTS is one form of dysautonomia, and many people with dysautonomia never meet POTS criteria at all. When two patients arrive with identical standing heart rates and still need different treatment, the reason is that the mechanism underneath differs. That is why we test rather than assume, and our diagnostic approach is built to identify which of the six are active for you.
Traveling for POTS treatment
Patients come to the clinic in Plano from outside Texas, and we help with the logistics. If you are considering traveling for care, see getting to treatment for how we assist with flights, accommodation and transport.
Getting evaluated
If your heart races when you stand and you have been told your tests are normal, orthostatic testing is usually the piece that is missing. The evaluation starts with your story and works toward which mechanism is actually driving your symptoms. We see patients in Plano and across the Dallas-Fort Worth area, and we work up all six Long COVID mechanisms rather than treating the tachycardia alone.
COVID Institute, 6957 W Plano Pkwy, Suite 2100, Plano, TX 75093
Request a consultation or call (214) 390-7557
Frequently asked questions
What does a POTS specialist do differently?
A POTS specialist does three things differently. They measure heart rate and blood pressure across a change in position rather than only at rest, because POTS is defined by what happens when you stand and a seated exam will miss it. They look for a secondary cause, such as a post-viral syndrome, thyroid disease or a B12 or thiamine deficiency, rather than stopping at the tachycardia. And they are explicit about whether they are treating the heart rate or the autonomic dysfunction underneath it.
Can I tell whether I have POTS from my symptoms?
No, and this is one of the more important findings in the recent literature. In a 2025 prospective study of 467 highly symptomatic Long COVID patients, the distribution of symptoms showed no significant difference between those who met POTS criteria, those who were tested and did not meet them, and those with no clinical signs of POTS. Objective orthostatic testing is what distinguishes them, in both directions.
Why do my test results come back normal?
Standard cardiac tests are usually performed lying down or sitting. POTS is defined by what happens when you stand, so a resting ECG, an echocardiogram and routine bloodwork can all be normal in someone with clear POTS. The autonomic nervous system is also not directly measurable on a standard blood panel or on routine imaging. The abnormality appears only when someone measures it upright.
Is POTS the same as dysautonomia?
No. Dysautonomia is the umbrella term for autonomic nervous system dysfunction. POTS is one specific, defined form of it, and many people with dysautonomia never meet POTS criteria.
Can Long COVID cause POTS?
POTS is well documented after COVID-19. In a 2025 prospective study of 467 nonhospitalized patients with highly symptomatic Long COVID, 31% met diagnostic criteria for POTS on formal cardiology evaluation. A significant number of Long COVID patients develop POTS-like symptoms, suggesting a post-viral autonomic neuropathy mechanism.
Does POTS go away?
Outcomes vary widely and no honest answer promises resolution. Secondary POTS, meaning POTS acquired from another cause rather than inherited, is potentially reversible. Many patients improve substantially with reconditioning, volume support and treatment matched to their subtype. Some see symptoms resolve, others manage a reduced but persistent version. Recovery trajectories in post-viral POTS are still being studied.
Do I need special salt for POTS?
No. Sodium chloride is sodium chloride, and sea salt or Himalayan salt offers no advantage over table salt for expanding blood volume. Sodium loading is also not appropriate for everyone, particularly with high blood pressure or kidney disease, so agree it with your clinician first.
References
- Björnson M, Wijnbladh K, Törnberg A, Svensson-Raskh A, Svensson A, Ståhlberg M, Runold M, Fedorowski A, Nygren-Bonnier M, Bruchfeld J. Prevalence and Clinical Impact of Postural Orthostatic Tachycardia Syndrome in Highly Symptomatic Long COVID. Circ Arrhythm Electrophysiol. 2025 Oct;18(10):e013629. doi:10.1161/CIRCEP.124.013629. PMID 41025260.
- Raj SR, Guzman JC, Harvey P, Richer L, Schondorf R, Seifer C, Thibodeau-Jarry N, Sheldon RS. Canadian Cardiovascular Society Position Statement on Postural Orthostatic Tachycardia Syndrome (POTS) and Related Disorders of Chronic Orthostatic Intolerance. Can J Cardiol. 2020 Mar;36(3):357-372. doi:10.1016/j.cjca.2019.12.024. PMID 32145864.
- Shaw BH, Stiles LE, Bourne K, Green EA, Shibao CA, Okamoto LE, Garland EM, Gamboa A, Diedrich A, Raj V, Sheldon RS, Biaggioni I, Robertson D, Raj SR. The face of postural tachycardia syndrome – insights from a large cross-sectional online community-based survey. J Intern Med. 2019 Oct;286(4):438-448. doi:10.1111/joim.12895. PMID 30861229.
- Fu Q, Levine BD. Exercise in the postural orthostatic tachycardia syndrome. Auton Neurosci. 2015 Mar;188:86-9. doi:10.1016/j.autneu.2014.11.008. PMID 25487551.
- Pearson L, Maina A, Compratt T, Harden S, Aaroe A, Copas W, Thompson L. Stellate Ganglion Block Relieves Long COVID-19 Symptoms in 86% of Patients: A Retrospective Cohort Study. Cureus. 2023 Sep;15(9):e45161. doi:10.7759/cureus.45161. PMID 37711269.
- Pearson L, Maina A, Compratt T, Harden S, Aaroe A, Copas W, Thompson L. Correction: Stellate Ganglion Block Relieves Long COVID-19 Symptoms in 86% of Patients: A Retrospective Cohort Study. Cureus. 2025 Sep 16;17(9):c295. doi:10.7759/cureus.c295. PMID 40964469.
This page is for education and does not constitute medical advice, diagnosis, or a treatment recommendation for any individual. Do not start, stop or change any treatment, supplement or exercise program based on it. Speak with a qualified clinician about your own situation. If you have chest pain, fainting, or a heart rate that will not settle, seek urgent medical care.