You stand up from the couch and your heart takes off like you just sprinted across a parking lot. Your vision narrows. Your legs feel heavy and strange. You grab the counter and wait for it to pass.
You have been to your primary care doctor, maybe a cardiologist, maybe a neurologist. Your bloodwork came back normal. Your EKG looked fine. Someone told you it was anxiety. Someone else said you needed to exercise more. And now you are sitting here searching the internet because you know, in your body, that something is actually wrong.
If that sounds familiar, you are not alone. And you are probably not anxious. You may have POTS, a type of dysautonomia that affects an estimated 1 to 3 million Americans and is misdiagnosed as anxiety in over 70% of cases.
We built this 28-question assessment based on the peer-reviewed clinical research cited throughout this article. It evaluates your symptoms against all four POTS subtypes, screens for commonly associated conditions like Ehlers-Danlos Syndrome and Mast Cell Activation Syndrome, and generates a personalized results profile you can print and bring to your doctor.
It takes about 5 minutes. No login or email required.
If you have already taken the quiz, keep reading to understand what your results mean.
Postural Orthostatic Tachycardia Syndrome (POTS) is a form of dysautonomia characterized by an abnormal increase in heart rate after standing up. It is not a heart condition in the traditional sense. It is a failure of the autonomic nervous system to properly regulate blood flow when you change position.
To be diagnosed with POTS, a patient typically meets these criteria:
These diagnostic criteria were established through decades of research, beginning with Schondorf and Low's landmark 1993 paper in Neurology and refined through the 2015 Heart Rhythm Society Expert Consensus Statement (Sheldon et al., Heart Rhythm 12:e41-63) and the 2019 NIH Expert Consensus Workshop (Vernino, Raj, Stiles et al., Autonomic Neuroscience 2021).
POTS predominantly affects young women (5:1 female-to-male ratio) with a peak onset age of 14, according to Shaw and colleagues' survey of 4,835 patients (Journal of Internal Medicine, 2019). The average patient waits 4.9 years and sees 7 different physicians before receiving a correct diagnosis.
That diagnostic delay is the reason this page exists.
This is the single most important distinction for anyone who has been told their symptoms are "just anxiety." The symptom overlap is real, which is why 77% of POTS patients are initially told their problem is psychiatric (Miller et al., Journal of Internal Medicine, 2019, n=4,835), and 69% receive an anxiety disorder diagnosis before anyone identifies the autonomic dysfunction.
Both POTS and anxiety can produce a racing heart, chest tightness, dizziness, shortness of breath, tremor, and a general sense that something is very wrong. But the pattern is different.
Symptoms that point toward POTS:
Symptoms that point toward anxiety:
The fastest way to start distinguishing the two: measure your heart rate lying down for 5 minutes, then measure it again after standing for 2, 5, and 10 minutes. If you consistently see a 30+ bpm increase on standing that resolves when you lie back down, that is not anxiety. That is an autonomic nervous system problem, and it has a name.
A study by Raj and colleagues at Vanderbilt confirmed that POTS patients are not more anxious than the general population. The sympathetic hyperactivation in POTS, especially the hyperadrenergic subtype, physiologically mimics anxiety because the body genuinely is in fight-or-flight mode. But the cause is autonomic, not psychological.
POTS is not a single disease. It is a collection of overlapping subtypes, each driven by a different mechanism. Most patients have features of more than one type, and a 2024 study of 378 patients by Angeli and colleagues in Nature Scientific Reports found no statistically significant symptom differences among phenotypes. Still, understanding your dominant pattern changes the treatment approach.
Mechanism: Damage to small nerve fibers (C-fibers and A-delta fibers) prevents proper blood vessel constriction in the lower body. Blood pools excessively in the legs and abdomen when you stand.
Key symptoms: Acrocyanosis (feet and legs turn purple or blue-red on standing), reduced sweating in the lower body, burning or tingling in the feet and hands, visible leg swelling after standing.
How common: Roughly 50% of POTS patients (Thieben et al., Mayo Clinic Proceedings, 2007, n=152).
Diagnostic clues: Abnormal QSART (sweat testing), reduced intraepidermal nerve fiber density on skin biopsy (sensitivity ~88%), standing plasma norepinephrine typically below 600 pg/mL.
Mechanism: Excessive norepinephrine (adrenaline) release creates an overactive fight-or-flight response. The sympathetic nervous system is stuck in overdrive.
Key symptoms: Blood pressure rises (not drops) on standing, tremor, excessive sweating (especially upper body), anxiety-like adrenaline surges triggered by position changes, pallor.
How common: 29 to 60% of patients depending on the diagnostic threshold used (Thieben et al., 2007).
Diagnostic clues: Standing plasma norepinephrine at or above 600 pg/mL, systolic blood pressure increase of 10+ mmHg upon standing. Shannon and colleagues identified the first genetic cause in the New England Journal of Medicine (2000): a mutation reducing norepinephrine transporter activity by over 98%.
Mechanism: Low total blood volume (typically about a 13% deficit) means there is simply not enough blood to fill the expanded vascular space when you stand up.
Key symptoms: Dramatic improvement with salt and fluid intake, heat intolerance, orthostatic headaches that worsen when upright and improve lying down, feeling best first thing in the morning before dehydration accumulates.
How common: Some degree of hypovolemia is present in the majority of POTS patients, making it arguably the most universal feature.
Diagnostic clues: Raj and colleagues at Vanderbilt (Circulation, 2005, n=29) documented the "renin-aldosterone paradox": despite significant hypovolemia, patients show paradoxically low renin and aldosterone levels, the opposite of normal compensatory physiology. Formal blood volume testing via DAXOR BVA-100 (I-131 labeled albumin) quantifies the deficit. Standard bloodwork cannot detect it because equal plasma and red blood cell losses yield a normal hematocrit.
Mechanism: Autoantibodies target receptors on the autonomic nervous system, blocking vasoconstriction and enhancing cardiac stimulation simultaneously.
Key symptoms: Post-viral onset (especially after COVID-19, mono, or flu), coexisting autoimmune conditions (Hashimoto's, celiac, Sjogren's, lupus), family history of autoimmune disease.
How common: Li and colleagues (Journal of the American Heart Association, 2014, n=14) found activating autoantibodies to adrenergic receptors in all 14 POTS patients tested. Gunning and colleagues (JAHA, 2019, n=55) found 89% had elevated alpha-1 adrenergic receptor antibodies.
Diagnostic clues: Ganglionic acetylcholine receptor antibodies (commercially available), adrenergic receptor autoantibodies (research labs, CellTrend GmbH in Germany offers ELISA panels). About 20% of POTS patients have a diagnosed coexisting autoimmune condition (Blitshteyn 2015; Raj et al. 2016).
If you have POTS, there is about a one-in-three chance you also have features of Ehlers-Danlos Syndrome, Mast Cell Activation Syndrome, or both. This overlap is so consistent that clinicians now recommend screening for all three whenever any one is present.
Ehlers-Danlos Syndrome (hEDS) involves lax connective tissue throughout the body, including blood vessel walls. When those vessels are too stretchy, blood pools more easily in the lower body on standing. Miller and colleagues (Autonomic Neuroscience, 2020) found that 31% of POTS patients met hEDS diagnostic criteria, and roughly 80% of hEDS patients reported POTS symptoms. Signs include joint hypermobility ("double-jointed"), easy bruising, stretchy skin, chronic joint pain, and frequent subluxations.
Mast Cell Activation Syndrome (MCAS) involves inappropriate release of histamine and other inflammatory mediators, causing flushing, hives, GI symptoms, food and medication sensitivities, and anaphylaxis-like reactions. When mast cells degranulate, the resulting vasodilation drops blood pressure and triggers reflex tachycardia, worsening the POTS pattern.
Cheung and colleagues (2021) found that among patients with both POTS and EDS, 31% also had MCAS, a 32-fold increase in odds compared to patients without both conditions. If you scored positive for EDS or MCAS flags on the quiz above, bring those results to a geneticist (for EDS) or allergist/immunologist familiar with MCAS.
Most POTS cases have an identifiable trigger. Knowing what started your symptoms helps clinicians determine your subtype and treatment approach.
COVID-19 has become the single largest driver of new POTS cases. A 2025 analysis of over 65 million patient records by Dulal, Grubb, and Maraey (European Heart Journal) found POTS incidence increased roughly 14-fold from pre-pandemic levels. A prospective study of 467 long COVID patients by Fedorowski and colleagues (Circulation: Arrhythmia and Electrophysiology, 2025) found that 31% met full POTS criteria. The Yale LISTEN cohort (n=578) confirmed 28.9% of long COVID patients reporting new-onset POTS.
Proposed mechanisms include autoimmune molecular mimicry against autonomic receptors, vagal nerve damage, mast cell activation triggered by spike protein (Theoharides et al., Annals of Allergy, Asthma, and Immunology, 2024), and disruption of the renin-angiotensin system. Post-COVID POTS typically develops 6 to 8 months after infection.
Other viral triggers include Epstein-Barr virus (mononucleosis), influenza, and cytomegalovirus. Post-viral onset accounts for 28 to 50% of all POTS cases.
This is where the story changes from what you will find on WebMD or Mayo Clinic's patient pages, because most POTS resources treat it as a purely cardiovascular problem. It is not. For a significant subset of patients, the problem starts in the brain.
The brainstem houses the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, and the rostral ventrolateral medulla. These are critical autonomic control centers that regulate heart rate, blood pressure, and vascular tone. They sit in a region that is particularly vulnerable to the rotational and shearing forces of concussion.
Kanjwal and colleagues (Cardiology Journal, 2010) described 8 previously healthy patients who developed POTS after TBI. Six of 8 experienced syncope, 6 of 8 developed significant cognitive dysfunction, and all were unable to maintain employment. Heyer and colleagues (Clinical Journal of Sport Medicine, 2016) found that over 40% of adolescents with persistent post-concussion symptoms showed evidence of orthostatic tachycardia. Notably, post-concussion POTS shows equal gender distribution, unlike typical POTS, suggesting a distinct pathophysiological mechanism (Pearson et al., Child Neurology Open, 2022, n=268).
Standard POTS medications (propranolol, midodrine, ivabradine) treat the downstream cardiovascular symptoms. They do not address the upstream brain injury driving the autonomic dysregulation. For patients whose POTS began after a concussion or head injury, treatment that targets the Central Autonomic Network, the brain circuit connecting the insular cortex, anterior cingulate cortex, hypothalamus, and brainstem nuclei, can address the actual cause rather than managing the effect.
Functional NeuroCognitive Imaging (fNCI) can identify which specific brain regions are underperforming, and the EPIC Treatment protocol targets those regions with intensive, individualized rehabilitation. This matters because a concussion patient on propranolol may get heart rate control but will never resolve the brain fog, fatigue, and exercise intolerance until the brain injury itself is treated.
You do not need a tilt table to get preliminary data. The active standing test (also called the NASA Lean Test or "poor man's tilt table") requires only a heart rate monitor or blood pressure cuff and a timer. Here is the protocol:
Step 1: Lie flat for 5 to 10 minutes in a quiet room. Record your resting heart rate and blood pressure.
Step 2: Stand up and lean your back against a wall (for balance, not support). Stay as still as possible.
Step 3: Record your heart rate and blood pressure at 2 minutes, 5 minutes, and 10 minutes. Write down any symptoms you experience and when they start.
What to look for:
Repeat the test on 2 to 3 different days at similar times of day for reliability. Avoid caffeine, large meals, and heavy exercise for at least 2 hours before testing.
This does not replace a formal tilt table test, which remains the diagnostic gold standard. But objective data is far more persuasive than describing vague symptoms when you walk into a clinic. Print the numbers and bring them to your doctor.
There are currently no FDA-approved drugs for POTS. Every medication used is off-label. But effective treatment exists, especially when matched to the right subtype.
Every POTS patient, regardless of subtype, should start here:
The most robust treatment evidence in POTS comes from structured exercise. Developed by Dr. Benjamin Levine at the Institute for Exercise and Environmental Medicine in Dallas, the protocol starts entirely with recumbent exercises (rowing, swimming, recumbent cycling) and gradually introduces upright activity over 7 to 8 months.
Fu and colleagues (Hypertension, 2010/2011, n=27) showed that 53% of completers no longer met POTS criteria, with increased cardiac mass, stroke volume, and blood volume. George and colleagues (Heart Rhythm, 2016, n=103 completers) confirmed 71% remission in community settings.
The critical caveat: about 60% of patients cannot complete the full program. If you also have ME/CFS with post-exertional malaise, standard graded exercise may be harmful. The approach must be tailored.
The most exciting recent development. Stavrakis and colleagues (JACC: Clinical Electrophysiology, 2024, n=25) published a double-blind, sham-controlled randomized trial of daily transcutaneous vagus nerve stimulation at the tragus of the ear. After 2 months, orthostatic tachycardia decreased from 26.4 to 17.6 bpm in the active group versus no change in the sham group. The treatment also decreased anti-adrenergic autoantibodies and TNF-alpha inflammatory markers. This is the first evidence of a non-pharmacological intervention that appears to modify the disease process rather than just managing symptoms.
This myth causes real harm when it leads to dismissive care. Yes, POTS patients are often deconditioned. But the deconditioning is a result of the disease, not the cause.
Oldham and colleagues (2016) demonstrated that POTS patients have low ventricular filling pressures during exercise, the opposite of what you see in simply deconditioned individuals. Telling a POTS patient to "just exercise more" without starting with recumbent exercise and progressing slowly is counterproductive and can make symptoms worse.
If you took the quiz above and scored in the moderate or high range, or if your symptom history matches what is described in this article, here is a practical path forward.
Start with the active standing test. Measure your heart rate lying down and standing on 2 to 3 separate days. Print the numbers and symptoms.
Request a tilt table test. Ask your doctor for a referral to a cardiologist or neurologist who specializes in autonomic disorders. This is the formal diagnostic gold standard. Expect it to cost $1,000 to $3,000 depending on location and insurance.
Screen for the trifecta. If you are unusually flexible, bruise easily, or have joint pain, ask about Ehlers-Danlos evaluation. If you get unexplained flushing, hives, or react to many foods and medications, ask about MCAS testing (serum tryptase, urine histamine metabolites).
Ask about subtype-specific testing. If you suspect neuropathic POTS, ask for a skin biopsy (intraepidermal nerve fiber density) and QSART. If you suspect hyperadrenergic POTS, ask for supine and standing plasma norepinephrine levels.
Do not accept "it's anxiety" without a standing heart rate test. A 30-second heart rate check lying down and standing is all it takes to raise or lower suspicion for POTS. If your doctor will not do this, find one who will.
Most POTS treatments target the symptoms. Beta-blockers slow your heart rate. Midodrine squeezes your blood vessels. Salt and fluids expand your blood volume. These can help, but if you still have brain fog, crushing fatigue, and exercise intolerance after months of standard treatment, the medications are managing the downstream effects without addressing what is actually driving the dysfunction.
At Cognitive FX in Provo, Utah, we start where other POTS programs stop: the brain.
On your first day, functional NeuroCognitive Imaging (fNCI) maps blood flow dynamics across 56 brain regions while you perform cognitive tasks. This shows us exactly which parts of your Central Autonomic Network are underperforming and how the dysfunction maps to your specific symptoms. Two patients with identical POTS diagnoses can have very different patterns of brain involvement requiring very different treatment.
Your results guide a personalized one-week Treatment program built around structured cycles of cardiovascular exercise, targeted neuromuscular therapy, vestibular recalibration, breathing mechanics training, and autonomic reconditioning. Each cycle takes advantage of the post-exercise cognitive boost, a window when your brain is optimally primed to adapt and rewire. You receive more therapeutic contact in one week than most patients get in 6 to 12 months of traditional appointments.
If your POTS started after a concussion, a viral illness like COVID, or if standard treatment has controlled your heart rate but left you still unable to function, the problem may not be cardiovascular. It may be neurological. And we can see it on imaging.
Your next step is a free consultation with our team to discuss your symptoms, review your history, and determine whether imaging-guided treatment is right for your situation.
