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POTS and Dysautonomia: Understanding and Managing Your Symptoms


You stand up. In those first few seconds, nothing. Then it starts. Your heart rate climbs, your vision blurs at the edges, a wave of heat or dizziness sweeps through you, and your heart is hammering as though you’ve just sprinted for a bus. You haven’t. You’ve just got up from the sofa.

That experience is one of the most commonly reported, and most misunderstood, symptoms in the hypermobility world. It has a name: Postural Orthostatic Tachycardia Syndrome, or POTS. It’s a form of dysautonomia, which is a broad term for when the autonomic nervous system doesn’t regulate the body’s automatic functions properly.

POTS is not rare. It’s not “just anxiety.” It’s not something you can think your way out of. It’s a genuine, physiologically measurable condition that affects an estimated one to three million people in the United States alone [1, 18], and is far more common in those with hypermobility and EDS than in the general population [2].

This page covers everything: what POTS actually is, how it’s diagnosed, why it’s so common in EDS and HSD, what the research says about treatment, and what you can realistically do about it. There’s a lot of ground to cover, so let’s get into it.

Table of Contents
  1. What Is POTS?
  2. What Is Dysautonomia?
  3. The POTS-Hypermobility Connection
  4. How POTS Is Diagnosed
  5. Common Symptoms
  6. Brain Fog: The Cognitive Cost
  7. Why Is Blood Pressure Often Low?
  8. Salt and Fluid: What the Science Actually Says
  9. Exercise: The Most Evidence-Based Treatment
  10. CO2 Tolerance and Breathing
  11. MCAS: The Third Part of the Triangle
  12. Medication Overview
  13. Living With POTS Daily
  14. References

What Is POTS?

POTS stands for Postural Orthostatic Tachycardia Syndrome. Broken down: postural means related to body position, orthostatic means upright or standing, and tachycardia means a fast heart rate. The syndrome part reflects the fact that it’s a cluster of symptoms with an underlying physiological cause.

Formally, POTS is defined as a heart rate increase of at least 30 beats per minute (bpm) within ten minutes of standing, without a significant drop in blood pressure. In adolescents aged 12 to 19, the threshold is 40 bpm. Symptoms must have been present for at least three months and include frequent lightheadedness, palpitations, brain fog, fatigue, or tremulousness, all of which get worse upright and improve when lying down [1].

That 30 bpm figure is important. A normal heart rate response to standing is an increase of around 10-20 bpm. In POTS, the response is excessive, and the heart is essentially trying to compensate for something going wrong in the circulation. When it comes to understanding which subtype you have, that something matters quite a lot.

The Three Main Types of POTS

POTS isn’t a single condition with one cause. It’s better understood as a “final common pathway” that several different mechanisms can produce [12]. The three main subtypes are:

In practice, many people have a mix of these mechanisms, and they can overlap with connective tissue disorders in ways that complicate the picture further [13]. Understanding which subtype predominates actually matters quite a bit, because the same medication that helps one person can make another significantly worse.

What Is Dysautonomia?

Dysautonomia is the umbrella term for any dysfunction of the autonomic nervous system. POTS is one of the most common forms, but it’s far from the only one.

When it comes to dysautonomia, the autonomic nervous system (ANS) is the place to start. It controls everything your body does automatically: heart rate, blood pressure, breathing rhythm, digestion, temperature regulation, bladder function, and more. It does this through two main branches. The sympathetic nervous system (often called “fight or flight”) accelerates things: it speeds up the heart, raises blood pressure, and redirects blood to the muscles. The parasympathetic system (often called “rest and digest”) does the opposite: it slows things down and promotes recovery and digestion.

In healthy people, these two systems work in a constant, seamless dialogue, adjusting to every change in posture, temperature, stress level, and activity. In people with dysautonomia, that dialogue breaks down. The responses are too big, too small, too slow, or simply wrong for the situation.

Other forms of dysautonomia include orthostatic hypotension (blood pressure drops on standing), neurocardiogenic syncope (fainting via vagal response), and multiple system atrophy (a progressive neurological condition). POTS is by far the most commonly encountered in the hypermobility community, though heart rate variability (HRV) changes and other subtle autonomic disturbances are also very common.

The POTS-Hypermobility Connection

If you have EDS or HSD, you’re significantly more likely to have POTS than someone in the general population. This isn’t just clinical observation. The data backs it up.

A 2020 study by Miller and colleagues evaluated 91 adults with POTS using the 2017 hEDS diagnostic checklist. 31% met formal criteria for hEDS, and an additional 24% had generalised joint hypermobility without meeting the full criteria [2]. So roughly half of all POTS patients in that study had some form of hypermobility.

In a large paediatric cohort of 362 young people with POTS, 22.7% had EDS and 39% had HSD, meaning over 60% had some form of hypermobility disorder [3]. Those with EDS also had earlier symptom onset and longer symptom duration. A separate study found that POTS prevalence was significantly higher in young women across the hypermobility spectrum than in healthy controls [19].

And in a 2025 study of women with HSD and hEDS, 58.3% had physician-diagnosed POTS, and one in four had the full clinical triad of hypermobility, POTS, and MCAS [4].

Why Does This Connection Exist?

The leading explanation involves connective tissue. In EDS and HSD, the connective tissue throughout the body is more elastic and less structurally stable than it should be. Blood vessels are also made of connective tissue. When those vessels are more compliant and less supportive, blood tends to pool more readily in the legs and abdomen when you stand up. The veins stretch and widen instead of maintaining tone, and the heart has to work harder to maintain circulation to the brain.

This is sometimes described as “venous pooling”. The upright circulatory system essentially leaks volume downward, triggering the compensatory tachycardia that defines POTS [2, 9].

There’s also emerging evidence around small fibre neuropathy (damage to the small autonomic nerve fibres in the skin and tissues), which is more common in hEDS than previously recognised, and may directly impair the blood vessel constriction that’s supposed to prevent pooling [1, 13].

It’s also worth noting that POTS is increasingly recognised after viral illness. One study found that 79% of long COVID participants met formal POTS criteria, suggesting post-viral illness can unmask autonomic vulnerability in those already predisposed [14]. If you’re still piecing together whether your symptoms point towards hypermobility, it’s worth reading about the full symptom picture of EDS and HSD and how the diagnosis process works.

How POTS Is Diagnosed

POTS is diagnosed primarily through a sustained orthostatic challenge. That means measuring what happens to your heart rate when you go from lying down to standing. There are three main methods.

The Active Stand Test

This is the simplest and most commonly used. You lie flat for at least five to ten minutes while your heart rate and blood pressure are measured. You then stand and measurements are taken at one, three, five, eight, and ten minutes. A sustained rise of at least 30 bpm (or 40 bpm in teenagers) on at least two of those readings, without a significant blood pressure drop, confirms POTS [1].

The Tilt Table Test

A more controlled version. You’re strapped to a table that tilts you to 60-70 degrees upright. This removes the effect of muscle pumping from the legs (which would normally help return blood to the heart during active standing), making it a purer test of autonomic cardiovascular control. It’s used when the active stand result is equivocal or when additional detail is needed.

The NASA Lean Test

A simplified version of the tilt table that can be done at home or in a GP surgery. You lean against a wall at roughly 70-75 degrees while heart rate is measured over ten minutes. It’s not quite as standardised as the active stand or tilt table, but it’s useful when formal testing isn’t immediately available.

Before the test, it’s standard to rule out other causes of tachycardia: anaemia, thyroid dysfunction, dehydration, medications, and arrhythmias all need to be excluded. POTS is a diagnosis of the pattern of response, not just an isolated fast heart rate [1].

It’s worth noting that because many people with EDS are diagnosed via specialist referral, there can be a significant delay between symptom onset and formal diagnosis. If you’re seeking a pathway to diagnosis, understanding how EDS and HSD are formally assessed can help you have more productive conversations with your doctors.

Common Symptoms of POTS

The hallmark symptom is obvious: a pounding, racing heart when you stand up or have been upright for a while. But POTS produces a much broader symptom picture than just tachycardia, and for many people it’s the non-cardiac symptoms that are most disabling.

Symptoms tend to be worse first thing in the morning, in hot conditions, after eating large meals, and during periods of physical deconditioning. They’re generally better when lying down, during cool weather, and when physically conditioned.

Brain Fog: The Cognitive Cost

Brain fog is one of the most debilitating features of POTS, and for a long time it was dismissed or attributed to anxiety. The research now tells a clearer story: there’s a measurable physiological cause.

When you stand up, blood needs to be actively redirected to the brain against gravity. In POTS, this process is impaired. Cerebral blood flow drops, and the brain doesn’t get the oxygen and glucose it needs to function properly. You feel slow, foggy, and unable to concentrate, not because something is psychologically wrong, but because your brain is quite literally getting less blood than it needs [6].

A 2020 study by Wells and colleagues demonstrated this directly. POTS patients showed a 7.8% reduction in cerebral blood flow velocity after a prolonged cognitive stress test, compared to just 1.8% in healthy controls. This translated into measurable psychomotor slowing and increased difficulty concentrating, and crucially, these effects occurred even while seated, not just on standing [6].

A 2025 SPECT imaging study went further, finding that 61% of POTS patients had abnormal cerebral blood flow even while lying down, not just on standing. The most affected regions were the lateral prefrontal cortex (associated with attention, working memory, and executive function) and the sensorimotor cortex [7]. This helps explain why brain fog in POTS isn’t just an “upright” problem. For many people, it’s present to some degree all the time.

There’s also a CO2 connection here, which we’ll cover shortly. When it comes to practical strategies for managing brain fog day to day, the detailed guide on brain fog in EDS, POTS, and long COVID covers the mechanisms and practical approaches in much more depth.

Why Is Blood Pressure Often Low?

POTS is technically defined as tachycardia without a significant blood pressure drop. But many people with POTS do have low blood pressure, particularly when upright, and it’s worth understanding why.

In hyperadrenergic POTS, blood pressure can actually be elevated. But in neuropathic and hypovolaemic subtypes, the inability of blood vessels to constrict properly on standing means that while the heart rate goes up (the compensatory mechanism), the blood pressure stays lower than it ideally should be. The tachycardia is essentially the body’s attempt to maintain adequate output despite low filling pressure.

Chronically low blood pressure, particularly when combined with poor circulation, contributes to fatigue, cognitive impairment, and that pervasive sense of not having enough energy for anything. For a deeper dive into the mechanisms behind low blood pressure and its wider effects on chronic pain and fatigue, that’s covered separately.

It’s also worth noting that some people have what’s called supine hypertension: normal or elevated blood pressure when lying down, dropping to lower levels on standing. This is particularly common in hyperadrenergic POTS and creates a management challenge, because treatments that raise blood pressure (like fludrocortisone) can make this worse.

Salt and Fluid: What the Science Actually Says

You’ve almost certainly been told to “increase salt and water intake” for POTS. This recommendation appears in virtually every POTS management guide, and it’s not wrong, but the picture is more complicated than “eat more salt and you’ll be fine.”

The rationale is straightforward: more sodium in the bloodstream helps retain water through the kidneys, which expands plasma volume. Expanded plasma volume means more blood available to circulate when you stand. The heart doesn’t need to race as hard.

A well-designed 2021 crossover trial by Garland and colleagues tested this directly. When POTS patients followed a high-sodium diet (300 mEq/day) compared to a low-sodium diet (10 mEq/day), their heart rate increase on standing dropped from 60 to 46 bpm, plasma volume improved, and standing norepinephrine decreased. These are meaningful improvements [8].

However, and this is worth emphasising: even on the high-sodium diet, POTS patients’ upright heart rates (117 bpm) and orthostatic tachycardia (46 bpm) remained significantly higher than healthy controls (85 bpm, 19 bpm increase). Salt helps, but it doesn’t fix POTS on its own. It’s a supportive measure, not a cure [8].

Current guidelines recommend 3 litres of fluid per day and 5-10g of salt per day for most adults with POTS [1]. Electrolyte drinks can help with compliance. For people with the hypovolaemic subtype, this is particularly important.

For much more detail on the research, including which forms of salt are most useful and how to approach this practically, the full guide on salt in POTS is worth reading.

Exercise: The Most Evidence-Based Treatment

Exercise is, without question, the most evidence-based intervention for POTS. It’s also the one most likely to provoke disbelief in people who’ve tried to exercise and felt dramatically worse. But those two things aren’t incompatible, and understanding why requires understanding the deconditioning cycle.

The Deconditioning Cycle

POTS is both caused and worsened by physical deconditioning. When you feel awful standing up, you naturally spend more time lying down. But lying down causes the heart to shrink slightly (cardiac atrophy), blood volume to decrease, and the muscles that pump blood back from the legs to weaken. All of which makes POTS worse. Which makes you spend more time lying down. Which makes everything worse again.

Research by Levine and colleagues at UT Southwestern demonstrated this clearly. POTS patients had significantly smaller hearts and lower blood volumes than healthy sedentary controls matched for age and sex. When those patients underwent a structured three-month exercise programme, their cardiac size and mass increased by around 12% and 8% respectively, their blood volume increased by 6%, and their peak VO2 improved by 8% [20]. Most importantly, 53-71% achieved remission of POTS by the end of the three months [9].

A 2025 systematic review confirmed that exercise is now considered first-line non-pharmacological treatment for POTS [10], and a 2023 randomised controlled trial found that a personalised, semi-supervised exercise programme produced significantly better improvements in aerobic fitness, orthostatic symptoms, and exercise tolerance than standard care [11].

The Levine Protocol: How It Works

The key to the protocol is starting horizontal. The reason so many people with POTS feel awful when they exercise is that they try to walk, stand, or do upright cardio, which immediately triggers their symptoms. The Levine approach bypasses this by beginning with exercise that doesn’t require you to be upright [9].

In the first month or two, everything is horizontal or recumbent: rowing machines, recumbent bikes, swimming. This allows the cardiovascular system to begin adapting without the orthostatic challenge that causes symptoms. As fitness improves and heart size and blood volume increase, upright exercise is gradually introduced.

The progression over three months looks roughly like this:

The resistance work is specifically for the lower body and core, because the leg muscles act as a venous pump. Stronger legs means better blood return to the heart on standing, which reduces the tachycardia [9].

For those with EDS or HSD, non-weight bearing options like swimming and rowing are particularly useful given the joint considerations involved. The full guide on exercise for POTS covers how to adapt this for hypermobility, including the specific first steps most people miss.

If you’re new to exercise in this context, the broader starting exercise with hypermobility guide is a sensible starting point.

CO2 Tolerance and Breathing

There’s a breathing component to POTS that doesn’t get nearly enough attention, and the research on it is genuinely striking.

Many people with POTS breathe in a pattern that keeps their CO2 levels lower than optimal. This might not sound like a big deal, CO2 is just what you breathe out, right? But CO2 is one of the primary signals the blood vessels use to regulate their diameter. Low CO2 causes blood vessels to constrict, including the cerebral vessels. It also increases heart rate.

A 2023 clinical study demonstrated this directly in POTS patients: when CO2 was experimentally lowered (hypocapnia), heart rate rose from 82 to 99 bpm, and stroke volume fell, possibly because of increased blood pooling in the capacitance vessels [16]. Another systematic review found consistent evidence linking hypocapnia to tachycardia specifically in POTS [15].

This means that dysfunctional breathing patterns, overbreathing in particular, can actively worsen POTS symptoms. It’s not just a co-occurring problem. When it comes to managing POTS, breathing retraining to improve CO2 tolerance can make a meaningful difference to both symptoms and exercise capacity. The full guide on CO2 tolerance and its impact on breathlessness, fatigue, and chronic pain is worth reading alongside this page.

MCAS: The Third Part of the Triangle

In many clinical and patient communities, you’ll hear about a triad: hEDS/HSD + POTS + MCAS. Mast Cell Activation Syndrome is a condition in which mast cells (immune cells that are involved in allergic responses) trigger excessively or without a clear cause, releasing histamine and other inflammatory mediators in ways that produce wide-ranging symptoms.

The clinical overlap between these three conditions is real and well-documented. A 2025 study of 84 women with HSD or hEDS found that 25% had all three diagnoses: hypermobility, POTS, and MCAS [4]. In a large paediatric POTS cohort, the frequency of MCAS varied from 2% to 87% depending on which diagnostic criteria were used, highlighting both the genuine overlap and the diagnostic uncertainty [5].

A 2021 study of 69 adult POTS patients found that 64% had non-orthostatic symptoms consistent with mast cell activation (including migraines, allergic complaints, skin rashes, and gastrointestinal symptoms), and 42% had both symptoms and at least one elevated biochemical marker (elevated prostaglandins, histamine, or methylhistamine) [17].

Why do these three conditions cluster together? One hypothesis involves the connective tissue: mast cells are concentrated in connective tissue, and in EDS/HSD, there may be local tissue changes that encourage mast cell dysregulation. There’s also likely a bidirectional relationship, mast cell mediators can directly affect blood vessel tone and autonomic function, potentially worsening POTS [17].

It’s worth being clear that the research on this triad is still evolving. Diagnostic criteria for MCAS remain contested, and not every claim you’ll see online about this overlap is based on solid evidence. The full guide on MCAS walks through what’s actually established and what’s still speculative.

Medication Overview

This section is for information only and is not medical advice. Medication decisions should always be made with a qualified clinician who knows your specific situation.

Several medications are used to manage POTS symptoms. None of them cure POTS, and none are approved by most regulatory bodies specifically for POTS (meaning they’re used off-label). They’re generally used to reduce symptom burden while lifestyle and exercise approaches take effect.

Beta Blockers (e.g., Propranolol)

The most commonly prescribed first-line medications. Beta blockers reduce the heart rate response to standing by blocking the effects of adrenaline on the heart. Low-dose propranolol (10-20mg, up to four times daily) has moderate evidence behind it and is the Canadian Cardiovascular Society’s recommended first-line medication option [1]. It’s particularly useful for hyperadrenergic POTS. It should be avoided in people with asthma or very low heart rate at baseline.

Ivabradine

A more selective heart rate reducer that doesn’t block adrenaline receptors, making it useful for people who don’t tolerate beta blockers. It targets the “funny current” in the heart’s pacemaker cells specifically. Evidence quality is moderate [1], and it’s generally better tolerated than propranolol for people with hypermobility-related exercise intolerance.

Fludrocortisone

A synthetic mineralocorticoid that promotes sodium and water retention by the kidneys, effectively expanding blood volume. It addresses the hypovolaemia component of POTS. Electrolyte monitoring (particularly potassium) is important. It can worsen supine hypertension and isn’t appropriate for hyperadrenergic POTS [1].

Midodrine

A vasoconstrictor that works by constricting the blood vessels in the periphery, reducing the pooling problem. It’s taken during the day (not near bedtime, because it raises blood pressure and can cause supine hypertension). Particularly useful for neuropathic and hypovolaemic subtypes [1].

Other options include pyridostigmine (improves nerve-to-blood vessel communication), clonidine or methyldopa (for hyperadrenergic POTS), and in some cases, low-dose desmopressin for severe hypovolaemia. Most people will try lifestyle measures first, then add medication if needed.

Living With POTS Daily

Beyond exercise, salt, and medication, there are several practical strategies that make a real difference to day-to-day life with POTS.

Pacing

One of the most important concepts for anyone with POTS. Pacing means deliberately managing your activity levels to avoid triggering post-exertional crashes. This isn’t about resting more, it’s about distributing activity more intelligently. The complete guide to pacing for EDS and chronic pain covers the evidence and practical strategies. For POTS, horizontal rest breaks throughout the day (not just at the end) can significantly reduce symptom burden.

Compression Garments

Waist-high compression garments (not just below-the-knee stockings) reduce blood pooling by applying external pressure to the legs and abdomen. Research suggests abdominal compression is particularly important, as a significant proportion of blood pools in the abdominal veins, not just the legs [1, 9]. Medical-grade garments (20-30 mmHg or higher) are more effective than standard compression stockings from a chemist.

Sleep Positioning

Sleeping with the head of the bed raised by 10-20 degrees (physically raising the head end, not just using pillows) encourages the kidneys to retain more sodium overnight, which helps maintain plasma volume during the day. This is called “nocturnal anti-Trendelenburg positioning” in the literature. It’s a small change that can have a meaningful cumulative effect. Sleep itself is often disrupted in POTS, and sleep in hypermobility is something worth addressing directly.

Diet Timing and Composition

Large meals divert significant blood flow to the gut for digestion, worsening circulatory distribution. Eating smaller, more frequent meals reduces this effect. High-carbohydrate meals are particularly problematic. Salt-loading before anticipated upright activity (such as before exercise or a long day out) can preemptively boost plasma volume. For more on dietary approaches in hypermobility-related conditions, the hypermobility and diet guide covers this well.

Managing Flares

POTS symptoms tend to flare with infections, heat, dehydration, sleep deprivation, and significant stress. Having a flare plan helps: oral rehydration salts, horizontal rest, compression, reduced activity, and not abandoning the exercise programme entirely but scaling back temporarily. The guide on managing EDS flares is applicable here. Avoid the trap of complete rest for extended periods, this accelerates deconditioning and makes recovery harder.

Physical Countermeasures

Simple physical manoeuvres can acutely reduce symptoms: leg crossing, calf raises, squatting, or tensing the leg muscles all increase venous return and can buy you time in situations where you need to stand. Some people find cooling strategies (cool packs, cold water on the face or neck) helpful for managing heat-triggered symptoms.

Napping is a double-edged sword. Short naps can help manage fatigue, but excessive horizontal time feeds deconditioning. There’s some practical guidance on this in the guide on napping in chronic conditions.

When it comes to the broader musculoskeletal picture, understanding the mechanisms behind chronic pain in fibromyalgia and hypermobility is valuable context for anyone navigating multiple overlapping diagnoses. And for those interested in nutritional support alongside exercise, creatine for hypermobility and EDS has some genuinely useful research behind it.

References

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