Types of POTS
At some point, you’ve probably been told there are three types of POTS and asked yourself which one fits your symptoms. It is a reasonable question and it has a slightly awkward answer. The different types of POTS aren’t boxes people fit into, and most patients carry symptoms of more than one. This distinction can sound academic until you notice it decides which treatment gets used first.
POTS subtypes
The subtype names describe what is driving the tachycardia in a given person. They are not separate diseases, and a patient is not assigned to one for life.
The Canadian Cardiovascular Society position statement, from a major cardiology society, describes POTS as a heterogeneous syndrome with likely several underlying pathophysiological processes, and states plainly that POTS is not a specific disease.1
A 2018 review in Drugs takes the same position from the other direction. It sets out five proposed subtypes based on pathophysiology, and then spends its argument on the overlap between them, concluding it’s crucial to understand each component of POTS in relation to the other symptoms rather than as distinct parts.2
So the honest framing is, subtyping is a clinical tool for deciding what to try first. If a page tells you there are exactly three types and that you are one of them, it is over-simplifying a condition the literature has not settled.
Two of these mechanisms come up most often in post-viral POTS.
Hyperadrenergic POTS
The hyperadrenergic pattern consists of excess sympathetic nervous system activity. The body behaves as though it is under threat, more or less continuously, and a racing heart is one expression of a much wider state.
What it tends to look like. A strong sense of internal adrenaline. Tremor. Anxiety alongside the physical symptoms instead of before them. Blood pressure up, not down, on standing. Sharp spikes under stress. Temperature and sweating changes.
How it is identified. In the ivabradine trial, the hyperadrenergic subtype was defined by a standing plasma norepinephrine above 600 pg per mL together with an abnormal tilt table test.3 That is a research threshold rather than something every clinic measures, and its absence does not mean the pattern is not there.
If your symptoms include sudden surges of adrenaline arriving without a trigger, go here to learn more about adrenaline dumps in POTS.
What tends to help. The mechanism here is sympathetic overactivity, not a shortage of circulating volume, which means loading up on fluid and salt can be disappointing, one of the more common sources of frustration in POTS.
Interventions aimed at the sympathetic system itself are the better match. For example, a stellate ganglion block places local anesthetic around the cluster of sympathetic nerves in the neck to quiet overactivity.
On medication, one trial is worth knowing about because it enrolled this subtype of POTS. In a randomized, double-blind, placebo-controlled crossover trial of 22 patients with hyperadrenergic POTS, ivabradine significantly lowered heart rate and improved both physical and social functioning on a standard quality-of-life measure.3
(Consult with your practitioner before trying any treatment options)
The trial was small and enrolled one subtype, which is exactly why the subtype question comes before the prescription. A medication helping hyperadrenergic POTS is not automatically the right choice for someone whose problem is blood volume.
Hypovolemic POTS
The hypovolemic pattern is inadequate blood volume to maintain circulation against gravity. There is not enough fluid in the system to keep the brain supplied when you stand, the heart beats faster to compensate.
What it looks like. Symptoms improve with fluids and salt. Symptoms worsen with heat, dehydration and prolonged standing.
Getting help. Because the shortfall here is volume, not signaling, the simplest measures often show the most impact, such as increased fluid and salt intake, and compression garments to reduce pooling in the legs.
One thing worth stating, because the supplement aisle suggests otherwise. Sodium chloride is sodium chloride. Sea salt and Himalayan salt is not better than ordinary table salt for blood volume.
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. Consult with your own practitioner instead of increasing salt intake on your own.
Why most people have both
If you read the two lists and recognized yourself in each of them, it’s not a sign you have misunderstood something.
Most people with POTS have variations of both mechanisms. What differs is the proportion, and the proportion is what changes the treatment order. Someone whose picture is mostly hypovolemic will often get further with volume expansion than with anything aimed at the sympathetic system. Someone whose picture is mostly hyperadrenergic tends to find the reverse, and can spend months on salt and fluids wondering why nothing shifted.
This is also why the published reviews keep returning to overlap rather than clean categories.2
The useful question in a consultation is “which half is louder in me right now”, not “which type am I”, and the answer can change over time.
Primary and secondary
There is a second way of dividing POTS, getting far less attention than the subtypes.
Primary dysautonomia is genetic, and includes conditions such as Ehlers-Danlos Syndrome. Secondary dysautonomia is acquired, caused by something else, and because it was acquired it is not necessarily permanent.
Post-viral POTS, including POTS after COVID, is secondary.
This makes it a different situation from an inherited condition, and it is the reason the workup should hunt for a cause rather than stop at the label. If you want to know where POTS sits inside the wider condition, see dysautonomia specialist and treatment.
Other proposed subtypes
The published classification runs wider than the two mechanisms above. The 2018 Drugs review names five proposed subtypes, adding neuropathic, joint-hypermobility-related and immune-related to the hyperadrenergic and hypovolemic patterns.2
If you have been given one of those labels, a label is a starting point for a conversation, not a fixed answer about what is happening in your body.
This page highlights those three subtypes because they stand in the published literature and does not attempt to define their mechanisms, because doing so properly needs more than a paraphrase.
How subtype gets worked out
Subtyping sits downstream of the diagnosis itself. POTS has to be confirmed against the published diagnostic criteria before any subtype question is worth asking. If you want to learn more about testing it’s covered on how POTS is diagnosed.
Once diagnosis is established, the subtype question is answered mostly by pattern and by response. What makes symptoms worse. What has already been tried and what it did. Whether blood pressure rises or falls on standing.
Because the answer can show up as a failure, a treatment you were disappointed with is diagnostic information, not wasted time. A course of salt and fluids changing nothing is a finding worth bringing to an appointment.
Getting evaluated
Working out which mechanism dominates is part of the evaluation, not something you settle at home in advance. POTS is one presentation of dysautonomia, and dysautonomia is one of six mechanisms assessed in post-viral illness. For what POTS is and how it is treated overall, see POTS specialist and treatment.
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Frequently asked questions
How many types of POTS are there?
Published reviews describe five proposed subtypes based on pathophysiology, and they overlap rather than acting as separate categories. Many clinic pages say three. The Canadian Cardiovascular Society position statement describes POTS as a heterogeneous syndrome with several underlying processes and states that it is not a specific disease, so the subtype names are best treated as descriptions of what is driving the tachycardia rather than as fixed diagnoses.
What is hyperadrenergic POTS?
Hyperadrenergic POTS is the pattern driven by excess sympathetic nervous system activity, not by low blood volume. It tends to present with a strong sense of internal adrenaline, tremor, anxiety arriving alongside the physical symptoms, blood pressure that climbs rather than drops on standing, and symptoms that spike under stress. In the trial that studied it most directly, it was defined by a standing plasma norepinephrine above 600 pg per mL together with an abnormal tilt table test.
Is hyperadrenergic POTS worse than other types?
Hyperadrenergic POTS is often harder to treat with the standard first steps, though not worse. The mechanism is sympathetic overactivity, not low blood volume, so fluid and salt loading tends to help less than it does in the hypovolemic pattern. The mismatch is a common reason people conclude treatment does not work for them, when the issue is the treatment was aimed at the other mechanism.
Can you have more than one type of POTS?
Yes, and most people do. Published reviews emphasize the overlap between subtypes and recommend understanding each component in relation to the others rather than as distinct parts. The practical question is which mechanism is dominant at the moment, and that can change over time.
Does the type of POTS change the treatment?
Yes, and it’s the main reason subtyping is valuable. Volume expansion with fluids, salt and compression addresses the hypovolemic mechanism most directly. Interventions aimed at the sympathetic nervous system suit the hyperadrenergic pattern better. Medication choice follows the same logic, which is why a drug studied in one subtype is not automatically the right choice in another.
Is POTS after COVID a specific type?
Post-viral POTS is classed as secondary, not primary, meaning it was acquired rather than inherited, and acquired is not the same as permanent. In terms of mechanism it commonly shows the hyperadrenergic pattern, with sympathetic overactivity and low parasympathetic tone, though features of low blood volume are frequently present alongside it.
References
- 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.
- Zadourian A, Doherty TA, Swiatkiewicz I, Taub PR. Postural Orthostatic Tachycardia Syndrome: Prevalence, Pathophysiology, and Management. Drugs. 2018 Jul;78(10):983-994. doi:10.1007/s40265-018-0931-5. PMID 29943373.
- Taub PR, Zadourian A, Lo HC, Ormiston CK, Golshan S, Hsu JC. Randomized Trial of Ivabradine in Patients With Hyperadrenergic Postural Orthostatic Tachycardia Syndrome. J Am Coll Cardiol. 2021 Feb 23;77(7):861-871. doi:10.1016/j.jacc.2020.12.029. PMID 33602468.
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.