Understanding POTS

I want to tell you about a patient. I'll call her Maria, though the details are changed to protect her privacy. When Maria first came to see me, she wasn't walking to the bathroom. She was crawling. Every time she stood, her heart would race, the room would spin, and she'd end up on the floor. She'd been to three emergency rooms and been told, more than once, that it was anxiety.

It wasn't anxiety. It was POTS, Postural Orthostatic Tachycardia Syndrome, and Maria's story is one I'm seeing more and more often since 2020.

Why you're hearing about POTS more than you used to

POTS isn't new. But it's become dramatically more common since the COVID-19 pandemic. A large U.S. database study tracking POTS diagnoses before and after 2020 found the incidence rate jumped more than tenfold: from about 1.4 cases per million person-years before the pandemic to over 20 per million after it, with new diagnoses climbing steadily into 2023. Some of that rise likely reflects better awareness and more doctors thinking to test for it. But the researchers behind that study, and others since, believe a real biological effect from COVID-19 infection itself is also driving new cases. POTS now appears to be one of the more common, and more treatable, faces of long COVID.

Dysautonomia: the umbrella term

POTS is one member of a larger family of conditions called dysautonomia: a general term for anything that disrupts the autonomic nervous system, the part of you that runs on autopilot, heart rate, blood pressure, digestion, temperature regulation. Dysautonomia isn't one disease; it's a category. POTS lives inside that category, alongside other conditions like neurocardiogenic syncope (the common fainting spell) and orthostatic hypotension.

What's actually happening in the body?

When you stand up, gravity pulls roughly half a liter of blood down into your legs and abdomen almost instantly. In a healthy system, the autonomic nervous system compensates in a fraction of a second: blood vessels constrict, heart rate ticks up slightly, and blood pressure holds steady. In POTS, that compensation is faulty, and there isn't one single agreed-upon reason why. A few explanations show up repeatedly in the research:

•  Low blood volume (hypovolemia). Many POTS patients are running with less circulating blood volume than they should have, so there's simply less to work with when gravity pulls blood downward.

•  Faulty vessel constriction. In some patients, the nerves that should tighten blood vessels in the legs on standing don't fire strongly enough, so blood pools instead of getting pushed back up, and the heart then races to try to compensate for the drop in return.

•  Autoimmunity. A growing body of research points to autoantibodies that interfere with receptors involved in blood vessel and heart rate regulation, particularly in cases that follow a viral illness.

•  Post-viral triggering. This is where COVID-19 fits in. One proposed mechanism is molecular mimicry: the immune response to the virus ends up cross-reacting with the body's own nerve tissue, disrupting autonomic signaling afterward.

None of these are mutually exclusive, and different patients likely land in different buckets. This is part of why POTS treatment is individualized rather than one-size-fits-all.

POTS vs. orthostatic hypotension

These two get confused constantly, including by physicians who don't specialize in this, so let's be precise:

POTS

When you stand up, your heart rate climbs excessively, by 30 beats per minute or more in adults (40+ in teenagers) within about 10 minutes of standing, while your blood pressure stays relatively stable. Your body is compensating for a circulation problem by racing the heart instead of losing pressure.

Orthostatic hypotension (OH)

When you stand up, your blood pressure itself drops significantly (a drop of 20 mmHg systolic or 10 mmHg diastolic within the first few minutes of standing). Heart rate may or may not change much.

Here's what makes them feel so similar: both are triggered by standing, both come from blood pooling in the legs instead of getting back to the brain efficiently, and both can produce the same dizzy, foggy, about-to-pass-out feeling. The difference is how your body tries, and fails, to compensate: with a racing heart in POTS, or with an outright pressure drop in OH. Diagnosing correctly matters, because the medications that help one can sometimes worsen the other.

A simple at-home self-check

Before you ever get to a specialist or a formal tilt table test, there's a rough screening test you can do at home with nothing more than a home blood pressure cuff and a clock. It's sometimes called the “poor man's tilt table test,” and it's a simplified version of the standing tests used in autonomic clinics.

1.  Lie down for 5 minutes before your first reading. Rest quietly, flat on your back, until you feel settled. Take your blood pressure and pulse. This is your baseline.

2.  Sit up and check again. Take another reading a minute or two after sitting.

3.  Stand up and check at intervals. Take your blood pressure and pulse right after standing, then again at 1, 3, 5, and 10 minutes if you can tolerate it. Standing still (not walking around) matters, leaning your shoulder blades against a wall, heels a few inches out, makes it easier to hold position.

4.  Write down the numbers, all three positions, with times, to bring to your doctor.

What you're looking for:

•  A heart rate rise of 30 bpm or more (40+ if you're a teenager) between lying down and standing, without a significant blood pressure drop, points toward POTS.

•  A blood pressure drop of 20 mmHg systolic or 10 mmHg diastolic or more on standing points toward orthostatic hypotension instead.

A word of caution: please don't do this alone if you have a history of fainting. Have someone nearby, and stop and sit or lie back down right away if you feel like you're going to pass out. This test doesn't replace a formal diagnosis, some people need a full tilt table test or additional autonomic testing to sort out what's really going on, but it's a genuinely useful first data point, and it's the same basic information I ask nearly every new patient with these symptoms to gather before our first visit.

Maria's turnaround

Back to Maria. We didn't start with anything exotic. In order:

1.  Water, a real volume, not a gesture. Most POTS patients are chronically underfilled on blood volume relative to what their circulation needs. We built her up to roughly 2.5–3 liters a day.

2.  Salt and electrolytes. Sodium holds water in the vascular space. Adding electrolyte mixes and increasing dietary salt gave her fluid intake somewhere to stay.

3.  Compression garments. Waist-high compression (not just knee-highs) counteracts the blood pooling in the legs and abdomen that starts the whole cascade.

These three alone took her from crawling to walking with a cane. Then we added the right medication for her physiology, and that's when things really turned: steadier heart rate, fewer crashes, days she could plan around instead of days that planned around her. At one point her volume depletion was severe enough that we sent her for IV fluids at the hospital, and that single infusion reset her system in a way oral fluids alone couldn't. That combination, fluids, salt, compression, targeted medication, and IV support when truly needed, is what got her her life back.

POTS is real, it's measurable, and, especially since 2020, it's far more common than most people realize. If standing up reliably makes you dizzy, foggy, or leaves your heart racing, this deserves a real workup, not a shrug. It's treatable, often with tools far simpler than people expect.

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And if your blood pressure actually rose rather than dropped when you did the home test above, that's not a fluke. There's a whole subtype, hyperadrenergic POTS, that looks different and is treated differently. More on that in a future post.

Selected sources: European Heart Journal – Quality of Care and Clinical Outcomes (2025) on POTS incidence pre/post-COVID; Johns Hopkins Medicine, POTS overview; Frontiers in Neurology (2026) on POTS vs. orthostatic hypotension classification; PMC (2025) review on COVID-19–induced POTS mechanisms (hypovolemia, autoimmunity, molecular mimicry); Frontiers in Medicine (2026) on POTS and platelet storage pool deficiency in long-haulers; Bateman Horne Center, 10-Minute NASA Lean Test clinician protocol, on at-home/passive standing test procedure and diagnostic thresholds.