Your Heart Isn't Overreacting. Your Nervous System Is Under-Regulated.
POTS — Postural Orthostatic Tachycardia Syndrome — is one of the most misunderstood and underdiagnosed conditions we see. The classic presentation: you stand up, your heart rate jumps 30+ beats per minute within ten minutes, and you feel dizzy, lightheaded, breathless, or like you might faint. You might also have brain fog, fatigue, nausea, headache, heat intolerance, and a general sense that your body is not cooperating.
For many patients, the path to diagnosis takes years. POTS is invisible on standard workups. Your labs are normal. Your ECG is normal. Your echocardiogram is normal. You're told you have anxiety, deconditioning, or are just "sensitive." Meanwhile you're building your life around how far you can stand from a place to sit down.
POTS is real, it's physiological, and it has identifiable mechanisms. It's also something we can meaningfully support.
What's Actually Happening
Normal blood pressure regulation depends on a rapid, coordinated response when you move from lying or sitting to standing. Gravity pulls blood toward the lower body — about 500-800ml shifts downward within seconds of standing. Your autonomic nervous system detects the drop in venous return to the heart, triggers vasoconstriction in the peripheral vessels (especially the legs), and increases heart rate modestly to maintain cardiac output and brain perfusion. In healthy individuals, this adjustment takes 15-30 seconds and is imperceptible.
In POTS, this regulatory response fails. The peripheral vasculature doesn't constrict efficiently. Blood pools in the lower extremities and abdomen. Venous return to the heart drops. Instead of compensating through vasoconstriction, the body over-relies on heart rate increase — a less effective mechanism. The heart races to try to maintain output. The brain gets less blood than it needs. Symptoms follow.
The diagnostic criterion is a heart rate increase of ≥30 beats per minute (or ≥40 in patients under 19) within 10 minutes of standing, without a significant drop in blood pressure (which would indicate orthostatic hypotension rather than POTS).
What's causing the failed vasoconstriction varies by POTS subtype — and understanding the subtype matters for treatment.
POTS Is Not One Thing
Hyperadrenergic POTS. Driven by excessive norepinephrine release on standing — the sympathetic nervous system is chronically over-activated. Heart rate and blood pressure both tend to rise with standing. Patients often feel anxious, tremulous, and jittery. Associated with genetic variations in norepinephrine transporter function.
Neuropathic POTS. Caused by damage or dysfunction of the small fiber autonomic nerves in the legs — the nerves responsible for constricting peripheral blood vessels when you stand. Without that vasoconstriction, blood pools. Often associated with prior viral illness, autoimmune processes, or metabolic nerve injury (diabetes). Small fiber neuropathy on skin biopsy is a common finding.
Hypovolemic POTS. Blood volume is chronically low — either from low aldosterone, impaired renin-angiotensin-aldosterone system function, or insufficient sodium and fluid intake. Less blood to begin with means more dramatic pooling when standing.
Post-viral and autoimmune POTS. Increasingly recognized since COVID-19. An immune-mediated attack on autonomic ganglia or adrenergic receptors. Autoantibodies against alpha-1, beta-1, and beta-2 adrenergic receptors, as well as muscarinic receptors, have been found in a subset of POTS patients. Long COVID POTS follows this mechanism in many cases.
Mast Cell Activation Syndrome (MCAS) overlap. A significant proportion of POTS patients have concurrent MCAS — mast cell dysregulation that causes episodic flushing, GI symptoms, skin reactions, and cardiovascular instability. The two conditions share a common thread of autonomic dysregulation and are commonly co-diagnosed.
Ehlers-Danlos Syndrome (hEDS) overlap. Hypermobility of connective tissue affects vessel wall compliance — vessels that should be stiff enough to constrict are instead stretchy, allowing greater blood pooling. POTS, hEDS, and MCAS form a well-recognized triad.
Where TCM Comes In
POTS maps closely onto several TCM patterns involving deficiency of the body's ability to hold and anchor qi and blood upward.
Spleen and Heart Qi Deficiency. The Spleen governs the raising of clear qi upward (the functional equivalent of maintaining venous return and adequate perfusion of the head). When Spleen Qi is deficient, things sink — blood pools, energy sags, and the brain doesn't receive adequate nourishment. Heart Qi deficiency produces the palpitations and poor cardiac response.
Kidney Yang Deficiency. The Kidney provides the foundational warming and driving energy for all organ function. When Kidney Yang is deficient, circulation is impaired, extremities are cold, and the body lacks the reactive capacity to compensate for positional changes.
Blood Deficiency with Empty Heat. Insufficient blood volume (which maps onto hypovolemic POTS) with compensatory false heat — palpitations, flushing, heat intolerance, anxiety, and night sweats.
Liver Wind. The tremulousness, palpitations, and nervous system dysregulation of hyperadrenergic POTS correspond closely to Liver Wind patterns — excessive upward and outward movement of nervous energy.
How We Approach It
POTS treatment at GoodMedizen is always individualized to the suspected subtype and the specific pattern presenting.
Acupuncture has documented effects on autonomic nervous system tone and heart rate variability — the measure of how flexibly the autonomic nervous system responds to changing demands. Improving heart rate variability is associated with better orthostatic tolerance. Specific point protocols address the TCM pattern driving the presentation, support blood volume and venous return, and calm sympathetic over-activation.
Chinese herbal medicine tailored to the TCM pattern — Spleen-raising formulas (Bu Zhong Yi Qi Tang and modifications), blood-nourishing formulas, and Kidney Yang tonics depending on what's operating.
Functional medicine assessment. We look at blood volume markers (plasma volume, aldosterone, renin), sodium and fluid regulation, adrenal function, small fiber neuropathy markers, autoimmune autonomic antibodies where clinically indicated, and MCAS markers (tryptase, histamine, prostaglandins). We also assess for hEDS overlap.
Lifestyle and foundational support. Increased sodium and fluid intake (for hypovolemic presentations), compression garments, recumbent and graduated exercise protocols, elevation of the head of the bed. These are first-line interventions with strong evidence and we guide patients in implementing them specifically.
Mast cell support when MCAS is part of the picture — dietary histamine management, mast cell stabilizing compounds, and addressing the gut dysbiosis that often underlies MCAS.
When to Consider Us
- You have a POTS diagnosis and want integrative support beyond beta-blockers and salt loading
- You have orthostatic symptoms (dizziness, palpitations, fatigue on standing) that haven't been formally evaluated
- Your POTS started after a viral illness, including COVID-19
- You have concurrent hypermobility (hEDS) or mast cell activation alongside the POTS
- You want to understand the subtype of your POTS and address the root mechanism
- Standard treatments haven't been sufficient and you want to add integrative layers
Selected References
- Raj, S. R. (2013). Postural tachycardia syndrome (POTS). Circulation, 127(23), 2336–2342.
- Fedorowski, A. (2019). Postural orthostatic tachycardia syndrome: Clinical presentation, aetiology and management. J Intern Med, 285(4), 352–366.
- Blitshteyn, S., & Chopra, P. (2018). POTS: A heterogeneous and multifactorial disorder. Prog Cardiovasc Dis, 61(3–4), 369–375.
- Vernino, S., et al. (2021). Postural tachycardia syndrome: State of the science. Auton Neurosci, 235, 102836.
- Goldstein, D. S., et al. (2002). Dysautonomias: Clinical disorders of the autonomic nervous system. Ann Intern Med, 137(9), 753–763.