POTS Is Misclassified as a Dysautonomia

POTS Is Misclassified as a Dysautonomia

Pradeep Chopra, MD

Introduction: A Problem of Labels, Not Physiology

Postural Orthostatic Tachycardia Syndrome (POTS) is almost universally described as a form of dysautonomia, meaning a disorder of the autonomic nervous system. This label is repeated in textbooks, medical websites, and patient education materials.

However, when one examines the actual physiology of POTS—particularly in patients with Ehlers-Danlos syndrome (EDS)—this classification becomes questionable.

In many cases, the autonomic nervous system is not failing. On the contrary, it is working exactly as it should. The problem lies elsewhere.

What Dysautonomia Actually Means

Dysautonomia implies that the autonomic nervous system:

• Fails to respond when it should
• Responds inappropriately
• Cannot maintain basic physiological stability

Examples include conditions where blood pressure collapses on standing, heart rate fails to rise when needed, or temperature and sweating are poorly regulated due to nerve failure.

In true autonomic failure, the system is unable to compensate.

This distinction is critical.

What Actually Happens in POTS (Especially in EDS)

In a large subset of POTS patients—particularly those with Ehlers-Danlos syndrome—the sequence of events is mechanical, not neurological:

1. Veins are excessively stretchy
2. Upon standing, blood pools in the pelvis, buttocks, thighs, and legs
3. Venous return to the heart drops
4. Cardiac output to the brain becomes threatened

At this point, the body does exactly what it is designed to do.

The Sympathetic Nervous System Is Doing Its Job

The sympathetic nervous system correctly detects reduced effective circulating volume and responds appropriately:

• Heart rate increases
• Cardiac output rises
• Blood pressure is maintained
• Loss of consciousness is prevented

This is not a malfunction.
This is textbook physiology.

If the autonomic nervous system were dysfunctional, patients would experience immediate hypotension and syncope. Most POTS patients do not.

Instead, they experience tachycardia with preserved blood pressure, which is evidence of an intact and responsive sympathetic system.

To take an example, when someone is running to exercise, they develop tachycardia (increased heart rate) so that more blood is pumped to their muscles. This does not mean they develop dysautonomia.

Tachycardia Is a Compensation, Not a Disease

The elevated heart rate in POTS is often portrayed as pathological. In reality, it is a rescue mechanism.

The heart beats faster because it must:

• Overcome excessive venous pooling
• Maintain cerebral perfusion against gravity
• Compensate for inadequate preload

Calling this response “dysautonomia” is akin to calling an elevated heart rate during exercise a disease.

The response is appropriate; the conditions forcing it are abnormal.

Why Symptoms Still Occur

Patients feel unwell not because the autonomic nervous system is failing, but because it is being pushed to extremes.

Even a correct response has limits:

• The heart cannot indefinitely compensate for severe venous pooling
• Cerebral blood flow may remain marginal
• Sustained sympathetic activation produces fatigue, palpitations, tremor, and brain fog

Symptoms arise from physiological strain, not autonomic incompetence.

How the Dysautonomia Label Became Entrenched

POTS was grouped under dysautonomia largely for practical reasons:

• It involves autonomic reflexes
• It produces orthostatic symptoms
• It does not fit neatly into cardiology or neurology

Over time, the label hardened into assumed truth.

But classification convenience is not the same as mechanistic accuracy.

Why This Mislabeling Matters

Misclassifying POTS as dysautonomia has real consequences:

• Patients are told their “nervous system is broken”
• Treatments focus on suppressing heart rate rather than improving venous return
• Mechanical contributors (such as connective tissue laxity) are underappreciated
• Patients may feel blamed for a “malfunction” rather than understood

For EDS-associated POTS in particular, the core issue is vascular mechanics, not autonomic failure.

A More Accurate Description

A more precise explanation would be:

“In many cases of POTS, especially those associated with Ehlers-Danlos syndrome, the autonomic nervous system is functioning appropriately. The elevated heart rate represents a compensatory response to excessive venous pooling caused by abnormally compliant veins. The problem is not autonomic dysfunction, but an abnormal mechanical load placed on an otherwise intact system.”

This framing aligns with observed physiology and patient experience.

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‍Conclusion

POTS is not a single disease, and it should not be explained with a single label.

In many patients—particularly those with connective tissue disorders—the sympathetic nervous system is not dysfunctional. It is working hard to maintain circulation under unfavorable mechanical conditions.

Calling this dysautonomia obscures the real problem.

Understanding POTS as a compensatory state driven by venous pooling, rather than a failure of the autonomic nervous system, leads to better explanations, better treatments, and better outcomes for patients.

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Olshansky B, Cannom D, Fedorowski A, Stewart J, Gibbons C, Sutton R, Shen WK, Muldowney J, Chung TH, Feigofsky S, Nayak H, Calkins H, Benditt DG. Postural Orthostatic Tachycardia Syndrome (POTS): A critical assessment. Prog Cardiovasc Dis. 2020 May-Jun;63(3):263-270. doi: 10.1016/j.pcad.2020.03.010. Epub 2020 Mar 25. PMID: 32222376; PMCID: PMC9012474.

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Zhao S, Tran VH. Postural Orthostatic Tachycardia Syndrome. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK541074/

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