POTS Is Neurological, Not Cardiogenic: Understanding Dysautonomia
- Marcia Cristiane Perretto

- 2 hours ago
- 4 min read

Postural Orthostatic Tachycardia Syndrome (POTS) is often misunderstood. Because the most noticeable symptom is a rapid heart rate, many people are told the problem must be cardiac. In reality, POTS is not a heart disease. It is a neurological disorder rooted in autonomic dysfunction3, and that distinction matters more than most people realize.
For individuals living with POTS, especially those with Ehlers-Danlos syndrome (EDS) or other hypermobility conditions, symptoms can be intense, unpredictable, and difficult to explain. Understanding why the heart is racing — and why the heart itself is not the primary issue — is a critical step toward effective management and long-term improvement.
What Is POTS and How It Affects the Autonomic Nervous System
POTS is a form of dysautonomia, meaning a disorder of the autonomic nervous system. This system controls involuntary functions such as heart rate, blood pressure, vascular tone, temperature regulation, and digestion.
Clinically, POTS is defined by a sustained increase in heart rate of at least 30 beats per minute (40 bpm in adolescents)5 within 10 minutes of standing, without a significant drop in blood pressure. Importantly, most individuals with POTS have structurally normal hearts.8 The heart is responding appropriately to faulty signals rather than malfunctioning on its own.
This distinction is central to understanding why traditional cardiology-based approaches often fail to fully address symptoms.
Why POTS Is Not a Heart Disease
In healthy individuals, standing causes blood to pool temporarily in the lower body.8 The autonomic nervous system compensates by tightening blood vessels and modestly increasing heart rate to maintain cerebral blood flow.
In POTS, this compensation system does not work efficiently. Blood vessels fail to constrict appropriately, blood volume may be low, and autonomic signaling becomes dysregulated. The brain senses reduced blood flow and responds by driving the heart rate higher.
The result is compensatory tachycardia, not heart disease.
Treating POTS as a cardiogenic condition often leads to partial or ineffective care. Managing heart rate alone without addressing autonomic regulation, vascular tone, and blood volume leaves the underlying problem unresolved.
Mechanisms Behind Heart Rate Changes in POTS
Several overlapping mechanisms contribute to autonomic dysfunction in POTS:
Blood pooling in the lower extremities due to impaired vasoconstriction
Low circulating blood volume (hypovolemia)
Sympathetic nervous system overactivation, particularly in hyperadrenergic POTS
Peripheral autonomic nerve dysfunction, including small fiber neuropathy
Impaired baroreceptor signaling, which disrupts blood pressure regulation
Each of these factors increases the workload on the autonomic nervous system and drives the heart rate higher as a compensatory response.1
Types and Causes of POTS
POTS is not a single condition but a syndrome with multiple contributing pathways1:
Neuropathic POTS
Often associated with damage or dysfunction of small autonomic nerve fibers, particularly in the legs. Poor vascular control leads to excessive blood pooling and orthostatic intolerance.
Hypovolemic POTS
Characterized by chronically low blood volume, making it harder to maintain adequate circulation when upright.
Hyperadrenergic POTS
Driven by excessive sympathetic nervous system activation, resulting in elevated norepinephrine levels, tremor, anxiety, and pronounced tachycardia.
POTS may develop after infections, surgery, trauma, pregnancy, or prolonged immobilization. Autoimmune mechanisms are increasingly recognized5, particularly in patients with overlapping connective tissue disorders.
POTS and Ehlers-Danlos Syndrome
The connection between POTS and EDS is well documented.7 Connective tissue laxity can impair vascular support, allowing excessive blood pooling and placing greater demand on autonomic regulation.
Individuals with hypermobile EDS often experience:
Increased orthostatic intolerance
Greater symptom fluctuation
Slower recovery from autonomic stress
This overlap is one reason comprehensive care for POTS frequently extends beyond cardiology and into neurology, physical therapy, and connective tissue–informed rehabilitation.
Common Symptoms of POTS
Symptoms typically worsen when upright and improve when lying down.4 Common features include:
Rapid heart rate upon standing
Dizziness or near-fainting
Fatigue and exercise intolerance
Brain fog and cognitive slowing
Cold or discolored extremities
Headaches, nausea, and visual disturbances
Because these symptoms overlap with anxiety, cardiac conditions, and metabolic disorders, careful evaluation is essential.
How POTS Is Diagnosed
Diagnosis is based on symptom history and objective testing, most commonly the tilt table test5 or active stand test. Diagnostic criteria include:
Sustained heart rate increase meeting POTS thresholds
Absence of significant blood pressure drop
Chronic symptoms of orthostatic intolerance
Additional testing may assess autonomic reflexes, blood volume, and comorbid conditions such as MCAS, EDS, or autoimmune disorders.
Treatment and Management Strategies for POTS
Because POTS is neurological, management focuses on supporting autonomic function,2 not correcting a heart defect.
Non-Pharmacological Strategies
Increasing fluids and sodium under medical guidance
Compression garments to reduce blood pooling
Recumbent and gradually progressive exercise programs
Postural retraining and pacing strategies
Lifestyle modifications to reduce autonomic stress
Medications
While no medications are FDA-approved specifically for POTS, off-label options may include volume expanders, vasoconstrictors, or agents that modulate heart rate and autonomic signaling.
Managing Comorbidities in POTS
Effective care often requires addressing overlapping conditions such as:
Autoimmune disorders
Small fiber neuropathy
A multidisciplinary approach improves outcomes and reduces symptom burden over time.
Prognosis and Long-Term Outlook
POTS can be life-altering, but it is not progressive heart disease. With appropriate education, targeted rehabilitation, and individualized care, many patients experience meaningful improvement.2
Understanding that POTS is neurological, not cardiogenic, helps patients and providers pursue strategies that actually align with the biology of the condition. Clinics like ActifyPT in Boca Raton specialize in this systems-based approach, integrating autonomic regulation, movement science, and connective tissue–aware care.
Key Takeaways: Understanding Neurological POTS
POTS is a disorder of the autonomic nervous system, not the heart
Tachycardia is a compensatory response, not cardiac failure
Management must address blood volume, vascular tone, and autonomic regulation
Physical therapy plays a critical role in improving orthostatic tolerance
Treating comorbid conditions is essential for long-term stability
References and Further Reading
References
Cleveland Clinic. (n.d.). Postural orthostatic tachycardia syndrome (POTS).https://my.clevelandclinic.org/health/diseases/16560-postural-orthostatic-tachycardia-syndrome
Dysautonomia International. (n.d.). Postural orthostatic tachycardia syndrome (POTS).https://www.dysautonomiainternational.org/page.php?ID=30
Johns Hopkins Medicine. (n.d.). Postural orthostatic tachycardia syndrome (POTS).https://www.hopkinsmedicine.org/health/conditions-and-diseases/postural-orthostatic-tachycardia-syndrome
National Institute of Neurological Disorders and Stroke. (n.d.). Postural orthostatic tachycardia syndrome (POTS).https://www.ninds.nih.gov/health-information/disorders/postural-orthostatic-tachycardia-syndrome
National Institutes of Health. (n.d.). Postural orthostatic tachycardia syndrome. In PubMed Central.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600095/
Osmosis. (n.d.). Postural orthostatic tachycardia syndrome (POTS).https://www.osmosis.org/learn/Postural_orthostatic_tachycardia_syndrome
POTS UK. (n.d.). Postural tachycardia syndrome (PoTS).https://www.potsuk.org
Vanderbilt Autonomic Dysfunction Center. (n.d.). Postural orthostatic tachycardia syndrome.
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