POTS
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding POTS
Postural Orthostatic Tachycardia Syndrome (POTS) is a form of autonomic dysfunction characterized by an excessive heart rate increase of more than 30 beats per minute (bpm) upon standing, without significant orthostatic hypotension. This condition involves impaired venous return and blood pooling in the lower extremities, causing reduced cerebral perfusion and symptoms of orthostatic intolerance such as dizziness, lightheadedness, and brain fog. POTS primarily affects young women and significantly impacts quality of life, with symptoms often worsening throughout the day and improving when lying down.
Recognizing POTS
Common symptoms and warning signs to look for
Severe dizziness or lightheadedness when standing up that improves when lying down
Heart racing (tachycardia) exceeding 30 bpm increase within 10 minutes of standing, often exceeding 120 bpm
Brain fog - difficulty concentrating, remembering, and processing information
Exercise intolerance and worsening of symptoms after physical exertion (post-exertional malaise)
Fatigue that is not relieved by rest and worsens with upright posture
What a Healthy System Looks Like
In a healthy individual, the autonomic nervous system maintains precise blood pressure and heart rate regulation through the baroreflex, a negative feedback mechanism centered in the brainstem. When standing upright, approximately 500-800mL of blood pools in the lower extremities due to gravity. The baroreceptors in the carotid arteries and aortic arch detect this decrease in stretch and signal the sympathetic nervous system to release norepinephrine, causing vasoconstriction (venoconstriction and arteriolar constriction) to maintain venous return. The muscle pump in the legs activates with movement, pushing blood back to the heart. Normal blood volume (normovolemia), healthy vascular tone, and responsive baroreceptors ensure adequate cardiac filling and cerebral perfusion. The heart rate increase upon standing is typically modest (10-15 bpm), stabilizing within seconds to minutes through baroreflex-mediated sympathetic overactivity modulation.
How the Condition Develops
Understanding the biological mechanisms
POTS involves multiple interconnected mechanisms of autonomic dysfunction: (1) Blood Pooling and Impaired Venous Return - hypovolemia (reduced plasma volume) and failure of venoconstriction cause severe blood pooling in the lower extremities upon standing, reducing cardiac filling and triggering compensatory tachycardia; (2) Baroreflex Dysfunction - impaired baroreceptor sensitivity fails to trigger adequate sympathetic overactivity response, while baroreflex buffering is compromised; (3) Hyperadrenergic POTS - excessive norepinephrine release (>600 pg/mL upon standing) causes heightened sympathetic overactivity, anxiety-like symptoms, tremor, and tachycardia; (4) Small Fiber Neuropathy - denervation of small unmyelinated autonomic nerve fibers impairs vasomotor control and sudomotor function, disrupting sympathetic outflow; (5) Hypermorphism and EDS - connective tissue hypermobility affects blood vessel integrity, causing vessels to distend inappropriately instead of constricting; (6) Deconditioning - reduced muscle mass and cardiovascular fitness impair the muscle pump mechanism and decrease stroke volume; (7) Mast Cell Activation - mast cell mediators (histamine, tryptase, prostaglandins) released upon upright posture cause inappropriate vasodilation and trigger orthostatic intolerance; (8) Autoimmune Mechanisms - autoantibodies targeting autonomic receptors (adrenergic and muscarinic) have been identified in many POTS patients, causing functional autonomic impairment.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| Norepinephrine (Supine) | 70-750 pg/mL | 100-300 pg/mL | Elevated supine norepinephrine indicates hyperadrenergic POTS with sympathetic overactivity; normal supine with elevated standing levels indicate postural orthostatic tachycardia |
| Norepinephrine (Upright) | 200-1200 pg/mL | 200-500 pg/mL | Excessive upright norepinephrine (>600 pg/mL) confirms hyperadrenergic POTS; exaggerated norepinephrine response indicates baroreflex failure and autonomic dysfunction |
| Renin Activity | 0.6-4.3 ng/mL/hr | 1.5-3.0 ng/mL/hr | Low renin suggests hypovolemia or impaired renin-angiotensin-aldosterone system (RAAS) activation contributing to POTS |
| Aldosterone | 4-31 ng/dL | 10-20 ng/dL | Inappropriately low aldosterone relative to orthostatic stress indicates impaired RAAS response and contributes to hypovolemia |
| Tilt Table Test - Heart Rate | Heart rate increase <20 bpm | <10 bpm | POTS is diagnosed with >30 bpm increase in heart rate upon standing or tilt without significant orthostatic hypotension; tilt table test is the gold standard diagnostic |
| Vitamin B12 | 200-900 pg/mL | 600-900 pg/mL | B12 deficiency can cause autonomic neuropathy and worsen POTS symptoms; common in POTS patients |
| Ferritin | 20-200 ng/mL | 50-100 ng/mL | Iron deficiency (even low-normal ferritin) contributes to reduced blood volume and worsens orthostatic intolerance |
| TSH | 0.4-4.0 mIU/L | 1.0-2.0 mIU/L | Thyroid dysfunction can mimic or worsen POTS symptoms; must rule out hyperthyroidism |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Autonomic Dysfunction (Baroreflex Failure)","contribution":"85% - Impaired baroreceptor sensitivity fails to trigger appropriate sympathetic overactivity response to orthostatic stress; baroreflex buffering is compromised","assessment":"Tilt table test, heart rate variability analysis, sudomotor function testing, baroreflex sensitivity testing"}
{"cause":"Hypovolemia (Low Blood Volume)","contribution":"70% - Reduced plasma volume decreases cardiac filling, triggering compensatory tachycardia; often due to reduced fluid intake, sweating, or impaired RAAS activation","assessment":"Blood volume studies, orthostatic vital signs, renin/aldosterone testing, iron studies"}
{"cause":"Small Fiber Neuropathy","contribution":"55% - Denervation of vasomotor and sudomotor autonomic fibers; confirmed via skin biopsy with reduced intraepidermal nerve fiber density","assessment":"Skin biopsy (quantitative sensory testing), autonomic function testing, QSART"}
{"cause":"Sympathetic Overactivity (Hyperadrenergic State)","contribution":"50% - Excessive norepinephrine release upon standing (>600 pg/mL); may be primary or secondary to hypovolemia and baroreflex unloading","assessment":"Plasma catecholamines (supine and upright), norepinephrine levels"}
{"cause":"Hypermorphism/EDS (Connective Tissue Dysfunction)","contribution":"45% - Joint hypermobility and connective tissue disorders affect blood vessel integrity and appropriate vasoconstriction","assessment":"Beighton score, EDS screening, genetic testing if indicated, clinical hypermorphism assessment"}
{"cause":"Autoimmunity","contribution":"35% - Autoantibodies targeting adrenergic and muscarinic receptors; autoimmune markers often elevated","assessment":"Autoimmune panel, anti-adrenergic receptor antibodies, ganglionic acetylcholine receptor antibodies"}
{"cause":"Deconditioning","contribution":"40% - Reduced cardiac mass and muscle pump efficiency from prolonged sedentary behavior; worsens after illness or bedrest; creates vicious cycle","assessment":"Exercise stress testing, cardiac MRI, physical assessment, 6-minute walk test"}
{"cause":"Mast Cell Activation","contribution":"30% - Histamine and inflammatory mediator release triggering inappropriate vasodilation and orthostatic symptoms","assessment":"Serum tryptase, urinary prostaglandins, histamine metabolites, response to antihistamine therapy"}
Risks of Inaction
What happens if left untreated
{"complication":"Progressive Symptom Worsening","timeline":"Months to years","impact":"Without treatment, POTS typically progresses; symptoms worsen throughout the day; exercise intolerance increases; quality of life declines progressively"}
{"complication":"Severe Exercise Intolerance","timeline":"Progressive","impact":"Inability to exercise or perform upright activities; deconditioning worsens symptoms; creates downward spiral of inactivity and worsening autonomic dysfunction"}
{"complication":"Cognitive Dysfunction","timeline":"Ongoing","impact":"Chronic cerebral hypoperfusion (reduced blood flow to brain) causes persistent brain fog; affects work, school, and daily functioning; may impact career and educational achievement"}
{"complication":"Mental Health Crisis","timeline":"Months","impact":"Depression and anxiety develop secondary to chronic illness; social isolation worsens; reduced quality of life increases suicide risk"}
{"complication":"Loss of Independence","timeline":"1-3 years","impact":"Unable to live independently; may require assistance with daily activities; may need to move back with family; housebound or bedbound state in severe cases"}
{"complication":"Inability to Work or Attend School","timeline":"Variable","impact":"Cannot maintain employment or education due to orthostatic symptoms; financial stress and loss of independence"}
{"complication":"Syncope and Injury","timeline":"Ongoing","impact":"Fainting episodes can cause falls and serious injury; driving restrictions; fear of standing; reduced safety and independence"}
{"complication":"Complete Social and Economic Marginalization","timeline":"2-5 years","impact":"Inability to maintain employment; loss of insurance; financial ruin; complete dependency on caregivers for daily activities"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Tilt Table Test","purpose":"Gold standard for POTS diagnosis","whatItShows":"Heart rate and blood pressure response to upright tilt; documents >30 bpm increase without significant hypotension; distinguishes POTS from other forms of orthostatic intolerance"}
{"test":"Heart Rate Variability (HRV) Analysis","purpose":"Assess autonomic nervous system and baroreflex function","whatItShows":"Reduced HRV indicates autonomic dysfunction; altered sympathetic/parasympathetic balance; impaired baroreflex sensitivity"}
{"test":"Plasma Catecholamines (Supine and Standing)","purpose":"Evaluate hyperadrenergic component and sympathetic overactivity","whatItShows":"Norepinephrine and epinephrine levels supine and upright; hyperadrenergic POTS shows >600 pg/mL norepinephrine upright"}
{"test":"Small Fiber Neuropathy Testing","purpose":"Identify autonomic neuropathy contributing to POTS","whatItShows":"Reduced intraepidermal nerve fiber density on skin biopsy; quantitative sensory testing abnormalities; sudomotor dysfunction"}
{"test":"Blood Volume Studies","purpose":"Assess hypovolemia and plasma volume status","whatItShows":"Radioisotope studies quantify plasma volume; POTS patients often show 10-20% hypovolemia; confirms volume depletion contribution"}
{"test":"Autoimmune Panel","purpose":"Identify autoimmune contributors to autonomic dysfunction","whatItShows":"ANA, anti-thyroid antibodies, rheumatoid factor; anti-adrenergic receptor antibodies if available"}
{"test":"Comprehensive Metabolic Panel","purpose":"Rule out differentials and assess metabolic contributors","whatItShows":"Electrolytes, kidney function, thyroid function, cortisol, iron studies"}
Our Treatment Approach
How we help you overcome POTS
Healers POTS Recovery Protocol
Healers POTS Recovery Protocol
Diet & Lifestyle
Recommendations for optimal recovery
Recovery Timeline
What to expect on your healing journey
{"initialImprovement":"Weeks 2-4: Reduced heart rate increase upon standing; improved orthostatic tolerance; decreased dizziness severity; better sleep quality; more stable blood pressure with compression therapy","significantChanges":"Months 2-3: Marked reduction in tachycardia; expanded upright tolerance; improved exercise capacity; reduced brain fog; better energy throughout day; less symptom fluctuation; improved baroreflex function","maintenancePhase":"Months 4-6+: Sustained orthostatic stability; able to stand for prolonged periods; returned to work and activities; maintained with lifestyle management; relapse prevention in place; normalized quality of life"}
How We Measure Success
Outcomes that matter
Reduced heart rate increase upon standing (<20 bpm from baseline)
Improved orthostatic tolerance (able to stand 10+ minutes without symptoms)
Increased exercise capacity (can exercise 20+ minutes without post-exertional crash)
Enhanced cognitive function (brain fog resolution)
Reduced dizziness and syncope episodes
Improved quality of life scores
Normalized heart rate variability
Stable blood pressure with posture changes
Return to work and activities of daily living
Maintained improvements at 6-12 month follow-up
Frequently Asked Questions
Common questions from patients
What is the difference between POTS and orthostatic hypotension?
POTS and orthostatic hypotension are both forms of orthostatic intolerance but differ fundamentally. Orthostatic hypotension involves a DROP in blood pressure (>20 mmHg systolic or >10 mmHg diastolic) upon standing, causing dizziness and fainting from insufficient cerebral perfusion. POTS (postural orthostatic tachycardia) involves a NORMAL or increased blood pressure but an EXCESSIVE heart rate increase (>30 bpm) upon standing. The treatments differ significantly - orthostatic hypotension requires different medications than POTS.
Can POTS be cured or will I have it forever?
POTS has a variable prognosis. Many patients, especially those with post-viral onset, experience significant improvement or complete resolution within 2-5 years with appropriate treatment. Young patients, those with shorter symptom duration before treatment, and those who respond well to volume expansion have better outcomes. While some patients have chronic POTS requiring ongoing management, most can achieve substantial symptom reduction and return to near-normal activities with proper treatment targeting the underlying mechanisms.
Why do my symptoms worsen as the day progresses?
POTS symptoms typically worsen throughout the day due to cumulative fluid loss through normal daily activities, upright posture, and possible mast cell activation. Blood volume becomes progressively depleted throughout the day (orthostatic diuresis). Additionally, autonomic fatigue accumulates, and baroreflex function may deteriorate with sustained orthostatic stress. Morning protocols including aggressive hydration, salt, and compression can help minimize this progression.
Is exercise safe with POTS?
Exercise is SAFE and RECOMMENDED for POTS but must be approached carefully to avoid worsening symptoms. The key is exercising in a recumbent or semi-recumbent position (rowing machine, cycling, swimming) initially to avoid upright stress that triggers blood pooling. Graded exercise starting at just 5-10 minutes and very slowly increasing is essential. High-intensity upright exercise can worsen symptoms and trigger post-exertional malaise. Working with a knowledgeable physical therapist experienced in POTS is ideal.
What causes POTS to develop?
POTS often develops after a trigger including viral illness (especially COVID-19, Epstein-Barr virus), surgery, trauma, pregnancy, or puberty. Other contributing factors include genetic predisposition, hypermorphism/EDS, small fiber neuropathy, autoimmune conditions, and deconditioning after illness. The common pathway is disruption of autonomic function (particularly baroreflex), blood volume regulation (hypovolemia), and/or sympathetic overactivity.
How is POTS treated with medication?
POTS medications include: Beta-blockers (propranolol, metoprolol) to control heart rate and reduce sympathetic overactivity; Fludrocortisone to increase blood volume and treat hypovolemia; Midodrine to promote vasoconstriction and reduce blood pooling; Ivabradine specifically for POTS heart rate control; Pyridostigmine for neuropathic POTS subtypes. Not all patients require medication - many improve substantially with lifestyle modifications including hydration, salt, compression, and exercise alone.
Medical References
- 1.1. Sheldon RS, Grubb BP 2nd, Olshansky B, et al. 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope. Heart Rhythm. 2015;12(6):e41-e63. doi:10.1016/j.hrthm.2015.03.029
- 2.2. Raj SR, Guzman JC, Harvey P, et al. Canadian Cardiovascular Society Position Statement on Postural Orthostatic Tachycardia Syndrome. Can J Cardiol. 2020;36(5):641-654. doi:10.1016/j.cjca.2019.12.010
- 3.3. Low PA, Sandroni P, Joyner M, Shen WK. Postural tachycardia syndrome (POTS). J Cardiovasc Electrophysiol. 2009;20(3):352-358. doi:10.1111/j.1540-8167.2008.01407.x
- 4.4. Benarroch EE. Postural tachycardia syndrome: a heterogeneous and multifactorial disorder. Mayo Clin Proc. 2012;87(12):1214-1225. doi:10.1016/j.mayocp.2012.08.013
- 5.5. Garland EM, Raj SR, Black BK, Harris PA, Robertson D. The hemodynamic and neurohormonal phenotype of postural tachycardia syndrome. Neurology. 2007;69(8):755-763. doi:10.1212/01.wnl.0000267633.68982.47
- 6.6. Fedorowski A. Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. J Intern Med. 2019;285(4):352-366. doi:10.1111/joim.12852
- 7.7. Arnold AC, Ng J, Raj SR. Postural tachycardia syndrome - Pathophysiology, diagnosis & management. Cleve Clin J Med. 2018;85(3):245-259. doi:10.3949/ccjm.85a.17050
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome POTS.