Low Blood Pressure & POTS
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Low Blood Pressure & POTS
Postural Orthostatic Tachycardia Syndrome (POTS) is a form of autonomic dysfunction where your heart rate increases excessively by more than 30 beats per minute when you stand up, without a significant drop in blood pressure. This condition involves impaired blood vessel constriction and blood pooling in the legs, causing reduced blood flow to the brain and resulting in dizziness, fatigue, brain fog, and exercise intolerance. POTS primarily affects young women aged 15-50 and can severely impact daily functioning, with symptoms typically worsening throughout the day and improving when lying down.
Recognizing Low Blood Pressure & POTS
Common symptoms and warning signs to look for
Severe dizziness or lightheadedness when standing up that immediately improves when lying down
Heart racing (tachycardia) with more than 30 bpm increase within 10 minutes of standing, often exceeding 120 bpm
Brain fog - difficulty concentrating, remembering things, and processing information clearly
Exercise intolerance with worsening symptoms after physical activity (post-exertional malaise)
Chronic 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 sophisticated negative feedback mechanism centered in the brainstem. When standing upright, approximately 500-800mL of blood naturally pools in the lower extremities due to gravity. The baroreceptors in the carotid arteries and aortic arch detect this decrease in arterial stretch and immediately signal the sympathetic nervous system to release norepinephrine, causing vasoconstriction of both veins and arterioles to maintain venous return to the heart. The skeletal muscle pump in the legs activates with movement, pushing blood back toward 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 beats per minute), stabilizing within seconds to minutes through baroreflex-mediated autonomic 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 of 10-20%) and failure of appropriate venoconstriction cause severe blood pooling in the lower extremities upon standing, reducing cardiac preload and triggering compensatory tachycardia; (2) Baroreflex Dysfunction - impaired baroreceptor sensitivity fails to trigger adequate sympathetic vasoconstrictor response, while baroreflex buffering is compromised, leading to excessive heart rate fluctuations; (3) Hyperadrenergic POTS - excessive norepinephrine release (>600 pg/mL upon standing) causes heightened sympathetic overactivity, anxiety-like symptoms, tremor, and palpitations; (4) Small Fiber Neuropathy - denervation of small unmyelinated autonomic C-fibers impairs vasomotor control and sudomotor function, disrupting sympathetic outflow to blood vessels; (5) Hypermobility and Ehlers-Danlos Syndrome - connective tissue hypermobility affects blood vessel integrity and collagen structure, 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, creating a vicious cycle; (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 adrenergic (alpha and beta) and muscarinic acetylcholine receptors have been identified in 30-50% of POTS patients, causing functional autonomic impairment through molecular mimicry.
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 baseline sympathetic overactivity; normal supine with elevated standing levels indicates postural orthostatic response |
| Norepinephrine (Upright - 10 minutes) | 200-1200 pg/mL | 200-500 pg/mL | Excessive upright norepinephrine (>600 pg/mL) confirms hyperadrenergic POTS subtype; exaggerated response indicates baroreflex failure and autonomic dysfunction |
| Renin Activity (Plasma) | 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 reduced blood volume in POTS |
| Aldosterone (Serum) | 4-31 ng/dL | 10-20 ng/dL | Inappropriately low aldosterone relative to orthostatic stress indicates impaired RAAS response and contributes to hypovolemia and orthostatic intolerance |
| Tilt Table Test - Heart Rate Response | Heart rate increase <20 bpm | <10 bpm increase | POTS diagnosed with >30 bpm heart rate increase upon standing or tilt without significant orthostatic hypotension; gold standard diagnostic test |
| Vitamin B12 (Serum) | 200-900 pg/mL | 600-900 pg/mL | B12 deficiency can cause autonomic neuropathy and worsen POTS symptoms; functional B12 deficiency common even with normal serum levels |
| Ferritin (Serum) | 20-200 ng/mL (women), 30-300 ng/mL (men) | 50-100 ng/mL | Iron deficiency (even low-normal ferritin <50 ng/mL) contributes to reduced blood volume, impaired oxygen delivery, and worsens orthostatic intolerance |
| TSH (Thyroid-Stimulating Hormone) | 0.4-4.0 mIU/L | 1.0-2.0 mIU/L | Thyroid dysfunction can mimic or worsen POTS symptoms; hyperthyroidism must be ruled out as it causes tachycardia and autonomic dysfunction |
| Comprehensive Metabolic Panel | Within reference ranges | Optimal organ function | Rules out kidney disease, electrolyte imbalances, and metabolic disorders that can cause orthostatic symptoms |
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 vasoconstrictor response to orthostatic stress; baroreflex buffering is compromised leading to excessive heart rate fluctuations","assessment":"Tilt table test, heart rate variability analysis, sudomotor function testing, baroreflex sensitivity testing, Valsalva maneuver"}
{"cause":"Hypovolemia (Low Blood Volume)","contribution":"70% - Reduced plasma volume (10-20% below normal) decreases cardiac filling, triggering compensatory tachycardia; often due to reduced fluid intake, excessive sweating, or impaired RAAS activation","assessment":"Blood volume studies (radioisotope), orthostatic vital signs, renin/aldosterone testing, iron studies, hydration status assessment"}
{"cause":"Small Fiber Neuropathy","contribution":"55% - Denervation of vasomotor and sudomotor autonomic fibers; confirmed via skin biopsy with reduced intraepidermal nerve fiber density; often post-viral or autoimmune in origin","assessment":"Skin biopsy with quantitative analysis, quantitative sensory testing (QST), quantitative sudomotor axon reflex test (QSART), autonomic function testing"}
{"cause":"Sympathetic Overactivity (Hyperadrenergic State)","contribution":"50% - Excessive norepinephrine release upon standing (>600 pg/mL); may be primary hyperadrenergic POTS or secondary to hypovolemia and baroreflex unloading","assessment":"Plasma catecholamines (supine and upright), norepinephrine levels, clonidine suppression test if indicated"}
{"cause":"Joint Hypermobility/EDS (Connective Tissue Dysfunction)","contribution":"45% - Joint hypermobility and connective tissue disorders affect blood vessel integrity, venous valve function, and appropriate vasoconstriction; vessels distend excessively instead of constricting","assessment":"Beighton score for hypermobility, EDS screening questionnaire, genetic testing if indicated, clinical assessment of skin elasticity and joint laxity"}
{"cause":"Autoimmunity","contribution":"35% - Autoantibodies targeting adrenergic (alpha-1, beta-1, beta-2) and muscarinic (M2, M3) acetylcholine receptors; autoimmune markers often elevated; molecular mimicry from infections","assessment":"ANA, ESR, CRP, anti-thyroid antibodies, anti-adrenergic receptor antibodies, ganglionic acetylcholine receptor antibodies, autoimmune panel"}
{"cause":"Deconditioning","contribution":"40% - Reduced cardiac muscle mass, stroke volume, and muscle pump efficiency from prolonged sedentary behavior; worsens after illness, surgery, or bedrest; creates vicious cycle with POTS","assessment":"Exercise stress testing, cardiac MRI, physical assessment, 6-minute walk test, VO2 max testing"}
{"cause":"Mast Cell Activation","contribution":"30% - Histamine and inflammatory mediator release triggering inappropriate vasodilation, increased vascular permeability, and orthostatic symptoms; often overlaps with POTS","assessment":"Serum tryptase during flares, 24-hour urinary N-methylhistamine, chromogranin A, prostaglandin D2, response to antihistamine trial"}
{"cause":"Post-Viral Trigger","contribution":"25% - Viral infections (COVID-19, EBV, CMV, HHV-6, enteroviruses) trigger autoimmune responses, autonomic dysfunction, and small fiber neuropathy; increasingly common post-COVID","assessment":"Viral titers, autoimmune markers, timeline correlation with infection, exclusion of active infection"}
Risks of Inaction
What happens if left untreated
{"complication":"Progressive Symptom Worsening","timeline":"Months to years without treatment","impact":"Without treatment, POTS typically progresses; symptoms worsen progressively throughout the day; exercise intolerance increases; quality of life declines significantly; patients may become housebound or bedbound"}
{"complication":"Severe Exercise Intolerance and Deconditioning","timeline":"Progressive over 6-12 months","impact":"Inability to exercise or perform upright activities; severe deconditioning worsens symptoms further; creates downward spiral of inactivity, muscle atrophy, cardiovascular deconditioning, and worsening autonomic dysfunction"}
{"complication":"Cognitive Dysfunction and Brain Fog","timeline":"Ongoing with chronic cerebral hypoperfusion","impact":"Chronic reduced blood flow to the brain causes persistent brain fog, memory problems, and difficulty concentrating; affects work performance, academic achievement, and daily functioning; may impact career trajectory and educational goals"}
{"complication":"Mental Health Crisis","timeline":"6-18 months of untreated symptoms","impact":"Depression and anxiety develop secondary to chronic illness and functional limitations; social isolation worsens mental health; reduced quality of life significantly increases risk of suicidal ideation; requires mental health intervention"}
{"complication":"Loss of Independence and Function","timeline":"1-3 years in severe cases","impact":"Unable to live independently; may require assistance with activities of daily living; may need to move back with family or into assisted living; housebound or bedbound state in severe untreated cases"}
{"complication":"Inability to Work or Attend School","timeline":"Variable, often within 1-2 years","impact":"Cannot maintain employment or education due to orthostatic symptoms and cognitive impairment; financial stress, loss of insurance, and dependency on disability benefits; significant economic impact"}
{"complication":"Syncope and Injury Risk","timeline":"Ongoing risk","impact":"Fainting episodes can cause falls resulting in head trauma, fractures, and serious injury; driving restrictions affect independence; fear of standing leads to further deconditioning"}
{"complication":"Social and Economic Marginalization","timeline":"2-5 years in severe cases","impact":"Inability to maintain employment; loss of health insurance; financial ruin; complete dependency on caregivers for daily activities; social isolation and relationship breakdown"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Tilt Table Test","purpose":"Gold standard diagnostic test for POTS","whatItShows":"Heart rate and blood pressure response to progressive upright tilt; documents >30 bpm heart rate increase (or >40 bpm in adolescents) without significant orthostatic hypotension; distinguishes POTS from other forms of orthostatic intolerance and vasovagal syncope"}
{"test":"Heart Rate Variability (HRV) Analysis","purpose":"Assess autonomic nervous system balance and baroreflex function","whatItShows":"Reduced HRV indicates autonomic dysfunction; altered sympathetic/parasympathetic balance; impaired baroreflex sensitivity; can track treatment response over time"}
{"test":"Plasma Catecholamines (Supine and Standing)","purpose":"Evaluate hyperadrenergic component and sympathetic overactivity","whatItShows":"Norepinephrine and epinephrine levels in both supine and upright positions; hyperadrenergic POTS shows >600 pg/mL norepinephrine upright; helps distinguish POTS subtypes and guide medication selection"}
{"test":"Small Fiber Neuropathy Assessment","purpose":"Identify autonomic neuropathy contributing to POTS","whatItShows":"Reduced intraepidermal nerve fiber density on skin biopsy; quantitative sensory testing abnormalities; sudomotor dysfunction on QSART; thermoregulatory sweat test abnormalities"}
{"test":"Blood Volume Studies","purpose":"Quantify hypovolemia and plasma volume status","whatItShows":"Radioisotope studies (iodine-131 albumin or chromium-51 labeled red cells) quantify plasma volume and red cell mass; POTS patients often show 10-20% hypovolemia; confirms volume depletion contribution and guides fluid management"}
{"test":"Autonomic Function Testing Battery","purpose":"Comprehensive assessment of autonomic nervous system","whatItShows":"Valsalva maneuver response, deep breathing heart rate response, cold pressor test, and orthostatic vital signs; identifies specific patterns of autonomic dysfunction and baroreflex impairment"}
{"test":"Autoimmune Panel","purpose":"Identify autoimmune contributors to autonomic dysfunction","whatItShows":"ANA, anti-dsDNA, ESR, CRP, anti-thyroid antibodies (TPO, TG), rheumatoid factor; anti-adrenergic and muscarinic receptor antibodies if available; helps identify underlying autoimmune etiology"}
{"test":"Comprehensive Metabolic and Nutritional Panel","purpose":"Rule out differentials and assess metabolic contributors","whatItShows":"Complete blood count, comprehensive metabolic panel, iron studies (ferritin, iron, TIBC), vitamin B12, vitamin D, magnesium, zinc, thyroid function tests (TSH, free T4, free T3), cortisol"}
{"test":"Echocardiogram","purpose":"Assess cardiac structure and function","whatItShows":"Rules out structural heart disease; assesses stroke volume and cardiac output; identifies postural orthostatic changes in cardiac function; small heart size (low stroke volume) common in deconditioned POTS patients"}
Our Treatment Approach
How we help you overcome Low Blood Pressure & POTS
Phase 1: Diagnostic Clarity and Hemodynamic Stabilization (Weeks 1-2)
{"phase":"Phase 1: Diagnostic Clarity and Hemodynamic Stabilization (Weeks 1-2)","focus":"Comprehensive assessment, accurate diagnosis, POTS subtype classification, and immediate symptom management","interventions":"Complete medical history with detailed symptom chronology and trigger identification. Advanced autonomic testing including tilt table test, heart rate variability analysis, and baroreflex sensitivity assessment. Plasma catecholamine testing (supine and upright) to identify hyperadrenergic subtype. Autoimmune panel to identify underlying causes. Small fiber neuropathy evaluation with skin biopsy if indicated. Blood volume assessment to quantify hypovolemia. Immediate interventions: aggressive hydration protocol (3-4 liters daily), salt supplementation (2-10g daily based on subtype), compression garment prescription (waist-high, 30-40 mmHg), pacing and symptom trigger education, sleep hygiene optimization with head-of-bed elevation (6-10 inches), and continuous heart rate monitoring during activities.\n"}
Phase 2: Volume Optimization and Autonomic Support (Weeks 3-8)
{"phase":"Phase 2: Volume Optimization and Autonomic Support (Weeks 3-8)","focus":"Restore blood volume, improve baroreflex function, reduce sympathetic overactivity, decrease blood pooling","interventions":"Continued aggressive hydration and electrolyte protocol with targeted sodium intake. Fludrocortisone therapy (0.1-0.2mg daily) if indicated for hypovolemia to increase blood volume. Midodrine (2.5-10mg TID) for vasoconstriction support and reduced blood pooling. Low-dose beta-blocker therapy (propranolol 10-20mg or metoprolol 25-50mg) for heart rate control in hyperadrenergic subtype. Ivabradine (5-7.5mg BID) as alternative heart rate control without blood pressure effects. Compression therapy optimization with abdominal binders if needed. IV fluid therapy (1-2 liters normal saline) for severely hypovolemic patients. Nutritional optimization addressing iron, B12, and magnesium deficiencies. Gentle recumbent exercise program (rowing, recumbent cycling, swimming) starting at 5-10 minutes. Pacing strategies and heart rate monitoring to prevent post-exertional malaise. Stress management techniques including meditation and breathwork.\n"}
Phase 3: Autonomic Restoration and Immune Modulation (Months 2-4)
{"phase":"Phase 3: Autonomic Restoration and Immune Modulation (Months 2-4)","focus":"Restore autonomic function, address autoimmune and neuropathic components, rebuild exercise tolerance","interventions":"Autoimmune protocols if autoimmune markers present: low-dose naltrexone (LDN), immune-modulating supplements (vitamin D, omega-3, curcumin), dietary modifications (autoimmune protocol diet). Small fiber neuropathy treatment: IV immunoglobulin (IVIG) if severe and autoimmune-mediated, alpha-lipoic acid, acetyl-L-carnitine. Mast cell management if MCAS identified: H1 and H2 antihistamines, mast cell stabilizers (cromolyn, quercetin), low-histamine diet. IV nutrient therapy: magnesium, B-complex vitamins, glutathione for antioxidant support. Gradual exercise progression from recumbent to upright activities, carefully monitored. Vagal tone enhancement through breathing exercises, cold exposure, and gargling. Gut health optimization with probiotics and gut-healing protocols. Continued volume management with adjusted medications. Beta-adrenergic receptor support and baroreflex training exercises.\n"}
Phase 4: Maintenance and Full Function Restoration (Months 5-12+)
{"phase":"Phase 4: Maintenance and Full Function Restoration (Months 5-12+)","focus":"Sustain improvements, optimize function, prevent relapse, return to normal activities","interventions":"Personalized maintenance nutrition plan with adequate hydration and electrolyte support. Continued exercise progression within individual tolerance, gradually increasing upright activity. Stress resilience building through ongoing mind-body practices. Relapse prevention strategies including recognition of early warning signs. Regular monitoring with quarterly autonomic function assessment. Quality of life enhancement through gradual return to social and occupational activities. Return to work and school planning with accommodations as needed. Long-term management planning with medication tapering if appropriate. Patient education for self-management and symptom recognition. Maintenance of healthy lifestyle habits for sustained autonomic health.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Aggressive hydration protocol: 3-4 liters water daily, starting with 16-20oz upon waking, Salt supplementation: 2-10g daily as tolerated and appropriate for POTS subtype (medical supervision required), Compression garments: Waist-high compression stockings (30-40 mmHg) or abdominal binders to reduce blood pooling, Avoid prolonged standing: Shift weight frequently, march in place, or use one-footed standing when unavoidable, Rise slowly from supine/sitting: 3-stage standing (sit up, dangle legs, stand slowly) to allow baroreflex adaptation, Sleep with head elevated: 6-10 inches to reduce nocturnal diuresis and morning orthostatic symptoms, Cool environment: Avoid overheating which causes vasodilation and worsens symptoms; cooling vests helpful, Heart rate monitoring: Continuous monitoring during all activities to stay within target zones and prevent PEM, Pacing and energy management: Activity planning to prevent post-exertional malaise; rest before and after activities, Recumbent exercise: Rowing machine, recumbent bicycle, swimming as primary exercise modalities, Counter-maneuvers: Leg crossing, muscle tensing, toe raises when feeling faint to increase venous return, Shower modifications: Cooler water temperature, shower chair, morning avoidance if symptoms severe
Recovery Timeline
What to expect on your healing journey
Phase 1 (Weeks 1-4): Initial stabilization with lifestyle modifications and medication if indicated; baseline diagnostics completed; some symptom relief begins with hydration, salt, and compression; sleep improvement with head-of-bed elevation.
Phase 2 (Weeks 4-12): Volume optimization and autonomic support; medication titration; marked reduction in heart rate response to standing; improved orthostatic tolerance; reduced dizziness severity; better energy throughout the day.
Phase 3 (Months 3-6): Autonomic restoration and exercise progression; significant symptom improvement (60-80% reduction); return to light activities; improved exercise capacity; brain fog resolution; normalized daily functioning.
Phase 4 (Months 6-12+): Maintenance and full function restoration; sustained orthostatic stability; return to work/school; maintained with lifestyle management; relapse prevention strategies in place; normalized quality of life with 80-100% improvement in compliant patients.
Note: Individual timelines vary based on POTS severity, subtype, adherence to treatment, number of root causes, and coexisting conditions. Post-viral POTS often has better prognosis than autoimmune-mediated POTS.
How We Measure Success
Outcomes that matter
Reduced heart rate increase upon standing to <20 bpm from baseline
Improved orthostatic tolerance - able to stand 10+ minutes without symptoms
Increased exercise capacity - can exercise 20+ minutes without post-exertional malaise
Enhanced cognitive function - resolution of brain fog and improved concentration
Reduced dizziness and syncope/presyncope episodes (80%+ reduction)
Improved quality of life scores ( validated questionnaires like COMPASS-31)
Normalized heart rate variability (HRV) indicating improved autonomic balance
Stable blood pressure with posture changes without excessive fluctuations
Return to work, school, and activities of daily living
Maintained improvements at 6-12 month follow-up without symptom relapse
Reduced need for medications or stable on minimal medication regimen
Improved sleep quality and unrefreshing sleep resolution
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 blood flow to the brain. POTS (postural orthostatic tachycardia syndrome) 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 and management than POTS.
Can POTS be cured or will I have it forever?
POTS has a variable prognosis depending on the underlying cause and subtype. Many patients, especially those with post-viral onset, experience significant improvement or complete resolution within 2-5 years with appropriate treatment. Younger 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 (60-80% improvement) and return to near-normal activities with proper treatment targeting the underlying mechanisms including hypovolemia, autonomic dysfunction, and any autoimmune components.
Why do my symptoms worsen as the day progresses?
POTS symptoms typically worsen throughout the day due to several factors: cumulative fluid loss through normal daily activities and upright posture; orthostatic diuresis (increased urination when upright) leading to progressive volume depletion; autonomic fatigue from sustained sympathetic activation; possible mast cell activation accumulating throughout the day; and natural cortisol decline in the afternoon. Morning protocols including aggressive hydration (16-20oz upon waking), salt intake, compression garments, and avoiding early morning upright activities can help minimize this progression.
Is exercise safe with POTS and what type should I do?
Exercise is SAFE and ESSENTIAL for POTS recovery but must be approached carefully to avoid worsening symptoms. The key is starting with recumbent or semi-recumbent exercises (rowing machine, recumbent stationary cycling, swimming) to avoid upright stress that triggers blood pooling. Graded exercise starting at just 5-10 minutes and very slowly increasing by 1-2 minutes per week is essential. High-intensity upright exercise can worsen symptoms and trigger severe post-exertional malaise. Working with a physical therapist experienced in POTS rehabilitation is highly recommended for safe progression.
What causes POTS to develop suddenly?
POTS often develops after a specific trigger including viral illness (especially COVID-19, Epstein-Barr virus, HHV-6), surgery, trauma, pregnancy, or puberty. The most common trigger is viral infection, with post-viral POTS representing 25-50% of cases. Other contributing factors include genetic predisposition, joint hypermobility/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 nervous system overactivity.
How is POTS treated with medication and do I need it?
Not all POTS patients require medication - many improve substantially with lifestyle modifications alone. When needed, medications include: Beta-blockers (propranolol, metoprolol) to control heart rate and reduce palpitations; Fludrocortisone to increase blood volume by promoting sodium retention; Midodrine to cause vasoconstriction and reduce blood pooling; Ivabradine specifically for heart rate control without affecting blood pressure; Pyridostigmine for neuropathic POTS subtypes; and DDAVP for severe hypovolemia. Medication selection depends on POTS subtype identified through testing.
Medical References
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- 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.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.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.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.Fedorowski A. Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. J Intern Med. 2019;285(4):352-366. doi:10.1111/joim.12852
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- 8.Miller AJ, Raj SR. Pharmacotherapy for postural tachycardia syndrome. Auton Neurosci. 2020;228:102689. doi:10.1016/j.autneu.2020.102689
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