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There are identifiable mechanisms that can be contributing to a patient's orthostatic intolerance. Many of these mechanisms may result in a lack of oxygen to the brain upon standing. Blood pooling in the veins of the lower body is a major factor in the vast majority of patients with orthostatic intolerance (Streeten, 1999).
The following is a partial list of proposed mechanisms that may be occurring in patients with orthostatic intolerance:
Alpha-receptor dysfunction may be occurring in some POTS patients (Gordon, Opfer-Gehrking, Novak & Low, 2000). Alpha-1 receptors cause peripheral vasoconstriction when stimulated. Alpha-1 receptor supersensitivity may be causing dysautonomia in some patients (Stewart & Erickson, 2002). Others with POTS may have an autonomic neuropathy that predominantly affects the lower extremities. This neuropathy may be resulting in alpha-1 adrenergic denervation hypersensitivity. Denervation hypersensitivity may be provoking the pooling of blood in a number of individuals with this disorder (Stewart & Erickson, 2002).
Beta-receptor supersensitivity may occur with hyperadrenergic states in some people with POTS (Low, 2000). The heart is responding to excessive catecholamine output in these patients. 
Brain-stem dysregulation may be occurring in some POTS patients (Novak, Novak, Opfer-Gehrking, O'Brien & Low, 1998). Researchers have identified a subset of patients with marked orthostatic hypertension, markedly labile blood pressure and troublesome orthostatic symptoms (Low, Schondorf, Novak, Sandroni, Opfer-Gehrking & Novak, 1997, pp. 686-687). These patients present as though they are suffering from baroreflex failure, although the baroreflexes are working. Excessive sympathetic activity is noted, which suggests the possibility of central (presumably brain-stem) dysregulation. One patient reportedly improved after microvascular decompression at the region of the left medulla (Low et al., 1997, p. 687).
Central autonomic regulation abnormalities leading to a hyperadrenergic state are a proposed cause of POTS. However, physicians have yet to determine whether a central abnormality of the autonomic nervous system is the primary mechanism or if the increase in sympathetic activity is an appropriate response to an underlying defect, such as a decreased blood volume or a circulating vasodilator (Jacob & Biaggioni, 1999). Circulating vasodilators are suspected of provoking dysautonomia in disorders such as hyperbradykininism, mast-cell activation and hyperdopaminergic states.
Delayed forms of orthostatic intolerance have been observed in POTS patients. Some physicians believe POTS symptoms should occur within 10 minutes of standing. However, studies on orthostatic intolerant patients prove that some display a delayed form of orthostatic intolerance in which orthostatic hypotension occurs after ten minutes of standing (Streeten & Anderson, 1992). One study showed that out of 23 chronic fatigue patients, 17 had orthostatic tachycardia alone during the initial period of head-up tilt. However, 22 eventually had obvious orthostatic hypotension after an extended period of time (Bou-Holaigah, Rowe, Kan & Calkins, 1995).
Hyperdopaminergic states maybe the underlying problem for some people with orthostatic intolerance. Some patients have been found to have a significant increase in upright (free + sulfconjugated) dopamine levels (Kuchel, Buu, Hamet, Larochelle, Gutkowska, Schiffrin, Bourque & Genest, 1985). Free plasma norepinephrine also tends to be higher in these patients. The excessive dopamine release might be causing natriuresis and vasodilatation, thus contributing to the pathophysiology of this disorder (Jacob & Biaggioni, 1999).
Orthostatic hypotension occurs in some patients with orthostatic intolerance. However, there are physicians who exclude orthostatic hypotension when defining POTS. Orthostatic hypotension is traditionally defined as a fall in systolic blood pressure of 20 mm Hg or more upon standing. Some physicians believe smaller drops in blood pressure associated with symptoms are also significant (Grubb & Karas, 1999). Orthostatic hypotension may become apparent only after prolonged standing. Baroreceptor-initiated reflex tachycardia is a potent physiological mechanism for correcting hypotension (Streeten, 1999). Hence, the standing tachycardia observed in POTS patients is sometimes occurring because the body is attempting to counteract falling blood pressure.
Some patients become more symptomatic than others when their blood pressure drops. Patients who experience few symptoms while hypotensive have a minimal decline in brain blood flow and good dilating blood vessels. Patients who become symptomatic when their blood pressure drops have a greater decline in blood flow to the brain (Coghlan, 2002).
Reduced cerebral blood flow has been noted in several studies of POTS patients.  However, one studydid not report this finding, and concluded that cerebral perfusion and autoregulation in many patients with POTS does not differ from that of normal control subjects (Schondorf, Benoit & Stein, 2005).
A reduction of cardiac output by arrhythmias, bradycardia, or intrinsic cardiac causes of pump failure can cause fainting, or other clinical manifestations of reduced cerebral blood flow (Streeten, 1999). Blood pooling in the lower body may also cause reduced blood flow to the brain. It has been reported that a person with POTS can have a 28% decrease in brain blood flow upon standing (Robertson, 2000). A normal person will have about a 9% decrease in blood flow to the brain upon standing. Transcranial Doppler ultrasonography is useful in detecting a reduction in cerebral blood flow (Fredman, Biermann, Patel, Uppstrom & Auer, 1995). Orthostatic symptoms have been attributed to impaired cerebral perfusion, even in the absence of a significant fall in blood pressure (Jacob & Biaggioni, 1999). 
Central nervous system abnormalities may be occurring in patients with reduced cerebral blood flow (Hermosillo, Jauregui-Renaud, Kostine, Marquez, Lara & Cardenas, 2002). One study reported that continuous observation of the Doppler recording in patients with postural tachycardia showed intermittent fluctuation of the cerebral blood flow velocity, with an oscillatory pattern (Hermosillo et al., 2002). This fluctuation in cerebral blood flow velocity occurred in spite of there being no systemic hypotension. This study also showed that when compared with neurocardiogenic syncope patients, those with postural tachycardia had larger variations of the pulsatility index (systolic velocity-diastolic velocity/mean velocity). The results suggest that patients with postural tachycardia, on standing up, could have an inefficient regulation of cerebral blood vessels (Hermosillo, et al., 2002). These findings led the researchers to conclude that central nervous system abnormalities may play a pivotal role in the pathogenesis of postural tachycardia syndrome (Hermosillo, et al., 2002).
Reduced venous return is one of the main mechanisms that results in POTS symptoms. Venous return can be reduced due to conditions such as low plasma volume (see hypovolemia), venous pooling and denervation (Low, 2000). A hyperadrenergic state may result as the body attempts to compensate for these abnormalities. Conditions resulting in reduced venous return often overlap or occur because of one another. The following are some abnormalities that can result in reduced venous return:
Sympathetic Overactivity is observed in many POTS patients. The sympathetic overactivity can be secondary to a number of factors, some of which may be peripheral denervation, venous pooling, or end-organ dysfunction (Low et al, 1998). Hyperadrenergic states with elevated norepinephrine levels are often found in patients with sympathetic overactivity. One study found that 29% of POTS patients had elevated norepinephrine levels upon standing, and the mean level was 531 pg/mL (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007). Norepinephrine is similar to adrenaline and is a natural vasoconstrictor. Genetic or acquired deficits in norepinephrine activation may result in hyperadrenergic states that lead to orthostatic intolerance (Shannon, Flattem, Jordan, Jacob, Black, Biaggioni, Blakely & Robertson, 2000). These deficits can cause patients to experience symptoms suggestive of not enough norepinephrine simultaneously with high norepinephrine levels. Many of the mechanisms listed here can result in states of chronic adrenergic activation that lead to orthostatic intolerance.
Sympathetic underactivty can also occur in some forms of orthostatic intolerance (Robertson, 2000), such as pure autonomic failure.
The above are some of the possible mechanisms that may be resulting in orthostatic intolerance. Physicians should attempt to discover the underlying mechanisms contributing to a patient's symptoms. This will ensure that treatment plans are tailored to target the specific mechanisms resulting in autonomic dysfunction, and that patients will receive the most effective care.
References
    1. Bou-Holaigah, I., Rowe, P. C.,  Kan, J., & Calkins, H. (1995). The   relationship between neurally mediated hypotension and the chronic fatigue     syndrome. Journal of the American Medical Association, 27, 961-967.     PMID: 7674527 [PubMed - indexed for MEDLINE]     2. Bush, V. E., Wight, V. L., Brown, C. M., & Hainsworth, R. (2000). Vascular     responses to orthostatic stress in patients with postural tachycardia   syndrome (POTS), in patients with low orthostatic tolerance, and in   asymptomatic controls. Clinical Autonomic Research 10, 279-284.   PMID: 11198483 [PubMed - indexed for MEDLINE]     3. Coghlan, H. C. (2002, July). Orthostatic Intolerance. National Dysautonomia   Research Foundation Patient Conference. Washington, DC.     4. Fredman, C. S., Biermann, K. M., Patel, V., Uppstrom, E. L., &  Auer, A. I.    (1995). Transcranial Doppler Ultrasonography during Head-Upright    Tilt-Table Testing. Annals of Internal Medicine 123, 848-849.         5. Gordon, V. M., Opfer-Gehrking, T. L., Novak, V., & Low, P. A. (2000).   Hemodynamic and symptomatic effects of acute interventions on tilt in   patients  with postural tachycardia syndrome. Clinical Autonomic   Research, 10(1), 29-33. PMID: 10750641     6. Grubb, B. P. (2000, July). Orthostatic intolerance. National Dysautonomia    Research Foundation Patient Conference. Minneapolis, Minnesota.     7. Grubb, B. P., & Karas, B. (1999) Clinical disorders of the autonomic nervous    system associated with orthostatic intolerance. Pacing and Clinical    Electrophysiology, 22, 798-810.    Full text: http://www.ndrf.org/PDF%20Files/disorders.PDF     8. Heitz, U. & Horne, M. M. (2005). Fluid, Electrolyte and Acid-Base Balance.   St. Louis, MO: Elsevier Mosby.     9.Hermosillo, A. G., Jauregui-Renaud, K., Kostine, A., Marquez, M. F., Lara,    J. L., Cardenas, M. (2002). Comparative study of cerebral blood flow   between postural tachycardia and neurocardiogenic syncope, during   head-up tilt test. Europace, 4, 369-74.   Full text: http://europace.oxfordjournals.org/cgi/reprint/4/4/369     .10.  Jacob, G., & Biaggioni I. (1999). Idiopathic orthostatic intolerance and   postural tachycardia syndromes. The American Journal of the     Medical Sciences, 317, 88-101. PMID: 10037112     11. Jacob, G., Robertson, D., Mosqueda-Garcia, R., Ertl, A. C., Robertson, R.   M., Biaggioni, I. (1997). Hypovolemia in syncope and orthostatic   intolerance: role of the renin-angiotensin system. American Journal of   Medicine, 103(2), 128-133. PMID: 9274896     12. Kuchel, O., Buu, N. T., Hamet, P., Larochelle, P., Gutkowska, J., Schiffrin,     E. L., Bourque, M., & Genest, J. (1985). Orthostatic hypotension: a    posture-induced hyperdopaminergic state. The American Journal of the     Medical Sciences, 289, 3-11. PMID: 3881951     13. Low, P. A. (2000, July). Orthostatic intolerance. National Dysautonomia    Research Foundation Patient Conference. Minneapolis, Minnesota.     14. Low, P. A., Schondorf, R., Novak, V., Sandroni, P., Opfer-Gehrking, T. L.,   & Novak, P. (1997). Postural Tachycardia Syndrome. In P.A. Low (Ed.),    Clinical Autonomic Disorders (pp. 681-697). Philadelphia:    Lippincott-Raven Publishers.     15. Novak, V., Novak, P., Opfer-Gehrking, T. L., O'Brien, P. C., & Low P. A.    (1998). Clinical and laboratory indices that enhance the diagnosis of    postural tachycardia syndrome. Mayo Clinic Proceedings, 73, 1141-50.   PMID: 9868411 [PubMed - indexed for MEDLINE]     16. Raj, S. R., Biaggioni, I., Yamhure, P. C., Black, B. K., Paranjape, S. Y.,   Byrne, D. W., & Robertson, D. (2005). Renin-aldosterone paradox   and perturbed blood volume regulation underlying postural tachycardia   syndrome. Circulation. 111(13), 1574-1582. Full Text     17. Robertson, D. (2000, July). General description of the autonomic nervous   system and orthostatic intolerance overview. National Dysautonomia   Research Foundation Patient Conference. Minneapolis, Minnesota.     18. Schondorf, R., Benoit, J., & Stein, R. (2005). Cerebral autoregulation is   preserved in postural tachycardia syndrome (POTS). Journal of   Applied Physiology, Apr 28; [Epub ahead of print] Full Text     19. Shannon, J. R., Flattem, N. L., Jordan, J., Jacob, G., Black, B. K.,   Biaggioni, I., Blakely, R. D., & Robertson, D. (2000). Orthostatic   intolerance and tachycardia associated with norepinephrine-transporter   deficiency. New England Journal of  Medicine, 24, 541-9.    http://content.nejm.org/cgi/content/abstract/342/8/541     20. Stewart, J. M. (2000, July). Pediatric and adolescent orthostatic intolerance   and CFIDS. National Dysautonomia Research Foundation Patient    Conference. Minneapolis, Minnesota.     21. Stewart, J. M., & Erickson, L.C., (2002). Orthostatic intolerance: an   overview. In Alejos, J. C., Konop, R., Chin, A. J., Herzberg, G., Neish, S.   (Eds.). emedicine Journal, 3, (1).   http://www.emedicine.com/ped/topic2860.htm     22. Stewart, J. M., & Weldon, A. (2001). Reflex vascular defects in the   orthostatic tachycardia syndrome of adolescents. Journal of Applied   Physiology, 90, 2025-2032.   Full text: http://jap.physiology.org/cgi/content/full/90/6/2025     23. Streeten, D. H. (1999). Orthostatic intolerance. A historical introduction to the   pathophysiological mechanisms. The American Journal of the Medical    Sciences, 317, 78-87. PMID: 10037111     24. Streeten, D. H., & Anderson, G. H. (1992). Delayed orthostatic intolerance.   Archives of  Internal Medicine, 152, 1066-72   PMID: 1580710 [PubMed - indexed for MEDLINE]     25. Thieben, M. J., Sandroni, P., Sletten, D. N., Benrud-Larson, L. M.,   Fealey, R. D., Vernino, S., Lennon, V. A., Shen, W. K.,  &   Low, P. A., (2007).  Postural orthostatic tachycardia syndrome: the   Mayo Clinic experience. Mayo Clin. Proc. 82, (3), 308-313.    

edriscoll
Dysautonomia means dysregulation of the autonomic nervous system. The autonomic nervous system is the master regulator of organ function throughout the body. It is involved in the control of heart rate, blood pressure, temperature, respiration, digestion and other vital functions. Dysregulation of the autonomic nervous system can produce the apparent malfunction of the organs it regulates. For this reason, dysautonomia patients often present with numerous, seemingly unrelated maladies.  
Diagnosis frequently requires a specialist familiar with autonomic dysfunction and the various disorders that result.  It is common for diagnosis to take a longer than many other disorders, however with the proper diagnostic testing the type of dysautonomia can be identified and effective treatment prescribed. 
DINET provides information , personal stories and articles written by patients about the types of dysautonomia, treatment and living with these chronic illnesses.   This site focuses on the following types of dysautonomia; please note, these are not the only types or subtypes of the disorders described.  Please explore the different categories under Information Resources to find out more about dysautonomia disorders. 
Postural Orthostatic Tachycardia Syndrome
Often more simply referred to as postural tachycardia syndrome, or POTS, this disorder is characterized by the body's inability to make the necessary adjustments to counteract gravity when standing up.
The defining symptom of POTS is an excessive heart rate increment upon standing. However, as you will discover, there are a multitude of other symptoms that often accompany this syndrome. As such, POTS can be a difficult disorder to detect and understand.
Our web site provides an overview of POTS and contains sections on symptoms, mechanisms, causes, tests, myths, links and research. There are also sections with information on what may help or hinder POTS patients. To read more about postural orthostatic tachycardia syndrome, explore the POTS category in our Information Resource section.
Neurocardiogenic Syncope (NCS)
Sometimes referred to as neurally mediated syncope or vasovagal syncope, this disorder is characterized by an episodic fall in blood pressure and/or heart rate that results in fainting (Robertson, 2002). The disorder occurs intermittently, with patients sometimes reporting good health between episodes.
Our web site provides general information on NCS, and also explores its symptoms, mechanisms, diagnosis and treatment. A page full of links to other neurocardiogenic syncope resources on the Internet is included as well. To read more about neurocardiogenic syncope, explore the  NCS category in the Information Resources section. 
Pure Autonomic Failure (PAF)
A degenerative disease of the peripheral nervous system characterized by a marked fall in blood pressure upon standing (orthostatic hypotension). The orthostatic hypotension leads to symptoms associated with cerebral hypoperfusion, such as dizziness, fainting, visual disturbances and neck pain (Mathias, Mallipeddi & Bleasdale-Barr, 1999). Other symptoms such as chest pain, fatigue and sexual dysfunction may also occur. Symptoms are worse when standing and are sometimes relieved by sitting or lying flat.
Our web site provides a page full of links to pure autonomic failure resources on the Internet.
Multiple System Atrophy/Shy-Drager Syndrome (MSA)
A degenerative disease of the central nervous system, MSA usually becomes apparent when one is in their fifties or sixties. Genitourinary dysfunction, impotence, headache, neck pain, dimming of vision, frequent yawning, orthostatic hypotension, gait disorder, sleep disorders and hoarseness may occur with multiple system atrophy (Polinsky, 1996). Loss of sweating, rectal incontinence, iris atrophy, external ocular palsies (paralysis of eye muscles), rigidity, tremor, fasciculations and wasting of distal muscles may also occur (Rehman, 2001). 
Loss of balance, difficulty moving, loss of fine motor skills, muscle aches and pains, changes (decline) in facial expressions, difficulty chewing or swallowing and a mild decline in intellectual function are among other symptoms patients may experience. (MEDLINEPlus, 2003, Multiple System Atrophy).
MSA is a very serious form of dysautonomia that can be fatal.  
Our website provides a page full of links to multiple system atrophy resources on the Internet.  
References
1. Mathias, C. J., Mallipeddi, R. and Bleasdale-Barr, K. (1999). Symptoms associated with orthostatic hypotension in pure autonomic failure and multiple system atrophy. Journal of Neurology, 246, (10), 893-898.
2. MEDLINEPlus Heath Information. (2003). Multiple System Atrophy. Retrieved September 8, 2003 from: http://www.nlm.nih.gov/medlineplus/ency/article/000757.htm
3. Polinsky, R. J. (1996). Multiple system atrophy and Shy-Drager syndrome. In Robertson, P. A. Low & R. J. Polinsky (Eds.), Primer on the autonomic nervous system (p. 222). San Diego, CA: Academic Press.
4. Rehman H. U. (2001). Multiple system atrophy. Postgraduate Medical Journal.  77, (908), 379-382.
5. Robertson, D. (2002, July). Drug therapy. National Dysautonomia Research Foundation Patient Conference. Washington, D.C.

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Newsletter Content
Patient Advocates by Reanna Mathis
Compression Stockings by Mona Hussein
Meet the member: Kat's story by Chelsea Goldstein
Medical Q & A, answers provided by DINET's Medical Advisory Team
Dysautonomia Research
Information Patient Guides
Looking Back and Looking Forward - 2017 to 2018
 
 
 
 
 
 
 
 
 
 
 
 
 

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Below are packets of information designed to help people living with dysautonomia.  The 1st guide  is written to help your family and friends understand your illness and help you all learn to live with it together. The POTS Guide for kids was created to be used as a handout for your child's teacher, coach, tutor, school nurse, their best friend's mom, or anyone else that may be responsible for your child when you are not there. There are links to pdfs in each article to make it easier to print, email or share.  The 3rd guide is to help patients with tips to prepare for a visit to the ER or a new medical provider. The Information Sheets are designed to help you remember the information you should have with you.
UNDERSTANDING DYSAUTONOMIA
A guide for family and friends
POTS GUIDE - for the family of children & teens living with POTS
I know a kid who has POTS  
Hydration and POTS
PATIENT'S GUIDE
Preparing for the ER and new medical visits
Information Sheets.
 

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Newsletter content
Walking out of the fog by Trudi Davidoff
How old words help me manage new illness by Missy Milton
Meet the member - Onva's Story by Chelsea Goldstein
Being truly helpful by Margeret Rose Lombardi
Medical Q & A
Research: Dysautonomia disorders and related chronic illness
Studies: Open recruiting studies for dysautonomia and related chronic illness
Survey Sundays:  Facebook followers answer questions by Lauren Mlack
2017 Age of onset survey results by Trudi Davidoff
We can't stand without support by Ellen Driscoll

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Dysautonomia through the ages by Chelsea Goldstein
Self-care, why it deserves a spot at the top of your to-do list by Amy Keys
Eating disorders and dysautonomia by Mona Hussein
Meet the Member: Caryn's Story by Chelsea Goldstein
I've changed my mind. I don't want to accept "acceptance" by Trudi Davidoff
How older chronically ill folks can help younger ones:;  Age-specific tools for managing illness by Missy Milton
Medical Q & A - Your questions answered by DINET's Medical Advisors
Updated Research Information for Dysautonomia and Related Chronic Illnesses
Updated Open Recruitment Studies
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edriscoll
POTS is a disorder that can easily be overlooked or misdiagnosed. Some patients have had to wait years before their condition was properly labeled. POTS is sometimes misdiagnosed because of the wide array of symptoms that accompany this syndrome. The symptoms of postural orthostatic tachycardia often mimic other illnesses. Entities such as thyroid disease, pheochromocytoma, hypoadrenalism, cardiac disease, autonomic neuropathies, medication side effects and anxiety disorders need to be ruled out before a patient is labeled with POTS (Low, 2000).

POTS is an easy disorder to overlook because physicians routinely take heart and blood pressure readings while the patient is sitting down. The POTS patient may have relatively normal vital signs while sitting down. Also, POTS symptoms can vary from day to day. Patients sometimes report good phases in which their symptoms are milder, followed by bad phases in which symptoms become more severe. This fluctuation in symptoms can also lead to difficulties in detecting POTS. Physicians that have experience in detecting and treating dysautonomia can be located on our Find a Physician database of dysautonomia specialists. 

There are a variety of tests that the POTS patient may undergo. Orthostatic symptoms are usually the most debilitating aspect of autonomic dysfunction readily amenable to therapy, and for this reason the blood pressure and heart rate response to upright posture should be the starting point of any autonomic laboratory evaluation (Robertson, 1996, p. 111).
To learn about the tests used to diagnose POTS and other forms of dysautonomia, please visit our Autonomic Testing page.
 

 

edriscoll
Autonomic nerve disorders (dysautonomia) refer to disorders of the autonomic nervous system (ANS) function. Dysautonomia is a general term used to describe a breakdown or abnormal function of the ANS. The autonomic nervous system controls much of your involuntary functions. Symptoms are wide-ranging and can include problems with the regulation of heart rate, blood pressure, body temperature, perspiration, and bowel and bladder functions. Other symptoms include fatigue, lightheadedness, feeling faint or passing out (syncope), weakness, and cognitive impairment. (1. Mayo Clinic, Autonomic Nerve Disorders 2019)
Some forms of dysautonomia include; Postural Orthostatic Tachycardia Syndrome (POTS), Orthostatic Hypotension (OH),  Orthostatic Intolerance (OI), Neurocarciogenic Syncope (NCS), Pure Autonomic Failure (PAF), Multiple System Atrophy/Shy-Drager syndrome (MSA). 
There are many advanced tests used for further diagnosis once some form of dysautonomia is detected.  The most common tests used are as follows.
The tilt table test is often the standard method used for detecting types of dysautonomia. A patient is strapped to a mechanical table, which will tilt them upright at an angle of at least 60 degrees. Measurements of heart rate and blood pressure are taken while lying flat and then again at intervals while tilted upright. The optimal duration of tilt testing in patients suspected of Autonomic Dysfunction is 40 minutes or until they faint, at which point the test is concluded (Carew, Cooke, O'Connor, Donnelly, Costelloe, Sheehy & Lyons, 2009). Some patients are given a drug called isoproterenol through an intravenous line during this test. Isoproterenol is used to test the sensitivity of beta-receptors. People who have POTS with beta-receptor supersensitivity and a hyperadrenergic state will generally have an exacerbation of symptoms due to this drug. Other drugs that are sometimes used in place of isoproterenol include nitroglycerin, edrophonium, adenosine triphosphate, ephedrine and nitroprusside (Grubb & McMann, 2001).
The tilt table test may be combined with transcranial doppler ultrasonography. Transcranial doppler ultrasonography is useful in detecting a reduction in cerebral blood flow (Fredman, Biermann, Patel, Uppstrom & Auer, 1995). A number of  patients with orthostatic issues will have a decrease in blood flow to the brain upon standing (Low, 2000). This can occur even if the patient does not become hypotensive (Low, 2000).
Bowel motility studies are useful in ascertaining the degree of gastrointestinal involvement present (Grubb, Kanjwal & Kosinski, 2006).
A catecholamine test is sometimes given to patients suspected of having chemical abnormalities. Testing one's levels of catecholamines and their metabolites is also useful in detecting certain tumors, such as pheochromocytoma. Some  patients will have abnormal catecholamine levels, particularly norepinephrine levels. Norepinephrine is the main chemical messenger of the sympathetic nervous system, and is often elevated in certain types of dysautonomia patients. A physician can determine one's total catecholamine levels through analysis of their blood or urine. 
The blood test is quite simple. The patient will have to lie quietly for a period of time (usually around 30 minutes) before their blood is drawn. Some doctors believe a more accurate reading is gained if an intravenous line is placed in the patient's arm before the resting period. This is because the fear and pain associated with needles may induce a rise in catecholamines that could obscure results.
Other doctors will use the 24-hour urine catch method to determine catecholamine levels. The patient is given a container to collect their total urine volume over a 24-hour period. The container is then returned to the physician and catecholamine levels are assayed. 
The cold pressor test is used to activate the blood pressure control system. The patient places their hand in ice water during this test. The physician will monitor blood pressure changes. This test can be used to localize a sympathetic lesion in the afferent or efferent limb of the baroreceptor reflex arc (Engstrom &  Aminoff, 1997). 
Deep breathing/Paced respirations are tests that evaluate autonomic function by measuring heart rate responses to controlled breathing.
Electromyography (EMG) is sometimes used to test the electrical activity of nerves and muscles. A needle electrode(s) is inserted through the skin into the muscle. The measured muscle response to nervous stimulation can detect nerve or muscle disorders. A nerve conduction study may be given concurrently with electromyography. During this test, muscles and nerves are stimulated with small bursts of electricity to determine if they are functioning in a normal manner.
The Hand-grip test is a simple and non-invasive test of sympathetic function. Some physicians feel its sensitivity and specificity compare favorably with the tilt table test (Khurana & Setty, 1996). During this test, a patient squeezes a hand-grip until their arm is fatigued. Those with autonomic dysfunction may have an excessive diastolic blood pressure response to this test.
Magnetic resonance imaging (MRI)/(MRA) can be used to diagnose some conditions thought to be associated with autonomic dysfunction, such as tumors, Chiari, cervical stenosis or the nutcracker phenomenon. This test encompasses a powerful magnet, low-intensity radio waves, and computer technology. The patient lies still inside the magnet. The magnetic field and different radio frequencies allow a specialized computer to generate detailed images of the inside of the body. The Stand-Up MRI may lead to interesting findings in POTS patients.
Microneurography is sometimes used to record traffic from the peripheral nerves. A small needle is placed into a nerve in the leg. Physicians can then measure nerve signals traveling from the brain to the blood vessels. Some POTS patients have nerve damage in their legs (Low, 2000)..
Sweat tests such as the thermoregulatory, resting sweat output and the quantitative sudomotor axon reflex are sometimes given to patients to determine if they are sweating appropriately. Many people with forms of dysautonomia will have impaired sweating abilities. Some patients report inappropriate sweating, including night sweats. 
During the thermoregulatory sweat test, the patient wears a disposable bathing suit and an orange powder is applied to the skin. The patient is then placed in a hot environment to induce sweating. The orange powder will turn purple where the patient sweats. In this way, physicians can determine if the patient has abnormal sweating patterns.
A small battery operated current may be used to stimulate the sweat glands directly during the resting sweat output test. 
The quantitative sudomotor axon reflex test (QSART) is used to determine sweat volume and latency of response. It can also be used to test for postganglionic lesions (Fealey, 1996, p. 297). A reduced or absent sweat response indicates postganglionic sympathetic sudomotor failure. Used in conjunction with the thermoregulatory sweat test, QSART can differentiate a pre- from the postganglionic lesion (Low, 2003, 407-421).
Some patients may be given a 24-hour urinary sodium test. This test is useful in determining if one's plasma volume is normal (Low, 2000). One study performed by researchers at the Mayo Clinic showed that 28.9% of POTS patients excreted less than 100 mEq in 24 hours and 66.4% excreted less than 150 mEq in 24 hours. These researchers concluded that an important first step in the assessment and treatment of POTS is to determine the patient's volume status and institute salt and fluid replacement in those with hypovolemia (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007).
A study of neurocardiogenic patients noted that those with a urinary sodium excretion <170 mmol/24 hrs. were more likely to have reduced plasma volume (El-Sayed & Hainsworth, 1996). These patients responded well to salt loading. 
A patient may also be given a test to determine total red cell mass and plasma volume. Hypovolemia is sometimes found in conjunction with POTS. Plasma volume may be reduced or red cell mass may be reduced in the POTS patient (Low, 1993).
Another test that is sometimes used to determine autonomic dysfunction is the Valsalva maneuver. This is a test of baroreflex responsiveness. A physician will have the patient blow into a tube while observing heart rate and blood pressure changes. Impaired baroreflex appears to be characteristic of moderate to severe forms of dysautonomia (Stewart, 2002). Patients may have an excessive blood pressure increment after cessation of the maneuver that is sometimes associated with headache (Sandroni, Novak, Opfer-Gehrking, Huck & Low, 2000). Some researchers report normal heart rate responses during the maneuver and conclude that the assessment of heart rate responses during this test does not contribute to the diagnosis of POTS (Braune, Wrocklage, Schulte-Monting, Schnitzer & Lucking, 1999).
A Patient may be given various tests to determine how dysautonomia is affecting their heart. Sinus tachycardia commonly occurs in those with dysautonomia. A patient may be asked to wear a Holter monitor to determine if their heart is functioning correctly. This device allows physicians to record the heart's activity over an extended period of time (usually 24 hours). Electrodes are placed at various locations on the patient's chest. These electrodes are attached to a small portable recorder. A patient may be asked to keep a written journal of any symptoms they experience while wearing the Holter monitor. Irregular heart rhythms are recorded and then evaluated by a physician.
Endless-loop recorders or event recorders are sometimes used instead of Holter monitors. These recorders are smaller and can be worn for months at a time. Patients will press a button after experiencing symptoms such as tachycardia or fainting. An ECG of the event will be recorded and transmitted via telephone for a physician to access.  
A stress test can be used to determine how exercise might affect the dysautonomia patient. The patient walks on a treadmill until a target heart rate is reached. The test is ceased if the patient becomes exhausted or develops complications. The heart's electrical activity is recorded while the patient exercises. Sometimes an echocardiogram will be performed along with the stress test. An echocardiogram is an ultrasound of the heart. This test helps physicians identify abnormalities in the heart's structure and function. 
The above are only some of the tests that may be given to a  patient suspected of having autonomic dysregulation. It is important for patients to ask their physician if they should discontinue their medication before taking specific tests. Some medications that have been reported to significantly affect autonomic testing results include chlorpromazine, thioridazine, tricyclic antidepressants, bupropion, mirtazapine, venlafaxine, clonidine, alpha blockers, beta blockers, calcium channel blockers, opiates and topical capsaicin (Sandroni, 1998). A patient taking medication to lessen symptoms will present with decreased symptoms upon testing. A patient should always consult their physician before discontinuing any medication.
Resources
1. Mayo Clinic, Autonomic Nerve Disorders, Full Text Link
2. Braune, S., Wrocklage, C., Schulte-Monting, J., Schnitzer, R., & Lucking, C.   H. (1999). Diagnosis of tachycardia syndromes associated with orthostatic    symptoms. Clinical Autonomic Research, 9(2), 97-101   PMID: 10225614 [PubMed - indexed for MEDLINE]     3. Carew, S., Cooke, J., O'Connor, M., Donnelly, T., Costelloe, A., Sheehy, C.,   & Lyons, D. (2009). What is the optimal duration of tilt testing for the   assessment of patients with suspected postural tachycardia syndrome?   Europace. 11(5), 635-637. PubMed   4. El-Sayed, H., & Hainsworth, R. (1996). Salt supplement increases plasma    volume and orthostatic tolerance in patients with unexplained syncope.    Heart, 75,  134-140. Full Text     5.  Engstrom,  J. W., &  Aminoff, M. J. (1997). Evaluation and treatment of     orthostatic hypotension. American Family of Physicians, 56(5).   PubMed     6. Fealey, R. (1996). Disorders of sweating. In D. Robertson, P. A. Low, & R. J.    Polinsky (Eds.), Primer on the autonomic nervous system (p. 293-299).    San Diego, CA: Academic Press.     7. Grubb B. P., Kanjwal, Y., & Kosinski, D. J. (2006). The postural   tachycardia syndrome: A concise guide to diagnosis and management.   J Cardiovasc Electrophysiol., 17, 108-112.     8. Grubb, B. P., & McMann, M. C. (2001). The Fainting Phenomenon:    Understanding why people faint and what can be done about it.    New York: Futura Publishing Company.     9. Khurana, R.K., &  Setty, A. (1996). The value of the isometric hand-grip    test--studies in various autonomic disorders. Clinical Autonomic     Research, 6, 211-218.    PMID: 8902317 [PubMed - indexed for MEDLINE]     10. Low, P. A. (1993). Postural Orthostatic Tachycardia Syndrome.    Department of neurology, Mayo Clinic.     11. Low, P. A. (2000, July). Orthostatic intolerance. National Dysautonomia    Research Foundation Patient Conference. Minneapolis, Minnesota.     12. Low, P. A. (2003). Seminars in neurology. In K. L. Ross and R. Freeman   (Eds.), Testing the Autonomic Nervous System (pp. 407-421). New York,   NY: Thieme Medical Publishers, Inc.     13. Robertson, D. (1996). Clinical assessment of autonomic failure. In D.    Robertson, P. A. Low, & R. J. Polinsky (Eds.), Primer on the    autonomic nervous system (p. 111-115). San Diego, CA:   Academic Press.     14. Sandroni, P. (1998, November/December). Testing the autonomic nervous     system. In C. B. Berde, & M. C. Rowbotham (Eds.) International    Association for the Study of Pain: Technical Corner From IASP   Newsletter. http://www.iasp-pain.org/TC98NovDec.html     15. Sandroni, P., Novak, V., Opfer-Gehrking, T. L., Huck, C. A., & Low, P. A.    (2000). Mechanisms of blood pressure alterations in response to the     Valsalva maneuver in postural tachycardia syndrome. Clinical    Autonomic Research, 10(1), 1-5.     16. Stewart, J. M. Heart rate and blood pressure variability. Retrieved March 23,    2002, from Center for Pediatric Hypotension.    http://www.nymc.edu/fhp/centers/syncope/heart%20rate%20variability%2   C%20blood%20pressure%20variability%20and%20the%20baroreflex.htm     17. Thieben, M. J., Sandroni, P., Sletten, D. N., Benrud-Larson, L. M.,   Fealey, R. D., Vernino, S., Lennon, V. A., Shen, W. K.,  &   Low, P. A., (2007).  Postural orthostatic tachycardia syndrome: the   Mayo Clinic experience. Mayo Clin. Proc. 82, (3), 308-313.  
 

edriscoll

POTS: An overview

By edriscoll, in POTS,

An overview of Postural Orthostatic Tachycardia Syndrome
Standing up is something most of us take for granted; we've been doing it since childhood. Our bodies automatically adjust to the pull of gravity by increasing vascular tone, heart rate, and cardiac output. Blood vessels contract, heart rates increase and our systolic blood pressure remains the same or decreases slightly while diastolic pressure increases slightly (Brunner & Suddarth, 2000, p. 546). Our bodies operate in perfect homeostasis and we stand up with little effort. 
However, the simple act of standing up can be a challenge for some people. There are disorders that affect the body's ability to appropriately adjust to the pull of gravity. When the body cannot effectively adjust to upright posture, a person is said to have orthostatic intolerance. Postural orthostatic tachycardia syndrome (POTS) is a disorder characterized by orthostatic intolerance.  POTS is a disorder that is a part of the dysautonomia family of disorders.
The criteria for diagnosis of POTS is: (1) a sustained increase in HR of at least 30 bpm within 10 minutes of standing (often with an absolute upright HR ≥ 120bpm); (2) in the absence of sustained orthostatic hypotension (drop in BP > 20/10mm Hg); (3) with symptoms of orthostatic intolerance for at least 6 months. In patients < 19 years of age, there is a higher HR threshold for POTS (increment  ≥40 bpm or absolute uprights HR  ≥ 120 bpm) due to physiological orthostatic tachycardia in adolescents and children (Singer et al., 2012)  (Arnold, Ng, Raj, 2018)
While the hallmark of POTS is an excessive heart rate increment upon standing, patients often exhibit numerous symptoms of autonomic nervous system dysregulation, and research by the Mayo Clinic suggests POTS is a limited autonomic neuropathy (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007). Many POTS symptoms seem to be caused by an imbalance of the Autonomic Nervous System's  (ANS) control over blood flow. It is the autonomic nervous system (ANS) that regulates the needed adjustments in vascular tone, heart rate and blood pressure upon standing. Some of the messages coming from the autonomic nervous system tell the blood vessels to relax or tighten. In people with POTS, the system seems to be out of balance and blood is not going to the right place at the right time to do what the body needs (Fischer, 2007).
The autonomic nervous system is responsible for regulating a multitude of organs and functions throughout the body. Some of these functions include temperature, respiration, pupil dilation and constriction, salivation and the digestive tract. A patient experiencing ANS dysregulation may experience abnormalities in the many organs and functions the ANS regulates. For example, around one third to one-half of POTS patients have digestive troubles (Fischer, 2007). The problem is that blood flow is not matching the need, so blood is not going to the right part of the intestinal system when it needs to. As a result, these people have trouble with nausea. For a smaller percentage of patients, the trouble is that there is too much blood in parts of the intestines. The body is attempting to digest food when there is no food to digest. This leads to cramping and colicky-like pains (Fischer, 2007).
Patients commonly suffer from cognitive dysfunction, sleep disturbances and exercise intolerance.  The symptoms can be exacerbated by numerous factors including dehydration, heat exposure, prolonged recumbency (resting, reclining), alcohol, menstruation, and acute exercise. Syncope (fainting) is not a predominant feature of POTS (only ~20–30% actually pass out, and this is usually thought to be due to vasovagal syncope) (Shen et al., 2017); however, many patients experience frequent pre-syncopal episodes that impair functional capacity. (Arnold, Ng, Raj, 2018)
POTS can be categorized as primary, meaning it is idiopathic and not associated with other diseases, or secondary, meaning it is associated with a known disease or disorder (Grubb, Kanjwal & Kosinski, 2006). Common comorbidities include chronic fatigue syndrome, hypermobility type of Ehlers-Danlos syndrome, migraine, bowel irregularities, autoimmune disorders, and fibromyalgia(Garland et al., 2015).
POTS is described as a clinical syndrome consisting of multiple heterogeneous disorders (disorders with diverse character). Some have taken to labeling "POTS Subtypes", with article published alluding to hyperadrenergic POTS ("Hyper POTS"), neuropathic POTS ("Neuro POTS"), or hypovolemic POTS.  It is important to note that these subtypes do not all have standard definitions therefore there is a non-exclusivity of names with patients often having overlapping clinical features and symptoms that involve more than one subtype.  Also, these subtypes do not have universally accepted definitions, so the labels can be misleading.  "While one doctor may use the term "Hyper POTS" to refer to a specific set of findings, another doctor might think that it refers to a different set of findings.  In theory, this could harm a patient's care.  In our experience, these "subtype" labels are not clinically helpful."  (Arnold, Ng, Raj 2018)

People generally develop POTS after becoming sick with a virus, giving birth, or being exposed to great bodily stressors (i.e. surgery, trauma or chemotherapy). Some people have had POTS their entire lives. Teenagers sometimes develop the disorder during the years of rapid growth, and 75-80% of them can look forward to being asymptomatic when they reach adulthood (Grubb, Kanjwal & Kosinski, 2006).
The symptoms of POTS are life-altering and debilitating at times. POTS patients use about three times more energy to stand than a healthy person (Grubb, 2002). It is as if these patients are running in place all the time. Activities such as housework, bathing, and even meals can exacerbate symptoms (Grubb, Kanjwal & Kosinski, 2006). Research shows that POTS patients' quality of life is similar to those with congestive heart failure and chronic obstructive pulmonary disease (Benrud-Larson, Dewar, Sandroni, Rummans, Haythornthwaite & Low, 2002) Twenty-five percent of people with POTS are disabled and unable to work (Goldstein, Robertson, Esler, Straus, & Eisenhofer, 2002). Most patients will have to make some lifestyle adjustments to cope with this disorder.
It was once estimated that nearly 500,000 Americans had POTS, which made standing up a challenge (Robertson, 1999). However, with research advances and growing physician education, the number of people found to have POTS symptoms is steadily rising. It is now estimated that one out of every hundred teens has POTS (Fischer, 2007).
The minimal requirements to detect POTS on initial evaluation are a detailed medical history, physical examination with orthostatic vitals and a resting 12-lead ECG (Sheldon et al, 2015)  The medical history should document medications, other medical conditions including personal and family history of cardiac disease, joint hypermobility, autoimmunity or neurological disorders, and the nature of tachycardia including potential triggers, frequency, time of day, association with pre-syncopal or syncopal episodes, symptoms, and impact on daily activities.  (Arnold, Ng, Raj 2018)
POTS has a strong female predominance (4–5:1), and primarily affects women of childbearing age. Most patients present with POTS between 13 and 50 years of age, with a family history of orthostatic intolerance reported in approximately 13% of patients (Thieben et al., 2007).The onset can be sudden or gradual. The quantity and severity of symptoms vary from day to day.
There are treatments for POTS symptoms which can be tailored to each individual patient, especially if an underlying cause is discovered. Researchers are attempting to identify and treat the mechanisms and causes of POTS. Studies show that most patients will eventually be able to stand up with fewer symptoms (Low, 2000). Most people with POTS can look forward to experiencing improvement with proper treatment.
For more information on POTS, please view our other POTS links and resources.
 
References
1.  Amy C. Arnold, Jessica Ng, Satish Raj
               Postural tachycardia syndrome: Diagnosis, Physiology and Prognosis    
               Autonomic Neuroscience, Vol 215 December 2018
               https://doi.org/10.1016/j.autneu.2018.02.005
 2. Benrud-Larson, L. M., Dewar, M. S., Sandroni, P., Rummans, T. A., 
  Haythornthwaite, J. A., &  Low, P. A. (2002, June). Quality of life in    patients with postural tachycardia syndrome. Mayo Clinic Proceedings,     77, 531-537.    Full text: http://www.mayoclinicproceedings.com/inside.asp?   AID=112&UID=     3. Brunner, L. S. & Suddarth, D. S. (2000). Assessment of cardiovascular   function. In S. C. Smeltzer & B. G. Bare (Eds.), Brunner and Suddarth's   textbook medical-surgical nursing (pp. 532-563). Philadelphia, PA:   Lippincott Williams and Wilkins.     4. Fischer, P. (2007). Postural orthostatic tachycardia syndrome. Mayo Clinic   Podcast. http://www.podcastingnews.com/details/www.   mayoclinic.org/rss/heart-podcast.xml/view.htm     5. Goldstein, D., Robertson, D., Esler, M., Straus, S., & Eisenhofer, G. (2002).   Dysautonomias: clinical disorders of the autonomic nervous System.   Ann Intern Med., 137, 753–763. Full Text     6. Grubb, B. P. (2000, July). Orthostatic intolerance. National Dysautonomia    Research Foundation Patient Conference. Minneapolis, Minnesota.     7. Grubb, B. P. (2002, October). The heterogeneity of symptoms related to    dysautonomia. Symposium conducted at the meeting of the   National Dysautonomia Research Foundation Northwest Ohio   Support Group. Toledo, Ohio.     8. Grubb B. P., Kanjwal, Y., & Kosinski, D. J. (2006). The postural   tachycardia syndrome: A concise guide to diagnosis and management.   J Cardiovasc Electrophysiol., 17, 108-112.     9. Grubb, B. P., & McMann, M. C. (2001). The Fainting Phenomenon:    Understanding why people faint and what can be done about it.      New York: Futura Publishing Company.     10. Low, P. A. (2000, July). Orthostatic intolerance. National Dysautonomia    Research Foundation Patient Conference. Minneapolis, Minnesota.     11. Robertson, D. (1999). The epidemic of orthostatic tachycardia and orthostatic   intolerance. The American  Journal of the  Medical Sciences, 317, 75-   77.     12. Thieben, M. J., Sandroni, P., Sletten, D. N., Benrud-Larson, L. M.,   Fealey, R. D., Vernino, S., Lennon, V. A., Shen, W. K.,  &   Low, P. A., (2007).  Postural orthostatic tachycardia syndrome: the   Mayo Clinic experience. Mayo Clin. Proc. 82, (3), 308-313.   Full Text

edriscoll
Postural Orthostatic Tachycardia is a syndrome. As such, there is a collection of symptoms that distinguish it. The symptoms are widespread because the autonomic nervous system plays an extensive role in regulating functions throughout the body. Many of these symptoms, such as low blood pressure,* may present only after prolonged standing. Symptoms will vary from person to person. The following is a list of symptoms reported by patients. When possible, we have included the percentage of patients that research reports have experienced a given symptom.
Symptoms presumed to be related to cerebral hypoperfusion:**
Lightheadedness  77.6 % (Grubb, 2000) Fainting or near fainting 60.5% of patients report near fainting (Grubb, 2000) Generalized weakness 50% (Low et al.)

  Symptoms presumed to be related to autonomic overactivity include the following:**
Palpitations 75% (Grubb, 2000) Tremulousness 37.5% (Low, Opffer-Gehrking, Textor, Benarroch, Shen, Schondorf, Suarez & Rummans, 1995) Shortness of breath 27.6 % (Grubb, 2000) Chest discomfort and/or pain 24.3 % (Grubb, 2000)

  Sudomotor symptoms include the following:**
Loss of sweating 5.3 % (Low et al.) Excessive sweating 9.2 % (Robertson, 2000)
Loss of sweating and excessive sweating are more common in patients with elevated norepinephrine levels (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007).

  Symptoms that may reflect dysautonomia:**
Delayed gastric emptying 23.7% of patients report gastrointestinal complaints, including bloating (Grubb et al., 1997) Bloating after meals (Grubb et al., 1997) Nausea 38.8% (Robertson, 2000) Vomiting 8.6% (Thieben et al., 2007) Abdominal pain  15.1% (Thieben et al., 2007) Diarrhea 17.8% (Jacob & Biaggioni, 1999) (sometimes with alternating constipation) Constipation 15.1% (Thieben et al., 2007) Bladder dysfunction 9.2% (Thieben et al., 2007) (this may include Polyuria(Jacob & Biaggioni, 1999) (excessive urination) Pupillary dysfunction 3.3% (Thieben et al., 2007) Pupillary dysfunction may or may not be responsible for some other reported symptoms, such as: Blurred Vision (Grubb, 2000) and Tunnel vision (Low et al.).

  Generalized Complaint symptoms:**
Fatigue 48% (Grubb, 2000) (which can be disabling)  Sleep disorders 31.6% (Low et al.) (can cause unrefreshing sleep and an increased need for sleep) Headache/migraine 27.6% (Grubb, 2000) Myofascial pain 15.8% (Thieben et al., 2007) (characterized by regional muscle pain accompanied by trigger points) Neuropathic pain 3% (Thieben et al., 2007)

  Other symptoms reported in research that are not categorized above include:
Dizziness (Grubb, 2000) Tachycardia(Grubb, 2000) Exercise intolerance (Grubb, 2000) Clamminess (Grubb, 2000) Anxiety (Grubb, 2000) Flushing (Grubb, 2000) Postprandial hypotension (Grubb, 2000) (low blood pressure after meals)  Blood pooling in limbs (Grubb, 2000) (can make legs feel heavy and appear mottled and purple in color)  Intolerance to heat (Grubb & Karas, 1999) Feeling cold all over (Grubb & Karas, 1999) Low blood pressure upon standing (Grubb, Kosinski, Boehm & Kip, 1997) (Some physicians feel orthostatic hypotension is a separate entity from POTS) Cognitive impairment (Grubb et al., 1997) (may include difficulties with concentration, brain fog, memory and/or word recall) Narrowing of upright pulse pressure (Jacob & Biaggioni, 1999) Cold hands (Low et al.) (and often feet & nose) Hypovolemia (Low et al.) (low blood volume) Chills (Low et al.) High blood pressure (Low et al.) Hyperventilation (Low et al.) Numbness or tingling sensations (Low et al.) Reduced pulse pressure upon standing (Low et al.) Low back pain (Mathias, 2000) Aching neck and shoulders (Mathias, 2000) Noise sensitivity (Stewart, 2001) Light Sensitivity (Stewart, 2001) Disequalibrium (Sandroni, Opfer-Gehrking, McPhee & Low, 1999)

  The above are symptoms reported by POTS researchers. Other symptoms sometimes reported by POTS patients include:
Arrhythmias (irregular heart beats) Chemical sensitivities (May have multiple chemical sensitivity and can be very sensitive to medications - may only need small doses) Easily over-stimulated  Feeling full quickly Feeling "wired" Food allergies/sensitivities (some foods seem to make symptoms worse) Hyperreflexia Irregular menstrual cycles Loss of appetite Loss of sex drive Muscle aches and/or joint pains Swollen nodules/lymph nodes Polydipsia (excessive thirst) Weight loss or gain Feeling detached from surroundings Restless leg syndrome POTS symptoms can vary from day to day. They tend to multiply and become exaggerated upon upright posture. Blood flow and blood pressure regulation are also abnormal while supine or sitting, but these abnormalities may not be as apparent and may require orthostatic stress to become evident (Stewart & Erickson, 2002). Some patients do report symptoms occurring while sitting or lying down. Heat, exercise and eating can exacerbate symptoms. Women sometimes report an increase in symptoms around menstruation.
If you are suffering from some of the above symptoms, you need to seek professional help. Please do not attempt self-diagnosis.
*Some of the above symptoms are specifically related to orthostatic hypotension, traditionally defined as an excessive fall in BP (typically > 20/10 mm Hg) on assuming the upright posture. Not all patients will experience a drop in blood pressure upon standing. Some physicians define orthostatic hypotension as a separate entity from POTS.
** The hypothesized origin of symptoms and their frequency came from the "Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience" by Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007. 
For more information about POTS, please view the additional articles, resources and links

References
1. Grubb, B. P. (2000, July). Orthostatic intolerance. National Dysautonomia               Research Foundation Patient Conference. Minneapolis, Minnesota.     2. Grubb, B. P., & Karas, B. (1999) Clinical disorders of the autonomic nervous    system associated with orthostatic intolerance. Pacing and Clinical    Electrophysiology, 22, 798-810.    Full text: www.ndrf.org/PDF%20Files/disorders.PDF     3. Grubb, B. P., Kosinski, D.J., Boehm, K., & Kip, K. (1997). The postural    orthostatic tachycardia syndrome: a neurocardiogenic variant identified    during head-up tilttable testing. Pacing and Clinical Electrophysiology,    20, (9, Pt. 1), 2205-12. PMID: 9309745 [PubMed - indexed for MEDLINE]     4. Jacob, G., & Biaggioni I. (1999). Idiopathic orthostatic intolerance and postural    tachycardia syndromes. The American Journal of the Medical Sciences,    317, 88-101. PMID: 10037112 [PubMed - indexed for MEDLINE]     5. Low, P. A., Oper-Gehrking, T. L., Textor, S. C., Benarroch, E. E., Shen, W.      K., Schondorf, R., Suarez, G. A., & Rummans, T. A. (1995). Postural    tachycardia syndrome (POTS). Neurology, 45, (4, Supplement 5), S19-25.   PMID: 7746369 [PubMed - indexed for MEDLINE]     6. Mathias, C. J. (2000, July). Other autonomic disorders. National Dysautonomia   Research Foundation Patient conference. Minneapolis, Minnesota.     7. Robertson, D. (2000, July). General description of the autonomic nervous system    and orthostatic intolerance overview. National Dysautonomia Research    Foundation Patient Conference. Minneapolis, Minnesota.     8. Sandroni, P., Opfer-Gehrking, T. L., McPhee, B. R., & Low, P. A. (1999).    Postural tachycardia syndrome: clinical features and follow-up study. Mayo    Clinic Proceedings, 74, (11), 1106-1110.    PMID: 10560597 [PubMed - indexed for MEDLINE]   9. Stewart, J. M., (2001, Spring/Summer). About being young and dizzy: overview    of dysautonomia. National Dysautonomia Research Foundation Youth    Network Fainting Robins Newsletter, "The Young and the Dizzy", 1, 1-2.     10. Stewart, J. M., & Erickson, L.C., (2002). Orthostatic intolerance: an overview.   In Alejos, J. C., Konop, R., Chin, A. J., Herzberg, G., Neish, S. (Eds.).    emedicine Journal, 3, (1). http://www.emedicine.com/ped/topic2860.htm     11. Thieben, M. J., Sandroni, P., Sletten, D. N., Benrud-Larson, L. M.,   Fealey, R. D., Vernino, S., Lennon, V. A., Shen, W. K.,  &   Low, P. A., (2007).  Postural orthostatic tachycardia syndrome: the   Mayo Clinic experience. Mayo Clin. Proc. 82, (3), 308-313.    

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