For a correct diagnosis of POTS there must be an absence of any other known cause of tachycardia, such as a specific heart condition.  POTS is usually accompanied by frequent spells of neurally mediated hypotension (NMH), but this is not always the case.  NMH means low blood pressure while standing, caused by a defect in the function of the autonomic nervous system.  Some patients may experience an increase in standing blood pressure due to an abnormal overcompensation of the autonomic nervous system to the orthostatic stress of the upright position.

     The brain is the most metabolically active organ in the body and requires a steady supply of oxygen and glucose to maintain healthy function.  Although the brain represents only 1-2% of the body's mass, it utilizes 20% of the body's oxygen consumption and 15% of cardiac output.  Our brains are thus highly dependent on adequate blood circulation to maintain our sense of health and well being.  The thought process, regulation of body temperature, hormone release, and many autonomic systems can be impaired by loss of proper blood pressure control.  Our survival is as dependent on adequate blood pressure regulation as on the fundamental process of breathing.

     A UCLA medical study found that women tolerate stress better than men, thus the claim by some uninformed doctors that POTS is caused by "stress" rather than an underlying physical disease process is not based on the scientific evidence.  If stress caused POTS, then men would develop POTS more often than women, the exact opposite of what accepted statistics indicates is the case.  Men have a stronger adrenaline fight or flight reaction to stress than women and are less prone to work out problems with friends and family.  Researchers found that women have higher levels of a hormone called oxytocin.  "Animals and people with high levels of oxytocin are calmer, more relaxed, more social and less anxious.  In several animal species, oxytocin leads to maternal behavior and to affiliation."

What causes POTS?  The answer to that question can be answered with a pie chart showing multiple causes, not by any one line statement.  Postural intolerance has been likened to a fever in that it is a symptom which can have many diverse root causes, both central and peripheral.  It is extraordinarily easy to induce orthostatic intolerance in human beings, and that is why most mammals have four legs, not just two.  Even our close genetic relatives, monkeys, chimpanzees, and apes, do not usually stand erect as humans do.  Just becoming dehydrated or overly heated can cause temporary orthostatic intolerance, so it should be no surprise that there are many proven and suspected causes of orthostatic intolerance.  Although gaps in our medical knowledge remain, most of the main root causes for the development of POTS have been identified and are listed below as general categories.

     Please remember that very little is ever 100% proven in the field of science.  Eternal doubt is an intrinsic part of the scientific method.  This page passes on the latest theories and accepted "facts," but does not guarantee that better facts and theories will not make some items on this list obsolete in the future.

1)  Viral and bacterial infections that damage the autonomic nervous system are a common cause.  Patients who develop POTS due to an infection, with no deeper underlying genetic cause, have the best chance for a spontaneous recovery over time.

2)  The development of POTS in women after childbearing is very common and may be due to changes in blood volume during pregnancy.

3)  Exposure to toxic chemicals which damage the autonomic nervous system can cause POTS.  This group includes adverse reactions to prescription drugs.  Some Gulf War veterans have developed POTS like symptoms after being exposed to small amounts of nerve gas, insecticides, and inadequately tested experimental drugs.

4)  POTS can be caused by genetically inherited neurotransmitter disorders, including disorders of catecholamine production and release, such as Norepinephrine-Transporter Deficiency.

5)  POTS can be caused by peripheral nerve damage due to rapid weight loss, diabetes, and alcoholism.  Doctors at the Mayo Clinic have identified autoantibodies specific for nicotinic acetylcholine receptors in the autonomic ganglia, which are believed to cause of approximately 10% of all POTS cases.  Doctors at Vanderbilt University believe that some POTS cases are caused by a partial sympathetic denervation, especially in the legs.

6)  POTS can be a phase in the gradual onset of Shy-Drager Syndrome.

7)  Damage to the vagus nerve can be a cause and there have been documented cases of patients developing neurally mediated hypotension and POTS after undergoing radiation treatment to the neck. 

8)  There is a mixed bag of less common potential causes, both genetic and acquired.  Ehlers-Danlos syndrome, a connective tissue disorder which permits veins to dilate excessively, is now an accepted cause of POTS.  Essentially anything that can damage the brain stem and important autonomic nervous system structures can cause POTS.

9)  Chronic Fatigue Syndrome (CFS), also known as Chronic Fatigue Immune Dysfunction Syndrome (CFIDS), is somewhat related to POTS, at least in terms of a similarity of many of the secondary symptoms.  In Europe CFS is called myalgic encephalomyelitis (ME).  Orthostatic intolerance, a broad title for blood pressure abnormalities such as neurally mediated hypotension (NMH) and POTS, is a common symptom of some types of CFS.  Neurally mediated hypotension refers to patients who get lightheaded when standing due to a defect in their nervous system's regulation of blood pressure.  Patients do not need to develop tachycardia to qualify for a diagnosis of NMH.  The Center for Disease Control now estimates that over 1,000,000 Americans have CFS.  Various studies suggest that more than 100,000 Americans have POTS.  Some percentage of patients have both POTS and CFS.  The Center for Disease Control has found at least four distinct forms of CFS, and that some forms of CFS cause abnormal heart rate and blood pressure issues (POTS and NMH) while others do not. 

     "The theory starts with the observation that infections that precede and may therefore induce CFS and related conditions act to induce excessive production of inflammatory cytokines that induce, in turn, the inducible nitric oxide synthase (iNOS).  This enzyme, in turn, synthesizes excessive amounts of nitric oxide which reacts with another compound (superoxide) to produce the potent oxidant peroxynitrite.  Peroxynitrite acts via six known biochemical mechanisms to increase the levels of both nitric oxide and superoxide which react to produce more peroxynitrite.  In this way, once peroxynitrite levels are elevated, they may act to continue the elevation, thus producing a self-sustaining vicious cycle.  It is this cycle, according to the theory, that maintains the chronic symptoms of CFS and it is this cycle, therefore, that must be interrupted to effectively treat this condition."  Also see "Kindling and Oxidative Stress as Contributors to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome".

     Cooperative new research conducted by the Pacific Northwest National Laboratory in Washington State and the University of Medicine and Dentistry in New Jersey has identified a unique subset of proteins in the spinal fluid of chronic fatigue syndrome patients that are not present in healthy control subjects.  "Because some of the proteins found in the spinal fluid of chronic fatigue syndrome patients also are implicated in Alzheimer's and Parkinson's diseases, the results support the idea that chronic fatigue syndrome has an underlying neurological cause."  Studies are currently being undertaken to see if the same proteins can be detected in the blood of patients in order to formulate a reliable blood test for Chronic Fatigue Syndrome.

Symptoms  

     POTS is diagnosed on the basis of heart rate increase and heart waveform signature revealed by electrocardiogram, not on the basis of a drop in blood pressure, as is the case with orthostatic hypotension and neurally mediated hypotension (NMH).  Neurally mediated hypotension is commonly associated with POTS, but having NMH is not a prerequisite for a diagnosis of POTS.  The secondary symptoms of POTS vary significantly from case to case.  The most commonly reported symptoms are listed below.    

     The length of time POTS patients can comfortably stand varies widely from case to case.  Patients may become dizzy, lightheaded, and develop chest and heart pain from standing beyond their limit.  Blood pooling in the legs and splanchnic bed (abdomen) may occur, which is felt in the same way you feel water fills your mouth when you get a drink.  Shortness of breath, blurry vision, tingling in the legs, sweating, and feelings of heat from increased adrenaline production are common symptoms of orthostatic stress.  Some patients pass out frequently, which is dangerous as well as uncomfortable.  Many patients experience spells of supine or standing vertigo, but this symptom is dependent on the root cause of the POTS.  Remember that POTS itself in not a specific disease like polio, but rather a symptom and a syndrome (a collection of symptoms).

     The current prevailing theory is that the heart pain associated with POTS is predominately non-ischemic, but further research may alter this perception.  It is believed the left sided heart pain so common among POTS sufferers is due to differences in heart chamber pressures, abnormal heart wall motions, and/or nerve damage.  It is not related to common angina which is usually caused by blocked arteries cutting off the supply of blood to the heart.  While uncomfortable and debilitating, this left sided heart pain is not believed to be immediately life threatening.

     With POTS and NMH you become lightheaded and weak even before you get a measured crash in blood pressure because the small blood vessels in the brain paradoxically constrict when you are under orthostatic stress.  This cerebral vasoconstriction cuts off the blood supply to brain cells while veins in the legs and splanchnic bed are dilated and pooling blood away from your heart. With inadequate filling of the heart's left ventricle and abnormal function of the alpha and beta adrenergic systems, it is no wonder that strange and irregular heart beats (palpitations) are a universal symptom of POTS.  These are often referred to as ectopic heartbeats, with frequent premature heartbeats the most common aberration reported. 

     POTS often generates a temporary rise in blood pressure immediately upon standing due to the rapid acceleration of heart rate.  Tachycardia is the body’s defense mechanism against a lack of sufficient venous blood returned to the heart.  Blood vessels, particularly veins, can become unnaturally dilated, causing blood pooling in the legs and splanchnic bed.  Thus the heart must beat more times in a minute to make up for the reduced blood volume transferred by each beat.  If a POTS patient stands up too suddenly, there may be so little blood in the heart that it may collapse upon itself, causing very painful heartbeats.  Patients often have measurably low standing pulse pressure, which can be an indicator of venous pooling.

     Frequent urination is a common symptom of POTS, NMH, and severe cases of CFS.  This problem is sometimes misdiagnosed as diabetes insipidus, which is a disease caused by reduced production of a pituitary hormone called vasopressin.  Some POTS patients develop a diabetes insipidus like syndrome which is believed to be caused by a variety of factors, including somewhat reduced vasopressin output, inadequate renin production, low blood volume, and disruption of the alpha adrenergic system, which helps the kidneys retain water and sodium.

     Reactive hypoglycemia is a common problem for both POTS and CFS patients, and occurs through a complex series of neural and hormonal interactions which are not yet fully understood.  The traditional definition of hypoglycemia is an abnormal lowering of blood sugar levels after the body overreacts to carbohydrates with excessive insulin production.  Researchers now understand that this lowering of blood sugar levels is not the only cause of symptoms.  Recent studies show that when patients with reactive hypoglycemia eat carbohydrates, which cause a sudden increase in blood glucose levels, their bodies abnormally produce excessive amounts of adrenaline and other stress hormones.  These stress hormones cause many negative symptoms in addition to the eventual crash in blood glucose levels due to excessive reactive insulin production.   

     Most patients with POTS have difficulty sleeping, which may result from a number of factors, including abnormally high adrenaline levels caused by increased orthostatic stress (the stress of standing).  Central sleep apnea is a problem for some people with POTS, which in some cases may be due to damage to the medulla, which controls important cardiac and respiratory functions.  Central sleep apnea causes breathing to temporarily stop while sleeping.

     Low grade fevers, mild chills, and general flu like symptoms are common with POTS.  This may be explained by a neurologically based loss of control of basic autonomic regulatory systems, an overactive immune system, or  abnormally high adrenaline levels effecting body heat production.  Many patients have positive anti-nuclear antibody tests (ANA test), which some doctors say is due to high adrenaline levels activating the immune system.  Other doctors suggest positive ANA tests may be due to an autoimmune disorder damaging nerve cells.  Patients are left in confusion as to which theory to believe.

     Chronic fatigue and weakness are common problems for POTS sufferers.  Those who have pure POTS, without CFS or significant immune system involvement, generally feel better and have greater postural tolerance despite tachycardia.  Many POTS patients have common allergies, uncommon food allergies, and are highly drug and chemical sensitive.  Many POTS and CFS patients experience severe night sweats.

     Nausea, bloating, and sore intestines are a frequent complaint.  The nausea can usually be eliminated by not stressing yourself beyond your capabilities.  Bloating is caused by low motility in the intestines.  Patients often develop irritable bowel syndrome, which leaves the intestines feeling raw and tender.  Difficulty swallowing (dysphagia - pronounced dis-FAY-jee-uh) is also a frequently reported problem.

     Numbness in palms and soles is a common symptom of POTS.  Legs, arms, and hands are often totally numb upon awakening from sleep.  Upper extremity somatosensory evoked potential studies are usually normal in POTS and CFS patients, but this is not always the case.  Unusual coldness of the hands is also common and is referred to as acral coldness.  Patients frequently experience sporadic itchiness, burning and tingling sensations all over the body, especially at night.  Some patients may also have dramatically reduced sweating, which can be tested for through a thermoregulatory sweat test. 

     Most POTS patients have poor balance, which may be caused by decreased blood flow to the brain and other disturbances in the vestibular system.  The patient's root neurological damage may also cause balance problems directly as well as causing the debilitating symptom of orthostatic intolerance.  Patients are often unable to pass a drunk test by walking with one foot placed directly in front of the other.  An abnormal gait is common.  Patients may walk with legs wide apart and feet flared out to the sides as an instinctive adaptive response to increase their stability.      

     Eye pain is another common problem, as is a feeling of pressure behind the eyes.  Patients can become so weak that their eye muscles are easily strained and focusing is difficult.  Many POTS and CFS patients see tiny little black dots floating in front of their eyes.  This is a problem of the fluid in the eyes which occurs naturally with age, but which can be made dramatically worse by the onset of CFS or POTS.  

     Supine blood pressure readings are usually normal or below normal in POTS patients.  This is in sharp contrast to multiple system atrophy (Shy-Drager syndrome), idiopathic orthostatic hypotension (Bradbury-Eggleston syndrome), and other forms of central autonomic failure typified by low standing blood pressure and high supine blood pressure.  Lack of supine hypertension (high blood pressure when lying down) is usually a sign you do not suffer from the classic forms of central autonomic failure.

     Most POTS patients will only have a few of the symptoms listed here, while others will have unique symptoms all their own.  A poor memory is a major symptom of POTS, and many patients will have a difficult time just remembering their own symptoms while conversing with doctors.  The total damage to the autonomic nervous system POTS sufferers experience, called dysautonomia, causes what Dr. David Robertson of Vanderbilt University refers to as “mild autonomic abnormalities.”  These symptoms, such as frequent urination and reactive hypoglycemia, are not life threatening, but they are quality of life destroying.

     People who do not have problems with low blood pressure have a difficult time understanding the concept of orthostatic stress.  They fail to realize that blood pressure is as basic and essential a bodily function as breathing.  How would you feel if your breathing were constricted for even one minute?  Low blood pressure can cause an enormous amount of symptoms and suffering, but those who don’t have it often miss that fundamental point.  Some patients with POTS have such a damaged regulatory system that they may get paradoxical wild swings in blood pressure from below 50 to over 200.  Complexly, POTS can be a low and high blood pressure problem combined.

Treatment  Treating patients with POTS and neurally mediated hypotension is often very difficult.  When you stand up your body should automatically constrict blood vessels to help maintain blood pressure in the face of increased orthostatic stress.  In the standing position, gravity wants to pull your blood down to your feet.  When you lie down, your body should automatically dilate blood vessels as gravity is no longer a force to fight against.  With POTS this automatic regulatory system breaks down and blood begins to pool in places where it should be flowing rapidly.  The heart is then stressed with the added work of trying to pull all that blood uphill without help from the much needed alpha adrenergic constriction process.

Non-drug treatments have the lowest risk of harm

     Adding lots of extra salt to the diet can increase both blood volume and blood pressure by increasing fluid retention.  One must increase fluid intake for salt to effectively expand blood volume.  The use of a large, stainless steel chef's style salt shaker can be helpful.  A high salt diet should only be tried under the recommendation and supervision of your doctor. 

     Pouring lots on ordinary table salt on food works better for most people than the use of salt tablets.  Salt tablets can irritate the stomach, cause vomiting, and tends to centralize body fluids in the digestive tract, which is not good for either blood volume or blood pressure.  For most people salt goes into the human body more smoothly and easily when mixed with food.  

     Patients with POTS and/or neurally mediated hypotension should avoid garlic and nitrates in food, which lower blood pressure.  Most patients also need to give up alcohol, coffee, tea, and adrenaline stimulating herbs like ginseng.  Try to avoid eating heavy meals as overloading the stomach decreases orthostatic tolerance by drawing blood to the digestive tract and away from main arteries which feed the brain.  

     Make sure you exercise every day when you are able.  Try to keep your muscles alive, as they produce the natural vasoconstricting hormone norepinephrine.  Good muscle tone, especially in the legs, helps limit abnormal blood vessel dilation and blood pooling.  Severely affected patients may find any amount of exercise difficult, but one can slowly increase activity over time as you improve.  Even just ten, two minute walks a day adds up to twenty minutes of walking, which can help maintain vital muscle mass and thus increase your orthostatic tolerance.  

     During the day it is better to rest in a recliner chair rather than lying in bed, as constant bed rest decreases orthostatic tolerance dramatically.  Astronauts often develop a temporary form of orthostatic tachycardia upon returning to earth due to the deconditioning effects of weightlessness, which are quite similar to prolonged bed rest.  When muscle mass is lost it is difficult to regain, therefore it is very important to avoid becoming deconditioned through inactivity.

     Activities that can aggravate POTS symptoms include working with your arms over your head, lifting heavy objects, and climbing stairs.  Warm temperatures have an especially negative effect on the exercise tolerance of POTS patients, as heat dilates blood vessels and diverts blood to the skin, thus reducing blood flow in key arteries that feed the brain.  Air conditioning during hot weather is essential for most POTS patients.  A few patients claim benefit from wearing medical support hose, which can be obtained from medical supply stores on the advice of a qualified physician.  These support garments look like long underwear and can reduce vasodilation in the legs by applying mild pressure.  Many patients, however, find them ineffective and/or uncomfortable to wear.  

     Meditation may help some patients reduce stress, feel more rested and alert, and often has a mild analgesic effect, reducing the perception of bodily aches and pains.  Meditation will not cure POTS or increase your comfortable standing time.  Meditation is a possible alternative to the use of sleep aids and sedatives, which often increase vasodilation and reduce orthostatic tolerance.  This Recliner Chair Meditation Technique may help patients who have the time and temperament for long periods of quiet sitting.

     It is impossible to replace the body’s dynamic, constantly changing system for controlling blood pressure with something as static as a simple dose of chemicals.   Drug therapy for POTS and neurally mediated hypotension often works much better in theory than in practice.  Patients who have neurally mediated hypotension or POTS due to Chronic Fatigue Syndrome are rarely helped by drug therapy, and often have bad drug reactions, ranging from mild to very serious.  Patients with a history of bad drug reactions should be extremely cautious when considering drug therapy for POTS.

Note - Below are brief descriptions of some commonly used drugs for the treatment of POTS.  This partial list is not a recommendation for any treatment, just the factual reporting of some of the drugs doctors most commonly prescribe.  I strongly urge all POTS patients to see specialists in the field and not ask ordinary doctors for treatment with these drugs.

Florinef is a common drug for the treatment of POTS and NMH.  It is used to stimulate the body’s retention of salt and water and it also has a very small alpha agonist effect (vasoconstricting effect).  The list of Florinef’s known potential side effects is hair raising, but at the small doses prescribed Florinef is not unusually dangerous.  Some patients have had bad reactions to Florinef, but that is true of all drugs.  Florinef makes you expel potassium so you must take potassium supplements to keep in balance.

Midodrine is a useful drug for many patients, and is probably the most effective alpha agonist currently available.  Alpha agonists work by constricting blood vessels, thus reducing blood pooling in the lower part of the body.  Sold in the United States as ProAmitine, Midodrine has the advantages of being long lasting and is most like the body’s own natural vasoconstricting hormones in effect.  Midodrine is a large molecule that does not pass through the blood brain barrier, which is helpful for patients who are drug sensitive.  Because you do not want your blood vessels constricted when you are supine, it is essential that alpha agonists should not be used before bedtime.  Supine hypertension is not only uncomfortable, it is dangerous.  Alpha agonists are usually only prescribed for those patients who are not seriously overweight, who have consistently low blood pressure, and whose main problem is vasodilation.  Florinef is usually tried first and Midodrine introduced for those who do not respond sufficiently to expansion of blood volume.

     Some patients have an abnormal supersensitivity to alpha agonists which can present serious problems during treatment.  Supersensitivity to alpha agonists can be caused by impaired amine uptake in the nerve endings of alpha receptors (denervation supersensitivity).  Abnormal sensitivity can also be produced by a prolonged lack of norepinephrine release from sympathetic nerve endings, which leads to enhanced receptor responsivity (decentralization supersensitivity).  These conditions usually produce a two to five times increase in sensitivity level, but there is a small subset of patients who are hundreds of times more sensitive than normal.  For these patients vasoconstricting alpha agonist drugs are dangerous to use because of their sheer potency.  If your physician prescribes any alpha agonist drug, consult with him about taking a very small test dose first in order to gauge your sensitivity level.

Beta blockers are used by many doctors to treat POTS and neurally mediated hypotension (NMH).  I have heard of more bad drug reactions to beta blockers than any other drug, especially for those patients who have NMH secondary to Chronic Fatigue Syndrome.  Beta blockers release histamines and should usually not be prescribed for patients who have significant allergies or asthma.  In a number of cases beta blockers have actually caused the onset of POTS.  Some patients have found beta blockers to be helpful, however, especially those patients who develop POTS because of an overly sensitive beta adrenergic system.  For these sensitive patients only very low doses of beta blockers are usually required.

Celexa (citalopram hydrobromide) is a selective serotonin reuptake inhibitor similar to Paxil, Zoloft, and Prozac, but with the claim of fewer side effects and less potential for negative drug interactions.  Serotonin reuptake inhibitors have been used for many years to treat neurally mediated hypotension and syncope (passing out).  The mechanism through which central serotonin levels affect blood pressure and heart rate has not been fully mapped out.  The net effect of Celexa appears to be to increase nerve communication and stimulation of the standing vasoconstriction reflex.  This limits venous blood pooling and increases orthostatic tolerance.  Celexa and the other serotonin reuptake inhibitors are known to increase norepinephrine release to varying degrees.

     Much has been made of the "placebo effect" in medicine, where a patient derives benefit from a pill, not through any chemical action of the medication, but through the purely mental belief that the pill is doing the patient some good.  It is my experience that this placebo effect has little affect on POTS patients, but many patients do fall victim to what I call the teddy bear effect.  The drugs used to treat POTS are not like antibiotics or anti-cancer agents.  They do not "cure" anything.  At best they can help your body cope with symptoms of a dysfunctional circulatory system, thus making you feel and function better.  If the drugs do not make you feel and function better, then consult with your doctor about stop taking the pills.

     All drugs have side effects, some of which are obvious, while others may build up slowly over time.  If you have chronic high blood pressure and your doctor tells you to stick with a drug, he is trying to save your life.  With POTS the situation is usually quite different.  If the drug works, you usually feel the benefit fairly quickly, have more energy, have longer comfortable standing time, and generally feel better.

     You would be surprised how many letters I receive from patients who keep taking drugs that they claim only makes them feel worse.  They continue to take the pills because they want to do something, anything, to fight this devastating illness.  For them, taking a medication may be comforting like a teddy bear, even if that pill has no discernible benefit, not even a positive placebo effect.  Generally speaking, patients should take a minimum number of drugs and only those drugs which have proven benefit.  I hear of some patients taking four or more drugs a day, but ask yourself this.  If any one of them really worked, or any reasonable combination of two drugs taken for synergistic effect really worked, then why would they need to take all the rest?  Over-medication is a serious potential problem, not just for POTS, but for any serious illness that has no swift or easy cure.

     It has also come to my attention that some doctors continue to advise POTS and NMH patients that sleeping with the heads of their beds slightly elevated at night will improve their orthostatic tolerance.  This method was originally developed to help patients with classic orthostatic hypotension diseases, such as Shy-Drager syndrome (multiple system atrophy) and Bradbury-Eggleston syndrome (idiopathic orthostatic hypotension).  Those diseases usually cause supine hypertension (high blood pressure while lying down).  It was simply assumed, without clinical studies, that elevating the head of the bed would help those with other orthostatic intolerance conditions as well.

     There is now documented evidence to suggest that some percentage of POTS and NMH patients experience supine hypotension (low blood pressure while lying down), which often manifests itself after the patient falls asleep.  If your blood pressure drops to below normal levels while sleeping, the last thing you want to do is to sleep with the head of your bed raised, thus draining even more blood and vital oxygen from your brain while you are unconscious.  It is therefore advisable that patients only elevate the head of their bed at night if they have proven supine hypertension. 

Finding Help  It is vital that you obtain proper professional medical help.  Do not try to diagnose or treat yourself.  The National Dysautonomia Research Foundation (a wonderful organization which I am not affiliated with) has a list of doctors who are educated in the diagnosis and treatment of POTS at: http://www.ndrf.org/physicia.htm.  Anyone interested in POTS can also read the following medical papers and books.  Some of the medical papers are from common medical journals, which can be obtained from local public, hospital, or college libraries.  Please do not ask me for copies.

"The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management" -  Satish R Raj MD MSCI, Indian Pacing Electrophysiol. J. 2006;6(2):84-99 

"Orthostatic Intolerance and Orthostatic Tachycardia," guest editor of special symposium issue on orthostatic intolerance David Robertson, M.D.,  The American Journal of Medical Sciences February 1999;317:#2: 75-124 

"The Fainting Phenomenon: Understanding Why People Faint and What Can Be Done About It," by Blair P. Grubb, MD, and Mary McMann, MPH.  This book is available on-line through the NDRF Reference Page or through amazon.com.

     If you read the above mentioned articles, you will know more about POTS and low blood pressure than your average cardiologist or neurologist.  Most doctors know about high blood pressure, not low blood pressure, and the first thing uninformed doctors will usually do is blame the patient for the symptoms.  I strongly suggest you consult an expert in the field instead of trying to educate your local doctor.  The drugs used to treat POTS can be dangerous and an experienced physician is needed to determine which drug or treatment is best for the patient.

     POTS is recognized as a physical, usually neurological based disorder by every major medical university in America.  Chronic Fatigue Syndrome is currently more difficult to diagnose, and thus skepticism in the medical community remains.  Research by Dr. Jonathan Kerr, Dr. Arnold Peckerman, and the Center for Disease Control has found credible evidence of serious measurable physical abnormalities in patients with Chronic Fatigue Syndrome.  These abnormalities include abnormalities in heart function and blood circulation, and abnormalities in gene expression in white blood cells and in brain cells that regulate metabolic and immune system response to stress, infection, and chemical exposure.  Doctors ridiculed people with MS, diabetes, and even polio for decades before a critical mass of evidence proved they were real diseases.  The same psychological torture (see Mind Experiment for Doctors) is now being inflicted on patients with Chronic Fatigue Syndrome.  It is essential that medical schools teach students humanity and humility instead of just teaching them how to prescribe drugs and mend bones.

     If you find any important research not mentioned on this page, please let me know.  Please read the brief Frequently Asked Questions page before you write me.

Christopher Calder        email = archive100 AT inbox DOT com

Useful POTS links

National Dysautonomia Research Foundation -  Has doctors list, discussion forum, and general information.

Center For Hypotension

"The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management" 

The Neuropathic Postural Tachycardia Syndrome

Autoantibodies to Ganglionic Acetylcholine Receptors in Autoimmune Autonomic Neuropathies

Norepinephrine-Transporter Deficiency

Chronic Fatigue Syndrome links

Novel Chronic Fatigue Syndrome (CFS) Theory Finally Produces Detailed Explanations for Many CFS Observations

CFS as Heart Failure Secondary to Mitochondrial Malfunction

Abnormal impedance cardiography predicts symptoms in chronic fatigue syndrome

European doctor also finds CFS genetic abnormalities in white blood cells

CFIDS Association of America