TILT TABLE TEST: What is it?

A tilt table test is also sometimes called a head-up tilt test. During one, your blood pressure and heart rate will be monitored by the minute. You lie down on the table and are strapped down while it is in a flat horizontal position. The table is gradually tilted up to different levels and you are monitored for changes in BP and HR.  You will have an IV inserted during the test in case medications are needed.

The purpose of the test is to help your doctors figure out what is causing your light-headedness and/or fainting spells, sometimes called syncope.

Syncope is when you lose consciousness due to a decrease in blood flow to your brain. This can be caused by a sudden drop in blood pressure or an increase in heart rate or by a large amount of your blood volume shifting to your lower extremities. It is frequently due to some medical condition related to your nervous system, heart or the amount of blood flow to your brain.

Depending on what the results are, your doctor can then determine the best course of treatment for you and if other tests might be needed.

A couple of things can happen when you have a Tilt Table Test or when you stand up. Depending on how your sympathetic nervous system reacts, you can have either POTS or NMH,(Neurally Mediated Hypotension).

NMH is most likely to occur is you have a decrease in norepinephrine and an increase in epinephrine. POTS is the opposite, it is most likely to result from an increase in norepinephrine and a decrease in epinephrine. These hormones are sometimes referred to as catecholamines.

Don't forget to watch the POTS videos at the bottom of the blog. You have to scroll down for them.

What Dysautonomia Patients Should Know About Antiphospholipid Syndrome or Hughes Syndrome

http://www.dysautonomiainternational.org/blog/wordpress/what-dysautonomia-patients-should-know-about-antiphospholipid-syndrome/http://www.dysautonomiainternational.org/blog/wordpress/what-dysautonomia-patients-should-know-about-antiphospholipid-syndrome/

This one is particularly important to me because I have suffered miscarriages. When I am in the hospital they usually give me blood thinners and use those pumps on my legs to keep me from developing clots. I go home with as much bruising on my abdomen as I have on my arms from IVs.

Dr. Vilardell from Barcelona : "There are two major "new" diseases of the twentieth century --AIDS and Hughes Syndrome."

It is also called Hughes Syndrome or sticky blood. It is associated with headaches, migraines, epilepsy, chorea, multiple miscarriages, peripheral thrombosis, demyelinating disease, Budd-Chiari syndrome, and renal vein thrombosis.

Symptoms include:

Headache or migraine
Giddiness
Memory loss
Visual disturbance
Thrombosis
Heart Attach
Stroke
Pulmonary Embolism
Multiple Sclerosis-like features
Gastrointestinal disorders
Problems with pregnancies

About 1/3 of women with Lupus have antiphospholipid antibodies, and a miscarriage rate of 20-50%.
About 20% of ALL miscarriages are caused by Hughes Syndrome. Treatment with aspirin or heparin results in a 90% success rate of normal pregnancy.

In younger people who have strokes, about 1 in 5 of them have undiagnosed Hughes Syndrome. The thickened blood causes TIAs, strokes and DVTs.


After you watch the antiphospholipid syndrome videos, don't forget to watch the POTS videos at the bottom of the blog. You have to scroll down for them.

This one is from a Lupus specialist, who first identified it in 1983, He has been published over 900 times in medical journals. I think it's fair to say he knows his stuff. 

Antiphospholipid Antibody Syndrome - Graham Hughes, MD, FRCP

What is Hughes Syndrome?

Muscarinic Antibody Research Study in POTS

http://www.dysautonomiainternational.org/page.php?ID=240

"Muscarinic receptors are part of the parasympathetic nervous system. When antibodies bind to these receptors, this may cause problems with parasympathetic nerve messaging, which can lead to dysautonomia symptoms. Muscarinic receptor antibodies have previously been associated with other forms of dysautonomia that may have an autoimmune basis, like Chagas disease, Sjogren's syndrome, and idiopathic tachycardia.

In a preliminary study of 16 POTS patients and 20 controls, Dr. Vernino's lab recently found that more than 87% of POTS patients had one or more of the muscarinic antibodies. The research team also found that M1 was associated with cognitive impairment ("brain fog") and M3 was associated with an abnormal QSART (a test that measures small fiber autonomic nerve function in the limbs). In the upcoming study, we hope to improve the method for measuring muscarinic antibodies, validate these findings, and obtain additional information by repeating this study on a larger group of POTS patients during the 2016 conference.

Identifying the percentage of POTS patients that have these antibodies and comparing the antibody profiles to patient reported symptoms is the first step in understanding how these antibodies impact POTS patients, which will lay the foundation for future research seeking to identify new treatments. "
Dysautonomia International

Don't forget to watch the POTS videos at the bottom of the blog. You have to scroll down to find them. Some of them also deal with receptors.

DIFFERENT TYPES OF POTS and SOME ASSOCIATED ILLNESSES

Neuropathic POTS ideology--POTS is an autonomic neuropathy. Nerves in the peripheral nervous system or,Small fibers that control autonomic functions and control pain are malfunctioning. About 50% of people with POTS have this type.

Hypo-adrenergic POTS--People with this type make more norepinephrine and epinephrine than normal people. NMH (ORTHOSTATIC HYPOTENSION) is most likely to occur is you have a decrease in norepinephrine and an increase in epinephrine. POTS is the opposite, it is most likely to result from an increase in norepinephrine and a decrease in epinephrine. About 33% of patients have this type.

Hypovolemic POTS--Blood Volume and urine sodium is low.About 33% have this type. Hypovolemia is Hypovolemia (also hypovolaemia or oligemia) when your body is in  a state of decreased blood volume. More precisely, you have a decrease in volume of blood plasma. It is what happens inside your blood vessels due to things like bleeding or dehydration.

Hypovolemia is related to sodium (salt) depletion which causes loss of water inside the blood vessels and is different from dehydration, which is excessive loss of body water. Symptoms of hypovolemia are tachycardia, low blood pressure, and lack of adequate blood flow which causes paleness of the skin and/or capillary refill on  the forehead, lips and nail beds. This is the time it takes  normal color to return to the skin or nail beds after pressure is applied. Other symptoms include feeling dizzy, faint, nauseated, or very thirsty. These are similar to the symptoms of shock.

Patients can have more than one type.

There is a genetic predisposition in some patients. Someone else in your family may have it. In my husband's family, his mother had it, but never got a diagnosis. And in my family, my father had it. There are major genetic things going on with my case. My father also had Parkinson's and it is genetic in our family. And in addition to this, my father had Rheumatoid Arthritis and a few secondary autoimmune conditions. I, in turn,  have,SLE (Systemic Lupus Erythematosus), Sjogren's Syndrome and other autoimmune conditions.

Typically, when you read about autonomic dysfunction, you read about a connection to Joint Hypermobility Syndrome or EDH(Ehlers-Danlos syndrome hypermobility type) . But they are autoimmune in nature, so Lupus and Rheumatoid Arthritis are not a stretch.

Parkinson's Disease is also common to read about in conjunction with autonomic dysfunction.

Other things that are connected are anemia, tumors, lightning injury(my husband was hit by lightning twice, see Page about it over on the side and read post about it here for more links), mitochondrial disease, porphyrias.


Don't forget to check out the videos at the bottom on POTS. You have to scroll down to find them.

IS POTS AN AUTOIMMUNE DISEASE? The Connection Between Dysautonomia and Autoimmunity

It is a recognized fact that some autoimmune diseases  also cause POTS, like Sjogren's Syndrome or Systemic Lupus Erythematosus. This is because these diseases cause damage called neuropathy by causing your body to produce autoantibodies that attack nerve cells/fibers.


But is POTS itself an autoimmune disease?

I happen to have both. I found this interesting article on the subject. New evidence of autoimmunity in POTS!  

There are a few other autoimmune diseases known to cause POTS. Guillain-Barre Syndrome and  CIDP, Chronic Inflammatory Demyelinating Polyneuropathy. Guillain-Barre works both like an infection and an autoimmune disorder simultaneously. It causes nerve inflammation and damages the protective myelin sheath covering the nerves. As a result, the nerve signals travel too slowly and can result in the nerve fibers being totally destroyed. It usually comes on suddenly after a GI infection or lung infection. The end result is some degree of motor function loss or damage to the motor nerves. CIDP is a more chronic form of Guillain-Barre.

They did a study to find out whether or not Lupus patients who also had Fibromyalgia were more likely to have Orthostatic Tachycardia, also called Neurally mediated hypotension.

They found that 47.9% of Lupus patients had Neurally mediated hypotension(NMH), Seven of the patients in the study had NMS and POTS. Two patients had borderline results because they didn't show enough of a drop in systolic BP when they stood. 23% of the SLE patients had fibromyalgia.

Eighteen (23.7%) SLE patients had FM and 51 (67.1%) had at least one tender point (TP). The frequency of NMH (first or second stage) in SLE with FM was 58.3% compared with 69.4% in SLE without FM. This indicates that fibromyalgia and NMH being associated with Lupus isn't because NMH causes fibromyalgia.
http://rheumatology.oxfordjournals.org/content/43/5/609.full

This study found in Rheumatology International, July 2006, Volume 26, Issue 9, pp 837–840, showed that 37% of patients in the study who had Lupus also had autonomic symptoms. 18% of them had lab results showing autonomic dysfunction. This dysfunction didn't appear to have anything to do with how long they had had Lupus, lupus activity, disease damage, any particular organ involvement or the presence/absence of peripheral neuropathy. This means they could have autonomic dysfunction without having peripheral neuropathy. http://link.springer.com/article/10.1007%2Fs00296-005-0093-0

Sjogren's Disease effects most notably, the lacrimal glands,(your eyes) and salivary glands(your mouth)  by damaging your ability to produce tears and saliva. It can also damage your lungs, kidneys, bladder, joints, etc.  Sjogren's Disease  sometimes causes autonomic, sensory, and motor neuropathy, as well as CNS lesions/inflammation in the spinal cord and brain. Besides hypotension and tachycardia, these patients often have gastrointestinal problems, difficulty swallowing, headaches, body aches and nerve pain in the arms and legs. They may have hypersensitivity to light, sound, and skin sensation, outside of any migraines.

The thing I find most interesting about POTS and Sjogren's is that dehydration is a symptom of both illnesses. And anhydrosis or the inability to sweat or decreased sweating is a symptom of both diseases. In this case, Sjogren's destroys the sweat glands and in POTS it is caused by nerve damage.  And it would be difficult to tell which one causes which.


Another study  I read at The National Center for Biotechnology Information found the following:

"Patients with POTS have a higher prevalence of autoimmune markers and co-morbid autoimmune disorders than the general population. One in four patients have positive ANA, almost one in three have some type of autoimmune marker, one in five have a co-morbid autoimmune disorder, and one in nine have Hashimoto's thyroiditis." http://www.ncbi.nlm.nih.gov/pubmed/26038344

Other autoimmune conditions that occur with POTS are Multiple Sclerosis (MS),
Ehlers-Danlos Syndrome (EDS) which is more of a connective tissue disease than an autoimmune disease, Celiac Disease, Crohn's Disease, Addison's Disease, Graves Disease, Hashimoto's Thyroiditis, and antiphospholipid syndrome, and Rheumatoid Arthritis.

A severe form of dysautonomia is called Autoimmune Autonomic Ganglionopathy(AAG). Only around 100 people are diagnosed with it each year.

Full of Piss and Vinegar?

A few months ago I went to the ER and they said I had a urinary tract infection AND shingles. And then more recently, I was in the hospital for bradycardia and low blood pressure, probably orthostatic tachycardia. While I was in there, they said I had another UTI. And then I had a third hospitalization.Needless to say, I am suffering from dehydration and have been pushing fluids.

I also have an ongoing problem of kidney stones, which means I am always trying to push fluids. Last week I did a 24-hour urine collection for my urologist because he repeats them every few months to monitor my urine calcium levels, to try to prevent the stones I already have from getting bigger and new ones from forming. And then two days later my internal medical doctor ordered another 24-hour urine study so that she could check my catecholamine levels.

This meme is my life this week.

Autoimmune Diseases and their Associated Antibodies: A Visual Chart

Diagrams of The Sympathetic and Parasympathetic Nervous Systems

Catecholamines

                                                                                         

Right now the thing on my mind is catecholamines. I just did a 24-hour urine study to check my catecholamine levels. So, I've been trying to understand them.

As part of our ability to survive as a species, the human body needs to be able to change internal things from one minute to the next, rather quickly and without our involvement, and regardless of what is happening in the environment outside the body, but also in response to it.

Changes in temperature, the humidity, and barometer or any danger we may find ourselves in, require the body to react quickly in order to maintain homeostasis (the body being in a stable state, normal operation). The hypothalamus does this through the Autonomic Nervous System and the endocrine glands.

The Autonomic Nervous System or ANS is one of the systems in our body that responds to changes in position. Around 25% to 30% of our blood volume is in the upper chest when we are laying down. But when we stand up between 300 and 800 mL of the blood moves to the lower body and extremities, helped along by gravity. This is a 25% to 30% drop in volume. Half of this happens during the first few minutes after we stand up.This causes a drop in the blood flow going back to the heart. That in turn, cause a drop in arterial pressure.

In order for you to remain standing and maintain adequate blood flow to the brain, several systems in your body have to be regulated.One of which is your blood pressure. Your blood pressure as to stabilize within about a minute after you stand up.

In Hyperadrenergic POTS, there is an abnormally large increase in plasma norepinephrine and a RISE of blood pressure instead of a drop when you stand up. The criteria for Hyperadrenergic POTS is an increase in systolic blood pressure >10 mmHg during 10 minutes of head-up tilt(HUT), as well as an increase of plasma norepinephrine, >600 pg/mL.

Patients usually have a rise in heart rate like other POTS patients, but also have symptoms like palpitations,anxiety, tachycardia and tremulousness. When a ganglionic blockade called trimethaphan is administered, they have a larger drop in BP than other patients, and their upright plasma norepinephrine levels are higher than non-hyperadrenergic POTS patients. When upright, individuals may experience a sense of anxiety, tremor, and cold sweaty hands and feet. Also, in a good portion of individuals, there is a significant urge to pass urine after even a short period of time upright (I wonder if this is why I have to run to the bathroom as soon as I stand up?). True migraine headaches are also common.

NMH or Orthostatic Tachycardia  is most likely to occur if you have a decrease in norepinephrine and an increase in epinephrine. POTS is the opposite, it is most likely to result from an increase in norepinephrine and a decrease in epinephrine.


An interesting article I read on Medscape.com said that people with Hyperadrenergic POTS have exaggerated pressor and sometimes tachycardia response to both orthostatic and other types of stress. It said it's important for them to minimize the reduction of blood flow back to the heart and pulse pressure. This can be helped by volume expansion, i.e. staying hydrated, and wearing an abdominal binder, which reduces vein capacity. Physical counter-maneuvers help too. Counter maneuvers are when you contract certain muscles in order to help blood flow back to the heart.

One really interesting thing the article said was that Inderal(propranolol0, which is a non-β-selective lipophilic agent, at about 10mg a day may work better than atenolol, which is a β-selective lipophilic agent. I happen to be on atenolol right now. Some people have such high BP jumps when they stand, (as much as 250/150 mmHg), that they have to be given phenobarbital. Sometimes they are helped
by clonidine or drugs in the same class.

I found the following on a Vanderbilt University website: "Some studies have labeled patients with “Hyperadrenergic POTS” if the patient’s upright plasma norepinephrine level is >600 pg/ml.  Other studies label patients with “Neuropathic POTS”if the QSART sweat test is abnormal.  Someone in the first study might say “I have hyperadrenergic POTS”, while the person in the second study might say “I have neuropathic POTS”.  The truth is that at least some (if not many) of those patients will have both abnormalities.  Often, these terms are not used to describe mutually exclusive subtypes, but to describe specific findings."

One related condition is pheochromocytoma (a norepinephrine producing tumor) and tests may be needed to differentiate between pheochromocytoma and hyperadrenergic POTS.

Another condition that is similar to Hyperadrenergic POTS is Norepinephrine Transporter (NET) Deficiency. It is thought to be an abnormality in a gene that leads to too much norepinephrine circulating in the body. It can be treated with a class of antidepressants called SNRIs, which will block these transporters. However, some people experience an increase in HR and can't take them.

Inappropriate sinus tachycardia or IST has similar symptoms to Hyperadrenergic POTS. IST patients have a high HR when they are laying down (around 90-100bpm), and slight exertion or emotional stress will cause rapid acceleration. Both conditions can overlap and may have the same underlying causes. Treatment options are similar.

I found an excellent explanation of what adrenergic receptors are at Dysautonomia International. "Think of adrenergic receptors like a TV antenna (if you are old enough to remember when TVs had antennas!). If the TV antenna picks up a signal, it transmits a message across the screen. In adrenergic receptors, the “signals” are chemicals present in the body called catecholamines (primarily epinephrine and norepinephrine). The “message” is what the catecholamine tells the receptor to do. For example, constrict a blood vessel or make the heart beat faster."

Some people have been found to have auto-antibodies called adrenergic receptor auto=antibodies. So instead of only fighting off a virus or something, their bodies have made auto-antibodies that have  attacked and damaged important sites on certain cell membrane proteins and altered their normal cell function. There are two kinds of adrenergic receptor auto-antibodies. One affects the blood pressure and causes it to drop and the other effects the HR and causes it to raise.

Did You Know That Lightning Sometimes Precipitates POTS?

My husband was hit by lightning, indirectly twice before he became ill with POTS symptoms. By indirectly, I mean both times he was touching things that were hit by lightning. The first time he was working on wiring inside a metal roofed car dealership's ceiling. The second time, he was welding on a rooftop of a building and a storm started rolling in.

Over the years, I mentioned it to his doctors, whichever one we were seeing at the time. They always looked at me like I was nuts, and that they didn't believe a person could be struck by lightning twice. not seek medical treatment either time and survive. But he was stubborn.

I found some articles about it and now feel somewhat vindicated. What I believe happened was that the lightning damaged the myelin sheath of his nervous system. But the exact mechanism by which lightning causes POTS isn't totally understood.

I'm here to tell you lightning can and does strike twice.

Central Hyperadrenergic State After Lightning Strike

New Onset Postural Tachycardia Syndrome Following Lightning Injury PDF file

Another Good Article I Found On THE MIGHTY

7 Stages I Experienced After My POTS Diagnosis

Nice Article-- How to Help A Loved One With POTS

This is written from the point of view of a patient who suffers from POTS.


how-to-help-a-loved-one-with-postural-orthostatic-tachycardia-syndrome

Poor Man's Tilt Table Testing- How To

Neurogenic Orthostatic Hypotension- Another Category for Orthostatic Hypotension

Things That Help or Hurt When You Have POTS or Orthostatic Hypotension And Contributing Factors

• Sitting or standing for long periods (shop in off-peak hours. Move your legs around)
• Warm environments (hot showers, saunas, hot tubs)
• Sodium/salt depletion 
• Prolonged bed rest
• Varicose veins
• High carbohydrate meals
• Diuretics, vasodilators, alpha-blockers
• Alcohol

  This is because they result in venous pooling and hypovolemia. 

• Stress
• Excercise
• Pain
• Hypoglycemia (low blood sugar)
• Albuterol
• Epinephrine

 They will increase catecholamines.

Some helpful things are:

• Raising the head of your bed
• Compression Garments i.e. support hose, body shapers/girdles. abdominal binders
• Waist high are better than thigh high which are in turn better than knee high 
• Standing with legs crossed
• squatting
• sitting knees to chest
• leaning forward when you are sitting
• elevating your knees when sitting (try using a foot rest)
• clenching your fists when you are standing up

All of these use your own muscles to pump blood. 

• Drink a minimum of 2 liters a day/0.52 gallons/67 ounces
• Drink at least every 2 hours
• Avoid sleeping more than 12 hours a day because you can't drink in your sleep
• Increase your salt according to your taste and add salt tablets

Even though you have exercise intolerance, some exercise is good. Being inactive is bad

• Avoid excessive bed rest/sleeping
• Start excise slowly and gradually increase
• Recumbent exercise bikes or lying on your back are good 
• Swimming
• Manual forms of Physical Therapy can be helpful

You need to be treated for any conditions that contribute to your orthostatic intolerance;

• food allergies
• anxiety
• depression
• pelvic vein incompetence
• EDS/JHS  ( Ehlers-Danlos Syndrome/Joint Hypermobility Syndrome)
• Chiari 1 malformations
• stenosis of the cervical spine
• Migraines
• movement restrictions
• Infection
• allergies/asthma because inhalants make you worse

Medications: Can be used alone or in combinations

• Vasoconstrictors: Midodrine, dexodrine, methylphenidate, SSRIs, SNRIs, aescin(horse chestnut seed extract), L-DOPS(Droxidopa) is being used in trials.
• volume expanders: Sodium consumption or IVs, fludrocortisone/Florinef, clonidine,
• catecholamine release inhibitors:beta blockers, disopyramide, SSRI's, ACE inhibitors
• Other treatments include but are not limited to:  pyridostigmine bromide

Common Findings in (POTS) Postural Orthostatic Tachycardia Syndrome

• More common in women than in men
• It often comes on slowly  or after infection, surgery, or trauma
• Symptoms are often disabling
• People suffer from: fatigue, exercise intolerance, palpitations
• Some of the Pathophysiologies are:

1.  Hyperadrenergic adrenergic/neuropathic forms
2.  Some classify into low, normal and high-flow POTS
3.  Sub categories include hypovolemia, elevated PRA/Aldosterone ratios, AChR ab positive,         NET deficiency

In both POTS and Orthostatic Hypotension, there is often acrocyanosis. This means that hands, lower legs and feet often have a purplish appearance from peripheral cyanosis. 

Symptoms of Orthostatic Hypotension

• Lightheadedness
• Syncope
• Diminished Concentration
• Headache
• Blurred vision
• Fatigue
• Exercise intolerance
• Dyspnea
• Chest Discomfort
• Palpitations
• Tremulousness
• Anxiety
• Nausea
• Nocturia

Common Things Found In Orthostatic Hypotension

• It is the most common cause of recurring syncope
• It is more common in women, young people, and people with low-normal to low BP.
• Common following infection
• Family members are also often affected with the condition
• Findings from physical and lab tests are frequently normal
• Hypotension or low BP goes undetected unless orthostatic stress is prolonged
• Fatigue lasts for hours after syncope

Synonyms for Orthostatic Hypotension

• Neurally Mediated Hypotension
• Vasovagal Syncope
• Neurocardiogenic Syncope
• Vasopressor Syncope
• Neurally Mediated Syncope

Orthostatic HYPERtension: What Is That?

I recently had a short stay in the hospital for low blood pressure and a slow heart rate(also called Bradycardia). I had a few EKG's, an Echocardiogram, and a Stress Test. The doctors took me off of my beta blocker that I have been on for years. When my blood pressure leveled out, they sent me home.

My doctor was out of town at the time and not expected to be back for a few weeks. A few days after I got home, I started having dizzy spells (Syncope). So, I started checking my blood pressure and it was high. I decided I didn't want to go back to the hospital and would wait it out and see what my doctor said when she got back. Since I had gone from really low BP and heart rate to having high BP and HR, I decided to look up how to do a "Poor Man's Tilt Table Test". You can read more on how to do this here. And there is a link to the right on what a tilt table test is.

I had some help doing it, but we did three of them. All three of them caused my BP and HR to raise over the requisite 30 beats above the resting BP and HR.

I knew what Orthostatic Hypotension was. It is sometimes also called Neurally Mediated Hypotension.But with it, your blood pressure drops 25 mmHg, without the increase in HR that I was having. When my husband was diagnosed, they didn't separate out Orthostatic Hypotension from POTS. And depending on who was talking to us, they were using the two terms interchangeably. Now they are two distinct diagnoses, although you can have both.

 I was pretty concerned because I had never heard of BP going up to the degree mine was when I stood up.  So, I did a google search.

I found out that there is a subclass of orthostatic intolerance that causes this called ORTHOSTATIC HYPERTENSION. This is what I could find out about it. There wasn't much information available.

In general, it is simply when your BP rises upon standing. Orthostatic hypertension was defined as either an increase in DBP (diastolic)  from <90 mmHg to ≥90 mmHg or an increase in SBP(systolic) from <140 mmHg to ≥140 mmHg.

Studies have shown that people who have Mast Cell Activation Syndrome and POTS sometimes have Orthostatic Hypertension. People with baroreflex failure also have bouts of it. Another rare condition  called norepinephrine transporter deficiency can also cause this increase in blood pressure on standing. And pheochromocytoma can also cause it. And finally, diabetes can cause it. Diabetics are prone to having neuropathy (nerve damage), and it is likely that neuropathy has some connection to Orthostatic Hypertension.

Patients usually have venous pooling in the lower legs. This means that a large amount of blood collects in your lower legs when you stand up. This causes a decrease in the cardiac output of your heart. That in turn, causes your sympathetic nervous system to become activated. And then your arteries become severely constricted. This is similar to the POTS occurs. POTS happens because of dysautonomia in the lower legs which results in venous pooling. But the difference is that POTS patients don't always have symptoms of Orthostatic Hypertension.

Different studies have used different criteria for diagnosing Orthostatic Hypertension.
One study used the following:  ≥20 mmHg increase in SBP upon assuming an upright posture ( head-up tilting to 70 degrees) from the supine position.

Generally, this result needs to be reproducible because people with conditions like essential hypertension (regular high blood pressure) or diabetes have more variation in blood pressure readings than otherwise healthy people.

Aside from the rise in BP when you stand there are other tests that need to be run in order to diagnose underlying causes. Your doctors need to know if there is something that needs to be corrected with surgery, or if you have baroflex failure.

To treat it, the most obvious line of treatment is to treat your high blood pressure, if you have it. Activation of the sympathetic nervous system should be controlled with things like alpha-1 adrenergic receptor antagonists such as prazosin, or central alpha-2 adrenergic receptor agonists such as clonidine.

More on this subject can be found here: Orthostatic Hypertension: When Pressor Reflexes Overcompensate

New Blood Pressure Monitor

When I was in the hospital last week, the first ER doctor that I saw said, "I'm not a big fan of patients taking their own blood pressure at home." He then went on to say that the reason was that they would fixate on their blood pressure and as a result, their blood pressure would be elevated and not accurate due to stressing. The implication being, that people are generally too stupid to do it at home.

I had been taking my blood pressure because my doctor and my rheumatologist had told me to. Then when I went to see my doctor yesterday, she said that my blood pressure monitor might not be accurate, since she got lower readings in the office.

I had been anticipating this. So earlier in the week, I went on Amazon and ordered a new one. It works with an app on my phone and is supposed to be medical grade equipment. It has excellent reviews. It is very simple to use.

Here's a link to it: iHealth Ease Wireless Blood Pressure Monitor for Apple and Android

A FUNNY VIDEO ABOUT POTS

When I started looking for information on POTS, one of the first things I ran across was this hilarious video. The idea behind it is, just how ignorant doctors are about POTS and how hard it is to get them to listen and learn. 

TEST

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Why Am I Blogging About This? My Life With POTS

I'm not sure what I want to say here. POTS or  Postural Orthostatic Tachycardia Syndrome is a terrible condition to live with. My late father had it. I don't know if it was secondary to his Parkinson's Disease or to his Rheumatoid Arthritis. My late husband had it as well. It was very debilitating for him. He had seizures as a result of it and ultimately he had a seizure and went into cardiac arrest and died. That is called SUDEP.

The Epilepsy Foundation defines SUDEP as "the sudden, unexpected death of someone with epilepsy, who was otherwise healthy. No other cause of death is found when an autopsy is done. Each year, more than 1 out of 1,000 people with epilepsy die from SUDEP. If seizures are uncontrolled the risk of SUDEPincreases to more than 1 out of 150."

There aren't enough doctors who even know what POTS is or how to diagnose it or even the difference between it and Orthostatic Hypotension or Hypertension.

I felt that POTS had taken enough from me. Then I recently started having symptoms of my own. It's a lot to handle. There is so much information to absorb and try to understand. And much of it is different than when my husband was diagnosed.

I figured as I find the information and learn from it, I could post it on this blog so that someone else might benefit from it. In the end, maybe there will be some benefit to this blog for me as well.