It's good to know that if there is money in it, they will be trying to find treatments for POTS.>insert sarcasm<
"Postural orthostatic tachycardia syndrome treatment market is expected to show significant growth over the forecast period owning to factors such as, increasing awareness and diagnosis. Unavailability of the specific treatment is a hindrance for the growth of postural orthostatic tachycardia syndrome but few drugs are under clinical trials which are expected to get marketing approval over the forecast period and fuel the growth of postural orthostatic tachycardia syndrome treatment market. "
I recently watched a video that was posted in a POTS support group. The man on the video is a chiropractor, Dr. John Bergman.
The makes it sound like things like beta blockers and tricyclic antidepressants are how POTS is typically treated. Later in the video he seems to imply that he can cure or treat POTS by doing chiropractic manipulation.
He does teach physiology, an offshoot of biology. But he really doesn't go into how the organs work much. His other field is biomechanics which is more akin to chiropractics than anything to do with neurology and internal organs. He also lists anatomy, but he pretty much skips over how the organs affect POTS.
I don't buy into the idea that you can use chiropractics for the treatment of orthostatic intolerance. And I hope you will consider all of the information here that disagrees with it. There are too many other mechanisms involved and you need to know what is causing YOUR POTS as opposed to someone else's. After you read this post, if you still think chiropractics is the way to go, there isn't much else I can say to disuade you. Underlying Causes of POTS What Is Causing Your POTS? And Why It IS A BIG DEAL: A Printable, Sourced Guide
Dr. Bergman gives very rudimentary explanations for the mechanisms that cause POTS. They are not always the same for every patient. That is why it is called a Syndrome vs Disease.
Not all POTS patients have low blood volume. It is very important to identify the type of POTS or the underlying condition that may be causing POTS because it can help your doctor decide what strategy to take for treatment. Different types of POTS include neuropathic POTS, hypovolemic POTS, hyperadrenergic POTS and POTS to due to de-conditioning. Some people have
more than one of these that cause their POTS. People with neuropathic POTS can have adrenal impairment and sudomotor denervation, which is nerve damage. This is why treatment is never a
one size fits all thing. There are even people who have autoimmune causes for their POTS, like autoimmune autonomic ganglionopathy POTS Subtype: Does It Really Matter?
"Another problem with these labels is that they are not mutually exclusive."
One of the first things he says is that doctors don't know what causes reduced blood flow returning to the heart. He quotes a NINDS Postural Tachycardia Syndrome Information Page But the dysautonomia information network gives an explanation for it. POTS mechanisms: dysautonomia information network It could be that no matter how fast the heart beats if the blood vessels in the lower body don't constrict enough to raise blood pressure, not enough
Beta blockers-- also known as beta-adrenergic blocking agents are drugs that block norepinephrine and epinephrine (adrenaline) from binding to beta receptors on nerves. Now just from that definition, you can understand that something is wrong with the adrenaline system or the receptors. He is indicating that they are bad for all patients and that they are routinely prescribed for all POTS patients, which they aren't. He says he watched a video or a speech where a Mayo Clinic doctor was saying that beta blockers work for most patients and that they work much better than calcium channel blockers. It is true that they work better than calcium channel blockers. But not that all doctors give them to all patients. And it isn't recommended to give ACE inhibitors or diuretics, but he has a slide up and makes it sound as if that is how it is commonly treated. At least some of the doctors at the Mayo Clinic say to try nonpharmacologic treatments before beta blockers. Postural orthostatic tachycardia syndrome and chronic fatigue in adolescents: Working toward recovery
"Beta blockers, including propranolol, block the receptors that are responsible
for the effects of epinephrine and norepinephrine (catecholamines produced
by the sympathetic system).We have shown in a placebo-controlled trial that
propranolol decreases heart rate and acutely improves symptoms in patients
with POTS. Interestingly, we found that symptoms were more improved by
low dose rather than high dose propranolol." Vanderbilt Autonomic Dysfunction Center--Propranolol
"The use of beta blockers in POTS is controversial, but we have seen many patients, including those who have previously failed beta blocker therapy, have success with propranolol.
They shouldn't be prescribed for all patients. However, some do benefit from a low dose."
"Some patients, particularly, those with partial dysautonomic POTS, improve on small doses
of beta blockers (e.g. metoprolol 25–50 mg once or twice daily), but the majority feel
worse on beta blockers." "The combined alpha1/beta blocker labetalol is useful in some
patients, as beta-blockade alone may worsen symptoms due to unopposed alpha-receptor
stimulation. A starting dose of 100–200 mg twice daily is used, and the maximum dose is
400 mg twice daily." Postural Orthostatic Tachycardia Syndrome (POTS): A Diagnostic Dilemma
Well, logic would tell you that for some people they will work and for some they will make things worse. That's why it's good to find out what is causing the POTS. For those who do take them, the goal is to find a dosage that slows down the tachycardia without lowering the BP too far. Sometimes it is a very low dosage. He says that it is recommended that beta-blockers be used to treat POTS and that isn't true. It is only used for some patients, not all. The above link basically talks about how it is necessary to find out what the cause of the POTS is in order to treat it properly.
Dr. Bergman points out that the heart rate speeding up is a good thing because it is your body's way of making sure blood gets to your brain and says it doesn't make sense to use beta blockers because they will slow your heart rate down and then you will get less blood flow to the brain. But he leaves out a very important fact: Studies show that long-standing persistent tachycardia in certain conditions has a potential to induce a dilated cardiomyopathy (or an enlarged and weakened heart). Tachycardia-induced cardiomyopathy can result from prolonged periods of rapid heart rates. Granted these studies were on people that had tachycardia from things like Afib or ventricular tachycardia, but it is believed that the same thing can happen from the tachycardia in POTS. Basically,where he was wrong was in indicating that the heart rate just raised and not that it raises too high, which is why it sometimes requires treatment. A resting heart rate that is over 100 bpm is tachycardia.High Heart Rate Increases Risk Of Death, Even In Fit People "resting heart rates over 90 beats per minute tripled the risk.... Every 10 to 22 additional beats per minute in resting heart rate raised the likelihood of death by 16%, overall, according to the authors." Myth: A Normal Heart Rate Is 60-100 beats per minute. " Many doctors think it should be lower. About 50-70 beats per minute is ideal, says Suzanne Steinbaum, MD, director of women's heart health at Lenox Hill Hospital." 5 Heart Rate Myths Debunked But aside from that, you won't necessarily have low blood because of a lower heart rate. Busting 5 Myths About Blood Pressure and Heart Rate He says that anything that reduces oxygen to the brain, i.e. a lower heart rate is bad. He uses the example of a giraffe and says that the giraffe would have to have a higher heart rate to get oxygen to its brain. But having a high heart rate isn't good either. "Circulatory shock, commonly known as shock, is a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function. The typical signs of shock are low blood pressure, rapid heart rate, signs of poor end-organ perfusion (i.e.: low urine output, confusion, or loss of consciousness), and weak pulses." Shock (circulatory)And then he says that water and appropriate nerve supply are the way to treat POTS. But those things can't always be fixed so easily either.
But it also necessary to understand how the autonomic system works and that it is not entirely controlled by the spine. You can't just fix the spine and think that will fix the whole system.
For instance, if you are one of the people who have serum auto-antibodies to alpha-3-acetylcholine receptors of the peripheral ganglia then you can't alter the autoimmune response by spinal manipulation.
It causes increased noradrenaline due to impaired clearance or decreased uptake of noradrenaline by the synaptic cleft. The synaptic cleft is a gap between neurons somewhere in your body. Not in your spine. Here's a video of how that works.
(Given how dumb that guy thinks people are, it's kind of amusing that the video
called A level biology. This is just basic biology/anatomy.)
The Brain—Lesson 2—How Neurotransmission Works
Hyperadrenergic state means that more adrenaline than usual is released, and then on top of that, it isn't reabsorbed like it should be. Again, you have both a gland that is being overactive as well as nerve receptors not working right either, i.e. some sort of neuropathy.
Selective serotonin reuptake inhibitors. The reason for those is because the nerves are not working properly and they basically reabsorb the serotonin before they should.You need the serotonin to help with vasoconstriction. And contrary to what he implies, it doesn't all originate in the gut. And some people are born with a genetic difference that causes their serotonin problem.
SSRIs will make existing bipolar worse, and that sometimes means that someone who was misdiagnosed with depression will suddenly become much more manic. But it doesn't cause them to be bipolar. That is an outdated idea. DSM-5 now says that it isn't the medicine it is that they were
misdiagnosed because bipolar often presents with several bouts of depression.
He points out that tricyclic antidepressants are on the list of drugs that make POTS worse, but those are an entirely different kind of antidepressant and work differently and he says they are one of the most prescribed drugs. But they really aren't recommended. POTS: What to Avoid He doesn't make clear whether or not he means in general or for POTS. There is no doubt that a certain percentage of people can become suicidal on antidepressants, but it's irresponsible to indicate that everyone or even a large percentage of people will or that they will become bipolar. For one reason, it's difficult to tell if a person who is put on an antidepressant might not have committed suicide regardless of whether or not they were put on medication. There is an increased risk in some studies, but in others there is a decreased risk. Antidepressants and Suicide in Adolescents and Adults
People usually become bipolar before the age of 25. He also says that the tricyclics are one of the most prescribed drugs for POTS. But that isn't true. SSRI and SNRI are the usual ones, particularly Celexa Autonomic Disorders: Syncope Dysautonomia & POTs or Postural Tachycardia Syndrome . That's why that list he was reading off said they would make POTS worse. It was so that doctors would be careful about using tricyclic antidepressants for POTS, not to suggest them for treatment. The dysautonomia information network says to avoid them. And they are quoting Dr. Blair Grubb at the University of Toledo Medical Center. He is one of the leading experts on POTS. So the experts are not recommending them as is implied.
I don't know if he figures the average person doesn't have a very good understanding of the body, or if he himself doesn't. I mean the way he presents the video is that he is trying to make a complicated subject easier to understand. But you don't do that by leaving out part of the information or being inaccurate.
He keeps saying that people just need more water and not beta blockers. Again, not everyone is prescribed beta blockers and some people have POTS because no matter how much water they drink, their body doesn't utilize it properly.
Sodium and potassium in the body are very important and besides controlling water in the body they also help with the voltage in the nerves and outside the nerves.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.This basically means that if you aren't adding extra salt to your diet, it won't matter how much water you drink. If for some reason your kidneys aren't releasing ADH (anti-diuretic hormone) then how much water you drink isn't going to help either.
"Patients should not drink excessive amounts of water because doing so can cause
essential electrolytes to become diluted in the bloodstream, which may affect heart
rhythm." POTS: What Helps
You can also find some basic information on how salt and your kidneys affect how your body uses water, despite how much you drink. If you drink more water than your kidneys can handle and the sodium in your body gets diluted it is called hyponatremia. The recommended amount of water
is about 64 oz. or about 2 liters. For men. the amount is higher, about 3 liters. That's about eight 8 oz. cups(13 for men). Preventing and treating orthostatic hypotension: As easy as A, B, C
You might want to drink more if you are in a hot climate or exercising. Then you could drink about twice that if you are a man. It's right after he tells people how much water they should be drinking and how much salt they should consume that he says there shouldn't be one guideline for anyone but different amounts for different people. This is kind of amusing considering for the rest of the video he is basically telling everyone to do the same thing. Even though he says that no two people will need the exact same spinal adjustment, he is still implying that everyone with POTS regardless of cause needs their spine adjusted.
Adrenal fatigue, he indicates that it is only caused by stress. It isn't even a proven medical condition. For those that believe in it, it is hypothesized that in the early stages there is too much adrenaline due to stress and then later not enough adrenaline. The theory is that the adrenaline is just slightly
low and that blood tests aren't sensitive enough to show it. But actual adrenal insufficiency can be found by tests. It is also known as Addison's disease. And that isn't caused by stress. It is an autoimmune disease. You can't cure that by reducing stress.
He says this unrecognized condition of adrenal fatigue causes autoimmune disease. But Addison's
disease an autoimmune disease itself and is often found with other autoimmune diseases like thyroid disease. To put that another way: he is saying that adrenal fatigue causes Addison's disease. Now how in the world does having a slightly lower than normal adrenaline level, (because that is what adrenal fatigue is) cause an autoimmune disease? All of the other symptoms he lists are caused by autoimmune diseases too.
POTS is often misdiagnosed as anxiety/stress or as this guy indicated it is said to be the cause of
it. It is true that POTS and anxiety are associated with over-activation of the sympathetic nervous system. But POTS happens because of things that are activated by standing or physical activity. But anxiety/stress can occur regardless of your body position. While he is talking about hyperadrenergic POTS and says that it can be caused by impaired clearance or decreased uptake by the synaptic cleft, he then turns around and says too much adrenaline is caused by physical, chemical or emotional stressors. But he just said that a Postgraduate Medical Journal said it was caused by not being reabsorbed like it should not by too much being released. One type of hyperadrenergic POTS is caused by a tumor called pheochromocytoma. That is most definitely not caused by a chronically stressed state.
He points out that he did a search for vaccines that cause POTS and got 9,440 results, allowing the viewer and his audience to believe that there are other vaccines that cause POTS. And he says not to take any vaccines even though HPV/Gardasil is the only one that he points out as causing POTS. If you do a search, that is probably the only one you are going to find either. And only 3 states mandate HPV vaccine for school, but he says they all do. He also says that boys have to take it even though it's just to prevent cervical cancer. It also isn't a vaccine for cervical cancer. It is for genital herpes, which can cause cervical cancer and genital cancer in boys and anal cancer in both. Besides preventing genital cancer in boys, the idea is to stop the spread of it because if a boy gives it to a girl she can then get cancer and so can he. I'm not recommending the vaccine, just pointing out how inaccurate the things he says are.
As it turns out he was wrong even about Gardasil causing POTS. So, it doesn't matter what anyone turns up in a search because the CDC determined that it doesn't and the old links are now outdated. "In November 2015, the European Medicine’s Agency completed a detailed review of available POTS data from young women who received HPV vaccines. The review found that the evidence does not support a causal link between HPV vaccines and POTS." Centers For Disease Control:Frequently Asked Questions about HPV Vaccine Safety I don't know when he made the video, but it was just uploaded a few days ago. So the information was out there for him almost a year ago.
Antibiotics: he names them off as bad too. What do you do if you have an autoimmune disease that causes your POTS and you are on an immunosuppressant and get an infection?
It seems like much of what he says is unfounded information. He could be correct about some things, but I wasn't able to find sources that backed him up, and it was a lot easier to find sources that contradicted him.
He recommends really high doses of vitamin D.(8000 IU per day).
Then he says chiropractic adjustment takes pressure off of the nervous system. But there is much more to the nervous system than just the nerves.
There are even three different parts to the nervous system, the central(CNS), peripheral(PNS), and autonomic nervous systems(ANS). You can think of it like this: The CNS sends commands out to the PNS. The PNS has receptors that are affected by chemicals and they send information back to the CNS which is the brain and spine.
Sometimes information goes straight to the brain so that the brain can decide what response to have. Other times, information goes to the spine and the spine basically makes the decision before it ever gets to the brain. This is called the reflex loop.
If this was what always happened, then it would make sense for spinal manipulation to work. But it isn't. You can work on the spine all you want, but it won't either make the brain work better or have any effect on those receptors on the other end of the PNS.
There are lots of things that can interfere with this communication system. For instance, the myelin sheath on nerves can be damaged. This happens with Multiple Sclerosis or a severe electrical shock or lightning strike. Myelin serves the same purpose as the plastic coating on an electrical wire. It keeps the electrical charge from leaking into the surrounding tissue. If it's damaged, the signals can fade or disappear. This is called demyelination. They don't get where they were supposed to be going.
He briefly touched on the parasympathetic and sympathetic nervous systems, which are the chemicals switching on some things and switching off some things. Those fight or flight hormones are also
countered by rest and digest hormones that control things like your digestive system.It cannot be helped by working on your spine.
The autonomic nervous system could also be called the automatic nervous system and it is controlled by your brain stem. It controls things like your internal organs. He refers to a journal that calls those organs your viscera. You would be well advised not to mess with your brain stem by doing some kind of adjustment, particularly in an effort to effect the heart. When he quotes a journal saying that it(manipulating the spine to affect the heart) MAY work, he is quoting a chiropractic journal(Journal of Manipulative and Physiological Therapeutics) and not a medical journal. If you look that journal up it says that this is at odds with classic views of neuroscientists about the potential for somatic stimulation of spinal structures to affect visceral function. http://www.jmptonline.org/article/S0161-4754(00)90076-9/abstract Why do you suppose he chose to leave out that neuroscientists don't agree with this theory?
When he starts talking about the sympathetic nervous system being located in the thoracic spine, that is true. But when it sends out signals, it also needs those chemicals/neurotransmitters like acetylcholine and norepinephrine sometimes called noradrenaline.
Part of the parasympathetic nervous system originates in the sacrum/lower spine and some of it up in the brain stem area called the medulla. It also requires acetylcholine. He says that if you work on one of these areas of the spine it will change the nerve supply and function of the organs.He seems to be talking about the sympathetic area of the spine and forgetting that the parasympathetic system
even plays a part. The reason I say this is because he refers to the thoracic area of the spine and
keeps talking about the "fight or flight" response and stress. But some people with dysautonomia
have problems with the parasympathetic nervous system. If you think of the sympathetic nervous
system as the ON switch and the parasympathetic as the OFF switch. A problem can be just as much a problem of the OFF switch not working as it can be of the ON switch working too much. The sympathetic nerves originate in the spinal area; they are fairly short and close to the organs they stimulate (a few inches in length). When they switch on, they do so quickly and the entire system is "on." The parasympathetic nerves, on the other hand, originate mostly from the brain, but some originate from the bottom of the spine, so they travel much longer distances to the organs which they stimulate (several yards); they are much slower to react and because of this it takes a much longer time for the body's systems to "turn off." You can easily see from this explanation that because some of these nerves originate in the brain, working on the spine won't fix problems with how they work.
If you think of this like a telegraph system, then he is talking about working on the telegraph machine itself. But then you still have the wires themselves as well as the telegraph machine on the other end that he isn't taking into account. Then you have to factor in the chemicals and hormones which are basically the electricity running through that wire.
He points out exercise as being a treatment for POTS. The problem is it doesn't work for everyone.
They have also done studies that show why it doesn't work. It is coauthored by Svetlana Blitshteyn
She is another expert on POTS.
"This study provides the first objective evidence that low ventricular filling pressures
in patients with POTS are contrary to what would be expected in deconditioned
patients—high filling pressures.Although the benefits of exercise have been acknow-
ledged in several studies, almost 60% of patients with POTS are unable to complete
an exercise training program despite their efforts. Importantly, Oldham et al.
demonstrate that exercise intolerance in POTS is not caused by a lack of maximum
effort from the patient but that low ventricular pressures occur despite the maximum
effort." Pulmonary Vascular Research Institute.
I can entirely understand not wanting to take medications that might have side effects.
But it is bad medicine to say that it is a viable option for everyone. If you keep an open mind and really want to understand how your nervous system works and watch these videos, you can learn. And once you do, it probably won't seem so much like what he says makes any sense. Just because he is recommending not taking medicine,which works for some patients, doesn't mean that everything else he says makes sense.
You will see that there is much more involved than just the spine. He way oversimplified it. For instance, spinal manipulation might help if you have bowel problems related to your POTS causing a balancing effect on the nerves that supply impulses to the intestinal tract.
But what about that serotonin that originates in the gut or other neurotransmitters? If those are out of balance, you may still have problems. That doesn't even factor in the enteric nervous system. It works like a secondary brain and has structures and chemicals similar to those in the brain. It has sensory and motor neurons and information processing circuits, as well as glial cells. It uses neurotransmitters: dopamine, serotonin, acetylcholine, nitric oxide, and norepinephrine. It even has benzodiazepines, similar to Valium and Xanax.
The Nervous System - CrashCourse Biology #26
Autonomic Nervous System: Crash Course A&P #13(This one explains how the parasympathetic
and sympathetic originate in different areas of the body)
Sympathetic Nervous System: Crash Course A&P #14 This one explains how hormones and neurotransmitters are necessary to the system. And they have nothing to do with chiropractics. And quite a bit to do with nerve receptors. If you pay close attention it touches on alpha and beta receptors, which are why beta blockers are used. And the adrenal glands, which if there is something wrong with them, cannot be fixed by spinal manipulation or drinking water.
Parasympathetic Nervous System: Crash Course A&P #15 This one explains how your parasympathetic system is supposed to keep your heart rate down. Remember that it doesn't originate in the thoracic area that this guy keeps referring to. And many of them don't even run through the spine. Check out the vagus nerve which goes from the brain directly to the heart, lungs, and stomach. No spine involved.
Peripheral Nervous System: Crash Course A&P #12 The peripheral nervous system doesn't start at the spine. It starts on the other end. And if the receptors, etc. on that end don't work right, they aren't going to send information back to the spine the way they should. And even though the information goes through the spine, ultimately it should end up in the brain. And the brain should affect the response.
I gave a lot of sources because at the end of his video he gave some sources. The first page
and a half of them are about side effects of medicines that I have shown are not always given for POTS and many of which aren't recommended by doctors who specialize in POTS, like cardiologists and neurologists.
Chiropractic manipulation has its place. It eases people's pain and that will help their overall health but in my opinion, it doesn't seem to be good science to say that it can do the things he claims.
There is a difference between Orthostatic Hypertension and Orthostatic Hypotension. It seems to be more unusual and there isn't much information to be found. I did, however, find some since that seems to be more in line with my personal symptoms. Here are the links to the PDF at two different sites. http://www.medscape.com/viewarticle/543590http://www.nature.com/nrneph/journal/v2/n8/full/ncpneph0228.htmlAt medscape, you have to create a username. But it is free and worth it because they have many medical articles that you can't find elsewhere. This is another one, AHA Journals: Orthostatic Hypertension Due to Vascular Adrenergic Hypersensitivity Orthostatic Hypertension in Patients With Type 2 Diabetes AHA Journals: Relationship Between Extreme Dippers and Orthostatic Hypertension in Elderly Hypertensive Patients I am going to try and give a brief overview (well as brief as possible). This is a direct quote from the first article: "Orthostatic hypertension—a rise in blood pressure upon assuming upright posture—is an underappreciated and understudied clinical phenomenon. There is currently no widely agreed-upon definition of clinical orthostatic hypertension, the current definitions being operational within the context of particular studies. The underlying pathophysiology is thought to involve activation of the sympathetic nervous system, but the actual etiology is poorly understood. Orthostatic hypertension is observed in association with a variety of other clinical conditions, including essential hypertension, dysautonomias, and type 2 diabetes mellitus. Orthostatic hypertension has been associated with increased occurrence of silent cerebrovascular ischemia and possibly with neuropathy in type 2 diabetes. So, appreciation of the true incidence of orthostatic hypertension, elucidation of the underlying pathophysiology, and an understanding of potentially effective treatment approaches and their associated risks and benefits might all have major clinical significance. Orthostatic hypertension is an aspect of hypertension that is in need of further focused investigation." Ordinarily, when you change from lying down or sitting up to a standing position, your blood pressure will drop slightly. This is because of "a redistribution of blood volume into the lower abdomen, buttocks, and legs under the influence of gravity".
For most people, the change is very slight and systems in your body quickly engage and compensate for the change in positions. Usually, baroflex receptors cause some of your arteries like the ones in your neck to stretch so that you can get more blood flow to your brain. And your body senses a decrease in BP in your chest and abdomen and your sympathetic nervous system kicks in and increases activity and there is also a corresponding decrease in the parasympathetic nervous system. Basically, this means that hormones in your body regulate your blood pressure to compensate for your change in position from prone to sitting and from sitting to standing.
Because your blood plasma volume decreases, your systolic blood pressure increases and your diastolic blood pressure drops slightly, as well as having a slight rise in heart rate. There is also an increase in norepinephrine, epinephrine, active plasma renin, aldosterone, and vasopressin. Your sodium reabsorption increases and your potassium excretion are increased by your kidneys. All of this is controlled by your sympathetic and parasympathetic nervous system, and in turn controlled by the baroflex response.
I have other posts here about orthostatic HYPOtension. That is when your BP drops 20/10 mmHg when you stand up. You also have of cerebral hypoperfusion, including dizziness or lightheadedness, visual changes, discomfort in the head and neck, fatigue, and frank syncope.
The first article above says that POTS frequently presents with no drop in blood pressure, or with a mild orthostatic HYPERtension.
Again, orthostatic HYPERtension is when your BP raises when you stand up. In order for there to be a diagnosis of Orthostatic HYPERtension, there needs to be an increase in systolic BP of 20 mmHg. How this plays out for me personally is very confusing. For instance, sometimes, my BP will raise by the required amount when I sit up from lying down, and then it will gradually drop as I am standing. Other times it has raised dramatically, even higher than the required amount. I do not have high hopes of getting a diagnosis, as I have been hospitalized recently for both low blood pressure and high blood pressure. I think at the very least I have some severe dysregulation. My late husband and father both had classic orthostatic HYPOtension and POTS. I would truly like to have a greater understanding of these conditions because I have children and grandchildren who could potentially develop them. Most people think that it any of these disorders are just a condition that you have to live with and they are just annoying. According to the article: " orthostatic hypertension might be a symptom of another treatable condition, such as pheochromocytoma or mast-cell activation disorder in the context of POTS.And "orthostatic hypertension resulting from any number of causes might be an important risk factor for silent cerebrovascular ischemia and infarct. Published studies from the Shimada laboratory indicate that, at least in populations of elderly Japanese people with essential hypertension, the incidence of silent cerebrovascular infarct detectable by MRI is higher in those patients who have clinically identifiable orthostatic hypertension."Some of these terms like pheochromocytoma are unfamiliar and confusing so I am going to link them to definitions when possible. I should have done that with my earlier posts. That one is basically a non-cancerous tumor on your adrenal gland.
These are the symptoms:
High blood pressure
Rapid or forceful heartbeat
Profound sweating
Severe headache
Tremors
Paleness in the face
Shortness of breath
Anxiety or sense of doom
Abdominal pain
Constipation
Weight loss
For some people, the spells last 15-20 minutes and can happen several times a day. Some people's BP is normal between spells and for others it stays elevated.These are some of the triggers:
Physical exertion
Anxiety or stress
Changes in body position
Bowel movement
Labor and delivery
Foods high in tyramine, a substance that affects blood pressure, also can trigger a spell. Tyramine is common in foods that are fermented, aged, pickled, cured, overripe or spoiled.
These foods may include:
Some cheesesSome beers and wines
Dried or smoked meats
Avocados, bananas, and fava beans
Pickled fishSauerkraut or kimchi
Certain medications that can trigger asymptomatic spell include:
Decongestants
Monoamine oxidase inhibitors (MAOIs), such as phenelzine (Nardil), tranylcypromine (Parnate) and isocarboxazid (Marplan)
Stimulants, such as amphetamines or cocaine
It is unknown what causes these tumors. Your body uses the adrenaline/epinephrine and norepinephrine produced by your adrenal glands, in the fight or flight response. Basically, in a stress situation, your body uses adrenaline to raise your BP and norepinephrine to slow down things in your body temporarily, like if a bear attacks you, you don't need to be digesting supper at that moment, so that would slow down in order to shift resources to more important things like running away. A pheochromocytoma causes an excessive release of these hormones. Less common signs or symptoms may include:I found it interesting that the cells that can cause one of these tumors can be found in other areas of the body. When they do, they are called paragangliomas. They can be in your heart, head, neck, bladder, back wall of the abdomen and along the spine. I believe my husband may have had one on his spine. I know he had what they called a benign tumor of some sort there. But doctors didn't connect it to his condition, and I was ignorant.
There are genetic conditions that predispose you to this condition.
These genetic conditions include the following:
Multiple endocrine neoplasia, type II (MEN II) is a disorder resulting in tumors in more than one part of the body's hormone-producing (endocrine) system. The locations of other tumors associated with MEN II include the thyroid, parathyroid, lips, tongue and gastrointestinal tract.
Von Hippel-Lindau disease can result in tumors at multiple sites, including the central nervous system, endocrine system, pancreas and kidneys.
Neurofibromatosis 1 (NF1) results in multiple tumors in the skin (neurofibromas), pigmented skin spots and tumors of the optic nerve.
Hereditary paraganglioma syndromes are inherited disorders that result in either pheochromocytomas or paragangliomas.
Interestingly, I have been told I have benign cysts on my liver, my kidneys, and on my thyroid. I also have had problems with my pancreas. My father had a tumor on his pituitary gland. So there may be something here for me.
Sometimes this requires the removal of the adrenal gland affected and it can be cancerous. I don't know what they do if the tumors are somewhere else in the body.
Mast cell activation syndrome is complicated. Mast cells, if you are familiar at all with them, are associated with allergic responses. They release histamines that cause itching and hives. They also have a role in healing the body and the immune system. Somehow they can also be paired on autonomic nerve fibers. Hence the association with dysautonomia.
They can release up to 200 different kinds of chemicals, and they produce, histamines, prostaglandins, and leukotrienes. For some people, there may be a malfunction in this system.
People with mast cell problems can have abdominal pain, cramping, diarrhea, flushing, itching, wheezing, coughing, lightheadedness, brain fog, and memory problems. Those symptoms can all be caused by other conditions. But there are some people who have these symptoms along with POTS.
There are tests for it. One is for tryptase, which is a protein that is made by mast cells. Elevated levels occur as a result of severe allergic reaction OR if your body makes too many of them, which is called mastocytosis. If you have too many, they will sometimes to a bone marrow biopsy. Mastocytosis is caused by a genetic mutation, that causes a cell to grow and divide uncontrolled. The treatment for it is different than for MCAS Most people with POTS don't have elevated tryptase or mastocytosis.
But they can have elevatedhistamines, prostaglandins and leukotrienes, which can be found in a 24 hour urine test. If they are elevated, then a diagnosis of MCAS, mast cell activation syndrome is usually made.
Here are the criteria:
Symptoms consistent with chronic/recurrent mast cell release
a. Recurrent abdominal pain, diarrhea, flushing, itching, nasal congestion, coughing, chest tightness, wheezing, lightheadedness (usually a combination of some of these symptoms is present)
Laboratory evidence of mast cell mediator (N-methyl histamine, prostaglandin D2 or 11-beta- prostaglandin F2 alpha, leukotriene E4 and others)
Improvement in symptoms with the use of medications that block or treat elevations in these mediators
The article I got this information from on dysautonomia international's blog says that the labs need to be sent on ice or they might come back falsely normal. And that they should be done after a flare-up of symptoms is possible. They also say that they are not always 100% accurate and should be interpreted carefully.
It says that if you have POTS or some other dysautonomia and also have some symptoms that seem allergic, you should ask your doctor about getting tested for MCAS. And it says that an allergist or immunologist is more likely to be familiar with MCAS.MCAS Mast Cell Activation Syndrome
Okay, back to the subject at hand, orthostatic HYPERtension.
Orthostatic hypertension
Systolic blood pressure increases by at least 20 mmHg upon standing(note:other studies only require a 10 mmHg change)
No change in diastolic blood pressure has been defined
That is different from Orthostatic HYPOtension, in which
Systolic blood pressure decreases by at least 20 mmHg upon standing
Diastolic blood pressure decreases by at least 10 mmHg upon standing
The older criteria for Orthostatic HYPERtension was a diastolic BP that was already 90mmHg and raised even higher when standing. While I am on beta blockers, mine tends to be just under that, at least part of the time.
People with Orthostatic HYPERtension also have a decrease in cardiac output, more venous pooling in the lower extremities and higher plasma norepinephrine levels when they are standing. I have no idea how they measure that. I assume with blood tests for the norepinephrine and possibly measuring your legs for swelling or just observing changes in color.
The theory is that the venous pooling in the lower body causes a decrease in cardiac output, which causes sympathetic nervous system response and an increase in diastolic BP.
Around 11% of older people who already have high blood pressure or hypertension also have orthostatic HYPERtension. And they are more likely to have silent cerebrovascular infarct.
About the same amount of people have orthostatic HYPOtension and they are also at risk of a
silent cerebrovascular infarct.
There are also people who are what they call an 'extreme dipper'. This means their systolic BP drops during the night. People who do this have a 72% likelihood of having orthostatic HYPERtension compared to the above 11%. They are also 53% more likely to have a silent cerebrovascular infarct. They are also more likely to have a regular stroke and don't recover as well.
Both people with Orthostatic HYPERtension and HYPOtension are more likely to have lesions on the central nervous system that can be detected by MRI.
The medical article I read said that a recent study showed that people with POTS and MCAS, mast cell activation syndrome, 38% of them had Orthostatic HYPERtension. I feel it necessary here for clarity to define POTS.
Dysautonomia International says that it is "a heart rate increase of 30 beats per minute (bpm) or more, or over 120 bpm, within the first 10 minutes of standing, in the absence of orthostatic hypotension".
So we are discussing BP changes, but POTS is a heart rate change, that can sometimes be concurrent with the orthostatic changes, but is a separate diagnosis.
Some of the patients in the study had orthostatic HYPERtension that was persistent in an upright position or sometimes they had a hypertensive crisis. A hypertensive crisis is a BP that is 180/120 and can go as high as 240/140. They say that it hasn't been observed in patients with POTS bub without MCAS.
People with Baroflex Failure can also have orthostatic HYPERtension.
Baroreflex Failure is a rare disorder characterized by a change of blood pressure with episodes of severe hypertension (high blood pressure). There can be increased heart rate during stress and hypotension (low blood pressure) with normal or reduced heart rate during rest.
Symptoms may include:
Headache
Excessive sweating
Extremely high or volatile blood pressure and heart rate with spikes in blood pressure in response to stress, with periods of normal or even low blood pressure during rest.
Heart rate that does not respond to medications intended to improve it.
Causes of Baroreflex
Possible causes may include:
Surgery and radiation for cancer of the throat
Injury to the glossopharyngeal and vagus nerves (nerves involved in sensing blood pressure)
Cell loss on both sides in the nuclei of the solitary tract (NTS, a column of cells located in the medulla) in the setting of a degenerative neurologic disease of the brain.
For many patients, the cause is unknown.
I'm leaning towards this for my own problems because I have had both low blood pressure and high blood pressure and the rise in heart rate. Also, my urine test didn't indicate Pheochromocytoma.
The treatment for Baroreflex Failure is medication to control blood pressure and heart rate and to reduce stress.
The purpose of Baroflexes is to buffer changes in arterial pressure so that excessive fluctuations of blood pressure are avoided. Baroreceptors are mechanoreptors in each carotid sinus brain stem and the aortic arch, and their function is to sense pressure changes caused by distention of the blood vessel walls send information about distention of the vessel wall by the glossopharyngeal nerves to the brain stem. There are baroceptors in the aortic arch and the large vessels of the thorax that transmit information through the vagal nerves to the same area of the brain stem. The blood volume in the thorax is sensed by low-pressure receptors that are linked to the vagal nerves and the brain stem.
Problems in the baroceptors, the glossopharyngeal or the vagus nerves or the brain stem all could cause baroflex failure. Sometimes the terms baroflex failure and autonomic failure are used interchangeably. But usually, autonomic failure caused orthostatic HYPOtension and baroflex failure and the accompanying anatomical lesions usually cause volatile hypertension.
Baroflex failure usually causes a loss of the buffering of blood pressure and volatility of BP and heart rate.
Baroflex failure can be documented by the inability of infusions of pressor and depressor drugs to cause reflex bradycardia and tachycardia.25 mmHg or higher. If you have a heart rate drop of 25 mmHg it indicates baroflex control of heart rate.
They can put you in a supine position(laying down) and inject you with phenylephrine and increase the dose until your systolic BP raises 25 mmHg or higher. If you have a heart rate drop of 25 mmHg it indicates baroflex control of heart rate.
They have also injected people with nitroprusside until your systolic BP drops by 25mmHg and causes a change in HR.
Apparently, there can be several causes of Baroflex failure. Some of the people in the study had previously had surgical damage of the glossopharyngeal nerve because of a neck injury. And some had radiation of the pharynx that caused problems and some other people had familial paraganglioma syndrome, which is a genetic problem that causes benign non-catecholamine producing tumors of the carotid body and glomus jugulare and glomus vagale. The tumors damage the glossopharyngeal and vagus nerves. One person also had cell loss in the nuclei of the solitary tracts of the brain stem that had been caused by a degenerative neurologic disorder. But some of the patients they coudn't find a cause for their baroflex failure.
I certainly hope there is some other way to find out if you have it besides being injected with stuff.
After they did the injection part of the test, the patients were monitored. In contrast to the 24-hour urine test I had, during the study they measured catecholamines were measured every so often. And the BP was taken every 4 hours in supine and upright positions and anytime they had symptoms.
They also did cold pressor tests. This is when they have you to put your right hand in a basin filled half with ice and half with water and keep it there for 1 minute. They measure your heart rate before and after. They did math tests by having people count backward from 200 by sevens. And they measured BP before and after this. And there is also a test called the isometric handgrip.
They also gave patients propranolol and atropine in order to measure sympathetic and parasympathetic responses that control heart rate. They gave them Clonidine and monitored BP afterward to see how it affected reduced the sympathetic response.
The patients BP would rise dramatically due to the cold pressor and math tests, which basically caused some mental stress.Some patients had increased nervousness or depression after they became ill. And it was worse with the patients with the worst BP elevation. When their BP was up, they had a sensation of flushing and were pale. They had palpitations and headache and sweating pheochromocytoma. But they had previously had this ruled out by urine and blood tests and radiographic tests and also by the improvement, or at least the absence of an increase, in hypertensive episodes during follow-up.
These patients had higher systolic BP than normal people. But they also had lower than normal BP at night, that "extreme dipper" thing. Their heart rates were also abnormal. Some of them had HR of 90 beats a minute, which could be from loss of parasympathetic control of the heart rate, caused by damage to the right vagal nerve.
When they were measuring the norepinephrine during the tests, they were much higher than normal. And they raised in some patients to more than 200 pg per milliliter (1.1 nmol per liter). Urinary excretion of epinephrine plus norepinephrine averaged 118 μg per 24 hours (697 nmol per 24 hours), more than twice normal (P = 0.015).
The cold pressor test caused a hypertensive paroxysm in some of the patients and lasted for a long time after they removed their hand from the cold water. That means their BP raised to a volatile level.
They were able to show a greater drop in BP during bouts of hypertension with Clonidine, more so than when their BP was at normal levels. Their norepinephrine levels decreased substantially too.
I would think that indicates that Clonidine is a pretty good treatment for it.
Propanolol didn't do much when the BP and heart rate was low in patients. But when they had tachycardia it would decrease the HR by about 12 beats a minute.
The study says that most of the patients could be treated with Clonidine and that many of them could eventually decrease the dosage after 2-4 years, and go onto diazepam 5mg three times a day.
It refers to an earlier study that concluded that baroflex failure could be differentiated from pheochromocytoma because pheochromocytoma doesn't respond to clonidine treatment.
They concluded the paper by saying that baroflex failure symptoms range from patients that have an acute hypertensive crisis to patients that have what they called habitual volatility of blood pressure and with heart rate and high BP surges in response to stress. But they could be punctuated by periods of normal or even low BP during rest. And that it is important to differentiate baroflex failure from other causes in order to treat the orthostatic HYPERtension properly.
Here is some information about people who are "extreme dippers" This medical journal article says that these extreme drops in BP at night are closely related to the abnormalities of autonomic nervous activity.
They defined orthostatic HYPERtension slightly differently than other places. They said it was a systolic BP rise of 10 mmHg when in the upright or standing position after 6-10 minutes. Whereas the above definitions required a 20 mmHg raise.
It also says that orthostatic HYPERtension isn't well known and that it hasn't been well defined. Some places define it as a rise from 90mmHg to above 90 mmHg. And that the older patients had higher systolic BP and lower diastolic BP.
"Although orthostatic hypotension is well recognized and commonly encountered, there are only a few reports of orthostatic hypertension. Most of the reported cases of orthostatic hypertension were related to excessive venous pooling, with an initial drop in cardiac output followed by overcompensation with an excessive release of catecholamines, or to nephroptosis, (also called floating kidney or renal ptosis is an abnormal condition in which the kidney drops down into the pelvis when the patient stands up.) with orthostatic activation of the renin-angiotensin system."
In this study, again from the American Heart Association, the patient had normal plasma and urinary catecholamines and renin release. Pharmacological tests of autonomic nervous system function showed an increased pressor sensitivity to norepinephrine (11 to 14 times normal), normal sensitivity to isoproterenol, diminished baroreceptor reflex sensitivity, and exquisite sensitivity to alpha blockers. This unusual case of orthostatic hypertension appears to be secondary to vascular adrenergic hypersensitivity. It also goes with the rise from 90 mmHg to above 90 mmHg on upright position. And refers to a man who had previously had orthostatic HYPOtension that was followed by HYPERtension. That is precisely what happened to me.
"Autonomic evaluation demonstrated diminished baroreflex sensitivity and an exaggerated pressor response to the cold pressor test and Valsalva phase 2. Combined autonomic blockade with propranolol and atropine abolished the postural BP changes. These data suggested that the exaggerated pressor response was due to an increase in systemic vascular resistance in excess of the demands arising from a transient postural fall in cardiac output."
They used the Valsalva maneuver to indicate baroflex failure. It is the action of attempting to exhale with the nostrils and mouth, or the glottis, closed. This increases pressure in the middle ear and the chest, as when bracing to lift heavy objects, and is used as a means of equalizing pressure in the ears. When you do that your pulse is supposed to drop when you let your breath out.
Just out of curiosity, I did this and my heart rate actually went up instead of down after I let my breath back out. I have one of those wristbands that measures your heart rate and steps and how many hours you are sleeping. It made my ears pop a lot. I repeated it and got the same response. (not a picture of me)
"Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome."Orthostatic hypertension—a new haemodynamic cardiovascular risk factor
There is still a lot of information here to absorb, even after I attempted to condense it. But I hope it is helpful to someone. I will be rereading it myself to try and get a grip on it.
I appologize for some of the weird formatting of this post. I don't know if it is something wrong with blogger or is related to the photos I included or what. I attempted to fix it about six times. Don't forget to watch the POTS videos at the bottom of the blog. You have to scroll down for them.
