TXPOTS

There is no contraindication for beta blockers and hyperadrenergic POTS.

Beta blockers are generally avoided in mast cell disease.

Ashelton,

If you are starting Dr. Levine's protocol, the beta blockers are not allowed to do the study. Only a physician with POTS knowledge can determine whether you are hyperadrenergic. Many POTS patients have higher levels of upright adrenaline, but it does not always mean they fit into the hyperadrenergic category according to the Vanderbilt review.

Issie,

I once had an infusion of albumin and saline to hold the fluid in my vessels longer. It made me feel much better at the time. I have little knowledge of intricacies of CHF and EDS. I only know the mechanisms of the drugs and the POTS research and review articles pertaining to medications. Sometimes drugs that seem counterproductive actually help patients. Also, drugs in various combinations help people. One drug may be a vasoconstrictor and another a beta blocker. Only a physician has the patient experience with prescribing and dosing, and only you know whether a medication is making a difference in the way you feel.

I looked up clonidine it seems to have the same qualities as the propranalol but it to warns of a rebound effect too. Since I have only been on 5mg of propranalol one to two times a day. I don't know why it's had such an effect. I know that I'm super sensitive to meds. I think for now, I'll stay off of it until I see the neuro at the end of next week. He would probably want me off of it any way to do his testing. I really liked that it had helped the tachy and chest/heart pains but sure didn't like my bp being so high upon standing when it was starting to wear off. Thanks for all the input - I appreciate your insights!!

Issie

Well, not the same qualities, but along similar lines. Clonidine is an alpha 2 agonist. It blocks the release of catecholamines from the brain stem, whereas propranolol blocks some of the receptor sites (beta 1 and beta 2). Clonidine works further up the chain of the events and only recommended for hyperadrenergic patients in the literature. Sometimes the increase in sympathetic tone is compensatory in POTS, so blocking adrenaline release or action at receptor sites may be counter productive. It depends on the mechanism causing POTS. With EDS, blood vessels may be more floppy, so the increase in sympathetic tone may be necessary to maintain perfusion upstairs. Good luck with the neuro visit, Issie. I hope your physicians can can up with a plan that gets rid of the tachy and chest pain without the high blood pressure. I'm super sensitive to meds as well. It's frustrating!

I would think this would only be a concern in central hyperadrenergic patients (upright NE > 1000 pg/ml), as opposed to the peripheral denervation variety (if we follow these classifications). Even the Vandy review article stress the importance of regulating NE centrally and peripherally, which is why clonidine or even methyldopa are popular choices (or even Labetalol and Coreg). I guess the only way to know is to try various medication combos under the watchful eyes of a responsible physician willing to work with us when the non-pharmacologic stuff fails. Dr. Grubb and Vandy do seem to be treating hyperadrenergic patients with different med combos than the more common variety of PD POTS.

I took propranolol for a week and it made my bp higher than normal as well. I don't think it was when it was worn off though. I chopped it up to the fact that since it was keeping my heartrate from being elevated then my body had to manage and keep me upright somehow, so it would raise bp. This is probably a good thing for some, but for me it made me feel worse. I have POTS and I can walk around for the most part without feeling like I'm going to pass out. When I was on propranolol I felt like I would pass out and vomit at the same time. My heartrate was nice and low and my chest pain was gone though. :/ I lasted a week on it before deciding it wasn't for me.

If the heart rate is low and the blood pressure is high on propranolol, it could be from unopposed alpha receptor stimulation or beta 2 antagonism from a non-selective beta blocker. For example in pheochromocytoma (a high adrenaline state from a tumor), pure beta blockers are contraindicated due to unopposed alpha stimulation. Alpha receptors on blood vessels cause constriction when stimulated. POTS patients can often produce high levels of adrenaline. It's interesting, but I notice Dr. Grubb mentions using Labaetalol or Coreg in hyperadrenergic POTS patients. He doesn't specifically mention other beta blockers in his review article. These are mixed beta/ alpha agonists. Even patients not on any medication may when heart rate is lower, blood pressure is higher.

Issie,

The higher bp could be rebound when the drug has worn off (hence the recommendation for UP TO 3-4x daily dosing) or less likely, beta 2 antagonism. It is a non-selective agent.

I would ask the prescribing doctor. It wouldn't be dosed four times daily in some patients with POTS if the twice daily dosing worked for everyone. So, you may be one of those patients needing more frequent dosing due to the way YOU metabolize the drug and the low dose. You have to decide how you feel on the drug and tailor a dose and schedule that works for YOU. Patients with POTS seem to have odd reactions to drugs that the non-dysautonomic population does not experience. You should keep working with your doctor on finding the right dose or decide it's not right for you. I would explain what is happening to your doctor and see what he/ she advises. Certainly, if your renin and aldosterone are low to begin with this is something to keep in mind since beta blockers do lower renin.

On a personal note, I sampled propranolol, and it made me feel worse. I was glad that I tried and ruled out another option. Initially, I thought I could not tolerate Florinef, but it just took time to mess around with the dose and timing.

Have you taken your heart rate and bp 60-90 minutes after taking propranolol? This is when the drug should be at peak effect.

Firewatcher,

Glad you have found success with propranolol and a dose that works for you. It can be a wonder for certain kinds of tremors and certain kinds of anxiety. I'll be sending you my revised article this week. The last week has brought lots of excellent beta blocker questions on the forum.

Bystolic at the 5mg dose is highly selective for beta 1 receptors in the heart and kidney. It also has nitric oxide stimulating, vasodilatory effects.

Propranolol is a non-selective agent, hitting beta 1 and beta 2. Beta 2 receptors are found, among other locations, in the blood vessels and actually cause vasodilation. By blocking beta 2, blood vessels become more constricted. Hence, the possible indication for migraines, though this is speculative since the cause of migraines is still debated. The net result is usually still a drop in blood pressure due to lowering of heart rate and renin/ aldosterone. However, beta 1 selective agents or mixed beta/ alpha agents may be better choices for those with hyperadrenergic POTS. Propranolol acts centrally which is why it is a good choice for anxiety, stage fright, and migraines.

It depends on the particular patient since we all metabolize drugs differently, but the advised dosing of the short acting propranolol is two up to 4 times daily. 5mg is the lowest dose and may be out of ones system more quickly. Raj and colleagues dose patients on 5-10mg bid to qid.

The immediate release is dosed two to four times daily.

The long acting is dosed once a day.

If you are on the immediate release, it is not meant to be taken once a day, unless it is being used on an as needed basis for stage fright/ anxiety.

I completely respect your desire to cut down on medications, but I urge you to taper one drug at a time. I would include your physician in the process to devise a bearable taper plan. Everyone responds differently to coming off SSNRIs and benzo, but occasionally withdrawal can be severe and delayed. I would include your doctor. I'm sure he will respect your wishes, if you explain to him your concerns.

Just wanted to pipe in that I also got this flavor of headache from too high a dosing of Florinef. I did find a happy medium, so I did not have to stop the drug entirely. The classic Florinef headache is one that you wake up with and can be migraine like. Not only can Florinef raise blood pressure, but it can increase intracranial pressure.

I saw an endocrinologist who ordered the renin and aldosterone. It is important not to consume a lot of salt before the tests as sodium can suppress renin. Beta blockers and clonidine can also reduce renin levels, but you did not mention being on those. Luckily, I have not noticed any puffiness or swelling, so that varies from patient to patient. I did gain weight, but I needed the extra fluid volume. Too much swelling should be evaluated by a physician.

Krissy,

Glad you are seeing your doctor to re-evaluate the Florinef. Sounds like you are not tolerating it well. The sweating and headaches can definitely be from the Florinef.

To preface, everyone responds differently to medications. So, the following is just my personal experience.

Florinef has been a wonder drug for me. I was bedridden before I started Florinef in January. I believe it worked well for me because my aldosterone levels were undetectable during several blood draws. I had a sunken in appearance to my face, salt cravings, and extremely dry mouth and eyes. I looked like a prune. The Florinef helped expand my blood volume. I was not able to this with salt alone. It did improve my mouth and eye dryness. With that being said, I only take 0.1mg/ day. My blood pressure gets too high on higher doses, and I get the classic Florinef headaches.

It's important to "start low and go slow". Florinef does not work right aways but builds in your system over a period of 2-3 weeks until steady state is reached. I get my potassium levels checked periodically because Florinef can lower potassium levels. It causes your body to retain sodium at the expense of potassium. Personally, my potassium levels have always been well within normal range. Florinef is also a weak vasoconstrictor. It can help blood vessels constrict, but is not as powerful as Midodrine in this regard.

The point of Florinef is really to help your body retain salt. The question is whether you are able to do this adequately without Florinef. You may ask your physician. Have you had aldosterone and renin levels checked?

Hope this helps a little.

Hi Jana,

I spent a good deal of 2009 bedridden and had similar episodes, which usually landed me in the hospital getting IV fluids. At the time, we did not know that I had POTS. If I had to guess, I would say that your blood pressure got too low and then your body sent out an adrenaline surge to compensate, resulting in the high blood pressure reading. Your pulse pressure was very narrow, perhaps indicating low blood volume. After these episodes, IV saline helped me tremendously. During my darkest days, I did not drive, and my mother stayed with us a lot. We have 2 young children, and I could barely care for myself, let alone them. I still have POTS, but these episodes ended after starting Florinef, DDAVP, and an exercise program. I know the Florinef is probably out for you if you have cardiomyopathy. Do these episodes happen often?

Regarding Lyrica, dizziness is one of the most common side effects and reasons patients stop taking it. I would definitely discuss this with your doctor, as you have planned. I know you have only been on the Lyrica for 2 weeks, but patients are supposed to taper off if they do decide to discontinue.

In the beginning, I was exhausted. I had trouble getting out of bed and spent half the day sleeping, but I also found myself tossing and turning at night. I was exhausted, but I never felt rested. I can recall being too tired to take a bath or even comb my hair. I still have disabling POTS symptoms that make it hard to function normally, but fatigue is no longer a major symptom. I sleep a regular 8 hours/ night and feel well rested. I also spend 2 hours exercising/ day. I wanted to give you some hope that things may improve over time and that yes, your symptoms sound familiar. Now if I could only get rid of the PAIN, dizziness, blurry vision, and brain fog.

Firewatcher-

What you describe happening when you exercise, is exactly what happens to me at rest. Then, I start to exercise, and my CO2 expiration normalizes.

We are going to start the search for a pulmonologist with an interest in metabolic issues, as suggested by the cardiologist. I'll let everyone know if he/ she can make heads or tails of the results or explain how this is related to dysautonomia. I read Stewart's article on hypocapnia, but I don't think hypocapnia necessarily equals high respiratory quotient. Stewart measured PetCO2 as a measure of hypocapnia. My PetCO2 was normal, but my respiratory quotient was high from increased CO2 expiration. I am out of my league in this area, as is the POTS cardiologist I see, so I need more clarification.

Sue and McBlonde,

I know we share many of the same symptoms, so I am curious if we have the same root issue.

Thanks for everyone's responses to my original post. We spoke with my POTS cardiologist yesterday who believes I have metabolic acidosis, though this has yet to be proven. My venous CO2 and pH have been mid range normal. The only definitive way to check for this would be an arterial blood gas. Other ideas would be drawing lactic acid and pyruvic acid samples. He mentioned supplemental oxygen therapy, which I am poo-pooing right now. I still think the high CO2 expiration is the result of autonomic dysfunction and not the cause. Plus, everything immediately is equalized once I start exercising.

After reviewing the symptoms and causes of metabolic acidosis, I believe IF this is actually transpiring, the acidosis must be mild. Erik, my thoughts are the same. I hypothesize that lactic acidosis would be the consequence of chronic hypoxia/ hypoperfusion. I agree that there appears to be a major miscalibration, and the hypothalamus needs a re-boot.

Thank you for the link, sue. I am reviewing it. I believe a pulmonologist with a metabolic speciality would be the best source regarding acid/ base disturbance.

In people with low aldosterone (from Addison's disease with high renin) their potassium levels are normally high. Aldosterone is supposed to retain sodium and excrete potassium, so if it's low then your sodium is too low and potassium too high. I'm simplifying it but that's the general idea. That's why websites are saying to avoid high potassium foods in Addison's patients.

Now for whatever reason those of us with low aldosterone, POTS with "adrenal fatigue" or whatever it is you want to call it, I don't tend to see high potassium levels. This paradoxical effect should make us wonder why that is happening! I personally haven't figured it out and don't offer any hypothesis either.

It is true that salt lowers aldosterone, but it lowers it when the body senses it has enough sodium. The lowering of aldosterone is a good thing in this case because if your body continued to make the same amount of aldosterone while your intake of sodium was high, you'd have too much sodium! If you have a real deficiency in aldosterone, then whether you take salt or not it's going to be low causing you to excrete too much sodium. I'm certainly not one that advocates taking lots of salt, but I think it's good to apply it to food to your taste.

It's best to check aldosterone while salt fasting to see the true levels in the body.

To complicate matters, people with diabetes insipidus have low potassium and high sodium. I ended up having both diabetes insipidus and low aldosterone. My electrolytes appeared normal though I had two major issues.

Got a copy of my labs today. My CO2 was 30 (ref range 16-30), Anion gap was 5 (ref range 6-16) and low insulin with normal fasting glucose. ACTH was normal.

So would the CO2 and anion gap (which shows a disturbance in acid/base balance) somehow fit in with the hypo/hypercapnia issue that Ramakentesh refers to?

I made a follow up appt with the endo for Friday so we'll see if he can shed any light on any of this.

Hmmmm.....

Definitely ask your endo, but I believe hypocapnia/ hypercapnia would be detected in arterial blood (arterial blood gases). The base metabolic profile CO2 is a sampling of venous blood. I only know that I expel high amounts of CO2 via respiration when upright, but I have no idea what the CO2 reads in my arterial blood. I have no intention of finding a pulmonologist to place an arterial line to test CO2 in various positions as suggested by my cardiologist. I am bunt out of all the testing for now. Was your albumin normal? Did they test venous pH? I have thought of bringing this CO2 issue up with my endo as well.

I caught myself holding my breath today while upright. There is something funny with my breathing when upright which should be unconscious. This must be related to OI.

Shingles is the chicken pox virus that becomes reactivated in one's own system. You don't get shingles from a child with chicken pox. You get shingles from your own past infection. However, a person with shingles can transit the virus to a person who has not been infected with chicken pox. So, a person with shingles should not be babysitting a child who has not received their varicella vaccine, or else the child may get chicken pox. There is a vaccine for patients over 60 that helps boost immunity to varicella and decrease the likelihood of reactivation/shingles.

It's interesting that the article notes "Hyperventilation that consists of an increased depth without an increased rate only occurs during orthostatic stress...." Seems to be what both TXPOTS and I have experienced. What I haven't experienced is getting relief of symptoms with rebreathing CO2. I've only tried it once, but it didn't seem to help. I actually did better with just slow focused timed breathing. I also don't recall a feeling of anxiety in those situations as much as just feeling REALLY BAD! I definitely get the paresthesias and tetany they mentioned in the article.

TXPOTS- No unfortunately I haven't found any particular treatment plan that has solved everything. I am better on my meds but still have days where I feel, as my children say, "I've been sniped". (As in shot by a sniper... as in I was doing well for a few days and then I feel like my wheels have been shot out from under me and I'm back in bed for a few days.) I have the same feeling you report of feeling like my breathing "is just OFF" many days. I find myself having a sense of needing to take frequent deep breaths/heavy sighs much of the time.

I haven't had CO2 measured on TTT. Wish it would have been but I've done 3 TTT that have all been miserable so don't want to repeat it again. Wish they would have done a transcranial doppler that some people on here have mentioned having done on TTT also.

My peripheral resistance was reported to be abnormally low in supine and "quite good" in upright. Not sure how that would relate to this situation.

I see the endocrinologist the end of August so am hoping he will test the angiotensn II, renin and aldosterone for me.

Still find this a very interesting topic. Thanks for all the input!

Chaos,

Did your endo test renin, aldosterone, and ang II? at the end of Aug. Curious, since we both have the breathing and CO2 issues. My renin and aldosterone were very low. My ang II was considered normal, but on the low end of the spectrum.

What kind of exercises help you?

Any kind of relatively strenuous activity like jogging, stairmaster, cross training... I believe the issue for me is compromised blood flow to the upper body and brain when upright, not moving. When you exercise, your stroke volume goes up and your skeletal muscle pump takes over. We rely on the ANS at rest to get the blood north. I think everyone with POTS is different, but the movement of my legs reduces my symptoms greatly.

Count me in. I have horrid posterior neck and head pain when upright or sitting up. The only thing that relieves it is exercise. I have not found a solution to this problem, though many of my other POTS symptoms have lessened since starting treatment. I agree with others that you should inquire about a repeat MRI. I went through a series of tests to rule out other causes for the pain, such as Chiari and CSF leak. I agree and sympathize. I detest the heavy head and terrible neck pain/ pressure. It is very annoying to live with day in and day out.

I have the headaches every day and every time I try to sit or stand up, unless I am exercising. I can not even sit up without being in a rocker or recliner due to the headaches. I am grateful that researchers are delving into this issue. Maybe it will save other patients from over aggressive CSF leak work-ups. I think migraines and POTS have been well established, but the orthostatic headaches and coat hanger pain are not always mentioned in the literature. Thank you for posting the full text, Dragon.

Can anyone get a full text pdf of this article? I really want to know if they found any good treatment strategies for these headaches, plus I want to give it to my neuro.

Thanks!

I'd love the full text too. My husband may be making a trip to the medical library. My quality of life would skyrocket if I could gain control over these headaches.

Thanks for the article, firewatcher. I was misdiagnosed with a CSF leak and underwent a year of extreme distress... 4 myelograms, 30 plus blood patches, and 5 hospitalizations because many doctors told me that an orthostatic headache= CSF leak. They discounted all my other symptoms consistent with POTS. The verdict after 18 months: a clear case of POTS and headaches caused by cerebral hypoperfusion. There are other patients out there being treated for invisible CSF leaks that probably have dysautonomia. A top POTS researcher even told my husband at one time that orthostatic headaches were not common in POTS. I will add this article to my collection. Thanks.