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High Hemoglobin, Hematocrit, Mcv, Mch


juliegee

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I can not comment on the calculation, but a higher osmo is a typical finding with diabetes insipidus. I take it you are not on DDAVP? Are you the gal who spends the day moving between recliners? I thought you wrote this in a post, and I can really relate, because that is so ME. I can exercise, but at home, I am in trouble if I am not moving and spend my time up and down between recliners.

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Yes, I am recliner friendly :huh: I usually can move around for about 5 minutes, or a few more, then go back to my handy dandy recliner. In my vehicle I have to somewhat recline also(not driving, a passenger!). But some days are bad and some days I can be upright for 10-15 minutes in my house. Just don't stress me out--then I have to be sitting!

My clueless endo ran the ADH for me last year at my request(isn't everything at the doctors done at my request these days!!). It came back low, so six weeks later he reran it and it was still low. So he prescribed vasopressin, but I never took it. After finding out from Firewatcher, there were a couple of reasons I didn't take it:

1. He did not run any serum osmo. along with it, so wasn't sure of its validity.

2. He never said anything about checking on my sodium levels as time goes on.

So, I figured he wasn't REAL familiar with it. He does label me on paperwork as "posterior pituitary deficient"(well, the back lobe that runs the ADH and oxytocin hormones). I now don't know if that is actually a fact or not. I guess I need an endo that might understand the dynamics of it all, as it could very well impact whether I continue to have POTS or possibly get my life back--I'll take the latter if given a choice!!

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In looking around at results for ADH, I have always seen normal as something like 0-4.8. I didn't understand how that pertained to my result, which was 0.8. My doctor said it was low.

I found a site that explains it in context to the serum osmolality:

http://www.muschealth.com/lab/content.aspx?id=150335

Looking through that, I see that my ADH is definitely low when compared to my high osmol.(guesstimate level).

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Yes, I am recliner friendly :huh: I usually can move around for about 5 minutes, or a few more, then go back to my handy dandy recliner. In my vehicle I have to somewhat recline also(not driving, a passenger!). But some days are bad and some days I can be upright for 10-15 minutes in my house. Just don't stress me out--then I have to be sitting!

My clueless endo ran the ADH for me last year at my request(isn't everything at the doctors done at my request these days!!). It came back low, so six weeks later he reran it and it was still low. So he prescribed vasopressin, but I never took it. After finding out from Firewatcher, there were a couple of reasons I didn't take it:

1. He did not run any serum osmo. along with it, so wasn't sure of its validity.

2. He never said anything about checking on my sodium levels as time goes on.

So, I figured he wasn't REAL familiar with it. He does label me on paperwork as "posterior pituitary deficient"(well, the back lobe that runs the ADH and oxytocin hormones). I now don't know if that is actually a fact or not. I guess I need an endo that might understand the dynamics of it all, as it could very well impact whether I continue to have POTS or possibly get my life back--I'll take the latter if given a choice!!

You are describing me to a tee!!!! I also have the seat reclined in our vehicle. The ADH should be run at the peak of water deprivation, and in that situation it should be above zero. If you have POTS, he/ she should also run a renin and aldosterone to make sure that you can properly retain sodium since the side effect of DDAVP is hyponatriemia. I have to take the Florinef along with the DDAVP and wait until my urine turns colorless again between doses. The tablet is less potent than the nasal.

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I don't know anything about the the blood measures involved here. However, those like Vemee who allude to chronic hypoxia (especially cerebral) being related sure seem to highlight a plausible connection. If these altered measurements coincide with "altitude" style reactions it seems to makes sense given a shoddy circulation associated with POTS, the apparent "cerebral autoregulation" problems, and NMH or NCS style tendencies to cut-off blood supply at inconvenient times.

In that sense, the potential link seems like a "no-brainer"... as in "no blood supply to brain"! :)

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Erik, yup, it makes sense that way to me too! But I'm not going to go to yet another doc who'll do a cranial doppler ultrasound to find out exactly that and then go: "Hmmm, it's not normal, but it must be normal for you!" :huh:

My PT asked me to research brain O2 levels and exercise and basically came to the same conclusion from the stack of articles I gave her and the ones she found. When I exercise, my brain thinks it is getting too much O2 and shuts the entire system down! She has asked me to breathe at half the pace of everyone else she trains so that I don't hyperventilate. I go from aerobic to anerobic in less than 10 seconds and then into just can't do anything anymore. It is very frustrating!

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I would like to add an interesting article about blood volume studies done at the Cleveland Clinic:

http://www.daxor.com/pdfs/Fouad%20Syncope.pdf

I personally don't yet take any meds for my POTS, but find it interesting about what they found in the people that do take fludro. and midodrine. Maybe some of you who take one or the other, or both, will find this useful. I find it interesting at the end of the article that it says that people really should have a TRUE blood volume analysis done to really know which treatment will work. I thought it was interesting that they found that in people with low blood volume using midodrine could actually be getting LESS brain perfusion.

I also found it interesting that it said that some people could have low RBC anemia and it not show up corresponding to the HCT.

I looked on the Daxor site and found a hospital in Houston that does this test. I put in a request for a referral to a physician who actually does the blood volume tests at thay hospital.

I find it interesting that that they say that a tilt table tells NOTHING related to blood volume, they found.

At the end, the last paragraph says that all patients with "syncope"(I assume postural intolerance too) should have a blood volume study to see their results, so then they will know what meds might work best for them. I personally know that alpha blockers make me feel awful, and I read today that alphas are not good for people with low ADH-volume issues.

I officially said the word "interesting" way too much in this post--SORRY!

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Erik, yup, it makes sense that way to me too! But I'm not going to go to yet another doc who'll do a cranial doppler ultrasound to find out exactly that and then go: "Hmmm, it's not normal, but it must be normal for you!" <_<

My PT asked me to research brain O2 levels and exercise and basically came to the same conclusion from the stack of articles I gave her and the ones she found. When I exercise, my brain thinks it is getting too much O2 and shuts the entire system down! She has asked me to breathe at half the pace of everyone else she trains so that I don't hyperventilate. I go from aerobic to anerobic in less than 10 seconds and then into just can't do anything anymore. It is very frustrating!

I would shut down during heavy physical activity, I still get out of breath and near syncope just doing simple yard work. I think it goes back to pooling and low blood volume, As your available circulating blood volume decreases your body tries to make up the o2 deficit by breathing faster. As the body tries to manage the lack of perfusion it starts to take blood away from the parts of the body that can do without it for a while and send it to the vital organs that start to die if the blood flow is stopped. After a while the body can not keep up and eventually cuts off more blood from more organs. I like to think of it as similar to hypovolumic shock and think it is a valid comparison since a lot of the symptoms are similar to what pots patients go through. I was told by a dr. at Vanderbilt that there was no proof of that happening but my pots dr. said that my body can not keep up with what I am doing which goes along with my theory. If there is a big drop in circulating blood volume what is the difference between it dropping out of circulation in our veins and bleeding out except that it is easier to recover.

I have forgotten the mechanics of hyperventilation except that our breathing is controlled by the level of carbon dioxide primarily and o2 levels secondarily so when we breathe fast we get rid of too much carbon dioxide and that somehow changes the chemistry in the body which causes the veins and arteries to constrict which causes the body to think it is not getting enough oxygen so it continues the fast breathing to bring in more oxygen. My question is that do those of us who have pooling really hyperventilate because we have blown off too much carbon dioxide by not controlling our breathing or is it just the body trying to make up for it not getting enough oxygen?

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Erik, yup, it makes sense that way to me too! But I'm not going to go to yet another doc who'll do a cranial doppler ultrasound to find out exactly that and then go: "Hmmm, it's not normal, but it must be normal for you!" <_<

My PT asked me to research brain O2 levels and exercise and basically came to the same conclusion from the stack of articles I gave her and the ones she found. When I exercise, my brain thinks it is getting too much O2 and shuts the entire system down! She has asked me to breathe at half the pace of everyone else she trains so that I don't hyperventilate. I go from aerobic to anerobic in less than 10 seconds and then into just can't do anything anymore. It is very frustrating!

I would shut down during heavy physical activity, I still get out of breath and near syncope just doing simple yard work. I think it goes back to pooling and low blood volume, As your available circulating blood volume decreases your body tries to make up the o2 deficit by breathing faster. As the body tries to manage the lack of perfusion it starts to take blood away from the parts of the body that can do without it for a while and send it to the vital organs that start to die if the blood flow is stopped. After a while the body can not keep up and eventually cuts off more blood from more organs. I like to think of it as similar to hypovolumic shock and think it is a valid comparison since a lot of the symptoms are similar to what pots patients go through. I was told by a dr. at Vanderbilt that there was no proof of that happening but my pots dr. said that my body can not keep up with what I am doing which goes along with my theory. If there is a big drop in circulating blood volume what is the difference between it dropping out of circulation in our veins and bleeding out except that it is easier to recover.

I have forgotten the mechanics of hyperventilation except that our breathing is controlled by the level of carbon dioxide primarily and o2 levels secondarily so when we breathe fast we get rid of too much carbon dioxide and that somehow changes the chemistry in the body which causes the veins and arteries to constrict which causes the body to think it is not getting enough oxygen so it continues the fast breathing to bring in more oxygen. My question is that do those of us who have pooling really hyperventilate because we have blown off too much carbon dioxide by not controlling our breathing or is it just the body trying to make up for it not getting enough oxygen?

I actually do "control" my breathing while exercising. Pilates is exceptional for that. The "thing" is that I am not huffing and puffing or even breathing hard, but if I breathe at what others would find to be a normal pace, it is too fast for me. That is why my PT is saying for me to breathe at half speed....basically take one breath for every two of my partner's. Otherwise, I'll just shut down. So I'm really hyperventilating at a normal respiratory rate since my diffusion capacity, RBC/hematocrit is so high......I think :blink:

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I appreciate all of the incite, but I have to admit I'm more confused than ever. Mack has the whole high RBC thing going on, but his serum osmolality is actually quite low....so it's NOT super-concentration of blood causing the abnormal labs. I suspect the blood pooling causes hypoxia, which, in turn causes Mack's body to make bigger and more RBC's.

The more I learn, the more confused I get <_<

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