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Hyperadrenergic Pots


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When used correctly this is the term for the type of POTS where sympathetic overactivity is the primary cause of the symptoms rather than it being an appropriate response to inappropriate circulatory activity (pooling, etc).

Its a theory rather than a proven science although most research bodies now accept that in at least some cases there appears to be a form of POTS that is caused by sympathetic excess.

Notable postulated causes include norepinephrine transporter deficiency, elevated angiotensin II levels and possibly even faulty parasympathetic activity.

Signs of this type of POTS are considered postural hypertension and excessive peripheral vasoconstriction rather than pooling.

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Guest tearose

My hyperadrenergic POTS was described to be my body having a normal response to an abnormal condition. Some of us with this form of POTS do not adjust to the changes in position and we then begin to have lack of oxygen to vital organs. In quick response we dump huge amounts of norepinepherine to make our heart beat faster and get blood to those organs. This happens so quickly it is extremely difficult to measure with the diagnostic tools now available. The Thermoregulatory Sweat Test did in fact capture signs of poor leg circulation in me. I do pool blood in my legs and splancnic bed and am very sensitive to temperature changes and need to wear compression hose to increase my bp and improve circulation.

tearose

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When used correctly this is the term for the type of POTS where sympathetic overactivity is the primary cause of the symptoms rather than it being an appropriate response to inappropriate circulatory activity (pooling, etc).

Thank you for the very useful "Cliff Notes" version of hyperadrenergic POTS!

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Tearrose - what you are describing is what some doctors call a hyperadrenergic response in POTS. The symptoms are kind of the same, but in true hyperadrenergic POTS the primary problem is this response in the face of no other (yet found) abnormalities according to some authorities.

Pooling in the extremities would not suggest primary hyperadrenergic POTS because these patients have increased rather than decreased peripheral resistance - that is excessive vasoconstriction either all the time or when standing - cold, white clammy skin.

Ultimately the symptoms are pretty similar, but anxiety related symtpoms are more common according to Grubb et al in the primary hyper types as is hypovolumia.

The causes could be very different though - in normal POTS reduced blood flow to the brain occurs because of sluggish blood return to the heart and head, whereas in hyperadrenergic POTS it occurs either because of something similar but from excessive vasoconstriction or cerebral vasospasm where the brain and head basically get a type of raynauds.

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Guest tearose

rama...if only it were that easy to connect the cause and effect but it is still not clear.

The problem with accurate diagnosis is multi fold. First, like me, some have an additional condition. I have lymphedema so my body is already working hard at maintaining fluid balance and I must limit sodium. Second, like me, when I am always doing behavioral modifications like maintaining electrolytes, using compression...we alter what can be captured as our treated status or regular status. For example, on my last TTT, I was without treatment and after 8 minutes of standing still with bp and hr in the okay range...boom, out of the blue comes a PSVT and then my bp and hr are going in opposite directions.

There was a study done on the effect of compression on the body and the facts are that some are able to maintain some improved level of constriction for 24-48 hours after we remove the compression!! This is very significant. When I was going for a pelvic CT scan, I was shown the study and learned that my pelvic floor collapse did not look as bad as it really was because I was always using compression. I share this because in the Thermoregulatory Sweat Test, the activity in my legs improved after using compression.

Anyway, I wanted to just make it clear that I have a normal response to an abnormal condition. This was an important fact for me to understand. IF I had an abnormal response to a normal condition, I would try to treat the abnormal response. In my case, the response is normal and saves me. The abnormal condition, whether it is from faulty nerve fibre response or lymphatic issues...is stil not known and so can't be treated.

I never get the anxiety some speak of. I do get clearly racing heart and fast speech which comes from my body trying to get O2 to where it needs to go. I sit down and usually manage better. I think the levels of norepinpherine during standing were the main reason I got the dx hyperadrenergic.

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While we are on the subject of "hyperadrenergic POTS", I have some questions for anyone who might know.

I was measured for possible inclusion into a study at NIH, so my exam was brief. My supine posture was followed by standing for 5 minutes only. My norepinephrine was measured first, while supine, and then, after standing for 5 minutes. I think my norepinephrine was in the 600's or 700's, I can't remember just now.

It was elevated.

Question: When people say their norepinephrine was high, is there a protocol as to how many minutes of standing is involved? My reading was done after 5 minutes of standing. Maybe others report their results after having stood longer?

Question: What is a normal reading of norepinephrine after standing for 5 minutes?

Question: Does the norepinephrine level continue to climb the longer we stand? If this is the case, then I cannot compare my reading of 700 + to anyone else's reading, unless they were standing for exactly 5 minutes like I had been? Maybe their reading is different because they stood longer, or I stood for less time than they did?

Thanks in advance.

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I had my catecholamines checked at Mayo and my supine norepinephrine was 250 and standing after 10 minutes was 1089. The neuro there told me I had a mild hyperadrenergic response to my pooling. So like Tearose, I have a normal (although slightly exaggerated) response to an abnormal condition.

When they were checking my upright catecholamines, they just told me to do whatever made me feel my worst. So I chose to stand, walk a bit, and talk.

Interesting comments about the compression hose. I've worn mine daily for over a year now. But I had to stop wearing them for about a week during the summer because of a skin infection on my feet. I felt gradually worse as the days went on, until by the seventh day I could hardly be upright at all. I really agree that wearing the compression regularly causes a cumulatively positive effect in my case. I wear 20-30mm thigh-high (sometimes with abdominal compression too).

The Mayo doc suggested that if I aim treatment at correcting the pooling that I'd have less symptoms of adrenaline. He's been right. Prior to wearing compression hose, I had chronically frostbitten toes because of the excessive vasoconstriction caused by high norepinephrine. Wearing the compression hose has actually helped the circulation in my legs because it decreases my body's need to produce so much norepinephrine by reducing the pooling.

Anyone can correct me on this, but I think that normal supine norepi level is in the 200's and normal standing levels are in the 400's.

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The best way to describe the suggested pooling problems in some POTS is that there are certain areas of the body where norepinephrine has less effect, so the body shoots off more (norepinephrine or sometimes epinephrine) to make that area constrict properly, but the areas of the body that are not desensitized to this increase feel its full effects.

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