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Hi Flow V/s Low Flow Pots


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Is there a way to tell if you have high flow or low flow POTS based on symptoms or test results? I am trying to understand this condition better.

Thanks!!!

Dr. Julian Stewart has published many articles on this subject. He measures blood flow in the calves, abdomen, pelvic, and thoracic areas to classify patients. It will be interesting to see if his research helps direct treatment choices.

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Different research groups break up POTS dependent on different parameters.

Some use neuropathic versus hyperadrenergic

Some use Posrt viral versus spontaneous

Vandy have an evolving framework with many hyper sub catagories.

And Medows and Stewart originally classified their POTS patients into grousp dependent on calf blood flow. On their OI document they state that this framework is evolving and will probably change to neuropathic versus autonomic or something similar.

High flow patients have increased peripheral (arm leg) blood flow, hot skin to too touch and pooling in their extremities. i think this is considered to be autoimmune, is considered to be the more benign form of POTS and correspondes with the small fiber autoimmune neuropathy.

Normal flow are patients that are completely normal supine and abnormal standing - these include stomach poolers, and a few others - and is the biggest group I believe - most have faulty upright cerebral vasoregulation caused by parasympathetic withdrawal.

Low Flow correspond with hyper patients (NET deficiency, increased angiotensin/decreased neuronal nitric oxide and vasomotor failure).

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Thanks, rama. I asked this in a previous thread.....symptom markers for types of POTS. Based on your descrip, I would tend to think I am normal-flow. I do not notice pooling, not hot to touch...also have normal catecholamines. I have a feeling I have stomach/trunk pooling - just a hunch based on how I feel, etc. - but, I am not 'normal' supine - my hr is usually hihg - nor does lying down resolve my episodes. I have more of a tripwire.....if I cross the line, I'm in for it for a good hour or more. It really seems like there is some involvement of the main control of nervous system for me (hypothalamus, etc) that gets stuck in the wrong gear - also unable to change gears w/o me manually doing it (by walking around after stairs, etc.....or marching in place while standing, etc). I feel I have to keep my blood moving actually. Walking around helps my migraines (tho they are menstrually caused), my episodes, my avoidance of episodes, etc. If I stop moving (esp too fast), things do not feel right. What does this mean?? - am I manually avoiding the pooling by using muscle pumps at a low level?

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Different research groups break up POTS dependent on different paramet

High flow patients have increased peripheral (arm leg) blood flow, hot skin to too touch and pooling in their extremities. i think this is considered to be autoimmune, is considered to be the more benign form of POTS and correspondes with the small fiber autoimmune neuropathy.

thanks Rama -

sure could recommend some docs for a CME course with you

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A few other interesting findings from Dr. Stewart's studies. I am sure they may evolve and change, but since we are on the topic.

Although 75-80% of POTS patients are female, low flow POTS patients were exclusively female. They tend to have reduced BMI. This may be to due to the low blood volume found in low flow POTS or from other hypothesized mechanisms. This may be the group of "skinny females" who get POTS?

Low flow POTS patients have total body hypovolemia, whereas normal and high flow patients actually have normal overall blood volume. Of course, thoracic blood volume is low in all subtypes when standing as blood pools in the legs and abdomen, but low flow patients have low blood volume to begin with.

Over half of low flow POTS patients have elevated angiotensin II. Many, but not all, have low renin and low aldosterone. High flow POTS patients have normal renin and aldosterone. Some normal flow patients have low renin and aldosterone.

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I think elevated Ang/AngII is an expected state if anyone is hypovolemic... however, it is supposed to trigger corrective actions which would then make it a temporary state (as in normal body regulation signals). So having high AngII seems expected for a population with low blood volume (and maybe even for a body condition simply mimicking that state?). It is the unexpected (paradoxical) lack of renin & aldosterone elevation that stands out as unusual in many.

I think the chronically elevated AngII is suspected of having especially untoward impacts on circulatory regulation (although it is by no means the only thing interacting in that realm)... so AngII comes heavily into the "Flow" subgroup theories.

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I think elevated Ang/AngII is an expected state if anyone is hypovolemic... however, it is supposed to trigger corrective actions which would then make it a temporary state (as in normal body regulation signals). So having high AngII seems expected for a population with low blood volume (and maybe even for a body condition simply mimicking that state?). It is the unexpected (paradoxical) lack of renin & aldosterone elevation that stands out as unusual in many.

I think the chronically elevated AngII is suspected of having especially untoward impacts on circulatory regulation (although it is by no means the only thing interacting in that realm)... so AngII comes heavily into the "Flow" subgroup theories.

It is also a paradox that renin is low in a state of high angiotensin II in this subgroup of patients. One of the several theories is that angiotensin II catabolism is impaired. I believe Dr. Stewart is starting a study to test losartan (an ARB) in patients with high angiotensin II.

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Walking around helps my migraines (tho they are menstrually caused), my episodes, my avoidance of episodes, etc. If I stop moving (esp too fast), things do not feel right. What does this mean?? - am I manually avoiding the pooling by using muscle pumps at a low level?

Hi mvdula,

You are the first person I've met who finds walking around helps migraine. I get chronic daily migraine and am on meds for it. But sometimes I get breakthrough pain and the best thing I can do is try to keep moving. I do find that I have to get up and move quite regularly as it helps relieve my migraine. Sleep can be torture for me. Most of my worst migraines start while I'm asleep. I have noted that when I stop walking (have to wait for a light to cross the road, say or standing in line) I come over all potsy and feel like I'm going to fall down. My pots doc told me the 'standing still after walking' thing is a fairly common symptom of POTS. I wouldn't mind it so much but it annoys me that because of POTS I can not walk very far anymore and somedays it's really hard to stay on my feet to stave off a more viscious migraine.

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Actually there are two forms of Low Flow POTS - and the angiotensin II low flow variety is almost but not exclusively female. The other - NET deficiency is more equal in terms of sexes.

There are POTS patients with hyperadrenergic presentations that are also low flow but have yet to be catagorised.

Low Flow POTS with elevated angiotensin II correlates with receptor hypersensitivity - there is an increased response to norepinephrine because increased angiotensin II through impaired catabolism causes increased oxidisive stress and less nitric oxide avaiable for neuronal activity where its chief role is to dampen sympathetic outflow. So these patients have an excessive response to relatively normal norepinephrine levels, vasomotor nerve failure, absolute hypovolumia, pallor from reduced cutaneous blood flow and reduced body mass index. And almost all of the patients are female.

And all low flow states impaire the skeletal muscle pump because they impaire blood flow to the legs and calves through excessive and inappropriate vasoconstriction.

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Actually there are two forms of Low Flow POTS - and the angiotensin II low flow variety is almost but not exclusively female. The other - NET deficiency is more equal in terms of sexes.

There are POTS patients with hyperadrenergic presentations that are also low flow but have yet to be catagorised.

Low Flow POTS with elevated angiotensin II correlates with receptor hypersensitivity - there is an increased response to norepinephrine because increased angiotensin II through impaired catabolism causes increased oxidisive stress and less nitric oxide avaiable for neuronal activity where its chief role is to dampen sympathetic outflow. So these patients have an excessive response to relatively normal norepinephrine levels, vasomotor nerve failure, absolute hypovolumia, pallor from reduced cutaneous blood flow and reduced body mass index. And almost all of the patients are female.

And all low flow states impaire the skeletal muscle pump because they impaire blood flow to the legs and calves through excessive and inappropriate vasoconstriction.

I have the low renin, aldosterone, absolute hypovolemia, and reduced body mass index with many of the hyperadrenergic symptoms. My blood pressure has been running high since becoming afflicted with POTS. Of note, I just received the results of my angiotensin II done by a reputable lab. It was well within the normal range, so I am happy to rule this particular pathophysiology out and move on.

Yes, I went back and reviewed the article, and Dr. Stewart mentioned a high percentage of low flow patients had high angiotensin II and this group with high angiotensin II were exclusively females and had low BMI. My understanding is that NET deficiency is very, very rare and tends to run in families. Is this true? One more question... are there are studies analyzing the NET in POTS? Could the transporter become damaged per say?

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I wonder which one I am. Can someone please give me their opinion, or best guess. I'm too cerebrally challanged! :huh:

Female: 110lbs. 5'5" LOW BMI (skinny girl)

Standing nori- 987

B/P HR. NORMAL supine

HR jumps immediately upon standing-30 bpm or more-120-130.

B/P decreases immediately upon standing, but sometimes goes high. Diastolic is usually a bit high, (80-90's) Except after resting supine at least 30 minutes.

Hypovolemic 14% less blood volume

Small fiber neuropathy dx by skin biopsy CC no treatment & no symptoms.

Mild mitro valve prolapse-no symptoms

Main symptoms---brain fog--constant lightheadedness-standing. Short term memory, bad. Confusion, unable to process information at normal speed.

BB did not work-HR went down but felt bad.

Adderall helps BUT only for a few days (10-12) then extreme muscle tightness, knots, stiff neck. And it's dehydrating.

It's my double edge sword medication. I can get a few semi- good days out of it, then suffer terrible withdrawals and body pains when I have to go off. I hate it however it IS a potent vasoconstrictor. AND it improves mood and energy. (Speed will do that).

I never see "pooling" in legs. But compression stockings help.

I'm on zyrtec and adderall (off and on). Tried midodrine, mestinon and florinef. Sometimes when I'm peeing a lot, I'll take 0.1mg. florinef. Stops excessive peeing. Don't feel any symptom relief. I can take a hot bath and not feel bad. This one is confusing to me. Perhaps because I'm lying down? Hot weather however, makes me worse.

So confusing. Anyone? Best guesses. I'm seeing yet another new neurologist in June. I don't have much confidence he'll be able to help :( either.

You guys know more!

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Yes, me too please!

No dizziness

PVCs - LOTS sometimes, sometimes none - goes in cycles for weeks/months at a time

Major exercise intolerance - if I do too much, will feel weak/hot/awful/dying for 1-2 hrs

bending over too much causes diff kind of 'episode' - weird chest pressure/discomofort and urgent/intense feeling

would characterize my POTS more as intense terrifying attacks....

also, tachycardia upon going up a flight of stairs or similar acitivty - does not settle down for a while

BP tends to go up (tho not dangerously) upon standing/activity

not usually any problems w/ standing

BMI low - now 5'1" 105#.....at beg of POTS: 98# or less

heat intolerance - seems much better - showering 'ok' - last summer fine, previous summer ****

need to move around after walking/climbing stairs, etc - can't stop too fast

menstrual migraines - controlled easily w/ pain med if taken soon enough

Klonopin helps - I think I can do more w/o symptoms

sleep usually fine, break any bad sleep cycle w/ one night of .25 Klonopin and it's fixed

gastro-bowel usually fine...but can have urgency both types at beginning of episode

don't pee too often at all

normal fertility

never Dx w/ anything else

normal catecholamines

onset>??

I think came on around onset of PSVT - no apparent viruses or trauma, but very mild.

Real onset about 9 months after 4th child - during cutdown of breastfeeding - just got worse & worse as I cut down more. Then crash when I quit altogether. Episodes were terrifying, heat intolerance was awful.

Basically have a tripwire where if I go too far/get too hot, I'm done for a period of time....pure **** and terror.

Feeling pretty good recently - had a nice remission last spring/summer

I think Vit D helps me - so far, this has proven true. Walking often - like a few blocks - slowly - w/ kids - seems to help too.

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As much as we all want answers, I think it is dangerous to ask any of us for diagnostic opinions. The doctors who study this aren't even sure of the subgroups, and there is even more debate on types here on the forum. Each clinical group of doctors has their own interests, classifications and treatments. We are all such individual cases, what works for one, won't work for the other and there is the possibility that some of us are anomalies: low flow, but not low BMI, viral onset but hyperadrenergic presentation. Please be careful!

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I totally agree with, firewatcher. The researchers still have not agreed on sub groups, although I personally find the research interesting and may mention interesting tid bits found in the articles I have read. Unfortunately, I don't think the sub groups translate well into individual therapy. My POTS physician said there is a data base with POTS patients and therapies, but the sub groups have not dictated therapy. Unless the cause is isolated in an individual patient, therapy seems to be trial and error though certain parameters may sway therapy in one direction or another. For example, a patient who is already hypertension, may want to avoid vasoconstrictors. On the flip side, a patient with orthostatic hypotension, may need to be more careful on drugs that lower peripheral resistance. The hypovolemic patient may want to start with volume expanders. There also seems to be overlap within subgroups. I wish there was a better way to target therapy! A good philosophy for all POTS patients is too start low and go slow with any new medication under the guidance of a trusted physician, since we seem to be prone to adverse drug reactions.

Notgivinup,

Since you are hypovolemic, have your physicians considered starting you on a tiny dose of Florinef. I know you mentioned taking it once and awhile, but Florinef actually needs to build in your system and then you should be tapering slowly off, if you need to stop or reduce the dose. I imagine, as with the Adderall, you'll have to keep a close eye on your blood pressure.

I wish we all knew WHY we had POTS.

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Unless the cause is isolated in an individual patient, therapy seems to be trial and error though certain parameters may sway therapy in one direction or another.

That's what I'm trying to do. I need a direction to start looking so I can figure out what to try next. I know I get pooling in my legs, that vasoconstrictors sometimes help, that vasodilators are always BAD, that klonopin doesn't do anything for me. That midodrine used to be great, before it stopped working. My most debilitating symptom is actually brain fog, not passing out or exercise intolerance. I'm hoping if I get enough little clues I'll be able to figure out where to go from there, since it's pretty obvious no doctor is gonna help me.

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Unless the cause is isolated in an individual patient, therapy seems to be trial and error though certain parameters may sway therapy in one direction or another.

That's what I'm trying to do. I need a direction to start looking so I can figure out what to try next. I know I get pooling in my legs, that vasoconstrictors sometimes help, that vasodilators are always BAD, that klonopin doesn't do anything for me. That midodrine used to be great, before it stopped working. My most debilitating symptom is actually brain fog, not passing out or exercise intolerance. I'm hoping if I get enough little clues I'll be able to figure out where to go from there, since it's pretty obvious no doctor is gonna help me.

I know how you feel. When the doctors don't have answers, you are forced to search for answers on your own. Has your doctor suggested Ritalin? There was a study that discussed Ritalin for patients that failed Midodrine. My POTS specialist also mentioned Provigil for brain fog.

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None of the therapies available for POTS are treating the underlying problem which is poorly understood at this stage. So therefore, none of them are completely helpful and some arent helpful at all (in my experience LOL).

When they understand the varied problems that seem to be causing POTS in all patients - then they can target treatments. There isnt any agreement currently on the causes and none of the explanations currently provided seem to explain all the problems found in most patients.

Small fiber neuropathy would suggest increased peripheral blood flow but the body often uses adrenaline to vasoconstrict when this occurs so you may have cold feet and hands.

Alpha agonists work wonders for a while for me, but then always wear off and they seem to leave me in a woprse state than when i started them. Most of my treatments that have been helpful have been focusing on reducing the sympathetic effects - beta blockers etc.

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Of note, I just received the results of my angiotensin II done by a reputable lab. It was well within the normal range, so I am happy to rule this particular pathophysiology out and move on.

Im pretty sure angiotensin II catabolises in half an hour - so it would probably need to be measured on tilt.

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Of note, I just received the results of my angiotensin II done by a reputable lab. It was well within the normal range, so I am happy to rule this particular pathophysiology out and move on.

Im pretty sure angiotensin II catabolises in half an hour - so it would probably need to be measured on tilt.

Actually, Ang II was measured supine, NOT on a tilt in Dr. Stewart's studies. This is the Quest lab that ran my test, so I am confident in my results. The sample must be frozen. I think the point is these patients had very high ang II, even when supine. Up to 200 ng/ml. In the control group the levels averaged 32 ng/ml. Mine was 13 ng/ml.

From Dr. Stewart's article.

Following a 30 min equilibration period, venous blood for assay purposes was collected from the catheter in the antecubital vein with subjects supine. All assays were performed by Quest Diagnostics Laboratory (Nichols Institute, San Juan Capistrano, CA, U.S.A.).

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I know how you feel. When the doctors don't have answers, you are forced to search for answers on your own. Has your doctor suggested Ritalin? There was a study that discussed Ritalin for patients that failed Midodrine. My POTS specialist also mentioned Provigil for brain fog.

My doctor refuses to prescribe it--despite recommendations from another doctor and my therapist (both are out of state and can't prescribe it themselves). I'm gonna try to convince him again on Tuesday. I HAVE to be able to function better than I am now.

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POTS was diagnosed by 70o upright tilt. Supine calf blood flow measured by venous occlusion plethysmography was used to subgroup POTS patients. 23 POTS patients were partitioned among 10 with low blood flow, 8 with normal flow, and 5 with high flow. There were 10 healthy volunteers. Blood volume was measured by dye dilution. Biochemical measurements were performed supine. Blood volume was decreased in low flow POTS (2.14?.12 L/M2) compared to control (2.76?.20 L/M2) but not in other subgroups. PRA was decreased in low flow POTS (0.49?.12 vs 0.90?0.18 ng/ml/hr), while plasma angiotensin-II was increased (89?20 vs 32?4 ng/L), but not in other subgroups. PRA correlated with aldosterone (r=+0.71) over all subjects. PRA correlated negatively with blood volume (r=-0.72) in normal and high flow POTS but positively (r=+0.65) in low flow POTS. PRA correlated positively with angiotensin (r=+0.76) in normal and high flow POTS but negatively (r=-.83) in low flow POTS. Blood volume was negatively correlated to angiotensin II (r=-0.66) in normal and high flow POTS, and in five low flow POTS patients. The remaining five patients had reduced blood volume and increased angiotensin-II uncorrelated to blood volume. Data suggest that plasma angiotensin-II is increased in low flow POTS patients with hypovolemia which may contribute to local blood flow dysregulation and reduced NO bioavailability.

Right you are - I thought I read otherwise.

Currently Vandy are evaluating hypovolumic patients to see whether kidney dopamine levels have a role - although sympo-excitation is probably the answer. unpublished data suggests that kidney sympathetic denervation is not found in POTS.

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  • 5 months later...

Yes, I went back and reviewed the article, and Dr. Stewart mentioned a high percentage of low flow patients had high angiotensin II and this group with high angiotensin II were exclusively females and had low BMI. My understanding is that NET deficiency is very, very rare and tends to run in families. Is this true? One more question... are there are studies analyzing the NET in POTS? Could the transporter become damaged per say?

Can someone direct me to the Dr. Stewart study that says low-flow patients with high angiotensin II are exclusively female? I've scoured his studies and haven't come across that. Thanks.

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