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Low, Normal And High Flow Pots


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I recently learned that the Center for Pediatric Hypotension at New York Medical College distinguishes between three kinds of POTS: high flow, normal flow, and low flow, POTS.

High flow POTS patients are characterized as having "high blood flow, low arterial resistance group with normal to decreased pv (peripheral venous pressure)"

Normal flow POTS is defined by "A normal blood flow, normal arterial resistance group with normal Pv..."

Low flow POTS is defined by "low blood flow, high arterial resistance, high Pv."*

Are these categories used by other clinics outside of New York Medical College? Are three subtypes known to be distinguishable by symptoms?

*http://www.nymc.edu/fhp/centers/syncope/circulatory_findings_in_pots_and_CFS.htm

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Green,

this site has more of the technical nitty-gritty on POTS and flow types:

http://www.nymc.edu/fhp/centers/syncope/circulatory_findings_in_pots_and_CFS.htm

Variants of postural tachycardia syndrome (POTS) are associated with increased (?high flow? POTS, HFP), decreased (?low flow POTS?, LFP) and normal (?normal flow POTS?, NFP) blood flow measured in the lower extremities while supine. We propose that postural tachycardia is related to thoracic hypovolemia during orthostasis but that the patterns of peripheral blood flow relate to different mechanisms for thoracic hypovolemia. We studied 37 POTS patients aged 14-21 years: 14 LFP, 15 NFP and 8 HFP patients and 12 healthy control subjects. Peripheral blood flow was measured supine by venous occlusion strain gauge plethysmography of the forearm and calf in order to subgroup patients. Using indocyanine green techniques we showed decreased cardiac index (CI) and increased total peripheral resistance (TPR) in LFP, increased CI and decreased TPR in HFP, and unchanged CI and TPR in NFP while supine compared to control subjects. Blood volume tended to be decreased in LFP compared to control subjects. We used impedance plethysmography to assess regional blood volume redistribution during upright tilt. Thoracic blood volume decreased while splanchnic, pelvic and leg blood volumes increased for all subjects during orthostasis, but were markedly lower than control for all POTS groups. Splanchnic volume was increased in NFP and LFP. Pelvic blood volume was increased in HFP only. Calf volume was increased above control in HFP and LFP. The results support the hypothesis of [at least] three pathophysiologic variants of POTS distinguished by peripheral blood flow related to characteristic changes in regional circulations. The data demonstrate enhanced thoracic hypovolemia during upright tilt and confirm that POTS is related to inadequate cardiac venous return during orthostasis.

It looks like it is based on peripheral blood flow.

Good luck

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Green,

this site has more of the technical nitty-gritty on POTS and flow types:

http://www.nymc.edu/fhp/centers/syncope/circulatory_findings_in_pots_and_CFS.htm

Thank you, Firewalker.

I am interested in learning whether these distinct forms of POTS belong to a theoretical framework unique to the New York clinic. A pubmed search on these terms didn't turn up any publications by non-NYC affiliated researchers, so I am inclined to think that these distinctions are either idiosyncratic or have alternative names. (although... I don't really know how pubmed works, and I imagine there must be peer-reviewed published research that DOESN'T end up in pubmed) I will write the NYC people as my next step.

Ultimately, my interest in this topic is driven by thoughts about how these different forms of POTS could be amenable to different kinds of treatment. For example, one of the articles on their website argues that "neuronal nitrous oxide is specifically decreased in low flow POTS." If this is true, then it would seem to merit investigating whether interventions that increase neuronal nitrious oxide would be helpful for people with low-flow, but not normal or high flow POTS.

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Its pretty confusing but Ive been told the following:

Grubb et al have broken up POTS into two distinct groups based on SYMPTOM PRESENTATION and also their clinical findings so far:

The PD form which accounts for 90% and of which 14% had positive antibody tests

Hyperadregenic POTS of which about half had faulty norepinephrine reuptake

Im not sure whether the Vandie people and the Baker Institute in Australia accept these two classifications. I was told at the Baker institute that there was NOT an accepted breakup of POTS until they could 100% confirm the causes of POTS.

Dr J Stewart in NY has broken up POTS into three groups based on peripheral/calf blood flow levels and has published work that suggests that these three subgroups might have different causes for symptoms. These classifications are based on his groups findings and not on symptoms. But one of the three - low flow now has a potential treatment being investigated.

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>These classifications are based on his groups findings and not on symptoms. But one of the three - low flow now has a potential >treatment being investigated.

>

What treatment are you referring too?

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I've come across some interventions that potentially improve peripheral blood flow:

Bodybuilders sometimes take "L-arginine" supplements because they improve NO availability and relax the small blood vessels.

Watermelon contains an amino acid called "Citrulline" that works the same way. Here is an article about it: http://www.biotech-weblog.com/50226711/cit...ike_effects.php (you have to get past the 'viagra-like effects' spin that the article has and attend to the theoretical significance of that)

Also, cholesterol medications may relax blood vessels.

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general vasodilators will increase peripheral blood flow, but they will also lower blood pressure and make POTS worse (generally in most people anyway).

I think the idea with this guy was to see if they could find distinguishable sub-groups of POTs patients based on laboratory findings and not symptoms, then see if they could find a cause.

I think Dr.Stewarts work looks quite promising - considering that he is looking at POTS from very different angles: (nitrous oxide and angiotenson II (1 is a vasodilator the other a vasoconstrictor) and also looking at elevated Carbon Dioxide as a possible cause of syncope/passing out and dizziness in some pots patients rather than lack of blood flow to the brain.)

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  • 2 weeks later...

Ok I think im across how these three catagories work now...

High Flow Pots is pretty much catagorised as vasodilation of the limbs - which I would expect would cause excessive blood pooling in the legs. On their website it demonstrates that people with High Flow POTS have more blood pooling in their legs than other places. This form is connected with the post-viral autoimmune peripheral neuropathy presentation suggested by Dr.Grubb

Normal Flow POTS is a redistributive form of POTS where the blood is pooling almost exclusively in the stomach. There is mention that this form often corresponds with EDS but Im not sure about that. Patients exhibit peripheral vasoconstriction so they do not seem to suffer denervation.

Low Flow POTS is where there is reduced peripheral blood flow even when supine and patients in this catagory may exhibit tachycardia even lying down, have clammy cold skin and sometimes blueish extremities. Peripheral vasodilation tends to reduce with orthostatic stress - blood pooling occurs primarily in stomach and pelvis but there is also some in legs.

From my reading I understand that Dr.J.Stewart isnt convinced that there is a form of POTS that is caused by excessive sympathetic activity although Normal Flow POTS might be.

Reduced NET activity or hyperadrenegic POTS - if it does exist and the jury is still out on this issue - would cause excessive vasoconstriction resulting in a form of Low Flow POTS.

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  • 11 months later...

gees I got that all a bit wrong. Ill try a bit harder if we include all the varied forms I think it looks like this:

Neuropathic POTS / High Flow POTS - reflex tachycardia, increased blood flow in the arms and legs, hot, warm hands and feet, autoimmune antibodies to a3 receptors implicated as well as distal neuropathy. Responds well to midodrine.

Neuropathic POTS / Normal Flow - reflex tachycardia, neuropathy specific to the stomach - pooling in stomach. Responds to octreotide?

Hypovolumia kidney - reflex tachycardia, low overall blood volume, respond well to volume increases.

Hypovolumia / sympathetic excess / Low Flow POTS. Tachycardia adrenergic, increased central and peripheral sympathetic excess, acyanotic skin, total body vasoconstriction, skeletal muscle pump failure, increased angiotensin II through reduced catabolism = decreased renin and low blood volume, sympathetic excess, decreased nitrergic neuronal nitric oxide = norepinephrine potentiation and increased MSNA. responds to losarten??

NET deficiency - tachycardia partly reflex partly adrenergic, increased peripheral resistance due to increased norepinephrine transduction, reduced norepinephrine uptake in heart, possible central reduced, pooling in stomach possibly from lack of norepinephrine through constant stimulation and transduction without reuptake protein. MSNA norma, decreased or increased, reduced cerebral blood flow may be due to pooling and or cerebral vasoconstriction?? Responds to alpha/beta blockers?? octreotide??

Parasympathetic withdrawal - reduced parasympathetic activity tonic or orthostatic which results in impaired cerebral vaso-regulation. tachycardia of nitrergic, cholinergic origin?? mestonin/beta blockers??

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What's "reflex" vs. "adrenergic" tachycardia. Can that be gleaned by something like the manner in which pulse rises upon standing? Like instantaneous vs slow delayed rise? Some other sign?

What does "tonic" mean in this context "reduced parasympathetic activity tonic or orthostatic"?

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So the phrase says that the subtype is characterized by either a persistent or a temporary-while-standing reduction to the parasympathetic activity... hence, "tonic or orthostatic". Am I parsing the sentence correctly?

I don't suppose there is a "poor man's" venous-occlusion-strain-gauge-plethysmography method out there? Something safe to do at home like the "poor man's tilt"? Any way to semi-reliably infer one's flow rates? :)

If a pulse increase is slow and steady and coincides with steady appearance & exacerbation of other "sympathetic" symptoms like sweating, trembling, tingling, etc. would that sound characteristic of a "sympathetic tachycardia"?

Would a reflex tachycardia be something like a reflex bradycardia (which is slowing of heart trying to counter a BP rise)? When the compensation is successful, one doesn't necessarily even see the BP change, however such reflex tachycardia is presumed in simple OH circumstances (where BP does drop) which is the case with hypovolemia. That reflex response is actually said to occur in normal people during orthostatic stress as part of an expected response to counter fluid shift. Perhaps there is a further distinction in the context of POTS, like "exaggerated" or hyper-reactive or something? Perhaps "baroreflex sensitivity" is the observation being alluded to... that is specifically measurable & studied in a number of ways (and its deviations enjoy correlations of various sorts such as with depression & essential hypertension, coincidentally).

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I mostly understand what the low/normal/high classification is saying, but I am clueless as how I could find out for myself which one I have.

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Hmmm.....I know I pool in both my hands and feet, it's minor pooling but it's definitely there. No clue how to tell about my stomach.

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