What do we actually know about orthostatic intolerance?

[Sasha]

For the time-chart, would there be an option to block in for reclining as well as for horizontal ?

The polling format here on Zenforo isn't sophisticated enough for that, I'm afraid.

Also, when I get slightly lightheaded its constant until it wears off, whether in bed or sitting or upright, so its not particularly related to postural change. So would my entry mess up the timeline pattern if any other light heads etc only occur on changing posture or standing ?

I'm not focusing on postural change but on when in the day our OI is forcing us to lie down. My impression is that most of us find that the pressure to lie down builds and builds over time until we're forced to lie flat, rather than our OI being just brought on by posture change. (I'm sure a much more sophisticated approach would be better but that would involve wearables and a proper study!)

 

[bicentennial]

The polling format here on Zenforo isn't sophisticated enough for that, I'm afraid.

I'm not focusing on postural change but on when in the day our OI is forcing us to lie down. My impression is that most of us find that the pressure to lie down builds and builds over time until we're forced to lie flat, rather than our OI being just brought on by posture change. (I'm sure a much more sophisticated approach would be better but that would involve wearables and a proper study!)

maye afterwards the recliners can be polled separately for comparison

my pattern is currently stable in thatIi must recline "by day" and go for flat out all "night"l(except by sleep cycle is rotating again), reason being that i cannot currently sustain the generation of energy to power load-bearing muscle (no stamina)

but other things happem when more upright. Some since covid and fitting long covid, some from the time before covid when I found I could sit up again after a long time flat out so long that then I would not lie down again so i sat up stubbornly in a captains chair all day and night til my head blacked out and hit the table, 24/7

thing is before the flattened time i could stubbornly sit up crosslegged in bed all day, despite it hurting my legs and so on and tiring out my muscle, but i cannot sit up at length any more now since the captains chair ejected me and returnedme to my bed, wimpo that I am

there is a keyboard warrior out there called Mr Riley who has not apologised to me for weaponising my story and turning it against me in dicatorial editored unedited unedifying edifying unexpurgated editorial fashion, Mr R being a dedicated follower of fashion and amusing someone who amuses him no doubt - in his spare time, but all is forgiven because he lay down his sword and shield Mahalia, by the rivers of babylon

 

[bicentennial]

the wearables may follow becasue Mr Wes Streeting announced the pilots and provisions are proceeding apace on the NHS as fully pioneered already in Plymouth Hoe for the remote monitoring of i think Parkinsons and soon to be bespoke to other conditions and rolled out across the uk so he wants us to turn up at the portal he is opening for ethical non-euthanising patient participation in this researchable and clinical experiment - see HIS new Delivery Plan for ME / CFS (UK)

Parkinsons Prioritsed for Pilot due to falls, so M.E / CFS is high upon the NHS waiting list for the next roll-out, high up there alongside the frail elders also waiting to be removed for the waiting lists

but we must must must speak for ours !!! !!!V!!! at the portal !!! !!! !!! elves now that the the MEA Trustees speaking for all af us with our blessing however can no longer differentiate between the 2 cohorts since falling into both at once .... with all due respects reciprocated

so this simple easy peasy poll emerged in the nick of time t indicate the profitable evidence base that can supersede rehab in all such cases once sold to the tech indsr=try

see the usa thread on wearable prospects here https://www.s4me.info/threads/impac...e-cfs-and-long-covid.41047/page-8#post-575993 because our Elon may be addng it to the Tesla portfolio, as we speak, the wearable sensors to measure and monitor your cases of chronic pain and its recesssions, making the diagnoisis of "woman" less challellenging

 

[bicentennial]

and see here https://www.s4me.info/threads/impac...e-cfs-and-long-covid.41047/page-7#post-575914

and when the time is ripe at the wearable rollout Wes Streeting portal, maybe change the name of this poll thread to ? what do we know about the horizontal (timeline)?

which implies there may also be a vertical timeline so if time has 2 axes as in 2D space x and y co-ordinates, maybe time has 3 timeline axes as in 3D space vectors, x..y..z .... no wonder we can't be mapped and a.i wants a try but what does a.i know about time passing

edit because the link was not translating to the post (after i had added the post number to the link in a prior edit but found it just reverted back to the original hyperlink in the event)

 

[dave30th]

Moved posts - there is some initial discussion about the possibility that anticipatory tachycardia is psychogenic

Well, yes the article is very much without sources.
I’m not sure it’s anything Andy needs to look for, I was just asking generally

there was a study from NYU that showed anticipatory tachycardia and patients with POTS who were told they were going to have a tilt table test. they interpreted that as suggesting that the tachycardia itself was psychogenic. It must have been 3-4 years ago.

 

[dave30th]

there was a study from NYU that showed anticipatory tachycardia and patients with POTS who were told they were going to have a tilt table test. they interpreted that as suggesting that the tachycardia itself was psychogenic. It must have been 3-4 years ago.

Fear conditioning as a pathogenic mechanism in the postural tachycardia syndrome - PMC

Despite its increasing recognition and extensive research, there is no unifying hypothesis on the pathophysiology of the postural tachycardia syndrome. In this cross-sectional study, we examined the role of fear conditioning and its association with ...

pmc.ncbi.nlm.nih.gov

 

[MrMagoo]

Well this seems like something the brain trainers could test scientifically. Y’know, it’s stats and data not qualitative interviews.
Also something that could be tested in a control (non ME/CFS non LC) at the same time.

 

[Turtle]

Fear conditioning as a pathogenic mechanism in the postural tachycardia syndrome - PMC

Despite its increasing recognition and extensive research, there is no unifying hypothesis on the pathophysiology of the postural tachycardia syndrome. In this cross-sectional study, we examined the role of fear conditioning and its association with ...

pmc.ncbi.nlm.nih.gov

I had a very bad experience with tilt table testing. 1 month of PEM, my brain all over the place.
I would fight anyone trying to put me on it again, my heart rate would go up big time.
Bad experience and prevention or anticipation?

 

[dave30th]

Bad experience and prevention or anticipation?

their argument was that the fact that people with POTS and tilt-table experience had anticipatatory tachycardia, while the comparison group didn't, indicated that the tachycardia itself might be psychogenic rather than that those with experience were having understandable anxiety upon knowing they would have a tilt-table test.

 

[Jonathan Edwards]

Tachycardia through anticipation is highly plausible, which maybe suggests that the tilt table test does not actually tell us anything useful about people with orthostatic intolerance. I don't think we have any evidence that it reflects important pathophysiology. It just seemed a neat idea to some physicians that it did.

 

[SNT Gatchaman]

Thread for the Fear Conditioning paper mentioned above. In the criticism, it was pointed out that some patients had a reduction in anticipatory HR and some controls had a similar increase to the patients.

Notwithstanding the ‘more pronounced anticipatory tachycardia’ found in the intervention than in the control group, a key challenge for the investigators’ hypothesis is the significant overlap between the two ranges of heart rates, as indicated in Fig. 1B of the paper.1 As is also clear from Fig. 1B, a subset of the POTS patients, like a subset of the healthy controls, experienced a decline rather than an increase in heart rate in anticipation of the tilt-table test. These salient details undermine the claim of psychogenic pathogenesis but are not addressed in the text of the paper.

 

[Sean]

their argument was that the fact that people with POTS and tilt-table experience had anticipatatory tachycardia, while the comparison group didn't, indicated that the tachycardia itself might be psychogenic rather than that those with experience were having understandable anxiety upon knowing they would have a tilt-table test.

Unfalsifiability, par excellence.

 

[rvallee]

their argument was that the fact that people with POTS and tilt-table experience had anticipatatory tachycardia, while the comparison group didn't, indicated that the tachycardia itself might be psychogenic rather than that those with experience were having understandable anxiety upon knowing they would have a tilt-table test.

Even though they are not mutually incompatible, which is a necessary condition for them to be correct about this. But I've never seen anyone give pause to anything psychosomatic when that happens.

And because honestly psychology is basically mostly Dunning-Kruger: they can't know that because they don't know that.

 

[Jonathan Edwards]

Something that seems odd about POTS is that if blood pressure is maintained, which is required by the definition of POTS, then there is no reason for brain perfusion to drop. For brain perfusion to drop one would have to posit some sort of reflex cerebral vasoconstriction as reflex in response to standing that was not in response to blood pressure drop. That would be a pretty strange reflex. Moreover, one could call it, in operational terms. a sort of 'anticipation' of an impending drop. That anticipation could be a conditioned reflex.

But the association of OI with tachycardia without a BP drop suggests much more that the unpleasantness of standing or sitting up relates to the reflex tachycardia itself rather than any loss of brain perfusion. We know from 'white coat syndrome' that such reflexes (in that case a rise in blood pressure and pulse) are very dependent on psychological environment. You cannot do anything about it with psychological therapy but the link is undeniable.

And as far as I can see none of this has anything much to do with PEM or 'fatigue' or anything that justifies the S after POT.

 

[InitialConditions]

Something that seems odd about POTS is that if blood pressure is maintained, which is required by the definition of POTS, then there is no reason for brain perfusion to drop. For brain perfusion to drop one would have to posit some sort of reflex cerebral vasoconstriction as reflex in response to standing that was not in response to blood pressure drop. That would be a pretty strange reflex. Moreover, one could call it, in operational terms. a sort of 'anticipation' of an impending drop. That anticipation could be a conditioned reflex.

But the association of OI with tachycardia without a BP drop suggests much more that the unpleasantness of standing or sitting up relates to the reflex tachycardia itself rather than any loss of brain perfusion. We know from 'white coat syndrome' that such reflexes (in that case a rise in blood pressure and pulse) are very dependent on psychological environment. You cannot do anything about it with psychological therapy but the link is undeniable.

And as far as I can see none of this has anything much to do with PEM or 'fatigue' or anything that justifies the S after POT.

I disagree.

The evidence points to brain hypoperfusion. We have reasonable evidence of reduced cerebral blood flow velocity from TCD studies — Novak, Raj etc.. The common symptoms of PoTS/OI certainly line up with that. I really don't think this has anything to do with the unpleasantness of tachycardia.

I don't think sustained peripheral blood pressure rules out cerebral vasoconstriction. In fact Novak has reported increased 'cerebral resistance' if I'm not mistaken. There may be different mechanisms at play within the brain.

Then there are all the known hemodynamic issues in PoTS/OI, including low blood volume and reduced cardiac output that would contribute to brain hypoperfusion. The issue is finding out what is driving each of them.

The tachycardia is just a (over)compensatory mechanism. Unfortunately it has been placed front and centre because of 'PoTS'. I think talking more broadly about orthostatic intolerance and dysautonomia is better. This paper suggests shared mechanisms in OI with and without tachycardia: https://pmc.ncbi.nlm.nih.gov/articles/PMC11562747/

I suppose condtioned response/reflex could fit into this picture. I don't know enough about how that would work.

 

[Felis Catus]

I didn't even know I was experiencing (postural orthostatic) tachycardia the first couple of years. Standing was making me feel unwell as well as sitting with feet on the floor but I didn't know what it was about. I was describing the unpleasant feelings in my body and if pushing through it getting to the point of fainting but I hadn't heard of POTS. Intuitively I realised I had to sit with legs raised and spend a lot of time horizontal.

 

[Jonathan Edwards]

The evidence points to brain hypoperfusion. We have reasonable evidence of reduced cerebral blood flow velocity from TCD studies — Novak, Raj etc.. The symptoms line up with that. I really don't think this has anything to do with the unpleasantness of tachycardia.

OK, there is some evidence of hypoperfusion but tachycarida would not in itself cause hypoperfusion. So what reason is there to think that the tachycardia is important? Why does it deserve to be diagnostic? Tachycardia is associated with poor brain perfusion in shock because it is a compensation for very low blood pressure. But in POTS it isn't.

I don't think sustained peripheral blood pressure rules out cerbral vasoconstriction. In fact Novak has reported increased 'cerebral resistance' if I'm not mistaken. There may be different mechanisms at play within the brain.

OK, so there may be a brain vasoconstriction syndrome but why should that be diagnosed by tachycardia if the two have no obvious relation?

Then there are all the known hemodynamic issues in PoTS/OI, including low blood volume and reduced cardiac output that would contribute to brain hypoperfusion.

But that does not add up. If BP is not low and pulse rate is high then low blood volume and poor cardiac output cannot be the reason for poor brain perfusion. These become non sequitur.


And to be honest, what we have found looking through the data in the past is that it is pretty much all over the plae and inconclusive.

 

[InitialConditions]

OK, there is some evidence of hypoperfusion but tachycarida would not in itself cause hypoperfusion. So what reason is there to think that the tachycardia is important? Why does it deserve to be diagnostic? Tachycardia is associated with poor brain perfusion in shock because it is a compensation for very low blood pressure. But in POTS it isn't.


OK, so there may be a brain vasoconstriction syndrome but why should that be diagnosed by tachycardia if the two have no obvious relation?



But that does not add up. If BP is not low and pulse rate is high then low blood volume and poor cardiac output cannot be the reason for poor brain perfusion. These become non sequitur.


And to be honest, what we have found looking through the data in the past is that it is pretty much all over the plae and inconclusive.

I don't think the tachycardia is that important. I think the tachycardia is compensatory. There are different upstream failures — hypovolaemia, venous pooling, sympathetic overactivation — driving reduced venous return and therefore compensatory tachycardia. The tachycardia is not causing the hypoperfusion.

Tachycardia is easily measurable/objective and so has taken centre stage in what we now call PoTS, but I'd prefer to just call it orthostatic intolerance until we know a bit more about what's going on.

But that does not add up. If BP is not low and pulse rate is high then low blood volume and poor cardiac output cannot be the reason for poor brain perfusion. These become non sequitur.

Cardiac output can be low despite high HR under reduced stroke volume (which is what you'd expect with poor venous return). HR cannot fully compensate.

I suspect there's something going on in the brain that's not reflected in peripheral blood pressure readings. But this is beyond my pay grade!

 

[ScoutB]

The tachycardia is just a (over)compensatory mechanism. Unfortunately it has been placed front and centre because of 'PoTS'. I think talking more broadly about orthostatic intolerance and dysautonomia is better. This paper suggests shared mechanisms in OI with and without tachycardia: https://pmc.ncbi.nlm.nih.gov/articles/PMC11562747/

So what reason is there to think that the tachycardia is important? Why does it deserve to be diagnostic?

I think everyone's in agreement that focusing on OI makes more sense than tachycardia?

And couldn't the OI be due to any number of subtle problems that we don't fully understand yet? E.g. (spitballing) could it be that 'neurovascular coupling' just isn't working as well as it should be?

 

[InitialConditions]

And to be honest, what we have found looking through the data in the past is that it is pretty much all over the plae and inconclusive.

I think we are much closer to understanding these issues than many others that appear in ME/CFS.