Normal versus abnormal: What normative data tells us about the utility of heart rate in postural tachycardia, 2019, Baker and Kimpinski

Hutan said:
From the above study:


Yes, I don't think we have to see the orthostatic tachycardia itself as pathologic. It may well be a very normal and helpful reaction to some sort of stressor - to blood or oxygen not getting to where it needs to get to, for example.
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This is my thinking as well. I have POTS, but my HR goes up a lot on bad days and not very much on better days. My resting HR is between 48 and 52, and on a bad day it will go up to over 100 when I stand up. But what really makes me think that my poor body is actually doing its best to keep me conscious is that I have postural hypertension too - when I had my tilt table test, my BP shot up from its normal 120/70 (bang on for my age) to 200/140 within about a minute of being upright. I

I had no idea this was happening so I’m very glad I had the test (and now I’m on meds for high blood pressure, annoyingly, even though technically I only need them when I’m upright!), but it makes sense as a physiological response if you consider that the rise in heart rate I might be your brain doing its best to keep itself oxygenated. A rise in BP would also do the same thing - my blood pools in my legs and feet really easily, to the point where my feet are blue within a very short time after standing, so I would assume that my rise in blood pressure is my brain telling my cardiovascular system that it’s not getting enough blood up there and thus squeezing everything as much as it can to try and shunt some oxygen upwards. So actually it’s reacting in an entirely sensible way. The real issue, of course, is why it needs to do all of that in the first place….
 
This kind of reminds me of the way journalists and aerosol scientists exposed the WHO's dogmatic adherence to the line "Covid can't be airborne, everyone knows that viral particles bigger than 5 microns can only be carried in droplets" and traced the source back to a single document from the CDC offering guidelines to hospitals. It seems like someone, somewhere proposed 30 bpm increase, and then perhaps it got taken up and generalised to other contexts, and came to be considered a clinically relevant threshold?

The Wired article I read on the question of airborne viral transmission had some poignant sections:

Part of medical rhetoric is understanding why certain ideas take hold and others don’t. So as spring turned to summer, Randall started to investigate how Wells’ contemporaries perceived him. That’s how she found the writings of Alexander Langmuir, the influential chief epidemiologist of the newly established CDC. Like his peers, Langmuir had been brought up in the Gospel of Personal Cleanliness, an obsession that made handwashing the bedrock of US public health policy. He seemed to view Wells’ ideas about airborne transmission as retrograde, seeing in them a slide back toward an ancient, irrational terror of bad air—the “miasma theory” that had prevailed for centuries. Langmuir dismissed them as little more than “interesting theoretical points.”
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....

What must have happened, she thought, was that after Wells died, scientists inside the CDC conflated his observations. They plucked the size of the particle that transmits tuberculosis out of context, making 5 microns stand in for a general definition of airborne spread. Wells’ 100-micron threshold got left behind. “You can see that the idea of what is respirable, what stays airborne, and what is infectious are all being flattened into this 5-micron phenomenon,” Randall says. Over time, through blind repetition, the error sank deeper into the medical canon. The CDC did not respond to multiple requests for comment.
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I wrote an overview of the problems I see with the POTS criteria, summarizing the studies posted in this thread.
https://mecfsskeptic.com/the-problems-with-pots/

A brief summary of the arguments looks like this:
  • A heart rate increase of 30 bpm (or 40 bpm in 12–19-year-olds) is far from abnormal. Many young and healthy people without OI symptoms also have this. This suggests that POT is not pathologic and not a good marker of underlying disease processes.
  • Most people with OI do not have POT. Only a minority of patients with OI symptoms has tachycardia upon standing.
  • The relationship between POT and OI is weak. Symptom severity often correlates poorly with the magnitude of postural tachycardia. Increasing the threshold to a value higher than 30 bpm is therefore unlikely to solve the problem.
  • Low reproducibility: POT measurements vary and are influenced by many factors including water intake, time of day, deconditioning, etc.
Many thanks to @Nightsong and @SNT Gatchaman for helping me find references. I hope it is ok that I've briefly mentioned you at the end of the blog post.
 
ME/CFS Skeptic said:
I wrote an overview of the problems I see with the POTS criteria, summarizing the studies posted in this thread.
https://mecfsskeptic.com/the-problems-with-pots/

A brief summary of the arguments looks like this:
  • A heart rate increase of 30 bpm (or 40 bpm in 12–19-year-olds) is far from abnormal. Many young and healthy people without OI symptoms also have this. This suggests that POT is not pathologic and not a good marker of underlying disease processes.
  • Most people with OI do not have POT. Only a minority of patients with OI symptoms has tachycardia upon standing.
  • The relationship between POT and OI is weak. Symptom severity often correlates poorly with the magnitude of postural tachycardia. Increasing the threshold to a value higher than 30 bpm is therefore unlikely to solve the problem.
  • Low reproducibility: POT measurements vary and are influenced by many factors including water intake, time of day, deconditioning, etc.
Many thanks to @Nightsong and @SNT Gatchaman for helping me find references. I hope it is ok that I've briefly mentioned you at the end of the blog post.
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A very useful account, though it perhaps leaves us with more questions than answers.
 
That's a really excellent overview. (You should post it as a new thread; it definitely deserves wider attention.)

I'll try and track down the Streeten paper. (It's not available in the online archives of the Journal of Laboratory and Clinical Medicine, which only go back to 1996 even when you access them through a university portal with full-text access to the journal, but there are other potential sources of old papers.)

Something else I was going to mention on one of these threads is that there also seems to be nontrivial diurnal variability of orthostatic tachycardia in healthy individuals (see e.g. this paper: This threshold HR was exceeded in the evening by 42% of POTS patients and 4% of control subjects. In the morning, the percentages increased to 60% of POTS patients and 31% of control subjects - and that was a 5-minute stand).
 
ME/CFS Skeptic said:
Thanks. To be honest I don't fully know what to make of it either. Am interested in what others think.
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What may have happened is the human tendency to want to fit diseases into neat boxes. POTS was a neat box where various kinds of orthostatic intolerances that lacked a box and a theoretical uderstanding could be fit into with relative ease.

The general phenomenon of not being able to tolerate upright posture for as long as others or of experiencing a decline in mental function while upright for too long needs to be investigated more.

I clearly have some kind of orthostatic intolerance, but "healthy" people also seem to experience some form of orthostatic intolerance in certain conditions (like sudden onset of hot weather). I suspect my OI is worse, can worsen more as exposure to triggers continues, and has a higher symptom ceiling but without a test there is no way to know for sure. I also used to meet POTS criteria but no longer do.

I frequently have a milder form of the same sensation in the head that accompanies initial orthostatic hypotension. It varies through the day but can occur just in response to climbing stairs, or after exertion. I suspect much of the time I'm getting suboptimal blood flow into the brain which has presumably a wide range of subtle negative effects. I also suspect one of the way the body reacts to this is to deprioritize nonessential brain functions like ability to socialize or be creative.
 
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ME/CFS Skeptic said:
Thanks. To be honest I don't fully know what to make of it either. Am interested in what others think.
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On a personal level though orthostatic intolerance is an important factor in managing my activity I don’t think (have not been formally assessed) that I have POTS. Consequently I found the overview oddly reassuring as it affirmed the validity of my experience, though it currently does not fit into a nice little box,
 
Nightsong said:
I'll try and track down the Streeten paper. (It's not available in the online archives of the Journal of Laboratory and Clinical Medicine, which only go back to 1996 even when you access them through a university portal with full-text access to the journal, but there are other potential sources of old papers.)

Something else I was going to mention on one of these threads is that there also seems to be nontrivial diurnal variability of orthostatic tachycardia in healthy individuals (see e.g. this paper: This threshold HR was exceeded in the evening by 42% of POTS patients and 4% of control subjects. In the morning, the percentages increased to 60% of POTS patients and 31% of control subjects - and that was a 5-minute stand).
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Thanks. I've found the Streeten data in his 1987 book which I assume is from the same experiment as the 1988 paper.
Orthostatic Disorders of the Circulation: Mechanisms, Manifestations, and ... - David H.P. Streeten - Google Books

Interesting paper on diurnal variability. In my view, further support that relying a single measurement of POT is questionable.
 
Thanks ME/CFS Skeptic Most interesting!

I have tried to figure out how much of my being I'm bedbound is because of ME or POTS or what combination of these to no success.

From a series of tests at an Autonomic Dystautonomia Centre run by a POTS specialist in Calgary it was concluded I don't have POTS. (My HR went up 29 bpm on the 10 min tilt table tests). I don't know how the other tests they ran figured into the conclusion.

On standing I become light headed, experience brain fog and need to sit down but I don't seem to get pooling of blood in my feet or ankles or at least don't have swelling or discolouration. Over the years the dysautonomia symptoms seem to correspond with the severity of my ME symptoms.

From these observations I've wondered if people with ME have a kind of autonomic dysautonomia different than POTS but after reading your article it seems that even the definition of POTS is unclear.

Edited for typo
 
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My POTS coincided with small fiber neuropathy and the treatment for POTS (salt water, and avoiding excessive exposure to triggers) were helpful. But even without POTS, on some days, if I I'm experiencing the typical symptoms of OI, half a liter of fairly salty water has a marked effect on these symptoms. It also improves mood, calming me and the irritability vanishes.
 
alktipping said:
I think that patients who have no previous experience with this test will have raised heart beats simply because it is a new procedure to them and do not fully understand everything that will happen . results would be skewed by this.
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Conversely, people who have done it before and suspect that they are going to feel quite unwell could also have a raised heart rate.
 
I’m afraid I can’t source this to a specific lecture, but Dr Satish Raj, when talking about TTT studies, mentioned that POTS patients feel unwell during the test, and then possibly faint, but healthy subjects feel fine during the test, and then possibly faint.

I will see whether I can find the lecture again.

Edit:

Here it is:


(Link looks odd but works if you click “Learn more”.)

The issues discussed in this thread and the comment I paraphrased above are covered early on, although not in huge detail.

He’s a good speaker so I recommend watching this if you haven’t seen any of his lectures before.
 
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Helene said:
On standing I become light headed, experience brain fog and need to sit down but I don't seem to get pooling of blood in my feet or ankles or at least don't have swelling or discolouration.
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I am not sure whether blood pooling is visible “from the outside”. I know people with POTS often report blotchy or red legs and POTS specialists mention acrocyanosis, but I don’t know that not having these signs means no pooling.

It’s covered briefly in this article:
https://www.ahajournals.org/doi/full/10.1161/circulationaha.112.144501

See paragraph just before Figure 2, and Figure 2.
 
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