Physiological assessment of orthostatic intolerance in chronic fatigue syndrome, 2022, Natelson et al

Hutan said:
They found some people had low end tidal Co2 levels when lying down, before doing the lean test. Yes, it's possible that the whole getting to the clinic and just being there is stressful, but why the variability between visits, with levels being low on some visits and not on others?

So, I'm hypothesising that the presence of PEM, or not, might account for the variability. And so it would be good to see a study that took into account whether the person with ME/CFS has PEM, or not.
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As with a lot of this OI stuff it has been explored in greater deal, often with controlled studies, in the POTS literature over the past decade or so.

For example: the hypocapnia seen here is clearly not a stress response to the test. Healthy controls have been used in similar POTS studies and do not show the significant drop in ETCO2 that we see in patients when put through the same stand/tilt table tests. The hypocapnic POTS patients also exhibit hyperpnea, not tachypnea, so don't fit an anxiety hyperventilation response - primary anxiety/HV patients have also been recruited to confirm this.

A leading theory is that the hyperventilation in POTS is caused by "a mechanism involving peripheral chemoreflex sensitization by intermittent ischemic hypoxia".

We know in these POTS patients CBF is reduced with orthostasis, hyperpnea and hypocapnia then follow - this has been observed and replicated in multiple controlled studies. The theory states that a reduction in CBF implies a reduction in carotid artery and carotid body blood flows. This is referred to as a stagnant or ischemic hypoxia, which the carotid body cannot distinguish from hypoxic hypoxia. So these patients are thought to have a type of chronic intermittent hypoxia, which increases the peripheral chemoreflex sensitivity to hypoxia. Lots of complicated words to suggest repeated orthostasis alters the patients breathing response.

Although ME/CFS patients don't necessarily exhibit the tachycardia issues defined by POTS, they can show reduced CBF, so presumably this theory and its chain of events could also apply here.
 
Jonathan Edwards said:
I am a bit sceptical that PWME actually have low CO2 levels though - other than maybe in some test situations or during episodes of distress. I also doubt that it would cause the other symptoms.
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For what it's worth - I looked at my old lab tests. There are 9 measures of my total CO2/bicarbonate, a measure of CO2 in the blood. They all have been within normal range, tending to the high side. The one time it was below normal range, my CRP was abnormally high, even for me, so perhaps something else was going on.

It still would be interesting to see how levels of CO2 in the breath and in the blood vary on good and bad days for people with ME/CFS.
 
Hutan said:
For what it's worth - I looked at my old lab tests. There are 9 measures of my total CO2/bicarbonate, a measure of CO2 in the blood. They all have been within normal range, tending to the high side. The one time it was below normal range, my CRP was abnormally high, even for me, so perhaps something else was going on.

It still would be interesting to see how levels of CO2 in the breath and in the blood vary on good and bad days for people with ME/CFS.
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Its not particularly difficult/painful to take an earlobe capillary blood sample and estimate arterial blood gases from that - I had this done with a respiratory workup at a chest clinic. Suspect it was preferable to an arterial puncture! From that sample I got HbO2%, PaO2, PaCO2, H2CO3 and pH.
 
Moved post

Move Over POTS – Hypocapnia May be a Bigger Deal in ME/CFS

https://www.healthrising.org/blog/2022/03/10/hypocapnia-chronic-fatigue-syndrome-pots/

The Gist

This is the first of a series of blogs on breathing and ME/CFS/FM and long COVID.
Dr. Natelson did the NASA Lean Test on people with ME/CFS three times over three years. He tested heart rate, blood pressure, and CO2 levels.
Contrary to perceived wisdom, Natelson found that hypocapnia (low CO2 levels) was the most prevalent orthostatic abnormality found. It was far more prevalent, for instance, than postural orthostatic tachycardia syndrome (POTS). Hypocapnia was even found in some people when they were lying down.
Hypocapnia is often a result of hyperventilation, which is characterized by rapid and deep breathing. Natelson found little evidence of rapid breathing; instead, he consistently found deeper than normal breathing. Natelson et al. called the condition POSH (postural orthostatic syndrome of hypocapnia).
We breathe more rapidly and deeply to get more oxygen to our muscles, and to remove CO2 from our blood, when we exercise. Exercise, however, was not a factor in this study.
Normal breathing is light breathing; it’s barely perceptible.
Other forms of orthostatic intolerance have recently been uncovered by Peter Novak MD, PhD of Harvard. Novak found hypocapnia was linked to low brain blood flows in a condition he called hypocapnic cerebral hypoperfusion.
Novak also uncovered a condition similar to what the Visser team has found in ME/CFS. In orthostatic cerebral hypoperfusion syndrome (OCHOS), low brain blood flows are found in the absence of increased hearts rates or drops in blood pressure.
A long list of possible causes (baroreceptor problems interfering with “respiratory drive”, compensation for metabolic acidosis, orthostatic ventilation-perfusion mismatch, problems with the respiratory centers in the brain) may be responsible for these conditions.

Treatment Possibilities

Treatment Takeaways

Treatment possibilities include:

Increasing blood volume by using oral rehydration salts, and compression hose
Having respiratory therapists use biofeedback techniques to try to reduce the depth of breathing.
Abdominal breathing (done slowly), breathing through pursed lips, meditation, mindfulness, relaxation exercises are recommended. We’ll check out more breathing options in this series.
Check out how to do an in-home test for hypocapnic hyperventilation – A Home Postural Hypocapnic Hyperventilation Test for Chronic Fatigue Syndrome and Fibromyalgia
 
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Really not my area but one interesting thing derived from this is that (in my limited understanding) the breathing reflex relies on CO2, not O2. So in a room with a slowly depleting oxygen saturation (from breathing) that can scrub out the CO2, the body wouldn't realize it is becoming hypoxic, would do nothing to compensate.

So if cells are poorly utilizing oxygen, by not producing much CO2 as a result it couldn't really compensate since the trigger to increase oxygenation relies on CO2.

But it'd be odd if this low CO2 hadn't been noticed before, rather than some artifact of a study or method.
 
Two Tests For Hyperventilation

A Simple Hyperventilation Test
  • Most people can hold their breath for 45 seconds or more. Take a breath and hold it: if you can only hold for your breath for 35 seconds or less you could be a chronic hyperventilator.
A Hyperventilation Test When Standing
  • Stand up straight for 8 minutes.
  • If you start to feel ill stop and rest for a while.
  • Repeat the test but time breathe into a paper bag held across your nose and your mouth. If your symptoms disappear when you are breathing into the bag you may be hyperventilating.
Source:
https://www.healthrising.org/forums...ilation-test-for-me-cfs-and-fibromyalgia.239/
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Holding my breath for 45 seconds felt horrible.
 
Note that hyperpnea causes sympathoinhibition which has been thought to be mediated by pulmonary stretch reflexes for several decades. https://pubmed.ncbi.nlm.nih.gov/2364488/ (1990)

The suggestion that hypovolemia or other blood flow issues may be a contributing factor to the hyperpnea is plausible. Another POTS study from 2008 found:
https://pubmed.ncbi.nlm.nih.gov/18502909/

Our data suggest that excessive splanchnic pooling and thoracic hypovolemia result in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.
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Another study suggested that reduced cerebral blood flow leads to a cascade: "resulting ischemic hypoxia of the carotid body causes chemoreflex activation, hypocapnic hyperpnea", however they found that sympathoexcitation was inversely proportional to end tidal CO2 levels.
https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.113.02824
So I guess it is possible the hyperpnea is a response to increased sympathoexcitation which is in turn a response to the increased blood pooling.

Reflecting on my own experiences - I don't suffer from POTS or OI on a daily basis since I started increasing my salt input and exercising briefly once a week.

But I still experience OI as a PEM symptom (delayed for several hours and persistent for around 24 hours) from exercise (which has a hypotensive effect due to splanchnic pooling), as well as increased susceptibility from certain medications - corticosteroids and amitriptyline, both of which cause sympathoinhibition and altered vascular resistance as a result.

One thing I'd like to mention is that some neurological diseases, such as Guillain Barre Syndrome have rapid-onset OI (among other symptoms) that cannot obviously be explained by deconditioning or dietary deficiencies - but rather blood flow problems due to disrupted nerve signals to/from the periphery.
 
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When things started going wrong for me, the very first symptom I noticed in myself (before I even realised my HR was 30-40 above normal) was abnormal breathing. I was sitting quietly at anchor enjoying a light salad in the early evening and had to intermittently stop eating and take a much deeper than normal breath.
 
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