• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

mechanism for normal Sp02 when short of breath?

WillowJ

คภภเє ɠรค๓թєl
Messages
4,940
Location
WA, USA
do we think our Sp02 (oxygen saturation in the blood of our finger, which is where it's convenient to test) stays normal, even when we're short of breath?

do we think this is because our tissues don't utilize oxygen well? Is this a mitochondria thing, or what?
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
I think it's a mitochondria thing and a perfusion thing.
Lately I am very interested in the Albert Donnay theories. He thinks that the mitochondria toxin - carbon monoxide - induced by heme oxygenase (HO) is the cause of CFS and CFS-like diseases. HO is induced by many stressors:

Koolmonoxide.JPG

I don't think that carbon monoxide is the main cause of CFS but I like the idea to monitor the disease with a carbon monoxide detector. He recommended a Fluke CO-220 and I will probably buy one.

He also mentioned that high venous SpO2 (>65%) and high pO2 (>35mmHg) are indicative for low cellular oxygen uptake and are easy to test with a blood gas analyzer.
For more info:
http://www.mcsrr.org
http://www.mcsrr.org/resources/articles/P11.html
www.bartlett.ucl.ac.uk/web/ben/CO Measurement Protocols.doc
http://www.mcsrr.org/graphics/poeposter.jpg
http://www.mcsrr.org/CO Protocol.pdf

My blood results:
HbCO - 2,7% (<1,5% for non-smoker)
Venous pO2 - 41 mmHg (< 35 mmHg)
Venous SpO2 - 79% (<65%)

I also believe that fat-soluble oxidants and low blood volume play a major role in low cellular oxygen uptake.



There are four basic types of hypoxia:

1. Hypoxic hypoxia occurs when there is a deficiency in oxygen exchange in the lungs.
Some causes include:
? Decreased partial pressure of oxygen available at altitude
? Conditions that block the exchange at the alveolar capillary level (e.g. pneumonia, pulmonary edema, asthma, drowning)

2. Anemic hypoxia occurs when the body cannot transport the available oxygen to the target tissues.
Causes include:
? Anemia from acute or chronic blood loss
? Carbon monoxide poisoning
? Medications such as aspirin, sulfonamides and nitrites
? Methemoglobinemia
? Sickle cell disease

3. Stagnant hypoxia occurs when there is insufficient blood flow.
Causes include:
? Heart failure
? Decreased circulating blood volume
? Excess vasodilatation
? Excess vasoconstriction
? Hyperventilation

4. Histotoxic hypoxia occurs when the bodys tissues are not able to use the oxygen that has been delivered to them.
Causes include:
? Hydrogen sulfide (mitochondrial toxin)
? Cyanide (mitochondrial toxin)
? Alcohol (mitochondrial toxin)
? Narcotics (mitochondrial toxin)
? Pesticides (mitochondrial toxin)
? Peroxynitrite (mitochondrial toxin)
? Antiretroviral drugs (mitochondrial toxin)
? Low CO2, hyperventilation (high oxygen affinity of hemoglobin)
? Carbon monoxide (high oxygen affinity of hemoglobin)
? Hypothermia (high oxygen affinity of hemoglobin)
? Alkalosis (high oxygen affinity of hemoglobin)
? Low phosphate (high oxygen affinity of hemoglobin)

Most important causes of hypoxia in ME/CFS:
? Anemic hypoxia: Low red cell mass
? Stagnant hypoxia: Low blood volume, Excess vasoconstriction (high norepinephrine/endothelin/angiotensin)
? Histotoxic hypoxia :All mitochondrial toxins, High oxygen affinity of hemoglobin*

* Oxygen affinity of hemoglobin (p50) is calculated from venous blood gas values.
Excel program to calculate p50 from venous blood gas values:
http://www.medsci.org/v04p0232.htm
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Is this a mitochondria thing, or what?

I haven't had the time to plunge into the mitochondria thing yet. But one aspect immediately comes to mind: can mitochondrial function change quickly? My SOB can change markedly in 24 hours, so I've been leaning towards a lung-centered explanation for me.

There's another thing: early on, the SOB was one of my main symptoms, so I tested myself by running (slowly). It seemed to me that any normal exertion, like walking, leads to some SOB. Yet on a slow run I surprisingly seemed to be the same as I ever was - not great but still the same as pre-CFS. My inclination is to think that my lung incapacity is in the upper lungs, so that on deeper breathing I use the lower parts which are okay. Whenever I take a fast, deep breath, I want to cough and I can feel that things are not right (almost ticklish) in the upper lung/airway area - say from the clavicles on down for several inches. That's been so for over two years.

Also, on giving myself the fingernail-pinch test sporadically over many months, I have seen seen anything unusual. I'd equate that to a normal PulseOx, though I might be mistaken. I do know that my PulseOx at 6 months before getting sick was 99%, because I was near a machine so I did it.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
4. Histotoxic hypoxia occurs when the bodys tissues are not able to use the oxygen that has been delivered to them.
Causes include:
...
? Peroxynitrite (mitochondrial toxin)

I'd immediately then wonder if there are two subgroups: those with hypotension and those (like me) with hypertension. If those who are hypo have excess Nitric Oxide, then that'd break down to lots of peroxynitrite. I'd also wonder if they are fibromyalgic (I'm not), do they also have excess bradykinin (the infamous pain-causer) which also leads to excess NO and is vasodilating in its own right.

Speaking of bradykinin, that's what is most responsible for pain in swollen nodes, as the proliferation of leukocytes stretches the node capsule from within. My submandibular nodes have been swollen for 2+ years yet have never been painful. So maybe I am in a subgroup not prone to overproduction of bradykinin, therefore no pain and no hypoT.

(A database that could establish correlations seems like such a good idea, but I wonder how many people would fill out the questionnaires?)
 
Messages
13
Lately I am very interested in the Albert Donnay theories. He thinks that the mitochondria toxin - carbon monoxide - induced by heme oxygenase (HO) is the cause of CFS and CFS-like diseases. HO is induced by many stressors:
...
I don't think that carbon monoxide is the main cause of CFS but I like the idea to monitor the disease with a carbon monoxide detector. He recommended a Fluke CO-220 and I will probably buy one.
...
He also mentioned that high venous SpO2 (>65%) and high pO2 (>35mmHg) are indicative for low cellular oxygen uptake and are easy to test with a blood gas analyzer.
For more info:
http://www.mcsrr.org
http://www.mcsrr.org/resources/articles/P11.html
www.bartlett.ucl.ac.uk/web/ben/CO Measurement Protocols.doc
http://www.mcsrr.org/graphics/poeposter.jpg
http://www.mcsrr.org/CO Protocol.pdf

My blood results:
HbCO - 2,7% (<1,5% for non-smoker)
Venous pO2 - 41 mmHg (< 35 mmHg)
Venous SpO2 - 79% (<65%)

Hi Emootje,

Thanks for your interest in my carbon monoxide theories all the way back to 2011, and especially for taking the time to test the biomarkers of CO poisoning that I recommended at the time.

Unfortunately, as you discovered, your COHb, venous PO2 and venous SpO2 results are all abnormally high -- in the range that I see in people with chronic CO poisoning.

It is now 2023 so I wonder if you ever found an external source of CO that was poisoning you or if this might be endogenous CO from some current or prior infection?

My current protocols are based on only non-invasive testing for body temp and CO in breath, which is much easier, faster, cheaper, safer, more accurate, and, of course, less painful than blood testing.

But you have to use a device with a CO sensor that is hydrogen compensated otherwise the hydrogen that we also have in our breath may be read as CO.
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
I am honored, the real Albert Donnay reacts :)
It is now 2023 so I wonder if you ever found an external source of CO that was poisoning you or if this might be endogenous CO from some current or prior infection?
Short answer: no
It's been a while but this what I can remember:
2008: UMC Utrecht stops providing (most) blood tests not ordered by a health professional, including COHb en blood gases.
2012: Bought a Fluke CO 210 (CO220 is to expensive) > no increased CO in my breath
2020: Bought two GEM OPL CO oximeters but both gave inconsistence results.
2022: Medische Laboratoria Dr. Stein & Collegae: CO-hemoglobine 1.2% Hb (good lab but it took 20 hours for my blood to arrive, still accurate?)
My current protocols are based on only non-invasive testing for body temp and CO in breath, which is much easier, faster, cheaper, safer, more accurate, and, of course, less painful than blood testing.

But you have to use a device with a CO sensor that is hydrogen compensated otherwise the hydrogen that we also have in our breath may be read as CO.
I love to hear more about your current protocols and which CO sensor you use nowadays.
 
Messages
58
do we think our Sp02 (oxygen saturation in the blood of our finger, which is where it's convenient to test) stays normal, even when we're short of breath?

do we think this is because our tissues don't utilize oxygen well? Is this a mitochondria thing, or what?
I’m in the low blood pressure ring. Vasodilated to disability 😞 I also have hyperventilation even-though im not purposely hyperventilating 😞