Free blood gases analysis [Netherlands]

[Valentijn]

@Emootje - Have you been able to test blood from your vein? I had ridiculously low PO2 and oxygen saturation when tested at a clinic recently. It was 24% for the saturation, which should be 70-80% for a venous sample.

 

[Lolinda]

@Emootje - Have you been able to test blood from your vein? I had ridiculously low PO2 and oxygen saturation when tested at a clinic recently. It was 24% for the saturation, which should be 70-80% for a venous sample.

Similar here. Then I asked at another department about these results... and why on earth nobody started panicking that I could be in life danger and why on earth I felt largely fine without much oxygen. And the PhD from the other department just laughed: "we always ignore these results... and hope that maybe this year they buy new equipment."

No way your results are any correct...Albeit not for venous but for arteriat SPO2, in this post you find some levels of SPO2 that are considered "hypoxia" or "likely organ damage", also, you find information on using standing-laying SPO2 to learn more about issues possibly affecting you

 

[CFS_for_19_years]

@Emootje - Have you been able to test blood from your vein? I had ridiculously low PO2 and oxygen saturation when tested at a clinic recently. It was 24% for the saturation, which should be 70-80% for a venous sample.

pO2 for a venous sample should be 28-48, not 70-80%.

http://www.globalrph.com/abg_analysis.htm

Normal Blood Gases
Arterial PaO2 80 to 100 mm Hg.
Venous PaO2 28 - 48 mm Hg

http://www.oxfordmedicaleducation.com/abgs/venous-blood-gas-vbg-interpretation/

Venous and arterial PO2 are also not comparable

• The arterial PO2 is typically 36.9 mmHg greater than the venous with significant variability (95% confidence interval from 27.2 to 46.6 mmHg).

Your pO2 is on the low side. Here are some possible reasons that should be confirmed with an arterial blood gas measurement:
https://www.glowm.com/lab_text/item/3

Decreased PO2 levels are associated with:

• Decreased oxygen levels in the inhaled air
• Anemia
• Heart decompensation
• Chronic obstructive pulmonary disease
• Restrictive pulmonary disease
• Hypoventilation

 

[Lolinda]

pO2 for a venous sample should be 28-48, not 70-80%.

Interesting data, @CFS_for_19_years .Would be interesting to learn her PO2. However his 24% were about the saturation, SPO2. @Valentijn did not give data about the partial pressure. No way SPO2 goes that low.

One can test venous SPO2 at home:
(using any commercial fingertip SPO2 gadget)
Just breathe out and hold breath for a while. During the first seconds, the finger will receive the blood from the lungs before holding breath. then SPO2 will drop a bit because the finger will get venous blood that was at the start of the experiment before the lungs! You wont be able to hold much longer But you will have measured venous SPO2.
- and I bet a good Champagne that whatever hard you try until your head gets purple, your eyes pop out and anyone nearby calls the (psychiatric ) emergency you will never ever see any SPO2 of 24%
(and if you had that value, you wouldnt see much anymore..... )

 

[Valentijn]

pO2 for a venous sample should be 28-48, not 70-80%.

24% was the oxygen saturation, not the PO2.

PO2 was was 2.2kPA (normal 4.0 - 6.7). That converts to 16.5mmHg.

Here's my full results, before and after climbing a big flight of stairs, since the internist wanted to see what it would do to my lactate. The ranges included with my results were already calibrated for venous samples, though the O2 saturation had no range listed. Most sources online say 75% or 70-75%, and one says 70-80%. This was at a very busy clinic in one of the best hospitals in the Netherlands - I'd be rather shocked if their equipment was outdated or faulty.

Home-tested lactate was 2.8 around 10pm, 5+ hours after exertion.

 

[Valentijn]

I tested three times with my finger pulse oximeter after fully exhaling and holding my breath for 30 seconds. I literally can't hold it any longer than that. Oxygen saturation got down to 83%, 78%, and 74%, which would be pretty normal for venous blood.

Vision did get a bit grey each time, but it also does that to a mild extent even under "normal" circumstances. Though it's usually just mildly shadowy/splotchy then and I can still see well enough.

 

[Lolinda]

one of the best hospitals in the Netherlands - I'd be rather shocked if their equipment was outdated or faulty.

that exactly matches my experience: the second most renowned academic hospital of a similar western country... but I wonder what the doctor commented on these results?

I tested three times with my finger pulse oximeter after fully exhaling and holding my breath for 30 seconds. I literally can't hold it any longer than that.

30 seconds are fully enough. you did the test well. (btw I can get you a patent writing in which they state and exploit these times for some fancy measurements. let me know and I am happy to dig it out. the times were specified for when the blood from where appears in the fingertip.)

Home-tested lactate was 2.8 around 10pm, 5+ hours after exertion.

that does not sound good. isnt that a very long time after the exertion?. To state my level of knowledge clearly, I am by no means any expert of lactate metabolism, in particular I do not know the natural curve after exertion nor the normal diurnal curve. nor do I know if you have eaten or had further exertion by going home. but back when I had cfs (is that your issue?) many doctors tested me for lactate. I guess with your impressive amounts of PR posts I really wont tell you anything new that elevated lactate is the hallmark of most mito diseases.
What could be, however, interesting: while I never had pathologically elevated lactate, I could lower my post-exercise lactate levels by breathing exercises. I took part in a research study and the experimenter revealed me that my second 5 threadmil trials were better than the first 5, and I have experienced myself that my performance improved. Yoga-like breathing is not the thing for everyone... If this is sthg you feel you want, let me know, I am glad to be of help. I base my idea on the fact that your PCO2 has still room for improvement. more CO2 means interestingly better oxygen exchange.
(though, I dont trust their measuremunts after doing so wrong with O2...repetition?)

then, what is your normal spo2, w/o holding breath?

have you tried increasing potassium? you seem to have room for improvement

 

[Valentijn]

that exactly matches my experience: the second most renowned academic hospital of a similar western country... but I wonder what the doctor commented on these results?

No comment yet. They have an online system for patients to access test results. They went up at the beginning of last week, then the country effectively had a 4-day weekend But wouldn't the PO2 support the low oxygen saturation, or are those generally unrelated? I haven't really looked into the PO2 much yet.

that does not sound good. isnt that a very long time after the exertion?. To state my level of knowledge clearly, I am by no means any expert of lactate metabolism, in particular I do not know the natural curve after exertion nor the normal diurnal curve.

Yes, I did look into lactate after my Adventures With Metformin. It's normal for it to go over the range given (that's the rested range). But it should peak about 5 minutes after exertion, then steadily drop over the next hour or so. I did a 4 minute step test at home (heart rate 140-145 for last three minutes), and mine didn't go particularly high, but it also didn't drop, and continued peaking for 2 hours.

This is a normal lactate curve:

This is my lactate:

So I think my lactate level shortly after the stair-climbing at the hospital was probably pretty normal, though possibly not for the level of exercise involved. The evening results aren't expected to be any higher from what I've read, though there isn't a lot of information online. I downloaded some medical books recently, so maybe those will have have some more concise answers.

nor do I know if you have eaten or had further exertion by going home. but back when I had cfs (is that your issue?) many doctors tested me for lactate.

I had dinner around 7pm, but no exertion after the stair climbing. We had my wheelchair at the hospital. It was a fairly bad day, however, even before leaving home. I started out with tachycardia pretty early, which usually means my pulse pressure is low.

What could be, however, interesting: while I never had pathologically elevated lactate, I could lower my post-exercise lactate levels by breathing exercises.

Altering my breathing tends to make me feel worse. It can help a bit if I temporarily breath deeper and faster, but it's too exhausting to do for long.

then, what is your normal spo2, w/o holding breath?

99%. At 97% my body seems to freak out and my heart rate rises until it's back to 99%.

have you tried increasing potassium? you seem to have room for improvement

My gut doesn't like electrolyte mixes, unless I use them very rarely. Disappointing, since they did seem to help with OI a bit.

 

[Emootje]

@Emootje - Have you been able to test blood from your vein? I had ridiculously low PO2 and oxygen saturation when tested at a clinic recently. It was 24% for the saturation, which should be 70-80% for a venous sample.

In critical care medicine they use central venous O2 saturation measurements (obtained from a central venous catheter) or a mixed venous O2 saturation measurements (obtained from the distal port of a pulmonary artery catheter) to determent the consumption of oxygen [Oxygen Consumption = Cardiac Output X Hb X (SaO2 - SvO2)]
Abnormal values of SvO2 are shown in table 1, clinical conditions in table 2:

http://icucare.blogspot.nl/2009/08/venous-oximetry-concept-of-svo2-and.html

Peripheral venous SPO2 measurements is never used as indicator for oxygen consumption so I guess it is not that reliable.

I have tested my peripheral venous blood PO2/SPO2 (26,5 mmHg and low = < 60%). I did not release the tourniquet during the blood draw which could induce local ischemia which could explain the lower PO2/SPO2.

Bides the low reliability of peripheral venous blood PO2 it also does not correlate well with arterial blood PO2:
"In conclusion, PVBG analysis compares well with ABG for pH estimations in adults but does not accurately reflect the partial arterial carbon dioxide concentration or partial arterial oxygen concentration. The differences between venous and arterial gas tensions are sufficiently large to be of clinical significance and suggest that venous and arterial blood gas analyses are not comparable." http://onlinelibrary.wiley.com/doi/10.1111/resp.12225/full

 

[CFS_for_19_years]

Interesting data, @CFS_for_19_years .Would be interesting to learn his PO2. However his 24% were about the saturation, SPO2. @Valentijn did not give data about the partial pressure. No way SPO2 goes that low.

24% was the oxygen saturation, not the PO2.

PO2 was was 2.2kPA (normal 4.0 - 6.7). That converts to 16.5mmHg.

Got it. Never mind.

 

[Valentijn]

I did not release the tourniquet during the blood draw which could induce local ischemia which could explain the lower PO2/SPO2.

I looked into that, and someone did a study showing tourniquets don't impact blood gases.

 

[Emootje]

I looked into that, and someone did a study showing tourniquets don't impact blood gases.

I saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).
Better safe than sorry?

Btw, my lactate levels after mild walking exercise are normal now (from ± 2,5 to ± 1 mmol/l). Don't know why but I suspect it's the benfotiamine, a pyruvaat dehydrogenase co-factor. Ever experiment with that Valentijn?

 

[Valentijn]

I saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).
Better safe than sorry?

Do you have a link for that one? I'm getting too many results to go through them all

But www.degroot.co.il/admin/Links/uploads/file1_76.pdf shows no impact on venous blood gases with short term use of a tourniquet. The ones where I'm seeing an impact are either lasting 5+ minutes, or involving imaging instead of blood samples.

Don't know why but I suspect it's the benfotiamine, a pyruvaat dehydrogenase co-factor. Ever experiment with that Valentijn?

Haven't tried it, sounds interesting though.

 

[Emootje]

Do you have a link for that one?

Here 's the link

 

[Valentijn]

I saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).

Here 's the link

Ah, that one took 10 minutes to drop that low. At one minute it was up a bit, and still pretty close to the starting level at 2 minutes:

Tourniquets are on very briefly in blood draws, typically less than a minute, and nowhere close to 10 minutes. So they have little or no impact upon blood gases in a blood draw.

 

[Emootje]

Tourniquets are on very briefly in blood draws, typically less than a minute, and nowhere close to 10 minutes. So they have little or no impact upon blood gases in a blood draw.

So true

 

[Valentijn]

So true

Always good to get things figured out! Too much info to sort through.

 

[Lolinda]

Btw, my lactate levels after mild walking exercise are normal now (from ± 2,5 to ± 1 mmol/l). Don't know why but I suspect it's the benfotiamine, a pyruvaat dehydrogenase co-factor.

Hey, I just came back to this thread in order to post that elevated lactate is a symptom of thiamine deficiency (= beri beri). So, benfothiamine indeed may have resolved the issue in you, @Emootje . Attached I post the best beri beri document I found. search for "lactic acidosis". I went through almost all the document and red some more papers. So to save you guys some time, here are the essentials:

• Beri beri is notoriously variable in symptoms. While there is some grouping into symptom clusters (neurologic beri beri, cardiovascular, brain) forget about them. One can have or not have any individual issue such as elevated lactate, brain fog, memory issues, edema, blood flow probs, muscle weakness, heart issues, delayed stomach emptying, ... and even diminished pancreas enzymes.
• The only sure way to diagnose or exclude thiamine deficiency is a transketolase TPP test in red blood cells. Thiamine in blood can be fine while you have a deficiency.
• Even if one consumes enough thiamine, one can have a deficiency: the attached document contains a lot of informations that any diseases drain thiamine. Body stores are tiny. So then imagine what a chronic disease will do to your thiamine! I could say: 'the fact of being on PR already qualifies a person as a candidate for thiamine deficiency.' @Gondwanaland taught me an interesting thing: gut bugs can produce or consume vitamin b1. One more reason that dietary intake cannot prove or disprove thiamine deficiency.

 

[Emootje]

Thank you Lolinda Doctor Antonio Costantini did also some excellent papers on thiamine and ME/CFS alike diseases: Fibromyalgia, Multiple Sclerosis, Parkinson's disease.

@Valentijn according to Cheney, almost all ME/CFS patients have low PvO2 (<30) . Unlike you, I have also a failure to desaturate after prolonged breath hold (low Bohr effect).
"Venous blood gases but not arterial blood gases are almost universally abnormal with low PvO2 (<30) and usually high PvCO2 (>50)... Finally, pulse oximetry, while normal, shows a failure to desaturate after prolonged breath hold suggesting a functional left shift on the oxy-hemoglobin dissociation curve."
njcfsa.org/wp-content/uploads/2010/09/Anesthesia-Recommendations-Dr-P-Cheney2.pdf

 

[Lolinda]

pulse oximetry, while normal, shows a failure to desaturate after prolonged breath hold suggesting a functional left shift on the oxy-hemoglobin dissociation curve."

I have just that!
(and I did not even think of the possibility to meat someone else having the same!)

I tried to find out a cause. The following is a possible explanation I found, which may be then an alternative explanation to the Cheney idea above:
elevated carbon monoxide fools cheap SPO2 meters

But then, where does the CO come from? I am not inhaling all the day some bad car exhaust fumes. So it will be endogenous. I found:

a) CO is a vasodilator in the gut (you may want to read this summary instead)

b) short RBC survival
"Estimates of RBC survival can be obtained from the rate of endogenous production of carbon monoxide"

c) endogenous CO production can be used as a biomarker for oxidative and inflammatory processes.

Here I dont know any further: how to find out where my CO comes from?