Free blood gases analysis [Netherlands]

[Emootje]

CO also causes a left shift on the oxy-hemoglobin dissociation curve and thus a failure to desaturate after prolonged breath holding :

Co-oximeters (with multiple wavelengths) aren't fooled by CO I think it would be a good first step to measure your CO by a lab or buy one yourself. I bought last year a cheap Gem-OPL co-oximeter on ebay but it wasn't a success like the Avovimeter 1000E (measures only oxygen saturation and Hb) I bought last year on ebay. Still looking for good co-oximeter like the OSM3, IL682, Masimo, Avoximeter 4000 or a better working Gem-OPL. Some day....

 

[Lolinda]

@Emootje your posts about alkalosis and the oxygen-hemoglobin bonding curve convinced me. I failed in the past when approaching a nice, knowledgeable, PhD pulmonologist with my ideas about endogenous CO production. I was not able to get out of him any tests, only got the advice that I should not hyperventillate before the breathholding test (which was useful). Would you give me some scientific fodder for a next doctor? My problem is that "Cheney thinks" does not convince doctors here...

@Valentijn according to Cheney

Ideal would be a research paper saying "failure to desaturate on breathholding = left-shift = alkalosis = less oxygen to tissues = symptoms x y z". ...or a paper for any single of these logical step. I guess such a paper could help also other people here to get tests...

I feel that the most important question is if a left-shift of the oxygen-hemoglobin binding curve in alkalosis has any important impact on real life, or it impacts only extreme conditions such as breathholding.

Where did you find the pic above about the oxygen-hemoglobin dissociation curve?

An unrelated comment to a previous post:

I had dinner around 7pm, but no exertion after the stair climbing

I would repeat the lactate measurement at a similar time after a simillar dinner, if you haven't done that yet. I mention it because doctors did that test for me. One can have elevated lactate from food (think mito diseases). I dont say anything such as that this would be your likely issue. I just say that it is worth to rule this out, or, if positive, this would give useful information about your issue. 5+h of elevated lactate after exertion is really really really long

 

[Butydoc]

Cheney uses a rebreather mask with the O2 so that CO2 rise:
"Oxygen through nasal prongs will not work. Oxygen alone in a mask will not work. It has to be a parietal rebreather mask, which has a bag attached. This allows you to rebreathe your expired carbon dioxide along with the oxygen that is flowing into the mask. Breathing increased levels of both CO2 and O2 at the same time is essential. The CO2 breaks the cycle. It corrects the alkalosis and frees the O2 in your blood to move into your cells. With proper functioning, vessels dilate and you start perfusing your brain and tissues, bringing out the toxins and brining in the nutrients"
http://www.prohealth.com/library/showarticle.cfm?libid=8812

For me, it's not entirely clear why he use oxygen when he thinks it's toxic...

Hi Emootje,

What isn't clear to me is why giving oxygen is essential. Most people with normal lungs have a O2 saturation of 99-100 percent. Giving oxygen at normal atmospheric pressure doesn't change the oxygen content of the blood significantly. Under greater pressure, like HBO, oxygen content can be increased. If the partial pressure of oxygen is increased under pressure, oxygen toxicity can occur. This can happen when people are breathing compressed air at great depths while scuba diving or receiving HBO for too long a period.

Best,
Gary

 

[Valentijn]

The charts I've seen with normal arterial oxygen and low venous oxygen indicate that oxygen therapy won't help. The two causes I've seen listed are anemic hypoxia and stagnant hypoxia. Stagnant hypoxia sounds like it's basically hypoperfusion, which might be caused by various things, including hypotension.

 

[Emootje]

Would you give me some scientific fodder for a next doctor?

Unfortunately, I don't know any 'failure to desaturate on breathholding' scientific papers

If you had a BGA in the past, an oxygen saturation gap > 5% is an indication for a left shift on the oxy-hemoglobin dissociation curve:

"The "oxygen saturation gap" is the difference between the calculated oxygen saturation from a standard blood gas machine and the reading from a pulse oximeter. If it is greater than 5%, the patient's hemoglobin may be abnormal, representing carbon monoxide poisoning, methemoglobinemia, or sulfhemoglobinemia"
Source

Where did you find the pic above about the oxygen-hemoglobin dissociation curve?

Found it here

 

[Emootje]

Found my Paul Cheney DVD
Here is the part about venous blood gases, oxygen-hemoglobin bonding curve and desaturate on breathholding:

 

[Lolinda]

thank you so much, @Emootje !!.
what do you think, does the textbook pic on the oxygen-hemoglobin binding curve refer to alkalosis in arterial or venous blood, or does this not matter?

If you had a BGA in the past

would you do an interpretation for my blood gas analyses? unfortunately, no doctor cared to explain me things. I learned from you more than all doctors together who did blood gas analysis on me. in particular I appreciate alkalosis / left shift of the oxygen hemoglobin binding curve. on the normal carb diet, I surprisingly often wanted to drink vinegar-water. it gave me clarity in my mind. if somebody wants a simple trick to get rid of brain fog for an hour, this was one of my favourites . could it be an intuitive attempt to correct alkalosis for a short time?
both test results are arterial blood gasses.

a while ago, on a normal diet:

last year, on keto diet:

What would you ask for, when I get a next blood gas test done?
I learned so far:
- if I have alkalosis and what causes it
- if I have a shift in the oxygen-hemoglobin binding curve
- test SPO2 both by blood gas machine and fingertip sensor ➞ oxygen saturation gap

I am unclear:
- is there any advantage to have both an arterial and venous blood gas test?
- is there any means to test tissue oxygen levels? (the very important X axis in the diagramm!!)

 

[Valentijn]

Here is the part about venous blood gases, oxygen-hemoglobin bonding curve and desaturate on breathholding:

That's interesting, because I didn't desaturate at first. Instead my entire body tensed. The 2nd time I tried, I realized I was tensing, and forced my muscles to relax after a few seconds, and then my O2 dropped to around 80%.

 

[Emootje]

would you do an interpretation for my blood gas analyses?

Of course I'm sorry to say but your blood gases are completely normal Also no sign of too much (endogenous) carbon monoxide (FCOHb < 1.5%) or other dyshemoglobinemia. No sign of left shift on the oxygen dissociation curve (calculated p50 almost perfect on 3.5 kPa spot). Electrolytes and lactate are normal. The only thing that's not perfect is that they switched the PaO2 and PaCO2 values on the last year results.

I surprisingly often wanted to drink vinegar-water... could it be an intuitive attempt to correct alkalosis for a short time?

Vinegar (acetate) is actually a bicarbonate precursors and quickly metabolize into this base. Lactate and citrate also behave this way in the body. Sulfur-containing amino acids are acid forming but the influence on blood pH is limited.

What would you ask for, when I get a next blood gas test done?

I do not expect much of additional blood gas tests, maybe I would ask for a venous blood gas test (more accurate for p50 calculations).

test SPO2 both by blood gas machine and fingertip sensor

The blood gas machine measures the saturation the same way as the finger pulse oximeter only without the skin and bones

is there any advantage to have both an arterial and venous blood gas test?

Yes... with the mixed venous blood from a pulmonary artery catheter you could calculate the consumption of oxygen. Don't know if blood gases from a normal venipuncture (peripheral venous blood) is meaningful to determine oxygen consumption .

(the very important X axis in the diagramm!!)

The X axis is the partial oxygen pressure in the blood. It goes from right (high oxygen pressure, after oxygenation in the lungs) to the tissue (20−50 mmHg capillary) to the venous side (left).

If you are bored:

 

[Lolinda]

can I give a 100 likes? I appreciate so much such detailed answers!! I wish doctors would explain things like you did... But I guess the majority of patients doesnt want to know / cannot understand... I want, a lot
So I see, there is really no indication for any left-shift of the oxygen-hemoglobin binding curve in me. I found it in this regard also interesting to learn about the P50, look it up, and indeed, looks like a useful marker for just that.
Then I was thinking: 'Ok, but I repeated my breathholding test a 20 times, in different health situations, time of the day, etc, and I haven't seen any desaturation in spite of torturing me to a 40 sec breathholding↯↯↯↯' And when re-reading my source for the breathholding test, I found an interesting line: " If SpO2 does not fall during this BH time, it is because SpCO in blood is rising more rapidly than O2 is falling as CO diffuses out of tissues into blood." Now, imo this makes sense. So if I combine all the parts, then my best guess is: my oxygen, breathing, CO, hemoglobin situation is completely fine. I may have a slightly elevated endogenous source of CO, which does not affect me normally, but gets released when breathholding. And actually, I am aware of one such source: my moderately diminished RBC survival, which causes more CO production (see a few posts above).
➞ consequence of all this is I guess as much as: I may not qualify as an apnea diver

Thank you once more, @Emootje

One more thing: I noticed the BE -3 (base excess strongly negative)
And I read:

• • metabolic acidosis if too low (less than −2 mEq/L)

Blood pH is determined by both a metabolic component, measured by base excess, and a respiratory component, measured by PaCO2 (partial pressure of carbon dioxide).​

So, this could then be why? I had an elevated anion gap, repeatedly, around the same time as the more recent blood gas. Here they say:

The serum anion gap is useful for determining whether a base deficit is caused by addition of acid or loss of bicarbonate.​

• • Base deficit with elevated anion gap indicates addition of acid (e.g., ketoacidosis).

While I do not have any ketoacidosis (tested), I am in ketosis, which inevitably adds some acids...

 

[Emootje]

can I give a 100 likes?

100X thanks

I repeated my breathholding test a 20 times, in different health situations, time of the day, etc, and I haven't seen any desaturation in spite of torturing me to a 40 sec breathholding

An alternative explanation could be that you have a shitty pulse oximeter, some do not track desaturation that well:

I have noticed that in my case there is a delay in desaturation after 40 sec of breath holding. No desaturation at 40 sec but when I'm breathing that delicious oxygen again my saturation drops about 3% (@30 sec after BH)

And when re-reading my source for the breathholding test, I found an interesting line: " If SpO2 does not fall during this BH time, it is because SpCO in blood is rising more rapidly than O2 is falling as CO diffuses out of tissues into blood

I think you need to hold your breath during the next CO test...

Also interesting but it's makes me really confused about the normal range of peripheral venous blood gasses:
"PaO2 is usually normal or low-normal in cases of CO poisoning but PvO2 is abnormally high, indicating substantial impairment of oxygen delivery from arterial blood plasma into tissue. Venous blood for the PvO2 analysis should be drawn at the elbow without a tourniquet. The optimum PvO2 level in healthy non-smoking adults is about 25mm Hg, while levels in CO poisoning (and CFS/FMS/MCS) patients are commonly in the range of 30 to 50"
Source

Btw, I have mildly elevated blood CO levels for a non-smoker: 2,2 %, 3.1 %, 2 % 2,7 % (0-1,5%) but no CO detected in my breath with a Fluke 220...

I noticed the BE -3 (base excess strongly negative)

My (old) reference says a BE of -3 is still normal... I think they have changed it...
But fair enough... maybe you can make your BE great again by using bicarbonate or bicarbonate precursors like acetate (vinegar) or citrate (lemons) and eat less sulfur-containing amino.
Ref.

Btw, more acid blood promotes vasodilatation.

 

[Lolinda]

Btw, more acid blood promotes vasodilatation.

hm... that could be me :
POTS, warm skin, super tolerance to heat, ...

But exactly which acidity is it that causes vasodilatation?

• blood PH?
• CO2?
• a negative BE?

An alternative explanation could be that you have shitty pulse oximeter, some do not track desaturation that well:

will retest. bought a shiny new Massimo, yeah
(Imagine, it measures while moving, even running. I am fascinated - whatever I do, no artifacts, no blank screen, etc.)

 

[Emootje]

But exactly which acidity is it that causes vasodilatation?

• blood PH?
• CO2?
• a negative BE?

Blood pH... don't know if there is vasodilation when the pH is normal and the CO2 high...
https://www.aana.com/newsandjournal/Documents/acidosis_0486_p148.pdf

bought a shiny new Massimo, yeah

Nice

 

[Lolinda]

Just for anyone attempting to test if they have an endogenous CO production issue (by measuring SpO2 on breathholding and checking for failure to desaturate):

An alternative explanation could be that you have a shitty pulse oximeter, some do not track desaturation that well

very right! thank you!! It turned out that my new Masimo MightySat fingertip SPO2 meter measured a big desaturation in me around 30 sec of breath holding, so everything is ok with me.
And that Chinese crap I used so far (details described at the end of this post) failed to do so and led me astray...

My (old) reference says a BE of -3 is still normal... I think they have changed it...
But fair enough... maybe you can make your BE great again by using bicarbonate or bicarbonate precursors like acetate (vinegar) or citrate (lemons) and eat less sulfur-containing amino.

I like vinegar!! always sprinkle it on all veggies. Thanks for the reference. I read there that these are the consequences of low BE:

These adaptive processes lower the urine pH and induce an
extensive change in urine composition, including hypocitraturia, hypercalciuria, and nitrogen and
phosphate wasting.​

indeed, my urinary PH is always constantly at 4.5. I guess that is around the lower end of normal. And I really do not need to loose Ca in the urine, because I anywise cannot eat enough, I barely meet 50% RDV on my ketogenic diet.
So thanks for the hint, I will keep happily eating vinegar or doing whatever else to not overtask my kidneys... I want them happy at 99y too

Hey, this inspires an idea: I always used urinary PH testing to measure postprandial gastric acid non-invasively. The testing scheme relies on the "urinary alkaline tide": when gastric acid is produced, the stomach secretes bicarbonate into the blood. Then, to keep blood PH constant, more base is peed out in urine, that is, urinary PH goes up. This is validated in several research studies and can be used to indirectly measure gastric acid. But it could be false on a ketogenic diet: if the body has anywise issues excreting a load of acid, then there might be a backlog. I dont know if a backlog is possible, but some acids could accumulate in tissues...? Thus when the precious base excess arises simultaneously to stomach acid production, it would not be peed out but could neutralise the acid backlog... This could explain why I never saw a normal alkaline tide in me...

 

[Lolinda]

update:

when doing the breathholding (30 sec, preceded by expiration), I noticed a surprising thing: my neuropathic pain & numbness in my left leg got less! what the heck?? I just realised, it is still less. Repeated the breathhold now once more to observe exactly: I feel sthg good happening in the leg. I could describe it like "a little warm happiness flowing through my leg". Normally, I dont have any pain nor numbness in legs, but yesterday sthg went wrong (long story involving thiamine, canned fish, MCAS and neuropathy....). To describe the issue exactly, it feels like when a leg sleeps away from too much sitting. Now, this is a bit influenced to the better by breathholding... huh??

Then, if I stand up and walk up stairs, this good feelinng increases. If I forcefully contract the leg a bum muscles it feels really good. and it is almost as if the neuropathy never had happened...

Other topic:
Thiamine testing and supplementation:
Previously on this thread, thiamine was discussed and its relationship to lactate / breathing. If anyone interested in
- different thiamine tests
- risks of supplementation
I posted all the details on this thiamine thread.

 

[Gondwanaland]

when doing the breathholding (30 sec, preceded by expiration), I noticed a surprising thing: my neuropathic pain & numbness in my left leg got less! what the heck??

Sounds like some severe vasoconstriction - caused by high lysine/not enough arginine intake?

 

[Lolinda]

Sounds like some severe vasoconstriction - caused by high lysine/not enough arginine intake?

Hey @Gondwanaland thank you so much!!! your post changed my life to the better. Instead of arginine, I had a box of citrulline at home. This is largely the same in the urea cycle as arginine and converts into NO (nitric oxide) thus improves blood flow.
Effect 1:
within 1-2h, this painful feeling that my leg sleeps away diminished to a level that I could sleep. Happy as a bird!! And very interesting, as I did not seem to have hypoperfusion: no cold limb.
Effect 2:
Less time in bed because of my POTS!! It has a nice effect on digestion speeding it up a lot.
Side effect:
I needed to go far over the recommended dosage, because the badly needed Effect 1 lasts only a few hours. After taking citrulline for two days, I got aggressive thoughts, pumped up mucles and a high desire to drink water with vinegar. These all fit high ammonia. Vinegar neutralises ammonia. Since then, I am drinking cups and cups of water with vinegar all the day.

Interpretation?
All this painful leg sleeps away problem came upon me after I happily supplemented increasing mini-doses of B1 and then ate 1 can of mackerel. Looking back, my previous two sudden worsenings of neuropathy also came after exactly this combo. Mast cells are triggered by thiamine and by not fresh fish.....
Maybe the leg sleeping away is not the real problem, but a useful feeling my body produces to trigger me to do things improving blood flow, to help neurons survive? After suffering the damage,, I immediately started massaging the leg, do sports, put hot water bottles and warm cloth on it ... then accidentally found that trick with the breathholding (which increases CO2, which is a strong vasodilator). The citrulline / NO could increase blood flow beyond normal? or improve microcirculation? The need for the bigger blood flow could be to enable repair of neurons?

I already had an unopened box of citrulline at home, bought a year ago for some unconcrete plans to experiment with tweaking NO production . It was clear to me that I have a problem: A previous experiment using a tiny 2mm morsel of Corvatone (Molsidominum, a NO donor) led to such an overwhelming effect that I prayed to all gods that it stops...

I still wonder how all this works, but it is wonderful! Thanks @Gondwanaland !!It seems like this time I escaped permanent neuronal damage. This was the best treatment suggestion I received in a long time!! Happy!!!

My lysine and arginine intakes during the days before the catastrophy happened:
09.06.2017 Arg: 2g, Lys 2.8g
08.06.2017 Arg: 2.8g, Lys: 3.5g
07.06.2017 Arg: 2.3g, Lys: 3g
06.06.2017 Arg: 2.5g, Lys: 3.2g
These correspond to my typical intakes.

 

[Gondwanaland]

your post changed my life to the better

I need someone like me in my life with such helpful suggestions too

 

[Emootje]

I have noticed that my blood pH is completely normal in the fasted state:

Possible explanation:
Fasting produces ketone bodies which lowers blood pH
Fating lowers sympathetic nervous system which lowers ventilation > more CO2 > Lower pH [1]
Less stomach acid is produced in the fasted state > less alkaline tide (Lolinda, thank you for introducing me with that phenomenon).

 

[ryan31337]

I have noticed that my blood pH is completely normal in the fasted state:

Possible explanation:
Fasting produces ketone bodies which lowers blood pH
Fating lowers sympathetic nervous system which lowers ventilation > more CO2 > Lower pH [1]
Less stomach acid is produced in the fasted state > less alkaline tide (Lolinda, thank you for introducing me with that phenomenon).

Unfortunately I haven't had a repeat ABG, but in repeat CPETs my low PETCO2 normalised after adopting ketogenic diet, so its interesting that you raise those points.

Good to see some plausible contributing factors rather than the usual naive explanation of "your breathing is dysregulated". I am quite aware of hyperventilating on orthostasis and during POTS flares (sympathetic overdrive), but I certainly wasn't hyperventilating during my CPETs - yet it was trotted out as the explanation when its clear something metabolic was going on in my view.