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."@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%.@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.
http://www.oxfordmedicaleducation.com/abgs/venous-blood-gas-vbg-interpretation/Normal Blood Gases
Arterial PaO2 80 to 100 mm Hg.
Venous PaO2 28 - 48 mm Hg
Your pO2 is on the low side. Here are some possible reasons that should be confirmed with an arterial blood gas measurement: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).
Decreased PO2 levels are associated with:
- Decreased oxygen levels in the inhaled air
- Anemia
- Heart decompensation
- Chronic obstructive pulmonary disease
- Restrictive pulmonary disease
- Hypoventilation
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.pO2 for a venous sample should be 28-48, not 70-80%.
24% was the oxygen saturation, not the PO2.pO2 for a venous sample should be 28-48, not 70-80%.
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commented on these results?one of the best hospitals in the Netherlands - I'd be rather shocked if their equipment was outdated or faulty.
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.)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.
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.Home-tested lactate was 2.8 around 10pm, 5+ hours after exertion.
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 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?
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.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.
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.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.
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.What could be, however, interesting: while I never had pathologically elevated lactate, I could lower my post-exercise lactate levels by breathing exercises.
99%. At 97% my body seems to freak out and my heart rate rises until it's back to 99%.then, what is your normal spo2, w/o holding breath?
My gut doesn't like electrolyte mixes, unless I use them very rarely. Disappointing, since they did seem to help with OI a bit.have you tried increasing potassium? you seem to have room for improvement
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)]@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.
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.
I looked into that, and someone did a study showing tourniquets don't impact blood gases.I did not release the tourniquet during the blood draw which could induce local ischemia which could explain the lower PO2/SPO2.
I saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).I looked into that, and someone did a study showing tourniquets don't impact blood gases.
Do you have a link for that one? I'm getting too many results to go through them allI saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).
Better safe than sorry?
Haven't tried it, sounds interesting though.Don't know why but I suspect it's the benfotiamine, a pyruvaat dehydrogenase co-factor. Ever experiment with that Valentijn?
Here 's the linkDo you have a link for that one?
I saw a 'no impact 'study and one that went from 39,3 mmHg to 27,8 mmHg (pO2).
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:Here 's the link
So trueTourniquets 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.
Always good to get things figured out! Too much info to sort through.So true
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: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.
I have just that!pulse oximetry, while normal, shows a failure to desaturate after prolonged breath hold suggesting a functional left shift on the oxy-hemoglobin dissociation curve."