Pulse Ox Vs PaO2

[roja]

So, after a multitude of discussions/arguements observed and participated in, today the same old damn arguement surfaced. And despite multiple google searches, I find nothing to awnser the question.


It seems apparant that at 100% pulse ox (in a patient with no tox stuff) the likelihood of having a very low Pao2 is exceptionally low.

At a pulse ox <95% then there is less correlation between the two.


However, I can find nothing to support either of the statements that there is a good or bad correlation.

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[docB]

One common situation is that you can have a high pulse Ox with a low PaO2 in anemia because the hemoglobin if fully saturated, there is just too little of it. Didn't we have a thread on this some time back? I'm goin' searchin'.

 

[docB]

OK, couldn't find it. Oh well.

 

[roja]

I am talking about more like your basic SOB breath patient or one with pneumonia. Essentially, using the PaO2 to decide on steroid use and thus using a an ABG to guide treatment.

Anemia, cold extremeties excluded. I was hoping someone might know of a reference of comparisons of Pa02 with Pulse ox. I found a european study but when I showed it to said attending, attending was like: we don't use those units. (kPa) *duh*

thanks the principle is still the same.

 

[beanbean]

Back in my previous life as a biomed engineer at a hospital we were always told that the accuracy of the pulse ox decreased as the SaO2 became lower. Like you mentioned, putting aside anemia, poor extremity circulation, meth- and carboxy- hemoglobin issues, etc; paO2 and SaO2 should correlate well. You may find some info from ECRI (Emergency Care Research Institute- they are a nonprofit group that is like the "consumer reports" of biomed devices. They test and evaluate all types of equipment and compare different models. They also track safety warnings and recalls. They publish the journal "Health Devices"; a fairly obscure journal not usually found outside the Clinical Engineering Department. Give them a call and ask to speak to the engineer for pulse ox - they would be a great resource.

 

[2ndyear]

I am talking about more like your basic SOB breath patient or one with pneumonia. Essentially, using the PaO2 to decide on steroid use and thus using a an ABG to guide treatment.

Anemia, cold extremeties excluded. I was hoping someone might know of a reference of comparisons of Pa02 with Pulse ox. I found a european study but when I showed it to said attending, attending was like: we don't use those units. (kPa) *duh*

thanks the principle is still the same.

I'd take a look in Miller's Anesthesiology. Dr. Tremper at UMich did a lot of SpO2 work and it's summarized there. Should be in the hospital library. Anecdotally, I have heard +/- 4% correlation, but I don't know how it functions on the extremes. Remember though that if you're talking COPD, PCO2 is really the variable that you're looking at on the ABG anyways to guide ventilation. But your question on oxygenation is good and I hope that you share the answer with all of us!

 

[ERMudPhud]

Roja,

Go here: http://www.nellcor.com/educ/List.aspx?S1=MON

and download the monograph on oximetry. It will give you everything that you need to know. Hint: docB isn't quite right. Anemia doesn't throw off the correlation but a patient with a Hgb of 6 and a sat of 100% has a crappy oxygen delivery despite good sats, good PaO2, and good circulation.

Other things like acidosis and extremes of body temp do throw off the correlation.

 

[roja]

Roja,

Go here: http://www.nellcor.com/educ/List.aspx?S1=MON

and download the monograph on oximetry. It will give you everything that you need to know. Hint: docB isn't quite right. Anemia doesn't throw off the correlation but a patient with a Hgb of 6 and a sat of 100% has a crappy oxygen delivery despite good sats, good PaO2, and good circulation.

Other things like acidosis and extremes of body temp do throw off the correlation.

Thanks so much. I am printing it out right now. Its a great review and I am going to carry it around so the next time someone asks me to draw an abg on someone who is 99% on room air to prove hypoxia I can whip it out.

 

[tBw]

Roja,

Go here: http://www.nellcor.com/educ/List.aspx?S1=MON

and download the monograph on oximetry. It will give you everything that you need to know. Hint: docB isn't quite right. Anemia doesn't throw off the correlation but a patient with a Hgb of 6 and a sat of 100% has a crappy oxygen delivery despite good sats, good PaO2, and good circulation.

Other things like acidosis and extremes of body temp do throw off the correlation.

ok, I was confused by this comment as I agreed with DocB - if anemic there is not a straight correlation between SaO2 (as reported by pulsox) and PaO2 - I'm not following the statement that the patient, in this particular example, would still have good PaO2 but poor oxygen delivery....

My impression was that:
in the example you gave of an anemic patient Hgb , a sat of 100% and good circulation
(a) the PaO2 would be poor
(b) the ODC (Oxygen Dissociation Curve) would probably right shift due to acidosis and thus
(c) the oxygen delivery would actually improve (easier unloading of Oxygen at the tissues) but that
(d) they could still have a deficit in total delivery

FWIW I looked over the monograph hoping it would shed light on my ignorance before posting this but reading it didn't change the above impression...??

 

[tBw]

hum, I turned to UpToDate for answers and there is an article there on it. I'm not sure if I am meant to reproduce it here but....


While pulse oximetry is a convenient way of measuring arterial oxygenation, it does not assess ventilation. Therefore, its use should be supplemented with arterial blood gas analysis when alveolar hypoventilation is suspected clinically [21]. The use of supplemental oxygen may prevent hypoxemia despite severe alveolar hypoventilation [26,27]. As an example, one inadvertently hypoventilated patient who was administered 100 percent oxygen during hip arthroplasty and monitored with pulse oximetry alone developed a PaCO2 of 265 mmHg and an arterial pH of 6.65, despite maintenance of oxygen saturations of 94 to 96 percent [26].

In addition, because it does not measure PaO2, overreliance on pulse oximetry can delay detection of clinically significant hypoxemia. A large decrease in PO2 will not produce a significant fall in SaO2 until the steeper portion of the oxygen hemoglobin dissociation curve is encountered at a PO2 of approximately 60 to 70 mmHg. This is particularly important in patients receiving supplemental oxygen. As an example, a fall in PaO2 in such a patient from 140 to 65 mmHg would be required before a significant decrease in oxygen saturation is detected. Furthermore, pulse oximetry results are signal-averaged over several seconds. Therefore, the pulse oximeter may not detect a hypoxemic event until well after it has occurred [8]. This delay may be of particular significance when the device is being used for monitoring during intubation.

Source: Mechem, C Crawford, Pulse Oximetry. In: UpToDate, Rose, BD (Ed), UpToDate, Wellesley, MA, 2005.

 

[typeB-md]

ok, I was confused by this comment as I agreed with DocB - if anemic there is not a straight correlation between SaO2 (as reported by pulsox) and PaO2 - I'm not following the statement that the patient, in this particular example, would still have good PaO2 but poor oxygen delivery....

My impression was that:
in the example you gave of an anemic patient Hgb , a sat of 100% and good circulation
(a) the PaO2 would be poor
(b) the ODC (Oxygen Dissociation Curve) would probably right shift due to acidosis and thus
(c) the oxygen delivery would actually improve (easier unloading of Oxygen at the tissues) but that
(d) they could still have a deficit in total delivery

FWIW I looked over the monograph hoping it would shed light on my ignorance before posting this but reading it didn't change the above impression...??

i don't know if this is what you were trying to figure out or not, but here gores:

regarding good PaO2 in the anemic patient, there is not a left or right shift in the OCD. Rather, the shift is better seen as a downward shift on a Oxygen Concentraion vs. PaO2 graph. Regardless of your total blood concentration, if you have normal Hb, the OCD graph should still be the same. What happens in the anemic situation is that at 100% SaO2, there is less TOTAL oxygen in the blood (but the Hb that is around still reacts normall... i.e. arterial is 100 mm Hg and venous is 40 mm Hg)

Here is the graphical representation of what i'm trying to say.

keep in mind that saturation values aren't shown. but if they were, they would be respective each Hb = x. In otherwords, at the upper limit, each Hb scenario is 100% saturated.

 

[tBw]

i don't know if this is what you were trying to figure out or not, but here gores:

regarding good PaO2 in the anemic patient, there is not a left or right shift in the OCD. Rather, the shift is better seen as a downward shift on a Oxygen Concentraion vs. PaO2 graph. Regardless of your total blood concentration, if you have normal Hb, the OCD graph should still be the same. What happens in the anemic situation is that at 100% SaO2, there is less TOTAL oxygen in the blood (but the Hb that is around still reacts normall... i.e. arterial is 100 mm Hg and venous is 40 mm Hg)

Here is the graphical representation of what i'm trying to say.

keep in mind that saturation values aren't shown. but if they were, they would be respective each Hb = x. In otherwords, at the upper limit, each Hb scenario is 100% saturated.

OCD? Obsessive Compulsive Disorder?? What are you saying about me?

Thanks, but no, I understand your statements above that reducing Hemoglobin will reduce oxygen content - that was the point - that the PaO2 would be reduced, even though SaO2 may still be 100%.

Mea Culpa if my original statements weren't clear

 

[southerndoc]

Roja,

Go here: http://www.nellcor.com/educ/List.aspx?S1=MON

and download the monograph on oximetry. It will give you everything that you need to know. Hint: docB isn't quite right. Anemia doesn't throw off the correlation but a patient with a Hgb of 6 and a sat of 100% has a crappy oxygen delivery despite good sats, good PaO2, and good circulation.

Other things like acidosis and extremes of body temp do throw off the correlation.

Nice link, thanks!

 

[ERMudPhud]

Be careful here. PaO2 is not a measure of total blood oxygen content. It is really a measure of the partial pressure of dissolved oxygen in the plasma. You could take the patients ABG, spin out all the red cells, assuming you have not in the process altered the serum pH or allowed the sample to equilabrate with room air, you could then measure the PaO2 in what is now a sample with a hgb of essentially 0 and still get the same Pa02. Pa02 is a measure of O2 concentration (partial pressure) in the aqueous phase of the blood sample not a measure of total blood O2 content. Total blood O2 content is indeed dependent on Hgb concentration and Hgb saturation but that is not what Pa02 measures. Assuming equal acid base status, equal pC02 and equal 2,3DPG the anemic and non-anemic patient will have equal ODC's and thus equally good Sa02 and PaO2 readings but drastically different blood O2 contents. That is why in septic patients and other shock states we transfuse for low crits even if the Sa02 and Pa02 are good because we want to improve oxygen delivery. If you don't believe me go to your lab and ask for printouts of the last few hundred ABG's they've run. Look for two samples with similar pC02, pH, and Sa02 but drastically different Hgb. You will find that the Pa02 in your two samples will be quite similar.

The up-to-date points are very good about the absolute need for an ABG to evaluate hypoventilation (unless you have capnography),AA gradient(especially in patients on supplemental O2), or acidosis. I think the value for hypoxemia in a patient with a sat of 100% on ROOM AIR is significantly less. Of course I live at 5000ft in the steep part of the curve anyway.

 

[tBw]

Well, I'm sure you're right with all of the following, but maybe you could indulge/educate me as there seems to be a significant error in my understanding of all this. My continued confusion relates to the following...

Be careful here. PaO2 is not a measure of total blood oxygen content. It is really a measure of the partial pressure of dissolved oxygen in the plasma. .

Absolutely agreed.

You could take the patients ABG, spin out all the red cells, assuming you have not in the process altered the serum pH or allowed the sample to equilabrate with room air, you could then measure the PaO2 in what is now a sample with a hgb of essentially 0 and still get the same Pa02. Pa02 is a measure of O2 concentration (partial pressure) in the aqueous phase of the blood sample not a measure of total blood O2 content. Total blood O2 content is indeed dependent on Hgb concentration and Hgb saturation but that is not what Pa02 measures.

again, absolutely agreed. PaO2 is measured by some form of polarographic oxygen electrode, which reflects dissolved O2 and could be identical in a spun out plasma sample.

Assuming equal acid base status, equal pC02 and equal 2,3DPG the anemic and non-anemic patient will have equal ODC's and thus equally good Sa02 and PaO2 readings but drastically different blood O2 contents.

Ok, this is where I fall down. I view these conclusions as correct if the assumptions are correct - but don't entirely agree that the assumptions are valid in real life ie outside of a spun down test tube. Although I agree with your spun-down plasma analogy I thought the whole point of measuring PaO2 was that we were making the assumption that, barring CO binding to hemoglobin, etc (which is a different situation altogether) we took PaO2 to be a guide, if an inaccurate one, of total oxygen content. Dissolved O2 is a very small fraction of total O2 and so the only reason (I thought) we cared about it was as an indicator if how much we might expect to be attached to hemoglobin. So, that being said, I realize it doesn't actually measure total oxygen, but if I'm wrong and we're not actually using it as even a rough indicator of that, why measure it at all?

Of course, if we do measure PaO2 as a rough indicator, as I had thought, then I am back to my original statement of the relationship of PaO2 to SaO2....hum, maybe type-B-md was right with that whole obsessive-compulsive disorder diagnosis after all...

 

[roja]

ERMudPhud-

thanks alot for the link. I am going to read the uptodate link next.

Its my understanding that the Pa02 measures the 1-2% of O2 in the blood that is dissolved. The Sa02 measures the 98% of Oxygen that is bound to hemoglobin. The Pulse ox machine measures the the oxyhemoglobin and deoxyhemoglobin and magically makes up a measurement of saturation.

The anemia makes perfect sense. I thought the picture was great.

If you have 4 Hg molecules at 100% saturation in and a person with 8 Hg molecules 100% saturated, they both have 100% sats but the one iwth 4 has significantly less oxygenation carrying capacity.


And looking at the ODC, a patient on room air, with a 98% will have good PaO2. (excluding hypothermia, toxicology, etc) and basically that there was NO need for me to do an ABG on this patient.

I'm going to check out the marino ICU book as well. I still find the whole Pa02 thing a little confusing, in terms of *really* understanding it. (I know what to look for and what to do)

 

[typeB-md]

Ok, this is where I fall down. I view these conclusions as correct if the assumptions are correct - but don't entirely agree that the assumptions are valid in real life ie outside of a spun down test tube. Although I agree with your spun-down plasma analogy I thought the whole point of measuring PaO2 was that we were making the assumption that, barring CO binding to hemoglobin, etc (which is a different situation altogether) we took PaO2 to be a guide, if an inaccurate one, of total oxygen content. Dissolved O2 is a very small fraction of total O2 and so the only reason (I thought) we cared about it was as an indicator if how much we might expect to be attached to hemoglobin. So, that being said, I realize it doesn't actually measure total oxygen, but if I'm wrong and we're not actually using it as even a rough indicator of that, why measure it at all?

Of course, if we do measure PaO2 as a rough indicator, as I had thought, then I am back to my original statement of the relationship of PaO2 to SaO2....hum, maybe type-B-md was right with that whole obsessive-compulsive disorder diagnosis after all...

my bad on the ocd

i didn't think the reason we got PaO2 was to calculate the total content. I thought the reason for PaO2 was to measure the effectiveness of O2 exchange between the alveolus and the arterial blood.

 

[ERMudPhud]

Ok, this is where I fall down. I view these conclusions as correct if the assumptions are correct - but don't entirely agree that the assumptions are valid in real life ie outside of a spun down test tube. Although I agree with your spun-down plasma analogy I thought the whole point of measuring PaO2 was that we were making the assumption that, barring CO binding to hemoglobin, etc (which is a different situation altogether) we took PaO2 to be a guide, if an inaccurate one, of total oxygen content. Dissolved O2 is a very small fraction of total O2 and so the only reason (I thought) we cared about it was as an indicator if how much we might expect to be attached to hemoglobin. So, that being said, I realize it doesn't actually measure total oxygen, but if I'm wrong and we're not actually using it as even a rough indicator of that, why measure it at all?

Of course, if we do measure PaO2 as a rough indicator, as I had thought, then I am back to my original statement of the relationship of PaO2 to SaO2....hum, maybe type-B-md was right with that whole obsessive-compulsive disorder diagnosis after all...

Pa02 is best used to calculate the Aa gradiet i.e. lots of oxygen into the aveoli but very little out into the blood equals problem with diffusion or more likely shunting of some sort.

Hgb times a measured(not calculated or estimated) Sa02 tells you exactly how much oxygen is being carried in the blood. Since Sp02 and Pa02 are directly, albeit nonlinearly, correlated with each other and Sa02 either can be used as a rough estimate of total blood oxygen content assuming no weird tox stuff etc and no severe anemia.

Your mistake is here

My impression was that:
in the example you gave of an anemic patient Hgb , a sat of 100% and good circulation
(a) the PaO2 would be poor
....

If your anemic patient has a good Sp02 and there is no weird tox stuff, acidosis, elevated 2,3DPG, etc. they will have a good PaO2 on their ABG but they will have a crappy total blood 02 content. The correct way to put it is that in severe anemia the ABG Pa02 and Sp02 still correlate well but normal values for either should not reassure you that you have good 02 delivery to tissues

Read the pages 19-25 of the 2nd edition of Marino's ICU book for a more intelligible explanation plus equations

 

[ERMudPhud]

And looking at the ODC, a patient on room air, with a 98% will have good PaO2. (excluding hypothermia, toxicology, etc) and basically that there was NO need for me to do an ABG on this patient.

Exactly!


Use ABG's if you're worried about hypoventillation (C02 retention) or acid base disturbances (you can't always rely on the bicarb on your chem panel to clue you in on the acid/base problem). Don't use it to measure hypoxemia in a patient with a normal sat on room air

Just curious, was this an EM, IM, crit care, or surgical attending

 

[ERMudPhud]

i didn't think the reason we got PaO2 was to calculate the total content. I thought the reason for PaO2 was to measure the effectiveness of O2 exchange between the alveolus and the arterial blood.

Exactly!

 

[tBw]

Your mistake is here



If your anemic patient has a good Sp02 and there is no weird tox stuff, acidosis, elevated 2,3DPG, etc. they will have a good PaO2 on their ABG but they will have a crappy total blood 02 content. The correct way to put it is that in severe anemia the ABG Pa02 and Sp02 still correlate well but normal values for either should not reassure you that you have good 02 delivery to tissues

Read the pages 19-25 of the 2nd edition of Marino's ICU book for a more intelligible explanation plus equations

aaaaahhhhh....the penny drops, thanks for the explanation!

 

[tBw]

my bad on the ocd

i didn't think the reason we got PaO2 was to calculate the total content. I thought the reason for PaO2 was to measure the effectiveness of O2 exchange between the alveolus and the arterial blood.

ahem!! And to think my pulm instructor told me "if there is one thing you should always remember it's that in pulmonary medicine the answer to any question is always 'ventilation-perfusion inequality'" (this is the part where I need the blushing smilie) ....well, sure, there is that whole thing of gas exchange....

my bad.

 

[GasPundit]

I haven't seen anyone bring up the following points:


1. Pulse-oximetry will fail in the presence of carbon monoxide. Why? It will see something bound to the hemoglobin, even something with a similiar absorption spectrum, but it's not oxygen.

2. In an anemic patient, the PaO2 can become quite significant. Remember, the oxygen delivery equation only gives you 0.003 as a multiplier for the PaO2, but if the Hct is low then a patient is receiving a significant portion of the oxygen delivery from the dissolved oxygen it is important NOT to ignore this.

3. Blood is supposed to be red; dyes such as indocyanine green or methylene blue will significantly change your reading, usually for the lower.

4. the oxygen-extraction ratio: How can a kid with a low Hct or low CO maintain adequate tissue perfusion? Take out more oxygen! It's amazing how some people can have SvO2 in the 30-40% range.

5. The "new thing" is obtaining SvO2 at the PA. It's possible for the light to bounce off of the walls of the vessel, reflecting back to the receiver before contacting any blood vessels, thus showing a SvO2 of 90%+. While your patient could be a good pumper, it's more likely this is due to reflectivity!

6. Motion artifact is a bugger. Try walking through a NICU someday, and you'll see plenty of wiggly kids with boxy signals on their pulse oximeters. The new Massimo machines are supposed to minimize this, with other companies coming up to speed soon too.

7. Last but not least: hemoglobinopathies!

 

[12R34Y]

Exactly!


Use ABG's if you're worried about hypoventillation (C02 retention) or acid base disturbances (you can't always rely on the bicarb on your chem panel to clue you in on the acid/base problem). Don't use it to measure hypoxemia in a patient with a normal sat on room air

Just curious, was this an EM, IM, crit care, or surgical attending

ERMudPHud,

just a question.........when I was on my PICU rotation we mostly used capillary/venous blood gases for CO2. I can't remember the exact answer that my attending gave me as to why, but something about venous and arterial CO2 should be pretty similar. So if one of the main reasons to obtain a blood gas is for hypoventilation why don't we just get venous blood gases instead as an indicator for CO2 retention.

Another question. Why can't you use "roughly" the serum bicarb as an indicator of acid/base status. I know on my inpatient medicine month we made mention of serum C02 in relation to acid/base now and then. Is this not reliable and why?

thanks a ton for enlightening the blood gas challenged.

later

 

[KGUNNER1]

Good points GasPundit but a few slight modifications

2. In an anemic patient, the PaO2 can become quite significant. Remember, the oxygen delivery equation only gives you 0.003 as a multiplier for the PaO2, but if the Hct is low then a patient is receiving a significant portion of the oxygen delivery from the dissolved oxygen it is important NOT to ignore this.

Oxygen content of blood (CaO2) = Hgb x 1.36 x SaO2 x (PaO2 x 0.003) where 1.36 is the volume of oxygen that can be bound by 1 gm of Hgb and 0.003 is the solubility coefficient of oxygen. You are correct in identifying the variables that directly affect the CaO2, but anemia doesn't affect the partial pressure of O2. The atmospheric pressure and FiO2 will. So the only way the pO2 will significantly contribute to oxygen delivery (CaO2 x C.O.) is when you achieve hyperbaric levels either in a hyperbaric chamber (to a much lesser extent breathing 100% O2 AND having healthy lungs).

4. the oxygen-extraction ratio: How can a kid with a low Hct or low CO maintain adequate tissue perfusion? Take out more oxygen! It's amazing how some people can have SvO2 in the 30-40% range.

Well, yes, kind of. The verbiage "oxygen extraction" makes it sound like this is an "active" process, where the cells are actively grabbing more O2 off the hgb like hungry lions picking off unsuspecting passengers on a train in Africa. In fact, O2 just diffuses down a concentration gradient. There is no active process involving wastage of ATP etc... Simplistically two things happen, DO2 increases (by increasing C.O. - assuming normal lungs and SaO2 remains high) and down-regulation of intracellular processes - sort of hibernation. Kids are remarkable in that they really can increase C.O. to amazing levels. Chronic heart failure patients slowly down regulate. When you cath these patients and check mixed venous sats, they are actually in the 50's and 60's. Very few people are walking around with SVO2 in the 30% range. But your point on compensation is well taken.

5. The "new thing" is obtaining SvO2 at the PA. It's possible for the light to bounce off of the walls of the vessel, reflecting back to the receiver before contacting any blood vessels, thus showing a SvO2 of 90%+. While your patient could be a good pumper, it's more likely this is due to reflectivity!

This isn't new. We've been measuring mixed venous gasses since Swan and Ganz popularized that silly catheter. If you want to be a purist, the only way you can measure a true SvO2 is from the pulmonary artery. A ScvO2 is obtained from either the SVC/RA junction or RA (distal port of a central line). I think what you're referring to is the Edwards continuous ScvO2 cath (Presep) http://www.edwards.com/MedicalProfe...x?ItemId=980B9C03-5CD7-472E-9EC9-E01B4D19F824 or the same thing in a PA cath. All this is is a fiberoptic bundle, much like the pulse ox, that now has been incorporated into the catheter. You can easily tell if your signal is poor by looking at the monitor and checking the SQI meter. There is a gauge of 4 boxes stacked on top of each other. If all 4 are lit up, you have a ton of artifact. You want to see only 1 or 2 boxes lit up.

Excellent topic all, this is really fun stuff. Some good articles to read
http://content.nejm.org/cgi/content/abstract/345/19/1368
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11436529&dopt=Abstract

 

[ERMudPhud]

ERMudPHud,

just a question.........when I was on my PICU rotation we mostly used capillary/venous blood gases for CO2. I can't remember the exact answer that my attending gave me as to why, but something about venous and arterial CO2 should be pretty similar. So if one of the main reasons to obtain a blood gas is for hypoventilation why don't we just get venous blood gases instead as an indicator for CO2 retention.

Another question. Why can't you use "roughly" the serum bicarb as an indicator of acid/base status. I know on my inpatient medicine month we made mention of serum C02 in relation to acid/base now and then. Is this not reliable and why?

thanks a ton for enlightening the blood gas challenged.

later

First, I'm glad that our intensivist has found this thread before I had a chance to go much more beyond the limits of my knowledge and make a fool of myself. I should probably leave your questions for KGUNNER but I'll take a shot at it.

The peds guys seem way ahead of the adult intensivists in their use of venous gases. I think this is partly because arterial sticks are harder in little kids and I would guess riskier as well. I don't know in adults how well venous CO2 reflects arterial CO2. KGUNNER?

Serum bicarb as an indicator of acid/base status is a problem because it doesn't tell you much about the primary process. Is your low serum bicarb a primary acidosis you need to work up or is it a compensation for respiratory alkalosis? Without the pH you can't actually say that they are acidemic because for all you know they might actually be alkalemic.

 

[KGUNNER1]

First, I'm glad that our intensivist has found this thread before I had a chance to go much more beyond the limits of my knowledge and make a fool of myself. I should probably leave your questions for KGUNNER but I'll take a shot at it.

The peds guys seem way ahead of the adult intensivists in their use of venous gases. I think this is partly because arterial sticks are harder in little kids and I would guess riskier as well. I don't know in adults how well venous CO2 reflects arterial CO2. KGUNNER?

Serum bicarb as an indicator of acid/base status is a problem because it doesn't tell you much about the primary process. Is your low serum bicarb a primary acidosis you need to work up or is it a compensation for respiratory alkalosis? Without the pH you can't actually say that they are acidemic because for all you know they might actually be alkalemic.

Too much to go into in one post. Suffice it to say, one way to approach acid-base problems is the physical-chemical approach (or Stewart approach). This approach accounts for all the charges at a physiologic pH from strong ions, weak acids, and proteins. Basically there are only 3 independent variables, pCO2, Strong Ion Difference (SID), and Atot (total amount of weak acids such as albumin and phosphates). Bicarb is dependent on these three. I can make it go up or down by altering either one of the SID, Atot, or pCO2.

Please check out these websites for a more complete explanation and some examples. You can also do a lit search on the keyword SID.

http://www.ccm.upmc.edu/education/resources/phorum.html
http://www.acidbase.org/
http://www.anaesthetist.com/icu/elec/ionz/Stewart.htm

Good luck.
kg

 

[KGUNNER1]

The peds guys seem way ahead of the adult intensivists in their use of venous gases. I think this is partly because arterial sticks are harder in little kids and I would guess riskier as well. I don't know in adults how well venous CO2 reflects arterial CO2. KGUNNER?

The pH is useful, not much difference. Same with venous Lactate. Not much clinically signifcant difference. pCO2 (A-VpCO2 difference) is different and is directly related to cardiac output (C.O.) Rember CO2 is generated by the cells. If your DO2 is decreased, you'll have an increased Venous (measured at the pulmonary artery) pCO2. Usually there is about a 5-7 mmHg difference between A-V. A-V pCO2 differences >10 usually represent decreased C.O.

Caviet.....dead cells (and people) don't produce CO2, so if your running a code, and you see your ETCO2 (end tidal -from the ET tube - different than venous) is below 15 for more than 10 min, your chance of recovery is dismal. Jay Falk, another EM/CCM beast out of Orlando, has done some great work on this.

kg