Sa02 versus Pa02 question

[cfdavid]

So, my new mantra 2 months out from residency is "ask now, or forever hold your peace"....

The question is based upon The ICU Book (by Marino), which seems to deemphasize Pa02 values from ABGs in favor of Sa02 from a pulse ox.

Now problem thus far given:

D02=CO x Hb x 13.4 (or 13.6 depending on what you read) x Sa02 + 0.003xPa02

Thus, the actual contribution (as we all know) of dissolved O2 is super weak to the extent that you can almost exclude it from the equation.

*****The question is can you ever have a scenario where you have adequate Sa02 (say >90%) with a very low Pa02???? (<50)

If so, can anyone elaborate on the mechanism?

I realize that ABGs for vent management rely mostly on PaC02 and pH versus the Pa02, but often it seems that too much emphasis IS placed on Pa02.....

cf

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[lord_jeebus]

The question is can you ever have a scenario where you have adequate Sa02 (say >90%) with a very low Pa02???? (<50)

If you're a fetus

 

[cfdavid]

ah, yes. ofcourse.

thanks.

 

[joshmir]

are you guys suggesting that with the curve left-shifted, and hgb holding onto the O2's more tightly, that a sat greater than 92% could be associated with a low po2?

or the above scenario (left shifted, sat>92) coupled with a high po2 results in possibly poor oxygen delivery?

 

[periopdoc]

D02=CO x Hb x 13.4 (or 13.6 depending on what you read) x Sa02 + 0.003xPa02

I believe that you have a misplaced decimal point.

- pod

 

[cfdavid]

are you guys suggesting that with the curve left-shifted, and hgb holding onto the O2's more tightly, that a sat greater than 92% could be associated with a low po2?

or the above scenario (left shifted, sat>92) coupled with a high po2 results in possibly poor oxygen delivery?

Actually, I was thinking of various mechanisms in which a blood gas would show a low Pa02 with an adequate Sa02.

A left shift in the Hb saturation curve would do this.

 

[pgg]

Edit - never mind, brain's in neutral today.

 

[DrN2O]

D02=CO x Hb x 13.4 (or 13.6 depending on what you read) x Sa02 + 0.003xPa02

Thus, the actual contribution (as we all know) of dissolved O2 is super weak to the extent that you can almost exclude it from the equation.

cf

Really? I disagree. In fact, increasing FiO2 thus increasing PaO2 can have as much effect on DO2 in an anemic pt (if he has healthy lungs and not much A-a gradient) as transfusing RBC and increasing the Hgb by 1g. And it's so much easier to do.

 

[Boujee]

please entertain me with the following question...

if u expose blood to O2 does it bind hgb prior to contributing to O2 tension...

i guess in other words, does the bound o2 on hgb contribute to po2?

 

[Licoricestick]

please entertain me with the following question...

if u expose blood to O2 does it bind hgb prior to contributing to O2 tension...

i guess in other words, does the bound o2 on hgb contribute to po2?

In order to bind to Hb the O2 must enter the capillary, therefore as the blood traverses the capillary a rise in PO2 happens from venous to arterial. For O2 to continue to diffuse from lung to blood there must be a concentration graient (remember Fick's law). That concentration gradient is generated as O2 combines with Hb.

But O2 combined with Hb does NOT contribute to PO2. PO2 is the partial pressure of oxygen in blood. Any gas bound to another substance does not contribute to partial pressure.

Therefore oxygen content (= [Hb(g/dL) x 1.34 x SpO2/100] + 0.003 x pO2) is actually more important than either PO2 or SpO2.

 

[Narcotized]

Really? I disagree. In fact, increasing FiO2 thus increasing PaO2 can have as much effect on DO2 in an anemic pt (if he has healthy lungs and not much A-a gradient) as transfusing RBC and increasing the Hgb by 1g. And it's so much easier to do.

You would need a pa02 of about 550 (1.36 divided by .003 then minus the roughly normal p02 of 90 or so) to have as much effect as transfusing a Hgb increase of 1. Maximum PAo2 is approximately 760 minus 47 minus another 50 (40 divided by .8), or 663. And then even with healthy lungs you will still have a shunt of about 5%.

So to do what you're saying you will need to keep the patient at roughly 100% FiO2, which you can only do so long, and if the problem is anemia you will have to transfuse eventually, so why wait?

To CF's point, dissolved O2 (about .3 ml/dl in a normal paO2) contributes very little to total oxygen delivery of about 20 in a normal healthy person.

 

[cfdavid]

I believe that you have a misplaced decimal point.

- pod

I wrote the equation for Delivery, which includes CO (as you know). So, to make the conversion in the Ca02 equation, expressed in ml/dl to become ml/L (to be used in D02 equation), it requires you multiply the 1.34 x 10.

Then, once you have ml/L and multiply by L/min, you get # ml/min Delivery.

probably should have just stuck to Content, as that was really the context of the original question....

cf

 

[Paseo Del Norte]

This does pose a curious question. How far left can you actually shift the curve? Even taking an extreme example of a pH of 7.60, we are looking at about a saturation of 83% at a tension of 40. In line with the OP's question, I think it would be rather difficult in most people to have saturations above 90% with a tension well below 50 regardless of a left shift.

Perhaps I am completely wrong; however, with such high PH's, the bonds that hold the protein structure in place will be altered and loss of conformation with all that other badness will eventually occur? Perhaps extreme alterations in temperature, 2-3-DPG and other variables could cause such conditions; however, at some point we run into a situation where conditions are incompatible with life?

The only situation that I have seen where the PaO2 makes a significant impact on CaO2 has been hyperbaric therapy.

 

[hoyden]

The question is can you ever have a scenario where you have adequate Sa02 (say >90%) with a very low Pa02???? (<50)

cf

If you have carbon monooxide poisoning your SpO2 is going to be in a 90s range, but your PaO2 is going to be low. All others when your Hgb-O2 dissociation curve is shifted to the left.

 

[Paseo Del Norte]

PaO2 would be normal assuming normal atmospheric pressure of oxygen, PAO2 and A-a. CO toxicity alone would not significantly alter PaO2 unless the patient came from a hypoxic environment. Of course, this may often be the case considering the environments that have elevated levels of CO.

 

[Licoricestick]

accidental double post...

 

[Licoricestick]

If you have carbon monooxide poisoning your SaO2 is going to be in a 90s range, but your PaO2 is going to be low. All others when your Hgb-O2 dissociation curve is shifted to the left.

Not so - three different things to consider for CO poisoning:

CO poisoning will not alter PaO2 as CO has no influence on the diffusion of O2 into the blood.

The SpO2 (ie pulse oximetry - two wavelengths of light and is only designed to diostinguish between oxyHb and deoxyHb, this is not SaO2) will be >90% as that is what carboxyhaemoglobin reads. However this does not represent an "adequate" SpO2 reading, rather it is a source of error in SpO2 readings as the Hb is tightly bound to CO and therefore unable to carry oxygen, thus significantly reducing oxygen content of blood and therefore oxygen delivery (DO2 being the major purpose of the cariorespiratory system).

The SaO2 (ie benchtop oximetry with multiple wavelengths that is therefore able to distinguish between different hb species/conformations) Should still give an accuarate SaO2 (ie low as very little Hb will be bound to O2).

I cannot stress this enough SpO2 IS NOT THE SAME AS SaO2. Yes, readings may be the same in the presence of only tiny amounts of Hb aside from oxyHb and carbaminoHb, but as soon as other species of Hb enter into the mix, the readings will be different.

 

[hoyden]

Not so - three different things to consider for CO poisoning:

CO poisoning will not alter PaO2 as CO has no influence on the diffusion of O2 into the blood.

The SpO2 (ie pulse oximetry - two wavelengths of light and is only designed to diostinguish between oxyHb and deoxyHb, this is not SaO2) will be >90% as that is what carboxyhaemoglobin reads. However this does not represent an "adequate" SpO2 reading, rather it is a source of error in SpO2 readings as the Hb is tightly bound to CO and therefore unable to carry oxygen, thus significantly reducing oxygen content of blood and therefore oxygen delivery (DO2 being the major purpose of the cariorespiratory system).

The SaO2 (ie benchtop oximetry with multiple wavelengths that is therefore able to distinguish between different hb species/conformations) Should still give an accuarate SaO2 (ie low as very little Hb will be bound to O2).

I cannot stress this enough SpO2 IS NOT THE SAME AS SaO2. Yes, readings may be the same in the presence of only tiny amounts of Hb aside from oxyHb and carbaminoHb, but as soon as other species of Hb enter into the mix, the readings will be different.

So why is it NOT SO? Your SpO2 IS going to be in the 90s range and your PaO2 may, or may not be that low, but usually IS low as well.
I know the reason the SpO2 is relatively high 😉)))

 

[pgg]

So why is it NOT SO? Your SaO2 IS going to be in the 90s range and your PaO2 may, or may not be that low, but usually IS low as well.

PaO2 is directly proportional to the amount of O2 dissolved in the blood and not bound to hemoglobin - even severe carboxyhemoglobinemia shouldn't affect that value in an arterial sample.

 

[Eta Carinae]

Not so - three different things to consider for CO poisoning:

CO poisoning will not alter PaO2 as CO has no influence on the diffusion of O2 into the blood.

The SpO2 (ie pulse oximetry - two wavelengths of light and is only designed to diostinguish between oxyHb and deoxyHb, this is not SaO2) will be >90% as that is what carboxyhaemoglobin reads. However this does not represent an "adequate" SpO2 reading, rather it is a source of error in SpO2 readings as the Hb is tightly bound to CO and therefore unable to carry oxygen, thus significantly reducing oxygen content of blood and therefore oxygen delivery (DO2 being the major purpose of the cariorespiratory system).

The SaO2 (ie benchtop oximetry with multiple wavelengths that is therefore able to distinguish between different hb species/conformations) Should still give an accuarate SaO2 (ie low as very little Hb will be bound to O2).

I cannot stress this enough SpO2 IS NOT THE SAME AS SaO2. Yes, readings may be the same in the presence of only tiny amounts of Hb aside from oxyHb and carbaminoHb, but as soon as other species of Hb enter into the mix, the readings will be different.

This is such an important distinction. And one that is infrequently made. Even on standardized exams, the SaO2 (though not explicitly labelled as such) is used interchangeably with what I would assume to be the SpO2 whenever O2 Sat is reported.

A minor enough detail on exams perhaps that the testers feel no need to be meticulous on that point.

Something to bear in mind however, in the acute mgmt of patients with elevated carboxyhemoglobin, methemoglobin or cyanohemoglobin levels.

Thanks.

 

[hoyden]

PaO2 is directly proportional to the amount of O2 dissolved in the blood and not bound to hemoglobin - even severe carboxyhemoglobinemia shouldn't affect that value in an arterial sample.

It(CO poisoning) does, however, but not through carboxyhemoglobin level.
I mean on the patient who is not breathing 100% O2, but just found near dead in his garage. His initial paO2 may or may not be low, depending on different physiologic mechanisms, not related to CO binding to Hgb.

 

[Paseo Del Norte]

It(CO poisoning) does, however, but not through carboxyhemoglobin level.
I mean on the patient who is not breathing 100% O2, but just found near dead in his garage. His initial paO2 may or may not be low, depending on different physiologic mechanisms, not related to CO binding to Hgb.

I'm not sure I follow you? The PaO2 will not really be effected. Yes, if you are not breathing, the PaO2 will eventually fall; however, it is a common misconception that you need to be exposed to significant amounts of CO for significant toxicity to occur.

CO has an affinity for HB of about 230 times more than oxygen. Essentially, a partial pressure of CO, 230 times less than oxygen will actually compete equally for HB binding. So, to keep the math simple assume you have a PaO2 of 100 mmHg. This is a pretty good PaO2 assuming a normal A-a and so on. However, you need only have a partial pressure of CO at about 0.44 mmHg to have a COHB of about 50%. A 50% COHB level is a pretty severe case of toxicity and it can occur at relatively tiny partial pressures of CO.

 

[Eta Carinae]

I'm not sure I follow you? The PaO2 will not really be effected. Yes, if you are not breathing, the PaO2 will eventually fall; however, it is a common misconception that you need to be exposed to significant amounts of CO for significant toxicity to occur.

CO has an affinity for HB of about 230 times more than oxygen. Essentially, a partial pressure of CO, 230 times less than oxygen will actually compete equally for HB binding. So, to keep the math simple assume you have a PaO2 of 100 mmHg. This is a pretty good PaO2 assuming a normal A-a and so on. However, you need only have a partial pressure of CO at about 0.44 mmHg to have a COHB of about 50%. A 50% COHB level is a pretty severe case of toxicity and it can occur at relatively tiny partial pressures of CO.

 

[hoyden]

I'm not sure I follow you? The PaO2 will not really be effected. Yes, if you are not breathing, the PaO2 will eventually fall; however, it is a common misconception that you need to be exposed to significant amounts of CO for significant toxicity to occur.

CO has an affinity for HB of about 230 times more than oxygen. Essentially, a partial pressure of CO, 230 times less than oxygen will actually compete equally for HB binding. So, to keep the math simple assume you have a PaO2 of 100 mmHg. This is a pretty good PaO2 assuming a normal A-a and so on. However, you need only have a partial pressure of CO at about 0.44 mmHg to have a COHB of about 50%. A 50% COHB level is a pretty severe case of toxicity and it can occur at relatively tiny partial pressures of CO.

Yes, it will. If the pt is unconsious with CO poisoning, his problems are not isolated to CO-Hgb, but to his alveolar ventilation as well and, sometimes, to V/Q balance. And I have underlined several times, that his PO2 may or may not be low - however, the longer time exposure to CO, the longer the pt is not being helped initially, the higher the possibility of PO2 being low. You have to view the pt with all possibilities involved, not just isolate CO binding to Hgb. it is not an in vitro experiment.

 

[Paseo Del Norte]

I apolagise if I come off being rather dull witted, but I am still not wrapping my head around your point. It was stated earlier that an example of a low PaO2/"normal" SaO2 situation is CO toxicity. *I do not see that as the SaO2 will likely be low in CO toxicity in spite of a normal PaO2. I could see a falsely elevated SaO2 if you simply went off of a calculated value; however, I am assuming we are talking about the actual SaO2 measured via Co-oximetry? I absolutely agree that eventually the PaO2 will fall with an unresponsive and apneic patient and that I am looking at this situation in a vacuum. I appreciate the continued discussion.

 

[hoyden]

I apolagise if I come off being rather dull witted, but I am still not wrapping my head around your point. It was stated earlier that an example of a low PaO2/"normal" SaO2 situation is CO toxicity. *I do not see that as the SaO2 will likely be low in CO toxicity in spite of a normal PaO2. I could see a falsely elevated SaO2 if you simply went off of a calculated value; however, I am assuming we are talking about the actual SaO2 measured via Co-oximetry? I absolutely agree that eventually the PaO2 will fall with an unresponsive and apneic patient and that I am looking at this situation in a vacuum. I appreciate the continued discussion.

There are TWO different issues here( relatively normal spO2 with relatively abnormal pO2), not connected with each other by direct causative relationship, but existing side by side - in a serious ( the one you get to see as anesthesiologist/intensivist) CO poisoning scenario - one is caused by specifics of CO binding to Hgb( and the resultant spO2 readings) and the other caused by hypoventilation + V/Q mismatch. You do not have to become apneic to decrease your pO2.

 

[Paseo Del Norte]

How is the SaO2 normal in the setting of CO toxicity?

 

[hoyden]

How is the SaO2 normal in the setting of CO toxicity?

spO2 - rarely anybody measures the direct oxygen content.

 

[Paseo Del Norte]

I understand, I just thought the OP was asking about SaO2. Being indirect and easy "fooled," I agree that SpO2 monitoring will be unreliable. However, CO toxicity or the suspicion of CO toxicity would be a primary indication for co-oximetry and a "direct" measurement of SaO2. Thanks again for the discussion.