ETCO2 questions

[Brandon O]

But understand that a "CO2 retainer", whether chronic or acute, is doing just that and the ETCO2 will be significantly lower than the patients PaCO2. Whether an acute asthma attack or COPD, the CO2 isn't being eliminated via exhalation because of obstructed airways.

In COPD, changes in the alveoli make gas exchange less efficient, so it is harder for C02 to diffuse from the blood through the alveoli into the expired gas. Because of this, higher than normal levels of C02 build up in the blood and this is why they are referred to as "retaining" C02. The EtC02 may be normal, a little high, or even a little low but the key point is that it is less than the blood (Pac02) levels.

Eh...

I think I have to disagree with this, guys.

COPD patients who "retain" don't have an elevated pCO2 because it's not diffusing into their alveoli. It's elevated because they can't exhale it from their alveoli. CO2 diffuses briskly, but is exhaled slowly, so it quickly forms an equilibrium (between PaCO2 and PACO2) and ceases to leave the blood. Bronchoconstriction is a problem of ventilation, not diffusion. So while less air is being exhaled overall, its contents should still accurately reflect blood levels. (In fact, if you're really worried about CO2 having a chance to diffuse, an obstructive patient should have a better correlation, because air is spending more time in their alveoli to swap gas back and forth.)

There are certainly cases where the ETCO2 is lower than the pCO2. And actually, I'm not sure how well this phenomenon is understood; I would love to see any good references. But I assume it is generally caused by technical matters (such as sidestream devices getting a diluted sample), perhaps combined with some true diffusion problems.

 

[E tank]

Eh...

I think I have to disagree with this, guys.

COPD patients who "retain" don't have an elevated pCO2 because it's not diffusing into their alveoli. It's elevated because they can't exhale it from their alveoli. CO2 diffuses briskly, but is exhaled slowly, so it quickly forms an equilibrium (between PaCO2 and PACO2) and ceases to leave the blood. Bronchoconstriction is a problem of ventilation, not diffusion. So while less air is being exhaled overall, its contents should still accurately reflect blood levels. (In fact, if you're really worried about CO2 having a chance to diffuse, an obstructive patient should have a better correlation, because air is spending more time in their alveoli to swap gas back and forth.)

There are certainly cases where the ETCO2 is lower than the pCO2. And actually, I'm not sure how well this phenomenon is understood; I would love to see any good references. But I assume it is generally caused by technical matters (such as sidestream devices getting a diluted sample), perhaps combined with some true diffusion problems.

Right...like I said, airway collapse creates a situation where the patient can't exhale the accumulated CO2 in the alveoli. That causes the a-A concentration gradient for CO2 to flatten out and cause the PaCO2 to rise. But the ETCO2 in patients with obstructive disease, when there is active obstruction as evidenced by the wave form, will be lower than the arterial CO2. It's why people get fooled trying to extubate what they think are normocarbic patients when the PaCO2 is much higher than what shows on the monitor.

 

[TXmed]

ETCO2 will never be higher than the PaCO2 but will give "false lows". In my experiance, a patients who is clearly having an asthma/copd attack will have a pretty high ETCO2 and then it will drop to the singles or teens (due to insuffeciant air movement) just prior to them going into respiratory arrest, as their muscles tire out and can no longer keep up with the demand.

False lows also clue you in to a PE and poor blood flow right-left.

Sorry if this was mentioned before i havent had a chance to read everyone elses responses.

 

[Carlos Danger]

Eh...

I think I have to disagree with this, guys.

I wrote:

In COPD, changes in the alveoli make gas exchange less efficient, so it is harder for C02 to diffuse from the blood through the alveoli into the expired gas. Because of this, higher than normal levels of C02 build up in the blood and this is why they are referred to as "retaining" C02. The EtC02 may be normal, a little high, or even a little low but the key point is that it is less than the blood (Pac02) levels.

You wrote:

COPD patients who "retain" don't have an elevated pCO2 because it's not diffusing into their alveoli. It's elevated because they can't exhale it from their alveoli. CO2 diffuses briskly, but is exhaled slowly, so it quickly forms an equilibrium (between PaCO2 and PACO2) and ceases to leave the blood. Bronchoconstriction is a problem of ventilation, not diffusion

I'm not seeing what it is that you disagree with?

Edit: actually one of the primary features of some types of emphysema (paracinar and distal acinar - I did have to look it up because I couldn't remember the names of the different forms) is alveolar damage which directly inhibits gas exchange. Granted these are much less common than the type induced by smoking.

 

[NPO]

@NPO - what was the pt’s body weight and height (to calc Ideal Body Weight)?

5'5", 122lbs as weight at the ED.

Pressure does not equal flow. People can have a normal/high pressure (high afterload) and minimal forward flow (Cardiac output).

Is an ETC02 of 25 necessarily bad in a post arrest patient? You should get an initial increase in ETC02 with ROSC since perfusion has now improved however once that has passed you still may have an underlying metabolic acidosis.

No, obviously I wouldn't always correlate BP with flow, but in this case, I suspect it did. The patient had a rapidly improving mental status, strong pulses and spontaneous respirations, all signs that, in a post arrest, I'd link to adequate perfusion, I'd think.

I'll chime in...All things equal, her ETCO2 trend would not concern me in the least given that she sounds like a bona fide save with plenty of cardiac output and I'm assuming good oxygenation because you didn't say anything about that. If I had to pick something to be concerned about it would be that HR and diastolic pressure, but that would probably be temporary given the circumstances.

If the BS's, SaO2 and perfusion is OK, I'd note it but not worry about it. I will say the most common reason for a lower ETCO2 without perfusion problems or obstructive lung dz is hyperventilation, like you pointed out, so, I got nothing for ya.

Yes, the most concerning was her BP. Her heart rate was 70-90 AFib, with a normalish EKG except some depression which I think was probably just strain pattern. No indication of STEMI. BGL was 205, and I agree the trend of ETCO2 wasn't my biggest concern since I expected a drop post arrest since she had been in a low perfusion state. I was just mostly curious is a ETCO2 this low is problematic or correctable.

 

[E tank]

I was just mostly curious is a ETCO2 this low is problematic or correctable.

Short answer, it should not be used in treatment decisions given what you've told us, not the least of which because it could very well represent a PaCO2 in the mid 30's. You just don't know.

 

[TXmed]

Short answer, it should not be used in treatment decisions given what you've told us, not the least of which because it could very well represent a PaCO2 in the mid 30's. You just don't know.

I fully agree with this. One thing ive come across is people become so engrossed with etco2 they neglect their other tools for assessment, and in some cases end up blaming the use of etco2 for "false numbers". Etco2 is just another tool in the box.

 

[E tank]

False lows also clue you in to a PE and poor blood flow right-left.
.

Explain. The low ET CO2 isn't false in a catastrophic PE. It's very real.

 

[TXmed]

Yes, youre correct the exhalation of CO2 in all the pathologies i mentioned is low and therefore real. I use the term false low as the patients PaCO2 is significantly high while the etco2 is low and people mistakenly think that in these pathologies they correlate giving a false impression. And some end up bashing the use of etco2 when in reality it was their poor understanding.

But thats why i use that term.

 

[Gurby]

I'm not seeing what it is that you disagree with?

I'll take a swing:

Diffusion will only occur if there is a partial pressure gradient. The way Brandon describes it, the alveoli equilibrate with the blood, and after that no more diffusion takes place because there is same amount of CO2 on either side. The CO2 can get into the alveoli but the patient can't ventilate the alveoli well enough to get the CO2 out of there.

In your description, there is a partial pressure gradient between the blood and alveoli, caused by damage to the alveoli that makes it such that the CO2 can't diffuse out effectively enough to equilibrate.

So Brandon is saying it's a ventilation issue, you're saying it's a diffusion issue. I would guess that it depends on the circumstances and there are probably lots of shades of gray?

 

[ThadeusJ]

Interesting that we haven't discussed the role of waveform analysis to look at whether its a diffusion issue or an airflow issue. You may be able to make a distinction between air trapping, diffusion issues or PE. Lots of online stuff on waveforms. Just sayin'...

 

[Carlos Danger]

I'll take a swing:

Diffusion will only occur if there is a partial pressure gradient. The way Brandon describes it, the alveoli equilibrate with the blood, and after that no more diffusion takes place because there is same amount of CO2 on either side. The CO2 can get into the alveoli but the patient can't ventilate the alveoli well enough to get the CO2 out of there.

In your description, there is a partial pressure gradient between the blood and alveoli, caused by damage to the alveoli that makes it such that the CO2 can't diffuse out effectively enough to equilibrate.

So Brandon is saying it's a ventilation issue, you're saying it's a diffusion issue. I would guess that it depends on the circumstances and there are probably lots of shades of gray?

I'm not saying it's necessarily a "diffusion issue" per se, but ultimately, what causes the increased C02 gradient is a failure of C02 to diffuse across the alveolar-capillary membrane into the alveolar sac. Whether that failure to diffuse is an actual problem with diffusing capacity (due to a problem with the alveolar-capillary membrane itself, as in the interstitial disease that follows PHTN, for instance), or a result of airway obstruction (and subsequent equalization of the partial pressure of C02, as Brandon described) seemed irrelevant to the OP's question, so I tried to keep it concise.

 

[Brandon O]

I'm not saying it's necessarily a "diffusion issue" per se, but ultimately, what causes the increased C02 gradient is a failure of C02 to diffuse across the alveolar-capillary membrane into the alveolar sac. Whether that failure to diffuse is an actual problem with diffusing capacity (due to a problem with the alveolar-capillary membrane itself, as in the interstitial disease that follows PHTN, for instance), or a result of airway obstruction (and subsequent equalization of the partial pressure of C02, as Brandon described) seemed irrelevant to the OP's question, so I tried to keep it concise.

Well -- the relevance is that we're talking about measuring the partial pressure of CO2 in the exhaled gas. In my model, there's little reason it should not equal the arterial partial pressure. In yours it should be much lower.

 

[Carlos Danger]

Well -- the relevance is that we're talking about measuring the partial pressure of CO2 in the exhaled gas. In my model, there's little reason it should not equal the arterial partial pressure. In yours it should be much lower.

OK, Brandon. Maybe you should re-read the OP’s question.

 

[Brandon O]

OK, Brandon. Maybe you should re-read the OP’s question.

Yes. I think your answer is wrong.

 

[Carlos Danger]

Yes. I think your answer is wrong.

Once again, Brandon, you said Co2 retention occurs, essentially, when Co2 is unable to leave the blood. I said Co2 retention occurs, essentially, when Co2 is unable to leave the blood.

We could squabble over the precise mechanisms that result in Co2 being unable to leave the blood, but I'd rather not. I think your explanation about mechanical obstruction being the sole cause leaves a lot of detail out. Because even though the classic description of COPD pathology is one of destruction of the small airways and loss of elasticity of the alveolar sacs resulting in impaired ventilation, there's actually more going on than that in moderate-advanced COPD, which is when C02 retention becomes an issue. Most of which is well beyond the scope of a reasonable answer to the original question.

Not sure what the issue is here but if you just need to have the last word, it's all yours.

 

[E tank]

Eh...

I think I have to disagree with this, guys.

COPD patients who "retain" don't have an elevated pCO2 because it's not diffusing into their alveoli. It's elevated because they can't exhale it from their alveoli. CO2 diffuses briskly, but is exhaled slowly, so it quickly forms an equilibrium (between PaCO2 and PACO2) and ceases to leave the blood. Bronchoconstriction is a problem of ventilation, not diffusion.

There are certainly cases where the ETCO2 is lower than the pCO2. And actually, I'm not sure how well this phenomenon is understood; I would love to see any good references. But I assume it is generally caused by technical matters (such as sidestream devices getting a diluted sample), perhaps combined with some true diffusion problems.

I can't tell if we're talking past each other, saying the same thing or we have a fundamental difference in day to day experience and practice. This statement:

"So while less air is being exhaled overall, its contents should still accurately reflect blood levels. (In fact, if you're really worried about CO2 having a chance to diffuse, an obstructive patient should have a better correlation, because air is spending more time in their alveoli to swap gas back and forth.)"

Cannot be reconciled with this in a mechanically ventilated patient:

Each subsequent breath arrives before the actual ET CO2 can be measured, evidenced by the continued increasing slope of the line on the vertical axis even as inspiration occurs, ie, the actual concentration measurement is being prematurely interupted by the next breath. This implies two things. One is that the alveolar CO2 must be higher than the ETCO2, and if that is true it then follows that the arterial CO2 is higher than the ETCO2. We demonstrate this objectively every single day in the OR by drawing arterial samples and comparing them against ETCO2 measurements.

Moreover, even in healthy lungs with no measurable obstruction, the a-ET gradient for CO2 can be 4 to 8 (or so) mmHg, so in lungs with obstructive disease, it reasonably follows, objective measurement aside, that the gradient would be even greater. Its why we adjust i:e ratios in order to optimize ventilation of these patients and how we measure our progress.

Sure, if you based your RR on true (complete) ETCO2 measurement, you'd get something approximating alveolar and therefore arterial CO2. But to do that you'd need to drop the RR to a point where ventilation and oxygenation would be inadequate.

 

[Brandon O]

Well, there's no better way to find truth than to go look for it.

Couple small studies on severe...
- COPD https://www.ncbi.nlm.nih.gov/pubmed/7750309
- and asthma https://www.ncbi.nlm.nih.gov/pubmed/16187465

Not much of a gradient; while they highlight the gradient in the first study, it is still quite low (<10 in all cases).

On the other hand, consider: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806812/

In this study of hypercapneic respiratory failure patients (mostly COPD), there WAS a large gradient at first (you have to pull up the graphics to see), which shrank with treatment.

The implication here is that a CO2 A-a gradient may exist in obstructive lung disease, but in most cases is quite minimal. During acute exacerbation, however, the gap might be larger.

Mechanistically, I don't think this has anything to do with gas exchange, for the reasons discussed; it has to do with dead space. Take the extreme example where a patient is only breathing tidal volumes of 30cc. Since this is less than the anatomic deadspace of the airway itself, no gas exchange occurs. The ETCO2 will therefore approximate that of the ambient air (i.e. will be low) -- since you're exhaling air largely unchanged -- while your PaCO2 climbs. The gradient will be high.

In less extreme examples the same principle will hold. Consider a PE creating large portions of dead spaced lung which will behave in the same way. And then, consider bronchospasm: the shark-fin capnogram, as I understand it, is caused by exhalation being so slow that you are mixing deadspace air with alveolar air throughout the entire breath (rather than briskly clearing the former at the beginning). As you point out, this does imply that ETCO2 is still rising at the end of the breath, and presumably will continue to rise until deadspace is fully cleared. However, what the data seem to suggest is that this gradient is numerically pretty small in patients not experiencing acute exacerbation, the graphics notwithstanding.

So I guess the upshot is that the answer to the OP's question is: mostly no, occasionally yes.

 

[E tank]

Well -- the relevance is that we're talking about measuring the partial pressure of CO2 in the exhaled gas. In my model, there's little reason it should not equal the arterial partial pressure. In yours it should be much lower.

In patients that have a diffusion barrier defect, ie, interstitial lung dz of one form or another, the problem isn't really hypercapnia or even CO2 retention. At the end of the day, it ends up being more hypoxemia. This is owing mostly to the diffusion rate of CO2 being so much greater than O2 (I get that you know that, I'm just pointing it out for lookers in that don't). So that means the ET value for CO2 here is more likely to be closer to the alveolar value and therefore the arterial value than it would be for obstructive dz, precisely because obstructed flow is not the issue. So, diffusion barrier defect = normal(ish) a-ET gradient and obstructive defect = greater a-ET gradient.

 

[E tank]

Well, there's no better way to find truth than to go look for it.

Couple small studies on severe...
- COPD https://www.ncbi.nlm.nih.gov/pubmed/7750309
- and asthma https://www.ncbi.nlm.nih.gov/pubmed/16187465

Not much of a gradient; while they highlight the gradient in the first study, it is still quite low (<10 in all cases).

On the other hand, consider: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806812/

In this study of hypercapneic respiratory failure patients (mostly COPD), there WAS a large gradient at first (you have to pull up the graphics to see), which shrank with treatment.

The implication here is that a CO2 A-a gradient may exist in obstructive lung disease, but in most cases is quite minimal. During acute exacerbation, however, the gap might be larger.

Mechanistically, I don't think this has anything to do with gas exchange, for the reasons discussed; it has to do with dead space. Take the extreme example where a patient is only breathing tidal volumes of 30cc. Since this is less than the anatomic deadspace of the airway itself, no gas exchange occurs. The ETCO2 will therefore approximate that of the ambient air (i.e. will be low) -- since you're exhaling air largely unchanged -- while your PaCO2 climbs. The gradient will be high.

In less extreme examples the same principle will hold. Consider a PE creating large portions of dead spaced lung which will behave in the same way. And then, consider bronchospasm: the shark-fin capnogram, as I understand it, is caused by exhalation being so slow that you are mixing deadspace air with alveolar air throughout the entire breath (rather than briskly clearing the former at the beginning). As you point out, this does imply that ETCO2 is still rising at the end of the breath, and presumably will continue to rise until deadspace is fully cleared. However, what the data seem to suggest is that this gradient is numerically pretty small in patients not experiencing acute exacerbation, the graphics notwithstanding.

So I guess the upshot is that the answer to the OP's question is: mostly no, occasionally yes.

Coming to too many conclusions from abstracts is kind of difficult and comparing the test subjects and methods in these studies to the patients and instruments that we each see in our daily practice may or may not be valid. The subjects in the first study were well enough to participate in it while those in the OR or ICU may have very different degrees of illness. I take those with a grain of salt and within the context of my own practice.

As far as abstracts go, there was one in the side bar of one of the above that found unequivocally that the P(a-ET)CO2 in pre-hospital patients was too great to base any ventilation decisions on the ET value. Annals of EM, I think. I use ETCO2 in the OR to make ventilation changes every time and the abg's correlate those changes consistently.

All that I can offer is that when caring for my patients with my instruments, if I see an obstructive pattern that is concerning for potential post extubation issues, I correlate with an abg. Depending on the degree of the slope, there is a corresponding difference, to one degree or another, every time.

Can't contribute anymore than that.