Monitoring intubated TBI patients with ETCO2

I wouldn't say that there is no evidence for the practice.

There's no evidence for it, in the absence of acute herniation, Once they start to herniate though, it can be an effective temporizing measure.

In TBI with severe multi-system trauma it gets more complicated. And frankly, very few of those patients survive without severe deficits, no matter what you do.
 
Remi, I think you misunderstood. This is not about hyperventilating brain-injured patients. It is about using ETCO2 to gauge your ventilations of patients with isolated TBI's in order to keep their blood CO2 levels in the normal range. As you probably know, it is believed that these patients do worse when they are over ventilated.
 
My bad
 
"In trauma patients the most robust evidence for the correlation between etCO2 and PaCO2 comes form a prospective observational study in Emergency department patients at a single center conducted by Lee et. al in 2009.(2) The median difference of PaCO2 and etCO2 was 3.6 mm Hg and greater in patients with severe hypotension and lactates > 7 mm/L."

"However in poly trauma patients especially those with severe chest and abdominal trauma there was as little as a 29% acceptable correlation of 5mmHg between the etCO2 and the paCO2.(3) In those cases Warner et al. in 2009 concluded that there is an unacceptable correlation between etCO2 and PaCO2 in the very sick and severely injured trauma patients. It is more likely that the etCO2 is artificially low"

Not much I can/will do about it as a paramedic, but good to know nonetheless.
 
"]Not much I can/will do about it as a paramedic, but good to know nonetheless."

You don't see how you can use this? If you've got someone with a head injury who is intubated and getting bagged, you can monitor the ETCO2 to guide your ventilation rate. This is especially useful if the patient is being manually ventilated and is not on a vent.
 
"]Not much I can/will do about it as a paramedic, but good to know nonetheless."

You don't see how you can use this? If you've got someone with a head injury who is intubated and getting bagged, you can monitor the ETCO2 to guide your ventilation rate. This is especially useful if the patient is being manually ventilated and is not on a vent.

I should have been more clear: I assumed it went without saying that we should use ETCO2 to titrate ventilations. That is a standing order protocol.

To me, the interesting thing about the article is that patients with multisystem trauma, hypotension, elevated lactate level, etc, will often have ETCO2 levels that are artificially low. Based on that fact, in the field with such a patient, one might be inclined to aim for a lower ETCO2 than the 35-40 that is recommended by protocols. When I said "not much I will do about it", I meant that I'm not going to be eager to deviate from protocols if I find myself in this situation.

For instance: I show up to a MVC, find patient unresponsive but alive with multisystem trauma, and decide to intubate. In this situation, since we can't do ABG's in the field, based on the article it might make sense to ventilate to ETCO2 level of 30 or even lower maybe (instead of normal 35-40). But that would be a deviation from protocol. If we had a long transport time I'd consider calling medical control about it.
 
Your protocols say base your ventilations on the ETCO2? That is not a great idea actually except in a specific situation like this. The ETCO2 will not match the true PaCO2 if there is any alteration in cardiovascular function.
 
Your protocols say base your ventilations on the ETCO2? That is not a great idea actually except in a specific situation like this. The ETCO2 will not match the true PaCO2 if there is any alteration in cardiovascular function.

In my state protocols under "routine care" it says, "Ventilation rates are to be titrated to goal EtCO2 recommendations" and "In patients who are not in cardiac arrest, all efforts should be made to avoid end-tidal carbon dioxide levels that have been shown to be detrimental and to ensure quality ventilation and oxygenation. In general this means that capno-ET-CO2 values should be kept between 35-40 mm Hg in these patients; specific exceptions should be discussed with online medical control."

Under the ROSC protocols it says, "Do not hyperventilate; goal ETCO2 of around 40 mmHg."

Under head trauma it says, "Provide advanced airway management only if patient is not adequately oxygenating (defined as SpO2 maintained at > 95%) or ventilating and not corrected by BVM. Maintain ETCO2 at 35-40 mmHg."


I think I see your point about "alterations in cardiovascular function": a patient in cardiogenic shock won't be able to carry as much CO2 back to the lungs, and so their ETCO2 will be artificially low compared to their PaCO2 - is that correct? So in that case it would be a big mistake to look at the CO2 and think that you're hyperventilating them and adjust ventilations accordingly. I hadn't thought of that!
 
"
a patient in cardiogenic shock won't be able to carry as much CO2 back to the lungs, and so their ETCO2 will be artificially low compared to their PaCO2 - is that correct? So in that case it would be a big mistake to look at the CO2 and think that you're hyperventilating them and adjust ventilations accordingly. I hadn't thought of that!"

Yes, you're right. Basically, when you measure CO2 levels with ETCO2, you are measuring the levels indirectly because you are not measuring the blood level directly, but rather what is exhaled through the lungs. What you are reading will correlate accurately to the blood level as long as the lungs are getting perfused normally. However, in any shock state, you can get an inaccurately LOW reading. (Note that you won't get an inaccurately high reading). So, in a 25 y/o asthmatic, you can bet that the ETCO2 you are seeing is accurate, but in the 75 y/o COPD'er with a big PE, you will only know that the ETCO2 reading is at least as high as the true PaCO2.
 
Now that I read the piece more closely, of course low perfusion states result in an artificially low C02. It's usually apparent by the capnogram. It's too bad that wasn't addressed in the article.

One piece that didn't make sense at all was in the last paragraph:
Case conclusion: Since the patient remained hemodynamically stable on the ventilator and only suffered from isolated TBI, you performed an initial ABG at found a PaCO2 of 37 mmHg and observed an etCO2 of 39-41 mm Hg by waveform capnography. For the next 3 hours in the ED you continued to monitor the etCO2 and did not perform any repeat ABGs

How do you get an EtC02 lower than the Pac02?
 
"How do you get an EtC02 lower than the Pac02?"

It's really not. The difference is only a few mmHg. It's meaningless. Either reading could have been off a bit in either direction. Or, perhaps the ABG was drawn a minute or two before the ETCO2 was observed.
 
it pains me to write this, because I remember when pre-hospital capnography first emerged and I thought it was a great addition.

But, honestly, it has little utility as a surrogate for PaCO2 in critically I'll patients. And if you are intubating in the field, you are treating a patient who is critically ill.

Anecdotally, I see little correlation in terms of numeric values. And there is litterature showing the same.

However, they do have very some very important roles: Confirmation of intubations. Effective chest compressions. Obstructive patterns. Even the trend of the CO2 is very important.

But the actual number you are getting- it's just not an accurate reflection of PaCo2 in critical illness.

There are texts that cite a fixed gradient between ETCO2 and PaCO2 which occurs due to gas washout in the dead space of the airways and the tubing of the capnography.

In a normal, healthy, well-inflated and well-perfused lung, that may hold true. A healthy patient under a general anesthetic, on the constant gas-flow of a ventilator usually correlate closely.

Patients who are intubated in the field do not have those conditions, nor physiology.
 
It's really not. The difference is only a few mmHg. It's meaningless. Either reading could have been off a bit in either direction. Or, perhaps the ABG was drawn a minute or two before the ETCO2 was observed.

Yeah, I get all that.

But given that the whole point of the article was the correlation between the serum and expired C02 values, it seems odd that they would use those values as an example.
 
Back
Top