ETCO2, PaCO2, dead space question

[hrmm]

In Baby Miller (p. 329, Anesthetic Monitoring: Capnography), it states that:

"Healthy, conscious people exhale gas from alveoli that are all essentially well perfused and ventilated; therefore, deadspace ranges from 2% to 3% and the differential between arterial and end-tidal CO2 is about 0.6 mm Hg."

I've always heard that the difference between PaCO2 and ETCO2 is ~2-5 mm Hg (with PaCO2 being 2-5 mm Hg more than the observed ETCO2). I also know that using an ETT will reduce your anatomic deadspace.

My questions:
1. What is the percentage of deadspace while using an ETT?
2. Why does a REDUCED amount of deadspace (while using an ETT) create an INCREASED difference between the arterial CO2 partial pressure (PaCO2) and the ETCO2? I would think that less deadspace would allow PaCO2 and ETCO2 to be more closely approximated.

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[pgg]

Even with healthy lungs, PPV in a surgical patient under anesthesia doesn't produce V/Q matching as good as spontaneous ventilation in an awake patient. As I understand it, this is the main reason why we routinely see PaCO2 and ETCO2 gaps of 5+ in the OR.


Edit - I'm not so sure an ETT really reduces dead space much. Deadspace of an ETT itself isn't hard to calculate, if we imagine 7mm internal diameter and 300mm length, that's 11545 mm^3 or or about 11 cc. There's a little more dead space proximal to the tube, until you get to the circuit Y piece, and a bit of dead space in the bronchi, but figure 20 cc roughly. 700 cc tidal volumes puts that about 3%, in line with what Miller quoted for the awake patient sans ETT. Again, I don't think it's the tube, but rather V/Q mismatch.

 

[Idiopathic]

pgg, the anatomic deadspace is a fraction of 0.3 or roughly 30%. the ETT bypasses some of that, due to eliminating the nose, mouth and oropharynx, but then the conduit is longer and there is a Y-piece, so im not sure exactly how much less it is.

as far as anesthetized patients, they have a more homogenized distribution of ventilation, even into areas that just can be perfused as well, turning normal physiology into functional dead space. i think its fair to say that this applies to anyone receiving PPV.

 

[pgg]

Erm, been a long time since I've looked at this but .3 seems high.

Vd / Vt = (PaCO2 - ETCO2) / PaCO2

Given PaCO2 of 40, and a typical under-GA gap of 5

Vd / Vt = (40-35)/40
Vd / Vt = .125

For a ratio of .3 you'd need a gap of 12, which seems high. Even in patients under GA, I don't often see gaps like that except in patients with lung disease. What am I missing? I'm sure it's something simple and embarrassing. 😳

 

[pie944]

The equation you utilized with end tidal carbon dioxide calculates alveolar dead space, but doesn't factor in anatomic dead space. To do that you need expired carbon dioxide which will give you the physiologic dead space(alveolar + anatomic), approximately 0.3.

 

[Idiopathic]

right, since the anatomic dead space isnt normally perfused to handle gas exchange, it isnt a source of CO2 retention necessarily, just a conduit. So when you have small tidal volumes and your PaCO2 goes up its because of the anatomic dead space, but that shouldnt widen your TRUE Pa-ET gradient, as they will equilibrate and once you ventilate the alveoli, you will see the ET wash out and resolution of the elevated CO2. This will not be the case with a true physiologic dead space problem, as you typically will have obstruction to flow and cant correct your elevated CO2 with better ventilation

 

[Idiopathic]

i guess thats also a good point to address for the OP, an ETT reduces ANATOMIC dead space but this does not function in gas exchange, so thats why it doesnt affect your CO2 gap - that increases due to other mechanisms