I did a spot on ETCO2 for Amal Mattu's podcast a couple of weeks ago. I try to clear up some of the myths on the use of ETCO2.
Of course the most pervasive and potentially dangerous myth is that ETCO2=PaCO2.
Long story short, in our patients, it doesn't.
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An ED Intensivist from NY. No conflicts of interest (coi).
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Thank you for your podcasts! They are perfect!
Hey Scott-
Quick question for ya:
What is it pathophysiologically that causes End-Tidal to drop as CPR progresses, despite continuing adequate compressions? If compressions are constant, and arterial CO2 is probably rising if anything, why does End-Tidal ever diminish (<10 after 20 mins, etc) ?
In cardiac arrest and shock states, ETCO2 is almost entirely a reflection of cardiac output and the amount of blood pumped to the lungs not the level of CO2 in the blood
Hey Scott,
I totally understand that point- but so then as long as we are performing excellent chest compressions, why should the End-Tidal ever get to less than 10-20 mm/Hg?
(The amount of blood circulating should generally theoretically stay the same, and the minor variable (CO2 in the blood) should only increase if anything)
During cardiac arrest the partial pressure of end-tidal carbon dioxide (PetCO2) falls to very low levels, reflecting the very low cardiac output achieved with cardiopulmonary resuscitation (CPR). Little part of lungs gets perfused thus lesser gas exchange area causing decreased PetCo2 though PaCO2 may be higher than normal as you said. ROSC achieves full perfusion in all lung zones( normal state) and larger gas exchange area causing increase in level of PetCO2.Higher levels of the PetCO2 in CPR indicate better cardiac output and thus quality of CPR.
At 9 minutes you mention dissociation between etCO2 and SpO2 when using supplemental oxygen. My attending does not believe this, do you have a reference I can show since it would be unethical to demonstrate on an actual patient?
what does your attending not believe. this is absolute physiology what are they contending