"If CO increases, EtCO2 rises, CO2 elimination increases, PaCO2 falls and this is also sustained."

The problem here is that if CO2 elimination increases, without a matching increase in production, dissolved CO2 will drop with a constant rate (elimination - production)

In ROSC, there is definitely an increase in CO2 production to maintain the new EtCO2.

I dont see how an increase in EtCO2 is not directly proportional to the amount of exhaled CO2 (unless the patient suddenly gets obstructive).

So when people use/study EtCO2 as indicator of fluid responsiveness, they look for a *temporary* increase in EtCO2? This is the model that makes sense to me, but I could not find it specified in any of the papers.

CaCO2 refers to the average CO2 in blood (arterial + venosus), right? The arterial concentration increase with ⬆️CO.

VCO2 = Exhaled + ΔCavCO2

At steady state the dissolved part is constant, so VCO2 = exhaled CO2.

I see how better V/Q will get EtCO2 closer to PaCO2.

But how can we sustain a higher EtCO2, if production is constant?
Assuming a square capnography curve, EtCO2 must be directly proportional to the volume of exhaled CO2, which must equal the production of CO2 (at steady state).

I find it more acceptable if it's formulated as: You ask a person with two kids: "is at least one of your kids a boy born on a Tuesday?" They say "yes". What is the probability that they have two boys?

Ah 👌 det giver jo egentligt god mening. TIL

Ok. Mit eksempel var grammatisk forkert ☺️ " ... med dens krig"

Men er den oprindelige overskrift ikke stadig god nok?

Er det ikke korrekt? "dansker banker" er grundled i sætningen.

Sætningen kunne forsættes "... med deres krig"

Great ... though it would have been nice to make this show 0✅

I have the same problem. If I only ever intend putting it on GitHub, is it reasonable to just ignore it? Escaping all these characters will make the code a lot less readable.

Thank you. With such praise, it is hard not to:
RSS: jenevoldsen.com/index.xml

It would be a reasonable regulatory mechanism, that lactate signals increased oxygen demand and raises CO, though I don't know whether it is possible, or even meaningful, to distinguish whether lactate is both fuel and a signal, or just fuel.

Just found that the same group also did this study, showing that lactate increases CO in healthy adults. pubmed.ncbi.nlm.nih.gov/39825426/

bsky.app/profile/johs...

Incredible effect sizes. Do we know what lactate does in a healthy heart? From a teleological perspective, it would make sense that lactate has a positive inotropic effect, regardless of it being a substrate. Simply as a signal of hypoperfusion.

I'm sorry you had to experience that. Unfortunately I don't know what determines which treatment is tried first, or whether e.g. cardioversion can be expected to work if the condition reoccurs, when it didn't work the first time.