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Epi-Respirations?


FL_Medic

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Okay, so the pulseless patient received Epi/Atropine down the tube. Dose not important just yet. Code worked, ROSC briefly, then back to cardiac arrest with spontaneous respirations, right?

So following the description of events, my thoughts would be:

The Epi/Atropine that was given down the tube had little/no effect on the situation immediately following administration.

CPR with IV Epi/Atropine/Bicarb got the vascular bed to return more CO2 to the central circulation (heart/brain)

Return of spontaneous circulation returned even more of the bodies CO2, and the CO2 that came with the administration of the Bicarb to the heart/brain.

The increase in the return of CO2 to the chemoreceptor areas of the brain stem caused the ventilations, not a direct response of the brain stem to the catecholamine. The fact that the patient continued to breath pseudo-normally after returning to cardiac arrest would indicate that there was a significant amount of CO2 that the brain chose to remove through ventilation.

I still doubt that Epinephrine, by itself would create and environment in the arrested patient to allow spontaneous respiratory patterns.

But, hell, not all patients are willing to read the instruction manual for what they are supposed to do anyway. Sure why not ?:)

lol, good answer. Thanks.

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Interesting discussion!

Just for the sake of argument. If the return of respirations are in fact a compensatory response to a high pCO2 s/p arrest (lol or just status?), wouldnt the resp rate be a little higher than 15? Compensatory rates in live patients tend to be a little higher to that-- are we saying that 15 is pretty much all this poor guy could manage since hes so otherwise compromised?

Is there a direct relationship between perfusion of the chemoreceptors and resp. rate? I feel like these types of patients are usually either breathing or not breathing... meaning I've never seen a depressed resp drive in a hypoxic patient-- depressed heart rate, yes-- but resps I usually find to be "on" (tachypnic perhaps) or "off." Is there physiology to back that up?

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Interesting discussion!

Just for the sake of argument. If the return of respirations are in fact a compensatory response to a high pCO2 s/p arrest (lol or just status?), wouldnt the resp rate be a little higher than 15? Compensatory rates in live patients tend to be a little higher to that-- are we saying that 15 is pretty much all this poor guy could manage?

Is there a direct relationship between perfusion of the chemoreceptors and resp. rate? I feel like these types of patients are usually either breathing or not breathing... meaning I've never seen a depressed resp drive in a hypoxic patient-- depressed heart rate, yes-- but resps I usually find to be "on" (tachypnic perhaps) or "off." Is there physiology to back that up?

The links above will get you started.

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Yea I read them. I didnt see anything about a direct relationship between chemoreceptor perfusion and a resulting variable respiratory rate. We're talking about a scenario where the pCO2 is high and yet respirations are still depressed (presumably 15 is fairly slow for this patient). Whats the pathophysiology?

Thanks for referring me to another site (again) though.

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Ahhh the shotgun approach, eh? Thats a ton of information for a pretty direct and specific question. Nonetheless I'll read and see what I can find.

Does anyone else know the answer?

The information is there, you just need to look..I gave you a few to help you have a number of different approaches to the info.

ACE

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