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Epi-Respirations?


FL_Medic

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Short answer: No

The epinephrine will increase the amount of oxygenated blood that is delivered to the brain. More importantly, the respiratory center in the medulla oblongata. When the heart stops, the brain loses perfusion and the respiratory center shuts down. Retun pulses, return perfusion to the medulla, the signals get sent from the brain, and respirations start up again.

Look up the Reticular Activating System for more:

Level of consciousness

Chemoreceptors-->Respiratory center

Baroreceptors-->Blood pressure center

Cardiac center-->Changes in heart rate

The perfusion of these areas follows a stepwise increase/decrease

The level of consciousness drops first, recovers last

The respiratory rate and depth next, then the blood pressure, then the heart rate

If the level of consciousness is good then the worst the vitals can be is compensated.

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Short answer: No

The epinephrine will increase the amount of oxygenated blood that is delivered to the brain. More importantly, the respiratory center in the medulla oblongata. When the heart stops, the brain loses perfusion and the respiratory center shuts down. Retun pulses, return perfusion to the medulla, the signals get sent from the brain, and respirations start up again.

Look up the Reticular Activating System for more:

Level of consciousness

Chemoreceptors-->Respiratory center

Baroreceptors-->Blood pressure center

Cardiac center-->Changes in heart rate

The perfusion of these areas follows a stepwise increase/decrease

The level of consciousness drops first, recovers last

The respiratory rate and depth next, then the blood pressure, then the heart rate

If the level of consciousness is good then the worst the vitals can be is compensated.

I had a cardiologist tell me otherwise. I also forgot to tell you the epi wasn't alone, there were other arrest drugs on board as well.

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The pharmacology of Epinephrine doesn't lend itself to the action you describe. Now, the cardiologist that you spoke to may have some greater insight into this mechanism than I do, but he also wouldn't be the first to be contradicted by this paramedic.

Renal dose Dopamine, prehospital 12 lead interpretation, prehospital CHF management, even ETT verification, and bradycardia management are all topics that I have taken doctors to task over. If this doctor is willing to discuss the mechanism, I am willing to listen, but I have not seen any evidence that it would.

The other code drugs would likely have less direct effect on the respiratory centers than epinephrine would. Unless the antidysrhythmic was able to convert the rhythm, and work with epinephrine to restore pulses, I would doubt they had much of an effect.

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What many consider post cholinergic response, such as Epi etc. after a code has ceased. There is sometimes agonal respirations, and gasps that one could associate with "breathing attempts" and the patient be pulse less or very bradycardic. There are still debates if there is truly an asystolic patient if one could perform a sensitive enough ECG. The pneumotaxic areas will respond sometimes to the levels of Co[sub:94b82267fe]2[/sub:94b82267fe] along with high doses of catecholimine rush, causing an increase in nervous response (hence- agonal breaths)

R/r 911

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No, Im talking aboout spontaneous resp. at 15/min.

here is the pt. I had...

Disp. possible cardiac arrest.

Showed up on scene and the wife said he just took his last breath and directed us to him.

We immediatley got him on the floor and began CPR.

EKG - PEA at a rate of 10

We got a tube in him and since the medic at the arm was unable to yet get an IV established he threw me drugs for the tube.

He threw me two prefilleds 1 epi(1:10,000), and 1 atropine(1:10,000), which is so wrong don't even get me started. Anyways he was the lead medic and said "just do it". so I did.

We continued CPR and he was able to establish a line. We stopped CPR to check rythm and saw idoventricular PEA coming and then going. So we continued CPR and got another Epi, atropine, and sodium bicarb on board.

After reassessing the rythm this time we saw V-Tach, Time to weld him.. First biphasic shock showed no change, and the second converted to asystole.

I changed the patches to AP and there must have been some serious hair cause it wasnt working so we continued CPR and started to notice some serious levidity.

The lead medic at this time decided we were gonna get permission to call him and phoned the ER. As soon as he left the room I decided we need to really make sure(because with the wife saying he just took his last breath on arrival we should have had a great chance at a save) and I said lets stop CPR one more time and check the rythm.

I saw a Narrow-complex tachy. I said "check a pulse". + carotid.

Next my airway guy said he is breathing... I said what???

and I confirmed it when we took off the bag and he had spontanious resp. 15/min.

At the hospital 30 min. after pt. transfer he coded again. I went into the room and watched the happenings. He basiclly went threw the same rythms in there.

Next I saw the doc put the dopler on him trying to find a pulse, and she couldn't. The doc called him and as the bag was removed we noticed he had spontaneous resp. at 12/min. The doctor reassessed her doplar andlooked at me like what the hell.

he ended up dying.

I asked a cardiolist and he told me that it was all the EPI/drugs

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[

He threw me two prefilleds 1 epi(1:10,000), and 1 atropine(1:10,000), which is so wrong don't even get me started. Anyways he was the lead medic and said "just do it". so I did.

Why do you think that tx was wrong? And what's with the atropine (1:10,000)?

You actually counted 15 times a minute?

I don't know what it was, honestly. I would go with agonal resps.

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[

He threw me two prefilleds 1 epi(1:10,000), and 1 atropine(1:10,000), which is so wrong don't even get me started. Anyways he was the lead medic and said "just do it". so I did.

Why do you think that tx was wrong? And what's with the atropine (1:10,000)?

You actually counted 15 times a minute?

I don't know what it was, honestly. I would go with agonal resps.

Yes I did count.. deffinatley not agonal.

the Atropine was 1mg. in 10cc

That tx is wrong:

Double the dose of EPI 1:1,000

Double the dose of Atropine.

you are suppose to follwo it with a flush, but if you are planning on repeated doses you need to concider the amount of flui and whether you are bagging good enough for it to get through the interstitial space.

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Don't get me wrong though he is a good medic, as are most of my coworkers. And it was his call, and barring the situation I can see why he didn't want to waste time. I don't think the outcome would have changed, and the purpose of this post isn't to question his skills but my original question.

Does EPI cause spontanious resp.

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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 ?:)

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