VASOPRESSIN OR EPI WHATS YOUR CHOICE

[Kiwiology]

We don't use vasopressin so no comment there. It seems our protocols have been change a lot recently: no more atropine or bicarb, only epi and we still have ETT drugs for some reason.

I remember back in the day standard cardiac arrest included lidocaine, epi, bretylium, atropine, maybe bicarb and Mg SO. Seems times have changed.

[usapride2004]

We don't use vasopressin so no comment there. It seems our protocols have been change a lot recently: no more atropine or bicarb, only epi and we still have ETT drugs for some reason.

I remember back in the day standard cardiac arrest included lidocaine, epi, bretylium, atropine, maybe bicarb and Mg SO. Seems times have changed.

No atropine? Like, at all? Why?

Do you guys even pretend to follow ACLS?

As for Vasopressin, ACLS makes it clear that neither is better than the other. We don't carry it at present, and I don't expect us to start any time soon. It seems unnecessary, since it's not any better than Epi...

[Dustdevil]

No atropine? Like, at all? Why?

Do you guys even pretend to follow ACLS?

Do you even pretend to read?

He -- and everybody else here except for you -- is talking about cardiac arrests only.

[AZCEP]

No atropine? Like, at all? Why?

Do you guys even pretend to follow ACLS?

Why should they? Since they are in Australia or other parts that are not in the bass-ackwards U.S. system, maybe we should try to emulate them rather than criticizing.

As for Vasopressin, ACLS makes it clear that neither is better than the other. We don't carry it at present, and I don't expect us to start any time soon. It seems unnecessary, since it's not any better than Epi...

Nice broad strokes you are painting with there. Did you bother to ocnsider that there are a number of situations that would not respond favorably to the strong beta effects that epinephrine will exert?

The cookbook seems to be getting to easy to follow for people to actually think anymore.

[Mateo_1387]

Nice broad strokes you are painting with there. Did you bother to ocnsider that there are a number of situations that would not respond favorably to the strong beta effects that epinephrine will exert?

The cookbook seems to be getting to easy to follow for people to actually think anymore.

Please elaborate how strong beta effects that epi exerts on the heart is not desirable for someone in cardiac arrest?

[Kiwiology]

Why should they? Since they are in Australia or other parts that are not in the bass-ackwards U.S. system, maybe we should try to emulate them rather than criticizing.

Nice broad strokes you are painting with there. Did you bother to ocnsider that there are a number of situations that would not respond favorably to the strong beta effects that epinephrine will exert?

The cookbook seems to be getting to easy to follow for people to actually think anymore.

It seems to me anyway, the cookbook is being rewritten from an evidence based approach (which if you read Circculation the 2005 AHA guidelines admit that randomized studies with cardiac arrest pharmacologics are few and didn't seem to show any great results)

Let's take bicarb as an example: The 1974 AHA guidelines said that along with Don McLean, Chevvy hightops (not sure if KKK-1822 was in force then) and really high gas prices all ACLS providers were to administer two 50mEq amps of sodium bicarbonate.

30 years later, we know that acidosis does not automatically occur in all cardiac arrests, so the guideline was changed. We don't use it at all (not sure how good/bad that is).

It seems to me that this is a bit of a grey area. I just want my paddles back!

[AZCEP]

Please elaborate how strong beta effects that epi exerts on the heart is not desirable for someone in cardiac arrest?

Cardiac arrest following an acute MI for one.

You wouldn't want to chemically induce a maximal effort from ischemic tissue when you don't have an adequate oxygen supply would you? You not only worsen the ischemia, but you also create the possibility of myocardial rupture through the ischemic tissue.

Hypovolemic cardiac arrest for another.

No fluid volume to pump, so do you really want to increase the amount of work the heart is doing without having anything to contract against?

Never mind the fact that epinephrine is well known to cause "stone heart" syndrome.

http://ajp.amjpathol.org/cgi/content/abstract/95/3/745

[Mateo_1387]

Hypovolemic cardiac arrest for another.

No fluid volume to pump, so do you really want to increase the amount of work the heart is doing without having anything to contract against?

I can see that epi for some body in hypovolemic arrest is not necessarily warranted.

You wouldn't want to chemically induce a maximal effort from ischemic tissue when you don't have an adequate oxygen supply would you? You not only worsen the ischemia, but you also create the possibility of myocardial rupture through the ischemic tissue.

But I do not see that epi is bad for someone who goes into cardiac arrest due to a MI. Maybe I am way off, but if somebody is in cardiac arrest due to MI they obviously do not have enough oxygen to support the function of the heart. The heart does not have any beta stimulation at this point. Also the brain is not being perfused. So I can see that epi's strong alpha and beta effects will cause vasoconstriction, increased inotropic, chronotropic, and dopaminergic effects to the blood vessels and heart, exactly what the patient's heart currently lacks. We have to increase the oxygen demand of the heart in order to make it function. Even if we watched a patient code in front of us, did two minutes of cpr, shocked once, and got return of pulses there is a good chance you will have to hang a drug like dopamine because the patient will be unstable.

Am I thinking way wrong? If so please explain.

[AZCEP]

But I do not see that epi is bad for someone who goes into cardiac arrest due to a MI. Maybe I am way off, but if somebody is in cardiac arrest due to MI they obviously do not have enough oxygen to support the function of the heart.

The hypoxic myocardium does not respond favorably to "maximal" beta stimulation. Prior to arrest the body will secrete huge amounts of endogenous catecholamines in an attempt to support function. When this fails the ischemia that is already present worsens. The heart fails as a pump, and is unable to provide perfusion to itself. Increasing vasoconstriction without the beta effects would be closer to physiologic neutral.

Also the brain is not being perfused. So I can see that epi's strong alpha and beta effects will cause vasoconstriction, increased inotropic, chronotropic, and dopaminergic effects to the blood vessels and heart, exactly what the patient's heart currently lacks.

The brain receives perfusion from vasoconstriction in the periphery. This can be better accomplished in the MI scenario with vasopressin because you won't worsen the ischemia. The inotropic/chronotropic/dromotropic effects are not what you should want to elicit from myocardium that has already failed from maximal stimulation. Give the heart an opportunity to recover a bit prior to forcing a maximal effort from it.

Epinephrine does not have any dopaminergic effects. That is an entirely different mechanism and does not belong here.

We have to increase the oxygen demand of the heart in order to make it function. Even if we watched a patient code in front of us, did two minutes of cpr, shocked once, and got return of pulses there is a good chance you will have to hang a drug like dopamine because the patient will be unstable.

Until vasopressin became available you had to increase the oxygen demand. At present, you don't absolutely have to unless you do not have a choice between the two agents in question.

In the scenario you mention, why would you restore circulation to an obviously irritable system only to worsen it by forcing more work from it. With the short time frame you are suggesting, allowing the pump to come back on its own would be much preferred. Dopamine is not necessarily recommended for someone that can maintain perfusion, as this situation probably could. There is a big difference between unstable and need to treat. You would be able to support perfusion with fluid boluses for a while, as you are watching this patient's MAP.

[bryan20w]

i am not one to be redundant but the outlook so far is cook book, i agree with the current ACLS guidlines that state to use it in place of first or second dose of epi however i have heard alot that people are using epi first because it is easier and this is bull. what is the most important thing to a pt in cardiac arrests? CPR if this is going on then you have time for getting the appropriate drugs. And as to which one to use, treat it based on how the drugs work, if you dont know how a drug works dont push it. Epi is a beta and alpha stimulator, where vasopressin is a sellective alpha stimulator, in the protocol for V fib you are giving your first dose as a pressor to increase vascular resistance and you are already dealing with and irritable heart so why increase your automaticity with epi. however in asystole you are dealing with no automaticity so increase it with epi. dont be a cookbook medic, think every call through, and know exactly how the drug that your are going to give a pt is going to work.