Current brain fart....

[gicts]

I was reviewing my mega codes today and really would like a why to a question.

Of course Epi is given in PEA v-tach and v-fib. How does epi, which speeds up the heart, convert such fast rhythms? :blush:

In my eyes it seems similar to giving Atropine to someone with an increased heart rate......ka boom! Obviously I am wrong. What am I missing? Does Epi mainly effect the AV?

 

[usafmedic45]

Of course Epi is given in PEA v-tach and v-fib. How does epi, which speeds up the heart, convert such fast rhythms?

The main effect in cardiac arrest is that it increases the coronary perfusion pressure increasing the delivery of oxygen to the tissues allowing for the increased chance of successful defibrillation. It also acts as a chronotropic (increases the rate), vasopressor (clamps down the peripheral vasculature) and inotropic (increases contractile force) agent in PEA which is not necessarily a fast rhythm. The vasopressor component is also there in any case, but I've never seen VT speed up from epinephrine and even if it did, it is not sufficient to warrant not giving epi. In fact, epinephrine probably has more evidence for its use than any other drug in ACLS for full arrest.

Does Epi mainly effect the AV?

No.

 

[gicts]

The main effect is that it increases the coronary perfusion pressure increasing the delivery of oxygen to the tissues allowing for the increased chance of successful defibrillation. It also acts as a chronotropic, vasopressor and inotropic agent in PEA which is not necessarily a fast rhythm.



No.

Thanks! That does make sense. The AV was my only guess and a very low shot in the dark at that.

 

[Smash]

In fact, epinephrine probably has more evidence for its use than any other drug in ACLS for full arrest.

Which is to say: next to none. There has never been a randomized, placebo controlled trial into epi in cardiac arrest, and unfortunately due to entrenched practice there is not likely to ever be one.

In fact there is no strong evidence to suggest that any pressor provides benefit in cardiac arrest.

Epi, as mentioned, is given for it's alpha agonist effects. Increased peripheral vascular resistance improves intra-aortic pressures, which then increases coranary perfusion pressure, which is shown (in dogs) to be a strong predictor of ROSC in arrest.

It is not given for it's beta effects. It's beta effects increase myocardial O2 demand, increase the likelihood of ventricular arrythmias, increase intrapulmonary shunt and decrease the ability of the heart to relax (and therefore pump should ROSC occur).

There is a nasty downward spiral when giving epi in cardiac arrest: the longer the arrest continues, the more epi is required to maintain CPP and the worse the myocardial dysfunction is subsequently.

Epinephrine also exacerbates neurological dysfunction post arrest by causing decreased cerebral blood flow and globally increased oxygen demand that cannot be met by CPR.

This is why there is so much interest in vasopressin in cardiac arrest as it is pure alpha, no beta. Unfortunately this has yet to lead anywhere useful either and there is no strong evidence to suggest that one, the other or both are of any use.

We need to concentrate on good quality CPR with minimal interruptions; defibrillation; and post-resus care. Post Cardiac Arrest Syndrome is something that is being investigated further, and it would not surprise me if in the future we are not only cooling and haemodiluting whilst maintaining MAP (as we are now) but also adding things like low dose steroids to combat post-resus adrenal insufficiency.

 

[Shishkabob]

Which is to say: next to none. There has never been a randomized, placebo controlled trial into epi in cardiac arrest, and unfortunately due to entrenched practice there is not likely to ever be one.

Maybe I missed something glaring, but how are you to placebo vasoconstriction, chronotropic and inotropic effects on dead people?

 

[Smash]

Maybe I missed something glaring, but how are you to placebo vasoconstriction, chronotropic and inotropic effects on dead people?

You give one lot of dead people the epi, you give the other lot of dead people the placebo (or nothing) and you see which stays deadest the longest...

The trouble is, epi is so entrenched as the standard of care that it will take a very, very brave ethics committee to ok such a trial.

 

[Shishkabob]

I know what a placebo test is. I don't get how you require one.

If you give one plant water, and another plant acid, I wonder which one will live.


Placebos only work on conscious, functioning brains. If you put saline in the body of a CA pt, the body will be like "oh, water". Put Epi and it goes and starts doing all it's little PROVEN effects it does.



That's how I don't get why you want a placebo test.

 

[usafmedic45]

Maybe I missed something glaring, but how are you to placebo vasoconstriction, chronotropic and inotropic effects on dead people?

You really can't do it because of the damn ethical concerns that hobble medical research. If I find out where Mengele, Rascher and the rest of those :censored::censored::censored::censored::censored::censored::censored:s are buried, I'm going to go take a crap on their graves because of it.

That said, the problem with Smash's comment is that it fails to take into account that there is evidence that epinephrine may have a positive effect versus nothing (and versus things like isoproterenol, etc) in regards to outcomes and this has been documented back into the 1950s (maybe further...I've never bothered to look any further), but some people (not pointing fingers at anyone) tend to have this opinion that if it isn't a double-blinded RCT with multiple centers that the value of the data is questionable at best. Now do I think epi is a miracle drug? No. Do I think it has some benefit? Yes. Is there evidence to back this up to a certain degree? Yes. Do I think we have answered all of the questions pertaining to it? No and if I ever start to feel that, I'll be checking myself into a psych ward because that means I'm a touch delusional.

 

[usafmedic45]

That's how I don't get why you want a placebo test.

"Placebo" and "placebo effect" are two separate terms and you seem to be confusing them. Placebo simply means something without the effect of the medication it is standing in for.

 

[Smash]

This is true, epi does show some favourable effects. It does improve CPP and it does improve the likelihood of ROSC. The question is whether this is worth the well documented and increasingly apparent detrimental effects that go with it that have been shown since the early/mid part of last century.

The resus was a success but unfortunately the patient died...

Like it or not, Level 1 evidence is what we should all be striving to find and incorporate in our practice. It isn't easy to achieve in the prehospital setting and there isn't much of it about, but this doesn't mean there is no value in looking for it.

In the meantime we settle for what we do have, and that is ok too, so long as we realise it isn't the best and it may need to change.

 

[usafmedic45]

The question is whether this is worth the well documented and increasingly apparent detrimental effects that go with it

If you look at the literature, most of the complications associated with epi were due to in patients given high-dose epi or with endotracheal administration (where you get a massive influx of the catecholamine with ROSC due to poor absorption prior to ROSC which taxes an already strained cardiac system). I can't recall any evidence that standard dose IV epi has been conclusively linked to detrimental effects. This could be because there is not a causal relationship or it might just not be possible to ascertain cause with the data currently available.

The resus was a success but unfortunately the patient died...

That is not likely due to the epinephrine. It is simply the price we pay for trying to unhinge the processes of death. We are going to fail most of the time. There are simply too many pathways that lead to a bad outcome and it is impossible to avoid all of them.

Like it or not, Level 1 evidence is what we should all be striving to find and incorporate in our practice.

I agree and don't recall anyone saying that we should not be trying to find a way to attain that lofty goal.

It isn't easy to achieve in the prehospital setting and there isn't much of it about, but this doesn't mean there is no value in looking for it.

There is a very good reason why in the case of resuscitation science it is more or less effectively impossible. In the literature, this conundrum (consent in emergency medicine) has been flogged more than a hypothermic arrest victim. The concerns about ethical research are cutting our legs out from underneath us and will keep us from getting to the point of having level I evidence for most interventions.

In the meantime we settle for what we do have, and that is ok too, so long as we realise it isn't the best and it may need to change.

I agree. However, I believe we will be settling until a sea change that I don't see coming in my lifetime hits the IRBs around the world in regards to implied consent and research.

BTW, prior to undertaking my current project, I worked with a professor who was part of a team working on a very large and long established in-hospital cardiac arrest outcomes project. He was an ethicist and statistician in terms of specialization and he and I had many long conversations on exactly what you and I are discussing here. It's a fascinating area of medical science but it is plagued by a terribly frustrating catch-22 when it comes to data acquisition.

 

[Ridryder911]

Awww... This reminds me of the old days Steve of intellectual debate and discussion.

It goes back to rating the outcome vs. resuscitation. Steve, you mentioned Isuprel. A wonderful drug that would even start a dead horses heart, and never not seen it work, even on Asystole. The problem was, I never seen one patient that ever exited the hospital either that was not in a bag. Successful resuscitation as in getting perfusion, you bet. However successful saves?... Never. Hence one of the reason(s) it was pulled as a primary resuscitation medication.

The same as Calcium Chloride for EMD (PEA) and others. Nice in theory but unfortunately in practicality the outcomes presented differently.

I remember being part of the studies for high dose Epi in the early 80's. We did alternating standard dosing vs. high dose, did we have better response from high dose Epi ? Yes, increase v-fib but usually became persistent and non-responsive to therapy... again as stated the outcome was dismal.

 

[akflightmedic]

I agree Rid...Steve I have missed ya man...don't know where ya been but welcome back!

 

[ResTech]

Just to make sure I understand correctly...

If you have a patient in VF/VT, the goal of giving Epinephrine is to increase peripheral vascular resistance (Alpha effect) to increase B/P-coronary artery perfusion?

How is the perfusion going to be increased when there currently is none except for whats being produced by CPR? Or does the Epinephrine make CPR more effective due to the vasoconstriction which in turn increase blood supply to the myocardium?

I've heard of Epinephrine being a form of "chemical defibrillation" but it sounds like the Epi has little effect on the conversion of the VF/VT... it just makes the heart respond more favorably to electrical defibrillation?

So the ability of Epinephrine to stimulate automaticity doesnt do any good in VF/VT and only in asystole?

 

[Shishkabob]

From what I understand, it makes the blood move just that much more easily through the constricted vessels.


You use amiodarone, adenosine, and lido for the actual conversion.


That's why Epi is used for all CA algorithms. That's also probably why many of the algorithms put "Give Epi or vasopressor" in the same step.

 

[ResTech]

But it also has the ability to increase automaticity and lower the threshold for defibrillation so it must be given with goals other than just its alpha effect to make blood flow more easily.

I would assume in asystole, the use of Epi would be also for its ability to cause automaticity and make the pacemaker cells start firing again.

I start cardiology in Sept so just curious about some of this to get a jump start on better understanding.

 

[Shishkabob]

Ditto, start Cardiology in August, so still a few weeks off and going simply off what I've read my self.

 

[Smash]

How is the perfusion going to be increased when there currently is none except for whats being produced by CPR? Or does the Epinephrine make CPR more effective due to the vasoconstriction which in turn increase blood supply to the myocardium?

You answered your own question. CPR is very inneffective when compared to physiological blood flow. So we need to try and improve that efficiency to ensure adequate blood/O2 supply (to the heart and brain primarily, but the kidneys and gut are also important)

To help us we give an alpha agonist (epi or vasopressin) to increase the pressure in the aorta. You'll recall that coronary circulation occurs during diastole (at rest) and that the coronary vessles arise just above the valves of the heart in the aorta. So between our emphasis on good CPR with adequate chest recoil and a bit of assistance from the alpha agonist, we improve coronary circulation. This means that the myocardium is better oxygenated and therfore more likely to sustain an organised rhythm should we achieve one. (and then we have the negatives as discussed above)

I've heard of Epinephrine being a form of "chemical defibrillation" but it sounds like the Epi has little effect on the conversion of the VF/VT... it just makes the heart respond more favorably to electrical defibrillation?

The only reason epi makes the heart respond more favourably is that it helps oxygenate the myocardium. The epi itself is not good for the myocardium. What would happen if you gave someone who had a beating heart 1mg of epi IV push? Chances are they would go into VT or VF. So epi actually makes the heart want to have arrythmias, which is the exact opposite of what we want to achieve.[/QUOTE]

You use amiodarone, adenosine, and lido for the actual conversion.

Adenosine is not used in cardiac arrest protocols, it is for reverting SVT.

Amiodarone/lidocaine are used essentially to try to prevent the heart fibrillating (simplifying things a touch). They are not used to convert the rhythm in cardiac arrest, merely to stabilise the cells to stop them going off in a little tantrum again. Defibrillation is what we use to terminate the rhythm in cardiac arrest.

Lidocaine (not sure about amiodarone, need to look it up) actually makes it harder to defibrillate.

So we kind of have a roundabout going on. We want to stop fibrillation by defib. Then we give epi which makes the heart want to fibrillate. Then we give lido which makes it harder to defib... round and round we go!

But it also has the ability to increase automaticity and lower the threshold for defibrillation so it must be given with goals other than just its alpha effect to make blood flow more easily.

I would assume in asystole, the use of Epi would be also for its ability to cause automaticity and make the pacemaker cells start firing again.

No, the only reason we give epi is for it's alpha effects. Epi can't cause automaticity; automaticity is an inherent function of cardiac cells. Epi can enhance automaticity (positive bathmotrope) but really too much automaticity is kind of the problem anyway.

 

[ResTech]

Smash... thanks for the great reply.... it makes sense and I understand now...

 

[Shishkabob]

Adenosine is not used in cardiac arrest protocols, it is for reverting SVT.

Where did I say it was in cardiac arrest protocols?

Amiodarone/lidocaine are used essentially to try to prevent the heart fibrillating (simplifying things a touch). They are not used to convert the rhythm in cardiac arrest, merely to stabilise the cells to stop them going off in a little tantrum again. Defibrillation is what we use to terminate the rhythm in cardiac arrest.

Convert in the way that I used it meant "to change" as in "to change from v-tach/v-fib in to normal sinus rhythm", not as in an electrical conversion. Sorry for the mis-communication.

Lidocaine (not sure about amiodarone, need to look it up) actually makes it harder to defibrillate.

Per Brady's drug book

"It is used to raise the threshold for ventricular dysrhythmias and to lower the threshold for defibrillation and cardioversion"