Acute MI to Cardiac Arrest

[d3653je]

I don't have a scenario but more of a few questions about cardiac emergencies we see daily.

Your patient is alert and oriented with vitals wnl. Has acute onset of chest pain with no known cardiac history. EKG shows signs of ischemia but you have seen worse. You have the pt on 15liters o2. No contraindicates to give 0.4 mg of Nitro S/L. You do with the general theory that it will cause vasodilation and open up the coronary arteries. One asprin chew and swallow. Pt has some relief with the nitro and o2. IV is patent. Vitals wnl s/p nitro. Lets say pain scale went from a 7 to a 3.

EKG looks a little better. Working theory is chest pain relieved with nitro and oxygen, rule out acute mi.

Pts. pain goes from 3 to 10, EKG shows VT. This has happened over a matter of a few seconds.

Pt. codes no pulse no breathing, PEA on the monitor. Start CPR and first drug pushed is 1mg of epi.

This is where we stop the scenario.

Epi has many effects on the body to include vasoconstrcition. Nitro work all be it a few minutes. Whatever amount of stenosis there is, the nitro did its job to open up the artery for as long as it could. Now we are giving the guy a med that causes vasoconstriction.

ACLS says give epi.

So the triple vessel stenosis this pt has was briefly treated with Nitro. It went from 80% in theory with nitro to 70%. However when the nitro ran out it went back to 80%. he codes Now we are giving him epi which will constrict by nature and now the stenosis is 100% due to the epi.

Question is... is epi a good drug to use in a cardiac arrest? Are we making things better or worse for this pt's heart?

 

[Veneficus]

So the triple vessel stenosis this pt has was briefly treated with Nitro. It went from 80% in theory with nitro to 70%. However when the nitro ran out it went back to 80%. he codes Now we are giving him epi which will constrict by nature and now the stenosis is 100% due to the epi.

It is not quite so simple.

Question is... is epi a good drug to use in a cardiac arrest? Are we making things better or worse for this pt's heart?

Depends on who you ask, but a respectable group of providers says "no."

 

[Lifeguards For Life]

It is not quite so simple.



Depends on who you ask, but a respectable group of providers says "no."

What do you think would be a better drug. I am doing a research paper for a class on alternative vasopressors in cardiac arrest.

 

[Veneficus]

What do you think would be a better drug. I am doing a research paper for a class on alternative vasopressors in cardiac arrest.

None in arrest.

after ROSC, then it would depend on the findings.

 

[Mex EMT-I]

This sound like a very interesting and common case.

Why don´t you post it on the ACLS part of the forum and lets hope someone gives us more information about this.

 

[Akulahawk]

I don't have a scenario but more of a few questions about cardiac emergencies we see daily.

Your patient is alert and oriented with vitals wnl. Has acute onset of chest pain with no known cardiac history. EKG shows signs of ischemia but you have seen worse. You have the pt on 15liters o2. No contraindicates to give 0.4 mg of Nitro S/L. You do with the general theory that it will cause vasodilation and open up the coronary arteries. One asprin chew and swallow. Pt has some relief with the nitro and o2. IV is patent. Vitals wnl s/p nitro. Lets say pain scale went from a 7 to a 3.

EKG looks a little better. Working theory is chest pain relieved with nitro and oxygen, rule out acute mi.

Pts. pain goes from 3 to 10, EKG shows VT. This has happened over a matter of a few seconds.

Pt. codes no pulse no breathing, PEA on the monitor. Start CPR and first drug pushed is 1mg of epi.

This is where we stop the scenario.

Epi has many effects on the body to include vasoconstrcition. Nitro work all be it a few minutes. Whatever amount of stenosis there is, the nitro did its job to open up the artery for as long as it could. Now we are giving the guy a med that causes vasoconstriction.

ACLS says give epi.

So the triple vessel stenosis this pt has was briefly treated with Nitro. It went from 80% in theory with nitro to 70%. However when the nitro ran out it went back to 80%. he codes Now we are giving him epi which will constrict by nature and now the stenosis is 100% due to the epi.

Question is... is epi a good drug to use in a cardiac arrest? Are we making things better or worse for this pt's heart?

I take it that the rhythm is now a pulseless VTach? Epi? Noo... Edison.. Calling Mr. Sparky... After that, then things get complicated.

 

[MrBrown]

Adrenaline has no real benefit in cardiac arrest and is a "can't hurt might do some good" drug really, amiodarone a little more towards might do some good but not shown to do much.

 

[zmedic]

There really isn't evidence that nitro saves lives in MI. The theoretical benefit of nitro in MI is mainly in it's effect on reducing preload and thereby reducing cardiac workload.

I also haven't seen data that epi reduces coronary artery perfusion. Remember that difference vessels have different levels of various receptors, so some drugs may act more on big vessels rather than smaller ones. So just because Epi has a certain effect on the arterioles doesn't mean it has the same effect on the heart.

The people who are having these huge MIs tend to have stiff coronary arteries with lots of plaque. I don't think they are quite as dynamic in terms of opening and closing as you are thinking. Furthermore, better to lose the heart muscle beyond the clot and get back a pulse than stay dead.

 

[lightsandsirens5]

Wait, epi for a pt in V-Tach? Something don't seem right there. :unsure:

Vene, why you say that no epi for an arrest. Are you referring to arrest as in asystole? I am no medic and I am no ACLS guy, but I have seen two people in the ER go from a line as flat as Kansas to a sinus with only epi.

I could be totally misunderstanding you also......

 

[lightsandsirens5]

Wait, epi for a pt in V-Tach? Something don't seem right there. :unsure:

Vene, why you say that no epi for an arrest. Are you referring to arrest as in asystole? I am no medic and I am no ACLS guy, but I have seen two people in the ER go from a line as flat as Kansas to a sinus with only epi.

I could be totally misunderstanding you also......

Bump. Cause I'm interested in this one.

 

[zmedic]

Epi is given for pulseless Vtach.

 

[ERMedic]

It's no longer V-tach according to the scnenario, its now PEA. Giving epi is the right drug per ACLS.

 

[LondonMedic]

In the scenario you give, there's only one curative pre-hospital intervention and that's thrombolysis. Adrenaline is not going to make the situation better or worse in the immediate term.

 

[Mex EMT-I]

For all those who are in doubt.

The 2005 ACLS protocol says that you give epinephrine 1mg every 3 to 5 min to the patients that are in:

- Ventricular fibrillation.
- Ventricular tachicardia.
- Electrical activity without pulse.
- Asystole.

So this almost covers everyone that is in cardiac arrest.

 

[Veneficus]

Vene, why you say that no epi for an arrest. Are you referring to arrest as in asystole? I am no medic and I am no ACLS guy, but I have seen two people in the ER go from a line as flat as Kansas to a sinus with only epi.

I could be totally misunderstanding you also......

I am aware of the ACLS algorithms.

From my own anecdotes, I have seen epi return asystole to an organized rhythm. Not always a perfusing one, and most often the rhythm doesn't last past the life of the drug.

I have on occasion seen people resusctated for the short and sometimes long term to discharge from both Asystole and PEA. They were very few, and multiple medications were involved, so to definitively say epi helped or not is not possible and unlikely as it was always the first medication given.

The most important thing to remember about ACLS is that it is not definitive treatment. They are guidlines that are based largely off of the epidemiologically most likely pathologies.

Specific treatments for specific conditions (that can be rapidly identified clinically and reversed) is the best medicine. I believe If the AHA was even remotely concered about it, I would think looking for and identifying reversible causes would be higher on the list of priorities and far more time spent on doing it than a simple mnemonic.

as for constricting arterioles, cerebral arterioles constrict with epi, so saving heart at potentially the cost of the brain, seems like a losing strategy to me unless organ donation is your goal.

I think there are arrest conditions which can be helped by epi, but they are pathology specific.

For a real brain teaser, since arrhythmia is a leading cause of cardiac arrest post MI, why does epi supercede "consideration an antiarrhythmic" in an arrest of unknown cause?

In any case, despite the fact "advanced cardiac life support" sounds like a very indepth course. It is simply BLS with some hospital toys. Nobody can take a 16 hour course, a large protion of which is psychomotor practice, and become an expert in resuscitative medicine.

I liken it more to a procedure than actual knowledge.

 

[MrBrown]

For a real brain teaser, since arrhythmia is a leading cause of cardiac arrest post MI, why does epi supercede "consideration an antiarrhythmic" in an arrest of unknown cause?
.

Something about the alpha effect of the adrenaline to cause vascular constriction in an attempt to get nutrient and oxygen rich blood back to the heart so that when we zap em at least one pacemaker site won't be hypoxic and acidotic?

oh and those beta inotropic and chronotropic effects probably fit in there somewhere too

 

[Smash]

oh and those beta inotropic and chronotropic effects probably fit in there somewhere too

They fit on the "Bugger, that's probably bad" side of the ledger. Or the "Oh, I'm sorry about your brain damage" side. Or the "How about some extra shunt to go with that hypoxia" side. Or the "You didn't really want a contractile myocardium anyway, did you?" side. Or the... well, you get the drift.

Chances are that epi is not all that it's cracked up to be in cardiac arrest. There is no compelling evidence that epi administration increases survival to discharge in cardiac arrest. There is good data from animal models that it is good at gaining ROSC, but not much else. However, due to these studies it's se is very firmly entrenched. I would like to think that a true placebo controlled RCT could be carried out in my lifetime, but I have my doubts.

 

[Kadian Mavik]

Something about the alpha effect of the adrenaline to cause vascular constriction in an attempt to get nutrient and oxygen rich blood back to the heart so that when we zap em at least one pacemaker site won't be hypoxic and acidotic?

oh and those beta inotropic and chronotropic effects probably fit in there somewhere too

That's about what I've learned as to the why we give epi. If you think about it, giving epinephrine puts the body in survival mode (fight or flight), and that vasoconstriction is going to force blood out of unnecessary organs and into the core where it is needed.

Also, that increase in blood pressure is going to give the important organs a better shot of getting some oxygen, preventing hypoxia to a degree.

The truth really is that resuscitation is grasping at straws. Early identification of a reversible cause and ridiculously good CPR are your patient's best shot at survival.

Epinephrine can maybe add a small percentage to their likelihood of survival?

They fit on the "Bugger, that's probably bad" side of the ledger. Or the "Oh, I'm sorry about your brain damage" side. Or the "How about some extra shunt to go with that hypoxia" side. Or the "You didn't really want a contractile myocardium anyway, did you?" side. Or the... well, you get the drift.

You're not pushing epi on people who are alive anyway. Whatever you have to do to reverse that is called for.

The beta-effects as far as I know aren't an all out bad thing. Sure you increase the cardiac workload and oxygen demand, and also preload and afterload, but if you don't get the beta effects, then the heart may have NO preload, and NO oxygen.. especially after being arrested for an extended period of time.. therefore making your resuscitation efforts useless.

Epi fits into the equation well. You need a HUGE combination of things to come together well in a code to actually be successful.

Chances are that epi is not all that it's cracked up to be in cardiac arrest. There is no compelling evidence that epi administration increases survival to discharge in cardiac arrest. There is good data from animal models that it is good at gaining ROSC, but not much else. However, due to these studies it's se is very firmly entrenched. I would like to think that a true placebo controlled RCT could be carried out in my lifetime, but I have my doubts.

It may not increase the survival rate, but it certainly doesn't decrease it. Giving epi to a dead person isn't going to kill them.

Again, I think the most important thing to remember is HIGH quality CPR and early recognition/treatment of causes. Get the pt in a unit, get an airway in place, and get some big firefighters doing compressions.

 

[Veneficus]

That's about what I've learned as to the why we give epi. If you think about it, giving epinephrine puts the body in survival mode (fight or flight), and that vasoconstriction is going to force blood out of unnecessary organs and into the core where it is needed..

It will also dialate arterioles in large muscle, which is certainly not in the core. Only in certain pathologies do people run out of catecholamine, which narrows the circumstances where additional epi is needed.

As was pointed out by both Smash and myself, cerebral arterioles contract in response to epi. The beta 2 dialation effects are primarily in the lungs and secondarily in coronary arteries. Consider however that the most likely cause of sudden death is an acute thrombotic event, how helpful is some dialation going to be? A thrombus is self perpetuating. There is also the question of whether or not a large amount of arteriosclerotic plaque will prevent and effect of the epi or the possibility that migratory intima smooth muscle contraction may further degrade vascular epithelium causing secondary thrombus or increasing the surface area of the original epithelial insult perpetuating the thrombus.

Given these possibilities and the complete lack of evidence that epi increases survival, is it possible then that epi can cause harm?

The studies I am aware of do not conclusively state whether there is help or harm, but since we are dealing with sudden death in most cases, it is possible that a specific treatment may make successful resuscitation less likely for a number of reasons. With epi not least of which is cerebral anoxia.

Also, that increase in blood pressure is going to give the important organs a better shot of getting some oxygen, preventing hypoxia to a degree.

We don't know that. as I pointed out, large muscle groups dialate to epi, there is more capilary area there than in central circulation. So you might actually be losing central pressure created with CPR. Considering the bellows effect of chest compressions and the normal dialation properties of the venous system, epi might be creating an avenue for blood to exit the central circulation and not return in greater amounts than it is preserving.

Not to be a jerk, but the brain is an important organ and we know that epi reduces circulation to it.

The truth really is that resuscitation is grasping at straws.

I do not agree with this. At least not if it is done right.

Early identification of a reversible cause and ridiculously good CPR are your patient's best shot at survival.

This I do agree with.

Epinephrine can maybe add a small percentage to their likelihood of survival?

It might also take it away. That doesn't make it better than nothing.

You're not pushing epi on people who are alive anyway. Whatever you have to do to reverse that is called for.

But there are indications for using an epi drip on people who are alive to keep them so, so it is not like you do not use epi on people who are alive.

The beta-effects as far as I know aren't an all out bad thing. Sure you increase the cardiac workload and oxygen demand,.

So what happens to hibernating cardiac cells when you increase this demand? The common wisdom is that they go from a reduced metabolic demand for survial to necrosis and apoptosis. (A fancy way to say you kill potentially salvagable myocardium)

but if you don't get the beta effects, then the heart may have NO preload, and NO oxygen..,.

That is what high quality cpr is for and why it helps so much.

especially after being arrested for an extended period of time.. therefore making your resuscitation efforts useless.

with an extended downtime and no cpr, short of a hypothermic event, resuscitation efforts are useless.

Epi fits into the equation well.

The jury on this is still out, but it doesn't look good.

You need a HUGE combination of things to come together well in a code to actually be successful.

That sort of defeats the idea of a identifiable reversable cause.

It may not increase the survival rate, but it certainly doesn't decrease it. Giving epi to a dead person isn't going to kill them. .

That is not in the evidence.

Again, I think the most important thing to remember is HIGH quality CPR and early recognition/treatment of causes.

The only thing we know here for certain.

Get the pt in a unit, get an airway in place, and get some big firefighters doing compressions.

Do people die often from not having a plastic tube in their throat?

I think that you will find that the more indepth you study resuscitation, the more inadequate ACLS is past the initial steps.

 

[Kadian Mavik]

It will also dialate arterioles in large muscle, which is certainly not in the core. Only in certain pathologies do people run out of catecholamine, which narrows the circumstances where additional epi is needed.

As was pointed out by both Smash and myself, cerebral arterioles contract in response to epi. The beta 2 dialation effects are primarily in the lungs and secondarily in coronary arteries. Consider however that the most likely cause of sudden death is an acute thrombotic event, how helpful is some dialation going to be? A thrombus is self perpetuating. There is also the question of whether or not a large amount of arteriosclerotic plaque will prevent and effect of the epi or the possibility that migratory intima smooth muscle contraction may further degrade vascular epithelium causing secondary thrombus or increasing the surface area of the original epithelial insult perpetuating the thrombus.

Given these possibilities and the complete lack of evidence that epi increases survival, is it possible then that epi can cause harm?

Absolutely it's possible. That's the nature of medicine isn't it? We don't know 100% of the time how things are going to work. So we go with what seems to work best. And then 10 years later we decide what we've been doing doesn't work as well as we hoped. But then 10 years after that we bring it back :huh:

The studies I am aware of do not conclusively state whether there is help or harm, but since we are dealing with sudden death in most cases, it is possible that a specific treatment may make successful resuscitation less likely for a number of reasons. With epi not least of which is cerebral anoxia.



We don't know that. as I pointed out, large muscle groups dialate to epi, there is more capilary area there than in central circulation. So you might actually be losing central pressure created with CPR. Considering the bellows effect of chest compressions and the normal dialation properties of the venous system, epi might be creating an avenue for blood to exit the central circulation and not return in greater amounts than it is preserving.

Not to be a jerk, but the brain is an important organ and we know that epi reduces circulation to it.

... I wonder what the use of a functioning brain is when you have no circulation though..

The problem inherent in ACLS treatment is that it is massively generalized. ACLS, as I understand it, is a treatment plan based on statistics, be them accurate or not.

It reminds me that the best medics aren't the ones who know their protocols/ACLS/PALS the best, but the ones who know their A&P and pharmacology.

I do not agree with this. At least not if it is done right.

Hrmm.. I think we're going to have to agree to disagree here. When I say Resuscitation is inherently grasping at straws, I don't mean it shouldn't be done, and that it doesn't ever work. I just mean that it rarely succeeds. Which the statistics show.

But there are indications for using an epi drip on people who are alive to keep them so, so it is not like you do not use epi on people who are alive.

Okay, yes, but I was talking about the use of Epi in arrested patients.

That is what high quality cpr is for and why it helps so much.

True.. then maybe we should be doing CPR for much longer periods of time before we call our patients? Giving their hearts a chance to take over without the use of Epi? I'd be interested to know if that worked better.

with an extended downtime and no cpr, short of a hypothermic event, resuscitation efforts are useless.

My county is bringing in induced hypothermia for this very situation

Do people die often from not having a plastic tube in their throat?

I think that you will find that the more indepth you study resuscitation, the more inadequate ACLS is past the initial steps.

People aspirate when they're on the way out. An ET/ Combitube/ King Airway can prevent that. I don't think there are any reasons to NOT drop an advanced airway on a coded patient?