# Acute MI to Cardiac Arrest



## d3653je (Sep 6, 2010)

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?


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## Veneficus (Sep 6, 2010)

d3653je said:


> 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.



d3653je said:


> 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."


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## Lifeguards For Life (Sep 6, 2010)

Veneficus said:


> 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.


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## Veneficus (Sep 6, 2010)

Lifeguards For Life said:


> 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.


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## Mex EMT-I (Sep 10, 2010)

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.


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## Akulahawk (Sep 10, 2010)

d3653je said:


> 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.
> 
> ...


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


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## MrBrown (Sep 11, 2010)

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.


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## zmedic (Sep 11, 2010)

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.


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## lightsandsirens5 (Sep 11, 2010)

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......


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## lightsandsirens5 (Sep 12, 2010)

lightsandsirens5 said:


> 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.


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## zmedic (Sep 12, 2010)

Epi is given for pulseless Vtach.


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## ERMedic (Sep 12, 2010)

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


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## LondonMedic (Sep 13, 2010)

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.


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## Mex EMT-I (Sep 13, 2010)

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.


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## Veneficus (Sep 13, 2010)

lightsandsirens5 said:


> 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.


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## MrBrown (Sep 14, 2010)

Veneficus said:


> 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


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## Smash (Sep 14, 2010)

MrBrown said:


> 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.


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## Kadian Mavik (Sep 20, 2010)

MrBrown said:


> 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?





Smash said:


> 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. 



Smash said:


> 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.


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## Veneficus (Sep 20, 2010)

Kadian Mavik said:


> 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. 



Kadian Mavik said:


> 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.



Kadian Mavik said:


> The truth really is that resuscitation is grasping at straws.



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



Kadian Mavik said:


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



This I do agree with.



Kadian Mavik said:


> 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.




Kadian Mavik said:


> 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.



Kadian Mavik said:


> 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)



Kadian Mavik said:


> 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.



Kadian Mavik said:


> 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.



Kadian Mavik said:


> Epi fits into the equation well.



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



Kadian Mavik said:


> 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. 



Kadian Mavik said:


> 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.



Kadian Mavik said:


> 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.



Kadian Mavik said:


> 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.


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## Kadian Mavik (Sep 20, 2010)

Veneficus said:


> 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:



Veneficus said:


> 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.
> 
> 
> 
> ...



... 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.




Veneficus said:


> 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.



Veneficus said:


> 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.




Veneficus said:


> 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.




Veneficus said:


> 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 



Veneficus said:


> 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?


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## Veneficus (Sep 20, 2010)

Kadian Mavik said:


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



I was trying to make the point that it is an all or nothing deal. If you focus on the heart at the cost of all else, the patient will not leave the hospital neurologically intact, making the resuscitation effort pointless.

However, an LVAD or a internal pacemaker may solve the problem post resuscitation. 



Kadian Mavik said:


> 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.



That is true, but the epidemiology is established. The real secret to ACLS is hoping your patient falls into it. Once you identify a reversible cause, ACLS goes right out the window.



Kadian Mavik said:


> 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.



I do not think it is a haphazard grasping at straws, I think it is a logical progression of trying to seek out and treat reversible causes. There are often times none can be identified, but how often do those patients survive to discharge when you can't find one?




Kadian Mavik said:


> 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..



Given that in an unwitnessed arrest best practice is shown to give 2 minutes of CPR prior to defib in vfib/pulseless VT, another 2 mnutes of CPR and shock prior to the first epi, as well as continuing CPR after the shock unless signs of life are present, I think there might be a move towards more CPR prior to giving medications. 

The salvage rate of asystole and PEA is so abysmal, I am not sure it will matter for that.




Kadian Mavik said:


> 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?



But do you get there before they go out very often? It is likely they aspirate before a tube is introduced. More importantly before you can worry about post resuscitation complications, you have to have a resuscitation.

Aside from lack of provider skill, I can see no reason not to use an advanced airway, but I also don't see the use in delaying CPR of other measures in order to get one either.


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## JPINFV (Sep 20, 2010)

Veneficus said:


> 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.



This was actually something comically (because we had 3 questions between two different professors regarding epi vs norepi) pounded into us during endocrine.

Epinephrine: Alpha, Beta 1, *2*, and Beta 3

Norepinephrine: Alpha, Beta 1, Beta 3 (no beta 2)

As such in a healthy patient the following effects are found:

Epinephrine: Increase in contractility, vasodilation of liver and skeletal muscles (which deceases PVR), vasoconstriction elsewhere, increase in systolic pressure, decrease in diastolic pressure and *increase in heart rate.*

Norepinephrine: Increase in contractility, vasoconstriction, increase in systolic pressure, increase in diastolic pressure, and because of feedback mechanisms, *decrease in heart rate. *

Now, the million dollar question is why not norepinephine in cardiac arrest than epinephrine, and from doing a cursory search online, norepi isn't supported for cardiac arrest in the studies done.


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## Veneficus (Sep 20, 2010)

JPINFV said:


> This was actually something comically (because we had 3 questions between two different professors regarding epi vs norepi) pounded into us during endocrine.
> 
> Epinephrine: Alpha, Beta 1, *2*, and Beta 3
> 
> ...



Actually, many years ago Levo was part of the cardiac arrest cocktail. (high dose epi, up to 5mg 1:1000 and levofed) hense the saying "leave 'em dead."

As it turned out, it did help with short term resuscitation (and many EMS groups jumped on the "pulse at ED delivery" stats. However when the chemical effect wore off, the patient was back to dead.), but fell flat on the dischage neurologically intact.


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## Kadian Mavik (Sep 20, 2010)

Veneficus said:


> I was trying to make the point that it is an all or nothing deal. If you focus on the heart at the cost of all else, the patient will not leave the hospital neurologically intact, making the resuscitation effort pointless.



It SHOULD be an all or nothing deal.. but it isn't, especially in a court of law. I personally don't want to be resuscitated if I'm brain dead, and I've made those wishes clear to my family, but some people don't agree. 

But, that being said.. alive and brain dead is better than dead to some people. 



Veneficus said:


> However, an LVAD or a internal pacemaker may solve the problem post resuscitation.



I get what you're saying to a certain degree.. The heart is more replaceable than the brain. But, is CPR effective enough to keep the brain oxygenated without the use of a vasoconstrictor? If I recall, even the best CPR can only output something like 35% of normal cardiac output. I seem to remember hearing that in class. 




Veneficus said:


> That is true, but the epidemiology is established. The real secret to ACLS is hoping your patient falls into it. Once you identify a reversible cause, ACLS goes right out the window.



Pretty much yea. 



Veneficus said:


> I do not think it is a haphazard grasping at straws, I think it is a logical progression of trying to seek out and treat reversible causes. There are often times none can be identified, but how often do those patients survive to discharge when you can't find one?



Maybe I should use a better phrase than grasping at straws.. Resuscitation is like.. I dunno.. it's a last ditch effort where you can try your absolute best, and you very well might fail regardless..



Veneficus said:


> Given that in an unwitnessed arrest best practice is shown to give 2 minutes of CPR prior to defib in vfib/pulseless VT, another 2 mnutes of CPR and shock prior to the first epi, as well as continuing CPR after the shock unless signs of life are present, I think there might be a move towards more CPR prior to giving medications.



That seems the way AHA is going anyway.. More CPR, more compressions. Considering the above fact that the best CPR is yielding something like 35% normal cardiac output, you probably need more than 5 cycles of CPR to adequately perfuse the heart. It's pointless to Defib/Push an antiarrythmic on a hypoxic heart. I think we might see better results if we go to a 50:2 ratio of compressions.



Veneficus said:


> But do you get there before they go out very often? It is likely they aspirate before a tube is introduced. More importantly before you can worry about post resuscitation complications, you have to have a resuscitation.



Again, there is no reason not to tube them anyway. Maybe if you're the only ALS provider, you might not prioritize it, but where I run, we have two ALS providers on a medic unit. And we get an engine/BLS unit on any code we run. There are more than enough hands to drop a combitube, do compressions and all that.

Once you have an advanced airway in place, you can assure adequate oxygenation, while performing continuous uninterrupted compressions, which I think is the most effective treatment anyway.



Veneficus said:


> Aside from lack of provider skill, I can see no reason not to use an advanced airway, but I also don't see the use in delaying CPR of other measures in order to get one either.



I agree, if those are your circumstances. I myself have never run a code with less than 4 people in the back of the unit, so there are plenty of folks to get the job done. One ALS on IV/Meds, one ALS on Airway and two BLS on compressions and BVM.


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## Veneficus (Sep 20, 2010)

Kadian Mavik said:


> It SHOULD be an all or nothing deal.. but it isn't, especially in a court of law. I personally don't want to be resuscitated if I'm brain dead, and I've made those wishes clear to my family, but some people don't agree.
> 
> But, that being said.. alive and brain dead is better than dead to some people.



I think this is why the healthcare provider needs to determine who is being resuscitated and when. (in many of the places I worked in the field ALS could decide to not inititate or discontinue efforts)

The fear of letting go or the idea that death can be forever avoided is rampant, but there are both emotional and serious financial ramifications of hopeless resuscitation.

As healthcare provders, EMS needs to be able to step up and have the objectivity and authority to decide when a resuscitation effort is futile. (the courage should be included in that too probably)



Kadian Mavik said:


> I get what you're saying to a certain degree.. The heart is more replaceable than the brain. But, is CPR effective enough to keep the brain oxygenated without the use of a vasoconstrictor? If I recall, even the best CPR can only output something like 35% of normal cardiac output. I seem to remember hearing that in class. .



But if the vasoconstrictor lowers the amount of oxygenated blood going to the brain, which seems the case with both epi, levofed, and by mechanism dopamine, then the efficency of CPR goes down lower. Which I think we both agree would be counter productive. That is one of the main arguments against the use of epi.




Kadian Mavik said:


> That seems the way AHA is going anyway.. More CPR, more compressions. Considering the above fact that the best CPR is yielding something like 35% normal cardiac output, you probably need more than 5 cycles of CPR to adequately perfuse the heart. It's pointless to Defib/Push an antiarrythmic on a hypoxic heart. I think we might see better results if we go to a 50:2 ratio of compressions.



If you didn't know, the 100 compressions per minute was actually based on the consensus of how many quality compressions the average person could do for 2 minutes. The actual most effective as I remember was around double, but the ability to compress properly dropped off sharply.



Kadian Mavik said:


> Again, there is no reason not to tube them anyway. Maybe if you're the only ALS provider, you might not prioritize it, but where I run, we have two ALS providers on a medic unit. And we get an engine/BLS unit on any code we run. There are more than enough hands to drop a combitube, do compressions and all that.



I have done the gambit of just me and my EMT-B partner would be the only response, 3 guys on the squad, 8 guys on the rescue company 3 of which were als providers, and the hospital with all the help you could want. I try to work with what is globally possible.



Kadian Mavik said:


> Once you have an advanced airway in place, you can assure adequate oxygenation, while performing continuous uninterrupted compressions, which I think is the most effective treatment anyway.



That is the ideal.


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## Hellsbells (Sep 22, 2010)

> 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)



Interesting, particularly because we are going in the induced hypothermic protocols in our service, It seems a bit counterproductive to give Epi while cooling the rest of the body, doing one thing to slow the metabolism and another to increase it. 

As to the question posed by the OP, I'd argue that the scenario he plays out is unlikely to occur quite the way he states it. Nitro typically works better for those with Angina, so its possible that at the outset of his scenario the pt had an incomplete block that progressed to a full blockage, leading to the V-Tach, then arrest. However, at the point of a full blockage, Nitro can no longer dilate the vessel enough for blood to pass through, which is why the pt coded in the first place, ergo he died because the Nitro had already failed to work. So the debate of Nitro vs Epi is moot. However, the debate for Epi vs No Epi rages on.


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## Smash (Sep 22, 2010)

Hellsbells said:


> Interesting, particularly because we are going in the induced hypothermic protocols in our service, It seems a bit counterproductive to give Epi while cooling the rest of the body, doing one thing to slow the metabolism and another to increase it.



It's an interesting conundrum, but not entirely new.  We have been striking this problem pretty much forever with resuscitation, vis a vis giving lidocaine (now amiodarone) and epi.  Epi is positively bathmotropic, that is, it increases excitability and therefore increases the desire of the myocardium to fibrillate.  So we give lido, to decrease that desire to fibrillate.  Unfortunately that then makes the myocardium more resistant to _de_fibrillation, which is the one thing we really want to work.  Bummer.

Thereapeutic hypothermia however is addressing a number of problems in the post-arrest patient (and maybe in the peri-arrest patient one day)  Have a look at the thread I started called "Post Cardiac Arrest Management" or some such thing for more on cooling the patient post arrest.


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## Charmeck (Oct 8, 2010)

Bumping.


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