ACLS Medications, ROSC, and Theraputic Hypothermia

[SeeNoMore]

Hey all,

I know this has been a thread before, but after some searching I can not find it (it was a long time ago) and as I recall it did not get many responses. In addition I can find nothing about it online.

So here is my question, if any can answer it or give me suggestions of where to look for information I would appreciate it.

Q) It seems that ACLS medications have show know decrease in patient mortality but can perhaps increase ROSC.

However, I know there has been a lot of work done on prehospital hypothermia for pt's who get ROSC.

Does it then follow that ACLS drugs could become more important with the increased use of hypothermia for cardiac arrest, given that the therapy is available for those who get ROSC? Or are the pts who benefit from this tx usually those who have regained a pulse from rapid defib?

Thanks

 

[Veneficus]

Does it then follow that ACLS drugs could become more important with the increased use of hypothermia for cardiac arrest, given that the therapy is available for those who get ROSC?

In my opinion, no, they will not be more important.

The major problem with survival to discharge is that the patient who arrests needs to have a disease process that is survivable past the acute phase.

As an example, if you have a patient go into cardiac arrest from arrhythmia secondary to cardiomyopathy, when all the toys and drugs get an ROSC, it doesn't increase the ejection fraction of the heart, and while that person can be maintained on life support, they may never have anything else. (obviously until LVADS become more common)

But the same can be true of other disease processes.

I think many people see a cardiac arrest as an acute event, and usually nothing can be farther from the truth. Most often it is the end result of the body failing to compensate for damage it has suffered for years if not decades. Only so much can be done for that.

 

[Shishkabob]

My honest, down to Earth view of long-term survivability and cardiac drugs?

Can't have more neurologically-intact survivals without having more ROSC, and cardiac drugs have shown an increase in ROSC and admissions. Now we just need to figure out how to translate ROSC to survival.


With the caveat that with some people, when it's their time to go, it's their time no matter how good we are and how far science progresses.

 

[Veneficus]

My honest, down to Earth view of long-term survivability and cardiac drugs?

Can't have more neurologically-intact survivals without having more ROSC, and cardiac drugs have shown an increase in ROSC and admissions. Now we just need to figure out how to translate ROSC to survival.


With the caveat that with some people, when it's their time to go, it's their time no matter how good we are and how far science progresses.

I once thought exactly the same way.

Then my physiology and biochemistry professors in medical school demonstrated the flaw in my logic.

When I first started in EMS, the combination of epi and levofed could get a heart to beat no matter the down time it seemed. So I figured that the problem with long term survival must be a hospital failure.

The problem is there are multiple important organs in the body. Not just the heart/brain/kidneys. Just because it is possible to save one, doesn't make it possible to save them all. By understanding how cells and organs die, I have been confronted with the futility of some of our efforts.

Scientifically, making a heart beat is a fairly simple task. The body is an electrical current in a watery medium. We can of course reproduce not only the current but the medium as well. Experiments are done almost daily on animals. The still beating hearts are removed, the animal euthanized, and then the heart is placed is a liquid medium that not only has nutrients, but maintains the electro/chemical polarities required. We can then chemically stimulate the heart. Mechanically stimulate it. Electrically stimulate it. Cut out the parts we don't want to study and leave only a still working atria or a ventrical. This can be done for days. Sometimes as long as a week or more on a single heart or piece of one.

We can play with the admixtures to see what the reactions are, but we cannot simply put the animal on a cardio bypass and put it all back.

In the grand game of homeostasis, certain organs operate on a very narrow margin. The kidney being the dominant one. Once Acute tubular necrosis sets in, the best we can hope for is lifelong dialysis. But when other organs start to fail, it becomes tougher for a save. So you save the heart at the cost of brain, already lost kidney, and now start to see liver and gut malfunctions. Nutrients cannot be absorbed, toxic metabolites cannot be converted, and we haven't talked about the initial loss, or reperfusion injuries.

Once apoptotic cascades start they are irreversible. On average it takes about 4 days. Sometimes more, sometimes less. Depends on a host of factors.

At some point the game is up. We cannot reverse the death. But we have the power to sustain some of the organism (notice I didn't say person) indefinately. They will not wake up, they will not go home, they will be utterly dependant on our machines and maniplation of the chemical environments. It is worse than a vegetable, because a vegatable can at least reproduce or react to its environment. Eventualy somebody will have to make the decision to remove this support. The emotionl and economic tolls not even spared a thought.

The ability to make a heart beat chemically, is of absolutely no use or importance at all. Like I said, with the right combination of chemicals, it doesn't even have to be in the body.

 

[Shishkabob]

Ah, but we only need look at therapeutic hypothermia and it's (relatively) drastic increase in survival-to-discharge from ROSC to show that more can survive than previously thought.

As science progresses, new things will be discovered to slightly push who CAN make it to discharge compared to those of today. But like I said, you can't have survival without having ROSC first. ROSC tends to happen more with the drugs we have. The studies I've read don't dispute the increase in ROSC from the cardiac drugs, just the rate of discharge, which tends to be minuscule in comparison.




Granted I'm not the biggest fan of Epi in cardiac arrest... and I DID state that just because we get more back doesn't mean all will live, due to the stress put on the body in the time it goes without adequate perfusion.

 

[Veneficus]

Ah, but we only need look at therapeutic hypothermia and it's (relatively) drastic increase in survival-to-discharge from ROSC to show that more can survive than previously thought.

As science progresses, new things will be discovered to slightly push who CAN make it to discharge compared to those of today. But like I said, you can't have survival without having ROSC first. ROSC tends to happen more with the drugs we have. The studies I've read don't dispute the increase in ROSC from the cardiac drugs, just the rate of discharge, which tends to be minuscule in comparison.




Granted I'm not the biggest fan of Epi in cardiac arrest... and I DID state that just because we get more back doesn't mean all will live, due to the stress put on the body in the time it goes without adequate perfusion.

But it is only ROSC if it lasts past the life of the drug. You cannot send people home on epi drips or whatever medication keeps the heart functioning.

 

[Shishkabob]

But it is only ROSC if it lasts past the life of the drug. You cannot send people home on epi drips or whatever medication keeps the heart functioning.

If they stay neurogically intact, why not?

Not really philosophically different from dialysis or any other long term, life sustaining treatment.

 

[Veneficus]

If they stay neurogically intact, why not?

Not really philosophically different from dialysis or any other long term, life sustaining treatment.

It is when you consider that you can have dialysis a few times a week, or for a few hours everyday, compared to how often you would have to change out a drip.

The other issue is while you can keep people alive, neuro intact is yet another very difficult stage to attain. Sure a GCS of 13 or better would be ideal, but where do you draw the line?

 

[jrm818]

I once thought exactly the same way.

Once apoptotic cascades start they are irreversible. On average it takes about 4 days. Sometimes more, sometimes less. Depends on a host of factors.

What if we could reverse the irreversible?

http://www.ncbi.nlm.nih.gov/pubmed/19628092




Granted I think this might arguably be preventing the beginning of the cascade, but I'm under-educated in cell bio, so I'm not sure.

 

[MrBrown]

The year was 1993, a gaggle of Ambulance Officers were in school upskilling to Paramedic (Advanced Care/Mobile Intensive Care Officer) and it was said that medications haven't been proven to work, all they do is change the environment slightly to make defibrillation more effective.

And yet nearly twenty years later we still cannot get that through our heads.

What is the five year survival rate for people who have cardiac arrest and leave hospital? Poor Brown bets you.

 

[Smash]

The trouble with ACLS meds is that while they improve your chances of getting ROSC, this seems to come at the expensive of longer term outcome, particularly neurological outcome. There is not much point in getting someone "back" if they are going to sit in the corner and be watered twice a day for the rest of their lives.

Therapeutic hypothermia is definitely an important part of post-arrest care, but at this stage there really isn't the evidence that it is an important part of prehospital post-arrest care.
My personal feeling is that it is important in the field, but that it needs to be part of a considered and targeted care bundle that includes hemodynamic optimization, hemodilution and hypothermia and early revascularisation (where indicated)

I personally think (with no evidence, merely my 'gut') that hypothermia should probably be started early (during the arrest) with cold fluid to mitigate the repercussion injury in a similar fashion to managing crush injury. I could be wrong but we will have to wait and see.

 

[Veneficus]

What if we could reverse the irreversible?

http://www.ncbi.nlm.nih.gov/pubmed/19628092




Granted I think this might arguably be preventing the beginning of the cascade, but I'm under-educated in cell bio, so I'm not sure.

According to the study it was supposed to up regulate the inhibitors of apoptosis. It is prevention, not a reversal.

 

[SeeNoMore]

So pts with ROSC from ACLS drugs are not the patients who have been able to walk out of the hospital with neurological function intact after hypothermic treatment?

I assume those pts are special cases where early cpr and defib has been performed and then they see the benefits of in hopsital hypothermia?


Anyway thanks for the respsonses, very interesting. My basic thinking was that if drugs resulted in more ROSC, and theraputic hypothermia was able to improve results for ROSC patients, it would therefore be important to use ACLS drugs. I see it's perhaps not so simple.

When do we get them of the truck then if they don't matter? It's a little odd to be practicing scenarios and memorizing drugs for treatments that don't matter. But I guess you can't change EMS over night.

 

[Ravemtech]

The new 2010 guidelines have suggested that with the introduction of Therapeutic Hypothermia, we will need to revisit the effectivness of many of the arrest drugs that gave ROSC but not increased discharge.

I think this basically sums it up. May be the cooling was the missing link that we needed. Until we restudy these drugs under ideal controlled trials, resonable response times, good apppropriate and measured CPR quality to ensure we are measuring apples against apples, and with the addition of Therapeutic Hypothermia, we do not know the answer.

So to answer your initial question, the 2010 Guidelines are asking the very same question. Only time will tell. Let the studies begin.

 

[jjesusfreak01]

No arrests leave the hospital unless you get ROSC at some point. Sure, some of the people we get back may not walk out of the hospital, but does this mean it isn't a good thing to get them that far? Remember, you may only be giving family members one last chance to say goodbye, but there's nothing wrong with that.

Think of our improved ability to get ROSC as practice for the future when new procedures allow us to get more of these patients walking out of the hospital intact.

 

[Veneficus]

If only life were simple

Resuscitation experts around the world have eliminated epi as a primary cardiac arrest drug yet the AHA still has it as the first drug in the algorythm?

Everytime some new guidlines come out everyone jumps on the "maybe it will work this time bandwagon."

At what point do you give up on outdated practices?
(In US EMS, never.)

Giving families a chance to say "goodbye" is not reason enough to go around abusing corpses, nor creating medical bills in the 10s of thousands for futile efforts. Those bills are not forgiven when patients die. Which can lead to very real and harsh consequences for the survivors.

There is a big difference between giving a patient every possible chance and making the provider feel better about themselves.

Both epi and atropine increase metabolism. The purpose of hypothermia is to decrease metabolism. (See the conflict?)

The use of an antiarrhythmic is to chemically alter the electrophyiological effects of the heart. In all emergency treatments, electrotherapy is demonstrated as the most beneficial and the most likely to improve outcome. If electrical doesn't work is there a realistic purpose to trying therapies that are not shown to work or have no statistical value?

If there was really an effort to identify reversible causes beyond epidemiology, perhaps these therapies would be more beneficial. If there were prehospital therapies directed at the underlying causes like clot dissolution maybe there would be a difference in outcome.

BUt the fact remains that the purpose of ACLS is to be simple. Bringing back people from the dead is anything but simple. It doesn't fit neatly into an algorythm. It doesn't follow a set order of operation. To think otherwise is just foolishness.

Increases in out of hospital arrest survival are going to come from bystander CPRnot from 4 or 6 or 8 or <9 minute response times 90% of the time. People in arrest for those times are likely dead unless there are mitigating factors that are rarely even mentioned in ACLS.

There is a Pittsburg physician who studies resuscitation extensively who has postulated perhaps we are doing just the opposite of what we need to.

What if CPR, defib, early hypothermia, and no oxygen is the formula as he has suggested? His save rates seem to suggest he is right.

Until people start working with the cellular, molecular, and biochemical mechanisms of an arrest, they are not going to be the "experts" needed to save lives.

Simply hoping to constantly work with oversimplified concepts and get different results doesn't demonstrate knowledge but desperation.

How heroic.

How many years and studies does it take to figure out when something is not dramatically helping?

 

[mgr22]

That's a top-ten post, Veneficus.

 

[Epi-do]

I was reading a similar thread on a different board, and someone posted the following:

Remember when we are coding someone we are attempting to reverse death. No one is ever the same after they die, the question is how will they be different.

This comment was made by an RN that works in the ICU and a large hospital in my area. I think it really helps to put into perspective what we are doing in a cardiac arrest.

I am not saying that 100% of cardiac arrests are futile and we should just walk away from all of them. However, maybe if we looked at cardiac arrest as "reversing death" as opposed to "treating death" we would begin to have a better understanding of what we are trying to accomplish when working towards ROSC.

 

[Mobey]

Resuscitation experts around the world have eliminated epi as a primary cardiac arrest drug yet the AHA still has it as the first drug in the algorythm?

Everytime some new guidlines come out everyone jumps on the "maybe it will work this time bandwagon."

At what point do you give up on outdated practices?
(In US EMS, never.)

Giving families a chance to say "goodbye" is not reason enough to go around abusing corpses, nor creating medical bills in the 10s of thousands for futile efforts. Those bills are not forgiven when patients die. Which can lead to very real and harsh consequences for the survivors.

There is a big difference between giving a patient every possible chance and making the provider feel better about themselves.

Both epi and atropine increase metabolism. The purpose of hypothermia is to decrease metabolism. (See the conflict?)

The use of an antiarrhythmic is to chemically alter the electrophyiological effects of the heart. In all emergency treatments, electrotherapy is demonstrated as the most beneficial and the most likely to improve outcome. If electrical doesn't work is there a realistic purpose to trying therapies that are not shown to work or have no statistical value?

If there was really an effort to identify reversible causes beyond epidemiology, perhaps these therapies would be more beneficial. If there were prehospital therapies directed at the underlying causes like clot dissolution maybe there would be a difference in outcome.

BUt the fact remains that the purpose of ACLS is to be simple. Bringing back people from the dead is anything but simple. It doesn't fit neatly into an algorythm. It doesn't follow a set order of operation. To think otherwise is just foolishness.

Increases in out of hospital arrest survival are going to come from bystander CPRnot from 4 or 6 or 8 or <9 minute response times 90% of the time. People in arrest for those times are likely dead unless there are mitigating factors that are rarely even mentioned in ACLS.

There is a Pittsburg physician who studies resuscitation extensively who has postulated perhaps we are doing just the opposite of what we need to.

What if CPR, defib, early hypothermia, and no oxygen is the formula as he has suggested? His save rates seem to suggest he is right.

Until people start working with the cellular, molecular, and biochemical mechanisms of an arrest, they are not going to be the "experts" needed to save lives.

Simply hoping to constantly work with oversimplified concepts and get different results doesn't demonstrate knowledge but desperation.

How heroic.

How many years and studies does it take to figure out when something is not dramatically helping?

This is a good read, but it would be nice to see some studies to back up your claims.

 

[Veneficus]

This is a good read, but it would be nice to see some studies to back up your claims.

Studies of what?

That electrical therapy is the prefered treatment in unstable cardiac patients like vfib, vtach, svt, etc?

Perhaps the the very AHA studies that are published in their instructor/experienced provider manual show no statistical benefit of the recommended cardiac arrest medications?

I cannot find the original copy of the oxgen study but here is a summary of the one I recall.

http://www.kevinmd.com/blog/2010/06/supplemental-oxygen-cardiac-arrest-resuscitation.html

Do you need a study to demonstrate epi and atropine increase metabolic demand? All I needed was a pharm class.

Why don't you look at the current NRP guidlines about supplemental oxygen. Perhaps an article or two on reperfusion injury.

Perhaps you doubt that finding and reversing an acute pathology will have better outcomes than mindlessly running a guidline?

What is next?