Acute MI to Cardiac Arrest

[Veneficus]

... 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.

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.

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?

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.

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.

 

[JPINFV]

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.

 

[Veneficus]

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.

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.

 

[Kadian Mavik]

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.

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.

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.

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..

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.

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.

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.

 

[Veneficus]

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)

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.

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.

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.

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.

 

[Hellsbells]

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.

 

[Smash]

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 defibrillation, 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.

 

[Charmeck]

Bumping.