STEMI and use of Nitro

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d3653je

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Asked this question in Medic Class and got a shrugged shoulder answer.

You are treating a pt. who is having an AMI, confirmed with your 12-lead. You give your pt. nitro with the hopes of dilating the coronary arteries...among other things/reasons as well. The pt. goes into cardiac arrest, lets say v-fib that converts to asystole with defibirlation. Per protocol you push 1mg of epi.

My questions are if the reason for the infarct is a blood clot in a coronary artery and nitro is given with the intention to dilate that vessel, would giving epi then constrict the same artery and cause more ischemia to the heart? Could vasoconstrictors be making things worse?

Also instead of starting another thread and it is along the same lines... the Lucas Device is now being rolled out in my neck of the woods. Medivacs in this region do not like to fly arrests... do you see that changing with the use of this device?
 
You can get worse ischemia and worse patient condition than cardiac arrest?
 
d3653je said:
Asked this question in Medic Class and got a shrugged shoulder answer.

You are treating a pt. who is having an AMI, confirmed with your 12-lead. You give your pt. nitro with the hopes of dilating the coronary arteries...among other things/reasons as well. The pt. goes into cardiac arrest, lets say v-fib that converts to asystole with defibirlation. Per protocol you push 1mg of epi.

My questions are if the reason for the infarct is a blood clot in a coronary artery and nitro is given with the intention to dilate that vessel, would giving epi then constrict the same artery and cause more ischemia to the heart? Could vasoconstrictors be making things worse?

Also instead of starting another thread and it is along the same lines... the Lucas Device is now being rolled out in my neck of the woods. Medivacs in this region do not like to fly arrests... do you see that changing with the use of this device?
Click to expand...

Once the patient is in cardiac arrest, treating the arrhythmia becomes the highest priority.
 
Yeah, the arrest is a bigger deal.

...and the Lucas device is great. We don't fly CPR, however.


Sent from my iPhone.
 
Epi is probably going to be demonstrated as being useless for cardiac. Some smaller pig studies have already done so.
 
Actually, Epi has been proven to be beneficial in cardiac arrests.




Just not quite in long term survival or survival to discharge.
 
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if the person goes into asystole, then treat them as a full arrest, no need to even bother with thinking about ischemia, and we currently use the lucas device down here, AMAZING tool, frees up alot of hands to help with other things on scene, however we do not fly any kind of arrest, only things we fly here are trauma, we are so close to hospitals it makes no sense for us to take a copter out of service to fly an arrest, and if a patient begins to arrest due to trauma we take them to the closest facility
 
I think the OP asks a very valid question. It does seem contradictory to one minute have the goal of venous and coronary artery dilation and than a few moments later when the patient arrests the focus is vasoconstricting.

In arrest though cardiac output even with maximized CPR is quite low. Without giving epi to increase the coronary and cerebral perfusion pressures, I'm not sure if we would be giving the patient the best chance of gaining a ROSC.

I honestly don't have the answer to the question and perhaps nobody does yet. There is a recent animal study dealing with vasodilation in cardiac arrest. It will be interesting to see if epi eventually disappears like atropine did for cardiac arrest. But don't foresee that happening for a really long time.
 
d3653je said:
Medivacs in this region do not like to fly arrests... do you see that changing with the use of this device?
Click to expand...
Only in very certain circumstances. A few points;

An arrest is almost always a dead body so it makes little sense to risk a helicopter and crew to transport to the morgue.

An arrest has a better outcome if it's treated on scene and not moved until perfusion has returned and stabilised. Moving patients in arrest stops CPR and empties the coronary circulation, worsening outcomes.

LUCAS is an excellent tool, however, I'm not sure whether it is cleared for use in aircraft - patients may not be flyable when it's connected.
 
d3653je said:
Asked this question in Medic Class and got a shrugged shoulder answer.

You are treating a pt. who is having an AMI, confirmed with your 12-lead. You give your pt. nitro with the hopes of dilating the coronary arteries...among other things/reasons as well. The pt. goes into cardiac arrest, lets say v-fib that converts to asystole with defibirlation. Per protocol you push 1mg of epi.

My questions are if the reason for the infarct is a blood clot in a coronary artery and nitro is given with the intention to dilate that vessel, would giving epi then constrict the same artery and cause more ischemia to the heart? Could vasoconstrictors be making things worse?

Also instead of starting another thread and it is along the same lines... the Lucas Device is now being rolled out in my neck of the woods. Medivacs in this region do not like to fly arrests... do you see that changing with the use of this device?
Click to expand...

18G said:
I think the OP asks a very valid question. It does seem contradictory to one minute have the goal of venous and coronary artery dilation and than a few moments later when the patient arrests the focus is vasoconstricting.

In arrest though cardiac output even with maximized CPR is quite low. Without giving epi to increase the coronary and cerebral perfusion pressures, I'm not sure if we would be giving the patient the best chance of gaining a ROSC.

I honestly don't have the answer to the question and perhaps nobody does yet. There is a recent animal study dealing with vasodilation in cardiac arrest. It will be interesting to see if epi eventually disappears like atropine did for cardiac arrest. But don't foresee that happening for a really long time.
Click to expand...

You can't kill a dead man. In the absence of a pulse you give epi.

In reference to crews not liking to fly arrests, depending on the aircraft's internal configuration it would be in useless to fly an arrest for this reason.

Federal Aviation Regulations (FAR's) state that ALL passengers will be seated and in full restraints during all critical phases of flight (take offs and landings) and as deamed necessary by the Pilot In Command (PIC). Because of this it is impossible (depending on configuration [which is all if not most aircraft]) to do effective CPR during take offs and landings resulting in the air crew delivering the ER a cadavar en lieu of a pt.
 
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Linuss said:
Actually, Epi has been proven to be beneficial in cardiac arrests.




Just not quite in long term survival or survival to discharge.
Click to expand...

Beneficial, but not in any way that is meaningful to patients...
 
Only in relation to Lucas. (Note the -B next to my name) Awesome tool, however the only instance we used it AND flew the arrest the flight crew looked at it, asked what it was, then took it off. Just a personal experience there.
 
Smash said:
If it doesn't benefit patients, in what way can it be said to be "beneficial"?
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If Epi increases the chance of getting a ROSC how is that not beneficial? I've yet to see anything contrary to that finding.
 
18G said:
If Epi increases the chance of getting a ROSC how is that not beneficial? I've yet to see anything contrary to that finding.
Click to expand...

Try asking the vast numbers of patients who get ROSC whether they think it is beneficial.

Oh wait, you can't, they're dead.

Increased ROSC as a result of the administration of epi does not result in increased survival to discharge. Survival to discharge (with some level of neurological function) is the only meaningful, patient orientated outcome there is. Epi does not improve this, and there is also a very valid argument that not only does it not improve such an outcome, but that it may in fact worsen neurological outcome.
 
Another point that's been missed is NTG has very little effect if the coronary vessels and is almost never going to have beneficial effect in the case of occlusive MI.
 
My school of thought is this when it comes to flying cardiac arrests of any etiology. I preface this by saying by ground/air the nearest level II is 20/10 minutes away. Nearest level I is 30/15 respectively.

With the lucas device in place, effective compression can be done during any part of the flight. In theory that would address some of the FAA concerns.

Another thing comes to mind as well and that is this pt who has expired is dead however the internal organs that could be removed and transplanted, could save countless lives. Of course this is case by case. I would be thinking more along the lines of single system traumas, ie gsw to head. if that goes to the local ER chances are slim the organs will be viable. Again case by case and hospital by hospital.

The theory is beyond our scope right now but suppose some type of in the field assessment could be done by a Paramedic and Med-Control to decide if these organs can be saved. the fact that driver's licenses state if one is a donor seems like a slam dunk consent wise.
 
Flying patients is dangerous enough. There's no excuse to put a dead body in the aircraft. Putting three lives at risk for someone who is confirmed to be dead is risk management.
 
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