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treatment for the brady MI


fiznat

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Your patient:

78 y/o female at a skilled nursing facility (SNF) complaining of nausea, weakness, and 8-10 "chest pressure" radiating down the left arm. Tingling in the fingers, skin cool/pale/diaphoretic. Mental status is AOx4, but the nurses on scene say that the patient is "not acting like herself." Blood pressure is 80/40, resps 20, and on the monitor you see a junctional (narrow complex, retrograde P waves) in the low 40's. Pulse ox is 80% on room air, up to 90% with 15lpm o2 via NRB. In the lungs you can hear some light rales in the bases. A 12 lead ECG reveals huge ST elevations in the inferior leads.

I did not have this patient, but my partner did during my day off last week. We were talking about potential treatments for this presentation, and I wanted to hear what you guys think.

There is of course the obvious: IV/Monitor/O2, ASA 324mg PO, 12 lead, transport quickly. The NTG is contraindicated (twice) by the presentation, so what else should we do for this patient? I dont think that there is any question about whether this patient is unstable, so in my medic school sparkyness I suggested pacing. The idea was perhaps we can get a little more perfusion with a better rate, and even though I realise that this does nothing to solve the root of the problem (inferior MI), there is still the hope that we can promote some better perfusion with a quicker, better organised rate. My (paramedic) partner was worried about damaging the already weak heart with the electricity, or perhaps sending the patient into a worse rhythm. Whatcha think about that? What about other treatments (Dopamine? Epi? anything else?)

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I had a similar patient not too long ago. A very tense transport, I tell you what.

Atropine might be a good temporizing measure, but once it is in you can't shut it off as it makes the MI bigger. Pacing should be a consideration, but it too will make the rate increase, and extend the MI. Dopamine and Epi, same problem.

Was a right sided view done on the ECG? It could have given you some very useful information. The patient presentation screams cardiogenic shock, so you wouldn't really be wrong with any of the standard treatments, but they will all make things worse as well. Use Dopamine just enough to get the pressure up, and balance it with some NTG or small doses of Morphine for the pain.

How good are you at walking a tight rope? That is what you are going to be doing.

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I would first try and consider pharmacological intervention. Pacing hurts, plain and simple, and her BP isn't nearly high enough for me to consider giving her sedation.

I'd be hesitant to consider atropine mainly due to the suspected ischemia as is shown on the 12-lead, and agree that Dopamine (or even Dobutamine if you carry it) would most like be best. And, the good thing about it, is if you carry Sodium Bicarbonate, there's a good possibility if you give that, you could deactivate it, same with lasix.

Here we would need to patch anyways, as Dopamine for us is only on standing order for a hypotensive patient post-arrest. Talk it over with the doc and see what they think.

Jacob

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Atropine was most definitely a consideration here, although in my classes I have been consistently told that the unstable patient should get electricity right away, not meds. Why shy away from pacing?

A right sided view was not performed. Truth be told, I cant think of ANY time where my medic partners have taken the time to do extra leads or extra views for a focused, diagnostic ECG. Not that the information wouldnt be valuable, it just seems like this either isnt in the average medic's daily skillset, or lazyness/time constraints get in the way. Another subject for another thread, perhaps.

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Not so much shy away from the TCP, just consider that while you are using it you will be making the MI bigger, and if you turn it off, you might not be able to re-capture the heart with it.

Patient comfort will also take a hit, but at this point I sure the patient wasn't feeling too well anyway.

With Dopamine, you would be able to monitor the rhythm better, and treat the pressure, which is the problem in the first place. You are right about the use of electrical therapy for the unstable patient, but keep the underlying problem in mind.

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Here we would need to patch anyways, as Dopamine for us is only on standing order for a hypotensive patient post-arrest. Talk it over with the doc and see what they think.

Jacob

We had a similar problem with Dopamine. 81 yo female acute pulmonary edema. Pulse Ox 80% on 15l. BP 60/30. Can't give Lasix or Morphine due to BP so we gave Dopamine to raise her pressure then the Lasix. When we got to the hospital she was talking. BP was 98/62. We got in a lot of trouble for not patching for the Dopamine however. Well you win some and you loose some. :oops:

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This type of patients makes one sphincter pucker... I agree I would probably either revert to pacing or Atropine. I agree with Azcep, I am thinking this is actually entering cardiogenic shock too or will be using the last of his heart up. The reason to shy away from pacing is I like a little sedation before hand... ever been shocked 60 times a minute?.. One would have to be cautious on sedation. Yet, a live heart is better than a dead one.

Sounds like a typical transmural infarct, and we really don't know if Dopamine would even do any good since there is no ejection fraction left. With this as well, we know we might be increasing the oxygen demand and increasing the infarct size.too I have sometimes used the pre-load : afterload trick . The effect of using Dobutamime and Dopamine together. This teeter totter effect appears to decrease the work load, until you can get the patient a transvenous or implanted pacemaker placed in them or place them on IABP if that does not correct the problem.

Like others stated it's a difficult case.

R/r 911

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What about epi? Good alpha effect, beta 1 for the rate and pressure (chronotropic/inotropic), beta 2 for perhaps some more effective resps, while at the same time getting that dilation of the coronary arteries.

...Of course you cant have your cake and eat it too-- with epi you're increasing myocardial O2 demand so again you get the balacing act.

Naturally this is what protocols and on-line medical control are for, but still its nice to think about what we *could* do given the tools we have and the permission to use them.

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Epi? Why not just defibrillate them? It would probably have the same effect but defibrillation would do it a lot quicker :wink:

NB, Epinephrine is a sympathomimetic, but it's also 2 forms down the line from Dopamine.

Tyrosine --> DOPA --> Dopamine --> NorEpinephrine --> Epinephrine

I would be EXTREMELY hesitant to give Epi to someone with a pulse, unless I'm using it for the B2 effects related to something such as anaphylaxis or severe asthma, and even then we don't give anymore then 0.3 mg 1:1000

Jacob

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Dopamine is a more titratable to effect medication than Epi is. You can increase it just enough to get the blood pressure back without increasing the heart rate too much.

For bradycardia, Epi is 2-10 mcg/min and it will do a bang up job of increasing the heart rate, but it can make the blood pressure worse. Alpha and Beta effects don't always play nice with each other. The infarcted area will become much bigger as well.

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