An astute paramedic

came in and said, hey, I saw an epsilon wave on our 12-8 EKG.

Here it is.

And it looks like an epsilon wave.

And on our repeat EKG, it didn't show up there.

And the patient got admitted to the hospital and had a defibrillator placed based off of this.

But this is a legitimate thing that patients have.

Yeah, that's not,

Can I just get you to speak to stepping back and looking at the wider cardiac patients, which maybe just doesn't tick that ST elevation box?

Yeah, so I think a couple of great questions in there, right? It's how much weight do I put in on my clinical gestalt? Because there's certainly patients we've walked in, and I'm sure you've had this too, right? You get the chest pain call, you walk in, you look at the patient, you're like, this is going to be a STEMI.

You hook them up, right? And you're like, this is the cleanest 12-lead ECG I've ever seen in my life.

What the heck, right? And then number two is what we're classically taught, that chest heaviness, clutching chest, is that the most accurate sort of thing to be suspicious for STEMI? So let me tackle that first question.

So how much weight should you put into your clinical gestalt? A lot, a lot.

We're still treating patients at the end of the day, right? I'm not sure if it's overseas the same as it is here in the U.S., but in the U.S., we hammer into our clinicians, treat the patient, not the monitor.

And there's some element of truth to that here, right? We're talking about very monitor-specific findings that could be considered with occluded arteries and a heart attack.

Could I get you to speak to just that systems change so that we can, to your earlier point, catch these patients, these high risk patients, which don't trigger the ST elevation criteria?

I didn't, I always thought it was just one.

Radiation, does it worsen with exertion? Does it go away with rest? Those are your classic ACS symptoms, right? The opposite are Prinzmetals angina, right? The patient may be exerting, they're fine.

Then they're sitting down and they have anginal symptoms.

That's called Prinzmetals angina.

That's vasospastic angina as opposed to occlusive angina.

So that's the only one that presents separately.

But classic ACS presents with chest discomfort with exertion.

And then just in general, how are we treating right-sided MIs differently or OMIs differently if we're suspecting that than

what's going on?

Yeah, so to Dr. Smith's credit, he does involve some cardiologists in there.

The names are escaping me right now, but It is.

So you'll see this with a lot of implementation of novel therapy.

Emergency and acute care clinicians, for the most part, are usually the most vocal about advocating for new implementation of new science.

Not that our cardiology colleagues are not.

They certainly are.

If you can't recognize these things and then go

And then you can start to see an acute change before your eyes in the patient.

Yeah.

So just as you alluded to, it's a very complex thing, right? You know, it almost seems as if they're competing guidelines or competing protocols, right? On one hand, we want to do permissive hypotension.

On the other hand, we want to perfuse more, right? So but what I would really say is like, appears competing protocols on paper and overtly, but they're actually calibration of that same dial.

Both of them really seem to say, and both those guidelines, yes, we want to try to reduce the amount of bleeding with permissive hypotension, but really at the end of the day, we resuscitate someone and they don't have an intact mental status then was it really you know all for naught um so you know i i have a fairly low threshold on what i consider an unreliable neuro exam or what could be a traumatic brain injury especially in the pre-hospital environment so i i really personally follow the the national association of ems physicians position statement over here uh not just because they're my parent organization as an ems physician but it's just a well-researched article and guideline as well as the BTF pre-hospital traumatic brain injury guidelines.

And what do those say? Based off our best look at the evidence, we know that we want to try to maintain cerebral perfusion pressure, or CPP.

So just as a quick refresher for what that is for everyone, it's the mean arterial pressure minus the intracranial pressure, or the MAP minus the ICP.

Could I get you to maybe just unpack for us, you know, if you haven't got access to blood, is it still a preferable agent of choice to give fluid?

Um, so why, why take it out fully with V-fib, V-tach? Why?

Yeah.

So I think that's a great question.

So, um, [clears throat] in VF and VT arrests, what we know is it's really a catecholamine sur- well, in particular for refractory VF, one of the theories is catecholamine surge.

So epinephrine is one of our endogenous catecholamines, which is a very big way of saying it's one of our body's own made catecholamines.

So if the body is already surging epinephrine, and that's one of the leading theories as to the reason people will go into refractory VF, it doesn't make sense for me to keep administering it in the sense of refractory VF.

That's where I started.

Like in a drip form, not the full milligram.

Yeah.

It's a very versatile drug, travels easy.

Um, again, but there's lots of problems with it within the cardiac arrest paradigm, especially how most people do cardiac arrest.

So the reason I share all that is that I'm writing this paper, um, that is, and, and talking about essentially how do people who identify as resuscitationists run a resuscitation? You know, if you look at the AHA CPR guidelines or really any national guidelines, you...

they are really made for the people that don't do CPR every single day.

You know, I, I think it's actually a little bit of a slap in the face slightly to make working EMS clinicians do Q2 year AHA ACLS, AHA CPR, et cetera, because, you know, most clinicians, especially at a high-functioning EMS agency, know how to do CPR.

Um, they're staying up on the literature.

... with that epinephrine delivered early and rapidly in asystole in PEA.