EKG: Ouch chest pain!

Anthony D. Chamblee, Paramedic

11/7/2010 10:44:06 AM #

Looks like an inferior, anterior, and high lateral MI w/ reciprocal depression (and possible posterior involvement). Treat with MONA as per usual. If unstable bradycardia develops again, I would go straight to TCP and avoid Atropine. Definitively, this man needs to get to the cath lab post haste.

Adam Thompson, EMT-P

11/7/2010 10:44:56 AM #

Given the pressure and the fact that the rate is slowing down leads me to believe that the right-side of the heart is involved.  

12-lead shows infero-lateral MI with probably posterior wall extension.  This leads me to believe that the patient has a proximal occlusion to their dominant RCA.

Give ASA and fluids.  Stretch receptors will improve HR & BP via the Bainbridge reflex.  I wouldn't want that HR much faster anyhow.  The hypoxia is another concern and we should assess lung sounds for an indication of cardiogenic shock.

Danielle Connell, EMT-P

11/7/2010 3:30:01 PM #

Anterioinferiolateral wall MI.    Because of the hypotention and the MI affecting the inferior wall of the heart, NO NITRO, NO MORPHINE ( decreasing the preload and afterload with that pressure will kill him).  Dopamine, ASA, and a pacemaker will help this guy.

Nick Adams

11/7/2010 4:02:04 PM #

Very good Adam.  I totally agree with you.  STEMI in leads II, II, aVF (inferior MI) with reciprcal ST depression in V1 and V2 indicates a right-sided dominant patient with posterior wall involement.  This indicates, atleast, a mid RCA occlusion.  With the pt presenting with hypotension and bradycardia, I would also agree that this is actually a proximal RCA occlusion.  Therefore, a quick 15 lead would be indicated.  I would assume that the V4R, V8 and V9 leads are also elvated, which a proximal RCA would then be verified.  The high left lateral leads of I and aVL are reciprocal ST segment depression from the Inferio MI.  I also see an Anterolateral ST segment elevation in V3 - V6 indicating an additional LAD occlusion.  Treatment for this patient shold be aimed at maintaining heart rate, preload, contractility, and coronary artery perfusion.  My treatment would include:  O2 to maintain an SpO2 of >90% or better.  Pacer pads on now,  4 mg of Zofran prior to ASA,  @ large bore IV's with generous fluid boluses for preload (lung sounds?).  This patient still needs Nitrates for vasodilation, so a Tridil gtt starting at 10mcg/min and titrating up to SBP and pain level is more managable then SL NTG.) Fentanyl for pain control without droping preload, and possibly Dopamine (last resort) for chromotrope and inotropic effects.  Reguardless, the definitive treatment is a rapid diesel bolus to a cath lab for a PTCA, IABP, CABG.

Mohammed Alo

11/7/2010 6:59:11 PM #

Everyone is mostly correct. The elevations in the inferior leads (II, III, aVF) indicate that this is a RCA infarct. As everyone has mentioned, the PDA (posterior descending artery) comes off the RCA, hence you have the Posterior MI. A posterior MI gives you ST depressions in V1-V3.

The Inferior leads are correctly reciprocating to AVL. That is where Inferior MIs always reciprocate too.

You also have ST elevations in the lateral leads (V5, V6) which demonstrates a lateral MI. When you have a mega dominant RCA, you can get ST elevations in V5 and V6, indicating a huge RCA travels past the inferior wall and goes all the way to the lateral wall. Normally, if you have a lateral MI only, you have ST elevations in AVL and I as well, but AVL is reciprocating to the INF leads and being depressed at this time.

You have ST depressions in the posterior leads (V1-V3), which is diagnostic of a posterior MI. Nothing else gives you that. The RCA normally supplies the PDA (posterior descending artery), hence you normally see INF and POST MIs together. The inferior leads do not reciprocate to the anterior leads (V1-V3), as someone mentioned.

The patient was also bradycardic and hypotensive. The RCA gives rise to the AV nodal branch and the RV branch. So this could be a very proximal RCA infarct and that could explain everything. Except for one problem.

You also have ST elevations in some of the Anterior leads (V4, V5). That is hard to explain? How can you have an acute MI in the anterior, posterior, lateral, and inferior leads? That doesn't make very much anatomic sense. It's not pericarditis, because the ST elevations clearly look like an acute MI and not pericarditis.  So then what is this?

One thing that could explain this is a dominant circumflex, but it'd have to be huge.

MONA is a very bad idea in any MI. Morphine has been demonstrated to kill people. The Crusade Trial has demonstrated that patients with chest pain had a 48-60%  higher mortality than those that didn't. It's because morphine is a vaso and veno dilator and drops perfusion pressure, and increases infarct size. Please don't give any one morphine.

Nitrates and Beta blockers are also a bad idea when the RCA is involved. Anything that would already block an ischemic AV node and or drop blood pressure that is already low, is a very bad idea. These are contraindicated in Right Sided MIs.

The treatment for Right sided MIs is lots and lots of fluids. The biggest help anyone can do for such patients is not give them nitro, or wipe off the nitro paste, and give them tons and tons of normal saline. 95% of RV infarct patients require about 18-20 liters of 0.9 normal saline in order to survive. From a paramedic standpoint, if you guys can recognize this immediately, since you get the first EKG, please don't give them nitro and load them up on normal saline, as much as you possibly can.

In order to diagnose a right ventricular infarct all you need is to see inferior elevations and hypotension. That's it! It's an RV infarct.

If you want more proof, if the ST elevations in lead III are higher than the ST elevations in lead II, then it's an RV infarct. Don't waste time getting a right sided EKG. There is no reason to get that. In this guys case, the ST elevations in III were taller than II, lending more credence to the RV infarct theory, which was his clinical presentation.

He did end up having unusual anatomy, but the outcome is the same, his RV was shot because the CIRC supplied the RCA distribution and most of the LAD distribution as well.

We took him to the cath lab, and he in fact had a massive and dominant circumflex artery, a tiny LAD and a tiny RCA. His CIRC supplied nearly his entire heart.

We had to put in an intra aortic balloon pump and temporary pacer, we had him on levophed, dopamine, and neosynephrine, at some point we switched to dobutamine. He was also intubated because he was starting to get more and more hypoxic. We were able to cross the circ lesion and balloon and stent it. He also had an obtuse marginal off the Circ that was a stub. Bad situation. He ultimately coded and after coding him for a long time, he didn't make it.