Recognizing a Subtle STEMI (Occlusion Myocardial Infarction)

For those who wish to hear our lecture on Youtube: here is the video

Normal Cardiac Cell Depolarization

It’s important to understand the effects of myocardial ischemia and how they manifest on the ECG. The normal resting potential is approximately -90 millivolts which is caused by the sodium potassium pump. This pump creates an electrolyte gradient with potassium in the cells and the sodium outside the cells. First, the sodium ions rush into the myocytes until the membrane potential hits around 20 millivolts. This causes depolarization and once the action potential hits 20, the sodium channels close. The next phase involves potassium and calcium. Remember potassium is still in the cells with all of the sodium ions. In the next phase, the potassium rushes out of the myocytes and calcium starts to enter. Since both are positively charged, there’s very little change in the action potential which you can see as the plateau for phase 2. After phase 2, the calcium channels close and the sodium potassium channels remain open. The potassium ions slowly leak out and because they’re positively charged, the membrane potential will decrease into the negative millivolts. You can see that in the phase 3 of the cardiac action potential which is called repolarization. In a normal and healthy cell, repolarization begins at the same point that depolarization happens. This continues until the resting membrane potential hits -90 millivolts. It then waits to start the whole cycle again. So now that we know the basics of cardiomyocyte action potential, let’s get into what causes the ischemia effects on a 12 lead.

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Patho of Ischemia

Now we all know that injured cells do not act the same way as healthy cells right? So why would damaged myocytes be any different? When myocytes are damaged, there’s a cascade of events that cause ECG changes. One of these events deals with electrical changes. The decreased sodium potassium pump activity delays phase 3 repolarization. As I said in the previous section, repolarization in healthy cells occurs at the same spot as depolarization, this is the opposite for ischemic cells! The repolarization will occur at the opposite site from where depolarization occurred. Now I think that’s enough patho for today. Let’s get into the meat and potatoes.

In school we’re mainly taught two different types of myocardial infarctions: STEMI and NSTEMI. One we can diagnose on a 12 lead ECG (STEMI) because it presents with marked ECG changes… One we need to use troponin to diagnose (NSTEMI) because it presents with limited ECG changes. But what if I told you there’s a third one that acts as the middle ground between them?

Now there are some extremely intelligent physicians out there who are very keen on occlusion myocardial infarctions (OMI). One of my favorite is Dr. Stephen Smith who runs Dr. Smiths ECG blog (http://hqmeded-ecg.blogspot.com/). He is an emergency room physician who has done a considerable amount of research on the topic so check out his website for hundreds of examples. But I will go into the basics here.

An occlusion MI is commonly diagnosed as a NSTEMI because people don’t know what to look for. The not so brilliant computer interpretation won’t catch this… Or as I call them the Doc in the box. OMIs produce subtle ECG changes that take place and often don’t meet STEMI criteria. So here are a few things we need to remember:

Normal T waves

T waves should be upright in every lead except for aVR and sometimes V1. These should be asymmetric in nature. They should present with a slow upslope and a fast downslope. Normal T waves have a concave morphology. Now we can get into some T waves with attitude.

OMI ECG Findings

As mentioned before, normal T waves are asymmetric in nature and have a concave morphology. When T waves start to have a wider base and become symmetric in nature think cardiac ischemia. In the example below, you can see the top T wave makes sort of a happy face. The one beneath the happy face has more of a convex morphology showing whats called the “R-T sign.” “R-T sign” is when the QRS complex leads straight into the T-wave with abnormal ST-segment morphology.

Hyperacute T waves are one of the earliest signs of a myocardial infarction besides a slight prolongation of the QTc (as the T wave broadens, it slightly increases the QTc). The average QTc for a STEMI is around 450 ms. When you start seeing elevation, there’s already dead myocardium. We need to catch these in an attempt to preserve ejection fraction. We want our patient’s to have the best outcomes possible.

So what is a hyperacute T wave? Well a hyperacute T wave is a fancy term for a T wave that is proportionately larger than the QRS complex. This is one of the most important finding in an OMI. Hyperacute T waves are a good sign in that the myocardium is at risk but not yet infarcted. A large hyperacute T wave is bad sign in that a lot of myocardium is at risk.

Yes those are dogs. We love dogs. Everybody loves dogs. So you get dogs to show proportionality. Before we go into OMIs, we need to make sure we are confident enough in diagnosing STEMIs. These are so easy to see, a taxi driver can see them.

STEMIs

These are super easy to see. I am not a huge fan when someone can be like “I just saved their life! I saw a STEMI!” Congrats… Their myocardium is already dead and it’s blatantly obvious. Now before the patient gets this bad, we need to recognize OMIs to save them and not wait for troponins to tell us there is myocardial death. Now let’s get into OMIs

OMI cases

Above is a 30 year old male with a chief complaint of chest pain. What do you guys notice? Well the first thing you may notice is T wave inversions in III and aVF. AVF’s best friend and most reciprocal lead is aVL. So if you look into aVL, you’ll see a small QRS and a massive, hyperacute T wave. This is diagnostic of an OMI. The Doc in the box didn’t catch this.

Above is the 12 lead of the 41 year old male complaining of some burning epigastric pain. What do you see? Notice the slight depression in aVL? Look at aVL’s best friend which Is lead III. See some symmetry in that T wave? Now let’s look around the 12 lead. II has a T wave that just shoots off the QRS complex and is looking large so that can be hyperacute. But look at aVF. Micro QRS and a massive T wave. That is your hyperacute T wave. There is also minute ST depression in V1-V3 indicating a possible posterior wall MI.

Above is a 56 year old female with chest pain. Look at those precordial lead T waves. Especially In V3. The T wave shoots off and you could fit the whole QRS complex inside of it. Now ER physicians didn’t recognize this as an OMI. But luckily they did a serial 12 lead. Keep a high index of suspicion and have a low threshold to run serial 12-leads. We’re supposed to obtain multiple sets of vitals right? We should be thinking the same way about 12 leads. Sometimes I’ll do one every 8-10 minutes and have 3-4 laying in front of me while I scrutinize them all. So lets look at that serial 12 lead they did 15 minutes later.

There is obvious ST elevation now with Q waves noted in the precordial leads.

Now we should be getting the hang of it. Look around and see if you notice anything. Minor depression in the inferior leads. Hyperacute in V2 and V3.

We should be close to pros now. What do you see? Inferior leads have hyperacute T waves with that flipped T wave in aVL.

This one is very similar to the previous one. Hyperacute Ts in inferior leads and you’ll also notice well formed Q waves in V1 and V2. T waves are also pretty acute so this could be a Type III LAD wrap around occlusion. The image below shows what a what a wrap around LAD looks like. You get elevation in the precordial leads and the inferior leads.

And for the final one!

This was sent in by a very astute paramedic who was able to recognize an OMI on a chest pain patient.  See that flipped T wave in aVL? Look at lead III. QRS is small and T wave isn’t too crazy but it’s sort of shooting out from the QRS complex showing the R-T sign. There’s also T wave inversions in the precordial leads hinting at a posterior wall infarction. Now lets see what she does next.

She did the right thing and obtained a serial 12 lead. Look at the changes! T waves are hyperacute with reciprocal T wave inversion. She was able to convince the hesitant ER physician to activate the cath lab because of the changes on the serial 12 leads.

Recap

Two big things. Serial 12 leads are a necessity! I can’t preface this enough. If it takes killing a few trees to convince a physician to activate the cath lab then do it.

Strive to always be a better provider and patient advocate. And finally, look for that frowny convex morphology and don’t forget about the QRS to T wave proportionality. Medicine is all about baby steps. Some of the 12 lead examples of OMIs were borrowed from Dr. Smith’s “The ECG of an Acute MI” book which you can download and look at for free using the link in the references.

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This site is meant to be used for educational use only. We strive to push evidence based medicine with no bias to help you obtain all the important information. You should always follow your protocols that have been set in place.

Scopeducation Team (Matt)

References

Dr. Smith’s “The ECG of an Acute MI” PDF

https://t.co/kRwzgmsaR5?amp=1

Levis, Joel T. “ECG Diagnosis: Hyperacute T Waves.” The Permanente Journal, The Permanente Journal, 2015, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500486/.

Meyers, Pendell. “Guest Post – Down with STEMI – The OMI Manifesto by Pendell Meyers.” EMCrit Project, 1 Apr. 2018, emcrit.org/emcrit/omi-manifesto/.

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