Triaging Triage ECGs

I’ve spent nine years working in an emergency department, which means I’ve also spent nine years performing electrocardiograms at triage. With a couple thousand waiting-room ECGs under my belt, I’ve noticed a few things:

  • A lot of ECGs are ordered at triage.
  • Many of them are performed on low-risk patients.
  • Very few of those ECGs lead to a change in initial management.

Oh, and one more thing:

  • Most physicians hate signing triage ECGs.

I can’t say I blame them. Triage ECGs interrupt their workflow and, worse than just slowing them down, that distraction can lead to errors. As an additional frustration, these patients often end up being seen by a different doctor in the department, and no one likes making diagnostic or treatment decisions that another provider will have to deal with. Plus, if the signing physician does happen to find something wrong, there’s always a nagging concern that the patient will end up being added to their already full group and need to be seen immediately—further interrupting flow.

Triage ECGs bring work and distraction.

So it’s understandable why many emergency physicians are rejoicing at the publication of a new study by Hughes, Lewis, Katz, and Jones: “Safety of Computer Interpretation of Normal Triage Electrocardiograms” [1].

Below are some great opinions on the article from the target demographic: emergency physicians.

They’re all well thought-out posts with perfectly reasonable conclusions. Dr. Salim Rezaie and Dr. Anand Swaminathan from R.E.B.E.L. EM also make it clear that they wouldn’t want to eliminate physician over-reads of “normal” triage ECGs, just delay them to reduce interruption.

My only issue with that approach is that the emergency physicians I’ve work with are always busy. Whether they read a triage ECG now or in fifteen minutes, they’re going to be doing something when I try to slide that paper in front of their screen.

As the only tech at triage, I’ve also got somewhere between one and thirty patients out in the waiting room, so if I don’t get that ECG signed right after it’s performed, I’ll get distracted myself and occasionally forget. It’s a lose-lose situation.

Maybe it’s just the practice at the hospital I worked at, but I think we’d make more progress at reducing interruptions by investigating a stricter triage protocol for ECGs. Though the rate of “normal” ECGs in this study was 26%, in my experience it’s somewhat uncommon to see a tracing with the words “Normal ECG” printed at the top in the ED (I’m just making this up, but I’d guess something < 10% at triage).

It’s not the “normal” ECGs that are weighing on my physicians.

I believe a bigger burden comes from ECGs that are read as “abnormal” in some way by the computer but were not indicated in the first place and do not change the patient’s management in the waiting room. If we could cut back on the number of triage ECGs that are performed on low-risk patients with non-cardiac complaints, I think that would make a bigger dent in reducing interruptions.

But I digress…

While seeing the computer spit out “Normal ECG” certainly stratifies a patient as lower risk, it’s not the same as “no risk.” That’s a problem, because triage ECGs are (or should be) performed in a moderate-to-high risk population with complaints suggestive of an acute cardiac process. In that cohort, the negative LR suggested by this study won’t “rule-out” concerns as well as it would in a general ED population getting ECGs as part of their routine workup.

As Dr. Steve Smith summarizes in his post on the topic, “Computer algorithms that make the diagnosis of ‘normal’ are usually correct, but is usually good enough?”

We don’t have an answer, and I don’t expect to make any headway on that issue with this blog post, but I thought it would be interesting to share a few subtle STEMIs from my collection that were read as normal by the computer.

It’s not data, and certainly not scientific, but it’s interesting (to the folks who like ECGs, at least).




  1. Hughes KE, Lewis SM, Katz L, Jones J. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med. 2017;24(1):120-124. doi: 10.1111/acem.13067

ECG Mixtape: Vol. 2

Welcome to the second installment in our ECG Mixtape series! It looks like this will be an irregular publication while we streamline our process of picking cases and getting permission to reproduce them. Enjoy!

Pick of the Week

This weeks top pick comes from cardiologist Dr. Gianni Manzo in São Paulo, Brazil, who shared this case on the Figure 1 app [note: the app and site require free registration to view cases].

A 78 year old male presented with a chief complaint of “oppressive” chest pain. The patient’s past cardiac history was significant for coronary artery bypass graft (CABG) surgery and pacemaker. The following ECG was obtained on arrival.

It shows an AV-sequential paced rhythm at approximately 70 bpm (probably a DDDR pacemaker). Most folks would just end their interpretation there (and the machine certainly will), but there’s a lot more to see on this tracing… like an infero-posterior STEMI!

Somehow the myth persists that you can’t identify ischemia in the setting of a paced rhythm. I don’t know it survives—I’ve got texts that Marriott wrote decades ago demonstrating STEMI’s with pacemakers—yet at least once a week I hear someone say, “He’s got a pacemaker; we can’t tell if there’s ischemia.”

The key is Sgarbossa’s criteria (and Smith’s modification), used to identify ischemia in the setting of left bundle branch block (LBBB); they can also be applied to paced rhythms! For an overview of how to understand and apply these simple criteria I recommend Tom Bouthillet’s three-part tutorial:

In this case we have excessively discordant (> 25%) ST-elevation in III and aVF in the distribution of an inferior STEMI. Even more impressive is the excessively discordant ST-depression in I and aVL—reciprocal changes just like we’d see in a non-paced inferior STEMI.

Sealing the diagnosis, we also see in appropriate concordant ST-depression in V1–V3. This is reciprocal to posterior ST-elevation, confirming that this is an infero-posterior STEMI. V5 and V6 show normal discordant ST-elevation (< 25%), while V4 is mixed between the findings in V3 and V5, showing an abnormal lack of the discordant ST-elevation we would expect not not meeting the criteria for frank ST-depression.

Angiography showed a 100% occlusion of the mid-right coronary artery (mid-RCA), confirming the diagnosis.

I have to add some caveats. First, Sgarbossa’s criteria hasn’t been as well-studied in pacemakers as it has in typical LBBB’s. This isn’t a big deal since: 1) It’s performed pretty well in the studies that have been done, and 2) people could still identify LBBB and paced-STEMI’s before Dr. Sgarbossa’s seminal paper; her work just gave concrete proof and objective measures to the concepts that experts has known for decades.  You’re gonna miss a lot of STEMI’s if you wait until there is large-scale, definitive proof of this pretty intuitive translation to pacemakers.

Second, and this is purely anecdote, but based on my experience, Sgarbossa’s criteria and Smith’s modification seem to be slightly less specific in the setting of paced rhythms. I can’t give you any real data (though Smith is currently studying this topic), but that’s my two cents on the matter. I still use the criteria routinely, I’m just slightly more careful when I apply the results.

Dr. Smith’s ECG Blog has a number of posts examining ischemia in the setting of paced rhythms: [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]


Our Favorite Blogs

Dr. Smith’s EGG Blog has been posting some fascinating cases the past few weeks so we’re actually going to highlight two of them here. The first concerns a 58 year old male patient who had been experiencing intermittent chest pain for two weeks and presented with the following 12-lead. The catch? Serial troponin levels were not only normal but undetectable! Make sure you click the image to see the full case description.


Our second case from Dr. Smith concerns another middle-age man presenting with chest pain and the following ECG. Is is a STEMI or just LVH? Follow the link for the answer and discussion.


I’m always looking for good examples of arrhythmias and their effects on invasive hemodynamic monitoring, and Mike over at Float Nurse shared a nice run of VT in a patient with an arterial line.


Next up are a pair of ECG’s obtained 15 min apart over at Dr. John Larkin’s ECG of the Week. What’s the cause of the T-wave inversions?


The Best of Social Media

In the Facebook group 12 Lead ECG – I’ve Got the Rhythm, Tomasz Adamski shared a great example of an antero-lateral STEMI visible through a LBBB—similar to our Pick of the Week showing a paced STEMI. Interestingly, the computerized interpretation managed to pick up the infarction.


From that same Facebook group we got another great LBBB anterior STEMI via Paul Halsey.


Heading over to the Twitter-verse, emergency physician Patricia van den Berg shared this awesome subtle “high lateral” STEMI—a diagnosis she made alone, in the middle of the night, when you really don’t want a false-positive activation. If you’re interested in more info on high lateral STEMI’s and why they look the way they do, I might suggest my own approach to the topic, located here.


Sticking to Twitter, cardiac electrophysiologist Janet K. Han, MD shared not one, but two cases of atrial flutter recently referred to her as “persistent sinus tachycardia.” Remember: sinus tachycardia will vary by at least a few bpm depending on the patient’s activity, positioning, treatment, mood, etc… If the monitor is stuck at one particular rate for 10+ minutes, strongly consider a non-sinus arrhythmia (usually flutter). I’ve collected more tips for spotting subtle flutter over here.


We’re not done with Twitter! Interventional cardiologist Dr. Eitan Friedman shared this uncommon rhythm. If you know the pattern it’ll take you 10 seconds to spot the diagnosis…


Well if you got the last one you’ll get this one too. Rajagopal Ramaswami‎ shared another manifestation of that same rhythm over in the EKG Club on Facebook.


I’m a sucker for dynamic acute coronary syndrome (ACS) so I love this case from Blake Bradley, NRP over on Twitter. Over 17 minutes his patient’s ECG evolved from subtle hyperacute T-waves in the inferior leads (superimposed on some diffuse subendocardial ischemia) to a full-blown obvious infero-posterior STEMI.


Shane Long was taking care of a patient with chest pain and a subtle anterior STEMI (check out that computerized interpretation)…

…when suddenly the patient went unresponsive. Whoops, that’s VF! One shock get him out of it. Don’t forget, even STEMI’s with only mild ST-elevation still carry a significant risk of sudden cardiac arrest.


Our last case was shared by Dr. Iliyas Sheikh in the EKG Club on Facebook. A routine EKG was performed on a 60 year old male:

If this patient had presented with acute chest pain our first thought would by hyperacute T-waves from an anterior STEMI, but it turns out this is just a normal variant in a patient with no acute symptoms.

For a similar ECG with more discussion check out this tracing from Dr. Smith’s ECG Blog. Thank you to EKG Club member Bartosz Kuczyński for finding this similar case!


I hope you find the cases interesting and take the time to check out the links to their original posts. Look forward to our next installment of the ECG Mixtape series returning… sometime soon!

ECG Mixtape: Vol. 1

Welcome to the start of a new series here at EMS 12-Lead. With the ECG Mixtapes we’ll compile some of the week’s best ECG’s from around the world of social media and #FOAMed. As High Fidelity taught us, “The making of a great compilation tape, like breaking up, is hard to do and takes ages longer than it may seem.” Please dig deeper into the cases that interest you.

Pick of the Week

This week’s top pick comes from Mohd Faried over at the EKG Club on Facebook.

2017.01.08 - Probable LMCA STEMI - Facebook - EKG Club - Mohd Faried

Click the image for a link to the original post on Facebook.

The patient, a 58 year old female, presented with chest pain x 1 hour with diaphoresis and signs of heart failure. This ECG shows sinus tachycardia, a (presumed) new RBBB, severe ST-depression in the inferior leads, and towering ST-elevation in aVR—which add up to quite a poor prognosis. It is important not to mistake the profound ST-changes in the limb leads for an extremely wide QRS (> 240 ms); the QRS in this tracing is really about 170 ms.

Now, despite common teaching, most cases of diffuse ST-depression with ST-elevation in aVR are not caused by acute occlusion of the left main coronary and often do not require immediate catheterization (for a lot more on this topic check out this post). The tracing above is unique for two reasons:

  1. The magnitudes of the ST-deviations in the limb leads are huge (though this can be seen in patients without obstructive coronary artery disease too).
  2. There are almost no ST-deviations in V1–V4.

This pattern is sometimes seen when anterior and posterior ST-elevation cancel each-other out and seems consistent with a true acute occlusion of the LMCA (a “left-main STEMI”). A patient with this ECG needs the cath lab now and, even with immediate intervention, the disease carries a very high mortality.

In this case the patient was intubated for worsening pulmonary edema and prepped for immediate angiography but, as often happens with these presentations, she did not survive long enough to make it to cath.

For more examples of true LMCA occlusion and a collection of ECG’s that share some of the features I describe, check out this post from our site.

Our Favorite Blogs

Dr. Steve Smith provides an in-depth discussion of a challenging wide complex tachycardia over at his eponymous ECG Blog.

2017.01.10 - WCT & Cyanosis - Steve Smith


Dawn Altman over at ECG Guru proves that you can spot a STEMI in a patient with a pacemaker.

PM AWMI - Dawn Altman - ECG Guru


Dr. John Larkin at ECG of the Week dissects a STEMI with anterior “tombstones” and almost no limb leads changes. Be warned! Some anterior STEMI’s look perfectly normal in the limb leads—typically those with mid-LAD lesions.

2017.01.11 - Mid-LAD STEMI - John Larkin - ECG of the Week


Dr. Arnel Carmona at ECG Rhythms shows you how the onset and offset of a wide complex tachycardia can be used to easily discern VT from SVT.

2017.01.11 - K. Wang WCT Logic - Arnel Carnoma - ECG Rhythms


Dr. Susan Torrey’s blog, Torrey EKG, explains why this otherwise healthy 48 year old male is bradycardic.

2017.01.11 - AV-dissociation - Susan Torry - Torrey EKG


Float Nurse posts a lot of quick, interesting, and accurate arrhythmia self-tests using real-world rhythm strips. Check out the latest one and make sure you have your basic arrhythmias down-pat before your next ACLS exam!

2017.01.09 - Non-conducted PAC - Rhythm Test 41 - Float Nurse


The Best of Social Media

How low can you go? Over at the Facebook group 12 Lead ECG – I’ve Got the Rhythm, Cam Warren shares a tracing from a patient who was conscious and alert with a heart rate of 17 bpm!

2017.01.10 - HR of 17 bpm - Cam Warren - I've Got the Rhythm - Facebook


12-Lead ECG – I’ve Got the Rhythm hosts another “Oh no! Too Slow!” rhythm with this case of tachy-brady syndrome from Luca Alfatti.

2017.01.10 - Tachy-brady - Luca Alfatti - I've Got the Rhythm - Facebook


And yet one more bradycardia! This time a type II AV-block from Dr. Michelle Connolly on Twitter.

2017.01.10 - Type II AV-block - Michelle Connolly - Twitter


Twitter brings us another spot-diagnosis arrhythmia with this beautiful ventricular tachycardia from Chris Evers.

2017.01.06 - VT - Chris Evers - Twitter


Speaking of VT… Don’t get distracted by this patient’s runs of tachycardia and miss the underlying cause. Make sure you check out the comments for more information on this interesting and instructive case from Kris Barraclough over at 12-Lead ECG – I’ve Got the Rhythm on Facebook.

2017.01.11 - VT w. STEMI - Kris Barraclough - I've Got the Rhythm - Facebook


Here’s a challenging one from our good friend Dr. Rohin Frances on Twitter. A 70 year old female with a history of schizophrenia and this ECG—can you spot the abnormality? Make sure you check out the serial ECG’s! Further discussion is also available in the EKG Club on Facebook.

2017.01.09 - Subtle a-tach - Medlife Crisis - Twitter


Here’s a subtle finding that’s vital to spot! At a glance the ECG looks normal, but there’s trouble brewing… From Dr. Sergio Pinski over on Twitter.

2017.01.09 - Atrial pacer dislodgement - Sergio Pinski - Twitter


And finally, here’s a facinating case from Dr. James Cranley on Twitter. A 31 year old female undergoes a liver transplant but suffers a bout of ventricular tachycardia soon after extubation. Her pre-op and post-VT ECG’s are shown below. What’s going on? Follow the link for the discussion.

2017.01.03 - Post-op Brugada - James Cranley - Twitter


I hope you find the cases interesting and take the time to check out the links to their original posts. Look forward to our next installment of the ECG Mixtape series returning again in a week!

Snapshot Case- No Day at the Beach

It is a beautiful summer afternoon when you and your partner are called to the beach for a “swimmer in distress”.

Upon your arrival, you find a 48 year old male sitting on a beach towel, appearing to be in some distress.

You are told that he was swimming in the ocean when he began to struggle, and was pulled out by bystanders.

Patient tells you that he developed a constant sharp pain in his chest, along with pain in his right arm, probably from overdoing the swimming he thinks. He says he feels a little better now.

He has no history, takes no meds, and tells you this has never happened before. He denies shortness of breath, lightheadedness, and nausea. Diaphoresis is hard to assess because the patient is still cool and wet from the water.


You get a set of vitals:

  • Pulse: 78 and regular
  • BP: 128/78
  • RR: 18 regular, lungs clear
  • SpO2: 96% on RA
  • Skin: cool and moist (out of the water)


You acquire a 12 lead ECG:




The community hospital is 12 minutes away by ground, and the STEMI center is 30 minutes away requiring Medevac transport.

For context, your system has had an issue with false positive cath lab activations, making activations from the field a little more difficult subject to system review.


Back to this call:

  • What is your ECG interpretation?
  • How will you treat your patient?
  • Will you take your patient to the closest hospital, or activate the cath lab?


59 Year Old Female: Intermittent Head Pain (Conclusion)

This is the conclusion to Wednesday’s post; if you haven’t seen it, I highly suggest checking out the original case description and initial ECG.

Wednesday’s case introduced a 59 year old woman with a chief complaint of intermittent occipital head pain for about 10 days. Recently, it had started radiating into her neck and upper back/shoulders. This was her initial ECG and it is clearly abnormal:

EKG #1

Figure 1. EKG on arrival at the ED.

The computer identifies it as showing left ventricular hypertrophy (LVH) with secondary ST and T-wave abnormalities (which we call a “strain pattern” or just “strain”). LVH with strain is quite common—in fact, it’s the predominant source of false-positive cath lab activations—but is that really what we’re looking at here? That’s a vital question because, if it’s not LVH w/ strain, then we’re probably looking at an inferior STEMI.

Does this tracing show a STEMI mimic? Or a true STEMI mimicking a STEMI mimic?

To start our analysis, I’d first caution anyone against trying to attribute ST/T abnormalities to a “strain pattern” in the absence of obviously large voltages or an old ECG showing a similar pattern. While Fig. 1 does meet a couple of different voltage criteria for LVH (which the computer is excellent at calculating—one of the few things I rely on it for), the voltages really aren’t that impressive. If you’re going to call LVH with strain based on a single ECG, you want it to be something obvious—like the tracing in Fig. 2.

LVH w/ strain

Figure 2. LVH with strain and massive QRS voltages.

On a side note, several commenters noted that they were swayed against the diagnosis of LVH by the absence of high voltage in the precordial leads of Fig. 1. While they were right to be skeptical of LVH, it was for the wrong reasons. Seeing high voltage in only one plane (large complexes in the limb leads but normal complexes in the precordials, or vice-versa) actually doesn’t do much to rule-out the diagnosis of LVH. Fig. 3 shows an ECG where the precordial leads demonstrate huge QRS complexes but the limb leads are perfectly normal.

LVH w/ strain and 2:1 AV-block

Figure 3. LVH with huge precordial QRS complexes but normal limb leads; there is also 2:1 AV-block.

Back to our case…

There are a couple of other findings that also weigh against a strain pattern:

  • Even if we believe there is LVH, the ST-deviations, especially in III and aVL, seem slightly excessive when considered in proportion to the size of QRS complexes. There is no good rule for determining excessive discordance with LVH (that 25% one is okay as a rule-in criteria and better than nothing, but terrible at ruling-out STEMI), but a seasoned eye will note that this seems like just a tiny bit too much elevation with a T-wave in III that is just a bit too tall for the QRS size.
  • There is a convex morphology to the ST-elevation in III that is slightly atypical for LVH.
  • There is a down-up morphology to the ST-depression in I and aVL. While sometimes normal with LVH, this has to be approached as abnormal and ischemic until proven otherwise.
  • There is concordant ST-depression in V2 and V3.
Concordant ST-depression in V2 and V3.

Figure 4. Concordant ST-depression in V2 and V3.

I’ve highlighted that last point because I think it’s the most important and pretty-much seals the diagnosis of STEMI for me. Since we’re already concerned about an inferior MI (based on the findings in III and aVL), and since inferior STEMI’s are often accompanied by posterior involvement, seeing right-precordial ST-depression consistent with posterior STEMI leaves me very confident that the ST/T abnormalities we see in III and aVL are indeed caused by an infero-posterior STEMI.

When we discuss the right-precordial leads in the setting of LVH on this blog [1] [2] [3] [4], it’s usually because the strain pattern often produces ST-elevation in V1 and V2 (and sometimes V3) that mimics STEMI (see Fig. 2). In those cases the ST-elevation is appropriately discordant and direct opposite the negative QRS complexes. It’s less common to see concordant right-precordial ST-depression in those leads when there is LVH.

Figure 5. LVH w/ strain and concordant ST-depression in V3.

Figure 5. LVH w/ strain and concordant ST-depression in V3. This is not a STEMI.

LVH w/ strain and concordant ST-depression in V2 and V3.

Figure 6. LVH w/ strain and concordant ST-depression in V2 and V3. This is not a STEMI.

When we do sometimes see concordant ST-depression with LVH, most of the time is due to chronic diffuse subendocardial ischemia from multi-vessel coronary artery disease or demand ischemia (as in Fig. 5 & 6). The key in those cases is that it’s usually associated with ST-depression in most of the limb leads and ST-elevation in aVR. Looking back on Fig. 1, the limb lead ST-depression in our case is confined to I and aVL and there is no ST-elelvation in aVR.

So that right-precordial ST-depression, combined with the other findings listed above, confirms that we are very likely looking at an infero-posterior STEMI. But we have another issue…

Note that I said it’s “very likely” that we’re dealing with a STEMI, not “certain.” Despite my confidence in the ECG findings, this still isn’t an easy diagnosis because things get much trickier when you take the patient’s symptoms into account. While acute coronary syndrome (ACS) was present on the differential for her initial presentation (hence, why we did the ECG), before we did the test it didn’t seem very likely that her symptoms were due to myocardial ischemia. In other words, her pretest probability (our assumed likelihood that she was experiencing a STEMI prior to performing the ECG) was pretty low.

Now, her pre-test probability of ACS clearly isn’t 0%, but it’s also not very high. As a result, it’s going to take a pretty convincing test to diagnose a STEMI in this patient. That’s unfortunate since we already determined that her ECG, while suggestive of STEMI, wasn’t 100% conclusive.

Large anterior STEMI

Figure 7. If a patient came in with toe pain and this ECG they’d still go for emergent PCI despite an incredibly low pretest probabilty. The ECG is so strongly indicative of acute anterior STEMI that it is capable of swinging us all the way from a pretest probabiltiy of almost 0% to diagnostic certainty. In the case of our 59 year old woman though, even though her pretest probability of ACS was a bit higher than someone with “toe pain,” the ECG is less clear-cut. While we are mildly confident that we are looking at a subtle STEMI, we are not certain because we have a hazy clinical picture combined with a non-pathognomonic ECG.

We’ve moved ACS way-up on the differential, but we haven’t clinched the diagnosis. [On a side note: The ECG is a very subjective test, and while an expert like Dr. Steve Smith would assign a lot of confidence to his interpretation and could very well diagnose STEMI here in-spite of a low pre-test probability, most providers could and should not.] When faced with a non-diagnostic ECG in the face of possible ACS, it’s almost always a smart move to repeat the ECG.

In our case I didn’t see this patient’ EKG until an hour after she arrived, but as soon as I did I expressed my concerns to the treating physician and requested a repeat EKG. To refresh your memory, here’s that initial tracing again, followed by the repeat:

Fig 1.

Fig. 1 (reprising its role).

EKG #2

Figure 8. Repeat ECG 1 hour later.

Well, that’s a bit different. There are several important findings in Fig. 8:

  • The ST-elevation in lead III has disappeared (normalization of the J-point).
  • There are now a terminal T-wave inversions in lead III (reperfusion T-waves).
  • The ST-depression in I and aVL has mostly resolved (normalization of the J-point).
  • The ST-depression in V2 has resolved (normalization of the J-point).
  • The T-waves in V2 and V3 are slightly taller and more symmetric (posterior reperfusion waves).

The most important of those changes is the new terminal T-wave inversions in lead III—these are reperfusion T-waves. Many providers are familar with Wellens syndrome affecting the anterior leads, but they are not aware that you can see similar T-wave inversions in other distubutions.

Wellens syndrome is due to spontaneous reperfusion of an anterior STEMI. When the patient’s LAD is blocked, it results in a typical anterior STEMI pattern…

Subtle Anterior STEMI

Figure 9. Subtle anterior STEMI.

But then if that previously closed LAD spontaneously re-opens, the leads that used to show ST-elevation sometimes develop these classic-looking T-wave inversions described by Dr. Wellens.

Wellens T-wave Inversions

Figure 10. Wellens T-wave inversions indicative of spontaneous reperfusion.

What Dr. Wellens didn’t mention in his original paper—and what is still not well known—is that you can see these sorts of T-wave inversions in any sort of STEMI. If a lateral STEMI suddenly reperfuses, you might see T-wave inversions in the lateral leads. If an inferior STEMI reperfuses, you might see T-wave inversions in the inferior leads (like we do here). And finally, if a posterior STEMI reperfuses, you can see T-wave inversions in the posterior leads. These posterior reperfusion waves are reflected on the standard 12-lead as subtly taller, upright T-waves in V2 and V3 (which we also see here).

Note the other important finding, listed in big text at the top of the Fig. 8: The patient’s pain, while present at a 3 out of 10 during EKG #1, was absent during EKG #2. That confirms that we are looking at reperfusion T-waves in EKG #2, which in-turn means that EKG #1 must have been showing an infero-posterior STEMI!

At this point in the patient’s course I was convinced but no one else was buying that this patient with a “headache” was actually experiencing an intermittent and spontaneously reperfusing STEMI.

Thankfully her troponin-I (ref <= 0.04 ng/mL) came back mildly elevated at 0.80 ng/mL right around that time, buying her some stronger consideration for ACS. She received aspirin, nitro paste, metoprolol, clopidogrel, and enoxaparin in the ED and preparations were made to admit her for an unstable angina/NSTEMI workup.

About 90 minutes after EKG #2 the patient began to complain of slight pain again and another EKG was recorded, including posterior leads:

Subtle infero-posterior STEMI

Figure 11. Repeat ECG showing subtle infero-posterior STEMI (again).

Inferior STEMI, Posterior ECG

Figure 12. Posterior ECG (V7–V9) showing no ST-elevation in the posterior leads.

The T-waves in lead III are now purely upright again—this is a phenomenon known as pseudo-normalization. Rather than being normal and reassuring, it is actually an indication of re-occlusion of the culprit artery. When dealing with reperfusion T-waves, an inverted T-wave becomes a good thing because it means the previously blocked artery is now open. A sudden reversion of an inverted reperfusion T-wave to a normal, upright configuration is usually associated with re-occlusion of that temporarily unclogged coronary artery.

As I was the electrocardiograph wires after EKG #4, the patient mentioned that her pain had completely resolved again, so of course I reattached her and ran another tracing:

Infero-posterior reperfusion

Figure 13. Infero-posterior reperfusion pattern… again.

This EKG suggest that she is in the process of reperfusion yet again, though there is still some mild residual ST-depression. The most important thing that that the T-wave in lead III has returned to its flipped “reperfusion” morphology—a good thing!

For a better visualization of changes across these last three EKG’s over the course of six minutes, check out the gif below.

Infero STEMI and reperfusion gif

Figure 14. The continuum between inferior STEMI and spontaneous reperfusion.

Follow each lead individually:

  • Lead III transitions from mild ST-elevation with an upright T-wave (STEMI) to an upright T-wave with no elevation to finally an inverted reperfusion T-wave.
  • aVL goes from showing ST-depression with a steep downslope (reciprocal changes) to an isoelectric J-point with very little downslope to the T-wave.
  • V3 initially shows concordant ST-depression with a small T-wave (posterior STEMI), but eventually evolves to showing a isoelectric J-point with a T-wave that is slightly taller than before (mirror image of a posterior reperfusion wave).

Just because we can, here’s a similar animation of all five ECG’s over the patient’s ED course.

Infero-posterior STEMI to reperfusion gif

Figure 15. The process of intermittent injury and spontaneous reperfusion over the patient’s ED course.

The patient was admitted to telemetry where her troponin-I values (ref <= 0.04 ng/mL) every 6 hours trended as:

  • 0.80 ng/mL
  • 0.75 ng/mL
  • 0.79 ng/mL

Echo the next morning showed normal left ventricular size and function with no regional wall motion abnormalities and a preserved EF of 55%. There was no echocardiographic evidence of LVH. That day she was transferred to the CCU at a nearby hospital where she experienced an uneventful course and underwent coronary angiography a couple of days later,  as planned.

Unremarkable left coronary system

Figure 16. Unremarkable left coronary system.

RCA culprit lesion

Figure 17. The right coronary system shows a culprit lesion in the RCA.

Cath showed a culprit lesion in the right coronary artery (RCA), perfectly consistent with the pattern of infero-posterior injury and reperfusion we were seeing on the patient’s ECG’s! She received a single drug-eluting stent and had a good outcome with no significant loss of LV function or other sequelae.

Open RCA

Right coronary artery status-post PCI and a single stent.

It might seem crazy that this patient was experiencing anginal pain in the back of her head, but that’s actually a well documented (though not really well known) presentation of myocardial ischemia known as “cardiac cephalgia.” We’ll discuss this a bit more in a couple of days but I think we’ve covered more than enough ground for today.

Let me know if you have any questions in the comments or in response to our links to this case on Facebook and Twitter!