Monday, March 2, 2020

A man in his 60s with chest pain. Could you have prevented his cardiac arrest?

Written by Pendell Meyers

A man in his 60s with HTN and AF presented with chest pain that started about 1 hour ago and started to subside during transport via ambulance. Vitals were normal except for a heart rate of 49 bpm at triage.

Here was his EMS ECG recorded just before arrival:

What do you think?

Sinus bradycardia with clear but subtle evidence of inferior OMI. The T-waves in III and AVF are certainly hyperacute, as they are fat and wide compared to their small, normal QRS complexes and are corroborated by the inappropriate T-wave inversion in aVL. Lead II would probably also be proven to be hyperacute in comparison to a baseline ECG if we had one with a clear baseline T-wave.

V3 also has a hyperacute appearance, but I am not sure how to reconcile this with the distribution of findings in the rest of the ECG.

The only available prior ECG in the system was this one in atrial flutter:
Despite flutter somewhat obscuring the T-waves, you can see that the inferior T-waves at baseline are not as big as the presentation ECG, proving they are indeed hyperacute. The T-wave in aVL is upright at baseline, and inverted in the presentation ECG.

The ED physician was worried about the EMS ECG and obtained an immediate repeat on arrival in the room:
Sinus bradycardia persists, but the hyperacute T-waves are deflating compared to the EMS ECG. It would seem that the patient is reperfusing at this time, which of course fits with the clinical data of decreasing pain. Of note, V3 is also improving, solidifying the notion that it was truly hyperacute in the first ECG.

It is unclear whether the cardiology team understood that the patient has an unstable ACS lesion causing intermittent OMI. They advised starting heparin drip (already received ASA) and no urgent cath at this time.

The initial troponin of course returned undetectable (our contemporary troponin T takes 4-6 hours from onset of persistent occlusion to rise).

Suddenly the family of the patient cried for help.

The team arrived in the room to find the patient in VF arrest.

He was successfully defibrillated with immediate return of mental status.

The team called the cardiologists back to bedside and obtained this repeat ECG:

I can't say I see a meaningful difference between the inferior leads on this ECG and the last one. Perhaps there is some new STD in V2. The T-wave in V3 has become hyperacute again, and now in retrospect it looks as if the entire anterolateral wall (V3-V6) may be affected by whichever artery is involved. The bottom line is: there is ongoing evidence of an unstable coronary lesion which is causing ongoing ischemic symptoms and a VF arrest!

They took the patient to cath and found a mid-RCA lesion which was barely open at that time (it is documented as 95% in one place in the report, 99% in another) but resulting in TIMI 2 flow. PCI was performed with excellent angiographic result. There was also disease in other arteries such as 75% LAD and 70% D1, which were not deemed acute lesions. They did not comment whether the RCA somehow supplied the anterior and/or lateral walls (which it appears to, based on the ECGs).

Here is the ECG after cath:

Clear inferior reperfusion findings in III and aVL, as well as V2-5.

For whatever reason, the cardiologists decided not to order any more troponins! So the only one on file is the initial troponin (prior to VF arrest) which was undetectable. It is obvious to me that the troponins would have risen, but I cannot prove it, and we do not know what the peak would have been.

Learning Points:

The RCA supplies the nodes (SA and AV), and RCA OMI frequently presents with sinus bradycardia and/or AV blocks.

You must be able to recognize subtle hyperacute T-waves. You must understand that they are proportional to their QRS complexes, and that ECGs with small voltage may have small absolute T-waves which are completely diagnostic of hyperacute T-waves.

This patient never met STEMI criteria, but had RCA OMI causing VF arrest. If this patient had been prospectively identified by an expert electrocardiographer as OMI and taken to the cath lab immediately, I think there is a strong possibility that we could have prevented his cardiac arrest and likely saved him some myocardium (and hopefully, then, long term sequelae).

MY Comment by KEN GRAUER, MD (2/28/2020):
Five ECGs are done in this case. I’ve labeled these — and focus My Comment on ECGs #1, 3 and 4 — which I’ve reproduced in Figure-1.

Figure-1: The 1st, 3rd and 4th ECGs shown above from this case (See text).

ECG #1: As per Dr. Meyers — the ST-T waves in each of the inferior leads are hyperacute. This is most marked for leads III and aVF, in which the T waves are disproportionately tall considering the tiny size of the QRS complex in these leads.
  • The ST-T wave change in lead II is more subtle — but it has to be considered in light of the definite hyperacute changes in the other 2 inferior leads (ie, my “threshold” for considering subtle change significant in the 3rd inferior lead is lowered — since both leads III and aVF are clearly abnormal). In this context — the T wave in lead II is indeed fatter-than-expected at its peak.
  • Confirmation that these inferior lead ST-T wave changes are real — is forthcoming from the ST depression with positive terminal T wave in lead aVL — that is nearly a mirror-image opposite change to the hyperacute T wave in lead III.
  • The ST segment in the other high-lateral lead ( = lead I) is also abnormal, in that it is uncharacteristically straight, with abrupt angulation at the onset of its T wave.
  • PEARL — On occasion, the T wave may be normally inverted as an isolated finding in leads III — aVF — and/or aVL. This is especially true when the QRS complex in the lead with T wave inversion is predominantly negative (ie, the T wave axis often follows close behind the QRS axis). However, when the QRS complex in lead aVL is positive (as it is in ECG #1) — ST depression as seen in lead aVL of this tracing is not a normal finding.
  • BOTTOM LINE — Each of the limb leads in this tracing (other than lead aVR) is abnormal. In the context of this man in his 60s with new-onset chest pain — the conclusion that ECG #1 represents acute OMI until proven otherwise is inescapable.

Looking further in ECG #1 — the reason I’ve numbered the beats in this tracing, is because of the variation in ST-T wave morphology in leads V2 and V3. Is it the ST-T wave of beat #5 — or beat #6 that is altered by artifact?
  • If ST-T wave morphology of beat #5 is real — then there appears to be some ST depression in lead V2 + a hyperacute T wave (fat at its peak and wide in its base) in lead V3.
  • On the other hand, if artifact is deforming the ST-T wave of beat #5 — and it is beat #6 that is showing the true ST-T wave morphology — then there may not be acute changes in the chest leads of ECG #1.
  • BOTTOM LINE — If decision-making depends on what is (or is not) going on in the chest leads — then ECG #1 should be promptly repeated. That said — I would not have needed to immediately repeat this tracing — because the limb leads alone are diagnostic.

ECG #3: The 3rd ECG shown above in this case ( = ECG #3) — was the initial tracing done in the ED. As per Dr. Meyers — there is improvement in the acute ST-T wave abnormalities noted in ECG #1 (which considering the associated decrease in chest pain — was consistent with spontaneous reperfusion).
  • The rhythm in ECG #3 is sinus bradycardia at ~50-55/minute.
  • Beat #5 is a PAC that conducts with slight aberration.

ECG #4: Some time after ECG #3 was done — the patient went into VFib. He was successfully defibrillated — and then ECG #4 was obtained.
  • As per Dr. Meyers — there does not appear to be a significant ST-T wave change in the appearance of the limb leads in ECG #4 compared to ECG #3.
  • On the other hand — there is subtle-but-real change in leads V3-thru-V6 of ECG #4 compared to ECG #3.
  • Lead V3 in ECG #4 provides the most interesting finding. Regardless of whether beat #6 or beat #7 in lead V3 of ECG #4 manifests the “true” ST-T wave morphology — both complexes show hyperacute changes in the form of slight ST elevation, ST segment straightening, and an extremely wide base to the T wave. This change is remarkable compared to lead V3’s appearance in ECG #3.
  • The ST segment in leads V4, V5 and V6 of ECG #3 is gently upsloping (curved RED lines). In contrast — the ST segment is straightened and/or slightly coved in these leads in ECG #4 (BLUE lines).
  • So WHY was there such a dramatic change in ST-T wave appearance in lead V3 of ECG #4? Normally acute changes aren’t seen in lead V3 when the “culprit artery” is the RCA (as was shown to be the case on cath). But this patient did have multi-vessel disease, including significant narrowing in the LAD — and, subtle-but-real changes are seen in leads V3-thru-V6 of ECG #4. Taken together, there have been subtle-but-real dynamic changes occurring over the course of the 3 tracings shown in Figure-1.
  • Beyond-the-Core — IF you interpreted the rhythm in the long lead V1 rhythm strip of ECG #4 as sinus — LOOK AGAIN! Isn’t there a change in P wave morphology between the first 2 P waves in the long lead V1 rhythm strip (which are positive, with a short PR interval) — compared to the P waves preceding the rest of the beats on this tracing (which are biphasic, with a longer PR interval)? While this shift in the site of the atrial pacemaker is unlikely to have clinical implications — it is good to train your eye to pick up this type of subtle finding. PEARL: By making it a practice to always spend the first 3 seconds (That’s all it takes!) in your interpretation of any ECG by looking to see if P waves are consistently present with constant PR interval in front of each QRS complex — You will not overlook subtle arrhythmia changes.

Our THANKS to Dr. Meyers for presenting this case.


  1. Mid-RCA subocclusion means that atrial and AV-nodal branches are uneffected. Or maybe it was not really mid-RCA, - rather proximal one.

    1. A mid-RCA lesion would spare the artery to the sinus node (which basically supplies the right atrium) IF the RCA actually provided the artery. Forty-five per cent of the time the LCx provides the SA nodal artery which has nothing to do with dominance. Since the artery to the AV node branches at the crux, if there is inferior LV wall involvement the AV nodal artery may also be affected as well.

    2. THANKS for your insights Jerry regarding expectations based on location of RCA occlusion! I’d add the following re Max's question and commentary in the post — namely that predictions about SA nodal and AV nodal involvement (as well as about manifestations of the resultant cardiac rhythm) are far from perfect — often being influenced by factors such as collateral flow, anatomic variants, coexistent coronary disease, duration of total vs less-than-total “culprit artery” occlusion, etc. In general, sinus bradycardia and/or AV blocks with narrow-QRS ventricular complexes tend to occur more often in acute inferior MIs with a relative increase in parasympathetic (compared to sympathetic) tone — especially during the early hours of acute inferior MI (which is why Atropine is more likely to work early on in these patients). But the “final decider” will be cardiac cath results — which in this case showed a mid-RCA lesion, as well as multi-vessel disease.

  2. Thanks for sharing this helpful article.

  3. Hi.

    I've tried finding where i could easiest contact the authors of this blog. I have, what i bellieve, is a rather interesting case with serial ECGs.

    1. Hello AndreJo. Dr. Smith lists an email address in the right hand column (it is down a bit ... ) — Send ECGs to: — Interesting cases are welcome! Please be sure ECGs are in the correct orientation ( = upright, and not sideways). THANK YOU — :)

    2. Thank you!
      I'm apparently blind!

    3. @ AndreJo — Not blind! We plan to move the Contact e-mail address closer to the top of the page (in the right-hand column) — and to make it more obvious. Interesting cases are WELCOME — so we need to be sure all know where to send them to! — :)

  4. Interessante essas alterações dinâmicas e sutis do eletrocardiograma desse caso e isto mostra quão atentos deveremos estar para análise desse exame nas emergências da dor torácica.

    1. Obrigado pelo seu comentário! Nosso objetivo é ajudar os clínicos e, esperamos em esse maneira, ajudar a melhorar o atendimento médico de emergência (TRANSLATION of Comment from Unknown and My Answer = Interesting subtle and dynamic ECG changes in this case, and this shows who attentive we need to be in the emergency evaluation of patients with chest pain. My Answer: THANK YOU for your comment! Our objective is to help clinicians, and we hope in this way to help to improve emergency medical care.)

  5. Thank you for sharing this case. Very insightful.

    I have a question regarding ECG #4: am I wrong in having the impression that the inferior leads have T waves that are wider based and more straight than the ones in ECG #3? It is stated twice that there is no significant change in comparison to ECG #3 but it seems to stand out to me.

    Another question if I may, this one regarding ECG #1: the T wave in aVL is bifasic with ST depression. Could one state that the positive deflection in the terminal fase of aVL is an early sign of reperfusion (as would be terminal T inversion in III had it been present)? I might be imagining now, but is there a small terminal T wave inversion in II as well?

    Thank you,
    Kris, Emergency Medicine Registrar, Belgium.

    1. THANK YOU for your comment Kris — and SUPERB observations on your part! YOUR 1st QUESTION: Changes in the inferior leads of ECG #4 are subtle — but as I take another look at them, I DO AGREE with you that although tiny in amplitude, the T waves in each of the 3 inferior leads of ECG #4 are fatter-at-their-peak and wider-at-their-base than they were in ECG #3. Because of their tiny amplitude, and because of what I felt were much more significant acute changes in the chest leads of ECG #4 — I did not comment on the inferior leads. This was an oversight on my part — since as YOU mention, there clearly IS a difference in inferior lead ST-T wave appearance (albeit subtle!) — which makes perfect sense in context with the more obvious changes we see in the chest leads of ECG #4. Re YOUR 2nd QUESTION: The history is critical in responding to your question — and as per the initial sentence in this case, the patient’s chest pain had begun ~1 hour prior to ECG #1, and had STARTED TO SUBSIDE during transport (and if I understand correctly just BEFORE ECG #1 was done = it wasn’t my case, so I’m not certain about time interval details). So YES — it seems we are MISSING an ECG at the onset of symptoms (there probably would have been more ST elevation at that time) — and this ECG #1 done ~1 hour later, at a time when chest pain was decreasing could certainly reflect some spontaneous reperfusion. YES, this could be the reason for the terminal positive component of the T wave in lead aVL — and YES, it does indeed look like there may be beginning T inversion in both leads II and III, at least for beat #1 in these leads of ECG #1. I did see this at the time I wrote my comment — but didn’t feel it definite enough to comment on at that time — but I DO agree with you. THANKS again for your “eagle eye” regarding these interesting details — :) (P.S. My Mom was born in Belgium — :)


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