Written by Pendell Meyers
An adult man presented with acute chest pain. He appeared critically ill. He had undergone stenting of the LAD several weeks ago (unclear whether elective for stable symptoms, or in response to acute coronary syndrome).
Here is his triage ECG:
Here is the digitized version with higher image quality:
He was rushed to the resuscitation area for "unstable VTach."
It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia?
If we look for P-waves, they are clearly visible:
Case continued
One of my former residents (who I taught about this pattern years ago!) recognized this ECG immediately and understood its significance and severity.
He sent it to me with no information, and I of course responded: "Definite LAD OMI, the worst pattern possible with ischemic RBBB and LAFB. Near 100% mortality without rapid reperfusion."
The ECG shows sinus tachycardia, RBBB+LAFB, and signs of anterolateral acute transmural ischemia (most likely due to acute coronary occlusion), with concordant STE in I and aVL, inappropriate STE in V4-6 (though limited a bit by motion, still definite). Of course there is reciprocal, concordant STD in inferior leads.
You can see above in the original ECG software used in actual practice, the QRS duration was grossly mismeasured at 284 msec (I have never seen an actual QRS duration of 284 msec, anything that widens the QRS kills the patient long before 284 msec). I fear that many learners would also not easily recognize where the QRS actually ends, and I fear that some may think that this is ventricular tachycardia due to inability to distinguish QRS from ST segment. You can see that our PM Cardio software measures the QRS duration more accurately in this case at 139 msec.
Here we show the median beat image, with J point marked by vertical dotted lines, to show where the QRS actually ends. The software is not perfect at this yet, but I generally agree with it in most leads here:
Queen of hearts of course recognizes OMI with extremely high confidence level overall.
Here is the explainability image of this ECG:
Unfortunately, despite immediate cath lab activation and medical therapy, the patient died on the cath lab table before emergent angiography could be performed.
If you can't instantly recognize this ECG and overcome its pitfalls, the patient will have even less of a chance than this one.
See our other cases with similar patters, to burn this deep into your brain files:
Smith: In my experience, these cases of LAD OMI with RBBB and LAFB are either about to arrest, post-arrest, and/or in cardiogenic shock. The ST Elevation is NOT typical. It is ofen downsloping
This one is also a wide complex tachycardia. The cath lab was activated but the interventionalist refused, saying that it was "Ventricular Tachycardia." The patient died of cardiogenic shock 8 hours later:
Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation
Acute chest pain, right bundle branch block, no STEMI criteria, and negative initial troponin.
An elderly woman with acute vomiting, presyncope, and hypotension, and a wide QRS complex
A man in his 40s who really needs you to understand his ECG
Cardiac Arrest at the airport, with an easy but important ECG for everyone to recognize
A woman in her 60s with 6 hours of chest pain, dyspnea, tachycardia, and hypoxemia
Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?
MY Comment, by KEN GRAUER, MD (1/11/2025):
- That despite all the "noise" and baseline motion artifact — sinus P waves are present! While difficult to see in many leads — definite upright P waves in lead II with a constant PR interval are consistently seen for each of the beats in the long lead II rhythm strip (RED arrows in Figure-1).
- That the chief complaint of today's patient was acute CP (Chest Pain) — with a history of known coronary disease and LAD stent placement a few weeks earlier. While of course possible for patients with sustained VT to present with acute CP — Think acute OMI with this clinical presentation.
- That (as per Dr. Meyers) — the combination of: i) Marked sinus tachycardia (rate ~120/minute) in a critically ill patient with acute CP; ii) RBBB/LAHB; — and, iii) ST elevation in multiple leads (in association with inferior lead ST depression) constitutes the "Must Recognize" pattern of acute proximal LAD occlusion + cardiogenic shock until proven otherwise.
- To quote Drs. Meyers & Smith — "When the QRS is wide, the J-point will hide. So, your next step is to Trace it down and Copy it over".
- In Figure-1 — the vertical RED line that runs through simultaneously-recorded leads V1,V2,V3 shows my starting point — because the EASIEST leads for defining the end of the QRS complex in this tracing are leads V1,V2.
- Continuing this vertical RED line downward through the simultaneously-recorded long lead rhythm strip shows the point in lead II where the end of the QRS lies.
- "Copying over" this point in lead II that defines the end of the QRS — allows us to extend upward vertical BLUE lines in each of the 3 remaining groups of simultaneously-recorded leads. The ST segment begins to the right of these vertical BLUE lines in each of the remaining 9 leads.
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| Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
- — 1st — recognizing the rhythm as sinus tachycardia (most easily done by looking beat-to-beat for P waves in the long lead rhythm strip).
- — 2nd — recognizing the obvious QRS widening (most easily done by looking at the QRS in leads V1,V2) — and seeing the bifascicular block = RBBB/LAHB (defined by the wide, all-upright QRS in lead V1 — and the almost-all-negative QRS in each of the inferior leads).
- — 3rd — seeing definite ST elevation in lead I, as well as in the other high-lateral lead ( = lead aVL). More subtle is the inferior lead reciprocal ST depression — though once that is also recognized, acute OMI is confirmed. On seeing the amount of ST elevation in lead I — I thought, "There is no way that this is not going to be an extensive ongoing STEMI."
- — 4th — recognizing definite ST elevation in lateral chest leads V4,V5,V6 (and by extension — beginning ST elevation also in lead V3).
- — 5th — thinking that the sharp T wave inversion in lead V2 was disproportionately deeper than I would expect from simple RBBB (therefore ischemic).
- — 6th — being impressed by the QS complex in lead V6 — and the very wide and deep Q wave in lead V5 (BLUE arrows in Figure-1).
- — 7th — seeing T-QRS-D in lead V4 (for more on Terminal-QRS-Distortion — See My Comment in the November 14, 2019 post and the February 18, 2022 post).
- In addition to the bifascicular block — additional indicators of adverse prognosis in today's case include: i) The marked sinus tachycardia; ii) The diffuseness of ST elevation with inferior lead reciprocal ST depression; — and, iii) Loss of lateral chest lead forces (especially the Qr in lead V5 and the QS in lead V6) — as well as the almost-all-negative inferior lead QRS complexes — with these findings suggesting already extensive necrosis with impending cardiogenic shock.
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