Teach your learners: when the QRS is wide, the J-point will hide, so trace it down and copy it over!

Case submitted by Alexis Cates, written by Pendell Meyers

A middle aged man with history of HTN, DM, and VSD repair at age 6, presented to the ED with chest pain and diaphoresis while exercising.

Here is his initial ECG:

What do you think?

Hopefully this is too easy for most readers, but it it shows a massive, obvious inferoposterior OMI, in the setting of sinus tachycardia with RBBB and LPFB. It may be too easy for you, but there is a very valuable teaching point for you as you spread ECG knowledge to your group, your residents, your learners.

Over the past 3 years I have shown this ECG and many similar ones to many residents and medical students, and it has become apparent to me that there is a very powerful pitfall in beginner ECG interpretation that happens when an abnormal and/or bizarre QRS complex attempts to hide the J-point from the learner. Their mental framework is to find the ST segment and then measure the ST deviation. This framework is obviously very inaccurate for its purpose of identifying Occlusion MI, but at least it provides an approach for the beginner. This is easily doable for the learner in regular QRS complex conduction, but then they encounter an abnormal QRS conduction and things get much more difficult because the classic STEMI paradigm teaching basically only applies to normal QRS complexes. In my medical school curriculum, there was essentially no teaching or understanding of what to do in the STEMI paradigm if the QRS is abnormal, or when the J-point isn't readily obvious, with the one exception of LBBB.

Here are the key take home points in my lecture to first year residents, which of course I first learned here on this blog:

1) "When the QRS is wide, the J-point will hide."

2) "When you aren't sure where the J-point is, your next move is to find it in any lead where you're more sure about it, then trace it down and copy it over."

"Trace it down and copy it over" means you find the J-point in any lead where you are more certain about it, then you trace it down to the rhythm strip to find the J-point on the rhythm strip, and now you can use that point on each QRS complex in the rhythm strip to find the J-point in all 12 leads.


Here is the result in this case:

Massive STE in leads III and aVF, with reciprocal STD in aVL. V2-V5 with clear STD, maximal in V2-4, indicating posterior OMI in addition to inferior. RBBB + LPFB would be concerning by itself for possible LAD occlusion even without clear STE, however would also be a consistent with many of the congenital heart disease surgeries, one of which this patient had at age 6. The morphology of the STE is somewhat unusual (downsloping), with reciprocal upsloping STD, but we have seen this morphology most often in the setting of RBBB + LAFB/LPFB (see this in several of our links at the end).

Another teaching point: New or possibly new RBBB, or RBBB + LAFB/LPFB, in a sick looking ACS patient is a very bad sign which correlates with LAD occlusion. The LAD supplies the bundles, and thus acute LAD OMI may present with new bundle blocks. In my experience the most likely blocks, in order of occurence, are first RBBB, second LAFB, last LPFB. I would be much more worried about a patient with new RBBB + LAFB than a patient with new LBBB (without any of the modified Sgarbossa criteria).

The 2017 ESC Guidelines partially address these issues by stating that left and right BBB are considered equal for recommending urgent angiography in the setting of persistent ischemic symptoms, however one could argue that we have already had the recommendation for years that ANY patient with ongoing ischemia (regardless of QRS, regardless of ischemic findings on ECG) should be considered for emergent angiography.

Back to the case:


The team taking care of this patient was not fooled and immediately understood that this patient likely had Occlusion MI. They activated the cath lab.

The cath report showed:
 - severe triple vessel disease
 - culprit: 100% ostial, large circumflex with TIMI 0 flow, with successful PCI with restoration of TIMI 2-3 flow
 - 100% occlusion of the prox RCA (TIMI 0), believed to be chronic due to L to R collaterals
 - 80% mid LAD, also with 99% stenosis after a large, believed to be intramyocardial vessel, probably "second LAD"

Initial troponin I: 9.91 ng/mL

Troponin I 6 hrs after cath: 968.3 ng/mL (enormous MI)


Learning Points:

When the QRS is wide, the J-point will hide

When you can't find the J-point, you first find it in any lead, then trace it down and copy it over.

Use this case and the following ones to train yourself and teach your learners:

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

Giant R-waves. What are they?

"Shark Fin": A Deadly ECG Sign that you Must Know!

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Comment by KEN GRAUER, MD (9/20/2019):

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Great case by Drs. Cates & Meyers for emphasizing the tremendously important concept, “When the QRS is Wide — the J-Point will Hide!"

• That said, I do disagree on one aspect of this case with Dr. Meyers = in that I did not in any way think this case “too easy for most readers”. Instead, I found interpretation of this ECG to be especially challenging.

PEARL: Dr. Meyers emphases that when you are unsure about where the J-point lies — Search for a lead in which you are sure! Then trace this J-point down to a simultaneously-recorded long lead rhythm strip — and copy this over for the other 3 sets of simultaneously-recorded leads.

• Starting with the ECG Figure in which Dr. Meyers’ vertical RED lines denote the J-Point (ie, the end of the QRS complex and beginning of the ST segment) — I have reproduced the initial ECG in this case in Figure-1. I’ve added thin vertical BLUE lines to denote the beginning of the QRS complex in each lead — and have then magnified 1 QRS complex in several of the leads that I discuss below.
• To me — leads V2 and V3 in Figure-1 depict the clearest boundaries for the beginning and end of the QRS complex. Following Dr. Meyers directions, allows us to determine where these beginning and ending boundary points lie on the simultaneously-recorded long lead V1 rhythm strip. We can then raise vertical BLUE and RED lines to denote the beginning and end of the QRS complex in simultaneously-occurring leads I, II, III — aVR, aVL, aVF — and V4, V5 and V6 (Figure-1).

Figure-1: Starting from Dr. Meyers ECG Figure that illustrates the J-point by vertical RED lines — I’ve added BLUE lines to denote the beginning of the QRS complex and, magnified the QRS in several leads (See text).

MY THOUGHTS on ECG #1: Sinus P waves are seen a number of leads (RED arrows in Figure-1). Although small in amplitude — these P waves are clearly upright in lead II with a fixed and normal PR interval that defines sinus rhythm.

• The QRS complex is exceedingly wide (I measure ~0.19 second) — and, QRS morphology is bizarre!
• Although the presence of a predominantly upright QRS complex in lead V1 — in association with fairly slender R waves in lateral leads I and V6, which both feature wide terminal S waves is consistent with RBBB (Right Bundle Branch Block) — QRS morphology in many of the leads in Figure-1 is bizarre! Have you ever seen an Rsr’S’R’’s’’ complex, as is evident in lead V2?

PEARL: The presence of such marked QRS widening + bizarre QRS morphology in so many leads + such unusual notching (fragmentation) in so many leads — tells us that this patient must have some form of significant underlying heart disease! This is not the type of QRS morphology seen with simple RBBB, with or without a hemiblock.

• When QRS morphology is as altered as we see in Figure-1 (especially in the magnified leads) — the usual process for assessing ST-T wave changes will also be altered.
• History is KEY. This patient underwent VSD (Ventricular Septal Defect) repair at age 6 — and he is now a middle-aged man.
• The ECG appearance of patients with VSD is highly varied — depending on age of the patient; size and location of the VSD; the extent of shunt flow and resultant hemodynamic changes; whether operative repair was or was not undertaken — to name a few. Brief pictorial review of the ECGs from several patients with VSD can be found on Dr. Mete Alpaslan’s BLOG post on this subject. Of interest — the only 1 of the 6 ECGs posted by Dr. Alpaslan that shows bizarre QRS morphology was from a patient with transposition of the great vessels in addition to a VSD. I then did a Google search of "VSD ECG" — and among the first 50+ tracings posted (CLICK HERE) — I didn't see a single one with as wide and bizarre a QRS as in Figure-1 above. Therefore, to ME — the bizarre QRS morphology we see in Figure-1 indicates the likelihood of much more than simple "VSD repair in a 6-year old" for this patient.
• What does the baseline ECG of this patient look like? “Baseline” ST-T wave appearance may possibly have been much more abnormal than we might think ... — and to me, this is what makes this case so challenging.
• That said — I do completely agree that there are marked ST-T wave deviations (ST elevation and ST depression) in multiple leads in Figure-1 (as defined by the J-point notation by Dr. Meyers) — so acute STEMI until proven otherwise must be assumed for this middle-aged patient with new-onset chest pain.
• That said — Are the very large inferior Q waves in Figure-1 new? How long have they been there?
• This patient was found to have severe 3-vessel disease. Is the ECG in Figure-1 reflective of just one of a bunch of MIs that this patient has already suffered? Has this patient’s QRS complex been this bizarre for many years? Again, as per Dr. Meyers — We have to assume acute STEMI until proven otherwise — but I suspect there's more ...

I would have loved to learn more about this patient’s prior history — and to have seen his “baseline” ECG.

Our THANKS to Drs. Cates and Meyers for presenting this instructive case!