Wednesday, December 12, 2018

Can you see through this wide complex rhythm?

Written by Pendell Meyers

A 76 year old man with history of CHF, moderate aortic stenosis, insulin-dependent diabetes, hypertension, stroke, CAD s/p stents, CKD, PVD, OSA presented to the ED with shortness of breath and chest pain off and on for 2 weeks. This afternoon his symptoms intensified so he called EMS.

In the ED he appeared acutely ill, with HR 100-115, RR 20-25, BP 93/52, hypoxic to 88-92% on 5L nasal cannula, afebrile.

Here is his presentation ECG, followed by his baseline ECG on file:
Presentation ECG.

Baseline ECG.

The presentation ECG shows ventricular paced rhythm at rate of approximately 120 bpm. The J-point in V3 is inappropriately isoelectric, and there is excessively discordant STD in V4-V6 and I. There is excessively discordant STE in aVR. These findings suggest diffuse severe supply-demand mismatch (a.k.a. diffuse subendocardial ischemia).

Back to the case:

The clinicians suspected cardiogenic shock and initiated resuscitation. He was also found to be in diabetic ketoacidosis. He was admitted to the CCU, and the cardiologists were worried that they were missing ECG findings because of the paced rhythm, so they decided to temporarily turn off the pacemaker to capture an ECG in normal rhythm.

Here are his two ECGs from that time, the first before suspending his pacemaker and the second after:

With pacing
Paced rhythm with the same findings as the presentation ECG.

Pacing suspended
Atrial fibrillation with narrow QRS. Large STD in V3-V6, I, II, III, and aVF, as well as STE in aVR and V1.

Because of these findings in normal QRS rhythm, he was then taken for urgent cath. He was found to have severe three vessel disease, with a proximal LCX lesion that was 95% stenosed with TIMI 3 flow at the time of cath. A stent was placed in the LCX, and an impella pump was placed for persistent cardiogenic shock.

Over the next 24 hours the ECG normalized:

The patient survived despite a complicated hospital course.


Just like Occlusion MI can be seen "through" left bundle and ventricular paced rhythms, so can other ECG findings such as those of diffuse subendocardial ischemia.

In our validation study of the modified Sgarbossa criteria, we performed an exploratory analysis for this very question. Here are a few relevant quotes from the study:

"We identified 4 patients who did not meet our definition of ACO, yet did have
notable catheterization findings and outcomes warranting immediate diagnosis.
These 4 patients were found to have AMI and new 3-vessel or left main coronary
artery disease with either an acute but non-occlusive culprit lesion or very high
troponin. Peak 24-hour troponin T levels were 0.25, 0.75, 1.04, and 6.61 ng/mL.
Two of these 4 required urgent or emergent CABG. We categorized these patients as
having “acute 3-vessel/left main disease myocardial infarction” (3V/LMD). Three of
these four patients had discordant ST elevation (STE/S ratio ≤-0.20 in lead aVR), but
only one of these three was positive by the -0.25 modified criteria. Two of the four
3V/LMD patients also met the overall discordance criteria (≤-0.30) due to
widespread ST depression (ST depression/R-wave ratio ≤-0.3) in various other
leads, including III, aVF, V5, and V6. None of the four met the weighted or
unweighted original Sgarbossa criteria."

"Our exploratory analysis of the four patients in our study with acute myocardial
infarction due to severe 3-vessel or left main disease (but without proven
ACO) suggests that this condition may also be identifiable in the context of LBBB. We
believe these patients’ ECGs may not be as reliably identified by the criteria
designed to detect ACO, mainly because they did not manifest concordant ST
elevation. In the same way that acute 3V/LMD presents in normal conduction as
diffuse ST depression with reciprocal ST elevation in aVR, we found that it usually
presented in LBBB with excessively discordant ST depression in V5 or V6 with
excessively discordant ST elevation in aVR (see Figures 7 and 9 in the online

Here are figures 7 and 9 from the online appendix:

 Figure 7: This ECG was recorded in a patient who was found to have a non-occlusive LAD culprit lesion in the setting of severe 3-vessel disease. Notice the extremely proportionally excessive discordant ST depression in leads V5 and V6, with proportionally excessive reciprocal ST elevation in lead aVR.

Figure 9: In this ECG the conduction pattern alternates between normal and LBBB, showing the equivalent findings of severe global ischemia (in this case due to severe 3-vessel disease with critical left main stenosis requiring emergent CABG) in both conduction patterns. The predominant findings are diffuse ST depression with reciprocal ST elevation in aVR, which manifest in LBBB as proportionally excessive discordant ST changes (with no concordant ST-elevation).

Learning Points:

Severe diffuse supply/demand mismatch ischemia (diffuse subendocardial ischemia) may be identified in the setting of LBBB and paced rhythms by identifying excessively discordant diffuse STD in multiple leads with STE in aVR, just as in normal QRS rhythm.

If you have the training and capability to change pacemaker settings, it may uncover ECG findings that you would not otherwise have noticed in paced rhythm. Otherwise, you should train with cases like this to be able to see "through" the wide complex rhythm.


  1. On the first ECG i think there is concordant STD in V4 and maybe AVF or am I wrong ?

  2. A great lesson, but it's really complicated for me. There are two issues that I have not understood yet, hope you can clarify.

    1. It is about the pacemaker. Apparently, from baseline ECG, this patient was placed a dual-chamber pacemaker, but why does ECG#1 only show a ventricular chamber working, and why can it create a 120bpm tachycarida? Could you please tell me what kind of this pacemaker and why does it work like that?

    2. It is about the ECG after turning off the pacemaker (ECG#4). What I see is a regularly irregular rhythm, that has P waves with lengthening PR intervals, so I think it can be a Wenckebach AV block. Could you clarify this for me?

    Thank you.

    1. 1) I'm not sure exactly what type of pacemaker it was, but I agree it must be dual chamber based on the baseline ECG. There are ventricular spikes at 120 bpm. this can happen when the pacemaker senses intrinsic atrial activity at 120bpm, then it simply matches the rate. I can't say I see clear P-waves, but the pacemaker would be able to detect them even if we can't see them.

      2) Hmm you may be right. It does look like there is regular grouped beating. The P-waves are not clear enough for me to be certain, but I think you are probably right, wenckebach type I second degree HB. Thanks!!

  3. Hi,
    Thank you for the post and the blog I've learned a lot through the years.
    I was wondering on the 4th ECG when the pacing was suspended was there ST elevation in AVL with the ST depression in inferior lead would you think it would be a STEMI by definition. It's unlikely giving the cath result, but wanted to hear your thoughts on that.
    thank you

    1. The definition of "STEMI" would require 2 leads with ST elevation meeting the criteria. aVL is up, but the only adjacent lead would be lead I which has STD rather than STE. So it does not meet STEMI criteria.

      Also interesting, the definition of STEMI technically has nothing to do with the cath results (unlike OMI). It the patient meets 4th universal definition of MI and has ECG findings meeting the STEMI criteria, then the patient has a "STEMI" by definition, no matter whether the cause of the MI is plaque rupture thrombotic ACS (type 1 MI) or not. For example, takotsubo cardiomyopathy may cause + STEMI criteria on ECG plus biomarkers that meet criteria for MI, thus "STEMI".


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