Sunday, February 20, 2022

ECG Blog #285 — A Wider Irregular Rhythm?

I was sent the ECG and 2-lead rhythm strip shown in Figure-1 — with the following 2 Questions:  
  • Is this a NSTEMI ( = Non-ST Elevation Myocardial Infarction)?
  • What is the Rhythm?

Figure-1: 12-lead ECG and non-simultaneous 2-lead rhythm strip that was sent to me.


NOTE: Some readers may prefer at this point to listen to the 8:30-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-60).



Today's ECG Media PEARL #60 (8:30 minutes Audio) — Reviews use of the "Mirror Test" to facilitate recognition of: i) Acute Posterior MI; ii) Acute High-Lateral or Inferior MI (ie, the "magical" reciprocal relationship between leads III and aVL)andiii) Anterior ST elevation due to LVH (that is not indicative of anterior MI).

  • NOTE: I've added LINKS to related ECG blog posts to better illustrate the concepts put forth in today's Audio Pearl (These LINKS are shown below at the end of this blog post).

My Approach to Today's Case:
I was not provided with any history for today's case. I immediately noted that the long 2-lead rhythm strip in ECG #2 of Figure-1 was not recorded simultaneously with the 12-lead ECG ( = ECG #1). Keeping in mind the systematic Ps, Qs, 3R Approach to rhythm interpretation (See ECG Blog #185) My Thoughts were the following:
  • Looking first at the 12-lead tracing ( = ECG #1) — the underlying rhythm is clearly supraventricular (ie, a narrow QRS in all 12 leads).
  • In the 12-lead — the rhythm looks to be quite Regular (taking into account that this smart phone photo is somewhat angled — therefore slightly distorted).
  • The Rate of the rhythm in the 12-lead ECG is ~85/minute
  • P waves are present in the 12-lead ECG. Although the P wave in lead II is upright — this P wave in lead II is tiny in size, and the PR interval appears to be shorter than expected (RED arrows in Figure-2)
  • In support that this tiny upright deflection in front of the QRS in lead II is real — is identification of P waves of similar small amplitude, with similar shorter-than-expected PR intervals in other leads (ie, the RED arrow in lead I — as well as unlabeled P waves in leads aVR, aVL and V1).
  • All of these P waves are Related to neighboring QRS complexes — as determined by a constant (albeit short) PR interval.
  • BOTTOM Line: I suspect that the underlying rhythm in the 12-lead ECG is a low atrial rhythm. To be emphasized — this is not necessarily a pathologic rhythm.

Figure-2: I've labeled KEY features from ECG #1 (See text).

The KEY to diagnosis of the tachycardia in ECG #2 lies with appreciation of the appeance of beat #4. WHY do I say this?

Note that the first 4 P waves in the long lead I rhythm strip are on time! (the 4 consecutive RED arrows in lead I of Figure-2). QRS morphology then changes with beat #4 — which begins a run of an irregular tachycardia with a different (wider) QRS morphology.
  • Isn't QRS morphology of beat #4 in both leads I and II of the long lead rhythm strip intermediate between QRS morphology of beat #3 and beat #5. This strongly suggests that beat #4 (that is preceded by an on-time P wave) is a Fusion beat! IF so — this identifies the run of tachycardia that follows as VT (Ventricular Tachycardia), albeit that beats #4-thru-20 are irregular, and the rate slows toward the end of the tracing (See ECG Blog #128 for review of Fusion beats).

  • I believe the YELLOW arrows in the long lead rhythm strip represent retrograde P waves. This 1:1 VA (retrograde) activity is seen following beats #5-thru-20 — but not after the initial beat in the run (which is the Fusion beat = beat #4).
  • I'm uncertain how wide the QRS is for the run of irregular tachycardia — because we only see 2 of the 12 leads. The QRS is wide — but does not look to be overly prolonged. Predominant negativity in both leads I and II could be consistent with origin near the left anterior hemifascicle — though without a 12-lead tracing during the tachycardia, it is impossible to know for certain the origin of tachycardia.
  • Although VT (and therefore also Fascicular VT) both tend to be regular (or at least fairly regular) rhythms — on occasion, these rhythms may be surprisingly irregular. I show my Laddergram for the proposed mechanism of the rhythm in the long lead rhythm strip below in Figure-3.

  • To Emphasize: The rate of the wide tachycardia in Figure-3 slows toward the end of the rhythm strip — with a rate of between ~80-100/minute for beats #16-to-20. Thus, the rhythm becomes more consistent with AIVR (Accelerated IdioVentricular Rhythm).

  • In further support that beats #4-thru-20 in Figure-3 represent a ventricular rhythm (becoming most consistent toward the end of the tracing with AIVR) — are the ECG findings in the remainder of the 12-lead tracing (Big HINT in the form of the "mirror-image" picture above the RED insert of inverted leads V2, V3 in Figure-2).

  • Acknowledgment: Although far more irregular than usual for a monomorphic (ie, similar QRS morphology) ventricular rhythm — I am otherwise at a loss to explain the irregular wide tachycardia from beats #4-thru-20, other than to call this rhythm VT that slows and evolves into an irregular AIVR. (AFib would not manifest a fusion beat — nor an on-time P wave before beat #4 — nor retrograde VA conduction during the entire run of tachycardia).

Figure-3: My proposed Laddergram for the rhythm in ECG #2. As noted above — the small size and short PR interval in lead II suggest a non-sinus mechanism for the rhythm (probably a low atrial rhythm). We see 4 consecutively-conducted P waves in lead I (RED arrows in this lead). Then follows a wider and irregular rhythm for beats #4-thru-20. There is 1:1 VA (retrograde) conduction beginning with beat #5 (YELLOW arrows). The fact that beat #4 is preceded by an on-time P wave, and manifests a QRS morphology intermediate between that of beat #3 and beat #5 defines beat #4 as a Fusion beat — which confirms a ventricular etiology for the irregular wide tachycardia.

Returning to the 12-lead ECG in Today's Case:
For clarity — I've isolated the 12-lead ECG in today's case in Figure-4As always — I favor the use of a Systematic Approach (which I review in ECG Blog #205):
  • Rate & Rhythm: We've defined the underlying rhythm in this 12-lead tracing as a low atrial rhythm at ~85/minute.
  • Intervals (PR/QRS/QTc): As noted — the PR interval is short, which is not unexpected with a non-sinus rhythm. The the QRS complex is narrow in all 12 leads. The QTc may be slightly prolonged.
  • Axis: The frontal plane axis is normal — as determined by predominant positivity in both leads I and aVF (probably about +50 degrees).
  • Chamber Enlargement: None. 

Figure-4: The 12-lead ECG in today's case (See text).

Regarding Q-R-S-T Changes:

  • Q Waves — There is a small Q waves in lead aVL.
  • R Wave Progression — There is a relatively tall R wave in lead V1 — with Transition (where the R wave becomes taller than the S wave is deep) occurring early, between leads V1-to-V2 (Transition normally occurs between leads V2-to-V4).
  • ST-T Wave Changes — There is diffuse ST segment flattening and depression in virtually all leads except leads I, aVR and aVL. These latter 2 leads show ST segment elevation.
  • Of note — the leads with ST segment flattening and depression all show terminal T wave positivity (with these terminal T waves being peaked and surprisingly tall).


Putting It All Together: 

There are a number of important points to consider in the interpretation of the 12-lead ECG shown in Figure-4:

  • The ECG finding of diffuse ST segment depression (ie, present in at least 7-8 leads) — in association with ST elevation in lead aVR (and sometimes in lead V1) — suggests the entity of diffuse Subendocardial Ischemia. Although this may be due to non-cardiac disorders (ie, shock, profound anemia, "sick" patient) — the most likely etiology in today's tracing, given the composite of ECG findings is severe coronary disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease).

  • PEARL #1: When the diffuse ST depression is maximal in leads V2, V3 and/or V4 (as it is in Figure-4)Posterior Infarction that may be acute is likely.

  • PEARL #2: In support of the likelihood of acute posterior infarction is the positive "Mirror" TestAs discussed in detail in the above Audio Pearl — the Mirror Test is used as a visual aid to facilitate recognition of acute posterior MI. The principle of this test is simple: It is based on the fact that the mirror-image view of anterior leads provides insight to the nature of electrical activity as viewed by the posterior wall of the left ventricle.
  • Note that I have vertically flipped anterior leads V2 and V3 in the RED insert of Figure-4 (to show the mirror-image view of these 2 leads). Doesn't the shape of the already tall R waves, the "shelf-like ST depression and terminal T wave positivity seen in leads V2 and V3 of Figure-4, when vertically flipped (as viewed in the Mirror Test) suggest deepening Q waves — worrisome shape and amount of ST elevation — and already deep T wave inversion?

  • PEARL #3: Isolated posterior infarction is possible, but uncommon. Instead — one usually sees inferior lead ST elevation in association with the anterior ST depression of posterior infarction. The fact that the ST depression with terminal T wave positivity is so diffuse — in association with maximal ST depression in leads V2-V4 — suggests a combination of diffuse subendocardial ischemia (from severe coronary disease) + acute posterior infarction may be present.

  • PEARL #4: Although the QRS complex in lead aVL is very small in amplitude — there is a Q wave + ST elevation + T wave inversion in this lead. This suggests acute high-lateral lead involvement. Acute occlusion of the LCx (Left Circumflex) coronary artery may cause the ECG picture of acute Postero-Lateral MI seen in Figure-4. Therefore — today's tracing is not a "NSTEMI" (in the sense of positive troponin but without coronary occlusion) — but rather a patient who likely has severe underlying coronary disease + acute occlusion of the LCx until proven otherwise.

  • PEARL #5: While impossible to date the infarction in today's case without knowing the history — there are a number of features that suggest spontaneous reperfusion has already occurred. These include: i) The surprisingly tall terminal T wave positivity in leads V2, V3, V4 (the mirror image of which [as shown in the RED insert] would show T wave inversion — See ECG Blog #258 and ECG Blog #266); ii) Reperfusion T wave inversion is also seen in lead aVL; and, iii) The rhythm in ECG #2 is an irregular AIVR — and this is an extremely common "reperfusion" rhythm in the context of recent infarction!

Case Follow-Up:
Cardiac cath was performed on the patient in today's case — and revealed multi-vessel coronary disease + recent acute occlusion with the "culprit" artery being the OM (Obtuse Marginal) branch of the LCx (Left Circumflex) coronary artery.

Acknowledgment: My appreciation to Ahmed Shaaban (from Cairo, Egypt) for the case and this tracing.



Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. (NOTE: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI).

  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
  • The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
  • The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

  • ECG Blog #108 — Reviews the ECG diagnosis of AIVR (Accelerated IdioVentricular Rhythm) — and clinical implications of this rhythm.

  • ECG Blog #128 — Review the concept of Fusion Beats (and clinical implications of their recognition).
  • ECG Blog #133 — Illustrates diagnostic use of Fusion Beats to confirm VT.
  • ECG Blog #129 — More on Fusion Beats.

How to Draw a Laddergram (Step-by-Step Demonstration) 

  • See ECG Blog #69 — for a Step-by-Step description on drawing a Laddergram.
  • See ECG Blog #188 — for a brief ECG Video review on the basics of what a Laddergram is — with LINKS at the bottom of the page to more than 50 ECG blog posts in which I review illustrative laddergrams.
  • See ECG Blog #164 — for a user-friendly rhythm solving approach to AV Wenckebach, followed by Step-by-Step construction of the Laddergram.
  • CLICK HERE — to DOWNLOAD my PowerPoint Laddergram STENCIL for  your use as desired.


ADDENDUM (2/18/2022): I've added below in Figure-5 review of a case in which there is an isolated posterior MI (ie, without accompanying inferior lead ST elevation).



Figure-5: KEY points in the recognition of isolated posterior MI (This figure is taken from ECG Blog #193 — in which I review the "Basics" for predicting the "culprit" artery).


  1. Very nice prof i well send more tracing for you but idont know how

    1. Go down the RIGHT-hand column of ANY page on my Blog — and you will come to a link that says, "To Send an E-mail" — You can then write me! — :)