Sunday, February 14, 2021

ECG Blog #194 — Did this OMI Reperfuse?

Today’s case is a Continuation of my previous post = ECG Blog #193. The tracing I’ll discuss is ECG #2, shown below in Figure-1:

  • The TOP tracing in Figure-1 was obtained from a man in his mid-30s, who presented to the ED with new chest pain. As discussed in detail in ECG Blog #193 — acute cardiac cath capability was not available, so the patient was immediately treated with thrombolytic therapy for his large acute infero-postero-lateral STEMI. The presumed “culprit” artery was a dominant LCx (Left Circumflex) Artery.
  • Within an hour of starting thrombolytic therapy — the patient’s chest pain was relieved — and, the BOTTOM 12-lead tracing and long lead II rhythm strip shown in Figure-1 was obtained.


QUESTIONS: In the context of the above-described events considering this patient’s initial ECG #1:

  • How would YOU interpret the 12-lead ECG and long lead II rhythm strip that is shown in ECG #2?
  • Is it likely that the “culprit” artery has reperfused?
  • Given clinical improvement and relief of this patient’s chest pain — Is specific treatment of the rhythm shown in ECG #2 needed?


Figure-1: Comparison of the initial ECG from this 30-something man with new-onset chest pain (that we discussed in detail in ECG Blog #193) — with the follow-up tracing obtained within an hour after starting thrombolytic therapy (See text).


NOTE: Some readers may prefer at this point to listen to my 6-minute ECG Audio PEARL before reading My Thoughts regarding ECG #2 in Figure-1. Feel free at any time to review to My Thoughts on ECG #2 (that appear below ECG MP-11).




Today’s ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.


MY Thoughts on ECG #2:

ECG #2 would be exceedingly challenging to interpret without the benefit of the above history and availability of this patient’s initial ECG. This is the art of clinical electrocardiography — which entails correlation of serial tracings with the history and clinical course.

  • First — Common things are common. In this patient who presents with new-onset chest pain — it is obvious from no more than a glance at ECG #1 — that this patient is in the midst of evolving a huge acute STEMI from acute occlusion of a major coronary artery. Therefore — we’ll be on the lookout for common sequelae of an acute STEMI.
  • BEST possible outcome from this presentation would be reopening of the acutely-occluded coronary artery — either spontaneously and/or by specific treatment measures.


As emphasized in the above ECG Media PEARL #11 — even without cardiac catheterization, there are clinical and ECG clues that can provide insight into the likelihood that the “culprit” artery has reopened. The 4 clues to look out for include:

  • Relief of chest pain (or at least a significant reduction in the amount of chest pain) that corresponds to the timing you’d expect after giving thrombolytic therapy that was successful.
  • Significant reduction in the amount of ST segment deviation (ie, including reduction in amount of both ST elevation and reciprocal ST depression).
  • Development of “reperfusion T waves”.
  • Development of reperfusion arrhythmias.


Common Things are Common: Although detailed interpretation of the long lead II rhythm strip at the bottom of ECG #2 is complex — Common things are common. Application of this commonsense truism facilitates clinical interpretation of this rhythm, even though precise elucidation of the mechanism of this rhythm may not be immediately evident. The KEY points to appreciate from assessment of Figure-1 in the context of the clinical course in today’s case include the following:

  • Acute reperfusion of the “culprit” artery is highly likely in today’s case because: i) Chest pain was relieved within an hour of starting thrombolytic therapy; ii) The amount of ST segment deviation (elevation and depression) has greatly decreased in the narrow beats of ECG #2, compared to the amount of ST deviation seen in the initial ECG; andiii) A very common reperfusion arrhythmia is seen.
  • There are 2 main QRS morphologies in ECG #2 — one of which is wide, and the other of which is narrow (This is best appreciated in the long lead II rhythm strip).
  • No P waves are seen anywhere in ECG #2. As a result — the underlying rhythm is not sinus.
  • Beats #2, 4, 6, 8 and 9 are wide. Each of these wide beats is preceded by a fairly long R-R interval (that varies from ~4-to-6 large boxes in duration). These wide beats are ventricular beats — which depending on the preceding R-R interval, are occurring at a rate of between 50-to-70/minute. Since the normal idioventricular escape rate is between 20-40/minute — the ventricular beats seen in the long lead II rhythm strip of ECG #2 represent a slightly irregular and slightly Accelerated IdioVentricular Rhythm ( = AIVR).


Common Things are Common: As emphasized in the above ECG Media PEARL #11 (and as we discussed in additional detail in ECG Blog #108) — AIVR is one of the most common rhythms associated with acute reperfusion.

Continuing with our interpretation of the rhythm in ECG #2:

  • Beats #1, 5 and 7 in the long lead II rhythm strip are narrow. These beats are not preceded by P waves. Comparing morphology of simultaneously-obtained leads I, II, and III for beat #1 — for leads aVR, aVL and aVF for beat #5 — and for leads V1, V2 and V3 for beat #7 — suggests little change in QRS morphology, but great reduction in the amount of ST segment deviation. This strongly suggests that the underlying rhythm in ECG #2 is a junctional escape rhythm (ie, narrow QRS; no P waves), with the “good news” being the marked reduction in ST elevation and depression in leads such as lead II (for beat #1)lead aVF (for beat #5) and leads V1 and V2 (for beat #7) — compared to what was seen in these same leads in ECG #1.
  • Beyond-the-Core: Look at beat #3 in the long lead II rhythm strip. Isn’t QRS and ST-T wave morphology of beat #3 intermediate between that of the purely ventricular beats (ie, beats #2, 4, 6 and 8) — vs the purely junctional escape beats (ie, beats #1, 5 and 7)? This is because beat #3 is a Fusion Beat, that occurs as a result of near-simultaneous occurrence of a junctional and ventricular escape beat.
  • Even more subtle — is recognition that beat #9 is also almost certainly a fusion beat, because that is the only way to explain why depth of the QS complex of beat #9 in the long lead II rhythm strip, and in simultaneously-obtained leads V4, V5, V6 is less deep than the QS complex of beat #8 in these leads. 
  • NOTE: For more on the recognition and clinical significance of Fusion Beats — Please CHECK OUT our ECG Blog #128 and Blog #129.


LADDERGRAM of the Rhythm in ECG #2: As discussed above — I believe the underlying rhythm in ECG #2 is junctional escape — with interposition of a slightly irregular and slightly accelerated AIVR.

  • Both of these rhythms would not be unexpected given the extensive acute infero-postero-lateral STEMI seen in ECG #1.
  • The absence of P waves in ECG #2 is represented in the laddergram by the empty Atrial Tier.
  • RED circles within the AV Nodal Tier of Figure-2 represent junctional escape beats.
  • RED circles at the very bottom of the Ventricular Tier represent ventricular beats.
  • Beats #3 and 9 are fusion beats. The double parallel line within the Ventricular Tier represents the point within the ventricles where junctional and ventricular beats meet. The reason I drew these double lines slightly higher up for beat #9 — is that the QRS complex of beat #9 is more similar in QRS morphology to the purely ventricular beats, therefore it "meets" with the AV nodal beat at a higher up point within the ventricles.
  • NOTE: For review on how to read laddergrams — See our ECG Blog #188.


Figure-2: For clarity — I’ve drawn a laddergram of the long lead II rhythm strip at the bottom of ECG #2 (See text).



Putting It All Together:

As I stated at the outset — precise interpretation of the rhythm in ECG #2 is complex. That said — Precise interpretation of this rhythm is not at all essential for recognizing the KEY clinical “Take Home” points about this case! Do NOT be concerned if you did not recognize the precise arrhythmia mechanism.

  • What is important to appreciate — is that compared to ECG #1 — this patient is much better off than he was prior to initiation of thrombolytic therapy because: i) His chest pain has been quickly relieved; ii) The relative amount of ST elevation and depression in narrow QRS beats is significantly less in ECG #2 than it was in ECG #1; andiii) Appreciation that the slightly accelerated ventricular beats we see in the long lead II rhythm strip is consistent with a variation of AIVR — that in the clinical context of today's case strongly suggests successful reperfusion with the use of thrombolytic therapy.


Follow-Up to this Case:

The patient improved clinically following thrombolytic therapy. No specific treatment of AIVR with the ventricular beats in Figure-2 was needed. The next ECG showed resumption of sinus rhythm.



Acknowledgment: My appreciation to Hosain Saleh (from Damascus, Syria) for the case and this tracing.


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