Thursday, May 19, 2016

ECG Blog #125 (Acute STEMI – Reperfusion – AIVR – IVCD)

This 12-lead ECG (with accompanying long lead II rhythm strip), was obtained from a 44-year old man who presented to the ED (Emergency Department) with new-onset chest pain. He was hemodynamically stable at the time this tracing was recorded. If no other history was available — How would you interpret this ECG? What do you suspect is going on clinically?
Figure-1: 12-lead ECG (with long lead II rhythm strip) obtained from a 44-year old man with new-onset chest pain. How would you interpret this ECG? What do you suspect is going on clinically? NOTEEnlarge by clicking on Figures.
Interpretation: This is indeed a challenging case! In the interest of conveying an approach to clinical decision-making — I will walk through my step-by-step thought process in analyzing this tracing:
  • We are told the patient was hemodynamically stable at the time this tracing was recorded. The “good news” — is that at least we have some time to work through our interpretation without need for instant intervention.
  • The history we are given is new-onset chest pain”. The obvious concern is whether acute infarction is evolving ...
  • Quick perusal of the 12-lead ECG suggests that the QRS complex is markedly widened, at least in most leads on the tracing. The reason the QRS complex does not initially appear to be wide in lead II — is that the terminal part of the QRS in this lead is nearly isoelectric to the baseline. That this is the case should be obvious from comparison of lead II with simultaneously-recorded leads I and III. Thus, although the QRS complex does not appear to be wide in the long lead II rhythm strip at the bottom of this tracing — the QRS is wide!
  • Normal sinus P waves are absent! That is, there is no consistent upright P wave preceding each QRS with constant PR interval — at least not for the majority of this tracing ...
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For me — further interpretation of this tracing required labeling P waves. I simply find interpretation of complex arrhythmias far easier once I am able to readily identify atrial activity. This case is an ideal example of this basic interpretation principle. This case also illustrates the importance of becoming facile in use of simultaneously-recorded leads — as I found myself going back-and-forth constantly between the long lead II rhythm strip (at the bottom of the tracing) — and various leads in the 12-lead ECG (Figure-2):
Figure-2: The 12-lead ECG in Figure-1 (with accompanying long lead II rhythm strip at the bottom) — has been labeled. Colored arrows indicate atrial activity. The beats in the rhythm strip have been numbered (See text).
In “real life” — I draw in arrows on a copy of the original tracing to facilitate instant recognition of atrial activity (Figure-2). I routinely use calipers to accomplish this — keeping in mind that there may often be slight variability in regularity of an underlying sinus mechanism rhythm (ie, sinus arrhythmia).
  • Numbering the beats greatly facilitates discussion of complex arrhythmias with colleagues. I chose different colors for the P wave arrows I drew in here purely for educational purposes. More than the “color” — what counts is determining whether there is or is not an underlying sinus mechanism vs an ectopic atrial mechanism, retrograde atrial activity — or, some combination of these features.
  • NOTE: You often will not clearly see P waves in each spot on the tracing where you think P waves are (or should be) occurring. This is common, and may be due to sinus arrhythmia, technical imperfections in the tracing, or hiding of P waves by simultaneous occurrence of the QRS complex or ST-T wave. That said, if you are able to otherwise march out a fairly regular rhythm with calipers — chances are atrial activity remains regular throughout even if you don’t clearly see P waves in every expected spot on the tracing ...
  • Finally — Remember that sinus (ie, forward-conducting) P waves should be upright in lead II (as well as in other inferior leads). In contrast, retrograde P waves should be negative in lead II. Retrograde P waves will also typically be upright in leads aVR and V1.
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Use of Figure-2 to Interpret this ECG:
Returning to the rhythm in this case — the QRS complex is wide, sinus P waves are absent — and, the R-R interval is fairly regular at a rate of ~80/minute for at least the first 10 beats on the tracing (Figure-2). These features define this initial part of the tracing as AIVR (Accelerated IdioVentricular Rhythm).
  • There is clear suggestion of ST segment elevation in leads I and aVL, in association with Q waves and deep symmetric T wave inversion. These features are not “normal” for a simple ventricular rhythm. The important point — is that at times, you may see QRS and ST-T wave changes in ventricular beats (or ventricular rhythms) that reflect ongoing ischemia/infarction. So, even though assessment of acute cardiac ECG changes is always more difficult in the presence of QRS widening from conduction defects, ventricular pacing, or ectopic ventricular beats — it is not impossible. QRST appearance of the AIVR rhythm in leads I and aVL of Figure-2 is virtually diagnostic of an acute STEMI (ST Elevation Myocardial Infarction) in evolution. Support of this diagnosis is forthcoming from: i) suggestion of reciprocal ST-T wave change in lead III; ii) what looks to be disproportionate J-point ST elevation for the AIVR beats in anterior leads V1,V2,V3; and iii) what is happening in leads V4,V5,V6 (See below).
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Why P Wave Arrows are Colored the way they are ...
Perhaps the most difficult part of this ECG and rhythm strip for me to interpret was deciphering of atrial activity. We simply do not see the entire QRS complex well in the single long-lead rhythm strip that we are given — because the last portion of the QRS complex in lead II for the most part occurs on the baseline. Therefore, even though the QRS complex for the first 12 beats in this lead II rhythm strip is wide — the QRS complex looks deceptively narrow in lead II ...
  • That said, there is an unmistakable double-hump following the QRS complex for at least the first several beats on the tracing. This looks to be real — and almost certainly represents atrial activity. I did not think this represented retrograde atrial activity — because the initial extra humps (WHITE arrows) are positive in this lead II rhythm strip.
  • The KEY — is beat #14, which is clearly preceded by an upright P wave with normal PR interval (RED arrow). Beat #14 is a sinus capture beat.
  • An upright P wave also precedes beat #13. However, the PR interval preceding beat #13 is clearly too short for normal conduction. Beat #13 is a fusion beat — in which the P wave preceding it (RED arrow) begins to conduct normally, but before travel through the ventricles is complete, the impulse fuses with a ventricular impulse arising from below at the site of the AIVR.
  • The reason sinus P waves appear after the QRS for the first 12 beats on this tracing — and only appear before the QRS for beats #13 and 14 — is that there is AV dissociation with an atrial rate that is close to the escape rate of the accelerated ventricular rhythm. Although initially, the RP’ interval (ie, distance from the QRS to the extra hump indicated by WHITE arrows) appears to be constant — beginning with the DARK BLUE arrows, we can see shortening of the RP’ interval. That the P waves appearing under each ARROW are not related to their neighboring QRS complex becomes obvious with onset of the LIGHT BLUE arrows, which clearly show these sinus P waves now receding backward to soon be hidden within the QRS complex. Finally, there is emergence of P waves from the QRS to a position preceding the QRS complex — resulting in partial conduction (fusion beat #13) and normal conduction (with the sinus capture beat #14).
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What does Sinus Beat #14 Show in Simultaneous Leads?
There is only 1 beat on this tracing that is entirely sinus conducted = beat #14. As a result, we focus on this beat #14 in simultaneously-recorded leads V4,V5,V6 to assess QRST morphology — since this is the only beat on the entire tracing that is not of ventricular origin. Unfortunately, the tracing in Figure-2 is cut off before completion of the ST-T wave for this last beat … In addition, the part of the ST segment that we see for beat #14 in lead V5 and lead II looks to be flat, most probably due to technical issues (and, inappropriate R wave progression in lead V5 suggests this electrode may be malpositioned ... ). But, we DO get a good look at the QRS complex and most of the ST-T wave in leads V4 and V6 for this sinus-conducted beat #14. Note there is no more than a vestigial (tiny) r wave in lead V4, with ST coving in this lead. The QRS complex is tiny in lead V6 for beat #14 — with presence of a probably significant Q wave and disproportionate (hyperacute) ST segment coving. In association with the ST-T wave changes described earlier in the other 9 leads for this patient with new-onset chest pain — these findings in leads V4 and V6 support our presumption of an acutely evolving antero-lateral STEMI.
  • Remember that AIVR is an extremely common reperfusion rhythm in the setting of evolving STEMI.
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Final Impression: Putting the “pieces” discussed above together — I thought the ECG in Figure-1 was highly suggestive of acute evolving STEMI, with probable reperfusion based on the presence of the AIVR rhythm. Maximal ST elevation in leads V2,V3 — in association with residual ST elevation in leads I,aVL plus reciprocal changes in leads III, aVF — suggest the proximal LAD (Left Anterior Descending) as the "culprit" artery.
  • Clinical Follow-Up: I later found out that the ECG in Figure-1 was obtained following thrombolysis with streptokinase of a large acute stemi.
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Acknowledgment: — My thanks to Haseeb Raza Naqvi (from Multan, Pakistan) for his permission to use this case and ECG.
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Additional Reading: For more on AIVR — Please check out my ECG Blog #108

4 comments:

  1. Replies
    1. My pleasure! My appreciation to you for sending me this case.

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  2. Very nice case and very nice interpretation and discussion.
    Thank you prof. Ken grauer

    ReplyDelete