Today's case offers a fascinating ECG in all regards — obtained from a 54-year old man with chest pain. As per Dawn — there is obvious acute inferior MI and AV block — but from a teaching perspective — there is so much more!

 

Beginning with the 12-lead ECG — I'd make the following points:

— Clearly there is acute inferior MI, with obvious ST elevation in each of the inferior leads. But what is the AGE of this inferior infarction? (See Blog #258). There are small-but-present q waves in leads II and aVF — with already a large Q wave in lead III. Not only is there ST elevation in lead III — but there is beginning T wave inversion, signaling the likely onset of reperfusion T waves.

— The ST-T wave in lead aVL is almost the mirror-image reciprocal picture of the ST-T wave in lead III — and this confirms that the MI is at least "recent" (See Blog #184) — but the unexpectedly tall T wave in lead aVL (which in its "mirror-image" corresponds to T wave inversion) confirms the presence of reperfusion T waves. Spontaneous reperfusion (without thrombolytics or angioplasty) is common during the course of acute MI — and this is undoubtedly ongoing in today's case.

— There is also associated acute posterior infarction — as signaled by the positive "Mirror Test" picture for the ST-T waves in anterior leads (See Blog #246), which is maximal in leads V2,V3. Further support of associated posterior MI is forthcoming from the taller-than-expected R waves in leads V2 and V3 (which in its "mirror-image" corresponds to increasingly deep Q waves).

— There is almost certainly also acute RV (Right Ventricular) infarction — as signaled minimal ST depression in lead V1 in the face of maximal downsloping ST depression in leads V2,V3 (See Blog #190). Lead V1 is in effect, a "right-sided" lead — and in the setting of acute proximal RCA (Right Coronary Artery) occlusion — there will often be infero-postero and RV infarction, as a result of anatomic areas supplied by the RCA. On ECG — the effect of simultaneous ST elevation in lead V1 (from acute RV MI) — together with the ST depression in lead V1 from acute posterior MI — will often yield a "net effect" of a nearly flat ST segment in lead V1. In neighboring leads V2, V3 (which are not "right-sided") — we don't see any effect from the ongoing acute RV MI, and as a result there will be disproportionately greater ST depression in other anterior leads. In contrast, with acute infero-postero MI but in the absence of acute RV MI — signficant ST depression will usually also be seen in lead V1, as well as other anterior leads.

— Note that there is much less ST depression in lateral chest leads (ie, leads V4, V5, V6) — but that marked T wave peaking persists. Although I would check serum K+ — I suspect this is not due to hyperkalemia — but rather extension of marked "mirror-image opposite" reperfusion T waves. Note that the History we were given did not specify the time symptoms began. Given the large Q in lead III, the taller-than-expected R waves in leads V2,V3 — and especially given diffuse and marked suggestion of reperfusion T waves — I'd suspect that although this extensive MI is "recent" — it is less likely to have just begun in the past couple hours (More history will probably help answer this question!).

— NOTE: Although chest lead T waves are tall and peaked — this is most probably not a manifestion of deWinter T waves from acute LAD (Left Anterior Descending) coronary artery occlusion because: i) There are very prominent changes of acute inferior MI in the limb leads; ii) I'd expect a different ST-T wave appearance in lead V1; and, iii) The duration of the depressed ST segments in the chest leads is relatively long (whereas with deWinter T waves, the slightly depressed J-point ST depression much more rapidly rises to form giant T waves than what we see in today's tracing — See Blog #266).

 

Regarding the Rhythm in Today's Case — I'd make the following points:

— I do not think definitive interpretation of the rhythm is possible from the single long-lead rhythm strip that we have been given. Additional monitoring would clearly be needed. That said — I believe we can define the principal rhythm abnormality, and speculate on the fascinating possibilities of a few unique findings.

— I have drawn a laddergram in the attached Figure to this post that presents 2 possible explanations for the ECG findings we see (For more on Laddergrams — See Blog #188). Panel A illustrates findings described by Dawn — in which there is a 2 beat grouping at the beginning of the tracing that suggests Mobitz I, 2nd-degree AV block with 3:2 AV conduction for beats #1 and 2 (PURPLE lines within the AV nodal tier in my Figure).

— Continuing with Panel A — There appears to be complete (3rd-degree) AV block, beginning with beat #3. ARROWS in the lead II rhythm strip show the occurrence of a regular atrial rhythm at the extremely fast rate of 155/minute. Whether this represents marked sinus tachycardia vs an ectopic atrial tachycardia is unknown from this single single tracing.

— As per Dawn, after beat #3 in Panel A — None of the P waves conduct. The way we know this — is that although the narrow-QRS ventricular rhythm is perfectly regular after beat #3 (at a rate of ~55/minute) — the PR interval continually changes (If you focus on each PINK arrow P wave before the QRS of beats #4, 5, 6, 7, 8 and 9 — you'll note a small-but-definitely-present continual change in the PR interval). This means that there is complete AV dissociation — because after beat #3, none of the P waves conduct! I suspect this represents complete AV block — although additional monitoring would be needed to confirm this. As an advanced Point — it is difficult to guarantee that all P waves fail to conduct despite adequate opportunity to conduct, because the ventricular rate is faster than 50/minute and because the atrial rate is so fast (See Blog #202).

— This raises the question of HOW can you have Mobitz I just 1 beat before you develop complete AV block? While hard to say that this is "impossible" — this rapid transition from 2nd-degree to 3rd-degree AV block in the space of a single beat seems highly improbable! As a result — I do not think Panel A represents a plausible mechanism for today's rhythm.

 

What about Panel B?

— The reason I do not think beats #1 and #2 represent a 3:2 Mobitz I grouping — is that the PINK arrow P wave just before beat #9 appears to have the same PR interval as for the P wave before beat #1 — yet we know that the P wave before beat #9 is not conducting.

— The "good news" about this 2nd laddergram that I propose in Panel B — is that instead of having to explain the path of several P waves (as per the several PURPLE lines in Panel A) — I only have to explain the path of 1 P wave ( = the RED arrow in the ST segment of beat #1). I suspect that the reason this 1 P wave in Panel B is able to conduct to the ventricles — is a result of "supernormal" conduction! This theoretical phenomenon is defined as, "better-than-expected conduction in the setting of depressed conduction during a short interval in the ventricular cycle" (See Friedman & Schweitzer).

— I fully acknowledge that the concept of "supernormal" conduction in humans remains controversial. Despite me being aware of this described phenomena for several decades — I count on the fingers of one hand the number of times that I thought I truly detected it. But for today's case, in which there is extensive recent inferior MI with what appears to be complete AV block with a junctional escape rhythm — I find theorizing "supernormal" conduction the BEST way to explain the early occurrence of beat #2. The P wave in the ST segment of beat #1 is appropriately located at a point where it would seem most likely to encounter that "magic point" in the cardiac cycle when depressed conduction might be transiently alleviated.

— P.S. — What I especially like about postulating the occurrence of "supernormal" conduction as the mechanism explaining why early beat #2 conducts — is that it supports my contention that it is all-but-impossible for a short grouping of Mobitz I to coincidentally interrupt complete AV block.

 

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For Additional Material on Subjects Covered Above:

 

ECG Blog #202 — How to quickly tell if there is Complete AV Block (Also check out the Audio Pearl in this post!).

 

ECG Blog #246 — What is the "Mirror Test" for Posterior MI (Also check out the Audio Pearl in this post!).

 

ECG Blog #258 — How to "Date" an MI? (Also check out the Audio Pearl in this post!).

 

ECG Blog #184 — The "magic" mirror-image opposite relationship between lead III and lead aVF with acuteMI.

 

ECG Blog #190 — How to Recognize RV MI (Also check out the Audio Pearl in this post!).

 

ECG Blog #188 — How to Read (and/or Draw) Laddergrams!

 

ECG Blog #266 — deWinter T waves or Posterior MI?

 

Friedman M and Schweitzer P: Transient Unexpected Improvement of AV Conduction: What is the Mechanism? (ie, Supernormal conduction?).