Sunday, December 12, 2021

ECG Blog #268 (76) — Mobitz I vs Complete AV Block vs Supernormal Conduction?

The ECG in Figure-1 was obtained from a 54-year old man, who presented to the ED (Emergency Department) with chest pain. There is obvious inferior MI and AV block — but from a teaching perspective — there is so much more!

  • In addition to inferior MI — What other areas of the heart are affected?
  • What is the probable age of the infarction?
  • What is the rhythm? Is this Mobitz I? — Complete AV block? — or something else? 


Figure-1: 12-lead ECG and 2-lead rhythm strip obtained from a 54-year old man with chest pain.



NOTE #1: I am indebted to Dawn Altman, RN, EMT-P — whose ECG Guru web site has been posting ECGs and Arrhythmias available for teaching purposes since 2011. My appreciation to Dawn for allowing me to expand on this case — that she originally posted on the ECG Guru.


NOTE #2: Some readers may prefer at this point to listen to the 3:10 minute ECG Audio PEARL before reading My Thoughts regarding interpretation of the rhythm in today's case. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-76).


Today’s ECG Media PEARL #76 (3:10 minutes Audio) — Briefly reviews the concept of "Supernormal" Conduction — in which conduction for a brief period in the cardiac cycle is better-than-thought-to-be possible.


MY Sequential Approach to the ECG in Figure-1:

There is a series of important ECG findings in this case — and the cardiac rhythm is fascinating. Although I used a Systematic Approach (as I always do) to interpret both the cardiac rhythm and the 12-lead ECG (See ECG Blog #185 and Blog #205 for details on my approach) — I did allow myself the "luxury" of a few seconds to take in the principal findings. Beginning with the 12-lead ECG — I'd make the following points:

  • Clearly there has been recent inferior MI, with obvious ST elevation in each of the inferior leads. But what is the AGE of this inferior infarction? 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 marked 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. This confirms that the inferior MI is at least "recent" (See Figure-2). That said — the unexpectedly tall terminal T wave in lead aVL (which in its "mirror-image" corresponds to T wave inversion) confirms the presence of what we saw in lead III = 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, which is maximal in leads V2 and V3 (See Figure-2). 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 suggested by minimal ST depression in lead V1 in the face of maximal downsloping ST depression in leads V2,V3 (See ECG Blog #190). This could be confirmed by obtaining right-sided leads. That said — 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 the anatomic distribution of 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 is much greater ST depression in other anterior leads. In contrast, with acute infero-postero MI, but in the absence of acute RV MI — significant ST depression will usually also be seen in lead V1, as well as other anterior leads. 
  • NOTE: Although in Figure-1 there is T wave inversion in lead V1 from reperfusion — the amount of ST depression in this lead is modest compared to the amount of ST depression in leads V2 and V3.
  • NOTE: As expected with posterior infarction, there is less ST depression in lateral chest leads (ie, leads V5 and V6). That said — tall T waves with marked T wave peaking persist through to lead V6. Although I would definitely check serum K+ — I suspect this picture is not due to hyperkalemia — but rather to extension of marked "mirror-image opposite" reperfusion T waves. Note that the History we were given did not specificy the time symptoms began. Given the large Q wave 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 would be needed to better determine the likely time of onset of the infarct).
  • Final NOTE: Although chest lead T waves are tall and peaked — this probably is 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 if the infarction was the result of acute LAD occlusion; andiii) The duration of 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 — as is discussed in more detail in ECG Blog #266).


Figure-2: I focus on the 12-lead ECG in today's case — to highlight the "magical" mirror-image-opposite relationship between lead III and lead aVL (which confirms recent inferior infarction). Application of the "Mirror Test" to the QRST complex in leads V2 and V3 confirms associated posterior MI (See text).


What about the Rhythm in Today's Case?

I do not think we have a sufficient period of ECG monitoring for definitive interpretation of today's rhythm. That said — I believe we can define the principal rhythm abnormality, and speculate on the fascinating possibilities of a few unique findings.

  • For clarity — I reproduce the simultaneously-recorded 2-lead rhythm strip in Figure-3. By the Ps, Qs & 3Approach — the QRS is narrow — a certain number of P waves are definitely present — and, the rhythm is almost, but not completely Regular (with a Rate of ~55/minute after beat #3). 

Figure-3: I focus on the rhythm strip in today's case (See text).


This initial rhythm assessment leaves us with QUESTIONS:

  • Are P waves regular throughout the rhythm in Figure-3?
  • IF P waves are regular — Are we seeing a 3:2 Mobitz I cycle ( = AV Wenckebach) at the beginning of the tracing?
  • After beat #3 — Are P waves Related to neighboring QRS complexes?


Are P Waves Regular throughout the Rhythm?

The challenge in assessing P wave regularity in today's case — is that many of the P waves are partially hidden within the ST segment.

  • Calipers provide invaluable assistance.
  • Find 2 P waves in a row that you are certain about. I chose the first 2 RED arrow P waves in Figure-4.
  • Setting your calipers to the P-P interval of these first 2 RED arrow P waves — you can now "walk out" regular P wave deflections throughout the entire rhythm strip (RED arrows in Figure-4).


Figure-4: Regular P waves are seen throughout this tracing (RED arrows).

MInitial Laddergram:

For those interested in a "primer" on how to read (and/or drawLaddergrams — Please check out ECG Blog #188.

  • My initial proposed laddergram for the mechanism of the rhythm in today's case is shown in Figure-5. This suggests a 2 beat grouping at the beginning of the tracing of Mobitz I, 2nd-degree AV block with 3:2 Wenckebach conduction for beats #1 and #2 (PURPLE lines within the AV nodal tier in Figure-5).
  • Continuing with the laddergram — 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 surprisingly fast rate of 155/minute. Whether this represents marked sinus tachycardia vs an ectopic ATach (Atrial Tachycardia) is unknown from this single single tracing.
  • None of the P waves after beat #3 in Figure-5 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 — Caliper measurement confirms 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 in Figure-5 despite being given adequate opportunity to do so (as would be required if there truly was complete AV block). This is because: i) The ventricular rate is faster than 50/minute; andii) Because the atrial rate is so fast. 

  • PEARL #1: Complete AV block is most reliably diagnosed when the ventricular rate is slow enough to guarantee that all P waves have adequate opportunity to conduct — yet still fail to do so (which optimally requires a ventricular rate of ~50/minute or less).
  • PEARL #2: Given rapidity of the atrial rate at ~155/minute (and the difficulty of distinguishing between a very rapid sinus tachycardia vs ectopic ATach) — it's impossible to know how much AV conduction might improve if the atrial rate were to slow down.


Despite these reservations (and assuming the rhythm after beat #3 truly is complete AV block) — 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 the mechanism I initially proposed in Figure-5 is "impossible" — such an abrupt transition from 2nd-degree Mobitz I — to complete AV block in the space of a single beat — seems highly improbable! As a result, on further reflection — I did not think this initial laddergram represented a plausible mechanism for today's rhythm.


Figure-5: My initial proposed laddergram for the mechanism of today's rhythm (See text).



MRevised Laddergram:

On further reflection — I revised my initial laddergram to the laddergram shown in Panel B of Figure-6. For the purpose of comparison — I show both laddergrams together in this Figure.

  • 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 have already established that the P wave before beat #9 is not conducting (because of the presence of complete AV dissociation).
  • 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 they pass through the AV Nodal Tier (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 "supernormalconduction! This controversial phenomenon is defined as "better-than-expected conduction" for a brief period during the cardiac cycle (See today's Audio Pearl — and the article bElizari et al).
  • I fully acknowledge the controversy surrounding the concept of "supernormal" conduction in humans. Despite me being aware of this described phenomenon 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 to be the most LOGICAL way to explain the early occurrence of beat #2. The P wave in the ST segment of beat #1 is located at a spot in the cardiac cycle where it would seem most likely to encounter that "magic point" when depressed conduction might be transiently facilitated.
  • KEY Point: What I especially like about postulating the occurrence of "supernormal" conduction as the mechanism for explaining why early beat #2 is conducted — is that this supports my contention that it is all-but-impossible for a short grouping of Mobitz I to abruptly interrupt complete AV block in the space of a single beat.


Figure-6: My revised proposed laddergram for the mechanism of today's rhythm is shown in Panel B. For comparison — I've reproduced my initial laddergrm in Panel A. Given how unlikely it would seem to abruptly change from Mobitz I to complete AV block in the space of a single beat — I feel my laddergram in Panel B is a much more logical proposal (See text).



Acknowledgment: My appreciation to Dawn Altman of the ECG Guru (Dawn lives in Tennessee, USA) for allowing me to use this tracing and this case.



Relevant ECG Posts to Today's Case: