Wednesday, June 8, 2022

ECG Blog #311: The Culprit of the Rhythm?

The ECG in Figure-1 — was obtained from a middle-aged man who presented with shortness of breath. No chest pain. Assuming the patient was hemodynamically stable:
  • How would YOU interpret the rhythm in Figure-1?
  • What are your diagnostic considerations?

NOTE: This is a challenging case! Both the rhythm and the 12-lead ECG manifest complexities without simple solution. My hope is to provide insight by presenting my thought process in the sequence that I used to approach this tracing. Are YOU up for the challenge?

Figure-1: 12-lead ECG and long lead II rhythm strip recorded from a middle-aged man with shortness of breath. No chest pain.

My Thoughts on Figure-1:
Instinctively applying the Ps, Qs, 3R Approach for assessment of the rhythm in Figure-1 (See ECG Blog #185) — my initial impression of this tracing (that I made within the first minute or so of seeing this ECG) — was the following:
  • The rhythm is supraventricular (ie, the QRS complex appears to be narrow in all 12 leads).
  • The rhythm is not completely regular. That said — there does appear to be "group" beating (with longer and shorter R-R intervals of a duration that repeats). 
  • P waves are present. I suspected that the atrial rhythm might be regular.
  • At least some P waves appear to be conducting (because some PR intervals repeat a number of times in this tracing!).

  • My Initial IMPRESSION: The findings of group beating — with P waves that look like they might be regular — a narrow QRS — and, a number of PR intervals of similar duration — when taken together, suggest that some type of Wenckebach conduction (if not 2nd-degree AV block of the Mobitz I type) is likely.

What About the 12-Lead ECG?
At this point I found myself continually looking at the exceedingly tall T waves in the anterior leads of Figure-1. From a Clinical Perspective — highest priority in assessing any case, is to quickly determine IF immediate treatment is needed. In today's case — Clarification of the rhythm beyond my above brief analysis is probably not needed for initial treatment decisions. As long as the patient remains stable (and the overall heart rate does not drop) — it is unlikely that a pacemaker will be needed. As a result — our priority shifts to assessing the 12-lead ECG regarding whether prompt cath and/or thrombolytic therapy is needed.
  • PEARL #1: An additional reason for turning our attention at this point to assessment of the 12-lead ECG — is that doing so may help in assessment of the rhythm (as I'll show momentarily).

Assessing the 12-Lead:
  • There is low voltage in the limb leads (ie, QRS amplitude does not exceed 5 mm in any of the limb leads).
  • The frontal plane axis is normal (Probably close to 0 degrees — though difficult to assess due to low voltage and Q waves of variable depth in the inferior leads).
  • There is no chamber enlargement.
  • There clearly has been a recent inferior MI (ie, Q waves are present in each of the inferior leads — in association with ST segment coving, at least 1 mm of ST elevation — and deep T wave inversion).
  • R wave progression is normal in the chest leads — with transition (where the R wave becomes taller than the S wave is deep) — occurring normally between leads V2-to-V3.
  • T waves are exceedingly tall and peaked in anterior leads V2, V3 and V4 (with a T wave = 15 mm tall in lead V3)
  • T waves are also disproportionately tall in leads I and aVL. 
  • The ST-T wave is flat in lead V6.

My Impression of the 12-Lead:
Despite the absence of chest pain — this patient has had a recent inferior MI. Without more history — it is difficult to determine when this occurred. Q waves are already quite deep (especially in leads III and aVF). ST elevation persists — although the amount of ST elevation is almost overshadowed by the very deep, symmetric T wave inversion in each of the inferior leads. A mirror-image opposite picture to this inferior lead T wave inversion is seen in the shape of the disproportionately tall T wave in lead aVL.
  • The composite picture in ECG #1 is consistent with a completed inferior STEMI from acute RCA (Right Coronary Artery) or possibly LCx (Left Circumflex) occlusion — now with reperfusion T waves in the inferior leads
  • Admittedly, the tall, peaked anterior T waves resemble deWinter T waves in their size and shape. However, to postulate that these are deWinter T waves would imply acute involvement of a 2nd coronary artery (ie, the LAD = Left Anterior Descending coronary artery). I think it far more likely that these tall anterior T waves represent part of the same acute process (ie, acute occlusion of the RCA or LCx — and not of the LAD).

  • Acute inferior MIs are frequently accompanied by posterior involvement — in which the anterior leads show a mirror-image of events occurring in the posterior wall of the left ventricle. As a result — anterior leads show ST depression (instead of ST elevation) with acute posterior MI — and anterior leads show tall, peaked T waves (instead of deep T wave inversion) when the posterior wall is reperfused.

  • Putting It All Together: I suspect today's patient had a recent infero-postero STEMI — and is now showing reperfusion T waves in these lead areas (ie, in the form of deep T wave inversion in inferior leads — and tall, peaked T waves in anterior leads). 
  • Additional history — serial troponins — Echo — and follow-up ECGs could all contribute to better understanding regarding the timing of this patient's event. Cardiac cath may be indicated — but given the ECG appearance in Figure-1 (that suggests this MI did not just happen) — cardiac cath will probably not be needed on an emergency basis as long as the patient remains stable.

PEARL #2: It is common to see 2nd-degree AV block of the Mobitz I type in association with acute or recent inferior MI. As a result — I immediately suspect some form of this conduction disorder in the setting of recent or acute inferior MI whenever I see group beating with a regular atrial rhythm and a number of similar PR intervals at the beginning of a number of groups. This is the situation in today's rhythm (See below).


A Closer Look at Today's Rhythm:
I found assessment of today's rhythm extremely challenging. My point in the above discussion — is that regardless of whether you were able to determine the precise etiology for each beat in the long lead II rhythm strip of Figure-1 — my basic assessment described above (ie, that this supraventricular rhythm with group beating in association with recent inferior MI is likely to represent some form of 2nd-degree Mobitz I AV block)  is more than adequate for initial management of this patient.
That said — Let's look closer.

  • Are the P waves in Figure-1 regular?

ANSWERSee Figure-2 ...

Figure-2: I've labeled the P waves in Figure-1 with RED arrows.

PEARL #3: As I have often emphasized — I have found the simple act of identifying all P waves to be invaluable for guiding me toward the right diagnosis.
  • Using calipers greatly facilitates the process. Set your calipers to the P-P interval between any 2 P waves that you clearly see in the long lead II rhythm strip (For example — Set your calipers to the P-P interval between the 2nd and 3rd RED arrows in Figure-2 — or between the 3rd and 4th RED arrows). Doing so readily allows you to "walk out" this interval throughout the entire rhythm strip (RED arrows in Figure-2).

My Next Steps in Rhythm Analysis:
Now that we have verified that the atrial rhythm is regular (at a rate just over 100/minute)LOOK again in Figure-2 at the QRS complexes that occur at the end of each of the longer R-R intervals (ie, at beats #3, 4, 6, 7, 9 and 10).
  • Are each of these beats preceded by a P wave? IF so — Is the PR interval of the P waves in front of beats #3,4; 6,7; and 9,10 long enough to conduct?
  • Is the PR interval identical before any of these beats?
  • Finally — LOOK to see IF a P wave precedes beats #2, 5, 8 and 11? IF so — Is the PR interval before each of these beats the same or different?

  • PEARL #4: You are looking for relationships that suggest the arrangement in this long lead II rhythm strip is not by chance! Finding such relationships is very characteristic of the likelihood that some form of Wenckebach block is present!

Figure-3: I've labeled P waves in the long lead rhythm strip according to their relationship with neighboring QRS complexes (See text).

I noted the following relationships between P waves in the long lead II rhythm strip — and their neighboring QRS complexes (Figure-3):
  • The P waves highlighted by WHITE arrows in Figure-3 all occur simultaneously with the onset of the QRS complex of beats #1, 4, 7 and 10. The PR interval of each of these WHITE-arrow P waves is clearly too short to conduct.

  • The P waves highlighted by RED arrows all manifest the same PR interval. These are the P waves before beats #3, 6 and 9. I measure the PR interval before these beats = 0.14 second, This is a long enough PR interval to conduct to the ventricles — although it is shorter-than-what-is-usually-seen for a patient with 2nd-degree AV Wenckebach. Because the PR interval in front of each of these beats is equal — I assumed that these RED-arrow P waves were conducting (but I could not be certain of this because of the relatively short PR interval).

  • The P waves highlighted by PINK arrows also all manifest the same PR interval, albeit a longer PR interval than that manifest by the RED-arrow P waves. These are the P waves before beats #2, 5, 8 and 11. I measure the PR interval before these beats = 0.24 second. I thought each of these PINK-arrow P waves were definitely conducting to the ventricles.

  • This left the 6 P waves highlighted by BLUE arrows — all of which occurred near the mid-point of one of the longer R-R intervals. I was not at all certain whether these BLUE-arrow P waves were conducting with a much longer PR interval — or whether they were not conducted.

NOTE: Today's rhythm is not typical for a simple Mobitz I, 2nd-degree AV block because: i) The PR interval before the QRS complex at the end of longer R-R intervals is not consistent as it usually is with typical Mobitz I (ie, alternating WHITE and RED arrows in front of beats #1, 3, 4, 6, 7, 9, 10); ii) The PR interval for RED-arrow P waves is shorter than is usually seen for conducting beats with Mobitz I ( = 0.14 second); and, iii) We never see 2 P waves in a row that are definitely conducting and manifesting progressive increase in their PR interval.
  • Unfortunately — the long lead II rhythm strip in today's tracing is not simultaneously-recorded with the 12-lead ECG above it. This negates use of a very helpful potential clue — which is that junctional escape beats can sometimes be distinguished from conducting beats because they may manifest slightly different QRS morphology.

LADDERGRAM Illustrations (Beyond-the-Core):
In my attempt to explain the mechanism of today's arrhythmia — I propose 2 potential solutions below: 

I show the simplest explanation for today's rhythm in Figure-4a
  • Most of the time with AV Wenckebach (ie, Mobitz I 2nd-degree AV Block) — there is a gradual increase in the PR interval with successive beats until a P wave is non-conducted. However, on occasion — dual AV nodal pathway physiology may be operative (Mani BC & Pavri BB: Dual AV Nodal Pathways Physiology — Indian Pacing Electrophysiol 14[1]:12-25, 2014). When this happens — there may be an abrupt change (increase) in the PR interval from one beat to the next due to sudden change in conduction from the fast pathway (which results in a shorter PR interval) — to conduction over the slower pathway (which results in abrupt PR interval lengthening). IF this is the mechanism in today's arrhythmia — it would look like the laddergram in Figure-4a.

Figure-4a: Proposed laddergram which presumes dual AV nodal pathway physiology — with abrupt switch to much slower conduction over one of the pathways accounting for the marked increment (increase) in PR interval from one P wave to the next — until a beat is dropped (ie, due to failed conduction over both AV nodal pathways).

I propose a 2nd potential explanation for today's rhythm in Figure-4b:
  • It could be that the reason the WHITE-arrow P waves are not conducted — is that a junctional "escape" beat occurs before these P waves have a chance to conduct. Since the R-R interval preceding beats #4,7,10 is just over 5 large boxes in duration — this would correspond to a junctional "escape" rate at ~58/minute (which is within the usual 40-60/minute escape rate range of the AV Node).
  • As shown in my proposed laddergram in Figure-4b — these junctional escape beats could be placed with a timing that also blocks conduction of the BLUE-arrow P waves occurring just before the WHITE-arrow P waves.
  • These junctional escape beats might also account for why the PR interval of the PINK-arrow P waves is longer than the PR interval of RED-arrow P waves (as suggested by the dotted line retrograde conduction from these junctional beats within the AV Nodal Tier that prolong conduction through the AV Node of the PINK-arrow P waves).
  • BUT — For the laddergram proposed in Figure-4b to be valid — the RED-arrow P waves would have to be able to conduct beats #3,6,9 with the relatively short PR interval = 0.14 second (which is a bit unusual in association with AV Wenckebach).

Figure-4b: My 2nd proposed laddergram for explaining the rhythm in today's case (See text).

PEARL #5: The path to achieving expertise in arrhythmia interpretation entails an appreciation of the following wonderful quote by Rosenbaum: “Every self-respecting arrhythmia has at least 3 possible interpretations.” 
  • We need to accept that the surface ECG is not always able to explain the precise mechanism of every arrhythmia. As a result — there may be more than a single potentially valid explanation to a complex rhythm. This is not a "weakness" of the ECG — but rather acknowledgment of the clinical reality, that sometimes the only way to prove what the true mechanism for a complex arrhythmia is — is through additional ECG monitoring on the patient or by EP (ElectroPhysiologic) Study.

  • I could have postulated additional laddergrams for today's case. For example — since the R-R interval preceding beats #3,6,9 is about the same as the R-R interval preceding beats #4,7 and 10 — it could be that all 6 of these beats represent junctional escape. IF that were the case — it would eliminate having to postuate that the RED-arrow P waves are conducting with the relatively short PR interval = 0.14 second. But it would mean postulating that there are 2 junctional beats in a row.

BOTTOM LINE for Today's Case:
Clinically — As intellectually interesting as it is to postulate the mechanism for today's rhythm — the answer to this question is not essential for appropriate management of today's case:
  • The initial ECG in Figure-1 tells us that this middle-aged man who presented with shortness of breath — most likely had a recent infero-postero MI that has evolved, and is now showing reperfusion T waves in the areas of infarction.
  • As a consequence of this recent event — he manifests a complex form of 2nd-degree AV block with Wenckebach conduction — but fortunately, with an overall ventricular rate between ~60-70/minute. 
  • There is no indication for pacing for the rhythm at this time. There is nothing to suggest that the conduction block is Mobitz II (especially since we never see 2 consecutively conducted P waves with the same PR interval). The rhythm is definitely not complete AV block because the ventricular rhythm is not regular — and there are several sets of repetitive PR intervals (which by definition would not be present if there was complete AV dissociation from 3rd-degree AV block).
  • Additional treatment decisions (including whether to cath the patient — and if so, when to do so) — will not depend on determining a more precise diagnosis of the rhythm.

  • My HOPE is that working through the above "thought process" will prove insightful for the process of interpreting a complex arrhythmia. I also think it worthwhile to appreciate when explanation of every beat on a tracing is not essential for appropriate initial management.


Acknowledgment: My appreciation to Abdullah Al Mamum (from Dhaka, Bangladesh) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).

  • ECG Blog #266 — Reviews a case illustrating distinction between deWinter T waves vs Posterior Infarction.

  • 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: The Audio Pearl in this post reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI. 

  • ECG Blog #80 — Reviews determination of the "culprit" artery and — application of the Mirror Test for recognition of acute Posterior MI.
  • ECG Blog #246 — Reviews use of the "Mirror Test" to facilitate recognition of acute Posterior MI.

  • ECG Blog #193 — Reviews the concept of "OMI" ( = Occlusion-based MI) — with an Audio Pearl that reviews the basics for predicting the "culprit" artery.

  • ECG Blog #294 — Reviews a case to illustrate keep concepts regarding predicting the "culprit" artery — and appreciating when reperfusion occurs.

  • ECG Blog #228 — Reviews the concept of "Silent" 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 #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
  • ECG Blog #183 — Reviews a case of deWinter T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern). 
  • ECG Blog #53 — Reviews another case of deWinter T Waves.

  • ECG Blog #186 — The AV Blocks (and when to suspect Mobitz I).
  • ECG Blog #224 — Reviews a case of Mobitz I with Inferior MI.
  • ECG Blog #262 — Another case of Mobitz I with Inferior MI.
  • ECG Blog #226 — A case of dual-level Mobitz I with Inferior MI.