ECG Blog #463 — Lots to Explain ...

I was sent the ECG shown in Figure-1 — told only that this tracing was obtained prior to elective electric cardioversion of a patient who had long been in persistent AFlutter (Atrial Flutter).

• Serum electrolytes were normal at the time of cardioversion.
• The patient tolerated cardioversion well — and later that day was discharged from the hospital. (The post-cardioversion tracing will be shown momentarily in Figure-3).
• Unfortunately — additional clinical details regarding today’s case are not known (nor is it known what medications the patient may have been taking).

QUESTIONS:

• How to interpret today’s initial rhythm? (shown in Figure-1).
• Why is the QRS wide? 

Figure-1: The initial ECG in today's case (obtained prior to elective electrical cardioversion).

My Thoughts on the ECG in Figure-1:

Limb leads and chest leads in Figure-1 show 2 short (~5 second) and somewhat different-looking rhythm strips.

• There is definite group beating in the limb leads (groups of 2 beats with alternating long-short cycles) — but no such organization in the chest leads.
• Very rapid and regular atrial activity is seen in a number of chest leads and limb leads (best seen in lead II — as highlighted by RED arrows in Figure-2). The P-P interval is slightly more than 1 large box in duration — which corresponds to an atrial rate just under 300/minute (and defines the underlying rhythm as AFlutter).
• As is often the case with AFlutter — flutter waves are well seen in some leads (ie, leads II,III,aVF; V1,V2) — but not in others.
• The QRS is wide — with a morphology consistent with LBBB (Left Bundle Branch Block) conduction in the chest leads (predominantly negative in anterior chest leads — and all positive in lead V6). 

QUESTIONS:

• Why is there group beating in the limb leads?
• Why no group beating in the chest leads?
• If there is LBBB conduction in the chest leads — Why is the QRS all negative in lead I?

Figure-2: RED arrows highlight very rapid and regular atrial activity in lead II. Atrial activity is also seen in leads III,aVF; V1 and V2.

The CASE Continues:

I then saw the repeat ECG obtained after cardioversion.

• Does this repeat ECG in Figure-3 provide answers to some of the above questions?

Figure-3: The repeat ECG obtained after cardioversion.

My Thoughts on the Repeat ECG in Figure-3:

Sinus rhythm has been restored following cardioversion. The overall heart rate is slow — and the QRS for most beats is now narrow.

• To facilitate interpretation of Figure-3 — I've numbered the beats and have labeled atrial activity in Figure-4.

Figure-4: I've labeled the post-conversion tracing.

The Post-Conversion Tracing:

Limb leads and chest leads in Figure-4 are continuous.

• RED arrows highlight sinus P waves in this brady rhythm (heart rate a bit under 50/minute).
• BLUE arrows highlight the presence of 2 PACs (Premature Atrial Contractions). Of interest — the QRS complex is wide in Figure-4 only for these 2 PACs ( = beats #2 and #7). Note that QRS morphology for both of these early beats is consistent with LBBB conduction (monophasic all upright R wave in leads I and aVL for beat #2 — and for beat #7, there is predominant negativity in the chest leads until the all upright R wave in lead V6).
• PEARL #1: The fact that the QRS was consistently wide during the faster rhythm (ie, while the patient was in AFlutter) — but now in Figure-4 shows a normal (narrow) QRS complex with the underlying post-conversion rhythm of sinus bradycardia except for the 2 early-occurring beats (beats #2 and 7, which are PACs) — suggests that the reason for QRS widening in the initial ECG is likely to reflect rate-related LBBB aberration (See ECG Blog #242 for more on rate-related BBB).
• PEARL #2: Did you notice in the post-conversion tracing that there is ST segment coving with fairly deep T wave inversion in the chest leads? In view of the clinical history (ie, that this patient had a history of longstanding AFlutter — but as far as we know, no chest pain) — this ST-T wave change most likely reflects a "memory" effect, in which there will often be ST-T wave abnormalities that persist for hours (up to a few days) following a long period of a sustained tachycardia. (Clinical correlation, and possibly Troponin levels — are needed to determine whether this deep T wave inversion needs additional evaluation).

QUESTIONS:

Take a LOOK at Figure-5 — in which I've put the initial ECG together with the repeat ECG recorded after cardioversion.

• Does this comparison in Figure-5 confirm why despite QRS widening with LBBB conduction in the chest leads of the initial ECG — the QRS complex in lead I of this tracing is all negative? (HINT: Look also at what happens to QRS morphology in lead aVR of ECG #1 compared to the appearance of lead aVR in ECG #2).
• P.S.: Did you figure out why there is group beating in the limb leads of the initial ECG?

Figure-5: To facilitate comparison — I've put the initial ECG together with the post-cardioversion tracing.

ANSWERS:

• Answering the 2nd question first — it is common with AFlutter for there to be group beating similar to that seen in the limb leads of ECG #1. As I'll illustrate momentarily in a step-by-step laddergram derivation (in Figures-8 thru -13) — this group beating is usually the result of dual-level Wenckebach conduction out of the AV Node. It is most often not the result of a pathological AV block — since normal 1:1 AV conduction usually returns with resumption of sinus rhythm.
• As to the lack of group beating for the 5 second rhythm in the chest leads — I interpreted this simply as AFlutter with a variable ventricular response. This probably occurred as a result of changing conduction ratios out of the dual levels within the AV Node.
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• Finally — The all negative QRS complex in lead I of the initial ECG is the result of LA-RA lead reversal!

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QUESTION:

• How do we know there is lead reversal in ECG #1?

ANSWER (Looking at the ECGs in Figure-5):

The technical misadventure of lead reversal is more common than is commonly appreciated. Of the lead reversals — the most common (by far) is a mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. When this happens — lead I resembles the QRST appearance normally seen in lead aVR — and vice versa.

• PEARL #3: Standard lead I is a left-sided lead. Since the heart lies toward the left — predominant electrical activity will almost always be directed toward the left. Even in the setting of a large lateral infarction — it is rare to see a predominant Q wave in lead I. Yet in ECG #1 — the QRS complex is all negative in lead I. Although possible for this to occur (ie, with a very unusual conduction defect) — Think dextrocardia or LA-RA lead reversal if you see an all-negative QRS in lead I.
• P.S.: We know that the all negative QRS in lead I is not the result of dextrocardia — because R wave progression in the chest leads of ECG #1 is exactly as expected for LBBB conduction (and R wave progression would be reversed if there was dextrocardia).

Additional confirmation of LA-RA reversal in ECG #1:

• Lead aVR is a right-sided lead. In the absence of marked RVH — One would not expect to see the all positive QRS that we see in lead aVR of ECG #1. But if lead I looked like lead aVR looks (and lead aVR looked like lead I looks) — then ECG #1 would look exactly as expected for this patient who manifests typical LBBB conduction in the chest leads.
• Lead V6 is a left-sided chest lead. Given that lead V6 is all positive in ECG #1 — We would not expect the QRS complex in left-sided lead I to be all negative!
• Final proof of LA-RA reversal is forthcoming in ECG #2. Note that beat #2 (which is the 1st PAC in this tracing that conducts with LBBB aberration) — now manifests typical LBBB morphology, with an all upright QRS in both lead I and lead aVL (within the dotted BLUE rectangle in Figure-5).

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What would ECG #1 look like IF there was not LA-RA reversal?

• I review multiple other examples of lead reversal in ECG Blog #396. As these example show — we can "correct" for the effects that each type of lead reversal has on the ECG (See Figure-6):

Figure-6: Correcting for the effects of LA-RA lead reversal.

And now substituting what ECG #1 would have looked like if all limb leads were correctly positioned — Take a LOOK at Figure-7 !

Figure-7: This is how Figure-5 would look — IF we correct for LA-RA reversal that was present in the initial ECG.

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Laddergram Illustration: Today's Dual-Level Wenckebach ...

I conclude today's case with laddergram derivation of the group beating pattern that we see in the limb leads of ECG #1.

• Figure-8 shows the rhythm I'll review. This is the 5-second lead II rhythm strip with flutter waves highlighted by RED arrows (taken from Figure-2).

Figure-8: RED arrows highlight flutter waves in this lead II excerpt from Figure-2. Note the group beating (alternating longer-shorter R-R intervals for beats #1-2; 3-4; 5-6). Note also the identical PR intervals that precede beats #3,5,7.

Figure-9: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. BLUE arrows show the onset of P waves (in this case, flutter waves) as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I drew in near-vertical lines in the Atrial Tier.
=  =  =  =  =
NOTE: Because I suspected dual-level AV block within the AV Node — I have divided the AV Nodal Tier into 2 parts (by drawing in a horizontal BLACK dotted line).

Figure-10: Laddergram STEP-2. I next fill in the Ventricular Tier.
 BLUE arrows show the onset of each QRS complex as my reference point for each of the QRS complexes in this tracing. 
=  =  =  =  =
KEY Point: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figures-9 and -10). Now the challenge begins — for trying to "solve" the laddergram by figuring out which of the P waves (in this case, flutter waves) in the Atrial Tier are being conducted to the ventricles.

Figure-11: While realizing that many complex tracings may have more than a single potential laddergram explanation — I find postulating 2:1 AV conduction in the upper AV Nodal level most often works for me when contemplating AFlutter with dual-level Wenckebach conduction.
= = = = =
KEY Point: Because of "concealed conduction" — flutter waves that are very close to a QRS complex are usually not able to conduct to the ventricles. For example — the 3rd RED arrow in this Figure-11 is unlikely to be conducting. As a result — flutter waves before-and-after this 3rd RED arrow probably are able to conduct through at least the upper AV Nodal level (PINK lines in this upper AV Nodal level).
This leaves me with the BLUE-lined path as the most logical conduction passageway to produce beat #3.

Figure-12: Continuing to postulate 2:1 conduction through the upper AV Nodal level once again suggests this next BLUE-lined path as the most logical conduction passageway to produce beat #4.

Figure-13: The pattern of beats repeats. My completed laddergram suggests the solution — which is AFlutter with dual-level conduction out of the AV Node (ie, with 2:1 conduction out of the upper AV Nodal level — and 3:2 Wenckebach conduction through the lower level).
NOTE: This pattern that we see for the first 6 beats changes for beat #7 — as there is no 2nd beat in this last grouping.

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Final PEARL #4: 

To remember: It is very common to see group beating with AFlutter — and — there will often be dual-level AV block of these rapid flutter waves out of the AV Node.

• Even without having to draw a laddergram — we can quickly recognize dual-level Wenckebach conduction out of the AV Node by seeing group beating that occurs in association with consecutive non-conducted flutter waves (as is evident in Figure-8) — especially when there are identical PR intervals before many of the beats.
• The "good news" — is that these consecutive non-conducted flutter waves generally do not represent a fixed (pathologic) form of AV block! Instead — normal 1:1 AV conduction usually resumes once AFlutter is converted to sinus rhythm.

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Acknowledgment: My appreciation to Samuel K. Sørensen (from Copenhagen, Denmark) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #264 — Reviews LA-RA Lead Reversal.
• ECG Blog #396 — for a list of lead reversals ...

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• ECG Blog #259 — Reviews step-by-step laddergram for a patient with Dual-Level AV Block.
• ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.
• ECG Blog #226 — Works through a complex Case Study (including an 11:00 minute ECG Video Pearl that walks you through step-by-step in the constrution of a laddergram with Wenckebach conduction and duallevel block within the AV Node).
• ECG Blog #416 — Case Study of acute OMI with step-by-step illustration of dual-level AV Wenckebach.
• ECG Blog #347 and Blog #439 — more examples of dual-level AV block.

 

ADDENDUM (1/3/2025): 

—  —

ECG Media PEARL #71 (5:45 minutes Audio) — Reviews the phenomenon of Dual-Level Wenckebach out of the AV Node (HOW to recognize this phenomenon — and how to distinguish it from Mobitz II).