ECG Blog #548 — More than One "Family"?

I was sent the ECG shown in Figure-1. I was told that the patient had "palpitations", but was hemodynamically stable. Her admission diagnosis was DKA (Diabetic KetoAcidosis).

QUESTIONS:

• How do you interpret the ECG that is shown in Figure-1?
• Can you explain the rhythm?

A

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My "Quick" ( = Initial) Impression:

Unfortunately, the information I was provided on this patient is limited. Nevertheless — I found a number of features in this initial ECG to be fascinating and worthy of discussion. Below my initial "quick thoughts" on Figure-1:

• The QRS is wide with a morphology consistent with RBBB (Right Bundle Branch Block) conduction (ie, predominant positivity in lead V1 — with wide terminal S waves in lateral leads I and V6).
• P waves are present in the long lead II rhythm strip — and without yet measuring, they appear to be at least fairly regular. And at least in front of beats #2,4,6,8 — the PR interval appears to be fixed and normal (therefore indicating at least some sinus conduction, as well as confirming that the rhythm is supraventricular with RBBB conduction).
• PEARL #1: There is group beating! (in the form of repetitive shorter-then-longer R-R intervals). When group beating is seen in association with a regular (or at least almost regular) P wave rhythm in which there is at least some sinus conduction — this suggests some form of Wenckebach conduction.

Turning my attention now back to QRS morphology:

• The QRS complex in leads V1 and V2 begins with a wide Q wave. Whether this Q wave is the result of previous infarction, pulmonary hypertension, or simply represents a less typical RBBB morphology is uncertain. But it’s worthwhile to be aware that the characteristic triphasic rsR’ of RBBB in lead V1 is for whatever reason, not seen in today’s tracing (therefore potentially worthy of follow-up as we learn more about the case).
• The T wave in lead V1, and in other anterior leads is upright in association with RBBB conduction. As reviewed in ECG Blog #204 (See the ECG Video and the Addendum in this ECG Blog #204) — normally with RBBB conduction, the ST-T wave should be oppositely directed to the last QRS deflection in lead V1 (and much of the time, also in other anterior leads).
• Instead — the T waves are surprisingly tall and peaked in leads V2,3,4 in this patient who presents with DKA! 
• PEARL #2: Acute acidosis is notorious for increasing extracellular serum K+ values ==> We need to find out the serum K+ level! (ie, One wonders how tall and peaked the anterior T waves in Figure-1 might really have been if ECG changes of hyperkalemia are not being superimposed on the ST-T wave depression that we would otherwise expect with RBBB conduction).
• PEARL #3: As emphasized in ECG Blog #275 — "All bets are off" regarding arrhythmias (especially forms of AV block) in the presence of hyperkalemia — with the "good news" being that much (most) of the time, these hyperkalemia-induced arrhythmias resolve once serum K+ is corrected. 
• As a result, since today's patient is hemodynamically stable in association with the rhythm in Figure-1 — determining the precise etiology of this fascinating rhythm is far less important than treating the patient's DKA (with treatment of DKA having an excellent chance of restoring a normal sinus rhythm).

The above said — I thought it instructive to explore how to go about assessing today's complex arrhythmia.

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Looking Closer at Today's Rhythm:

As I often emphasize — the simple step of numbering the beats and labeling P waves is often of invaluable assistance for both determining if the atrial rhythm is in fact regular — and for facilitating determination as to whether P waves are (or are not) related to neighboring QRS complexes.

• RED arrows in the long lead II rhythm strip at the bottom of Figure-2 — confirm that an underlying sinus rhythm is present, albeit with a very slight variation in the P-P interval (ie, ventriculophasic sinus arrhythmia — that is so commonly seen in association with 2nd- and 3rd-degree AV blocks).
• NOTE: For practical purposes and simplicity — I'll refer to the atrial rhythm in this blog as "regular", realizing that there is slight variation in the P-P interval.

Figure-2: RED arrows highlight an underlying sinus mechanism, with no more than minimal variation in the P-P interval.

To facilitate looking even closer at the mechanism of today’s arrhythmia — I’ll focus on the long lead II rhythm strip (See Figure-3 below):

• As noted a moment ago — the P waves in front of beats #2,4,6,8 are all upright and manifest a constant PR interval of 0.16 second. This tells us that at least these even-numbered beats — are all sinus-conducted with a normal PR interval.

Figure-3: Focusing on the long lead II rhythm strip …

Surprisingly (as shown in Figure-4) — BLUE arrows highlighting the P waves in front of beats #3,5,7 also manifest a constant (albeit much longer) PR interval.

• This suggests that these BLUE arrow P waves (despite their long PR interval of 0.44 second) — are also in some way being conducted!
• Had the rhythm strip in Figure-4 been started a little bit earlier — it most probably would have shown another BLUE arrow P wave with a similar prolonged PR interval of 0.44 second occurring before beat #1.

Figure-4: Since the PR interval preceding beats #3,5,7 is constant — these QRS complexes must be conducted (albeit with a very long PR interval). 

This leaves us with the YELLOW arrow P waves that I highlight in Figure-5 — as the only P waves that have not yet been addressed.

• By the process of elimination (ie, since each of the 8 QRS complexes in Figure-5 have been accounted for) — these YELLOW arrow P waves can not possibly be conducting. 
• This defines today's rhythm as representing some form of 2nd-degree AV block — because some (but not all) of the “on time” sinus P waves are conducting — but others are not.
• That is, there are a total of 15 P waves in Figure-5.
• 7 of these P waves (highlighted by the RED and BLUE arrows) are conducting 7 of the QRS complexes in this figure ( = beats #2-thru-8).
• The remaining 8 P waves (highlighted by YELLOW arrows) — are not conducted.

Figure-5: The YELLOW arrow P waves are not conducted.

A Laddergram is needed …

Today’s rhythm is complex! This tracing provides an example of one of the few times in which although I immediately recognized the general mechanism of today’s rhythm — I need to devise a laddergram in order to prove my theory.

KEY Points: I want you to walk away with the following concepts:

• Although it takes time and practice to become comfortable drawing laddergrams — knowing how to draw laddergrams is not necessary for optimal clinical management.
• In contrast — Learning to read laddergrams is EASY (as I'll demonstrate momentarily) — and this can help in selecting optimal management options.
• For interested readers — I review how to read and draw laddergrams in ECG Blog #188 (where I provide over 140 examples of laddergrams — many with step-by-step analysis). 

The “Quick” Answer to Figure-5:

We’ve already established that today’s rhythm manifests a supraventricular rhythm with RBBB conduction, regular P waves and group beating in which a number of “on time” P waves are conducting — but other “on time” P waves are not conducting.

• This establishes the rhythm as some form of 2nd-degree AV block — with the group beating strongly suggesting some form of Wenckebach conduction.
• As implied in the title of this ECG Blog post — there is more than a single “family” of PR intervals that conduct to the ventricles. Specifically: 
• RED arrow P waves conduct with a normal PR. 
• BLUE arrow P waves conduct with a longer PR.
• 
  
• PEARL #4: The most logical explanation for why a large PR interval "increment" may exist between 2 "families" of constant PR intervals — is that there are dual AV Nodal pathways that alternate conduction of sinus impulses:
• RED arrow P waves conduct with a normal PR interval of 0.16 second.
• BLUE arrow P waves conduct with a prolonged PR interval of 0.44 second.

My proposed Laddergram …

What follows is my step-by-step derivation of this laddergram: 

Figure-6: It's easiest to begin by completing the Atrial Tier (as shown by the vertical GREEN arrows that mark the onset of P waves).

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Figure-7: It's usually easiest to then complete the Ventricular Tier (GREEN arrows marking the onset of each QRS).

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Figure-8: It's now time to begin "solving" the laddergram — by postulating which P waves are most likely to be conducting to which QRS complexes. Depending on the complexity of the laddergram — this may entail some "trial and error". I start by connecting those P waves that I am most certain about (in this case — the RED arrow P waves that conduct with a normal PR interval to beats #2,4,6,8).

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Figure-9: I next connected the BLUE arrow P waves to beats #3,5,7. Because of the large PR interval "increment" between RED and BLUE arrow P waves — I used light BLUE lines to represent conduction over the slower AV nodal pathway.

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Figure-10: If conduction of the BLUE arrow P waves to the ventricles is over the slower AV nodal pathway — this means that the faster AV nodal pathway must be blocked at this time (which I represent by RED butt ends within the AV Nodal Tier). 

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Figure-11: This means that when normal conduction of the RED arrow P waves is occurring over the faster AV nodal pathway — the slower AV nodal pathway must be blocked (which I represent by adding the BLUE butt ends within the AV Nodal Tier).
= = = = = = =
NOTE: This leaves us with the 8 YELLOW arrow P waves — none of which are conducting ...

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Figure-12: Since none of the YELLOW arrow P waves are conducting to the ventricles — I complete the laddergram by schematically representing with RED and BLUE butt ends that both AV nodal pathways are blocked at this time.
= = = = = = =
Impression: One possible explanation of the mechanism for today's rhythm is that there may be 3:1 AV block in the faster AV nodal pathway that alternates with 3:1 AV block + 1st-degree AV block in the slower AV nodal pathway.

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More than One Possibility ...

What follows below goes way beyond-the-Core!

• My purpose in presenting an alternative laddergram to the one that I just derived in Figure-12 — is to illustrate the principle that with complex arrhythmias — there will often be more than a single possible explanation! 
• Without EP (ElectroPhysiologic) study — it will be impossible to know for sure which explanation is correct.
• Knowing which explanation is the "correct" one is not important for optimal clinical management.
• Unless your goal is to "dive in" to the specifics of complex arrhythmia interpretation — there is no need to concern yourself with the "Hows" and "Whys" of drawing this alternative laddergram.
• For those readers interested in "diving in" — I offer an alternative laddergram that I feel is more likely than postulating the simultaneous 3:1 AV blocks in both AV nodal pathways that Figure-12 suggests.

What follows is my derivation of this alternative laddergram: 

Figure-13: We can begin with the foundation established in Figure-7 — in which all P waves and QRS complexes are noted in the Atrial and Ventricular Tiers. 

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Figure-14: This alternative laddergram is based on the premise that when consecutive non-conducted "on time" P waves are seen in association with group beating suggestive of Wenckebach conduction — that there may be more than a single level of Wenckebach conduction out of the AV Node. I've presented this complex arrhythmia concept a number of times in this ECG Blog (See ECG Blog #259 — for a brief Audio Pearl and step-by-step laddergram demonstration of this phenomenon).
= = = = = = =
NOTE: I schematically represent the concept of dual-level AV block by drawing a BLACK dotted line within the AV Nodal Tier.

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Figure-15: I fully acknowledge that I tried several combinations before coming up with a plausible one that worked, which I show above. I postulate that over the faster AV nodal pathway — there is 2:1 block in the upper AV Nodal level — and then again 2:1 block in the lower AV Nodal level (RED butt ends in the upper and lower AV Nodal Tiers, respectively).

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Figure-16: This means that somehow, conduction to the ventricles of beats #1,3,5,7 must be occurring over the slower AV nodal pathway (BLUE arrows in the Ventricular Tier).

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Figure-17: I postulate that conduction of the BLUE arrow P wave makes it through both AV nodal levels — with retrograde conduction in the lower AV Nodal level preventing the YELLOW arrow P wave from passing through this lower AV Nodal level.

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Figure-18: If my Figure-17 is correctly drawn — then it would seem logical that conduction over the slower AV nodal pathway is blocked elsewhere in this rhythm strip (which I show in the next figure).

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Figure-19: I complete this alternative laddergram by schematically representing with RED and BLUE butt ends where AV nodal pathways are blocked throughout the rhythm strip.
= = = = = = =
Impression: This alternative laddergram postulates that there is dual-level block out of the AV Node with alternating 2:1 block in dual AV nodal pathways.

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In Summary:

The "quick answer" to today's complex arrhythmia is that the presence of regular P waves with 2 "families" of conducting PR intervals with a large PR interval increment — in association with group beating — strongly suggests there are dual AV nodal pathways.

• In addition — the finding of consecutive "on time" P waves that fail to conduct suggests there may be dual-level Wenckebach block out of the AV Node.
• Construction of a laddergram that works supports my theory that this is a plausible mechanism for today's arrhythmia.
• 
  
• CASE Follow-Up: As noted — this patient had DKA. Serum K+ at the time she presented = 7.0 mEq/L. Treatment of her DKA (with correction of her hyperkalemia) resulted in restoration of normal sinus rhythm. Along the way — today's initial rhythm provides arrhythmia enthusiasts with a fascinating account of the likely mechanism for this complex conduction disturbance.

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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ECG Blog #547 — What Happened When?

 The ECG in Figure-1 was obtained from a mid-30s man — who presented with CP (Chest Pain) that began ~1 hour earlier.

• The patient had previously been well. He had some risk factors — but no known history of heart disease.
• He reports a similar episode about a week earlier. He did not seek care at that time — because the episode resolved spontaneously. 

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• What happened when?
• What is the “culprit” artery?

Figure-1: The ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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My Thoughts on Today’s CASE:

The challenge in this case is not to diagnose that there is an ongoing acute MI, since that is obvious. Instead — the objective is to figure out what may have happened when?

• The rhythm in Figure-1 is sinus at the relatively fast rate of ~95/minute.
• QRS duration looks to be at the upper limit of normal. The QTc is no more than borderline prolonged. There is no clear sign of chamber enlargement.

The remainder of this tracing is markedly abnormal. I’ve labeled the principal findings in Figure-2: 

• The most “eyecatching” findings are in anterior leads V1,V2,V3 (within the RED rectangle in Figure-2).
• Deep QS complexes are seen in these first 3 anterior leads (YELLOW arrows in leads V1,V2,V3).
• The T waves in leads V2,V3 are hyperacute — in that they are huge (taller than the S waves are deep in these leads) — with symmetric rise-and-fall, with a “fattened” peak and widened base. We instantly know that the cath lab needs to be activated! That said — I found it impossible to identify the J-point defining the amount of ST elevation, because the ascending limb of these hyperacute T waves is so smooth (I suspect there is at least 2-3 mm of ST elevation — but can’t prove this on the basis of this initial tracing).
• PEARL: T waves do not have to be as tall as they are here in order for them to be "hyperacute". There admittedly is some subjectivity in defining one or more ST-T waves as 'hyperacute". I generally classify ST-T waves in this way when, in a patient with acute symptoms — ST-T waves exceed "expectations" (ie, When there are one or more acutely angled or straightened ST segment takeoffs — with a "fatter"-than-expected peak and/or wider-than-expected T wave base).
• With experience — You'll know when an ST-T wave is "hyperacute".
• 
  
• It’s insightful to recognize that the ST-T wave in lead V1 is clearly abnormal! The coved shape that we see here, with ≥1 mm J-point ST elevation — is not normal in lead V1 (and this abnormal appearance provides an important clue regarding the “culprit” artery).
• In contrast to the hyperacute anterior T waves in Figure-2 — is the scooped ST depression in lateral chest leads V5,V6 (BLUE arrows in these leads).
• I interpreted lead V4 as a “transition” lead — in that it shows an “intermediate” pattern with less hyperacuity than its neighboring anterior leads, and less ST depression than its neighboring lateral chest leads.

There are comparable ST-T wave abnormalities in the limb leads:

• There is marked reciprocal ST depression in the inferior leads (BLUE arrows in leads II,III,aVF).
• Lead aVL is especially abnormal — with a deep and wide Q wave indenting a fragmented QRS, followed by an obvious hyperacute ST-T wave (showing ST segment straightening, ≥1 mm of J-point ST elevation with “fattened” T wave peak and widened T wave base).
• The other high-lateral lead ( = lead I ) shows less marked, but still hyperacute ST-T wave changes.
• NOTE: I am not as strict when defining neighboring leads as "hyperacute". For example, by itself — I might not classify lead I as being "hyperacute". But in the context of this patient with new CP — in association with such obvious hyperacuity elsewhere, especially in neighboring lead aVL — the "fatter"-than-expected peak and wide base of the lead I T wave qualifies by my subjective definition as being "hyperacute".

Figure-2: I've labeled today's ECG. What do you see?

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Putting It All Together:

Despite the younger age and seemingly benign prior history of today’s 30-ish year old man — determining the “culprit” artery, as well as “What happened when?” does not change the obvious need for prompt cath as soon as this can be accomplished. Virtually all leads on this tracing show marked ST-T wave abnormalities! 

• Q waves have been documented to develop in as short a time period as 1-2 hours. That said — it would seem unlikely for Q waves as large as we see in leads V1,V2,V3 (and in fragmented lead aVL) to develop over the 1 hour that this patient has had symptoms. I therefore suspected that some event had occurred prior to this patient's onset of CP (that only began 1 hour before he came to the hospital).
• The patient acknowledges "a similar episode about a week earlier" — so perhaps he had an initial event at that time.
• "Silent" MI (in which an acute MI occurs in the absence of CP) is a real entity (See ECG Blog #228). That said — "true" Silent MI is less common among previously healthy younger adults. As a result — it would be worthwhile to revisit the History — since sometimes patients overlook past symptoms unless specifically asked to, "Think back over recents days to weeks as to whether at any time you had chest discomfort or other symptoms that concerned you for a period of hours or a day or two".
• For as much as the very deep QS complexes in Figure-2 do not seem acute — the huge hyperacute T waves in leads V2,V3, with marked ST-T wave abnormalities in virtually all other leads clearly do look acute — and strongly suggest acute proximal LAD (Left Anterior Descending) occlusion (The abnormally coved ST elevation in lead V1 + hyperacute leads V2,V3 + scooped ST depression in leads V5,V6 — strongly suggest a Precordial Swirl pattern — as described in ECG Blog #380).

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The CASE Continues:

On seeing this patient's initial ECG — providers promptly activated the cath lab.

Cath Findings = multi-vessel disease:

• Left-dominant coronary system.
• 100% proximal LAD occlusion.
• 80% distal LCx stenosis.
• 95% left PDA stenosis.
• PCI was successfully performed in the proximal LAD, the distal LCx (Left Circumflex), and the left PDA (Posterior Descending Artery).
• Post-procedure ejection fraction was surprisingly preserved!

Final Thoughts:

Despite the patient's younger adult age and seemingly benign past medical history — cardiac cath revealed severe multi-vessel disease with acute proximal LAD occlusion as the cause of his acute event.

• Presumably the patient had an acute extensive anterior infarction superimposed on previous anterior infarction.
• The "good news" is that despite severe underlying coronary disease — this patient did survive, and left ventricular function following PCI was relatively preserved. 
• Discharge management clearly needs focus on risk factor reduction, consideration of preventive and maintenance medication (ie, antiplatelet therapy, statin, beta-blocker, ACE-inhibitor or ARB, etc.) — with need for good compliance with close clinical follow-up.

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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ECG Blog #546 — Which Beat is Key?

 

I was sent this tracing ...

• The patient whose ECG is shown in Figure-1 is a man in his 60s with CKD (Chronic Kidney Disease) — who presented with "dizziness".

QUESTIONS:

It is immediately understandable why this patient may have dizziness — as the cardiac rhythm is obviously abnormal. 

• How to begin to assess this rhythm?
• HINT: Which one beat is KEY for our understanding of the etiology of the rhythm?

• And — What might be causing this rhythm?

Figure-1: I was sent this tracing — knowing only that it was from a man in his 60s with CKD. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

I fully acknowledge that it took me a moment to know how to proceed for assessing this rhythm. That's because the rhythm is clearly irregular with a number of different elements.

• PEARL #1: When you encounter a rhythm with multiple different elements (some of which are clearly more complex than others) — Start with the EASIER part(s)!
• Save those parts of the tracing that are more challenging to interpret for later ...

I was initially uncertain as to what I was seeing in Figure-1.

• I focused my attention on the long lead II rhythm strip. I highlight in Figure-2 the one beat that caught my "eye".

Figure-2: The KEY to today's rhythm is beat #2.

The KEY to Today's Rhythm ...

Beat #2 is the KEY to today's rhythm.

• Beat #2 is a sinus-conducted beat (RED arrow in the long lead II rhythm strip showing an upright sinus P wave with normal PR interval preceding this beat). I've highlighted this beat #2 within a RED rectangle in the picture of lead II from the 12-lead tracing.
• 
  
• PEARL #2: The reason beat #2 is so essential to understanding today's rhythm — is that this is the only beat that shows us what a "normal T wave" looks like!

QUESTION:

• Does PEARL #2 explain why the ST-T waves of beats #1,3,4,6,8,9 and 11 look different than the ST-T wave of beat #2?
• HINT: Check out Figure-3 ...

Figure-3: What is suggested by the YELLOW arrows?

ANSWER:

Beat #2 is the only sinus-conducted beat in this tracing.

• All beats in Figure-3 (with the exception of beat #10) manifest a narrow QRS complex. This confirms that all of these narrow beats are supraventricular. Since no P wave precedes beats #1,3,6,8,9 and 11 — these must be junctional escape beats.
• 
  
• PEARL #3 (Advanced concept!): Although the shape of the junctional escape beats looks similar to the shape of sinus-conducted beat #2 — the escape beats following each of the short pauses in the long lead II rhythm strip ( = beats #1,3,6,8,9,11) all appear to be slightly taller than the one sinus-conducted beat #2.
• On occasion in complex arrhythmias — it may be difficult to tell if one or more beats are sinus conducted vs escape beats from the AV Node. Awareness of a slight difference in appearance in the QRS complex of escape beats in such a tracing may provide a subtle clue as to whether or not these beats are being conducted. (An example of this advanced concept in which awareness of a slightly different QRS shape immediately tells you which beats are "escape" vs conducted beats — is seen in ECG Blog #63).

PEARL #4: The most plausible reason for the negative deflections that are highlighted by YELLOW arrows in the long lead II rhythm strip of Figure-3 — is that these negative deflections are the result of retrograde P waves that arise from the junctional escape beats.

• Note that the RP' interval (ie, the distance from the R wave of beats #1,3,6,8,9,11 in Figure-3 — until the negative deflection that follows) is the same!
• Note also that another QRS complex follows the retrograde P waves of beats #3, 6, 8 and 9 to produce beats #4,7, and 10. These beats #4,7 and 10 are called "Echo" beats (because rather than conducting down to the ventricles, the atrial impulses prior to these beats "turned around" and were directed back to the atria).

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Laddergram Illustration:

Today's rhythm is admittedly complex. That said — it offers a superb example of how drawing a laddergram serves to facilitate our understanding the mechanism of an "escape-capture" rhythm in which "capture" is the result of retrograde P waves that produce "echo" beats.

• I guarantee that this complex mechanism will become clearer by following my sequential derivation of today's laddergram — beginning with the legend in Figure-4.

Figure-4: As discussed above — beat #2 is the only sinus-conducted beat in today's tracing (as it is the only beat that is preceded by an upright P wave in this long lead II rhythm strip).

Figure-5: The next step in drawing today's laddergram — is to fill in the Ventricular Tier. I do this by drawing in near-vertical RED arrows to represent rapid conduction through the ventricles of narrow beats #1,3,4,5,6,7,8,9, and 11 (I'll explain beat #10 momentarily).
The large BLUE arrows in this figure schematically show that I timed each of the RED arrows in the Ventricular Tier to the occurrence of these beats in the rhythm strip.

Figure-6: As discussed in my explanation before beginning to draw this laddergram — We know that beats #1,3,6,8,9,11 are all junctional "escape" beats, because each of these beats follows a similar duration short pause, and none of these beats are preceded by P waves. I represent the AV Nodal origin of these escape beats by RED circles placed within the AV Nodal Tier.

Figure-7: I next represent the timing retrograde P waves by dotted BLUE lines that schematically show conduction back to the atria.

Figure-8: Conduction through the AV Node is slower than conduction through the atria. I schematically show this by the angled dotted BLUE lines that I've added in Figure-8 to represent retrograde conduction back to the atria from each of the junctional escape beats. This leaves me with having to explain how beats #4,5,7 and 10 come about! (which I do in Figure-9). 

Figure-9: The most plausible way to explain beats #4,7 and 10 — is that these must be "echo" beats, in which the retrograde impulse arising from junctional beats #3,6 and 9, turns around to produce forward conduction of beats #4,7,10. But this now leaves me having to explain how beat #5 comes about! (which I do in Figure-10).

Figure-10: Beat #5 must be another "echo" beat. And the only way I can explain how this might come about — is if during the forward path of conduction through the AV node on the way to produce beat #4 — there once again is retrograde conduction back to the atria (dotted BLUE line in this Figure-10).

Figure-11: The solid BLUE line that I've now added in this Figure-11 completes the laddergram. Thus, this figure shows the presence of 2 successive "echo" beats ( = beats #4 and 5).
Note in this Figure-11 that retrograde conduction back to the atria, followed by forward conduction to produce another QRS complex does not always occur. The reason why it sometimes does, and sometimes does not occur is not clear.

Figure-12: This is the completed laddergram. All that remains is to explain why the QRS of beat #10 is wide? (which I do in today's Figure-13 by going back to the original 12-lead tracing).

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Putting It All Together: 

Whenever we encounter a complex arrhythmia — it's important to always go back to the clinical situation and the original 12-lead tracing.

• The only history we were provided with for today's patient — is that this man in his 60s presented with "dizziness" — and that he has a history of CKD (Chronic Kidney Disease).
• Armed with awareness that hyperkalemia is notorious for producing unusual arrhythmias that are often featured by bradycardia and unusual forms of AV conduction disturbances — checking the serum K+ level is essential in today's case.
• Although subtle — I thought a number of chest lead T waves to be more peaked than expected, leading me to suspect some degree of hyperkalemia as a contributing factor. (Unfortunately — I was unable to find out the serum K+ level in today's case).
• Attention to the ST segments in leads V3,V4,V5 (within the BLUE rectangle in Figure-13) — suggests ST segment straightening and some ST depression. Perhaps this represents a recent or acute posterior OMI that may be responsible for the bradycardia with junctional escape beats? (Unfortunately — I was unable to obtain follow-up regarding this possibility in today's case).
• Finally — If we look in Figure-13 at the simultaneously-recorded chest leads for beat #10 — it becomes apparent that this beat is conducted with RBBB aberration (rsR' for beat #10 in lead V1 — with a wide terminal S wave in lead V6 for beat #10). This explains why beat #10 in the long lead II rhythm strip looks different and is slightly wider than other beats in this tracing. 
• It also explains why beat #7 in the long lead II rhythm strip is shorter than other beats in this tracing (Beat #7 is being conducted with incomplete RBBB aberration — as suggested by the rSr' morphology of beat #7 in simultaneously-recorded lead V1).  

Figure-13: Returning to today's original 12-lead tracing (See text).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) and M Shah (from Srinagar, India) — for allowing me to use this case and this tracing.
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