ECG Blog #465 — A Tale of Syncope & 2 Rhythms

The ECG in Figure-1 was obtained from an older woman who presented to the ED (Emergency Department) because of a syncopal episode. She was asymptomatic at the time this ECG was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
•   Is there AV block?  If so — What kind?

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

MY Thoughts on Figure-1:

As always — I favor the Ps, Qs, 3R Approach as an optimally time-efficient way to assess any arrhythmia, including the AV blocks (See ECG Blog #185).

• As shown in the long lead II rhythm strip at the bottom of Figure-1 — the Rhythm is regularly irregular (ie, there is group beating, with repetitive short-long cycles). As a result — the Rate of the rhythm is not constant, although the overall ventricular rate is not overly rapid.
• P waves are present.
• The QRS is wide (ie, more than half a large box in duration). Looking at the 12-lead ECG that appears above the long lead II rhythm strip — QRS morphology appears to be consistent with LBBB (Left Bundle Branch Block) conduction, in that the QRS is all upright in left-sided leads I,V6 — and predominantly negative in right-sided lead V1, as well as in other anterior chest leads.

This leaves us with needing to assess the 5th Parameter — which is determining whether those P waves that are present, are Related to neighboring QRS complexes?

• To answer this question — I’ve labeled the P waves that we see in the long lead II rhythm strip with RED arrows (Figure-2).
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• PEARL #1: To facilitate determining if any of the P waves that you see are conducting — Label the P waves you identify! Doesn't this simple step of labeling P waves make it easier to determine which P waves are (or are not) Related to neighboring QRS complexes?

Figure-2: I've labeled P waves in today's initial ECG with RED arrows.

Are P Waves Related to Neighboring QRS Complexes?

Focus on QRS complexes that end each of the pauses in Figure-2 (ie, on beats #3,5,7,9 and 11).

• Isn't the PR interval that precedes beats #3,5,7,9,11 constant? This tells us that each of these beats is being conducted to the ventricles. (NOTE: Although we do not see far enough in front of beat #1 to assess the PR interval — by its similarity to the overall pattern in this tracing, we can presume that beat #1 is also being conducted to the ventricles).
• Next — Focus on the 2nd beat in each group (ie, on beats #2,4,6,8,10,12). Although somewhat difficult to tell because the P wave in front of each of these beats is partially hidden within the preceding T wave — Doesn't it appear that the PR interval before beats #2,4,6,8,10,12 is also constant, as well as being equal to the PR interval before beats #1,3,5,7,9,11?

For clarity in Figure-3 — I've drawn a laddergram of the long lead II rhythm strip from today's initial ECG. Note the following:

• Group beating (repetitive 2 beat groups throughout the tracing).
• A fairly (albeit not completely) regular atrial rhythm.  
• QRS widening (that we determined is consistent with LBBB conduction).
• All 12 QRS complexes in Figure-3 are preceded by P waves that manifest the same constant PR interval (ie, the slope of the RED lines within the AV Nodal Tier remains constant). 
• The PR interval of conducted beats is not prolonged.
• Every 3rd P wave is not conducted (ie, every 3rd P wave fails to make it out of the AV Nodal Tier).

Conclusion: The finding of a fairly regular atrial rhythm with failure of one or more on-time P waves to conduct to the ventricles defines today's initial rhythm as a form of 2nd-degree AV block.

• QUESTION: Which type of 2nd-degree AV block? 

Figure-3: Laddergram of the long lead II rhythm strip from Figure-2.

PEARL #2: As reviewed in detail in the ADDENDUM below — there are 3 Types of 2nd-degree AV block. These are:

• Mobitz I, 2nd-degree AV block ( = AV Wenckebach) — in which the PR interval increases until a beat is dropped.
• Mobitz II — in which the PR interval remains constant for consecutively conducted beats until one or more QRS complexes are non-conducted.
• 2nd-degree with 2:1 AV block — in which because of the fact that we never see 2 consecutively conducted beats — We are not able to tell if the PR interval would lengthen before dropping a beat IF given the chance to do so.
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• BOTTOM Line: By the above definitions — the rhythm in Figure-3 appears to be the Mobitz II form of 2nd-degree AV block because: i) The QRS is wide; ii) On-time sinus P waves are not conducted to the ventricles (which happens with every 3rd P wave in Figure-3); — and, iii) The PR interval remains constant for consecutively conducted beats.
• KEY Point: Distinction between the Mobitz I and Mobitz II forms of 2nd-degree AV block is important — because the clinical course of Mobitz I is often fairly benign — whereas patients with Mobitz II are much more likely to need a permanent pacemaker.

PEARL #3: There are a number of ECG and clinical Clues that may help to determine IF the type of 2nd-degree AV block you are looking at is more likely to be a Mobitz I or Mobitz II block. These clues include the following:

• Mobitz II is rare. In my experience — well over 90-95% of all 2nd-degree AV blocks will turn out to be Mobitz I.
• The QRS complex will most often be wide with Mobitz II. As a result — Mobitz II is very unlikely if the QRS is not wide. In contrast — the QRS is most often narrow with Mobitz I (although exceptions exist IF in a patient with Mobitz I — there is preexisting bundle branch block).
• Mobitz I is most often associated with recent or acute inferior infarction. In contrast — Mobitz II is most often associated with anterior infarction.
• The PR interval for beats that conduct with Mobitz I is often prolonged (sometimes markedly so). In contrast — the PR interval of conducting beats with Mobitz II is more often normal, or no more than minimally prolonged.
• It is unlikely to switch back-and-forth from Mobitz I to Mobitz II (or vice versa). Therefore, IF on review of additional monitoring on your patient you see clear evidence of Mobitz I (ie, progressive PR interval lengthening until a beat is dropped) — then it is likely that all tracings on that patient (including those with 2:1 AV block) — are also Mobitz I.

Regarding Today's CASE ...

• Because of the implication that pacing will be needed if today's rhythm is Mobitz II — We want to be as certain as possible that the PR interval is not increasing with consecutively conducted beats. As noted earlier — it is difficult to be certain of this in Figure-2, because the onset of the 2nd P wave in each 2-beat group is partially hidden within the preceding T wave.
• The 12-lead ECG that is seen in Figure-2 does show LBBB — but there is no clear sign of acute, recent or previous infarction.
• Conclusion: I strongly suspect the rhythm is Mobitz II — but I cannot be 100% certain this from this single ECG.

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The CASE Continues:

Today's patient had another syncopal episode. Her ECG at that time is shown in Figure-4.

QUESTIONS:

• How would YOU interpret the ECG in Figure-4?
•   Is there AV block?  If so — What kind?

Figure-4: Repeat ECG obtained following another syncopal episode.

MY Thoughts on Figure-4:

The rhythm in Figure-4 is now slower, but regular. The R-R interval is ~8 large boxes in duration — corresponding to a rate a bit less than 40/minute. P waves are seen. The QRS is obviously wide.

• As per PEARL #1 — Assessment of whether P waves are (or are not) related to neighboring QRS complexes is most easily accomplished by labeling P waves — which I have done in Figure-5.

Figure-5: I've labeled the P waves in Figure-4.

Are P Waves in Figure-5 Related to the QRS?

In Figure-5 — I've labeled those P waves that we can readily identify with RED arrows. Although there is slight variation in the P-P interval — this type of ventriculophasic sinus arrhythmia is common with 2nd- and 3rd-degree AV blocks.

• Given that it makes more sense for the underlying atrial rhythm to remain regular (rather than to all-of-a-sudden drop several beats) — I added PINK arrows in Figure-5 where I expected to find 2 additional P waves. (Slight distortion at the beginning of the QRS of beat #3 — and at the end of the T wave of beat #3 — strongly suggests that P waves do lie below these 2 PINK arrows).

Putting Together what we've determined in Figure-5:

• The QRS is wide.
• The ventricular rhythm is essentially regular (with minor variation in the R-R interval due to ventriculophasic sinus arrhythmia). The ventricular rate is just under 40/minute.
• An almost regular atrial rhythm is present (colored arrows in Figure-5). Focusing on the P waves before each of the 6 beats in the long lead II rhythm strip — the PR interval continually changes. Thus, P waves “are marching through” the QRS — such that there appears to be complete AV dissociation (ie, None of the P waves in Figure-5 are being conducted to the ventricles).

PEARL #4: Clearly, there is at least 2nd-degree AV block in Figure-5 — because many of the on-time P waves are not being conducted to the ventricles (ie, There are many more P waves than QRS complexes in this tracing). 

• As discussed in ECG Blog #405 — the KEYs for determining if complete (3rd-degree) AV block is present are: i) Whether there is an underlying regular (or almost regular) atrial rhythm; and, ii) Whether all P waves fail to conduct despite having an adequate opportunity to conduct. To satisfy these conditions — the rhythm strip must be long enough for P waves to occur during all parts of the R-R interval, and still fail to conduct.
• PEARL #5: Escape rhythms from the AV Node, the His or the ventricles — tend to be regular. As a result — the BEST clue for suggesting that AV block is not complete — is if the ventricular rhythm is not regular. The occurrence of one or more QRS complexes earlier-than-expected usually means that those earlier beats are being conducted.
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• Conclusion: As a result, I strongly suspect that the rhythm in Figure-5 is complete AV block because: i) The QRS is wide; ii) The ventricular rate is slow and regular; iii) The atrial rate is regular; — and, iv) None of the P waves appear to be conducting to the ventricles despite many of these on-time P waves occuring in parts of the cycle during which we would expect P waves to be able to conduct.
• Beyond-the-Core: Technically, we can not rule out the possibility that some P waves might be able to conduct if "given the chance" — since we do not truly see P waves occurring over all parts of the R-R interval. To see this — we would probably need another 20-to-30 seconds of monitoring. That said — the failure to conduct consecutive P waves at many points in this 10-second rhythm strip suggest at the very least, that there is high-grade (if not complete) AV block. 

QUESTIONS:

Take another LOOK at the 2 ECGs in today's case. To facilitate comparison — I have placed these tracings together in Figure-6. 

• Did YOU notice how different the QRS complex looks in each tracing? — WHY is this so?
• What about the appearance of ST-T waves in ECG #2?

Figure-6: Side-by-side comparison of the 2 ECGs in today's case. 

 

ANSWER: QRS morphology in ECG #1 (TOP tracing) is consistent with LBBB conduction (ie, all positive in left-sided leads I and V6 — but predominantly negative in the anterior chest leads). The constant PR interval preceding each beat in ECG #1 tells us that each of the 12 QRS complexes in this tracing is being conducted — although every third P wave is not. Thus, the rhythm in ECG #1 is 2nd-degree (not 3rd-degree) AV block.

• In contrast — the QRS complex is wider in ECG #2, with a very different QRS morphology (ie, resembling RBBB conduction in lead V1 — albeit with marked right axis in the limb leads). In association with the much slower ventricular rate and the constantly changing PR interval throughout this tracing — this suggests there is now a ventricular "escape" focus (which supports our assumption that the rhythm is now complete AV block).
• If any of the P waves in ECG #2 were to be conducting — we would expect to see a return to the LBBB conduction morphology that we saw in ECG #1.
• The laddergram in Figure-7 schematically illustrates failure of all atrial impulses to conduct in ECG #2 — because there is now complete AV block (dotted line in the AV Nodal Tier) — with resultant slow ventricular "escape".

Figure-7: Laddergram showing complete AV block in ECG #2.

To conclude the case — Take another LOOK at ST-T wave morphology in ECG #2 (BOTTOM tracing in Figure-6). Although none of the QRS complexes in this tracing are being conducted — Doesn't ST-T wave morphology look abnormal? (ie, There is ST segment coving with deeper-than-expected T wave inversion in leads V1-thru-V4).

• It's possible that the reason for the slower heart rate and progression to complete AV block is the result of a recent event. Serial troponins and ECGs are indicated to rule out an acute or recent MI.

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Summary of Today's CASE:

The patient in today's case is an older woman who presented to the ED for a syncopal episode. Although she was asymptomatic at the time her initial ECG was recorded — this initial tracing (shown in Figure-1) showed frequent non-conducted P waves as a result of 2nd-degree AV block of the Mobitz II type.

• As emphasized — clinical implications of Mobitz II are clearly more worrisome than for the much more common Mobitz I type of 2nd-degree AV block. For this reason — permanent pacing will often be needed when the rhythm is Mobitz II.

Today's patient then had a 2nd syncopal episode. Her repeat ECG at this time (shown in Figure-4) — now showed complete AV block, with a slow ventricular "escape" rhythm.

• Final Follow-Up: A recent event was ruled out. Thus, this case showed progression of Mobitz II to complete AV block. The patient received a permanent pacemaker.

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Acknowledgment: My appreciation to Rajeesh R Pillai (from Kollam, Kerala, India) for the case and this tracing.

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ADDENDUM (1/18/2025): 

• I've included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.

—  —

ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

My GOAL in the 15-minute ECG Video below — is to clarify ECG diagnosis of the 2nd-Degree AV Blocks, of which there are 3 Types:

• Mobitz I ( = AV Wenckebach).
• Mobitz II.
• 2nd-Degree AV Block with 2:1 AV conduction.

This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.

• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
• Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not! (This is a free download).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• 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 #256 — and Blog #342 — Review  of SSS (Sick Sinus Syndrome).
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• ECG Blog #295 — Reviews the concept of bradycardic-induced BBB ( = Phase 4 block). This is discussed near the bottom of the page (ie, in Pearl #5 — that appears just under Figure-6).
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• The July 5, 2018 post in Dr. Smith's ECG Blog — (Please see My Comment at the bottom of the page for Review on the ECG diagnosis of Sick Sinus Syndrome).
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• ECG Blog #192 — The 3 Causes of AV Dissociation.
• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #251 — Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach.
• ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach). 
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• ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
• ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).
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• ECG Blog #63 — Mobitz I, 2nd-degree AV block with junctional escape.
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• ECG Blog #405 — ECG Video presentation that reviews the distinction between AV Dissociation vs Complete (3rd-degree) AV Block (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).

 

 

ECG Blog #464 — Why a Dilated Heart?

The ECG in Figure-1 was obtained from a previously healthy 15-year old male — who presented with a 2-week history of palpitations, dizziness and dyspnea. He was hemodynamically stable in association with this tracing.

QUESTIONS:

In view of the above history:

• How would YOU interpret the ECG in Figure-1?
•    How would you treat the patient? 

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

MY Initial Thoughts:

Since the patient in today's case is hemodynamically stable in association with the rhythm in Figure-1 — there is at least a moment of time to contemplate the rhythm. As always — I favor the Ps, Qs, 3R Approach (See ECG Blog #185).

• The rhythm is a regular WCT (Wide-Complex Tachycardia) at ~160-170/minute, without clear sign of sinus P waves.
• The QRS measures 0.12 second in certain leads.
• Looking closely at the inferior leads — it appears that there may be retrograde P waves (YELLOW arrows in Figure-2).

QUESTIONS:

• Does the fact that we see retrograde P waves in today's initial ECG indicate that there is AV dissociation?
• Does this prove that the rhythm is VT (Ventricular Tachycardia)?
• Should we expect to see VT in an otherwise healthy 15yo?

Figure-2: I've labeled the negative deflections after each QRS in the inferior leads with YELLOW arrows.

PEARL #1: The phenomenon known as AV dissociation — is said to occur when "on time" P waves are not related to neighboring QRS complexes. AV dissociation may be transient (occurring for as little as a single beat) — or persistent (as occurs when there is complete AV block). The diagnostic value of recognizing AV dissociation in a WCT rhythm — is that it virtually proves the rhythm to be VT, since if "on time" P waves are not being conducted to produce the regularly-occurring wide complexes — then these wide beats must be arising from below the AV node (See ECG Blog #151 and Blog #133).

• The problem is that most of the time when confronted with a WCT rhythm of uncertain etiology — the rate of the WCT will be too fast to allow us to reliably detect underlying sinus P waves. Therefore, you will not often see AV dissociation in faster VTs (and it is the faster VTs rather than VT at slower rates — that challenge our diagnostic abilities).
• In my experience — AV dissociation is overdiagnosed. There is a tendency to think AV dissociation is present whenever one sees "extra deflections" in a WCT rhythm. The clinical reality is that artifact (rather than true AV dissociation) is the usual cause of these deflections. As a result — I favor undercalling AV dissociation unless I can truly "walk out" underlying regular P wave throughout much (if not all) of the tracing.
• We do not see AV dissociation in Figure-2. Instead — the RP' interval remains constant (ie, the distance from the QRS until each retrograde P wave does not change). Both VT and reentry SVT rhythms (AVNRT and AVRT) may conduct retrograde. As a result — the finding of retrograde P waves is of no help diagnostically for distinguishing between VT and SVT rhythms.

The CASE Continues:

Providers initially thought it unlikely for an otherwise healthy adolescent to be in VT.

• Carotid massage was tried — but was unsuccessful.
• 2 doses of Adenosine failed to convert the rhythm.
• At this point — Verapamil (5 mg IV) was given. Over the next several minutes — the WCT rhythm gradually slowed, and then converted to normal sinus rhythm.

Shortly after giving IV Verapamil — the rhythm in Figure-3 was recorded.

• Does the Figure-3 recording help solidify your diagnostic impression of what today's WCT rhythm was?

Figure-3: Rhythm strip recorded within minutes after treatment with IV Verapamil. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Figure-3:

The "good news" on seeing the 3-lead rhythm strip shown in Figure-3 — is that the WCT rhythm is slowing — and that sinus P waves are now at least intermittently seen.

• How many sinus P waves can you identify?

ANSWER:

In Figure-4 — I've highlighted with RED arrows the sinus P waves that are clearly seen in Figure-3.

• As per these RED arrows that I've added in Figure-4 — beats #2 — #5,6 — #9,10 — and #13,14 all appear to be normal sinus-conducted impulses.
• Interspersed between these sinus beats are ventricular couplets (ie, beats #3,4; 7,8; 11,12, and 15,16). Over the next few minutes (as Verapamil had time to work) — these ventricular couplets resolved, and normal sinus rhythm resumed. 

QUESTION:

• Are there more sinus P waves present? (ie, More sinus P waves than the ones highlighted in Figure-4?).

Challenge Question: Do all of the sinus-conducted beats in Figure-4 look the same? 

• HINT: Look carefully in lead III ...

Figure-4: I've added RED arrows to highlight the sinus P waves in Figure-3 that are clearly seen. Are there more?

PEARL #2: The easiest (and fastest) way to find the additional P waves in Figure-4 that are "hiding" — is to use calipers.

• Rather than there only being only the intermittent sinus P waves highlighted by RED arrows in Figure-4 — Wouldn't it seem logical for the underlying P wave rhythm to be regular? 
• If this were the case — then the P-P interval suggested by the shorter distance between any 2 RED arrows will probably continue throughout the entire tracing.

I illustrate applying this concept in Figure-5. 

• PINK arrows highlight partially hidden on-time sinus P waves that continue throughout this entire rhythm strip.

PEARL #3: By "walking out" regular on-time sinus P waves throughout the entire Figure-5 rhythm strip — we have established that there is now at least transient AV dissociation (because the colored arrows in Figure-5 demonstrate that there is now an underlying regular sinus rhythm — and the on-time PINK arrow P waves are unrelated to the wide QRS beats).

• Demonstrating AV dissociation in Figure-5 proves that beats #3,4; 7,8; 11,12; and 15,16 are of ventricular origin. And, the fact that QRS morphology in leads I,II,III from today's initial ECG (ie, from Figure-1) is virtually identical to QRS morphology of these ventricular beats in Figure-5 — provides even more proof that today's initial ECG was VT!

Figure-5: PINK arrows highlight on-time sinus P waves that continue throughout this tracing.

ANSWER to the Challenge Question:

Take another LOOK at lead III in Figure-5. Isn't the QRS complex of the 2nd sinus-conducted beat in each group a little bit smaller than the 1st sinus-conducted beat?

• The answer is that the QRS of sinus-conducted beats #2,6,10 and 14 is slightly smaller than the QRS of beats #1,5,9,13.
• This is because beats #2,6,10,14 are fusion beats! There is a subtle-but-real shortening of the PR interval before beats #2,6,10,14 compared to the PR interval before beats #1,5,9,13 (seen best in leads I and II). This sets up the possibility for beats #1,5,9,13 to conduct part of the way through the ventricles — until they encounter the wave of depolarization initiated by near-simultaneous occurrence of a ventricular beat.

PEARL #4: The clinical significance of finding fusion beats in an otherwise regular WCT rhythm — is that like AV dissociation, this proves that the rhythm is VT.

• The mechanism for fusion in Figure-5 is best illustrated by the laddergram drawn in Figure-6. We need to remember that moments before this rhythm was recorded — the patient had been in a sustained WCT. Administration of IV Verapamil is now in process of converting the rhythm to sinus.
• Looking at the Ventricular Tier in the laddergram — Rather than the persistent WCT rhythm (that was present moments earlier) — there are now only salvos of 3 ventricular beats in a row (beats #2,3,4; 6,7,8; 10,11,12; and 14,15,16). These salvos are interupted by periodic capture beats ( = on-time sinus P waves occurring at just the right moment to be able to conduct beats #1; 5; 9; and 13 to the ventricles).
• In contrast — PINK arrow P waves in Figure-6 occur during the absolute refractory period — and are therefore not able to conduct to the ventricles.
• This leaves the P waves before beats #2,6,10 and 14 — which are able to conduct into the ventricles (at least up until the moment that they meet up with near-simultaneously occurring ventricular impulses). This results in fusion. (For more on the concept of fusion beats — See ECG Blog #128 and Blog #129).

Figure-6: Laddergram illustration for the mechanism in Figure-5.

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Today's CASE Continues:

Shortly after IV Verapamil restored sinus rhythm — an Echo was obtained:

• Echo showed dilation of all 4 cardiac chambers with global reduction in contractility = DCM (Dilated CardioMyopathy).

QUESTIONS:

• Do these Echo findings change your impression on the sequence of events in today's case?
• Why should a previously healthy 15-year old develop DCM with severely reduced ejection fraction?
• Could the patient have had a viral infection with relatively silent involvement of the heart (ie, myocarditis)? If so — Could myocarditis have been the cause of this patient's VT?
• OR — Could it be that this patient was having frequent and prolonged episodes of sustained VT over the 2 week period that he reported having symptoms for, with the end-result that prolonged tachycardic episodes caused his cardiomyopathy?

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PEARL #5: Be aware of TiCM (Tachycardia-induced CardioMyopathy)

While definitive answers to the above questions are not forthcoming — the most likely scenario (given that this 15yo had previously been healthy) — is that sustained tachycardic episodes did precipitate development of TiCM (Huizar, Ellenbogen et al — JACC 73(18):2328-2344, 2019 — and — Kim et al — Korean Circ J. 49(9):808-817, 2019).

• TiCM — is defined as the presence of a reversible form of LV dysfunction due solely to an increase in ventricular rate from any type of frequent or sustained tachycardia (rapid AFib being the most common precipitating rhythm — but TiCM has also been shown to arise from AFlutter, reentry SVT rhythms, ATach, frequent PVCs, episodes of VT).
• The risk of developing TiCM depends not only on the type of tachycardia — but also on the duration and the rate of the tachycardia.
• The time that it takes to develop TiCM is variable — potentially being as short as 3 days vs persistent tachycardia episodes over a period of months (ie, The 2-week history of symptoms in today's case was enough time for TiCM to develop).
• The mechanism for developing TiCM is uncertain (persistent epinephrine release; intracellular calcium handling issues?).
• A range of symptoms may be seen. Most commonly patients complain of palpitations — but there may be dyspnea, dizziness and/or fatigue. Surprisingly, a significant percentage of patients are asymptomatic — with TiCM only discovered when Echo reveals an unexpected reduction in cardiac function. Heart failure may develop.
• Typical Echo findings include dilated cardiac chambers with moderate to severe biventricular systolic dysfunction. Septal and left ventricular wall thickness is not increased (ie, there is no LVH). Secondary mitral insufficiency may be seen.
• The "good news" — is that LV function often improves, and may even return to normal IF the tachycardia can be controlled. Treatment options include ß-blockers, other antiarrhythmic agents, RFCA (RadioFrequency Catheter Ablation). When treatment is successful — recovery of LV function may begin within weeks. Patients who recover usually do so within 6 months of achieving rate control.
• Bottom Line: It may be extremely challenging to determine whether the finding of DCM on Echo is the cause or result of a recurrent tachycardia rhythm.

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Back to the Initial ECG:

Take another LOOK at the initial ECG in today's case — that I show again in Figure-7. 

• QUESTION: Are there clues that this regular WCT is VT?

Figure-7: Taking another look at today's initial ECG. 

MY Thoughts on Figure-7:

There is a mistaken impression among many clinicians that otherwise young, healthy adults or adolescents do not develop VT.

• It is true — that ischemic VT is generally not seen in the absence of underlying heart disease.
• However — approximately 10% of all VT rhythms are the result of Idiopathic VT, in which VT that occurs in patients without underlying structural heart disease.
• 
  
• Fascicular VT — is one of the most common forms of idiopathic VT. It is named because of its origin in one of the ventricular hemifascicles. As a result — QRS morphology with fascicular VT most often resembles either RBBB/LAHB or RBBB/LPHB.

PEARL #6: Recognition of fascicular VT is facilitated by: i) Realizing that this form of VT is much more common than is generally appreciated, especially when the patient is an otherwise healthy adolescent or young adult without known heart disease; — and, ii) Recognizing that fascicular VT becomes more likely in such patients when QRS morphology is similar but not completely typical for one of the forms of bifascicular block.

• Today's ECG shows a regular WCT rhythm at ~160-170/minute, without clear sign of sinus P waves. (As discussed earlier — there may be retrograde 1:1 VA conduction in the initial ECG — but this does not help with differential diagnosis).
• QRS morphology in Figure-7 superficially resembles RBBB/LAHB conduction but: i) The QRS complex in lead V1 is amorphous. It lacks the typical triphasic (rSR' with taller right rabbit ear) configuration that so often is seen in otherwise healthy, younger adults; — and, ii) Most of the time when there is LAHB conductionn in otherwise healthy, younger adults — there will be more of an initial r wave and not quite so much QRS widening in the inferior leads.
• 
  
• To Emphasize: While I was not 100% certain — my strong suspicion on seeing the initial ECG in today's case was that the above atypical features in QRS morphology made it much more likely than not that Figure-7 represented fascicular VT (from the left posterior hemifascicle). 
• On seeing this tracing in this previously healthy 15yo — my initial treatment would have been IV Verapamil, which is the drug of choice for fascicular VT (and which will also usually work if the rhythm is a reentry SVT with aberrant conduction instead of VT).
• Given the severity of symptoms in this patient (with resultant development of TiCM) — optimal treatment after conversion of the WCT would entail EP referral for ablation. Hopefully — LV function will return to normal following control of the rhythm.

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Acknowledgment: My appreciation to Fardeen Baray (from Kabul, Afghanistan) for the case and this tracing.

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ADDENDUM (1/11/2025):

I summarize KEY features regarding Idiopathic VT in Figure-8.

Figure-8: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio):

 — What is Idiopathic VT? — WHY do we care? 

Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT.

 

==============================

Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews systematic rhythm interpretation, using the Ps, Qs & 3R Approach.
• 
  
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
• 
  
• ECG Blog #220 — Reviews approach to the regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT rhythm.
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
• 
  
• ECG Blog #197 — and Blog #323 — review Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• 
  
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.

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.
• 
  
• 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).
• 
  
• ECG Blog #264 — Reviews LA-RA Lead Reversal.
• ECG Blog #396 — for a list of lead reversals ...

• 
  
• 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).