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.

 

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews systematic rhythm interpretation, using the Ps, Qs & 3R Approach.
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• 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.
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• ECG Blog #220 — Reviews approach to the regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT rhythm.
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• 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?
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• ECG Blog #197 — and Blog #323 — review Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• 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.