ECG Interpretation: ECG Blog #301 — 40yo Man: VT vs Aberrancy?

The ECG in Figure-1 was sent to me for my interpretation. It was obtained from a previously healthy 40-ish year old man — who presented to the ED (Emergency Department) with “palpitations”. He was hemodynamically stable.

QUESTION:

What is the rhythm: VT vs Aberrancy?

Figure-1: 12-lead ECG and long lead II rhythm strip obtained for a 40-ish year old man with palpitations.

MY Thoughts on the ECG in Figure-1:

We are told that the patient in today’s case is hemodynamically stable with the rhythm in Figure-1. Therefore, by definition — we have at least a moment in time to contemplate the rhythm without need for immediate cardioversion. By the Ps, Qs, 3R Approach (which I review in ECG Blog #185):

The rhythm for ECG #1 is rapid and Regular — at a Rate of ~190/minute (Use of the Every-Other-Beat Method to estimate this heart rate is explained below in the legend to Figure-2).
The QRS complex is wide.
I do not see any evidence of atrial activity (ie, there are no P waves — and therefore no "Relation" between atrial and ventricular activity).
IMPRESSION: In this hemodynamically stable 40-ish year old man — use of the Ps, Qs, 3Rs allows us to describe the ECG in Figure-1 as a regular WCT ( = Wide-Complex Tachycardia) rhythm at ~190/minute, without clear sign of atrial activity. Before going further — it is well to remember the differential diagnosis of a regular WCT of uncertain etiology (Figure-2).

Figure-2: This is my LIST #1: Causes of a Regular WCT (Wide-Complex Tachycardia) of Uncertain Etiology (ie, without clear sign of sinus P waves).

KEY POINTS Regarding the Above Differential Diagnosis:

My reason for repeating VT no less than 8 times in Figure-2 before listing another possibility — is to emphasize that statistical odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT begin at ~80%. As per ECG Blog #196 — these odds increase to ≥90% if the patient is of a "certain age" (ie, middle-aged and beyond) and has underlying heart disease. As a result — Assume VT until proven otherwise!
PEARL #1: Because of the above "statistical odds" — When assessing a hemodynamically stable patient in a regular WCT rhythm without P waves — our "mindset" should be that we need to prove that the rhythm is not VT, rather than the other way around.
That said — 90% is not 100% — so there will be cases in which a regular WCT rhythm will turn out to be supraventricular. We simply need to approach our differential diagnosis with the "starting point" of assuming a regular WCT rhythm without sinus P waves is VT until proven otherwise.

In Today's Case: — I Did Not Think the Rhythm was VT:

Despite the above statistical odds in favor of VT — Figure-3 illustrates why I did not think ECG #1 was VT.

PEARL #2: Although far from perfect — QRS morphology can be helpful for distinguishing between supraventricular vs ventricular rhythms. Many supraventricular rhythms resemble some form of known conduction defect (ie, RBBB, LBBB, LAHB, LPHB, or RBBB with either LAHB or LPBH).
In contrast — ventricular rhythms are less likely to resemble any known form of conduction defect (because these rhythms originate in the ventricles, usually from a site not in contact with the conduction system).
Of course — Exceptions to the above generalities clearly exist! (ie, Fascicular VT resembles RBBB with a hemiblock — whereas some SVT rhythms may not resemble any known conduction defect IF the preexisting ECG during sinus rhythm showed an unusual form of IVCD).
BUT — IF a completely typical QRS morphology for RBBB is present in each of the 3 KEY leads ( = left-sided leads I, V6 — and right-sided lead V1) — then a supraventricular etiology is highly likely. This is precisely what we see in Figure-3 because: i) A very typical RBBB conduction pattern (rsR') is seen in right-sided lead V1, in the form a small, initial positive deflection (r wave) — followed by an s wave that descends below the baseline — and ending in a "taller right rabbit ear" with a slender and tall R' complex; ii) Left-sided lead I is consistent with LPHB conduction (rS) — in that a slender initial r wave is followed by a very steep descent to a wide terminal S wave; and, iii) Left-sided lead V6 also manifests a triphasic (qRS) pattern (the opposite of the rsR' pattern in lead V1) — with wide terminal S wave that is highly characteristic of RBBB conduction.

Figure-3: I’ve outlined in RED a QRS complex in each of the 3 KEY leads to highlight the very typical QRS morphology of RBBB conduction (See text). In lead aVF — I illustrate application of the Every-Other-Beat Method for rapid estimation of heart rate (this method discussed in full in ECG Blog #210). It takes a little more than 3 large boxes (RED numbers in lead aVF) — to record 2 beats (BLUE numbers). If it would have taken exactly 3 large boxes to record 2 beats — then 1/2 the rate would have been 300 ÷ 3 = 100/minute. This means that 1/2 of the rate is a little bit slower than 100/minute — which means that the ventricular rate is ~190/minute.

PEARL #3: There is a tendency to simplify the differential diagnosis of a regular WCT rhythm down to 2 entities: VT vs "aberrant" conduction.

As shown above in LIST #1 (Figure-2) — this simplification overlooks the possibility that the reason for QRS widening in a WCT rhythm could be that the QRS complex was already widened at a time when the patient was in sinus rhythm (ie, as would be the case if there was a preexisting BBB). Unless a prior ECG on the patient is available — there may be no way to know IF the reason for QRS widening in a supraventricular tachycardia is: i) A rate-related conduction defect (ie, "aberrant" conduction); or, ii) A preexisting conduction defect on the baseline tracing.
LIST #1 also serves to remind us that in addition to VT and SVT with either preexisting BBB or aberrant conduction — other potential reasons why a tachycardia might manifest QRS widening include: i) A WPW-related tachyarrhythmia that travels first down the Accessory Pathway (anterograde); ii) Hyperkalemia; and/or, iii) Some other toxic effect that results in QRS widening.

PEARL #4: IF our assessment of QRS morphology in Figure-3 is correct — then the WCT rhythm in this tracing will be a regular SVT (SupraVentricular Tachycardia) at ~190/minute, without clear sign of atrial activity. As discussed in the Audio Pearl (ECG-MP-64) in the ADDENDUM below — my LIST #2 that I favor for the differential diagnosis of a regular SVT rhythm consists of 4 Causes:

Sinus Tachycardia (Sinus Tach).
Atrial Flutter (AFlutter).
A Reentry SVT (ie, AVNRT or AVRT).
Atrial Tachycardia (ATach).

Of these 4 Causes — the least common in my experience is Atrial Tachycardia (ATach). Consideration of the heart rate may provide an important clue to the etiology of a regular SVT without clear sign of atrial activity.

In a supine adult (ie, an adult who has not just exercised) — it is not common for sinus tachycardia to exceed ~170/minute. This is not to say that you will never see sinus tachycardia this fast in a non-exercising adult — but rather to suggest that the very rapid heart rate in today’s case (ie, ~190/minute) makes sinus tachycardia much less likely.
Untreated AFlutter most commonly presents with 2:1 AV conduction, in which the atrial rate of flutter is close to 300/minute (ie, ~250-to-350/minute range) — and the ventricular rate close to half that, or ~150/minute (ie, ~130-to-160/minute range). The ventricular rate of ~190/minute in today's case would imply an atrial rate of 190 X 2 = 380/minute, which is much faster than the usual atrial rate for AFlutter.
From these points — it can be seen that when the rate of a regular SVT rhythm is not more than 150-160/minute — any of the entities on the SVT LIST could be operative. However, when the ventricular rate is greater than ~170/minute (as it is in Figure-3) — then a reentry SVT rhythm becomes much more likely!

PEARL #5: Practically speaking — IF the rhythm in Figure-3 turned out to be VT — it would probably be a Fascicular VT. Appreciation of this fact has important clinical implications.

As emphasized in ECG Blog #197 — Approximately 10% of all VT rhythms fall into the category of Idiopathic VT rhythms, in which VT occurs in the absence of underlying structural heart disease.
Idiopathic VT is more likely to be seen in a previously healthy, younger adult population — which fits the profile of the patient in today's case.
Fascicular VT is one of the 2 most common forms of idiopathic VT. Morphologically — the QRS complex in Fascicular VT (as implied in its name) tends to resemble a RBBB pattern with either left anterior or left posterior hemiblock (ie, a "hemi-fascicular" block pattern).
Fascicular VT responds surprisingly well to IV Verapamil. On occasion — it may also respond to Adenosine, but IV Verapamil is the drug of choice for known Fascicular VT. In contrast — Verapamil is contraindicated for treatment of scar-related or ischemic VT.
BOTTOM LINE: I thought the rhythm in today's case was most likely to be a reentry SVT rhythm — because of the highly suggestive QRS morphology (as shown in Figure-3) that is perfectly consistent with typical RBBB conduction. But if it turned out that this rhythm was VT — its resemblance to RBBB/LPHB conduction would strongly suggest a Fascicular VT. As a result — IV Verapamil would have been my drug of choice, since this drug is 1st-line treatment for both reentry SVT rhythms and Fascicular VT.
IV Adenosine that was used in today's case was a perfectly suitable alternative — because this drug is generally safe — it is highly effective in terminating reentry SVT rhythms — and on occasion, it also may convert Fascicular VT.

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CONCLUSION of Today's CASE:

The patient in today's case was treated with IV Adenosine. The 2-lead rhythm strip in Figure-4 shows the result of such treatment.

QUESTION:

Was IV Adenosine effective in converting the rhythm?
What was the cause of QRS widening in the initial tracing?

Figure-4: Comparison of the initial ECG in today's case — with a 2-lead rhythm strip obtained after administration of IV Adenosine (See text).

ANSWER:

Unfortunately — I do not have a 12-lead ECG to show after administration of IV Adenosine. That said — even though I would have greatly preferred a lead V1 (rather than lead V2) rhythm strip — I believe ECG #2 in Figure-4 confirms my impression that the regular WCT rhythm in the initial tracing was supraventricular (in the form of a reentry SVT rhythm), in which the reason for QRS widening was preexisting bundle branch block.

Even though we do not have a left-sided monitoring lead (ie, lead I or V6) — and we do not have a lead V1 monitoring lead — the post-Adenosine tracing ( = ECG #2) shows conversion to sinus rhythm with persistent QRS widening and a QRS morphology in leads II and V2 that is virtually identical to the QRS morphology in these same leads during the WCT!
P.S.: To emphasize that IV Adenosine works rapidly — with antiarrhythmic effect usually complete with 1-2 minutes after administration. It's BEST to run a continuous hard-copy rhythm strip during the entire ~2-minute period after Adenosine administration — since the etiology of the arrhythmia will usually be evident during the process of conversion to sinus rhythm.

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Acknowledgment: My appreciation to M Shah (from Srinagar, India) for the case and this tracing.

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Relevant ECG Blog Posts to Today's Case:

ECG Blog #185 — Reviews my System for 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 in detail the differentiation in "List #1" for the causes of a Regular WCT ( = Wide-Complex Tachycardia).
ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm.
ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types.
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 ECG Media Pearl #21 in this blog post.
ECG Blog #211 — Reviews in detail WHY Aberrant Conduction occurs (and why RBBB aberration is the most common form).
ECG Blog #250 — Reviews in detail the differential in "List #2" for the causes of a Regular SVT ( = SupraVentricular Tachycardia).

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ADDENDUM #2 (5/3/2022):

My appreciation to JJ for their comment — in which they bring up the point that "some kind of electrical alternans can be seen in leads V3,V4".

I agree. I review the subject of Electrical Alternans in ECG Blog #83 — in which I emphasize the definition of this phenomenon = "a beat-to-beat variation in any one or more parts of the ECG recording — that may occur with every-other-beat — or with some other recurring ratio (3:1, 4:1, etc.)."

Leads V3,V4 do show variation in the height of the R wave — not strictly every-other-beat — but indeed with a recurring ratio.
The finding of electrical alternans is most common with reentry SVT rhythms (especially when there is an accessory pathway) — but on rare occasions, this phenomenon has been reported in monomorphic VT. So seeing electrical alternas supports (but does not prove) a supraventricular etiology.

My appreciation again to JJ for their observation!

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ADDENDUM #1 (4/22/2022):

I've added below from previous Blog posts a series of educational material regarding assessment of the Regular WCT — and the basics of Aberrant Conduction.

Figure-5: Use of the "3 Simple Rules" for distinction between SVT vs VT (taken from ECG Blog #196).

Figure-6: Use of lead V1 for assessing QRS morphology during a WCT rhythm (taken from ECG Blog #196).

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ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).