ECG Interpretation: April 2026

The ECG in Figure-1 was obtained from an older woman who presented with new-onset palpitations. She was hemodynamically stable in association with this tracing.

QUESTIONS:

How would you interpret the ECG in Figure-1?

How specific can you be with your interpretation?

What is the treatment of choice?

Figure-1: The initial ECG in today's case.

MY Thoughts on this Tracing:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~185/minute without clear sign of atrial activity.

QRS morphology is consistent with LBBB conduction in the chest leads (ie, predominantly negative QRS in the anterior leads — with an all-positive QRS in lateral chest leads) — with an inferior frontal plane axis (as determined by the all-positive QRS in inferior leads — with an equiphasic QRS in lead I).

Impression:

The above description is virtually diagnostic of RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia).

PEARL #1: Once you are familiar with the entity of RVOT VT — You should be able to make this diagnosis with high accuracy within seconds of seeing an ECG that looks like today’s tracing.
As we’ve shown on multiple posts on this ECG Blog — RVOT VT is one of the two most common forms of idiopathic VT (See ECG Blog #489 — Blog #346 — Blog #323 — among many others). This term “idiopathic” VT simply refers to the ~10% of patients who present with VT without underlying heart disease.

I review the KEY distinguishing points of the idiopathic VTs in the ADDENDUM to today’s post (See my summary info sheet in Figure-4 — and my 8-minute Audio Pearl below).

Many (admittedly not all) of the idiopathic VTs are readily recognizable by their QRS morphology (described in Figure-4).
Because the QRS complex in idioventricular VT is typically not overly wide — and because of the resemblance to QRS morphologic features of known conduction blocks (ie, RBBB with a Hemiblock in the limb leads, as in fasicular VTs — and LBBB in the chest leads, as in outflow track VTs) — there is a tendency to misdiagnose the idiopathic VTs as some form of reentry SVT with aberrant conduction (instead of recognizing them as VT).

PEARL #2: One of the most helpful clues that a regular WCT without P waves is likely to be idiopathic VT (and not some form of reentry SVT with aberrant conduction) — is that there are subtle atypical features that are not consistent with any known form of conduction block. For example — in Figure-1:

Although the predominant negativity of the QRS complex in leads V1,V2 is consistent with LBBB conduction — with typical LBBB, transition tends to occur later than what is seen in Figure-1 (ie, with simple LBBB — no more than a tiny r wave usually persists past lead V3 — and this R wave does not become predominant until at least lead V5). Instead, as we look at Figure-1 — the R wave is already enlarging in lead V3, and it is already predominant in lead V4.
With LBBB — septal depolarization moves right-to-left (instead of left-to-right) — followed by slow, progressive leftward depolarization of the left ventricle (that overwhelms electrical activity arising from the much smaller right ventricle). As a result — the QRS vector in left-sided lead V6 and in lead 1 manifest an all-positive widened R wave. However, the small isoelectric QRS complex that we see in lead I of Figure-1 should not be seen with a typical LBBB (unless there has been prior infarction and/or extensive scarring or myocardial infiltration). The fact that this small isoelectric complex in lead I begins with a negative deflection — and the finding of an all negative QRS in high-lateral lead aVL are especially atypical for LBBB conduction.
To Emphasize: It’s impossible from Figure-1 alone to be 100% certain that this ECG represents VT. But the findings of LBBB-like conduction in the chest leads with an inferior frontal plane axis are completely typical for RVOT VT — and — the atypical QRS morphology features described in this PEARL #2 strongly suggest VT until proven otherwise.

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The CASE Continues:

Today's patient was successfully cardioverted — but the WCT rhythm in Figure-1 returned. Lasting conversion to sinus rhythm was finally achieved after a 2nd cardioversion (as shown in Figure-2).

QUESTIONS:

Does the ECG in Figure-2 solidify the diagnosis of VT for the initial ECG that was seen in Figure-1?

What other interventions might have been considered?

Figure-2: The repeat ECG, recorded after the 2nd cardioversion.

My Thoughts:

The repeat ECG in Figure-2 shows restoration of a normal sinus rhythm (RED arrows in Figure-3 highlighting upright sinus P waves in the long lead II) — with the exception of a single early wide beat toward the end of the tracing ( = beat "X").

PEARL #3: We know with 100% certainty from Figure-3 that beat X is a PVC (Premature Ventricular Contraction) and not an aberrantly conducted supraventricular beat — because underlying "on time" sinus P waves continue thoughout this long lead II rhythm strip (ie, The PINK arrow P wave shows continuation of these "on time" sinus P waves — and this can only happen if the wide beat originates "from below", since a supraventricular beat would have delayed the next sinus P wave).
PEARL #4: Note that QRS morphology in Figure-3 of the PVC is identical in simultaneously-recorded leads V4,V5,V6 (within the BLUE rectangle) — to QRS morphology in leads II,V4,V5,V6 during the WCT rhythm in ECG #1. This finding highlights the utility of the post-conversion ECG for retrospectively making a definitive diagnosis of the etiology of a WCT rhythm if one or more similar QRS morphology PVCs are seen.

Figure-3: Comparison between the 2 ECGs in today's case.

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Final Thought: Regarding treatment of the WCT rhythm in ECG #1:

There is no single "correct" answer for how best to treat the regular WCT rhythm that today's patient presented with. And, the treatment path chosen in today's case was successful.
Synchronized cardioversion is clearly the intervention of choice if there is any concern about hemodynamic stability in association with a WCT rhythm. Sometimes, "Ya just gotta be there" to judge when to go ahead with synchronized cardioversion.
That said — today's patient was stable on presentation, so options are available. As noted below in Figure-4 — RVOT VT often responds to Adenosine, which could have been tried.
Recurrence of the WCT after the 1st synchronized cardioversion in today's case was a signal that a longer-acting intervention (ie, perhaps IV Amiodarone) might be needed to maintain sinus rhythm, rather than repeat cardioversion.
I do not have further follow-up as to whether or not this patient was referred for EP evaluation.

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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Johore, Malaysia) for making me aware of this case and allowing me to use this tracing.

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