ECG Blog #135 (Regular WCT – Fascicular VT – RBBB – LPHB – SVT)

The ECG in Figure-1 was obtained from a 55-year old man who presented for emergency care with palpitations and fatigue. Blood pressure was 80/50 mmHg at the time this tracing was recorded.

• Is this VT (Ventricular Tachycardia)?
• How certain are you of your answer?

Figure-1: 12-lead ECG obtained from a 55-year old man with palpitations. Is this VT? 

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Interpretation: The rhythm is a regular WCT (Wide-Complex Tachycardia) at 180-190/minute without clear sign atrial activity. Although QRS appearance resembles RBBB (Right Bundle Branch Block) with LPHB (Left Posterior HemiBlock) — QRS morphology is not completely typical for this conduction defect because:

• Instead of a discrete rsR’ pattern in lead V1 — there is a double notch to the initial deflection in this lead, and — we do not see a clear s wave that descends below the baseline.
• The initial slender positive deflection (r wave) in lead I, followed by a predominant deep negative deflection is consistent with LPHB — but lack of a predominant R wave in lead II is not.

IMPRESSION: As emphasized in ECG Blog #134 — statistically, more than 80-90% of all regular WCT rhythms that lack sinus P waves will turn out to be VT. As a result — VT should always be assumed until proven otherwise! And, in view of slightly atypical features for RBBB/LPHB (as described above) — the likelihood that this rhythm represents fascicular VT would seem to be at least 90%. That said, given the presence of symptoms plus low blood pressure at the time this tracing was recorded — immediate cardioversion was indicated regardless of whether the etiology of this rhythm turned out to be VT or SVT (SupraVentricular Tachycardia) with either preexisting bundle branch block or aberrant conduction.

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Follow-Up: The patient received an electrical shock. This resulted in conversion of the rhythm to that seen in Figure-2.

• What happened? Does the post-conversion 12-lead ECG shown in Figure-2 prove what the etiology of the initial rhythm in Figure-1 was?

Figure-2: Post-conversion ECG after electrical shock. Is the etiology of the initial rhythm seen in Figure-1 now clear?

Discussion of Figure-2: The post-conversion 12-lead ECG seen in Figure-2 now shows sinus rhythm with QRS widening consistent with RBBB/LPHB. The KEY diagnostic observation is that QRS morphology in Figure-2 is virtually identical to QRS morphology during the tachycardia (that was seen in Figure-1). This proves that the initial rhythm was not VT — but rather SVT with preexisting bifascicular block.

• Note fragmentation of the widened QRS complex in several leads of both tracings. This is especially well seen in lead V2 (in which there is distinct angular notching of the S wave) — but it is also seen in the irregularity of the S wave in lead I, the R wave in leads III and aVF, and the notched initial r wave in lead V1. Fragmentation was also seen in Figure-1 during the tachycardia. During the WCT rhythm — such fragmentation contributed to our impression of a somewhat atypical RBBB appearance that made VT more likely. But its persistence after conversion to sinus rhythm suggests that in addition to the underlying conduction defect — the patient has underlying heart disease (ie, scarring from prior infarction and/or cardiomyopathy).
• QRS morphology can only go so far in predicting the etiology of a regular wide tachycardia. When ECG features of simple RBBB are completely characteristic (ie, distinct tri-phasic rsR’ complex in lead V1, with s wave descending below the baseline, and taller right rabbit ear) with smooth, wide terminal S waves in leads I and V6 — this appearance tends to be highly specific in predicting a supraventricular etiology. But the reverse is not true, such that atypical RBBB features are far less specific in their predictive value (See ECG Blog #42 for additional details).
• Sometimes one is surprised by the ultimate etiology of an arrhythmia. The ECG during a wide tachycardia is not a perfect predictive tool. That said, the correct diagnostic procedure was followed in this case. As always — Treat the patient, NOT the monitor. Since the patient was hemodynamically unstable because of the rapid rate of the presenting rhythm — immediate cardioversion was the intervention of choice regardless of the etiology of the arrhythmia!

Final Semantic Point — The reason for QRS widening in Figure-1 was not aberrant conduction! Instead, there was preexisting bifascicular block (RBBB/LPHB). If the reason for QRS widening would have been “aberrant conduction” — then the QRS widening would have resolved once the heart rate slowed.

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Acknowledgment: — My thanks to Darren Butcher (from London, UK) for his permission allowing me to use this case and ECG.

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For More on this Subject:

• See ECG Blog #38 — for review of Fascicular VT.
• See ECG Blog #42 — for my user-friendly approach to assessing the regular wide tachycardia.
• See ECG Blog #134 — for recent review of a WCT rhythm that we can definitively say is VT from the initial ECG.