Thursday, December 22, 2016

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? NOTE — Enlarge by clicking on the Figure.
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.
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.
Acknowledgment: — My thanks to Darren Butcher (from London, UK) for his permission allowing me to use this case and ECG.
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.


  1. Prof. Grauer, from the learnig point of view, one of the most helpful point is the fact that fragmentation can led astray and can lead us to the wrong diagnosis of VT. Very helpful post!

    1. We all are always learning! Nothing is 100% — so this was a very insightful case to me also — :)