A regular wide QRS tachycardia with right bundle branch block morphology and left QRS axis deviation

Abstract

A 76-year-old male called an emergency medical service after his smartwatch detected rapid heart rate. ECG obtained on ambulance recorded a regular, wide QRS tachycardia (150 bpm) having a morphology of right bundle branch block and left QRS axis. Two main diagnoses were discussed: a) any type of supraventricular tachycardia associated with ventricular aberration; b) ventricular tachycardia originating close to the posterior fascicle of the left ventricle. The final diagnosis was made after performing carotid sinus massage.

1. Case presentation

A 76-year-old male called an emergency medical service after his smartwatch detected rapid heart rate. ECG obtained on ambulance arrival is shown in Fig. 1.

Fig. 1.

Twelve lead ECG obtained on ambulance arrival.

Considering the good hemodynamic tolerance of the tachycardia, the physician in the emergency room preferred first to perform carotid sinus massage (CSM) rather than to give an antiarrhymic drug. CSM resulted with the tracing shown in Fig. 2.

Fig. 2.

Three leads ECG tracing recorded during carotid sinus massage in the emergency room.

Due to thoracic chest discomfort, the patient underwent direct-current cardioversion with restoration of sinus rhythm. Post-cardioversion ECG is shown in Fig. 3.

Fig. 3.

ECG recorded after electrical cardioversion of the arrhythmia.

Questions:

• 1)What is the differential diagnosis of the initial ECG?
• 2)What is the final diagnosis?

2. Discussion

Our patient presented with regular wide QRS tachycardia having a RBBB morphology pattern an a left QRS frontal axis. Tachycardia rate was 150 bpm.

Two main diagnoses should be discussed: a) any type of supraventricular tachycardia (SVT) associated with RBBB and left anterior fascicular block (LAFB); b) ventricular tachycardia (VT) originating close to the posterior fascicle of the left ventricle (LPF-VT). Although the presence of atrioventricular (AV) dissociation, capture, or fusion beats should avoid the misdiagnosis of the arrhythmia, the ECG diagnosis may remain challenging [1] when fusion or capture beats are absent, when a 1:1 atrioventricular relationship is present, or when P waves are not well visible.

In the present case, an obvious P wave, negative in inferior ECG leads, was present preceding each QRS complex that rendered the diagnosis more difficult.

Among SVT associated with RBBB and LAFB, 4 main diagnoses should be discussed:

a) Atrial tachycardia with 1:1 AV conduction; b) Atypical AV nodal reentry tachycardia (fast-slow AV nodal reentry); c) Orthodromic AV junctional reentrant tachycardia involving a slow conducting accessory pathway in the retrograde direction; d) Atrial flutter with 2:1 AV conduction in which only one P wave is visible. The least plausible of these 4 diagnoses is the first one considering the very short PR interval during tachycardia.

Michowitz and coworkers [1] were the first to provide a prediction model based on 4 simple morphological criteria that may facilitate achievement of correct diagnosis of LPF-VT compared with SVT with RBBB plus LAFB.

• a)QRS width ≤ 140 ms (odds ratio, 7.7; 95 % CI, 2.9–20.3; P < 0.001).
• b)atypical V1 morphology (odds ratio, 5.1; 95 % CI, 1.7–15.6; P = 0.004).
• c)positive QRS in aVr (odds ratio, 19.2; 95 % confidence interval [CI], 4.3–86.5; P < 0.001).
• d)R/S ratio in V6 ≤1 (odds ratio, 6.7; 95 % CI, 1.6–28.5; P = 0.01).

In the present case, all these 4 ECG criteria would rather support the diagnosis of LPF-VT over the diagnosis of SVT with RBBB plus LAFB. Actually, the following QRS characteristics were found:

• a)QRS width was 120 ms.
• b)The QRS morphology in V1 (qR) was atypical for conventional RBBB.
• c)A tall R wave was observed in aVR.
• d)There was a rS pattern in V6 with a small r/S ratio.

Contrasting with the ECG criteria above which would suggest LPF-VT as the tachycardia mechanism in our patient, simple CSM enabled to appropriately identify the type and mechanism of the tachycardia by inducing transient AV block and revealing an underlying atrial flutter with 2:1 conduction. The presence of isolated RBBB in sinus rhythm without LAFB suggests that the latter was rate-dependent. Although CSM has largely been replaced by the intravenous injection of adenosine compounds for this purpose, it should remain a valuable tool [2], especially when these compounds are not available or contra-indicated. Finally, the tachycardia rate observed in our patient (150 bpm) should always raise a possible diagnosis of atrial flutter with 2:1 conduction.

3. Editorial commentary (Mohammed Mhanna, Brian Olshansky)

We read with great interest the case report by Belhassen et al. describing a 76-year-old man with a wide QRS tachycardia of right bundle branch block (RBBB) morphology and left axis deviation, ultimately diagnosed as atrial flutter with 2:1 conduction following carotid sinus massage (CSM). This is an instructive and thought-provoking case, yet certain aspects of the mechanism merit further discussion.

Indeed, it is difficult to make a final call on the exact underlying arrhythmia mechanism(s). On the presenting ECG, there is consistent atrial activity with an apparent short PR interval. The presence of underlying atrial flutter, however, does not necessarily rule out ventricular tachycardia (VT) as a separate entity.

The QRS morphology during tachycardia is clearly different from the RBBB present in sinus rhythm, raising doubt about a purely supraventricular origin of the wide QRS tachycardia even with the possibility of progressive aberration. The tall R in aVR during tachycardia suggests inferior-to-superior activation, a finding typically associated with fascicular or ventricular tachycardia and not expected in supraventricular tachycardia, especially when the QRS axis in aVR is negative in sinus rhythm.

The ECG tracing after CSM is equally intriguing. It is not entirely clear that carotid massage affected the tachycardia cycle length, as QRS complexes can be marched through in leads I and III without a clear pause. Only between complex 9 and 10 does there appear to be transient slowing. Why the QRS narrowed subsequently remains uncertain. While atrial flutter with 2:1 conduction is a plausible explanation for the wide QRS complex tachycardia, the explanation cannot be considered definitive. The temporal relationship between tachycardia termination (or wider QRS morphology tachycardia) and CSM remains uncertain. Without more data on the time relationship, it is possible that the tachycardia termination was not necessarily due to CSM despite their concomitance. As effects of CSM are transient, it is important to clarify whether the same wide QRS tachycardia recurred during resumption of continued robust AV conduction.

Vagal stimulation can stop some idiopathic VTs. This been known for quite some time [3]. Similarly, we, and others, reported that adenosine can stop some idiopathic ventricular tachycardia (albeit for VTs with LBBB inferior axis morphology) [4]. Hence, suppression of tachycardia by CSM or even adenosine alone does not exclude VT.

The lack of intracardiac electrogram documentation of tachycardia mechanism is a limitation, as such recordings remain the gold standard for distinguishing SVT with aberrancy from fascicular or other forms of VT.

A side note of concern relates to subsequent management. The patient underwent direct-current cardioversion despite an unknown duration of atrial flutter and absence of oral anticoagulation. While chest discomfort was present, it is not clear that ischemia was the established. We favor an initial rate control with pharmacologic therapy and prolonged anticoagulation (or transesophagel echo with anticoagulation) before cardioversion to minimize risk of a thromboembolic catastrophe.

Taken together, while the enduring value of CSM in arrhythmia diagnosis and management are apparent, further diagnostic testing is necessary to rule out VT tachycardia. The case also highlights that a wide QRS tachycardia at 150 bpm should always raise the possibility of atrial flutter with 2:1 conduction, but that careful correlation with morphology and intracardiac data remains essential.

We commend the authors for presenting this educational case. Nevertheless, we remain cautious regarding the proposed mechanism and believe that additional data are needed to reach a definitive conclusion regarding the mechanism of the wide QRS tachycardia.

Consent form

The patient was a 76-year-old male who gave full written consent for all treatments which were delivered to him.

Ethical statement

All authors significantly contributed to the conception, writing and editing of the case report.

Yotam Kolben: Writing original and final preparation, Reviewing and Editing.

Marianna Vander: Data curation, Writing Original draft preparation.

Bernard Belhassen: Conceptualization, Methodology, Writing, Reviewing and Editing.

Funding

None.

Declaration of competing interest

We, certify that none of the following authors listed below, have something to declare.