This figure demonstrates the transition from a wide QRS complex tachycardia to a narrow QRS complex tachycardia. The first question is whether the patient has supraventricular tachycardia with aberrancy or ventricular tachycardia with a transition to a supraventricular tachycardia. Typically, one would not expect the tachycardia rate to increase with the disappearance of aberrancy and careful measurement of the wide QRS complex tachycardia shows that it has a longer cycle length than the subsequent narrow QRS tachycardia. Does this mean that the wide complex tachycardia is ventricular tachycardia and it somehow induces a supraventricular tachycardia?

Evidence to support that this is a supraventricular tachycardia can be found in careful analysis of the T wave just preceding the onset of the arrhythmia. Note that this T wave shows a peaked contour compared with the preceding T waves and this strongly suggests that a P wave is inscribed on the T wave. This is most compatible with the onset of a supraventricular tachycardia. If the bundle branch system were used in supraventricular tachycardia, one might indeed anticipate a shorter cycle length with the disappearance of the bundle branch block. This is characteristic of AV reentry (AVRT) utilizing an accessory pathway for retrograde conduction. In such an instance, the cycle length will prolong in approximately 85% of patients who have a bundle branch block occurring on the side of the accessory pathway, in this instance a left-sided accessory pathway with left bundle branch block (LBBB) aberrancy. This is because of an increase in the circuit time reflected in the ventriculoatrial interval due to transseptal conduction time from the right to left ventricle in the presence of LBBB. The disappearance of the LBBB will shorten the reentrant circuit by allowing the left side of the heart to be activated sooner and thus shorten the tachycardia cycle length.

This patient had a concealed left free wall accessory pathway that was used in AVRT that was successfully ablated.

The 12-lead electrocardiogram shows a regular tachycardia with LBBB morphology and a cycle length of approximately 220 milliseconds. While not “classic” for a typical LBBB pattern, the QS complex appears to be more typical than atypical for LBBB. Note the lack of a Q wave in ECG leads 1 and aVL and a rather rapid downstroke of the initial portion of the QRS in the early precordial leads. Figure 2–2B demonstrates the mechanism of tachycardia. Because the patient was stable in the emergency room setting, the treating physician administered intravenous verapamil with the assumption that this was a supraventricular tachycardia. As an aside, this should not be done, of course, when VT remains in the differential diagnosis as it surely is in this case. Regardless, the mechanism of tachycardia was revealed when this was performed and the patient has atrial flutter shown well in ECG leads 2, 3, and aVF. Note also that after block the slower tachycardia has half the ventricular rate of the wide QRS tachycardia. Agents such as propafenone and flecainide are well known to allow the emergence of atrial flutter in patients with atrial fibrillation and 1:1 AV node conduction can occur if an AV node blocking agent is not present. This can lead to a cardiac arrest, which fortunately did not occur here.

In the ECG rhythm strip designated A, note sinus rhythm with a short PR interval and a broad QRS complex consistent with ventricular preexcitation. The onset of tachycardia in B is shown in the lower rhythm strip. Careful analysis of the ST segment of the second sinus complex demonstrates a deformation that is most likely a P wave that results in a narrow QRS complex and the onset of tachycardia. Note that this premature atrial complex initiates tachycardia not only with loss of preexcitation but also with a markedly prolonged PR interval of approximately 360 milliseconds. This almost surely represents conduction over a slow AV nodal pathway. There is a P wave noted just at the end of the QRS complex during tachycardia. While this could be AV reentry with retrograde conduction over an accessory pathway and anterograde conduction over a slow AV nodal pathway, the V to retrograde P interval is very short (approximately 80–100 milliseconds) and this would be “borderline” for retrograde conduction over an accessory pathway. In this instance, the mechanism identified at EP study and ablation was slow–fast AV node reentry. The accessory pathway was not capable of retrograde conduction, and it was just by chance that a PAC blocked anterograde conduction over the accessory pathway while starting AV node reentry.

This patient demonstrates sinus rhythm with RBBB QRS morphology and a Mobitz 1 Wenckebach sequence on the left-hand side of the tracing (Fig. 2–4). The PR interval does prolong slightly before the third P wave in the sequence blocks. Carotid sinus massage was performed on the right side of the rhythm strip, and the sinus cycle slows with resumption of 1:1 AV conduction. These findings indicate block in the His–Purkinje system and not in the AV node. The relatively short PR interval at the start of the Wenckebach sequence, a small PR interval increase prior to the nonconducting P wave, and a relatively fast sinus rate are consistent with His–Purkinje pathology and block. Slowing of the rate with carotid massage allows resumption of 1:1 AV conduction, contrary to what one would expect if block were in the AV node. This patient underwent electrophysiology study where infra-Hisian block was confirmed and a pacemaker was implanted.

In the upper rhythm strip (A), note that there is an irregular narrow QRS complex rhythm with P waves that are variable. The seventh QRS complex demonstrates an intermediate QRS morphology compared with the wide QRS complexes that are seen on the right-hand portion of ECG strip A as well as the left-hand portion of the bottom strip (B). The differential diagnosis is ventricular tachycardia, a preexcited tachycardia, or supraventricular tachycardia with aberrancy.

Several features strongly suggest aberrancy. First, there is a relatively long–short interval preceding the incomplete BBB of the seventh QRS complex. This is followed by an even longer pause and a short interval, now with a persistent wide QRS complex noted. The cycle length is mostly regular with some slight variability. The RR intervals of the wide complex tachycardia and the P–P intervals noted at the end of the rhythm strip in B are nearly identical. This suggests SVT with aberrancy during 1:1 AV conduction.

Most compellingly, there is a relatively short interval between the last BBB complex and the first narrow complex seen on the right-hand side of strip B. This interval is approximately 280 milliseconds, and it would be extremely unusual for a supraventricular complex to conduct so quickly after termination of ventricular tachycardia, because ventricular tachycardia produces retrograde concealed conduction into the AV node preventing subsequent rapid supraventricular conduction. The seventh complex might be considered partially preexcited, suggesting preexcited tachycardia, but the initial, not the latter, part of the ECG complex should have reflected this. This patient did have supraventricular tachycardia with aberrancy.