Reentrant tachycardias involve continuous propagation of an activation wavefront. Exceptions are limited to physiologic (non-reentrant) sinus tachycardia and automatic atrial tachycardias. Most of the above-mentioned tachycardias have a reentrant mechanism. SVT: Supraventricular tachycardia AVRT: Atrioventricular reentrant tachycardia IVCD: Intraventricular conduction defect AVNRT: Atrioventricular nodal reentrant tachycardia. This frequently results in a QRS complex that is wider than a typical LBBB aberrant complex, and explains why Q waves may be recorded in the left-sided ECG leads. Electrical impulses travel in a delayed fashion, and may propagate rightward (away from the lateral leads) before exciting the bulk of the left ventricle (Figure (Figure2 2). They arise from the ventricular myocardium. In contrast, LBBB-like morphologic tachycardias are not confined to the specialized conduction system. Q waves will not be seen in the lateral leads on a surface ECG (Figure (Figure1). Because there is no antegrade conduction via the left bundle branch, the electrical impulse must propagate in a cell-to-cell fashion, resulting in delayed conduction to the left ventricle. The interventricular septum is depolarized via the His-Purkinje system with subsequent activation of the left ventricle. Atriofascicular accessory pathways bypass the AV node and His bundle and insert directly into (or extremely close to) the right bundle branch. In most instances, activation of the right bundle branch occurs via the AV node and His bundle. The ECG appearance of typical LBBB depends on antegrade ventricular activation occurring via the right bundle branch. Kindwall and colleagues used the following criteria to distinguish ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberrant conduction in patients with LBBB-like morphology: (1) R wave in lead V1 or V2 > 30 ms (2) any Q wave in V6 (3) a duration of ≥ 60 ms from the onset of the QRS to the nadir of the S wave in V1 or V2 and (4) notching of the downstroke of the S wave in V1 or V2. In typical, or “classic” LBBB, lead V1 will demonstrate either an rS or QS complex, and, more importantly, Q waves will be absent from the left lateral leads. Most algorithms define LBBB-like morphology as a QRS complex that is predominantly negative in the right precordial leads (specifically, V1) and predominantly positive in the lateral leads (I, aVL, V5, V6). There are secondary ST and T-wave changes in the opposite direction of the major QRS deflection. There is delayed onset of the intrinsicoid deflection (the beginning of the QRS to the peak of the R wave is > 50 ms) in leads I, V5 and V6. LBBB is defined as a prolonged QRS duration (≥ 120 ms) with broad monophasic R waves in leads I, V5 and V6 that are usually notched or slurred.
It is important to understand the distinction between “LBBB- like” patterns and a typical LBBB morphology. However, committing these algorithms to memory can be challenging and overreliance on them may impede cardiologists from understanding the underlying tachycardia mechanism.
Many of these algorithms use specific features of the QRS complex, and subcategorize tachycardias into “right bundle branch-like” and “left bundle branch like” morphologies. Complex algorithms have evolved (from 1978 to 2008) to assist the treating physician in making this distinction (Table (Table1 1). While the presence of atrioventricular (AV) dissociation during wide complex tachycardia is highly specific for a ventricular origin, this finding is often not present or is difficult to discern on the surface electrocardiogram (ECG). Most physicians understand that the pivotal diagnostic challenge focuses on determining whether the tachyarrhythmia is of supraventricular (with aberrant ventricular conduction) or ventricular origin. Even the presence of hemodynamic stability is not helpful in determining the tachycardia mechanism. The process of determining the correct diagnosis can be confusing and cumbersome. The evaluation of wide QRS complex tachycardia (WCT) remains a common clinical dilemma.