Wide Complex Tachycardias: Understanding this Complex Condition Part 2 - Management, Miscellaneous Causes, and Pitfalls

INTRODUCTION Patients who present with electrocardiograms (ECGs) demonstrating wide complex tachycardias (WCTs) are often challenging to clinicians. Not only may the patient present with (or be at risk for) hemodynamic compromise, but their treatment may result in hemodynamic collapse if the incorrect pharmacologic agent is selected. In Part 1 of this article, 1 the identification, epidemiology, and electrophysiology of WCTs were discussed. In this article, treatment of WCTs and miscellaneous causes of this condition will be described. In patients presenting with WCTs, correct interpretation of the ECG should not be the primary concern of emergency physicians. In fact, it is appropriate (and may be preferred) to " diagnose " the ECG as " wide complex tachycardia of unknown (or uncertain) etiology. " This may allow the treating clinician to focus on the patient and his or her hemodynamic status, rather than the academic exercise of ECG interpretation. The most important aspect of treating patients who present with WCTs is to select a therapeutic approach that does no harm. Several diagnostic algorithms were provided for the interpretation of WCTs, although none have proven superior over others, and great debate continues among researchers as to the preferred approach. Given this circumstance of uncertainty, proper treatment will be described for conditions resulting in WCTs. It is critical to note that once a WCT is identified, the Figure 1. ECG representing Wolff-Parkinson-White Syndrome (WPWS) with Atrial Fibrillation (AFIB). Note the wide QRS complexes, and the irregularly irregular rhythm. In lead II, the axis changes. A slurred delta wave can be identified in the left precordial leads, since the overall rate is not as fast as it might be when these conditions coexist. The R-R interval of the first two QRS complexes seen in leads V1-3 approaches 300, which is extremely dangerous. use of certain pharmacologic therapies may have deleterious effects on patients. Verapamil and diltiazem are calcium channel blockers (CCBs) that should be avoided in WCTs, as cardiac arrests from hemodynamic collapse have been reported following their administration. 2,3 This is especially true in infants. Not only do these agents cause negative inotropy and at times profound vasodilation, but they may also allow WCTs to degenerate into VFIB. CCBs slow conduction at the AV node so that accessory pathways can be preferentially used; this results in ventricular rates that approach atrial rates. In addition, verapamil may shorten the effective refractory period of accessory pathway …