Wide Complex Tachycardias
Introduction
The major differential diagnoses of a regular wide complex tachycardia (WCT) are 1) ventricular tachycardia (VT), 2) supraventricular tachycardia (SVT) with aberration or bundle branch block (BBB), and 3) preexcited tachycardia. Hyperkalemia- and pacemaker-mediated tachycardia, however, should be excluded (Fig. 17-1). The clinical history provides valuable clues for diagnosis. A WCT in the setting of a prior myocardial infarction, congestive heart failure, or recent angina pectoris has a high likelihood of being VT (Fig. 17-2).1 A WCT in the presence of a type Ic antiarrhythmic drug for paroxysmal atrial fibrillation should raise suspicion of “drug flutter” with 1:1 atrio-ventricular (AV) conduction and rate-related aberration (Fig. 17-3).
The purpose of this chapter is to:
Differentiate VT from SVT with aberration by the 12-lead ECG.
Differentiate VT from preexcited tachycardia by the 12-lead ECG.
Diagnose WCT by intracardiac recordings, pacing, and vagal maneuvers.
12-LEAD ECG
BASELINE
The sinus rhythm ECG provides important information about the substrate to develop WCT including the 1) morphology of underlying BBB or aberrantly conducted QRS complexes, 2) morphology of spontaneous PVCs, 3) infarction patterns, 4) preexcitation, and the 5) status of AV conduction. A WCT whose QRS morphology is identical to underlying BBB suggests an SVT, except for the possibility of His-Purkinje type VT (e.g., bundle branch reentrant tachycardia [BBRT], interfascicular VT (see Figs. 21-2 and 21-15).2 Conversely, a WCT whose QRS morphology is different or even narrower than underlying BBB or identical to spontaneous PVCs argues for VT.3 A WCT in the setting of pathologic Q waves or preexcitation suggests VT or preexcited tachycardia, respectively. A WCT in the presence of AV block also favors VT because of inability for SVT to conduct rapidly to the ventricle.
VT VERSUS SVT WITH BBB
ECG clues differentiating VT from SVT with BBB include analysis of 1) QRS morphology, 2) QRS intrinsicoid deflection and width, 3) frontal QRS axis, 4) AV relationship, and 5) zones of transition.
QRS Morphology
WCTs are categorized either into right bundle branch block (RBBB) (terminal QRS positivity in V1) or left bundle branch block (LBBB) (terminal QRS negativity in V1) tachycardias. Bundle branch morphology itself is determined by the site of earliest ventricular activation. Because true aberrant conduction causes specific QRS morphology patterns, any deviation from the “typical aberration” suggests VT.
Morphologic features of LBBB tachycardias favoring VT over SVT with BBB include 1) initial r wave >30 ms in V1 or V2, 2) onset of the r wave to the nadir of the S wave in V1 or V2 >60 ms, 3) notching on the downstroke of the S wave in V1 or V2, and 4) q wave in V6 (Kindwall-Josephson criteria) (Fig. 17-4).4 The first three criteria reflect the intrinsicoid deflection, which is narrow and rapid for aberration but slow and wide for VT (see below). LBBB alters normal left to right septal activation, causing loss of septal q waves in V6. Therefore, the presence of q waves in V6 during LBBB tachycardia favors VT.
Typical LBBB Tachycardias
WCT with typical LBBB morphology are a unique group and include 1) SVT with LBBB, 2) antidromic tachycardia using an atrio-fascicular or nodo-fascicular accessory pathway (AP) (whose distal insertion is in the right bundle), and 3) typical (counterclockwise) BBRT (whose exit site is from the right bundle) (see Figs. 11-20 and 21-10).5
 FIGURE 17-1 Hyperkalemia. Hyperkalemia mimics VT with RBBB (top) and LBBB (bottom) morphology. P waves are not visible because high potassium levels affect atrial depolarization. Note the “M” type pattern in lead I and V4, respectively, reflecting QRS widening/T wave peaking. Initial QRS forces are relatively rapid, while terminal forces are slurred and delayed because the His-Purkinje system is more resistant to hyperkalemia than ventricular muscle. Note also in the top ECG that hyperkalemia can cause ST segment elevation mimicking acute myocardial infarction (“dialyzable current of injury”) or Brugada syndrome (“Brugada phenocopy”). |
 FIGURE 17-2 VT in the setting of an old myocardial infarction. Top: NSR with an old anterior infarct. Bottom: Relatively narrow, triphasic (rsR′)/left superior QRS complexes suggest origin near the LPF. 2:1 VA block (arrows) and initial aVR q wave >40 ms indicate VT. |
 FIGURE 17-3 Atrial flutter with 1:1 AV conduction. The ventricular rate during 1:1 conduction (bottom) is exactly twice that during 2:1 conduction (top) resulting in RBBB aberration. The initial aVR q wave <40 ms. |
 FIGURE 17-4 LBBB tachycardias. Top: Typical AVNRT with LBBB. The initial V1 r wave <30 ms and aVR Vi/Vt >1. Bottom: RVOT VT. The initial V1 r wave >30 ms and aVR Vi/Vt <1. The intrinsicoid deflection is narrower and more rapid during aberration. |
 FIGURE 17-5 RBBB tachycardias. Top: ORT with RBBB. The aVR q wave <40 ms. Bottom: Idiopathic LV VT. Idiopathic LV VT mimics SVT with RBBB/LAFB because of origin near the LPF; however, the aVR q wave >40 ms. |
Morphologic features of RBBB tachycardias favoring VT over SVT with BBB include 1) monophasic R, biphasic Rr′ (R > r′), and qR patterns in V1 and 2) R/S ratio <1 in V6 (Wellens criteria) (Fig. 17-5).6 In contrast, right bundle branch aberration produces a triphasic rsR′ complex in V1 (the initial r wave reflects normal [left to right] depolarization of the interventricular septum and the R′ represents late activation of the right ventricle [RV]) and R/S ratio >1 in V6.
Typical RBBB Tachycardias
WCT with typical RBBB morphology include 1) SVT with RBBB, 2) idiopathic left ventricular (LV) VT (because it arises from/near the left posterior fascicle [LPF]), and 3) interfascicular reentrant tachycardia [IFRT]) (because macroreentry involves the LPF and left anterior fascicle [LAF]).
Absence of an RS complex in all the precordial leads is a specific morphology pattern that also favors VT (Brugada criteria).7 It encompasses positive and negative concordance (precordial QRS complexes all positive or negative, respectively) and precordial qR patterns (q waves reflect prior infarction that are preserved during VT) (Fig. 17-6).
Concordance
Negative QRS concordance indicates tachycardia origin from the ventricular apex and strongly favors VT. However, SVT with LBBB can rarely show negative concordance due to laterodorsal rotation of the heart (Fig. 17-7).8,9,10 Positive QRS concordance indicates tachycardia origin from the ventricular base and can be seen with VT or preexcited tachycardia using a left-sided AP (the ventricular insertion of most typical left-sided APs is at the basal mitral annulus) (Fig. 17-8; see also Fig. 18-7).
QRS Width and Intrinsicoid
The width of initial forces (intrinsicoid deflection or R/S interval [onset of R wave to nadir of S wave]) and the QRS width itself are a function of conduction velocity or slew rate (dV/dt). The His-Purkinje system is the most rapidly conducting electrical structure in the heart.11 Initial, rapid His-Purkinje conduction is preserved during BBB resulting in narrower intrinsicoid deflections and QRS widths than during VT (pure muscle-to-muscle conduction). An R/S interval in any precordial lead >100 ms indicates VT (Brugada criteria).6 For RBBB and LBBB tachycardias, QRS durations >140 ms and >160 ms, respectively, also favor VT.12 However, antiarrhythmic drugs (e.g., Classic Na channel blockers causing “drug flutter” with 1:1 AV conduction) slow His-Purkinje/myocardial conduction causing SVT with BBB to mimic VT (false-positive VT).
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