Approach to the Patient with Wide Complex Tachycardia
Approach to the Patient with Wide Complex Tachycardia
John M. Miller
Deepak Bhakta
Gopi Dandamudi
Rahul Jain
Vikas Kalra
INTRODUCTION
Arriving at the correct diagnosis of wide complex tachycardia (WCT) can be one of the most anxiety-provoking tasks facing most cardiologists and trainees. Although many algorithms have been developed to assist in this process, these are often not easily recalled or applied. The purposes of this chapter are to try to simplify the methods used to make the correct diagnosis, as well as to provide a guide to initial patient management. For the following discussion, WCT is defined as heart rate >100/min with QRS duration >120 ms. WCT may be uniform morphology (all QRS complexes identical) or polymorphic (varying QRS configuration). Left bundle branch block (LBBB) pattern is characterized by negative terminal vector in V1, whereas right bundle branch block (RBBB) pattern has a positive terminal vector in V1.
In order to establish the correct diagnosis of WCT, one must know what the possible diagnoses are. These include:
Ventricular tachycardia (VT)
Supraventricular tachycardia (SVT) with:
a. Aberrant (AB) interventricular conduction
i. Fixed (present during baseline rhythm)
ii. Functional (present only during WCT)
b. Atrioventricular (AV) conduction over accessory pathway (Wolff-Parkinson-White)
c. Abnormal QRS configuration not due to aberration or preexcitation
i. Present at baseline—hypertrophy, cardiomyopathy, congenital heart disease
ii. Situational—drug toxicity, electrolyte disorders
Ventricular pacing
Electrocardiographic artifact
All WCTs can be categorized as one of these causes; Table 14-1 gives their relative prevalence and typical clinical settings. Ventricular pacing and ECG artifact are rare causes, but their correct recognition is critical to prevent inappropriate testing and treatment for rhythm disturbances that are not present. The Key Points at the end of this chapter lists some important concepts in WCT diagnosis and management. In almost all published series, VT is the most common cause of WCT (in some series, 75%); therefore, if there is uncertainty as to the correct diagnosis, the WCT should be assumed to be VT. This is especially true in patients with structural heart disease, in whom VT accounts for >95% of all WCTs. Although special populations have different proportions of the remaining diagnoses (e.g., pediatric centers with congenital heart disease patients), in most clinical situations, the differential diagnosis of uniform-morphology WCT is between VT and SVT-AB. The following discussion deals with this distinction. Since the vast majority of both SVT-AB and VT are very regular, varying by no more than 30 ms in cycle length, they are generally readily distinguished from atrial fibrillation with either aberration or conduction over an accessory pathway (Wolff-Parkinson-White syndrome). The latter possibilities will thus not be considered further here.
TABLE 14-1 Relative Frequency and Clinical Settings of WCTs
Supraventricular tachycardia (SVT) with aberration
++
Younger patient; no SHD; history of prior tachycardia episodes
SVT with abnormal baseline QRS
++
History of cardiomyopathy, heart surgery
Preexcited SVT
+
Younger patient; Wolff-Parkinson-White
SVT and pronounced antiarrhythmic drug effect
+
History of use of antiarrhythmic drug +/- change in dose or metabolism
SVT with hyperkalemia
Rare
Acute renal failure, rhabdomyolysis
Ventricular paced rhythm
Rare
Pacing system present
ECG artifact
+
Asymptomatic; patient motion
a Number of + signs indicates relative frequency in a typical group of patients presenting with WCT. SHD, structural heart disease; VT, ventricular tachycardia; WCTs, wide complex tachycardias.
VENTRICULAR TACHYCARDIA VERSUS SUPRAVENTRICULAR TACHYCARDIA WITH ABERRATION
The ECG appearance of VT can have immense variety, whereas that of SVT-AB has far fewer possible manifestations. Therefore, if one is familiar with all the configurations SVT-AB can have, and the WCT being analyzed looks like one of those, it probably is SVT; if not, it is probably VT. All of the published diagnostic algorithms take advantage of this distinction in one way or another. A brief summary of ECG distinctions follows; Table 14-2 summarizes many of these. The specificities of most criteria are tempered by whether or not the baseline QRS complex is fairly normal or not; if very distorted, such as in patients with cardiomyopathy or repaired congenital heart disease, ECG distinctions are blurred.
TABLE 14-2 ECG Distinctions between VT and SVT
SVT with Aberration
VT
QRS Duration
≤140 ms
>140 ms
QRS Axis -90° to 180°
Rare
Occasional (20%)
Precordial concordance
Rare
Occasional (20%)
QRS in V1 (LBBB type)
– Initial R wave duration
≤40 ms
>40 ms
– QRS onset to S nadir
≤60 ms
>60 ms
R/S ratio in V6 (RBBB type)
>1
<1
RS complex any precordial lead
Present
Absent (30%)
Vi/Vt in multiphasic lead
≥1
<1
QRS in aVR
– Narrow initial Q
Common
Rare
– Tall R wave
Rare
Frequent (40%)
– Wide/slurred Q
Rare
Occasional (20%)
R wave peak time in lead 2
<50 ms
≥50 ms
AV Relationship
– Dissociation
Extremely rare
Common
– Non-1:1 relationship
Occasional (30%)
Frequent (40%)
Initiating complex
P wave
QRS complex
AV, atrioventricular; LBBB, left bundle branch block; RBBB, right bundle branch block; SVT, supraventricular tachycardia; VT, ventricular tachycardia.
QRS duration—The wider the QRS complex, the less likely it is SVT-AB. In the setting of RBBB-like WCT, a QRS duration more than 140 ms suggests VT, whereas for LBBB-like WCT, a QRS duration more than 160 ms suggests VT. Caveats: sodium channel blocking agents (type 1A or IC antiarrhythmic drugs, amiodarone, hyperkalemia, etc.) can cause nonspecific widening of the QRS complex and thus an SVT QRS that would otherwise be only 125 ms may increase to 145 ms and suggest VT. Contrariwise, patients with VT in the absence of structural heart disease typically have relatively narrow QRS complexes during VT, which may then be misdiagnosed as SVT.
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