Fast and Wide
Wide Complex Tachycardia—Overview
Both supraventricular and ventricular mechanisms underlie wide complex rhythms.
Monomorphic VT—ECG Features
There are several features that may help diagnose monomorphic VT as the underlying cause of a regular, wide complex tachycardia.
Widening of the QRS complex beyond 160 msec in precordial leads with LBBB morphology or beyond 140 msec in precordial leads with RBBB morphology suggests VT.
QRS axis more negative than −90 degrees or more positive than +180 degrees (northwest axis) indicates VT. QRS waves are negative in leads I and aVF. This is a form of extreme axis deviation that is less likely to occur in SVT.
The direction of the QRS waves in the precordial leads is uniformly positive (pointing upward) or uniformly negative (pointing downward). Negative precordial concordance is most often VT.
This is a hybrid beat that results from a ventricle simultaneously activated by the reentrant circuit of VT and by another focus. This focus can be supraventricular or ventricular. The QRS complex morphology differs from the other QRS complexes in the ECG and the patient’s native QRS complex (that which would appear in the patient’s normal sinus rhythm).
In VT, the sinus impulse continues to fire but most often arrives at the ventricles when they are in a refractory state. If properly timed, however, a sinus impulse traveling down the normal conduction system may reach the ventricles no longer in their refractory period. The QRS complex of a capture beat has the same morphology as the patient’s native QRS complex.
AV dissociation is considered to be a hallmark finding in VT but is seldom present on the 12-lead electrocardiogram. When atrial and ventricular conduction are occurring independently, P waves are often difficult to discern because they are often buried by T waves or wide QRS complexes.
AV dissociation can also occur in SVT; this finding is not entirely specific for VT.
Ventriculoatrial Association: Retrograde conduction from the ventricles to the atria is not uncommon. Retrograde P waves may be seen following QRS complexes.
VT versus SVT with Aberrancy—Algorithms
Several algorithms have been published to help differentiate VT from SVT with aberrancy. Sensitivity and specificity of these criteria in validation studies are lower than those reported in derivation cohorts, and no particular algorithm has demonstrated superiority.1 Interobserver agreement is also suboptimal (approximately 80% in the application of Brugada criteria).2,3 For reference, several of the more common algorithms are listed below.
In clinical practice, it is safer to assume that a wide complex tachycardia is ventricular in origin. VT is much more common than SVT with aberrancy. Clinical stability is not a useful variable for differentiating ventricular and supraventricular causes of wide complex tachycardia (i.e., patients with VT can remain stable, and patients with SVT with aberrancy can become unstable).4
As the name suggests, the QRS complexes in polymorphic VT change in width, shape, and axis. The rhythm is irregular. Polymorphic VT with a normal QTc is most often secondary to acute myocardial ischemia. Some complexes may appear pointing upward while others appear pointing downward.
Catecholaminergic Polymorphic VT
This type of VT is either bidirectional or polymorphic and is induced by exercise or emotional stress. Approximately half of these patients are found to have mutations in genes coding for the ryanodine receptor or the protein calsequestrin. Treatment includes betablocker therapy and placement of an ICD.
Torsades de Pointes
If polymorphic VT is associated with QTc prolongation, the rhythm is torsades de pointes. The QTc interval can be measured before the onset of or after the termination of the tachycardia. The waves of VT gradually increase and decrease in amplitude. The rate ranges from 180 to 250 bpm. This rhythm often self-terminates after seconds. It can degenerate into ventricular fibrillation.
Commonly, the onset of torsades occurs after a long R-R cycle is followed by an early depolarization.
This is a regular monomorphic tachycardia resulting from a macroreentrant ventricular rhythm similar to the atrial reentrant circuit of atrial flutter. The ECG morphology may appear as a sine wave. This is a nonsustainable rhythm that deteriorates into ventricular fibrillation.
ECG changes secondary to motion artifact can look remarkably similar to ventricular flutter. Narrow QRS complexes will interrupt the large amplitude waves generated by motion artifact.
Ventricular fibrillation is a disorganized rhythm with rates exceeding 300 bpm. The shape and amplitude of each wave vary. VFib with very low-amplitude undulations may be mistaken for asystole.
Supraventricular Causes of Wide Complex Tachycardia
VT is far more common than supraventricular tachycardia with aberrancy. SVT with aberrancy should still be considered, however, in the differential of wide complex tachycardias as treatment and outcomes differ.
SVT can result in a wide complex tachycardia if the AV node is bypassed by conduction down an accessory pathway or if a normal conduction pathway (bundle branch) distal to the AV node is blocked.
A slurring of the initial inscription of the QRS wave may represent a delta wave. This results from ventricular preexcitation by an accessory pathway. A similar pattern of preexcitation seen on a patient’s previous ECG makes the diagnosis of SVT more likely.
SVT with aberrancy is the likely diagnosis if identical QRS morphology in the setting of normal sinus rhythm can be seen on a previous ECG.
Triphasic morphology in leads V1 and V6 (Fig. 11.4) is an unlikely QRS morphology to result from an impulse generated by a single ventricular focus and is therefore suggestive of SVT.
Antidromic Atrioventricular Reciprocating Tachycardia
This rhythm is also known as wide complex atrioventricular reciprocating tachycardia (AVRT). In patients with Wolff-Parkinson-White syndrome, narrow complex AVRT due to orthodromic conduction is far more common than wide complex AVRT due to antidromic conduction.
The reentrant circuit of AVRT is triggered by an ectopic impulse. In antidromic AVRT, the ectopic impulse encounters an AV node still in its refractory period and a bypass tract that is out of its refractory period and ready to conduct to the ventricles.
Activation of the ventricles occurs by anterograde conduction down the bypass tract. Ventricular impulse spreads from myocardial cell to myocardial cell. Conduction then continues in a retrograde fashion from the ventricles to the atria through the AV node before reentering the reentrant circuit.
Rarely, retrograde conduction from the ventricles to the atria can occur through a second bypass tract.
QRS complexes are wide and regular. Because the ventricle is activated solely through the bypass tract, each QRS wave should show evidence of preexcitation (delta wave).
Left-sided bypass tract: The left ventricle is the first to be activated. Spread of ventricular impulse occurs in a left-to-right direction. This results in positive QRS complexes in the right precordial lead V1. This is similar to the QRS morphology seen in RBBB.
Right-sided bypass tract: Ventricular activation spreads from the right ventricle to the left ventricle, away from the direction of V1. The QRS complex in V1 is therefore predominantly negative and similar to the morphology of an LBBB.
Atrial Fibrillation Down an Accessory Pathway
This is the most dangerous rhythm that can occur in a patient with a bypass tract capable of anterograde conduction.
Conduction from the disordered supraventricular rhythm of atrial fibrillation reaches the ventricles via both the AV node/Purkinje system and the bypass tract (Fig. 11.8A).
The variability in QRS morphology (Fig. 11.8B) results from the variable contributions of the bypass tract and the normal conduction pathway to ventricular activation.
QRS morphology varies from one beat to the next. Each QRS complex is a fusion complex generated by simultaneous conduction coming from the normal and bypass pathways. QRS complexes show varying degrees of preexcitation and delta wave morphology.
The ventricular rate is extremely rapid because the bypass tract is capable of conducting impulses much faster than the AV node.
This rhythm can deteriorate into ventricular fibrillation or lead to hypotension and cardiac ischemia. Bypass tracts with a shorter refractory period are capable of conducting impulses to the ventricle at dangerously rapid rates.
Drugs to Avoid
The accessory pathway and pathway of normal ventricular conduction are not completely independent. Impulses carried through the His-Purkinje system can, in retrograde fashion, inhibit the bypass tract and thereby decrease the number of atrial impulses successfully conducted down the accessory pathway (dotted blue arrow, Fig. 11.8A). Any medication that inhibits the AV node can facilitate more rapid conduction down the accessory pathway and increase the risk of ventricular fibrillation. These medications include adenosine, beta-blockers, calcium channel blockers, and digitalis. If the patient is stable, the preferred treatment is procainamide. Direct current cardioversion is indicated if the patient is unstable.