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.

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.

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.

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.

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.

Ventricular Tachycardia

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.

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.