The normal activation of the ventricles occurs after impulse generation in the sinoatrial (SA) node and conduction through atria and the atrioventricular (AV) node, and then through the specialized conduction tissues of the His–Purkinje system. This conduction system leads to rapid depolarization of the ventricles via their respective bundles. This normal activation pattern results in the surface electrocardiogram (ECG) showing normal (narrow) QRS complex morphology with duration of less than 0.12 s. When a rhythm is found to have a QRS complex width greater than 0.12 s in duration and is at a rate greater than 100 bpm (beats per minute), it is referred to as a wide complex tachycardia (WCT). In children, heart rates and QRS complex widths vary with age – consequently, children may present with WCT, including ventricular tachycardia (VT), with QRS duration of less than 0.12 s; age‐related values of the QRS complex duration and ventricular rate define WCT in younger children.

WCTs (Box 7.1) may originate from any atrial, nodal, or ventricular site. “Supraventricular” WCTs can originate from cardiac tissues “above the ventricle,” including foci in the SA node, atrial tissues, or the AV node. In these cases, the widened QRS complex results from abnormal conduction through the ventricles. “Ventricular” WCTs originate from the ventricular conduction system or ventricular myocardium (i.e. VT), or they may be the result of a ventricular paced rhythm (i.e. an extrinsic pacemaker). In each of these cases, the site of rhythm generation is located lower in the conduction system, leading to a wide QRS complex due to slower, less efficient conduction through the ventricular myocardium.

Ventricular Tachycardia – Monomorphic and Polymorphic

Although not the most common of all WCTs (supraventricular rhythms with aberrant conduction are more common), VT is the most concerning of the wide complex tachydysrthymias (Box 7.2). VT is defined as three or more beats of ventricular origin at a rate of 100 bpm or greater, although generally the rate is less than 200 bpm. While some minimal irregularity may be seen – particularly at the onset – the ECG in VT typically reveals a rhythm with very regular R–R intervals and a widened QRS complex (>0.12 s). “Normal” beats (those correlating to the patient’s baseline or underlying rhythm with a narrow QRS complex) may be visible on rhythm strips before the initiation or after the termination of VT.

The morphology of the QRS complexes of VT may be one of two basic types, monomorphic or polymorphic. Monomorphic VT arises from impulses generated by a single ventricular focus, whereas polymorphic VT arises from multiple foci of impulse generation. The monomorphic type is much more common and is characterized by a regular WCT in which each of the QRS complexes in a given lead has the same appearance (Figure 7.1). In contrast, polymorphic VT has a wavy, undulating appearance (Figure 7.2) that indicates several electrical foci, leading to morphology that varies from beat to beat. Torsade de pointes VT (Figure 7.3) is a very specific subtype of polymorphic VT that is encountered in patients with an underlying prolonged QT interval.

Certain electrocardiographic findings can aid in the diagnosis of VT and can differentiate SVT with conduction aberrancy. These include AV dissociation as well as capture beats and/or fusion beats. The presence of these findings provides strong evidence suggesting that the rhythm is VT rather than a supraventricular rhythm with aberrant conduction. Unfortunately, these findings are not always obvious on rhythm strips and 12‐lead ECGs; the clinician should review both the standard 12‐lead ECG and a longer single‐lead rhythm strip for their presence in a patient who presents with WCT.