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Ventricular tachycardia (VT) is protean in form, duration, clinical setting, and prognosis. There is no uniformly accepted classification of VT, and this arrhythmia may be subdivided using many factors, as noted in Table 8-1. Unfortunately, no single subcategory provides enough information for correct classification of all patients with VT, and in many instances there is substantial crossover. For example, in many patients the mechanism of tachycardia is not certain. Whereas reentry is the presumptive mechanism for sustained VT in patients who have coronary artery disease with a previous myocardial infarction and ventricular scar, the mechanism of exercise-induced VT may include enhanced automaticity, triggered activity, and probably reentry. Thus, our present state of knowledge regarding mechanism of VT precludes use of this sole criterion for classification. The other potential classification variables listed in Table 8-1 also have deficiencies. It is often more useful to define a set of variables for a particular type of tachycardia so as to provide the clinician with a meaningful approach to the patient who has that arrhythmia. For example, patients with no definable structural heart disease who have right bundle branch block, left axis morphology sustained VT are a select subgroup for whom the location of this tachycardia is known and response to therapy—for example, endocardial radiofrequency catheter ablation or oral verapamil—has been well-documented.1-3 We will approach the classification of VT by clinical presentation in order to aid the clinician taking care of these patients.

TABLE 8-1Classification of ventricular tachycardia.


Accelerated idioventricular rhythm (AIVR) is a form of VT that is probably due to automaticity. The rate of tachycardia is usually between 50 and 110/min, and it becomes manifest in most instances as sinus slowing occurs. Thus, the sinus node competes with the idioventricular focus for capture of the ventricles. Although this arrhythmia usually occurs in the presence of heart disease, we have noted it in patients with no definable structural heart disease. The arrhythmia is self-terminating and rarely requires any therapeutic intervention. In some prolonged episodes of AIVR with sinus nodal dysfunction, there may be a decrease in blood pressure because of the ventricular origin of the arrhythmia and lack of atrioventricular synchrony, and enhancement of the sinus rate or suppression of the ventricular focus may be necessary. The former can be accomplished with drugs such as atropine or isoproterenol if not contraindicated, or by atrial pacing. Examples of AIVR are noted in Figures 8-1 and 8-2. Note that in Figure 8-1 the fourth QRS complex is slightly premature, 120 ms in duration, and ventricular in origin. The PR interval is suddenly shortened, consistent with the ventricular origin of the QRS complex. The last 4 QRS complexes represent ...

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