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Sustained monomorphic ventricular tachycardia (VT) presents as a wide QRS tachycardia that has the same QRS configuration from beat to beat indicating an identical sequence of ventricular depolarization for each beat (see Fig. 247-3A). VT originates from a stable focus or reentry circuit. In structural heart disease, the substrate is often an area of patchy replacement fibrosis due to infarction, inflammation or prior cardiac surgery that creates anatomical or functional reentry pathways (see Fig. 247-5). Less commonly, VT is related to reentry or automaticity in a diseased Purkinje system. Idiopathic VT occurs in the absence of structural heart disease and is due to a focal region of automaticity or reentry involving a portion of the Purkinje system.
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The clinical presentation varies depending on the rate of the arrhythmia, underlying cardiac function, and autonomic adaptation in response to the arrhythmia. While rapid VT, >200 beats/min, usually causes hypotension that may present as syncope, patients with normal cardiac function might tolerate rapid VT, and those with severe left venricular (LV) dysfunction may experience symptoms of hypotension, even if VT is slower than 150 beats/min. Monomorphic VT that is rapid or associated with structural heart disease may deteriorate to ventricular fibrillation (VF), which may be the initial cardiac rhythm recorded at the time of resuscitation of a cardiac arrest.
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Sustained monomorphic VT has to be distinguished from other causes of uniform wide QRS tachycardia. These include supraventricular tachycardia with left or right bundle branch block aberrant conduction, supraventricular tachycardias conducted to the ventricles over an accessory pathway (Chap. 241), and rapid cardiac pacing in a patient with a pacemaker or defibrillator. In the presence of known heart disease VT is the most likely diagnosis of a wide QRS tachycardia. Hemodynamic stability during the arrhythmia does not exclude VT. A number of ECG criteria have been evaluated to distinguish supraventricular tachycardia with aberrancy from VT. The presence of AV dissociation is usually a reliable marker for VT (Fig. 249-1), but P-waves can be difficult to define. A P-wave following each QRS does not exclude VT because 1:1 conduction from ventricle to atrium can occur. A monophasic R wave or Rs complex in AVR or concordance from V1 to V6 of monophasic R or S waves are also relatively specific for VT (Fig. 249-1). A number of other QRS morphology criteria have also been described, but all have limitations, and are not very reliable in patients with severe heart disease. In patients with known bundle branch block, the same QRS morphology during tachycardia as during sinus rhythm suggests supraventricular tachycardia rather than VT, but is not absolutely reliable. An electrophysiological study is sometimes required for definitive diagnosis. Occasionally, noise and movement artifacts on telemetry recordings can simulate VT; prompt recognition can avoid unnecessary tests and interventions.
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