Sustained monomorphic ventricular tachycardia (VT) is a ventricular arrhythmia with a wide QRS lasting for 30 s or requiring an intervention for termination. Each QRS complex resembles the others, indicating either a site of origin from either an automatic focus or fixed reentry circuit. In structural heart disease, the substrate is most often an area of patchy replacement fibrosis due to infarction, fibrosis, inflammation, or prior cardiac surgery that creates anatomic or functional reentry pathways. Less commonly, VT is related to reentry or automaticity in diseased conduction pathways in the Purkinje system. While scar-related reentrant VTs are associated with risk of sudden death, idiopathic VT is a more benign form of VT that occurs in structurally normal hearts and can be due to a focal region of automaticity in the myocardium or reentry involving a portion of the Purkinje system.
The clinical presentation varies depending on the rate of the arrhythmia, underlying cardiac function, and autonomic adaptation in response to the arrhythmia. Rapid VT can produce hypotension that may present as syncope, particularly in patients with significant ventricular dysfunction. In contrast, patients with normal cardiac function might tolerate their sustained VT, even presenting with simple palpitations, despite rapid rates. Monomorphic VT that is rapid or associated with structural heart disease may eventually deteriorate to ventricular fibrillation (VF), which may be the initial cardiac rhythm recorded at the time of resuscitation of an out-of-hospital cardiac arrest.
Sustained monomorphic VT (Table 254-1) 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, and rapid cardiac pacing, appropriate or inappropriate, in a patient with a ventricular pacemaker or defibrillator. In the presence of known heart disease, VT is the most likely diagnosis of a wide QRS tachycardia, independent of QRS morphology. When left ventricular (LV) function is depressed or there is evidence of structural myocardial disease, scar-related reentry is the most likely cause of sustained monomorphic VT. Scars are suggested by pathologic Q waves on the electrocardiogram (ECG), segmental LV or right ventricular wall motion abnormalities on echocardiogram or nuclear imaging, and areas of delayed gadolinium enhancement during magnetic resonance imaging (MRI).
TABLE 254-1Sustained Ventricular Arrhythmias ||Download (.pdf) TABLE 254-1 Sustained Ventricular Arrhythmias
Idiopathic ventricular tachycardia (VT) without structural heart disease
Outflow tract origin
Right ventricular (RV) outflow tract: left bundle branch block pattern in V1 with inferior axis (tall QRS in inferior leads) and late transition in the precordial leads
Left ventricular (LV) outflow tract: similar inferiorly directed axis but with early precordial transition with prominent R wave in V2–V3
LV fascicular VT: Typical right bundle branch block pattern in V1 with sharp intrinsicoid deflection and left axis deviation (arising ...