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There are myriad types of ventricular arrhythmias (VAs), affecting patients with normal hearts and those with structural heart disease ranging from benign to life-threatening. An understanding of an approach to these arrhythmias is critical to being appropriately parsimonious with benign forms, while understanding an approach to the malignant forms.
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VAs can arise from focal sites of origin or from reentrant circuits. Focal VAs can originate from myocardial or Purkinje cells capable of automaticity or triggered activity. Reentrant VAs often involve areas of scar such as old myocardial infarction or a cardiomyopathic process. Less commonly, diseased Purkinje conduction pathways can also result in reentrant circuits. VAs are characterized by their electrocardiographic appearance and duration. Conduction away from the ventricular focus or reentrant circuit exit, propagating through the ventricular myocardium, is slower than activation of the ventricles over the normal Purkinje system. For this reason, the QRS complex duration during VAs will be wide, typically >0.12 s, though there are unusual situations that can arise with narrow QRS duration as well.
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Premature ventricular beats (also referred to as a premature ventricular contractions [PVCs]) are single ventricular beats that fall earlier than the next anticipated supraventricular beat (Fig. 252-1). PVCs that originate from the same focus will have the same QRS morphology and are referred to as unifocal (Fig. 252-1A). PVCs that originate from different ventricular sites have different QRS morphologies and are referred to as multifocal (Fig. 252-1B). Two consecutive ventricular beats are ventricular couplets.
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Ventricular tachycardia (VT) is three or more consecutive beats at a rate faster than 100 beats/min. Three or more consecutive beats at slower rates are designated an idioventricular rhythm. VT that terminates spontaneously within 30 s is designated nonsustained, whereas sustained VT persists for >30 s or is terminated by an active intervention, such as administration of an intravenous medication, external cardioversion, antitachycardia pacing, or a shock from an implanted cardioverter defibrillator (Fig. 252-2).
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Monomorphic VT has the same QRS complex from beat to ...