Premature ventricular complexes (PVCs)
Premature ventricular complexes (PVCs) result from depolarizations that originate from the ventricles and occur prior to the next normally conducted sinus beat. PVCs often occur in the absence of structural heart disease and are increasingly frequent with age. Potential triggers are similar to those for PACs (smoking, alcohol, adrenergic stimuation).
The EGG reveals a premature QRS complex with a bizarre morphology typically greater than 120 milliseconds in duration, with a T-wave polarity opposite to that of the QRS complex.
PVCs typically require no therapy. When patients are symptomatic, therapy should be directed toward correction of underlying abnormalities. Specific antiarrhythmic agents may be effective in suppressing PVCs, but adverse effects (e.g., arrhythmia aggravation, proarrhythmia, death) preclude their widespread use. In the setting of acute myocacardial ischemia or infarction, IV lidocaine may suppress PVCs, but toxic effects (e.g., increased risk of asystole and CNS effects) appear to outweigh potential benefits in most cases.
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