A premature ventricular contraction occurs when a focus in the ventricle generates an action potential before the next scheduled sinoatrial nodal action potential.
There are four main characteristics of premature ventricular contractions:
- Premature, occurring earlier than expected if measured against previous R-R intervals.
- Ectopic, originating outside of the SA node, and thus the QRS morphology would be different from the normal morphology when the action potential travels through the normal conduction system.
- Wide complexes; because they come from the ventricles and do not use the normal ventricular conduction system, action potentials need to travel from myocyte to myocyte, which is much slower, creating a wide QRS complex. Unlike premature atrial contractions, or PACs, usually narrow-complexed because they use the normal ventricular conduction system (unless a baseline right or left bundle branch block is present).
- Compensatory pause following the contraction; the extra action potential causes the SA node to become refractory to generating its next scheduled beat, and thus it must “skip a beat” and will resume exactly two P-P intervals after the last normal sinus beat.
Ventricular bigeminy occurs when every other beat is a PVC.
No treatment is necessary for PVCs. If symptomatic, beta-blockers or antiarrhythmic drugs can be effective. Rarely, ablation of PVCs is needed.
No treatment is necessary for PVCs after myocardial infarction. Lidocaine was tried after MIs to suppress PVCs. Although the drug was successful, there was no clinical or mortality benefit from this therapy. This is not the same as ventricular tachycardia, which frequently requires urgent therapy to terminate. The CAST trial demonstrated increased mortality using encainide, flecainide and moricizine to suppress PVCs after an acute coronary syndrome.