Premature Ventricular Contraction Medication
- Author: James E Keany, MD, FACEP; Chief Editor: David FM Brown, MD more...
Medication Summary
Therapy for complex ventricular ectopy depends on the setting and the underlying cause. In drug toxicity, specific therapies are available. With electrolyte imbalances, correction of abnormalities is therapeutic. Lidocaine is the drug of choice (DOC) in the setting of complex ectopy in the peri-MI period if the patient is symptomatic, yet no firm evidence supports this practice.
Antiarrhythmics
Class Summary
These agents alter the electrophysiologic mechanisms responsible for PVCs.
Amiodarone (Cordarone)
Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Effective in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence; low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose 200 mg/d).
During loading, patients must be monitored for bradyarrhythmias. Before administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.
Lidocaine (Dilocaine)
Class IB agent that stabilizes cell membranes and blunts phase 0 of action potential and shortens repolarization. Net effect is to decrease firing of ectopic foci and allow normal rhythm to reassert itself.
Procainamide (Procanbid)
Class IA agent for PVCs. Increases refractory period of atria and ventricles. Myocardial excitability reduced by increasing threshold for excitation and inhibition of ectopic pacemaker activity.
Bretylium (Bretylate)
Class III agent for treatment of PVCs. Because of catecholamine-releasing properties and adverse effects, should not be used as initial treatment. Limit use to PVCs refractory to class I antiarrhythmics. Increases fibrillation threshold and causes refractory period by decreasing potassium conductance.
Beta-adrenergic blockers
Class Summary
This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.
Metoprolol (Lopressor)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.
Esmolol (Brevibloc)
Excellent drug for patients at risk of complications from beta-blockade, particularly those with reactive airway disease, mild-moderate left ventricular dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if necessary.
Propranolol (Inderal)
Class II antiarrhythmic, nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Electrolytes
Class Summary
These agents are considered to be therapeutic alternatives for refractory PVCs. Patients with persistent or recurrent PVCs following antiarrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmias. Hypomagnesemia is associated with the onset of PVCs.
Magnesium sulfate
Acts as antiarrhythmic agent; diminishes frequency of PVCs, particularly those due to acute ischemia.
Calcium channel blockers
Class Summary
Calcium is involved in the generation of action potentials in specialized automatic and conducting cells in the heart. The calcium channel blockers share the ability to inhibit movement of calcium ions across the cell membrane. This effect can depress both impulse formation (automaticity) and conduction velocity.
Verapamil (Calan, Covera, Verelan)
Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AVN, can restore normal sinus rhythm in paroxysmal supraventricular tachycardia.
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