eMedicine Specialties > Emergency Medicine > Cardiovascular
Premature Ventricular Contraction: Treatment & Medication
Updated: Nov 16, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- Perform telemetry.
- Secure intravenous (IV) access.
- Administer oxygen.
- Complex ectopy in the setting of myocardial ischemia or causing hemodynamic instability should be suppressed. Use lidocaine for patients with myocardial ischemia.
Emergency Department Care
- The decision to treat premature ventricular contractions (PVCs) in the emergency or outpatient settings depends on the clinical scenario. In the absence of cardiac disease, isolated, asymptomatic ventricular ectopy, regardless of configuration or frequency, requires no treatment. With cardiac disease, certain toxic effects, and electrolyte imbalances, treatment may be required. Establish telemetry and IV access, initiate oxygen, and obtain a 12-lead ECG.
- Hypoxia: Treat the underlying cause; secure the ABCs and provide oxygen.
- Drug toxicity: Specific therapy is indicated for certain toxic effects. Examples include digoxin (Fab antibodies), tricyclics (bicarbonate), and aminophylline (GI decontamination and possibly hemodialysis).
- Correct electrolyte imbalances, particularly those of magnesium, calcium, and potassium.
- Acute ischemia and/or infarction
- Early diagnosis and treatment of acute infarction/ischemia are the cornerstones of therapy.
- The routine use of lidocaine and other type I antiarrhythmic agents in the setting of acute MI is no longer recommended because of their toxic effects.
- Acute ischemia or infarction includes patients with ectopy in the period immediately after receiving thrombolytic agents, during which complex ectopy frequently is seen.
- First-line therapy for ectopy without hemodynamic significance in patients post-MI is beta-blockade.
- Only in the setting of symptomatic, complex ectopy is lidocaine likely to benefit a patient having an MI.
- Lidocaine is especially useful when symptomatic ectopy is associated with a prolonged QT interval as it does not lengthen the QT interval as other antiarrhythmic agents do.
- Amiodarone is also a useful agent to suppress ectopy/VT if hemodynamically significant. Additional beneficial effects include coronary vasodilation and increased cardiac output via a reduction in systemic vascular resistance.
Consultations
Involvement of a cardiologist may be indicated if the patient's condition is refractory to standard therapy.
Medication
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
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.
Adult
150 mg IV over 10 min, then 1 mg/min continuous infusion for 6 h, then maintenance infusion at 0.5 mg/min IV
Oral dosing generally 400 mg/d after load
Pediatric
Not established; weight-based dosing suggested; consider for refractory ventricular arrhythmias in children
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers, may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong QT interval; coadministration may increase myopathy/rhabdomyolysis risk associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs that prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk
Documented hypersensitivity; complete AV block and intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Known to cause serious (possibly fatal) toxicities, including pulmonary and liver toxicities; may cause prolonged proarrhythmic effects; may cause optic neuritis/neuropathy or hypothyroidism or hyperthyroidism; CNS and GI toxicity may occur and typically dissipates with dose reduction
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.
Adult
1-1.5 mg/kg IV bolus; repeat 1.5 mg/kg boluses q3-5min prn to total of 3 mg/kg; follow with 2 mg/min continuous IV infusion after return of perfusion; if continuous infusion not started, additional boluses of 0.5 mg/kg should be administered q10min to maintain effect ET dose is 2-2.5 times IV dose
Pediatric
Loading dose: 1 mg/kg IV/ET/IO; repeat twice q10-15min prn
Maintenance dose: 20-50 mcg/kg/min continuous IV infusion
Cimetidine or beta-blockers increase toxicity; procainamide or tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Documented hypersensitivity; Adams-Stokes syndrome; Wolff-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block, if artificial pacemaker not in place
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use solution without preservatives; caution in CHF, hepatic disease, hypoxia, hypovolemia or shock, respiratory depression, and bradycardia; may increase risk of CNS and adverse cardiac effects in elderly; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities
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.
Adult
30 mg/min IV infusion until arrhythmia suppressed, hypotension occurs, QRS widens 50% above baseline, or maximum dose of 17 mg/kg administered
After arrhythmia suppressed, may continuously infuse at 1-4 mg/min
Pediatric
Not established; following doses have been suggested:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
Maintenance: 20-80 mcg/kg/min IV continuous infusion; not to exceed 100 mg/dose or 2 g/d
Cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine increase levels of procainamide metabolite NAPA; may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion and may increase bioavailability; sparfloxacin may increase risk of cardiotoxicity
Documented hypersensitivity; complete heart block or second- or third-degree heart block (if pacemaker not in place); torsade de pointes; systemic lupus erythematosus
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for hypotension; plasma concentrations of procainamide and active metabolite NAPA may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency
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.
Adult
5 mg/kg (undiluted) IV over 1 min; 10 mg/kg (undiluted) over 1 min for persistent arrhythmia; repeat q15-30min prn; not to exceed 30-35 mg/kg/24 h
Maintenance: 1-2 mg/min IV
Pediatric
Not established
Suggested dose: 10 mg/kg over 1 min IV q15min prn; not to exceed 30 mg/kg
Maintenance: 5-10 mg/kg/dose IV q6h
Pressor catecholamines and digitalis may increase toxicity; ofloxacin may increase risk of cardiotoxicity
Documented hypersensitivity; systemic lupus erythematosus; digitalis-induced arrhythmias; complete heart block or second- or third-degree heart block if pacemaker not in place; torsade de pointes
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hypotension, especially in patients with fixed cardiac output (eg, aortic stenosis); caution in renal insufficiency, severe pulmonary hypertension, and aortic stenosis; half-life increases in the elderly; with renal clearance of 10-50 mL/min, administer 25-50% of usual dose; rapid IV injections may result in transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site
Beta-adrenergic blockers
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.
Adult
5 mg IV q2min for 3 bolus injections
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; sparfloxacin, phenothiazines, astemizole (withdrawn from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase toxicity; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; 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.
Adult
Loading dose: 500 mcg/kg/min IV infusion for 1 min
Maintenance dose: 50 mcg/kg/min IV infusion for 4 min; if adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion of 100 mcg/kg/min IV; continue titration procedure, repeating loading infusion and increasing maintenance infusion by 50 mcg/kg/min (for 4 min); as desired heart rate or therapeutic end point (eg, lowered BP) approached, omit loading infusion and reduce incremental dose in maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min or lower; if desired, increase interval between titration steps from 5 to 10 min
Pediatric
Not established
Suggested dose: 100-500 mcg/kg IV; administered over 1 min
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; sparfloxacin, astemizole (withdrawn from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents increase toxicity
Documented hypersensitivity; cardiogenic shock; CHF; bradycardia; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication abruptly withdrawn; withdraw drug slowly and monitor patient closely
Propranolol (Inderal)
Class II antiarrhythmic, nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Adult
1-3 mg (with careful monitoring) IV; not to exceed 1 mg/min to avoid lowering BP and causing cardiac standstill
Allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn; thereafter, do not give additional drug in <4 h
Do not continue doses after desired alteration in rate or rhythm achieved; switch to PO ASAP; 10-30 mg tid/qid PO usual dose
Pediatric
2-4 mg/kg/d PO divided bid (ie, 1-2 mg/kg bid)
IV use not recommended; however, for arrhythmias, dose of 0.01-0.1 mg/kg IV has been recommended; not to exceed 1 mg/dose by slow push; change to PO ASAP
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; may increase toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines
Documented hypersensitivity; uncompensated CHF; cardiogenic shock; bradycardia; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely
Electrolytes
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.
Adult
1-2 g diluted in 100 mL of D5W IV over 1-2 min for refractory ventricular fibrillation and known or suspected hypomagnesemia (magnesium <1.4 mEq/L); not to exceed 30-40 g/d, or maintenance infusion of 1-2 g/h
Pediatric
Not established
Suggested dose for hypomagnesemia: 25-50 mg/kg/dose IV q4-6h for 3-4 doses; maximum single dose of 2 g may also be administered and repeated if hypomagnesemia persists
Nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone; may increase cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
May alter cardiac conduction, leading to heart block in patients receiving digitalis; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte administered parenterally; caution when administering dose, as may produce significant hypertension or asystole; in overdose, may give calcium gluconate 10% solution as antidote for clinically significant hypermagnesemia
Calcium channel blockers
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.
Adult
80-160 mg PO tid
Pediatric
Not established
May increase levels of carbamazepine, digoxin, and cyclosporine; amiodarone can cause bradycardia and decrease in cardiac output; beta-blockers may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hepatocellular injury may occur; transient elevations of transaminases with or without elevations in alkaline phosphatase and bilirubin have occurred (elevations transient and may disappear with continued treatment); monitor liver function periodically
More on Premature Ventricular Contraction |
| Overview: Premature Ventricular Contraction |
| Differential Diagnoses & Workup: Premature Ventricular Contraction |
 Treatment & Medication: Premature Ventricular Contraction |
| Follow-up: Premature Ventricular Contraction |
| Multimedia: Premature Ventricular Contraction |
| References |
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References
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Further Reading
Keywords
premature ventricular contraction, premature ventricular contraction causes, premature ventricular contraction treatment, PVC, ectopic cardiac pacemaker, paroxysmal tachycardia, arrhythmias, dysrhythmias, acute myocardial infarction, MI, ventricular ectopy, myocarditis, dilated cardiomyopathy, hypertrophic cardiomyopathy
