eMedicine Specialties > Emergency Medicine > Cardiovascular
Premature Ventricular Contraction
Updated: Nov 16, 2009
Introduction
Background
Premature ventricular contraction (PVC) is caused by an ectopic cardiac pacemaker located in the ventricle. PVCs are characterized by premature and bizarrely shaped QRS complexes usually wider than 120 msec on with the width of the ECG. These complexes are not preceded by a P wave, and the T wave is usually large, and its direction is opposite the major deflection of the QRS.
The clinical significance of PVCs depends on their frequency, complexity, and hemodynamic response.
For additional information, see Medscape's Cardiology Specialty page.
Pathophysiology
Premature ventricular contractions (PVCs) reflect activation of the ventricles from a site below the atrioventricular node (AVN). Suggested mechanisms for PVCs are reentry, triggered activity, and enhanced automaticity.
Reentry occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, the area of slow conduction activates the blocked part of the system after the rest of the ventricle has recovered, resulting in an extra beat. Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia.
Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).
Enhanced automaticity suggests an ectopic focus of pacemaker cells in the ventricle that has a subthreshold potential for firing. The basic rhythm of the heart raises these cells to threshold, which precipitates an ectopic beat. This process is the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly hyperkalemia.
Ventricular ectopy associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract beneath the pulmonic valve. The mechanism is thought to be enhanced automaticity versus triggered activity. These arrhythmias are often induced by exercise, isoproterenol (in the EP lab), the recovery phase of exercise, or hormonal changes in female patients (pregnancy, menses, menopause). The characteristic ECG pattern for these arrhythmias is a large, tall R wave in the inferior leads with a left bundle-branch block pattern in V 1 . If the source is the left ventricular outflow tract, there is a right bundle-branch block pattern in V 1 . Beta-blocker therapy is first-line therapy if symptomatic.
Factors that increase the risk of PVCs include male sex, advanced age, African American race, hypertension and underlying ischemic heart disease, a bundle-branch block on 12-lead ECG, hypomagnesemia, and hypokalemia.
Frequency
United States
Premature ventricular contractions (PVCs) are one of the most common arrhythmias and can occur in patients with or without heart disease. The prevalence of PVCs varies greatly, with estimates of less than 3% to more than 60% in asymptomatic individuals.
Data from large, population-based studies indicate that the prevalence ranges from less than 3% for young white women without heart disease to almost 20% for older African American individuals with hypertension.
Mortality/Morbidity
The clinical significance of premature ventricular contractions (PVCs) depends on the clinical context in which they occur.
- PVCs in young, healthy patients without underlying structural heart disease are usually not associated with any increased rate of mortality.
- PVCs in older patients, in particular those with underlying heart disease, are associated with an increased risk of adverse cardiac events, particularly sustained ventricular dysrhythmias and sudden death.
- In patients who have had a MI, the risk of malignant ventricular arrhythmias and sudden death is related to the complexity and frequency of the PVCs. Patients with PVCs in Lown classes 3-5 are at greatest risk (see Lown grading criteria below).
Race
African American race is associated with an increased frequency of PVCs on routine monitoring.1 In a large population-based study of PVC prevalence, African American race alone increased the risk of PVCs by 30% compared with the risk in white individuals.
Sex
Ventricular ectopy is more prevalent in men than in women of the same age. Male sex alone increases the risk of identifying PVCs on routine screening, with an odds ratio for male sex of 1.39 compared with women.
Age
PVC frequency increases with age, reflecting the increased prevalence of hypertension and cardiac disease in aging populations.
Clinical
History
The important elements in obtaining a history from patients with ventricular ectopy are a history of cardiac disease or structural heart disease. Current medications that may be proarrhythmic or that may increase the risk of abnormal potassium or magnesium levels and use of drugs or medications that are sympathomimetic (eg, ephedrine-containing products, cocaine), may also provide important clues to the source of the premature ventricular contractions (PVCs).
Symptoms pertinent to the management of the PVCs are those that suggest underlying ischemic cardiac disease, such as chest pain or its anginal equivalent, or those suggesting hemodynamic compromise, such as lightheadedness or syncope.
- Patients are usually asymptomatic.
- Cannon A waves or the increased force of contraction due to postextrasystolic potentiation of contractility can cause palpitations and neck and/or chest discomfort.
- The patient may report feeling that his or her heart "stops" after a PVC.
- Patients with frequent PVCs or bigeminy may report syncope. This symptom is due to either inadequate stroke volume or decreased cardiac output caused by the condition effectively halving the heart rate.
- Long runs of PVCs can result in hypotension.
- Exercise can increase or decrease the PVC rate.
Physical
Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy.
- Blood pressure: Frequent premature ventricular contractions (PVCs) may result in hemodynamic compromise. Frank hypotension is rare, but relative hypotension is not uncommon, particularly in patients with underlying cardiac disease.
- Pulse: The ectopic beat may produce a diminished or absent pulse depending on the force of the ventricular contraction.
- Pulse oximetry: Hypoxia may precipitate PVCs.
- Cardiac findings: Cannon A waves may be observed in the jugular venous pulse if the timing of the PVC causes an atrial contraction against a closed tricuspid valve.
- Cardiopulmonary findings: Findings in conjunction with longstanding hypertension (elevated BP and an S 4 ) or CHF (S 3 and rales) are important clues to the cause and clinical significance of PVCs.
- Neurologic findings: Agitation and findings of sympathetic activation (eg, dilated pupils, warm and dry skin, tremor, tachycardia, hypertension) suggest that catecholamines may be the cause of the ectopy.
Causes
- Cardiac
- Acute MI or ischemia
- Myocarditis
- Cardiomyopathy, dilated or hypertrophic
- Myocardial contusion
- Mitral valve prolapse
- Hypoxia and/or hypercapnia
- Medications (eg, digoxin, sympathomimetics, tricyclic antidepressants, aminophylline, caffeine)
- Illicit substances (eg, cocaine, amphetamines, alcohol, tobacco)
- Hypomagnesemia, hypokalemia, hypercalcemia
Differential Diagnoses
Acute Coronary Syndrome
Myocardial Infarction
Myocarditis
Ventricular Fibrillation
Ventricular Tachycardia
Workup
Laboratory Studies
- Obtain serum electrolyte levels, in particular potassium levels. Consider checking the magnesium level, especially in patients with low potassium levels.
- In selected patients, a drug screen may be helpful.
- For patients taking medication with known proarrhythmic effects (eg, digoxin, theophylline), drug levels may be useful.
Other Tests
- ECG allows for characterization of the ventricular ectopy and determination of cause. In addition to the standard 12-lead ECG, a 2-minute rhythm strip may help in determining frequency of the ectopy and capture infrequent premature ventricular contractions (PVCs). Findings may include the following:
- Left ventricular hypertrophy
- Active cardiac ischemia (ST-segment depression or elevation and or T-wave inversion)
- In patients with previous MI - Q waves or loss of R waves, bundle branch block
- Electrolyte abnormalities (hyperacute T waves, QT prolongation)
- Drug effects (QRS widening, QT prolongation)
- On ECG, PVCs may be premature in relation to the next expected beat of the basic rhythm. The pause after the premature beat is usually a fully compensatory pause. The R-R interval surrounding the premature beat is equal to double the basic R-R interval, showing that the ectopic beat did not reset the sinus node.
- PVCs may appear in a pattern of bigeminy, trigeminy, or quadrigeminy, which describe a pattern of PVCs occurring every other, every third, or every fourth beat, respectively.
- PVCs with identical morphologies on a tracing are called monomorphic or unifocal. If the PVCs demonstrate 2 or more different morphologies, they are referred to as multiform, pleomorphic, or polymorphic.
ECG shows frequent, unifocal PVCs with a fixed coupling interval between the ectopic beat and the previous beat. These PVCs result in a fully compensatory pause; the interval between the 2 sinus beats surrounding the PVC are exactly twice the normal R-R interval. This finding indicates that the sinus node continues to pace at its normal rhythm despite the PVC, which fails to reset the sinus node.
On this ECG, the PVCs occur near the peak of the T wave of the preceding beat. These beats predispose the patient to ventricular tachycardia or fibrillation. This R-on-T pattern is often seen in patients with acute myocardial infarction or long Q-T intervals. In the latter case, the triggered arrhythmia would be torsade.
- PVCs usually are described in terms of the Lown grading system for premature beats. The higher the grade, the more serious the ectopy.
- Grade 0 = No premature beats
- Grade 1 = Occasional (<30/h)
- Grade 2 = Frequent (>30/h)
- Grade 3 = Multiform
- Grade 4 = Repetitive (A = Couplets, B = Salvos of = or > 3)
- Grade 5 = R-on-T pattern
- Holter 24-hour monitors are useful in quantifying and characterizing ventricular ectopy.
- Holters also have been used to determine treatment efficacy in patents with frequent or complex PVCs.
- Suppression of ectopy on Holter monitoring is not always predictive of survival.
- The most important role for Holter monitoring is risk stratification of patients with a recent MI or known left ventricular dysfunction.
- More than 60% of healthy, middle-aged men have ventricular ectopy on Holter monitoring.
- Signal-averaged ECG
- Signal-averaged ECGs (SAECGs) may have a future role in identifying patients at risk for complex ventricular ectopy and nonsustained ventricular tachycardia (NSVT).
- SAECGs may have a role in identifying patients with complex ectopy who may benefit from electrophysiologic studies (EPS).
- Echocardiography is useful not only in evaluating the ejection fraction, which is important in determining the prognosis and also in identifying valvular disease or ventricular hypertrophy.
Procedures
- Exercise stress testing (EST) is best used complementary to Holter monitoring. In patients with complex ectopy, EST can unmask NSVT triggered by increased catecholamines or myocardial ischemia.
- The role of EPS in complex ventricular ectopy is an area of both intense research and debate. A joint American Heart Association (AHA)/American College of Cardiology (ACC) statement suggested the following:
- Routine EPS are not indicated in low-risk patients after MI. Low risk refers to simple ectopy, good left ventricular function, and low congestive heart failure (CHF) class.
- EPS are indicated in high-risk patients with complex ectopy.
- EPS are though to be beneficial in patients with sustained ventricular tachycardia more than 48 hours after MI.
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.
Dosing
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
Interactions
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
Contraindications
Documented hypersensitivity; complete AV block and intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Precautions
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.
Dosing
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
Interactions
Cimetidine or beta-blockers increase toxicity; procainamide or tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Contraindications
Documented hypersensitivity; Adams-Stokes syndrome; Wolff-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block, if artificial pacemaker not in place
Precautions
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.
Dosing
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
Interactions
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
Contraindications
Documented hypersensitivity; complete heart block or second- or third-degree heart block (if pacemaker not in place); torsade de pointes; systemic lupus erythematosus
Precautions
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.
Dosing
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
Interactions
Pressor catecholamines and digitalis may increase toxicity; ofloxacin may increase risk of cardiotoxicity
Contraindications
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
Precautions
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.
Dosing
Adult
5 mg IV q2min for 3 bolus injections
Pediatric
Not established
Interactions
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
Contraindications
Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Precautions
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.
Dosing
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
Interactions
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
Contraindications
Documented hypersensitivity; cardiogenic shock; CHF; bradycardia; AV conduction abnormalities
Precautions
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.
Dosing
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
Interactions
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
Contraindications
Documented hypersensitivity; uncompensated CHF; cardiogenic shock; bradycardia; AV conduction abnormalities
Precautions
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.
Dosing
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
Interactions
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
Contraindications
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Precautions
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.
Dosing
Adult
80-160 mg PO tid
Pediatric
Not established
Interactions
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
Contraindications
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Precautions
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
Follow-up
Further Outpatient Care
- Catheter ablative therapy has a role in the management of patients with PVCs. This is in the setting of PVCs from the right or left ventricular outflow tract that occur in structurally normal hearts. Ablation is indicated for frequent, symptomatic PVCs despite medical therapy. Success is variable depending on frequency and inducibility at the time of electrophysiologic study. Guidelines on the use of catheter ablation in ventricular arrhythmia are available from the European Heart Rhythm Association (EHRA) and the Heart Rhythm Society (HRS) in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA).2
Prognosis
- In asymptomatic patients without underlying heart disease, the long-term prognosis is similar to that of the general population. Asymptomatic patients with ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. Therefore, in patients with absence of heart disease on noninvasive workup, reassurance is appropriate. One caveat to this is that emerging data suggest that very frequent ventricular ectopy (>4000/24 h) may be associated with the development of cardiomyopathy related to abnormal electrical activation of the heart. This mechanism is thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy.
- In the setting of acute coronary ischemia/infarction, patients with simple PVCs rarely progress to malignant arrhythmias. However, persistent complex ectopy after MI is associated with increased risk of sudden death and may be an indication for EPS.
- Patients with underlying chronic structural heart disease (eg, cardiomyopathy, infarction, valvular disease) and complex ectopy (eg, >10 PVCs/h) have a significantly increased rate of mortality.
- Understanding of the role of antiarrhythmic therapy in the months after MI is poor. The Cardiac Arrhythmia Suppression Trial (CAST) studied patients with ventricular ectopy after MI to see if antiarrhythmic therapy improved survival rates.3 Despite suppression of ectopy on Holter monitoring, patients treated with encainide, flecainide, or moricizine had increased rates of sudden death and death from all causes. Findings have suggested a role for amiodarone in this patient population and have had significant reductions in rates of post-MI ventricular arrhythmias and death. Moricizine (Ethmozine) was discontinued in July 2007 because of diminished market demand.
- Left ventricular dysfunction has a stronger association with increased mortality rate than do PVCs. Many now believe that PVCs reflect the severity of heart disease rather than contribute to arrhythmogenesis.
- EPS has a primary role in risk stratification of patients with frequent or complex PVCs. Patients with PVCs that are noninducible (ie, unable to trigger ventricular tachycardia during stimulation) have a low risk of sudden death.
Miscellaneous
Special Concerns
- Children
- PVCs are less common in children than in adults, but PVCs do occur in healthy children.
- About 20% of healthy boys aged 10-13 years have PVCs on routine Holter monitoring.
- PVCs in healthy newborns generally resolve by the 12th week and usually require no treatment once the presence of a healthy heart is confirmed. This finding probably is related to developmental factors associated with the autonomic nervous system.
- In older children, PVCs often are related to transient or exogenous factors, including mild viral myocarditis, excessive caffeine, or sympathomimetic drugs (cold or asthma medications). They usually resolve without treatment.
- When complex ectopy is seen in pregnancy, or immediately after, obtain an ECG for possible peripartum cardiomyopathy.
- Closely monitor and admit to an appropriate monitored setting patients with presentations that indicate an ischemic basis for their PVCs (eg, chest pain, dyspnea, syncope) or who are hemodynamically unstable while in the ED.
Multimedia
Media file 1: ECG shows frequent, unifocal PVCs with a fixed coupling interval between the ectopic beat and the previous beat. These PVCs result in a fully compensatory pause; the interval between the 2 sinus beats surrounding the PVC are exactly twice the normal R-R interval. This finding indicates that the sinus node continues to pace at its normal rhythm despite the PVC, which fails to reset the sinus node.
Media file 2: On this ECG, the PVCs occur near the peak of the T wave of the preceding beat. These beats predispose the patient to ventricular tachycardia or fibrillation. This R-on-T pattern is often seen in patients with acute myocardial infarction or long Q-T intervals. In the latter case, the triggered arrhythmia would be torsade.
References
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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
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James E Keany, MD, FACEP, Medical Director, JetWest International Air Ambulance; Consulting Staff, Department of Emergency Services, Mission Hospital Regional Medical Center; Host of Healthbuzz at Jim.MD
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Aseem D Desai, MD, FACC, Cardiac Electrophysiologist, Mission Internal Medicine Group, Inc
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