Premature Ventricular Contraction

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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.

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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.

Epidemiology

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.

Race

African American race is associated with an increased frequency of PVCs on routine monitoring.[2] 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.

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.

Physical

Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy.

Causes

Laboratory Studies

Other Tests

Procedures

Prehospital Care

Emergency Department Care

Consultations

Involvement of a cardiologist may be indicated if the patient's condition is refractory to standard therapy.

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.

Amiodarone (Cordarone)

Clinical Context:  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)

Clinical Context:  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)

Clinical Context:  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)

Clinical Context:  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.

Class Summary

These agents alter the electrophysiologic mechanisms responsible for PVCs.

Metoprolol (Lopressor)

Clinical Context:  Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.

Esmolol (Brevibloc)

Clinical Context:  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)

Clinical Context:  Class II antiarrhythmic, nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

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.

Magnesium sulfate

Clinical Context:  Acts as antiarrhythmic agent; diminishes frequency of PVCs, particularly those due to acute ischemia.

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.

Verapamil (Calan, Covera, Verelan)

Clinical Context:  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.

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.

Further Outpatient Care

Prognosis

Author

James E Keany, MD, FACEP, Associate Medical Director, Emergency Services, Mission Hospital Regional Medical Center, Children's Hospital of Orange County at Mission

Disclosure: Nothing to disclose.

Coauthor(s)

Aseem D Desai, MD, FACC, Cardiac Electrophysiologist, Mission Internal Medicine Group, Inc

Disclosure: Nothing to disclose.

Specialty Editors

Assaad J Sayah, MD, FACEP, Chief, Department of Emergency Medicine; Senior Vice President, Primary and Emergency Care, Cambridge Health Alliance

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eddy S Lang, MDCM, CCFP(EM), CSPQ, Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

References

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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.

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.