Premature Ventricular Contraction

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Background

A 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 that are unusually long (typically >120 msec) and appear wide on the electrocardiogram (ECG). These complexes are not preceded by a P wave, and the T wave is usually large and oriented in a direction opposite the major deflection of the QRS.

The clinical significance of PVCs depends on their frequency, complexity, and hemodynamic response.

Pathophysiology

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 one-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 electrophysiology laboratory), 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 V1 . If the source is the left ventricular outflow tract, there is a right bundle-branch block pattern in V1 . Beta-blocker therapy is first-line treatment for symptomatic patients.

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,[1] and hypokalemia.

Etiology

Cardiac causes of premature ventricular contractions include the following:

Other causes of PVCs include the following:

Epidemiology

United States statistics

PVCs are one of the most common arrhythmias and can occur in patients with or without heart disease. Their prevalence varies greatly, with estimates ranging from 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.

Race-, sex-, and age-related demographics

Black race is associated with an increased frequency of PVCs on routine monitoring.[5] In a large population-based study of PVC prevalence, black race alone increased the risk of PVCs by 30% in comparison with the risk in white individuals.

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 as compared with female sex.

PVC frequency increases with age, reflecting the increased prevalence of hypertension and cardiac disease in aging populations.

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 no evidence 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 hr) 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 electrophysiologic studies (EPS).

In patients with underlying chronic structural heart disease (eg, cardiomyopathy, infarction, valvular disease) and complex ectopy (eg, >10 PVCs/hr), mortality is significantly increased. The following points should be kept in mind.

First, 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.[6]  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 was discontinued in July 2007 because of diminished market demand.

Second, 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. Some studies in recent years suggest that increased variability of the PVC coupling interval in patients with underlying heart diseases, including left ventricular dysfunction, is a predictor of cardiac death; however, this remains a matter of debate.[7, 8]

Third, 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.

Frequent PVCs may be associated with increased risk of stroke in patients who do not have hypertension and diabetes.[9]

Mortality/morbidity

The clinical significance of PVCs depends on the clinical context in which they occur, as follows:

History

The important element in obtaining a history from patients with ventricular ectopy is 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. Note the following:

Physical Examination

Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy, including the following:

Laboratory Studies

In young, healthy patients without concerning concomitant symptoms, laboratory tests are not typically necessary. The following diagnostic measures may be necessary, depending on the patient's history and underlying illness(es):

Echocardiography

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.

Electrocardiography

Electrocardiography (ECG) allows characterization of the ventricular ectopy and determination of the cause. In addition to the standard 12-lead ECG, a 2-minute rhythm strip may help in determining the frequency of the ectopy and capturing infrequent premature ventricular contractions (PVCs). Findings may include the following:

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 one. 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 (ie, may occur every other beat, every third beat, or every fourth beat). PVCs with identical morphologies on a tracing are called monomorphic or unifocal. PVCs demonstrating two or more different morphologies are referred to as multiform, pleomorphic, or polymorphic. (See the images below.)



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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 compensa....



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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 fibril....

PVCs usually are described in terms of the Lown grading system for premature beats, as follows (the higher the grade, the more serious the ectopy):

Holter 24-hour monitoring

Holter 24-hour monitors are useful in quantifying and characterizing ventricular ectopy. Holters also have been used to determine treatment efficacy in patients 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 myocardial infarction (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 ECG (SAECG) may have a future role in identifying patients at risk for complex ventricular ectopy and nonsustained ventricular tachycardia (NSVT). SAECG may have a role in identifying patients with complex ectopy who may benefit from electrophysiologic studies (EPS).

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[10, 11] :

Medical Care

The optimal indications for therapy for premature ventricular contractions (PVCs) have not yet been elucidated.[4] Involvement of a cardiologist may be indicated if the patient's condition is refractory to standard therapy.

Prehospital care

Perform telemetry, and secure intravenous (IV) access. Administer oxygen, if any hypoxia exists. 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 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 electrocardiogram (ECG). Note the following:

Acute ischemia or infarction

Early diagnosis and treatment of acute infarction/ischemia are the cornerstones of therapy. Note the following:

Catheter Ablation

Catheter ablative therapy has a role in the management of patients with PVCs.[13, 14] 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 that occur despite medical therapy. Success is variable, depending on frequency and inducibility at the time of electrophysiologic study (EPS).

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).[15]

Fichtner et al evaluated the outcome and success of PVC ablation in 408 patients in the German Ablation Registry from March 2007 to May 2011.[16] The acute ablation success rate was 82%; all patients were discharged alive after a median of 3 days; and no patient suffered an acute MI, stroke, or major bleeding. After 12 months of follow-up, 99% of patients were still alive, and 76% showed significantly improved symptoms.

Im et al investigated ECG criteria for predicting successful ablation of PVCs from the right coronary cusp (RCC). They found that the presence of a dominant positive lead I, an R-wave duration index (RWDI) higher than 43.6%, and an S-wave amplitude lower than 0.95mV in aVL predicted RCC PVCs in patients with a sensitivity of 83% and a specificity of 94%.[17]

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.

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

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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.

Chief Editor

Erik D Schraga, MD, Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

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

Disclosure: Nothing to disclose.

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.