AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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

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 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 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

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 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. 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

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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 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 S₄) or CHF (S₃ 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

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab 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 the physician to characterize the ventricular ectopy and determine its 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 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.
  • 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

Section 6 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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 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

Section 7 of 12  

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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

Drug Category: Antiarrhythmics

These agents alter the electrophysiologic mechanisms responsible for PVCs.

Drug Category: 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.

Drug Category: 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.

Drug Category: 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.

FOLLOW-UP

Section 8 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

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.¹ 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

Section 9 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

ACKNOWLEDGMENTS

Section 10 of 12  

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• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Sarah A Stahmer, MD, and Edwin Williams, MD, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.
	View Full Size Image
Media type:  ECG

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.
	View Full Size Image
Media type:  ECG

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

1. CAST Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. Aug 10 1989;321(6):406-12. [Medline].
2. Burkart F, Pfisterer M, Kiowski W, et al. Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS). J Am Coll Cardiol. Dec 1990;16(7):1711-8. [Medline].
3. Cairns JA, Connolly SJ, Roberts R, Gent M. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Lancet. Mar 8 1997;349(9053):675-82. [Medline].
4. Califf RM, McKinnis RA, Burks J, et al. Prognostic implications of ventricular arrhythmias during 24 hour ambulatory monitoring in patients undergoing cardiac catheterization for coronary artery disease. Am J Cardiol. 1982;50:23-31. [Medline].
5. Hallstrom AP, Bigger JT Jr, Roden D, et al. Prognostic significance of ventricular premature depolarizations measured 1 year after myocardial infarction in patients with early postinfarction asymptomatic ventricular arrhythmia. J Am Coll Cardiol. Aug 1992;20(2):259-64. [Medline].
6. Hammill SC, Trusty JM, Wood DL, et al. Influence of ventricular function and presence or absence of coronary artery disease on results of electrophysiologic testing for asymptomatic nonsustained ventricular tachycardia. Am J Cardiol. Mar 15 1990;65(11):722-8. [Medline].
7. Hargarten K, Chapman PD, Stueven HA, et al. Prehospital prophylactic lidocaine does not favorably affect outcome in patients with chest pain. Ann Emerg Med. Nov 1990;19(11):1274-9. [Medline].
8. Jouven X, Zureik M, Desnos M, et al. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med. Sep 21 2000;343(12):826-33. [Medline].
9. Kennedy HL, Whitlock JA, Sprague MK, et al. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med. Jan 24 1985;312(4):193-7. [Medline].
10. Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation. Jul 1971;44(1):130-42. [Medline].
11. Maggioni AP, Zuanetti G, Franzosi MG, et al. Prevalence and prognostic significance of ventricular arrhythmias after acute myocardial infarction in the fibrinolytic era. GISSI-2 results. Circulation. Feb 1993;87(2):312-22. [Medline].
12. Rehnqvist N, Olsson G, Erhardt L, Ekman AM. Metoprolol in acute myocardial infarction reduces ventricular arrhythmias both in the early stage and after the acute event. Int J Cardiol. Jun 1987;15(3):301-8. [Medline].
13. Simpson RJ, Cascio WE, Schreiner PJ, et al. Prevalence of premature ventricular contractions in a population of African American and white men and women: the Atherosclerosis Risk in Communities (ARIC) study. Am Heart J. Mar 2002;143(3):535-40. [Medline].
14. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials. JAMA. Oct 6 1993;270(13):1589-95. [Medline].

Article Last Updated: Apr 15, 2008