Premature Ventricular Contraction Treatment & Management

  • Author: James E Keany, MD, FACEP; Chief Editor: David FM Brown, MD   more...
 
Updated: Mar 11, 2010
 

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.
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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.
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Consultations

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

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Contributor Information and Disclosures
Author

James E Keany, MD, FACEP  Medical Director, TravelMDAssist; Staff Physician, Department of Emergency Services, Mission Hospital Regional Medical Center

James E Keany, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, and California Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

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

Aseem D Desai, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Assaad J Sayah, MD  Chief, Department of Emergency Medicine, Cambridge Health Alliance

Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians

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

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

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

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

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

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

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.
 
 
 
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