Premature Ventricular Contraction Workup

  • Author: James E Keany, MD, FACEP; Chief Editor: David FM Brown, MD   more...
 
Updated: Apr 24, 2012
 

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.
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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 couECG 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 TOn 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 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 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.
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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 thought to be beneficial in patients with sustained ventricular tachycardia more than 48 hours after MI.
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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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