eMedicine Specialties > Emergency Medicine > Cardiovascular

Premature Ventricular Contraction: Differential Diagnoses & Workup

Author: James E Keany, MD, FACEP, Medical Director, JetWest International Air Ambulance; Consulting Staff, Department of Emergency Services, Mission Hospital Regional Medical Center; Host of Healthbuzz at Jim.MD
Coauthor(s): Aseem D Desai, MD, FACC, Cardiac Electrophysiologist, Mission Internal Medicine Group, Inc
Contributor Information and Disclosures

Updated: Nov 16, 2009

Differential Diagnoses

Acute Coronary Syndrome
Myocardial Infarction
Myocarditis
Ventricular Fibrillation
Ventricular Tachycardia

Workup

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.

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 co...

      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.

      ECG shows frequent, unifocal PVCs with a fixed co...

      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 ...

      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.

      On this ECG, the PVCs occur near the peak of the ...

      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.

    • 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.

More on Premature Ventricular Contraction

Overview: Premature Ventricular Contraction
Differential Diagnoses & Workup: Premature Ventricular Contraction
Treatment & Medication: Premature Ventricular Contraction
Follow-up: Premature Ventricular Contraction
Multimedia: Premature Ventricular Contraction
References

References

  1. 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].

  2. [Guideline] Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F, Calkins CH, Delacretaz E, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace. Jun 2009;11(6):771-817. [Medline][Full Text].

  3. 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].

  4. Bala R, Marchlinski FE. Electrocardiographic recognition and ablation of outflow tract ventricular tachycardia. Heart Rhythm. Mar 2007;4(3):366-70. [Medline].

  5. 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].

  6. 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].

  7. 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].

  8. 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].

  9. 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].

  10. 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].

  11. 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].

  12. 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].

  13. Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation. Jul 1971;44(1):130-42. [Medline].

  14. 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].

  15. 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].

  16. 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].

Further Reading

Keywords

premature ventricular contraction, premature ventricular contraction causes, premature ventricular contraction treatment, PVC, ectopic cardiac pacemakerparoxysmal tachycardia, arrhythmias, dysrhythmias, acute myocardial infarction, MI, ventricular ectopy, myocarditis, dilated cardiomyopathy, hypertrophic cardiomyopathy

Contributor Information and Disclosures

Author

James E Keany, MD, FACEP, Medical Director, JetWest International Air Ambulance; Consulting Staff, Department of Emergency Services, Mission Hospital Regional Medical Center; Host of Healthbuzz at Jim.MD
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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

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, Assistant 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.

 
 
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