Premature Ventricular Contraction Clinical Presentation

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

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.
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Physical

Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy.

  • Blood pressure: Frequent premature ventricular contractions (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 S 4 ) or CHF (S 3 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.
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Causes

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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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