eMedicine Specialties > Cardiology > Arrhythmias

Ventricular Premature Complexes: Differential Diagnoses & Workup

Author: Jatin Dave, MD, MPH, Instructor, Department of Medicine, Department of Internal Medicine, Division of Aging, Harvard Medical School; Staff Physician, Brigham and Women's Hospital
Coauthor(s): Revat Lakhia, MD, Visiting Staff, Department of Internal Medicine, Brigham and Women's Hospital; Graduate Student in Public Health, Department of Health Science, West Chester University of Pennsylvania; Shivkumar H Jha, MD, Chief Resident, Department of Psychiatry, St Elizabeth's Medical Center, Tufts University School of Medicine; Fellow, Brain Imaging Center, McLean Hospital, Harvard Medical School
Contributor Information and Disclosures

Updated: Aug 24, 2009

Differential Diagnoses

Other Problems to Be Considered

Differentiating VPCs from other arrhythmias can be challenging because the following arrhythmias may mimic VPCs:

Aberrant premature atrial contractions: The presence of ectopic P waves, usually absence of full compensatory pause (R-R interval containing the premature contraction is <2 times the R-R interval of basic rhythm), and a relatively narrow QRS complex morphology help differentiate atrial premature complexes from VPCs. In general, the sinus node is not always reset by VPCs because the ectopic impulse meets the sinus impulse more distal to the sinus node (either at the AV node or in the ventricles). Thus, VPCs frequently cause a fully compensatory pause (R-R interval containing the premature contraction is equal to 2 times the R-R interval of basic rhythm). On rare occasions, the ectopic impulse conducts retrogradely to the sinus node; resets the sinus node; and a shorter, noncompensatory pause occurs. If the sinus impulse is able to conduct despite the VPC, then the VPC is termed interpolated and no compensatory pause occurs.

Fusion beat: Simultaneous activation of the ventricle by 2 sources can lead to a beat with characteristics between the conducted sinus beat and the ectopic beat.

Premature junctional contractions: The origin of this arrhythmia is automaticity or reentry in AV junctional tissues. The P waves usually are inverted because of retrograde atrial depolarization. If the ectopic beat originates in high nodal tissue, the QRS complex can be narrow.

Idioventricular escape rhythms: A very slow pacemaker in the ventricle takes over when sinoatrial node and AV junctional pacemakers fail to function. The rate usually is less than 45 beats per minute, which helps to differentiate it from other arrhythmias.

Ventricular tachycardia: When 3 or more consecutive ventricular contractions occur, they are called VT. VT that persists for 30 seconds or causes hemodynamic collapse is called sustained VT.

Parasystole: Parasystole occurs when a protected focus discharges independently of the dominant pacemaker. The characteristics of parasystole include wide QRS complexes with a varying coupling interval between the ectopic (parasystolic) and the dominant (usually sinus) complex, fusion beats, and variable coupling interval.

Fixed versus variable coupling interval: Fixed coupling refers to a fixed interval between the sinus QRS complex and the VPC; this indicates reentry or a triggered focus as the possible cause. Variable coupling could be due to parasystole or multifocal ectopy.

Interpolated VPC: When the sinus rate is slow, a short-coupled VPC can occur between sinus beats. If concealed retrograde conduction occurs, the subsequent PR interval can be prolonged.

VPCs as a proarrhythmic effect: VPCs can be exacerbated by catheters in the heart or pacemaker leads. They can occur in response to an antiarrhythmic drug. If they are worsened with an antiarrhythmic drug and the QT is prolonged from the drug, a risk of torsades de pointes exists.

Workup

Laboratory Studies

  • Look for correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI.
  • Obtain serum electrolyte and magnesium levels.

Imaging Studies

Look for underlying structural heart abnormalities that can predispose to VPCs.

  • Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging.
  • Echocardiography may be preferable because it also provides structural information about the heart.

Other Tests

  • In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
    • The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
    • Suppression of VPCs by beta-blocker or calcium blocker, together with a typical VPC morphology (inferior axis, LBBB morphology) can be helpful in establishing typical right ventricular outflow tract ectopy.
    • Suppressing the VPCs themselves is not the focus of treatment unless patients are significantly symptomatic.
    • Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
  • ECG should be performed to look for structural cardiac abnormalities. Diagnostic criteria include the following:
    • Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
    • No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
    • The T wave usually is in the opposite direction from the R wave.
    • Full compensatory pause is common.
    • VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
    • VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
    • Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle inferior axis morphology.
  • Electrophysiologic study
    • Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
    • According to current American College of Cardiology/American Heart Association guidelines, class I indications for EPS are patients with CAD, low EF (<0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
  • Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.

Procedures

In patients suspected of having coronary artery disease, a noninvasive evaluation to rule out this possibility or even a cardiac catheterization may be helpful diagnostically. This is based on not just the presence of VPCs, but on all risk factors and symptoms. Onset in an elderly patient should be a red flag to consider the possibility of progressive structural heart disease.

Staging

VPCs can be classified in different ways. The Lown classification was introduced to gauge effects of antiarrhythmic drugs.

Table 1. Lown Classification

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Table
ClassArrhythmia
0None
1Unifocal; <30/h
2Unifocal; ³ 30/h
3Multiform
4A2 consecutive
4B³ 3 consecutive
5R-on-T phenomenon
ClassArrhythmia
0None
1Unifocal; <30/h
2Unifocal; ³ 30/h
3Multiform
4A2 consecutive
4B³ 3 consecutive
5R-on-T phenomenon

The Lown classification does not necessarily imply a continuum of increasing risk.
  • Clinical classification is as follows:
    • Benign
    • Potentially malignant
    • Malignant
  • Classification according to frequency is as follows:
    • Frequent - 10 or more VPCs per hour (by Holter monitoring) or 6 or more per minute
    • Occasional - Fewer than 10 VPCs per hour or fewer than 6 per minute
  • Classification according to relationship to normal beats is as follows:
    • Bigeminy - Paired complexes, VPC alternating with a normal beat
    • Trigeminy - VPC occurring every third beat (2 sinus beats followed by VPC)
    • Quadrigeminy - VPC occurring every fourth beat (VPC following 3 normal beats)
    • Couplet - 2 consecutive VPCs
    • Nonsustained VT - 3 or more consecutive VPCs (<30 s)
  • Classification according to origin is as follows:
    • Number of foci
      • Unifocal/unimorphic - Beats originate from 1 focus, ie, all VPCs have the same morphology
      • Multifocal/multimorphic - VPCs have more than 1 morphology and may originate from more than 1 site
    • Site of origin
      • Left ventricular
      • Right ventricular
    • Associated heart disease
      • None (idiopathic)
      • Structural heart disease present

More on Ventricular Premature Complexes

Overview: Ventricular Premature Complexes
Differential Diagnoses & Workup: Ventricular Premature Complexes
Treatment & Medication: Ventricular Premature Complexes
Follow-up: Ventricular Premature Complexes
Multimedia: Ventricular Premature Complexes
References
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Further Reading

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Keywords

ventricular premature complexes, ventricular extrasystole, ventricular ectopic beats, benign ventricular arrhythmia, missed beats, VPC, PVC, premature ventricular complex, VPD, ventricular premature depolarization, VPB, ventricular premature beat, ventricular arrhythmia, beta-blockers, myocardial infarction, MI, postmyocardial infarction, post-MI, congestive heart failure, CHF, coronary artery disease, CAD, ventricular ectopy, ventricular tachycardia, VT

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Contributor Information and Disclosures

Author

Jatin Dave, MD, MPH, Instructor, Department of Medicine, Department of Internal Medicine, Division of Aging, Harvard Medical School; Staff Physician, Brigham and Women's Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

Revat Lakhia, MD, Visiting Staff, Department of Internal Medicine, Brigham and Women's Hospital; Graduate Student in Public Health, Department of Health Science, West Chester University of Pennsylvania
Revat Lakhia, MD is a member of the following medical societies: Medical Council of India
Disclosure: Nothing to disclose.

Shivkumar H Jha, MD, Chief Resident, Department of Psychiatry, St Elizabeth's Medical Center, Tufts University School of Medicine; Fellow, Brain Imaging Center, McLean Hospital, Harvard Medical School
Shivkumar H Jha, MD is a member of the following medical societies: American Psychiatric Association, International Society for Heart Research, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

 
 
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