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Pediatric Ventricular Fibrillation Workup

  • Author: Elizabeth A Stephenson, MD, MSc; Chief Editor: Howard S Weber, MD, FSCAI  more...
 
Updated: Jan 29, 2015
 

Laboratory Studies

The workup in patients who have been resuscitated from ventricular fibrillation is aimed at determining any preventable triggers or risk factors for the ventricular arrhythmias that may degenerate into ventricular fibrillation. A detailed discussion of triggers and risk factors is offered in Ventricular Tachycardia.

Note the following:

  • Electrolyte levels: In particular, serum magnesium, potassium, and calcium levels are most relevant to assessing ventricular arrhythmia vulnerability.
  • Blood gases: Blood gases, particularly pH, are determined because acidemia promotes arrhythmia susceptibility.
  • Drug levels: Clinicians may want to obtain drug levels, particularly to assess for any of the medications that may prolong the QT interval and any proantiarrhythmic agents to which the patient may have been exposed. Medications such as procainamide and amiodarone have arrhythmogenic potential, as do many antiarrhythmic drugs.
  • Toxicology screen: In particular, stimulant drugs of abuse, such as cocaine and amphetamines, may promote ventricular arrhythmias. Other illicit drugs, including phencyclidine, lysergic acid diethylamide (LSD), ecstasy, and even marijuana may increase vulnerability to arrhythmias, including ventricular fibrillation. Legal stimulants, such as caffeine, theophylline, and pseudoephedrine, may promote ventricular arrhythmias, particularly in individuals with underlying susceptibility.
  • Genetic testing: Extensive research is ongoing regarding identification of cardiac channelopathies which cause many of the primary electrical diseases. Commercial testing is becoming available for some of these channelopathies; however, many genetic variants have yet to be identified.
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Imaging Studies

Obtain the following imaging studies:

  • Chest radiography
  • Echocardiography
  • Cardiac MRI: This should particularly concentrate on the potential for arrhythmogenic right ventricular dysplasia. Fibrofatty infiltration may be evident in patchy distribution within the right, and sometimes left, ventricle.
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Other Tests

Other studies include the following:

  • Electrocardiography: A 12-lead ECG is most helpful in formulating differential diagnoses following ventricular fibrillation arrest.
  • Holter monitor
  • Event monitor

Additional tests indicated based on suspected precipitating factors, such as the following:

  • Provocative testing to elicit arrhythmias may be helpful in determining the electrophysiologic etiology.
  • Noninvasive provocative testing is predominantly by means of exercise stress testing.
  • Less commonly, infusion of cardioactive medications, such as isoproterenol or epinephrine, has been used to provoke ventricular arrhythmias in individuals with potential susceptibility.
  • In addition, infusion of sodium channel blocking antiarrhythmic drugs, such as ajmaline or procainamide, has been used to provoke an electrocardiographic phenotype of Brugada syndrome.
  • These tests may increase sensitivity in the identification of individuals with potential susceptibility, although specificity may be sacrificed. The value of the use of these provocative tests in pediatric patients has not yet been fully defined.
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Procedures

Electrophysiologic studies

An invasive electrophysiologic (EP) study may be warranted in patients at high risk for ventricular fibrillation (eg, sustained or nonsustained ventricular tachycardia, averted sudden cardiac death). An EP study usually consists of programmed atrial and ventricular stimulation to determine the presence or absence of inducible ventricular tachycardia/ventricular fibrillation. Other potential arrhythmia substrates such as WPW with rapid antegrade conduction may also be examined.

Pharmacologic provocation studies (eg, using isoproterenol or other catecholaminergic agents for arrhythmia induction) may also be used during an EP study. Medications that may promote ECG signatures for specific disease states, such as a type I antiarrhythmic agents (eg, flecainide, ajmaline), may be administered to unmask the classic ECG pattern found in patients with Brugada syndrome.

Because diagnostic predictive value is limited, negative EP study findings do not exclude the possibility of a sudden cardiac event in the future, particularly in patients with structural congenital heart disease.

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Contributor Information and Disclosures
Author

Elizabeth A Stephenson, MD, MSc Associate Professor of Pediatrics, University of Toronto Faculty of Medicine; Consulting Staff, Division of Cardiology, The Hospital for Sick Children

Elizabeth A Stephenson, MD, MSc is a member of the following medical societies: American Heart Association, Heart Rhythm Society, Canadian Cardiovascular Society, Pediatric and Congenital Electrophysiology Society

Disclosure: Nothing to disclose.

Coauthor(s)

Charles I Berul, MD Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, Heart Rhythm Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, American College of Cardiology, American Heart Association, Society for Pediatric Research

Disclosure: Received grant/research funds from Medtronic for consulting.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Alvin J Chin, MD Emeritus Professor of Pediatrics, University of Pennsylvania School of Medicine

Alvin J Chin, MD is a member of the following medical societies: American Association for the Advancement of Science, Society for Developmental Biology, American Heart Association

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Additional Contributors

Christopher Johnsrude, MD, MS Chief, Division of Pediatric Cardiology, University of Louisville School of Medicine; Director, Congenital Heart Center, Kosair Children's Hospital

Christopher Johnsrude, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology

Disclosure: Nothing to disclose.

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Ventricular fibrillation with polymorphic morphology and cycle lengths varying from 80-280 milliseconds.
 
 
 
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