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Pediatric Ventricular Fibrillation Clinical Presentation

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

History

Ventricular fibrillation is usually preceded by other ventricular arrhythmias, and prevention of ventricular fibrillation may be best accomplished through prevention of those arrhythmias. Thus, obtain a thorough history focusing on identification of symptomatic arrhythmias and exercise-associated symptoms.[11] Note the following:

  • Patients with ventricular ectopy may present with dizziness, palpitations, chest pain, or syncope, all of which should be explored.
  • Recreational and prescribed drug use may increase the risk of ventricular ectopy. Cocaine use is of specific concern because it can lead to coronary perfusion abnormalities. The extensive list of medications that can prolong the QT interval are also of specific concern.
  • Genetic influences may be present, such as long QT syndrome, Brugada syndrome, or inherited cardiomyopathies; therefore, the family history should be explored for syncope, arrhythmia, or sudden death, especially in young people. A family history of congenital deafness associated with syncope, palpitations, or sudden death should raise the suspicion of Jervell and Lange-Nielsen inherited long QT syndrome. Often, the family history does not clearly indicate a cardiac cause but simply shows unexplained deaths, such as drownings, early "heart attacks," or single motor vehicle accidents. Occasionally, the syncope and myoclonic movements that can be seen with long QT syndrome–associated arrhythmias are misdiagnosed as seizures.
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Physical

Focus the physical examination on detection of structural heart disease because these patients may be at increased risk of malignant ventricular arrhythmias. Note the following:

  • Conditions such as long QT or Brugada syndromes may not have any physical examination correlates, although congenital nerve deafness is associated with Jervell and Lange-Nielsen syndrome.
  • Signs of congestive heart failure, low cardiac output, myocarditis, abnormal heart sounds, or cholesterol deposits may indicate underlying conditions that increase the risk of serious ventricular arrhythmias.
  • Identify findings compatible with hypertrophic cardiomyopathy and ventricular outflow obstructive lesions (eg, aortic stenosis).
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Causes

Various factors can lead to the lowering of the ventricular fibrillation threshold and, thus, increase the likelihood of an arrhythmia proceeding to ventricular fibrillation. These precipitating factors include electrolyte abnormalities, proarrhythmic medications, alterations in the sympathetic-parasympathetic balance (particularly increased catecholamines), hypothermia or hyperthermia, primary electrical disease (eg, long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia), and hypoxia/ischemia. These variables may influence myocardial susceptibility to an R-on-T phenomenon, causing depolarization of partially repolarized tissue, potentially initiating ventricular fibrillation.

Ventricular tachycardias

Because ventricular fibrillation is usually a degeneration of ventricular tachycardias, the role ventricular tachycardias play in the evolution of the rhythm disturbance must be considered.

The triggers for ventricular tachycardia are diverse. For more information, see Ventricular Tachycardia and Cardiomyopathy, Hypertrophic.

Briefly, the triggers for ventricular tachycardia include a long QT interval (eg, congenital, acquired), drug use (eg, digoxin, antiarrhythmics, antidepressants, phenothiazines, terfenadine, erythromycin), alcohol intake, metabolic imbalance (eg, electrolytes, hypoxia, acidemia), coronary artery disease, myocarditis, cardiomyopathy (eg, idiopathic, hypertrophic cardiomyopathy, Chagas disease), mitral valve prolapse(possibly), intracardiac tumors, and congenital heart disease, especially postsurgical interventions.[12, 13]

Wolff-Parkinson-White syndrome

Atrial fibrillation (AF) in the presence of an accessory pathway (bypass tract) that allows extremely rapid antegrade stimulation of the ventricle (>300 beats per minute [bpm]) presents a potential risk for degeneration to ventricular fibrillation in patients with Wolff-Parkinson-White (WPW) syndrome. The risk of rapidly conducting AF depends on the conduction and refractory characteristics of the accessory pathway. These electrophysiologic properties may vary during the day (eg, with catecholamine state associated with exertion, anxiety), by age, and with other clinical variables.

Commotio cordis

Commotio cordis is an uncommon syndrome of abrupt ventricular fibrillation following blunt chest wall trauma that typically occurs in young participants in sports (notably, ice hockey, lacrosse, baseball, and softball).[14, 15, 16]

Commotio cordis is unusual and appears to particularly affect individuals aged 5-15 years; boys are affected more often than girls. Whether this is secondary to increased participation of boys in higher-risk sports activities or differences inherent to each sex is unclear.

Commotio cordis is characterized by a relatively low-energy impact that does not cause structural damage to the chest wall, myocardium, coronary arteries, or elsewhere within the thorax. Ventricular fibrillation is the most common rhythm recorded after an event, although complete heart block and idioventricular rhythms have also been observed. Commotio cordis is notably difficult to convert to sinus rhythm, and survival rates from this type of arrhythmic event are unfortunately quite low.

In an animal study by Link et al, timing of low-energy chest wall impact was coordinated with the cardiac cycle.[15] They found that ventricular fibrillation could be produced when impact occurred at 15-30 milliseconds before the peak of the T wave on ECG; it was not produced at any other time during the cardiac cycle. Ventricular fibrillation was initiated at the time of impact and was not preceded by ventricular ectopy, ischemic changes in ECG, or heart block.

Whether individual susceptibility to commotio cordis occurs or whether it is solely an issue of an electrical timing vulnerability remains unclear. Regardless, survivors of commotio cordis are recommended to wear adequate chest protection during future contact sports participation.

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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.

References
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  2. Mogayzel C, Quan L, Graves JR, et al. Out-of-hospital ventricular fibrillation in children and adolescents: causes and outcomes. Ann Emerg Med. 1995 Apr. 25(4):484-91. [Medline].

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  13. Leenhardt A, Lucet V, Denjoy I, et al. Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients. Circulation. 1995 Mar 1. 91(5):1512-9. [Medline].

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  19. Berg RA, Samson RA, Berg MD, et al. Better outcome after pediatric defibrillation dosage than adult dosage in a swine model of pediatric ventricular fibrillation. J Am Coll Cardiol. 2005 Mar 1. 45(5):786-9. [Medline].

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  21. Valdes SO, Donoghue AJ, Hoyme DB, et al. Outcomes associated with amiodarone and lidocaine in the treatment of in-hospital pediatric cardiac arrest with pulseless ventricular tachycardia or ventricular fibrillation. Resuscitation. 2014 Mar. 85(3):381-6. [Medline].

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