Pediatric Ventricular Fibrillation

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Ventricular fibrillation (VF) is rare in the pediatric population; when it does occur, ventricular fibrillation is usually a degeneration of other malignant arrhythmias, such as ventricular tachycardia (VT). The period of arrhythmia may not be extensive, but ventricular fibrillation that occurs without a few initial beats of ventricular tachycardia is unusual. In adults, ventricular fibrillation is preceded by ventricular tachycardia in approximately 80% of cases. [1]

Primary ventricular fibrillation is uncommon in children. In a study of pediatric out-of-hospital arrests, ventricular fibrillation was the initial recorded rhythm in 19% of cardiac arrests. [2] Causes of ventricular fibrillation varied and included medical illness, overdose, drowning, and trauma; only 2 of 29 patients had congenital heart disease. Thus, ventricular fibrillation as a terminal rhythm in cardiac arrest may result from various causes. [3]

The outcome in patients with ventricular fibrillation is better than in patients with asystole or pulseless electrical activity (PEA), and outcome may be further improved by prompt recognition and treatment of ventricular fibrillation. In a population of patients with known ventricular arrhythmias, individuals who had ventricular fibrillation were more likely to have underlying significant heart disease (eg, cardiac tumors, long QT syndrome, structural congenital heart disease) than patients with ventricular tachycardia. [4]

After initial resuscitation, therapy in patients with ventricular fibrillation is primarily focused on preventing the antecedent ventricular tachycardias. However, technologic advances in both implantable and external automated defibrillators have made these devices an important part in the management of malignant ventricular arrhythmias. [5]

The electrical activity in ventricular fibrillation is characterized by chaotic depolarization of cells throughout the ventricular myocardium. The lack of coordinated depolarization prevents effective contraction of the myocardium and, thus, ejection of blood from the heart. Surface ECG demonstrates no identifiable QRS complexes, although a wide range of amplitude of electrical activity is present, from sine-wave ventricular flutter to fine ventricular fibrillation, which may be difficult to distinguish from asystole (see image below). This arrhythmia is maintained by multiple re-entrant circuits because portions of the myocardium are constantly depolarizing. Ventricular fibrillation may be initiated when an area of myocardium has refractory and conducting portions, and, as in any reentrant circuit, this combination promotes a self-sustaining rhythm. [6]

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The incidence of ventricular fibrillation from all causes is very low in the pediatric population. In studies of pediatric cardiac arrests, ventricular fibrillation was the first identified rhythm in 6-19% of patients, with asystole or PEA as the most frequent rhythm identified first. [7, 8] Overall incidence is likely to be higher because cardiac rhythms frequently change during an arrest, and ventricular fibrillation may have preceded asystole in some patients.


The short-term prognosis of a patient with ventricular fibrillation is primarily dictated by time to defibrillation, and long-term issues are modulated by any underlying conditions that may have led to the ventricular fibrillation event.

One study demonstrated a good outcome in 17% of patients presenting with cardiac arrest and ventricular fibrillation, all of whom had early defibrillation. [9]


Without prompt and aggressive therapy, sustained ventricular fibrillation is uniformly lethal. Polymorphic ventricular tachycardia (eg, torsade de pointes) may be sustained or nonsustained, and morbidity is related to the duration of the arrhythmia and to the cardiac output. Some ventricular arrhythmias allow adequate cardiac ejection for a limited period, but once a rhythm degenerates to ventricular fibrillation, ejection is minimal. Until the rhythm is converted, cardiac output is not effective; thus, patients are extremely vulnerable to ischemia and death. [3] In one study, 17% of patients with cardiac arrest and a presenting rhythm of ventricular fibrillation had a good outcome (ie, absent or mild disability), all of whom received early defibrillation. [9] Clearly, early defibrillation is essential to a good outcome.

Although some predisposing factors may demonstrate genetic trends, ventricular fibrillation can be observed throughout all populations.

Vulnerability to ventricular fibrillation is not significantly different between males and females, although, at least in adults, torsade de pointes is more commonly observed in females than in males. In preadolescent children, this sex difference in QT interval range and propensity to torsade de pointes is not evident.

Sudden cardiac death is unusual in pediatric populations, even in children with known cardiac disease; however, patients with congenital heart disease may encounter increasing risk of arrhythmias with or without surgical intervention and as they age. Although terminal rhythms are not often documented in sudden death populations, ventricular fibrillation may represent a final common pathway for these patients.

Various forms of congenital heart disease have been associated with an increased incidence of late sudden death, including tetralogy of Fallot, aortic stenosis, and the atrial switch operations for D-transposition of the great arteries. This may represent an increased incidence of both ventricular tachycardia and ventricular fibrillation vulnerability in this population because the sudden death is presumed to be of arrhythmic etiology. [10]

Safranek DJ, Eisenberg MS, Larsen MP. The epidemiology of cardiac arrest in young adults. Ann Emerg Med. 1992 Sep. 21(9):1102-6. [Medline].

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].

Walsh CK, Krongrad E. Terminal cardiac electrical activity in pediatric patients. Am J Cardiol. 1983 Feb. 51(3):557-61. [Medline].

Pedersen DH, Zipes DP, Foster PR, Troup PJ. Ventricular tachycardia and ventricular fibrillation in a young population. Circulation. 1979 Nov. 60(5):988-97. [Medline].

Cecchin F, Jorgenson DB, Berul CI, et al. Is arrhythmia detection by automatic external defibrillator accurate for children?: sensitivity and specificity of an automatic external defibrillator algorithm in 696 pediatric arrhythmias. Circulation. 2001 May 22. 103(20):2483-8. [Medline].

Vlay S. A Practical Approach to Cardiac Arrhythmias. Boston, MA: Little Brown & Co; 1996.

Benson DW Jr, Benditt DG, Anderson RW, et al. Cardiac arrest in young, ostensibly healthy patients: clinical, hemodynamic, and electrophysiologic findings. Am J Cardiol. 1983 Jul. 52(1):65-9. [Medline].

Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol. 1985 Jun. 5(6 Suppl):118B-121B. [Medline].

Garson A Jr, Smith RT, Moak JP, et al. Ventricular arrhythmias and sudden death in children. J Am Coll Cardiol. 1985 Jun. 5(6 Suppl):130B-133B. [Medline].

Berul CI, Hill SL, Geggel RL, et al. Electrocardiographic markers of late sudden death risk in postoperative tetralogy of Fallot children. J Cardiovasc Electrophysiol. 1997 Dec. 8(12):1349-56. [Medline].

Alexander ME, Berul CI. Ventricular arrhythmias: when to worry. Pediatr Cardiol. 2000 Nov-Dec. 21(6):532-41. [Medline].

Morady F, Scheinman MM, Hess DS, et al. Clinical characteristics and results of electrophysiologic testing in young adults with ventricular tachycardia or ventricular fibrillation. Am Heart J. 1983 Dec. 106(6):1306-14. [Medline].

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].

Link MS. Commotio cordis: sudden death due to chest wall impact in sports. Heart. 1999 Feb. 81(2):109-10. [Medline].

Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med. 1998 Jun 18. 338(25):1805-11. [Medline].

Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med. 1995 Aug 10. 333(6):337-42. [Medline].

American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005 Dec 13. 112(24 Suppl):IV1-203. [Medline]. [Full Text].

American Heart Association. 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: pediatric advanced life support. Pediatrics. 2006 May. 117(5):e1005-28. [Medline]. [Full Text].

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].

Stephenson EA, Batra AS, Knilans TK, et al. A multicenter experience with novel implantable cardioverter defibrillator configurations in the pediatric and congenital heart disease population. J Cardiovasc Electrophysiol. 2006 Jan. 17(1):41-6. [Medline].

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].

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.

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, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, Society for Pediatric Research

Disclosure: Received research grant from: Medtronic.

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

Disclosure: Nothing to disclose.

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: Society for Cardiovascular Angiography and Interventions

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

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.

Pediatric Ventricular Fibrillation

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