eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Ventricular Fibrillation

Author: Elizabeth A Stephenson, MD, MSc, Assistant Professor of Pediatrics, University of Toronto; Consulting Staff, Division of Cardiology, The Hospital for Sick Children
Coauthor(s): Charles Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Contributor Information and Disclosures

Updated: Jul 17, 2008

Introduction

Background

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

Pathophysiology

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 Media file 1). 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

Frequency

United States

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.

Mortality/Morbidity

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.

Race

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

Sex

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.

Age

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

Clinical

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

• 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 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.

Physical

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

• Conditions such as long QT syndrome 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).

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), 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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