Pediatric Ventricular Fibrillation Treatment & Management
- Author: Elizabeth A Stephenson, MD, MSc; Chief Editor: Howard S Weber, MD, FSCAI more...
Evaluate patients presenting with ventricular fibrillation arrest or averted sudden death for evidence of risk of repeated events (see Workup).
Appropriate follow-up care is determined by any substrate for further arrhythmia that is identified.
Resuscitation from ventricular fibrillation is occasionally successful if performed in a timely fashion; the longer the myocardium is allowed to fibrillate, the more difficult conversion to a sinus rhythm becomes. The use of antiarrhythmics, such as lidocaine and amiodarone, may assist in maintaining sinus rhythm once successful defibrillation is achieved. Note that bretylium has been removed from the current American Heart Association (AHA) pediatric advanced life support (PALS) pulseless arrest guidelines, secondary to risk of hypotension and unclear efficacy.[17, 18]
The AHA recommendations for treatment in pediatric patients with pulseless (ventricular tachycardia/ventricular fibrillation/PEA) arrest are as follows:
Perform cardiac and pulmonary rehabilitation (CPR).
Support ABCs, and provide airway management with 100% oxygen.
Additionally, if ventricular fibrillation or pulseless ventricular tachycardia occurs, use the following methods:
Defibrillate with 2 J/kg, 4 J/kg, and 4 J/kg.
Administer epinephrine intravenously (IV) or intraosseously (IO) at a rate of 0.01 mg/kg (1:10000, 0.1 mL/kg) or via endotracheal tube (ET) at a rate of 0.1 mg/kg (1:1000, 0.1 mL/kg)
Identify and treat causes.
Defibrillate with 4 J/kg within 30-60 seconds after each medication.
Consider treatment with one of the following antiarrhythmics:
- Amiodarone 5 mg/kg bolus IV/IO
- Lidocaine 1 mg/kg IV/IO/ET
- Magnesium 25-50 mg/kg IV/IO (not to exceed 2 g) for torsade de pointes or hypomagnesemia
Defibrillate with 4 J/kg within 30-60 seconds after medication infusion.
Defibrillation is the definitive treatment for ventricular fibrillation. Electric shocks (delivered in an asynchronous fashion for ventricular fibrillation) are aimed at depolarizing the myocardium to terminate the fibrillating rhythm and allow an intrinsic cardiac pacemaker to resume control. If the shocks delivered have successfully terminated ventricular fibrillation or ventricular tachycardia, defibrillation has been achieved.
Several factors can influence whether attempts at defibrillation are successful, including transthoracic impedance, paddle placement, energy dose, type of waveform used, and metabolic environment. Note the following:
Impedance: The electrical impedance of the defibrillating circuit is affected by paddle size and the electrode–chest wall interface. Larger paddles reduce impedance, but paddles or electrodes cannot be in contact with one another or bridging can occur and the electrical current is shunted and does not travel through the patient. Similarly, use electrode cream generously to lower the high impedance of the skin and to avoid serious skin burns.
Placement of paddles: The goal of paddle placement is to direct most of the electric current through as much myocardium as possible.
- In larger children, this is usually achieved by placing the paddles in the standard adult position of one paddle over the right upper chest and the other paddle over the apex of the heart. However, paddles may also be placed in the anterior-posterior or, alternately, in the side-to-side position. This may allow larger paddles to be used in children when pediatric paddles are not available.
- Rarely, simultaneous defibrillation may be necessary through two separate pairs of pads/paddles because of markedly high defibrillation energy requirements (>360 J).
- In children with congenital heart disease, recognizing that the heart may not be located in the left hemithorax is important. In this case, if the cardiac position is known, attempt to position the paddles to capture as much myocardium as possible.
Energy dose: Standard energy recommendations are 2 J/kg for the first shock, followed by 4 J/kg for subsequent shocks if defibrillation is not achieved with the first dose. If the patient is successfully defibrillated but ventricular fibrillation resumes, the energy dose does not need to be increased because a critical mass of myocardium was captured with the first shock. At that point, concentrating on improving the metabolic environment and raising the myocardial fibrillation threshold becomes important. Some antiarrhythmic medications may affect the defibrillation threshold; therefore, the defibrillation dose may need to be modified, particularly if the initial attempts are unsuccessful. 
Waveform: Defibrillators use biphasic or monophasic waveforms; biphasic waveforms have been shown to be more effective at lower energy doses and have a lower probability of defibrillation thresholds than monophasic waveforms. Recently, biphasic waveforms have been used more frequently in modern external defibrillators than monophasic waveforms, although both modalities are effective.
Metabolic environment: The metabolic environment influences the ability to defibrillate the patient and the ability to maintain a perfusing rhythm after successful defibrillation. Thus, while correction of hypoxia, acidosis, and pharmacologic therapy should not delay the initiation of electric shocks, concomitant therapy aimed at correction of these factors should be attempted.
Automated external defibrillators (AEDs) have been introduced into communities and adult populations. AEDs offer the opportunity to vastly improve outcomes from cardiac arrests, primarily by providing earlier defibrillation.
Currently, AEDs are standardized for adult resuscitation and, until 2001, were not recommended for use in children younger than 8 years. Work by Cecchin et al has shown a high specificity and sensitivity for ventricular fibrillation and nonshockable rhythms in a pediatric population using an adult-based algorithm. Recently in a swine model, Berg et al demonstrated that outcomes were improved using pediatric rather than adult electrical dosages. This may indicate that AEDs are indeed accurate (in algorithm-based rhythm diagnosis) for use in all age groups, and using AEDs with pediatric pads or cables may improve survival rates following ventricular fibrillation arrests.
The US Food and Drug Administration (FDA) has approved AED models for use in children. These systems incorporate the option of pediatric-modified pads or cables. If the pediatric output is plugged into the AED, the system decreases the output current to approximately one third of the standard 150-J output for adult AED defibrillation.
Consult with a pediatric electrophysiologist.
A patient who has experienced any life-threatening arrhythmia should have an electrophysiologic evaluation, ideally by a pediatric electrophysiologist; transfer to a facility with appropriate staff and an EP laboratory may be required.
In addition to therapy with medications, implantable cardioverter-defibrillators (ICDs) are often indicated in patients who have survived ventricular fibrillation arrest. Note the following:
The use of ICDs has dramatically expanded since the first human implant in 1980 and has changed the clinical treatment of patients with malignant ventricular arrhythmias. Technological advances are rapidly improving the features available with ICDs and expanding the indications and patient populations in which they can be used.
Originally, ICDs were quite large and required a sternotomy or thoracotomy for implantation. Therefore, usage was limited in the pediatric population, especially in small patients.
Modern devices are significantly smaller than the original devices, allowing for nonthoracotomy implantation, even in smaller patients. Features may include high- and low-energy defibrillation, as well as antibradycardia and antitachycardia pacing.
Modern devices can be deployed through epicardial patch or transvenous lead placement, although the transvenous route may be limited in the smallest patients secondary to the lead-to-vessel lumen ratio. Patients with congenital heart disease with significant intracardiac shunting or single ventricle anatomy would also be most likely to have an ICD placed via the epicardial route.
Current technology allows the ICD generator to be used as part of the defibrillation circuit (ie, "hot can"), thereby lowering defibrillation thresholds. The lead has several parts, including 1 or 2 coils for internal defibrillation, pacing and sensing electrodes for detection of ventricular rate and rhythm, and antibradycardia and antitachycardia pacing. Subcutaneous arrays can also be used, when necessary, in patients who have demonstrated high defibrillation thresholds. In unique circumstances, such as infants, a subcutaneous array has been used alone without a transvenous shocking coil or epicardial patch. This technique has been successfully demonstrated in both an immature piglet model and a series of pediatric patients. 
The ICD generators use lithium batteries with an average lifespan of 4-8 years and may use monophasic or biphasic pulses. A biphasic pulse often results in lower defibrillation thresholds; therefore, a biphasic pulse is typically preferred.
No specific diet restrictions are recommended for management or prevention of ventricular fibrillation beyond the nutritional recommendations for prevention of coronary artery disease.
Restrictions on activity are dictated by the conditions that may have led to ventricular fibrillation; for example, the arrhythmias in long QT syndrome or catecholaminergic ventricular tachyarrhythmias may be triggered by exercise.
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].