Ventricular Fibrillation

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 VF, which may be difficult to distinguish from asystole  The rhythm is maintained by multiple reentrant circuits because portions of the myocardium are constantly depolarizing. It 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.

Frequency:

• The incidence of VF from all causes is very low in the pediatric population. In studies of pediatric cardiac arrests, VF was the first identified rhythm in 6-19% of patients, with asystole or pulseless electrical activity (PEA) as the most frequent first identified rhythm. The overall incidence is likely to be higher because cardiac rhythms frequently change during an arrest, and VF may have preceded asystole in some patients.

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

Race: Although there are some predisposing factors that may demonstrate genetic trends, VF can be observed throughout all populations.

Sex: Vulnerability to VF is not significantly different between the sexes, although, at least in adults, torsade de pointes is more commonly observed in females than 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 those with known cardiac disease; however, patients with congenital heart disease may encounter increasing risk of arrhythmias with surgical intervention and as they age. Although terminal rhythms are often not known in sudden death populations, VF may represent a final common pathway for these patients.

• There are various forms of congenital heart disease that 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 VT and VF vulnerability in this population, as the sudden death is presumed to be of arrhythmic etiology.

• Because VF is usually a degeneration of ventricular tachycardias, one must consider the role these play in the evolution of the rhythm disturbance. The triggers for VT are multiple and diverse; they are expanded upon in the articles  Briefly, the triggers for VT include long QT (eg, congenital, acquired), drugs (eg, digoxin, antiarrhythmics, antidepressants, phenothiazines, alcohol, terfenadine, erythromycin), metabolic imbalance (eg, electrolytes, hypoxia, acidemia), coronary artery disease, myocarditis, cardiomyopathy (eg, idiopathic, hypertrophic cardiomyopathy, Chagas disease), possibly mitral valve prolapse, intracardiac tumors, and congenital heart disease, especially postsurgical interventions.

• 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 bpm) presents a potential risk for degeneration to VF. The risk of rapidly conducting AF is dependent 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 sports participants (notably ice hockey, lacrosse, baseball, softball).

• The condition is unusual and appears to particularly affect individuals aged 5-15 years, with boys afflicted 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. VF is the most common rhythm recorded after an event, although complete heart block and idioventricular rhythms also have been observed. Commotio cordis is notably difficult to convert to sinus rhythm, and survival from this tragic type of arrhythmic event is unfortunately quite poor.

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

• It is not yet clear whether an individual susceptibility to commotio cordis exists or whether it is solely an electrical timing vulnerability issue. Regardless, survivors of commotio cordis are recommended to wear adequate chest protection during future contact sports participation.

Other Problems to be Considered:

Torsade de pointes
Asystole
Electrocardiographic artifact (electrode/lead failure)

Lab Studies:

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

• Electrolytes: In particular, serum magnesium, potassium, and calcium are most relevant to ventricular arrhythmia vulnerability.

• Blood gas, particularly the pH, as acidemia promotes arrhythmia susceptibility.

• The clinician may want to obtain drug levels, particularly any of the medications that may prolong the QT interval, as well as any pro-antiarrhythmic agents to which the patient may have been exposed. Medications such as procainamide and amiodarone have arrhythmogenic potential, as do many anti-arrhythmic drugs.

• Toxicology screen: In particular, stimulant drugs of abuse, such as cocaine and amphetamines, may promote ventricular arrhythmias. Other illicit drugs, including phencyclidine, LSD, "ecstasy," and even marijuana may also increase vulnerability to arrhythmias, including VF. Legal stimulants, such as caffeine, theophylline, and pseudoephedrine, may also promote ventricular arrhythmias, particularly in individuals with an underlying susceptibility.

Imaging Studies:

• Chest radiograph

• Echocardiogram

• Cardiac MRI, particularly concentrating on potential for arrhythmogenic right ventricular dysplasia. Fibrofatty infiltration may be evident in patchy distribution within the right (and sometimes left) ventricle.

Other Tests:

• ECG

• Holter monitor

• Event monitor

• Perform additional tests as indicated based on suspected precipitating factors. Provocative testing to elicit arrhythmias may be helpful in determination of the electrophysiological 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 utilized to provoke ventricular arrhythmias in potentially susceptible individuals. In addition, infusion of sodium channel blocking antiarrhythmic drugs, such as ajmaline or procainamide, has been utilized for provocation of an electrocardiographic phenotype of Brugada syndrome. These tests may increase sensitivity of identification of vulnerable individuals, although specificity might be sacrificed. The value of these provocative tests has not yet been fully defined in pediatrics.

Procedures:

• Electrophysiologic studies

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

• Pharmacological provocation studies also may be utilized during EP study, such as isoproterenol or other catecholaminergic agents for arrhythmia induction. Medications that may promote ECG signatures for specific disease states, such as a type I antiarrhythmic agent (eg, flecainide, ajmaline), may be administered to unmask the classic ECG pattern of the Brugada syndrome.

• However, because of limited diagnostic predictive value, negative EP study findings do not rule out the possibility of a sudden cardiac event in the future, particularly in patients with structural congenital heart disease.

Activity: Restrictions on activity are dictated by the conditions that may have led to VF, for example, the arrhythmias in long QT syndrome or catecholaminergic ventricular tachyarrhythmias may be triggered by exercise.

Patients who have been resuscitated from VF arrests should be evaluated for risk of recurrence. If VF was secondary to degeneration of another arrhythmia that may recur, medication and other therapies (eg, radiofrequency catheter ablation [RFCA], pacemaker placement, automatic ICD [AICD], surgery) may be aimed at prevention of that arrhythmia. This would likely be arrhythmias that occurred without evidence of severe electrolyte disturbance, metabolic derangement, hypoxia, myocardial infarction (MI), or drug toxicity. These medications are discussed in Ventricular Tachycardia. Some evidence suggests that vasopressin may play a role in the treatment of adult shock-refractory VF; however, the safety and efficacy of this drug in children has not been evaluated.

Drug Category: Antiarrhythmic agents -- These agents alter the electrophysiologic mechanisms responsible for arrhythmia. When used during cardiac arrest, follows administration of epinephrine and attempted defibrillation.

Drug Name	Amiodarone (Cordarone) -- May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.
Adult Dose	Cardiac arrest: 300 mg IV bolus; may repeat with 150 mg in 2-5 min; not to exceed 2.2 g/d
Pediatric Dose	Cardiac arrest: 5 mg/kg bolus IV/IO
Contraindications	Documented hypersensitivity; complete AV block, if pacemaker not in place; intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Interactions	Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels; avoid use with other drugs that prolong QT interval
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in thyroid, kidney or liver disease; may cause hypotension; may prolong QT interval and increase risk for polymorphic VT

Drug Name	Lidocaine (Xylocaine) -- Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Consider as alternate treatment for VF or pulseless VT.
Adult Dose	1-1.5 mg/kg IV bolus over 2-3 min; may repeat doses of 0.5-0.75 mg/kg in 5-10 min; not to exceed a cumulative dose of 3 mg/kg Maintain with continuous infusion: 30-50 mcg/kg/min IV (typically 1-4 mg/min)
Pediatric Dose	Loading dose: 1 mg/kg IV/IO/ET; may repeat in 10-15 min for 2 doses Maintain with continuous infusion: 20-50 mcg/kg/min IV/IO
Contraindications	Documented hypersensitivity; Adams-Stokes syndrome and Wolff-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block, if artificial pacemaker not in place
Interactions	Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly or very young patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities; reduce maintenance dose with liver impairment or low CO that is compromising hepatic and renal blood flow

Drug Name	Magnesium sulfate -- Used for suspected hypomagnesemia or torsade de pointes. Consider use in refractory VT following lidocaine.
Adult Dose	Cardiac arrest: 1-2 g IV rapid bolus over 5 min (dilute prior to administration)
Pediatric Dose	25-50 mg/kg IV/IO infusion (administer over 10-20 min); not to exceed 2 g/dose
Contraindications	Documented hypersensitivity; heart block, if pacemaker not in place; Addison disease, myocardial damage, or severe hepatitis
Interactions	Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Pregnancy	A - Safe in pregnancy
Precautions	Magnesium may alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering magnesium dose because may produce significant hypotension or asystole; in overdose, calcium gluconate (10-20 mL IV of 10% solution) can be given as antidote for clinically significant hypermagnesemia; may cause hypotension and bradycardia with rapid administration; caution in renal failure (adjust dose)

Drug Category: Vasopressors -- Patients most likely to respond adequately are those in whom physiological parameters (eg, urine flow, myocardial function, blood pressure) have not profoundly deteriorated.

Drug Name	Epinephrine (Adrenalin) -- Used for asystole or pulseless arrest. Also used for symptomatic bradycardia unresponsive to oxygen and ventilation.
Adult Dose	1 mg (10 mL of 1:10,000 solution) rapid IV bolus q3-5min or 0.1 mg/kg IVP q3-5min; higher doses up to 0.2 mg/kg may be used if 1 mg dose fails Alternatively, 2-2.5 mg ET (dilute in 10 mL normal saline)
Pediatric Dose	0.01 mg/kg (1:10,000; 0.1 mL/kg) IV/IO; may repeat with higher doses of 0.1-0.2 mg/kg (1:1000; 0.1-0.2 mL/kg) q3-5min Alternatively; 0.1 mg/kg (1:1000; 0.1 mL/kg) ET
Contraindications	Documented hypersensitivity; cardiac arrhythmias, angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue
Interactions	Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in elderly persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Further Inpatient Care:

• Evaluate patients presenting with VF arrest or averted sudden death for evidence of risk of repeated events . Appropriate follow-up care is determined by any substrate for further arrhythmia that is identified.

Transfer:

• 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 EP laboratory may be required.

Prognosis:

• The short-term prognosis of a patient with VF is primarily dictated by time to defibrillation, and long-term issues are modulated by any underlying conditions that may have led to the VF event. One study demonstrated a good outcome in 17% of patients presenting with cardiac arrest and VF, all of whom had early defibrillation.

Patient Education:

• It is essential that the families of patients with life-threatening arrhythmias, such as VF, be competent in bystander cardiopulmonary resuscitation (CPR); they must be aware of the need for early defibrillation.

• Any patient who has averted sudden death or has been identified as at risk for such an event is likely to require psychological support and counseling, as may family members.

• Driving can be an issue in adolescents with life-threatening arrhythmias. Individual states have restrictions that must be followed, which often are based on a certain length of time the driver is free of any event.

• In patients with long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, familial dilated or hypertrophic cardiomyopathy, and other inherited arrhythmia disorders, family members also should be evaluated for presence of the disease.

Constructed by Dr N.A. Nematallah Consultant in perioperative medicine and intensive therapy, Al Razi Orthopedic Hospital , State of Kuwait, email : razianesth@freeservers.com