Pediatric Ventricular Fibrillation Workup

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

Laboratory Studies

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

Note the following:

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

  • Blood gases: Blood gases, particularly pH, are determined because acidemia promotes arrhythmia susceptibility.

  • Drug levels: Clinicians may want to obtain drug levels, particularly to assess for any of the medications that may prolong the QT interval and any proantiarrhythmic agents to which the patient may have been exposed. Medications such as procainamide and amiodarone have arrhythmogenic potential, as do many antiarrhythmic drugs.

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

  • Genetic testing: Extensive research is ongoing regarding identification of cardiac channelopathies which cause many of the primary electrical diseases. Commercial testing is becoming available for some of these channelopathies; however, many genetic variants have yet to be identified.

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Imaging Studies

Obtain the following imaging studies:

  • Chest radiography

  • Echocardiography

  • Cardiac MRI: This should particularly concentrate on the potential for arrhythmogenic right ventricular dysplasia. Fibrofatty infiltration may be evident in patchy distribution within the right, and sometimes left, ventricle.

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Other Tests

Other studies include the following:

  • Electrocardiography: A 12-lead ECG is most helpful in formulating differential diagnoses following ventricular fibrillation arrest.

  • Holter monitor

  • Event monitor

Additional tests indicated based on suspected precipitating factors, such as the following:

  • Provocative testing to elicit arrhythmias may be helpful in determining the electrophysiologic 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 used to provoke ventricular arrhythmias in individuals with potential susceptibility.

  • In addition, infusion of sodium channel blocking antiarrhythmic drugs, such as ajmaline or procainamide, has been used to provoke an electrocardiographic phenotype of Brugada syndrome.

  • These tests may increase sensitivity in the identification of individuals with potential susceptibility, although specificity may be sacrificed. The value of the use of these provocative tests in pediatric patients has not yet been fully defined.

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Procedures

Electrophysiologic studies

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

Pharmacologic provocation studies (eg, using isoproterenol or other catecholaminergic agents for arrhythmia induction) may also be used during an EP study. Medications that may promote ECG signatures for specific disease states, such as a type I antiarrhythmic agents (eg, flecainide, ajmaline), may be administered to unmask the classic ECG pattern found in patients with Brugada syndrome.

Because diagnostic predictive value is limited, negative EP study findings do not exclude the possibility of a sudden cardiac event in the future, particularly in patients with structural congenital heart disease.

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