Pediatric Tachycardia Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.^[10]

Class Summary

Alter the electrophysiologic mechanisms responsible for arrhythmia.

Adenosine (Adenocard)

First-line medical treatment for termination of PSVT. Short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. Effective in terminating both AVNRT and AVRT. More than 90% of patients convert to sinus rhythm with adenosine 12 mg. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion.

Procainamide (Pronestyl)

Class I-A antiarrhythmic. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. Indicated in recurrent VT not responsive to lidocaine, refractory SVT, refractory VF, pulseless VT, and AF with rapid rate in WPW.

Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Total digitalizing dose (TDD): Initially administer 50%; then, administer the remaining two 25% portions at 6-12 h intervals (ie, 1/2, 1/4, 1/4).

Propranolol (Inderal)

Class II antiarrhythmic. Nonselective, beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. Do not administer IV dose faster than 1 mg/min.

Epinephrine (Adrenalin)

Has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects. Indicated for ventricular fibrillation and pulseless VT (after defibrillation).

Amiodarone (Cordarone)

Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit A-V conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.

Has low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.

Lidocaine (Xylocaine)

Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Magnesium sulfate

DOC for torsade de pointes, it also may be useful to treat conventional VT, especially where hypomagnesemia is confirmed. When treating with magnesium sulfate, monitor for hypermagnesemia since an overdose can cause cardiorespiratory collapse and paralysis.