eMedicine Specialties > Emergency Medicine > Pediatric

Pediatrics, Tachycardia

Mirna M Farah, MD, Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Division of Emergency Medicine, Children's Hospital of Philadelphia
Christine S Cho, MD, MPH,, Attending Physician, Division of Emergency Medicine, Children's Hospital and Research Center of Oakland; HS Assistant Clinical Professor, Department of Pediatrics, University of California, San Francisco School of Medicine

Updated: Sep 23, 2009

Introduction

Background

Tachycardia is an abnormal rapidity of heart action that usually is defined as a heart rate more than 100 beats per minute (bpm) in adults. In children, the normal heart rate is age dependent, and the definition of tachycardia varies, as shown below.1

  • Age 1-2 days - 123-159 bpm
  • Age 3-6 days - 129-166 bpm
  • Age 1-3 weeks - 107-182 bpm
  • Age 1-2 months - 121-179 bpm
  • Age 3-5 months - 106-186 bpm
  • Age 6-11 months - 109-169 bpm
  • Age 1-2 years - 89-151 bpm
  • Age 3-4 years - 73-137 bpm
  • Age 5-7 years - 65-133 bpm
  • Age 8-11 years - 62-130 bpm
  • Age 12-15 years - 60-119 bpm

Pathophysiology

The heart is innervated primarily by the vagus nerve and the sympathetic ganglion. Pain sensation travels through afferent fibers associated with the sympathetic ganglia. In most patients, the sensation of a normal heartbeat is not felt. Some children may complain of palpitations or rushing or pounding in the ears.

Clinical

History

  • Chest pain
  • Palpitations
  • Syncope
  • Dizziness
  • Shortness of breath
  • Diaphoresis (for infants—while feeding)
  • Color changes
  • Neurologic changes (mental status, motor/sensory deficits)
  • Decrease in intake and output
  • Trauma
  • Pain
  • Fever
  • Onset/duration of illness
  • Relationship to exercise, meals, and stress
  • Medical history, especially history of tachycardia or other cardiac problems
  • Medications - Amphetamines, cocaine, caffeine, ephedrine, antihistamines, phenothiazines, antidepressants, theophylline, appetite suppressants, albuterol
  • Allergies
  • Family history of sudden death, deafness (Jervell-Lange Nielsen syndrome) or cardiac disease

Physical

  • General appearance
  • Temperature
  • Heart rate
  • Respiratory rate
  • Blood pressure
  • Oxygen saturation
  • Assessment of pain
  • Decreased level of consciousness, decreased level of activity
  • Jugular venous distention
  • Neck mass
  • Dyspnea, increased work of breathing, retractions
  • Crackles, wheezing
  • Cardiac gallop
  • Cardiac murmur
  • Increased liver size
  • Abdominal mass
  • Decreased urine output
  • Poor peripheral perfusion (delayed capillary refill >2 sec, cool extremities, pallor)
  • Cyanosis
  • Edema

Causes

Tachycardia can be due to a physiologic response of the heart to noncardiac stimuli or to a true dysrhythmia.2,3

  • Hyperdynamic cardiac activity
    • Increased heart rate and contractility are physiologic responses to catecholamine release.
    • Catecholamine release may occur with stress or anxiety, exercise, fever or infection, pain, anemia, seizure, hypovolemia, hypoxia, drugs or medications/stimulants (eg, amphetamines, cocaine, caffeine, ephedrine, antihistamines, phenothiazines, antidepressants, tobacco, theophylline, general anesthesia), vasodilation (eg, anaphylaxis), oncologic mass (pheochromocytoma, neuroblastoma), hypoglycemia, hyperthyroidism, or acidosis.
  • True dysrhythmias
    • Supraventricular tachycardia (SVT)
      • Drug induced (eg, amphetamines, cocaine, caffeine, ephedrine, antihistamines, phenothiazines, antidepressants, tobacco, albuterol, theophylline, general anesthesia)
      • Wolff-Parkinson-White syndrome (WPW)
      • Hyperthyroidism
      • Congenital heart disease
      • Postoperative cardiac repair
      • Atrial ectopic tachycardia
    • Atrial fibrillation or atrial flutter
      • Drug induced
      • Wolff-Parkinson-White syndrome (WPW)
      • Postoperative cardiac repair
      • Congenital or rheumatic mitral disease
      • Hyperthyroidism
    • Junctional ectopic tachycardia (JET) - Postoperative cardiac repair
    • Ventricular tachycardia (VT)
      • Drug induced (eg, tricyclics, phenothiazines, antiarrhythmics, chloral hydrate, organophosphates, hydrocarbons, digoxin, amphetamines, cocaine, arsenic)
      • Prolonged Q-T syndrome/torsades de pointes
      • Myocarditis
      • Rheumatic fever
      • Mitral valve prolapse
      • Cardiomyopathy
      • Myocardial ischemia
      • Postoperative cardiac repair
      • Hyperkalemia (peaked T waves, prolonged QRS and QT intervals)
      • Hypocalcemia (increased QT intervals secondary to ST-segment prolongation)
      • Hypokalemia (especially in association with digoxin use due to its synergistic effects on automaticity and conduction)
      • Hypomagnesemia (associated with hypocalcemia and hypokalemia)
      • Cardiac tumors
      • Arrhythmogenic right ventricular dysplasia

Differential Diagnoses

Anemia, Chronic
Toxicity, Cocaine
Atrial Fibrillation
Toxicity, Cyclic Antidepressants
Atrial Flutter
Toxicity, Digitalis
Hyperthyroidism, Thyroid Storm, and Graves Disease
Toxicity, Hallucinogen
Hypoglycemia
Toxicity, Organophosphate and Carbamate
Pediatrics, Bacteremia and Sepsis
Toxicity, Sympathomimetic
Pediatrics, Dehydration
Toxicity, Theophylline
Pediatrics, Diabetic Ketoacidosis
Toxicity, Thyroid Hormone
Torsade de Pointes
Ventricular Tachycardia
Toxicity, Amphetamine
Wolff-Parkinson-White Syndrome
Toxicity, Anticholinergic
Toxicity, Antidepressant
Toxicity, Antihistamine

Workup

Laboratory Studies

Laboratory studies for tachycardia may include the following:

  • Electrolyte levels - Particularly potassium, bicarbonate, calcium, and magnesium
  • Blood glucose level
  • Complete blood count
  • Toxicology screen
  • Arterial blood gas measurement
  • Thyroid function tests
  • Urine catecholamine metabolites (homovanillic and vanillylmandelic acid)

Imaging Studies

Imaging studies for tachycardia may include the following:

  • Chest radiography (posteroanterior and lateral)
  • Echocardiogram


This ECG belongs to an asymptomatic 17-year-old m...

This ECG belongs to an asymptomatic 17-year-old male who was incidentally discovered to have Wolff-Parkinson-White (WPW) pattern. It shows sinus rhythm with evident preexcitation. To locate the accessory pathway (AP), the initial 40 milliseconds of the QRS (delta wave) are evaluated. Note that the delta wave is positive in lead I and aVL, negative in III and aVF, isoelectric in V1, and positive in the rest of the precordial leads. Therefore, this is likely a posteroseptal AP.


Other Tests

Other tests may include the following:

  • 12-lead electrocardiogram


This is a 12-lead ECG from an asymptomatic 7-year...

This is a 12-lead ECG from an asymptomatic 7-year-old boy with Wolff-Parkinson-White (WPW) pattern. Delta waves are positive in leads I and aVL; negative in II, III, and aVF; isoelectric in V1; and positive in the rest of the precordial leads. This again predicts a posteroseptal location for the accessory pathway (AP).


  • Cardiac rhythm strip
  • Holter monitoring
  • Event recorder
  • Electrophysiology testing

Treatment

Prehospital Care

  • Assess and stabilize airway, breathing, and circulation.
  • Administer oxygen.
  • Start intravenous (IV) fluids when indicated.
  • Place a cardiorespiratory monitor.

Emergency Department Care

Treatment depends on the condition of the patient and the etiology of the tachycardia.4 The child who appears ill with tachycardia requires rapid assessment for the presence of hypoxemia, shock, hypoglycemia, or life-threatening dysrhythmia.5

  • Assess and support airway and breathing as needed. Direct treatment of sinus tachycardia toward reversing the underlying medical condition.
  • Supraventricular tachycardia
    • Asymptomatic patients or those with mild heart failure
      • Ice to face and vagal maneuvers: The diving reflex causes peripheral vasoconstriction and a vagally mediated decrease in cardiac output.
      • Adenosine: Dose for infants and children is 0.1 mg/kg (not to exceed 6 mg/dose) rapid IV push; if ineffective, the dose can be doubled to 0.2 mg/kg (not to exceed 12 mg/dose). Complications may include bronchospasm (relatively contraindicated in patients with asthma), bradycardia, headache, shortness of breath, dizziness, and nausea.
      • Propranolol: Usual dose for children is 1 mg/kg/dose PO q6h (may initiate at 1 mg/kg/day PO divided q6h, then titrate upward).
      • Digoxin: Total digitalizing dose (initial dosing) is 10 mcg/kg IV in infants, 20 mcg/kg IV in older children; administer 1/2 dose stat, then 1/4 dose q8-12h X 2 (contraindicated in WPW).
      • Procainamide: 15-50 mg/kg/d PO divided in 6 doses
    • Patients with moderate heart failure
      • Ice and vagal maneuvers
      • Adenosine IV (see above)
      • Amiodarone: 5 mg/kg IV over 20-60 min or procainamide 15 mg/kg IV over 30-60 min (do not routinely administer amiodarone and procainamide together)
      • Cardioversion, synchronized: 0.5-1 J/kg, doubling dose prn (up to 2 J/kg)
      • Propranolol: 0.01-0.1 mg/kg slow IV over 10 min
      • Digoxin IV (see above)
      • Rapid atrial pacing (esophageal or intracardiac)
    • Patients with severe heart failure
      • Cardioversion, synchronized - Initial dose 0.5-1 J/kg (see above)
      • Adenosine IV (see above)
      • Amiodarone IV or procainamide IV (see above)
      • Propranolol IV (see above)
      • Digoxin IV (see above)
      • Rapid atrial pacing (esophageal or intracardiac)
  • Atrial fibrillation or flutter
    • For stable patients
      • Beta-blocker (eg, propranolol - 1 mg/kg/dose PO q6h)
      • Digoxin: Total digitalizing dose (initial dosing) is 10 mcg/kg IV in infants, 20 mcg/kg IV in older children; administer 1/2 dose stat, then 1/4 dose q8-12h X 2 (contraindicated in WPW).
      • Amiodarone: 5 mg/kg IV over 20-60 min
      • Cardioversion: 0.5-1 J/kg; may repeat prn up to a total dose of 2 J/kg. Administer cardioversion earlier if signs of severe cardiac failure manifest or if deterioration occurs during medical treatment. If patient is stable and presenting with >48 hours of signs of atrial dysrhythmia, consider anticoagulation prior to cardioversion.
    • For patients in shock
      • Immediate cardioversion: 0.5-1 J/kg; may repeat prn up to a total dose of 2 J/kg.
  • Ventricular tachycardia6
    • For stable patients, consider the following medications in consultation with a pediatric cardiologist:
      • Amiodarone: 5 mg/kg IV over 20-60 min or procainamide 15 mg/kg IV over 30-60 min (do not routinely administer amiodarone and procainamide together)
      • Cardioversion: 0.5 J/kg; may increase to 1 J/kg, then 2 J/kg if initial dose ineffective. Administer cardioversion earlier if signs of severe cardiac failure manifest or if deterioration occurs during medical treatment.
    • Patients in shock and those with pulseless VT or ventricular fibrillation
      • Assess ABCs and secure IV access.
      • Start cardiopulmonary resuscitation (CPR) and ventilate with 100% oxygen (Do not delay defibrillation with these interventions).
      • Defibrillate once with 2 J/kg. May use AED for children aged >1 year. Use the pediatric AED system, if available, for children aged 1-8 years.
      • Give 5 cycles of CPR.
      • Check rhythm and if shockable, defibrillate once with 4 J/kg.
      • Resume CPR immediately.
      • Administer epinephrine 0.01 mg/kg (1:10,000: 0.1 mL/kg) IV/IO or if via endotracheal tube (ET) 0.1 mg/kg (1:1000: 0.1 mL/kg). Repeat epinephrine q3-5min.7
      • Give 5 cycles of CPR.
      • Check rhythm and if shockable, defibrillate once with 4 J/kg.
      • Consider lidocaine 1 mg/kg IV/IO/ET bolus.
      • Consider amiodarone 5 mg/kg IV/IO.
      • Consider magnesium 25-50 mg/kg IV/IO.
      • If rhythm is nonshockable, resume CPR immediately and administer epinephrine as stated above.

Consultations

Consult a cardiologist for all cases of true dysrhythmia, particularly if the patient is unstable.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.8

Antiarrhythmic agents

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.

Dosing

Adult

Initial dose: 6 mg rapid IV bolus over 1-2 sec followed by a fluid bolus through a widely patent IV site; if no response within 1-2 min, give 12 mg rapid IV bolus; repeat 12 mg dose a second time
Single doses >12 mg not generally recommended

Pediatric

0.1 mg/kg IV rapid bolus (not to exceed 6 mg/dose); if first dose ineffective, repeat with 0.2 mg/kg, not to exceed single dose of 12 mg/dose
Alternatively; 0.05 mg/kg IV and if not effective within 2 min, increase dose by 0.05-mg/kg increments q2min not to exceed 0.25 mg/kg

Interactions

Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects of adenosine; methylxanthines may antagonize effects of adenosine

Contraindications

Documented hypersensitivity; second- or third-degree AV block or sick sinus syndrome (except in patients with functioning artificial pacemaker), atrial flutter, atrial fibrillation, and ventricular tachycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adenosine-induced bronchoconstriction in patients with asthma may occur; adverse effects include bronchospasm, flushing, chest pain, and brief asystole


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.

Dosing

Adult

30 mg/min IV at continued infusion rates until arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered; may infuse at a continuous rate of 1-4 mg/min once arrhythmia is suppressed

Pediatric

Not established
Suggested dosing: 15-50 mg/kg/d PO divided q3-6h; 20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d; 3-6 mg/kg/dose infused over 5 min; 20-80 mcg/kg/min administered as continuous infusion maintenance; not to exceed 100 mg/dose or 2 g/d

Interactions

Expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim and quinidine; may increase effect of skeletal muscle relaxants, quinidine and lidocaine and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Contraindications

Documented hypersensitivity; complete heart block or second- or third-degree heart block, if a pacemaker is not in place; torsades de pointes; systemic lupus erythematosus

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypokalemia and hypomagnesemia; monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency


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).

Dosing

Adult

Total digitalizing dose (TDD) to be administered over 24 h; first dose is one-half the TDD; second dose is one-fourth the TDD, administered 8 h later; third dose is one-fourth the TDD, administered 8 h after the second dose: 0.75-1.5 mg PO in divided doses over 1 d; alternatively 0.5-1 mg IV/IM in divided doses over 1 d
Maintenance dose: 0.125-0.5 mg PO qd or 0.1-0.4 mg IV/IM qd

Pediatric

Total digitalizing dose (TDD) to be administered over 24 h; first dose is one-half the TDD; second dose is one-fourth the TDD, administered 8 h later; third dose is one-fourth the TDD, administered 8 h after the second dose:
Preterm infant: 20-30 mcg/kg PO or 15-25 mcg/kg IV in divided doses
Term infant: 25-35 mcg/kg PO or 20-30 mcg/kg IV in divided doses
1-24 months: 35-60 mcg/kg PO or 30-50 mcg/kg IV/IM in divided doses
2-5 years: 30-40 mcg/kg PO or 25-35 mcg/kg IV/IM in divided doses
5-10 years: 20-35 mcg/kg PO or 15-30 mcg/kg IV/IM in divided doses
>10 years: 10-15 mcg/kg PO or 8-12 mcg/kg IV/IM in divided doses
Maintenance:
Oral:
Preterm infant: 5-7.5 mcg/kg/d PO divided bid
Term infant: 6-10 mcg/kg/d PO divided bid
1-24 months: 10-15 mcg/kg/d PO divided bid
2-5 years: 7.5-10 mcg/kg/d PO divided bid
5-10 years: 5-10 mcg/kg/d PO divided bid
>10 years: 2.5-5 mcg/kg PO qd
Parenteral:
Preterm infant: 4-6 mcg/kg/d IV divided bid
Term infant: 5-8 mcg/kg/d IV divided bid
1-24 months: 7.5-12 mcg/kg/d IV/IM divided bid
2-5 years: 6-9 mcg/kg/d IV/IM divided bid
5-10 years: 4-8 mcg/kg/d IV/IM divided bid
>10 years: 2-3 mcg/kg IV/IM qd

Interactions

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Contraindications

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis


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.

Dosing

Adult

1 mg slow IVP over 10 min; repeat q5min; not to exceed 5 mg total cumulative dose

Pediatric

0.01-0.1 mg/kg slow IVP over 10 min; not to exceed 1 mg/dose
Asymptomatic SVT or those with mild heart failure: 1 mg/kg/dose PO q6h

Interactions

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely


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).

Dosing

Adult

1 mg IVP; may repeat q3-5min
Alternatives: 2-5 mg IV q3-5min; escalating 1-, 3-, and 5-mg doses at 3-min intervals; 0.1 mg/kg q3-5min

Pediatric

First dose: 0.01 mg/kg IV/IO (0.1 mL/kg of 1:10,000 solution)
Subsequent doses: 0.1 mg/kg IV/IO (0.1 mL/kg of 1:1000 solution); repeat q3-5min
Intratracheal: 0.1 mg/kg IV/IO (0.1 mL/kg of 1:1000 solution)

Interactions

Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; do not use during labor (may delay second stage of labor)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in older persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias; adverse effects include tachycardia, palpitations, and anxiety


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.

Dosing

Adult

150 mg IV infused over 10 min, follow with 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min
Oral dosing generally 400 mg/d following load

Pediatric

Not established; weight-based dosing suggested; consider for refractory ventricular arrhythmias in children; suggested dose is 5 mg/kg IV infused over 20-60 min; not to exceed 300 mg/dose

Interactions

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone 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; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong QT interval; coadministration may increase myopathy/rhabdomyolysis risk associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs that prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk

Contraindications

Documented hypersensitivity; complete A-V block and intraventricular conduction defects; patients taking ritonavir or sparfloxacin

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Known to cause serious (and at times fatal) toxicities including pulmonary and liver toxicities; may cause prolonged proarrhythmic effects; may cause optic neuritis/neuropathy or hypothyroidism or hyperthyroidism; CNS and GI toxicity may occur and typically dissipates with dose reduction


Lidocaine (Xylocaine)

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

Dosing

Adult

1-1.5 mg/kg IV bolus initially over 2-3 min; repeat doses of 0.5-0.75 mg/kg in 5-10 min, not to exceed a total of 3 mg/kg, followed by 2-4 mg/min IV

Pediatric

1 mg/kg IV/IO bolus initially, not to exceed 100 mg/dose, followed by 10-50 mcg/kg/min IV continuous infusion

Interactions

Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Contraindications

Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and WPW syndrome; avoid in severe sinoatrial, AV, or intraventricular block, if artificial pacemaker not in place

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure (decrease bolus and maintenance doses), hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression and bradycardia; may increase risk of CNS and cardiac adverse effects in older persons; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities


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.

Dosing

Adult

1-2 g diluted in 100 mL of D5W IV over 1-2 min for refractory VT and known or suspected hypomagnesemia (Mg+2 <1.4 mEq/L); not to exceed 30-40 g/d; maximum rate of infusion for maintenance not to exceed 1-2 g/h

Pediatric

Not established
Suggested dose: 25-50 mg/kg IV q4-6h for 3-4 doses; maximum single dose of 2 g also may be administered and repeated if hypomagnesemia persists

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen 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

Contraindications

Documented hypersensitivity; heart block, Addison disease, myocardial damage, or severe hepatitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Magnesium may alter cardiac conduction leading to heart block in digitalized patients; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering magnesium dose since 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

Follow-up

Patient Education

  • For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Supraventricular Tachycardia and Palpitations.

Multimedia

This ECG belongs to an asymptomatic 17-year-old m...

Media file 1: This ECG belongs to an asymptomatic 17-year-old male who was incidentally discovered to have Wolff-Parkinson-White (WPW) pattern. It shows sinus rhythm with evident preexcitation. To locate the accessory pathway (AP), the initial 40 milliseconds of the QRS (delta wave) are evaluated. Note that the delta wave is positive in lead I and aVL, negative in III and aVF, isoelectric in V1, and positive in the rest of the precordial leads. Therefore, this is likely a posteroseptal AP.

This is a 12-lead ECG from an asymptomatic 7-year...

Media file 2: This is a 12-lead ECG from an asymptomatic 7-year-old boy with Wolff-Parkinson-White (WPW) pattern. Delta waves are positive in leads I and aVL; negative in II, III, and aVF; isoelectric in V1; and positive in the rest of the precordial leads. This again predicts a posteroseptal location for the accessory pathway (AP).

References

  1. Custer JW, Rau RE, eds. Johns Hopkins: The Harriet Lane Handbook. 18th ed. Philadelphia, PA: Mosby Elsevier Inc; 2008.

  2. Wiley JF. Tachycardia/palpitations. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 5th ed. 2006:657-668.

  3. Kaltman J, Shah M. Evaluation of the child with an arrhythmia. Pediatr Clin North Am. Dec 2004;51(6):1537-51, viii. [Medline].

  4. [Guideline] 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 12: Pediatric Advanced Life Support. Circulation. 2005;112(24 Suppl):IV167-87. [Full Text].

  5. Gewitz MH, Woolf PK. Cardiac emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 5th ed. 2006:717-758.

  6. Samson RA, Atkins DL. Tachyarrhythmias and defibrillation. Pediatr Clin North Am. Aug 2008;55(4):887-907, x. [Medline].

  7. Perondi MB, Reis AG, Paiva EF, et al. A comparison of high-dose and standard-dose epinephrine in children with cardiac arrest. N Engl J Med. Apr 22 2004;350(17):1722-30. [Medline].

  8. Physicians' Desk Reference. 63rd ed. Thomson Healthcare; 2009.

Keywords

tachycardia in children, supraventricular tachycardia, SVT, atrial fibrillation, AF, atrial flutter, junctional ectopic tachycardia, JET, ventricular tachycardia, VT, torsade de pointes, ventricular fibrillation, VF, dysrhythmia

Contributor Information and Disclosures

Author

Mirna M Farah, MD, Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Division of Emergency Medicine, Children's Hospital of Philadelphia
Mirna M Farah, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Christine S Cho, MD, MPH,, Attending Physician, Division of Emergency Medicine, Children's Hospital and Research Center of Oakland; HS Assistant Clinical Professor, Department of Pediatrics, University of California, San Francisco School of Medicine
Christine S Cho, MD, MPH, is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David A Peak, MD, Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Further Reading

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)