Updated: Sep 23, 2009
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
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.
Tachycardia can be due to a physiologic response of the heart to noncardiac stimuli or to a true dysrhythmia.2,3
| 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 |
Laboratory studies for tachycardia may include the following:
Imaging studies for tachycardia may include the following:
Other tests may include the following:
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
Consult a cardiologist for all cases of true dysrhythmia, particularly if the patient is unstable.
The goals of pharmacotherapy are to reduce morbidity and prevent complications.8
Alter the electrophysiologic mechanisms responsible for arrhythmia.
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.
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
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
Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects of adenosine; methylxanthines may antagonize effects of adenosine
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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adenosine-induced bronchoconstriction in patients with asthma may occur; adverse effects include bronchospasm, flushing, chest pain, and brief asystole
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.
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
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
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
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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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).
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
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
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
Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
1 mg slow IVP over 10 min; repeat q5min; not to exceed 5 mg total cumulative dose
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
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
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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).
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
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)
Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
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)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
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
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
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
Documented hypersensitivity; complete A-V block and intraventricular conduction defects; patients taking ritonavir or sparfloxacin
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
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
Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.
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
1 mg/kg IV/IO bolus initially, not to exceed 100 mg/dose, followed by 10-50 mcg/kg/min IV continuous infusion
Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
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
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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
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.
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
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
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
Documented hypersensitivity; heart block, Addison disease, myocardial damage, or severe hepatitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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
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Physicians' Desk Reference. 63rd ed. Thomson Healthcare; 2009.
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
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.
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.
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.
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
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.
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.
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.
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