eMedicine Specialties > Cardiology > Arrhythmias

Paroxysmal Supraventricular Tachycardia: Treatment & Medication

Author: Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Coauthor(s): Phillip L Kraft, MD, Director, Interventional Cardiology and Cardiac Catheterization Laboratory, William Beaumont Hospital
Contributor Information and Disclosures

Updated: Aug 12, 2009

Treatment

Medical Care

Most of the patients who present with paroxysmal supraventricular tachycardia have AVNRT or AVRT. These arrhythmias depend on AV nodal conduction and therefore can be terminated by transiently blocking AV nodal conduction.

Vagal maneuvers are the first-line treatment in hemodynamically stable patients. Vagal maneuvers, such as breath-holding and the Valsalva maneuver (ie, having the patient bear down as though having a bowel movement), all slow conduction in the AV node and can potentially interrupt the reentrant circuit.

Carotid massage is another vagal maneuver that can slow AV nodal conduction. Massage the carotid sinus for several seconds on the nondominant cerebral hemisphere side. This maneuver is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this maneuver. Do not perform carotid massage on both sides. A Valsalva maneuver, if performed properly by the patient, can frequently avert an attack.

Synchronized cardioversion starting at 50 J can be used immediately in patients who are hypotensive, have pulmonary edema, have chest pain with ischemia, or are otherwise unstable.

  • Short-term medical management
    • When SVT is not terminated by vagal maneuvers, short-term management involves intravenous adenosine or calcium channel blockers. Adenosine is a short-acting drug that blocks AV node conduction; it terminates 90% of tachycardias due to AVNRT or AVRT.39,11,13,16,48 Adenosine does not usually terminate atrial tachycardia, although it is effective for terminating SNRT.39,11,13,21,48 Typical adverse effects of adenosine include flushing, chest pain, and dizziness. These effects are temporary because adenosine has a very short half-life of 10-20 seconds.44
    • Other alternatives for the acute treatment of SVT include calcium channel blockers like verapamil, diltiazem or beta-blockers like metoprolol or esmolol. Verapamil is a calcium channel blocker that also has AV blocking properties. Verapamil has a longer half-life than adenosine and may help maintain sinus rhythm following the termination of SVT. It is also advantageous for controlling the ventricular rate in patients with atrial tachyarrhythmia.20,12,13,31,55,21,44,24
    • Acute management of a wide complex tachycardia in a hemodynamically unstable patient requires immediate cardioversion whereas in a stable patient, IV procainamide, propafenone, or flecainide is acceptable. Amiodarone is preferred in patients with impaired left ventricular function or in patients with heart failure or structural heart disease.9
    • Treatment of AF and atrial flutter involves controlling the ventricular rate, restoring the sinus rhythm, and preventing embolic complications. The ventricular rate is controlled with calcium channel blockers, digoxin, amiodarone, and beta-blockers. The sinus rhythm may be restored with either pharmacological agents or electrical cardioversion. Pharmacological agents such as ibutilide convert AF and atrial flutter of short duration to sinus rhythm in approximately 30% and 60% of patients, respectively.
    • Electrical cardioversion is the most effective method for restoring sinus rhythm. If AF has been present for longer than 24-48 hours, defer cardioversion until the patient has been adequately anticoagulated to prevent thromboembolic complications.39,11,13,31,40,21,44,48
  • Long-term medical management
    • The choice of long-term therapy for patients with SVT depends on the type of tachyarrhythmia and the frequency and duration of episodes, symptoms, and risks associated with the arrhythmia (eg, heart failure, sudden death). Evaluate patients on an individual basis, and tailor the best therapy for the specific tachyarrhythmia.
    • Patients with paroxysmal supraventricular tachycardia may initially be treated with calcium channel blockers, digoxin, and/or beta-blockers. Class IA, IC, or III antiarrhythmic agents are used less frequently because of the success of radiofrequency catheter ablation.39,11,13,31,40,21,44,48,56 Consider radiofrequency ablation for any patient with symptomatic paroxysmal supraventricular tachycardia in whom long-term medical treatment is not effectively tolerated or desired. In addition, because of the risk of sudden cardiac death, perform catheter ablation on patients with symptomatic WPW syndrome. Radiofrequency catheter ablation is more than 90% effective in curing paroxysmal supraventricular tachycardia.20,39,55,48,19
    • Radiofrequency ablation involves focally ablating the crucial component of the arrhythmia mechanism. For example, in AVNRT, the slow pathway is ablated, which prevents the reentry cycle. The accessory pathway is targeted in patients with AVRT. Focal atrial tachycardia, atrial flutter, and, in some cases, AF can also be cured with ablation. Radiofrequency ablation has a high success rate and is performed using conscious sedation in an outpatient setting or with overnight hospitalization. Complications, which occur at a rate of 1-3%, include deep vein thrombosis, systemic embolism, infection, cardiac tamponade, and hemorrhage. The risk of death is approximately 0.1%. The lifetime risk of fatal malignancy as a result of radiation exposure is low.
    • Radiofrequency ablation is cost-effective for patients who have frequent episodes of SVT that require antiarrhythmic agents and frequent emergency visits. It is also indicated for patients with incessant tachycardia and for patients with symptomatic WPW syndrome. The optimal management strategy for patients with asymptomatic preexcitation syndromes remains uncertain.42,45,30,20,19

Surgical Care

Prior to the advent of percutaneous radiofrequency catheter ablation, open cardiac surgical procedures were the only means of curing paroxysmal supraventricular tachycardia. Currently, open surgical procedures are rarely performed.

Consultations

  • A cardiologist should be consulted for patients with frequent episodes of paroxysmal supraventricular tachycardia, syncope, and/or preexcitation syndromes.
  • Consultation with a cardiologist should also be obtained for patients in whom medical management has failed.
  • An electrophysiologist should be consulted for patients considered for radiofrequency catheter ablation.

Diet

Dietary changes depend on underlying medical problems.

Activity

Changes in physical activity depend on underlying cardiac problems and other comorbidities.

Medication

The goals of pharmacotherapy are to correct arrhythmia, to prevent complications, and to reduce morbidity.

Antiarrhythmic agents

Used to treat or prevent arrhythmia.


Flecainide (Tambocor)

Blocks sodium channels, producing dose-related decrease in intracardiac conduction in all parts of heart. Increases electrical stimulation of threshold of ventricle, HIS-Purkinje system. Shortens Phase 2 and 3 repolarization, resulting in a decreased action potential duration and effective refractory period.
Indicated for the treatment of paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms and PSVT, including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and other supraventricular tachycardias of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. Indicated also for prevention of documented life-threatening ventricular arrhythmias, such as, sustained ventricular tachycardia. Not recommended in less severe ventricular arrhythmias even if patients are symptomatic.

Adult

100 mg PO bid q12h; increase q4d to a maximum of 400 mg/d

Pediatric

3-6 mg/kg/d or 100-150 mg/m2/d PO divided tid to 11 mg/kg/d or 200 mg/m2/d

May increase toxicity of digoxin; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; CYP4502D6 inhibitors (ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity of flecainide

Documented hypersensitivity, preexisting second- or third-degree AV block, right bundle branch block associated with left hemi-block (bifascicular block) or trifascicular block), unless a pacemaker is present to sustain the cardiac rhythm if complete heart block occurs; concurrent use of ritonavir or amprenavir; recent MI

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 pre-existing sinus node dysfunction, history of congestive heart failure, sick-sinus syndrome, post-MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only due to deaths associated with proarrhythmic effects of Class IC antiarrhythmics; adjust dose in renal or hepatic impairment


Propafenone (Rythmol)

Shortens upstroke velocity (Phase 0) of monophasic action potential. Reduces fast inward current carried by sodium ions in Purkinje fibers, and to a lesser extent myocardial fibers. May increase diastolic excitability threshold and prolong effective refractory period prolonged. Reduces spontaneous automaticity and depresses triggered activity.
Indicated for the treatment of documented life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. Appears to be effective in the treatment of supraventricular tachycardias including atrial fibrillation and flutter. Not recommended in patients with less severe ventricular arrhythmias, even if patients are symptomatic.

Adult

150 mg PO q8h and increase at 3-4 d intervals up to 300 mg q8h

Pediatric

Not established

Rifampin may decrease plasma levels; quinidine may increase pharmacologic effects; propafenone may increase plasma levels of beta-blockers, cyclosporine, warfarin, and digoxin; CYP4502D6 inhibitors (ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity of propafenone

Documented hypersensitivity, second or third-degree AV block, right bundle-branch block associated with left hemi-block (bifascicular block) or trifascicular block; concurrent use of ritonavir or amprenavir

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 pre-existing sinus node dysfunction, history of congestive heart failure, sick-sinus syndrome, post MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only due to deaths associated with proarrhythmic effects of Class IC antiarrhythmics; adjust dose in renal or hepatic impairment


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 (Pieper, 1995; Orejarena; 1998; Siberry, 2000; Trohman, 2000).
Effective in terminating both AVNRT and AVRT. More than 90% of patients convert to sinus rhythm with adenosine at 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 (Pieper, 1995; Orejarena; 1998; Siberry, 2000; Trohman, 2000).

Adult

Initial: 6 mg rapid IV bolus (antecubital vein), followed by saline flush; second bolus of 12 mg may be given if initial bolus is unsuccessful

Pediatric

0.1-0.2 mg/kg rapid IV push, increasing increments of 0.05 mg/kg IV bolus q2min until PSVT resolves; not to exceed 12 mg

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

Third-degree heart block, asthma, or sick sinus syndrome; documented hypersensitivity; atrial flutter or AF in setting of ventricular preexcitation (WPW syndrome)

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

Associated with flushing, chest tightness, dyspnea, lightheadedness, nausea, and palpitation; patients may have sinus bradycardia or sinus arrest; due to ultrashort half-life, adverse effects rarely require specific interventions; adenosine-induced bronchoconstriction may occur in patients with asthma

Class IV calcium channel blockers (nondihydropyridine)

Decrease conduction velocity and prolong refractory period.


Verapamil (Isoptin, Calan)

Calcium channel blockers prevent calcium influx in slow channels of AV node, decrease conduction velocity, and prolong refractory period, which effectively terminates reentrant conduction.

Adult

2.5-5 mg IV over 2-3 min; repeat in 5-10 min if arrhythmia is not slowed or converted to sinus rhythm; monitor BP and pulse
240-480 mg SR PO qd to prevent recurrent PSVT

Pediatric

<1 year: Not established
>1 year: 0.1 mg/kg IV bolus; not to exceed 0.3 mg/kg; continuous ECG monitoring

Risk of serious bradycardia and AV block with beta-blockers; increases digoxin blood levels, leading to arrhythmia and complete AV block; may increase levels of carbamazepine, digoxin, cyclosporine, and theophylline; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; cimetidine may increase levels

Children <1 year; documented hypersensitivity; cardiogenic shock, sick sinus syndrome, or severe CHF; second- or third-degree AV block

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 patients on beta-blockers, digoxin, antidysrhythmics, and antihypertensives because effects may be additive, resulting in serious conduction abnormalities and hypotension; adjust dose with renal insufficiency; hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); periodically monitor liver function


Diltiazem (Cardizem, Tiazac, Dilacor)

Similar to verapamil, this agent decreases conduction velocity in AV node. Also increases refractory period via blockade of calcium influx. This, in turn, stops reentrant phenomenon.

Adult

0.25 mg/kg IV bolus converts 75-100% of PSVTs; usual dose is 20 mg IV over 2 min

Pediatric

1.5-2 mg/kg/d IV

Levels increased with cimetidine; increases levels/effects of cyclosporins, carbamazepine, theophylline, fentanyl, digoxin, and beta-blockers; with amiodarone, may cause bradycardia and decreased cardiac output

Sick sinus syndrome, second- or third-degree heart block, heart failure, acute MI; documented hypersensitivity; hypotension (<90 mm Hg systolic)

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

Warn patients that headache, nausea, vomiting, and dizziness may occur; caution in patients on beta-blockers or digoxin because effects may be additive and result in serious conduction abnormalities and hypotension; caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

Class II beta-blockers

Increase refractory period of AV node.


Propranolol (Inderal)

Beta-blockers abolish reentry-induced PSVT by increasing refractory period of AV node. Other beta-blockers effective in treating PSVT are esmolol, metoprolol, atenolol, and nadolol.

Adult

IV: 0.5-1 mg bolus; not to exceed 5 mg
PO: 10-30 mg tid/qid; 80-160 mg qd long-acting formulation

Pediatric

0.01-0.1 mg/kg IV over 10 min, repeat q6-8h prn; not to exceed 1 mg/dose for infants or 3 mg/dose for children

Calcium channel blockers result in additive effects and increase risk of AV block; barbiturates, rifampin, and indomethacin may decrease effects; cimetidine, quinidine, chlorpromazine, and verapamil may increase effects; aluminum salts, NSAIDs, penicillins, calcium salts, and cholestyramine may decrease effects; loop diuretics and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Asthma, second- or third-degree heart block, heart failure; documented hypersensitivity; bradycardia, cardiogenic shock

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

D - Fetal risk shown in humans; use only 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


Esmolol (Brevibloc)

Short-acting beta-blocker that abolishes reentry-induced PSVT by increasing refractory period of AV node.

Adult

Loading dose of 0.5 mg/kg IV over 1 min, followed by a maintenance infusion of 50 mcg/kg/min for 4 min; if unsuccessful, a second bolus of 0.5 mg/kg is infused over 1 min, with a maintenance rate of 100 mcg/kg

Pediatric

Not established; suggested dose is 100-500 mcg/kg administered IV over 1 min

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock, and AV conduction abnormalities

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

Category D in second or third trimester; beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Cardiac glycosides

Increase vagal activity, which decreases conduction velocity through AV node.


Digoxin (Lanoxin)

Indirectly increases vagal activity, thereby decreasing conduction velocity through AV node, which can result in termination of PSVT.

Adult

0.125 mg PO qod to 0.375 mg PO qd

Pediatric

<5 years: Not established
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose is 25-35% of PO loading dose

Medications that may increase levels include quinidine, verapamil, diltiazem, amiodarone, alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, aminoglycosides, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, and tolbutamide
Drugs that increase hepatic microsomal enzyme activity (eg, rifampin, phenobarbital, phenytoin) may increase metabolism; diuretics may result in hypokalemia, which may increase risk of digoxin toxicity
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, kaolin/pectin, and aminosalicylic acid

Ventricular dysrhythmia; documented hypersensitivity; beriberi heart disease, hypertrophic cardiomyopathy, constrictive pericarditis, and carotid sinus syndrome

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

Dose adjustment in patients with renal insufficiency; monitor levels to avoid toxicity or symptoms (eg, confusion, headache, ataxia, vomiting, weakness, visual disturbances, delirium, diarrhea); most serious effects of toxicity are dysrhythmia and PVC (most common), but ventricular tachycardia and AV block also occur; monitor for electrolyte abnormalities because hypokalemia may increase risk of toxicity; toxicity can be treated with Digibind IV calcium but may produce arrhythmia in digitalized patients; hypercalcemia predisposes patients 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

More on Paroxysmal Supraventricular Tachycardia

Overview: Paroxysmal Supraventricular Tachycardia
Differential Diagnoses & Workup: Paroxysmal Supraventricular Tachycardia
Treatment & Medication: Paroxysmal Supraventricular Tachycardia
Follow-up: Paroxysmal Supraventricular Tachycardia
Multimedia: Paroxysmal Supraventricular Tachycardia
References
[ CLOSE WINDOW ]

References

  1. [Guideline] Advanced cardiovascular life support, Introduction to ACLS 2000. Overview of recommended changes in ACLS from Guidelines 2000 Conference. Circulation. 2000;102:186-189.

  2. Akhtar M. Supraventricular tachycardias. Electrophysiologic mechanisms: Diagnosis and pharmacological therapy. In: Josephson ME, Wellens HJ, eds. Tachycardias: Mechanisms, Diagnosis, Treatment. Philadelphia, Pa: Lea & Febiger; 1984:137.

  3. Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S, Dhala A. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations. Circulation. Jul 1993;88(1):282-95. [Medline].

  4. Al-Khatib SM, Pritchett EL. Clinical features of Wolff-Parkinson-White syndrome. Am Heart J. Sep 1999;138(3 Pt 1):403-13. [Medline].

  5. Atie J, Brugada P, Brugada J, et al. Clinical and electrophysiologic characteristics of patients with antidromic circus movement tachycardia in the Wolff-Parkinson-White syndrome. Am J Cardiol. Nov 1 1990;66(15):1082-91. [Medline].

  6. Bardy GH, Packer DL, German LD, Gallagher JJ. Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation. Sep 1984;70(3):377-91. [Medline].

  7. Basta M, Klein GJ, Yee R, Krahn A, Lee J. Current role of pharmacologic therapy for patients with paroxysmal supraventricular tachycardia. Cardiol Clin. Nov 1997;15(4):587-97. [Medline].

  8. Bellet S. Clinical Disorders of the Heart Beat. Philadelphia, Pa: Lea & Febiger; 1963:144-5.

  9. [Guideline] Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. Oct 15 2003;42(8):1493-531. [Medline].

  10. Brugada P, Wellens HJ. The role of triggered activity in clinical ventricular arrhythmias. Pacing Clin Electrophysiol. Mar 1984;7(2):260-71. [Medline].

  11. Campbell RW, Smith RA, Gallagher JJ, Pritchett EL, Wallace AG. Atrial fibrillation in the preexcitation syndrome. Am J Cardiol. Oct 1977;40(4):514-20. [Medline].

  12. Campbell RW. Supraventricular tachycardia. Doing the right things. Eur Heart J. May 1997;18 Suppl C:C50-3. [Medline].

  13. Connors S, Dorian P. Management of supraventricular tachycardia in the emergency department. Can J Cardiol. Mar 1997;13 Suppl A:19A-24A. [Medline].

  14. Coumel P, Gourgon R, Fabiato A, Laurent D, Bouvrain Y. [Studies of assisted circulation. I. Methods of repetitive provoked extrasystole and slowing of effective heart rate]. Arch Mal Coeur Vaiss. Jan 1967;60(1):67-88. [Medline].

  15. Denes P, Wu D, Dhingra RC, Chuquimia R, Rosen KM. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation. Sep 1973;48(3):549-55. [Medline].

  16. Etheridge SP, Judd VE. Supraventricular tachycardia in infancy: evaluation, management, and follow-up. Arch Pediatr Adolesc Med. Mar 1999;153(3):267-71. [Medline].

  17. Farre J, Wellens HJ. The value of the electrocardiogram in diagnosing site of origin and mechanism of supraventricular tachycardia. In: Wellens HJJ, Kulbetus HE, eds. What's New in Electrocardiography. The Hague, Belgium; Martinus Nijhoff; 1981:131-71.

  18. Gallagher JJ, Sealy WC. The permanent form of junctional reciprocating tachycardia: further elucidation of the underlying mechanism. Eur J Cardiol. Nov 1978;8(4-5):413-30. [Medline].

  19. Ganz LI. Approach to the Patient with Supraventricular Tachycardia. In: Ganz LI, ed. Management of Cardiac Arrhythmias. ed. Totowa, NJ: Humana; 2002.

  20. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med. Jan 19 1995;332(3):162-73. [Medline].

  21. Gold MR, Josephson ME. Cardiac arrhythmia: current therapy. Hosp Pract (Minneap). Sep 1 1999;34(9):27-8, 31-2, 35-8 passim. [Medline].

  22. Habibzadeh MA. Multifocal atrial tachycardia: a 66 month follow-up of 50 patients. Heart Lung. Mar-Apr 1980;9(2):328-35. [Medline].

  23. Jazayeri MR, Hempe SL, Sra JS, et al. Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia. Circulation. Apr 1992;85(4):1318-28. [Medline].

  24. Josephson ME, Zimetbaum PJ, Buxton AE, Marchlinski FE. Tachyarrhythmias. In: Harrison TR, Resnik WR, Isselbacher KJ, et al, eds. Harrison's Online [serial online]. New York, NY: McGraw-Hill; 2001.

  25. Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med. Sep 1977;87(3):346-58. [Medline].

  26. Josephson ME, Wellens HJ. Electrophysiologic evaluation of supraventricular tachycardia. Cardiol Clin. Nov 1997;15(4):567-86. [Medline].

  27. Klein GJ, Sharma AD, Yee R, Guiraudon GM. Classification of supraventricular tachycardias. Am J Cardiol. Aug 31 1987;60(6):27D-31D. [Medline].

  28. Klein GJ, Bashore TM, Sellers TD, Pritchett EL, Smith WM, Gallagher JJ. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. Nov 15 1979;301(20):1080-5. [Medline].

  29. Krahn AD, Yee R, Klein GJ, Morillo C. Inappropriate sinus tachycardia: evaluation and therapy. J Cardiovasc Electrophysiol. Dec 1995;6(12):1124-8. [Medline].

  30. Lesh MD, Van Hare GF, Epstein LM, et al. Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms. Circulation. Mar 1994;89(3):1074-89. [Medline].

  31. Levy S, Ricard P. Using the right drug: a treatment algorithm for regular supraventricular tachycardias. Eur Heart J. May 1997;18 Suppl C:C27-32. [Medline].

  32. Montoya PT, Brugada P, Smeets J, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. Eur Heart J. Feb 1991;12(2):144-50. [Medline].

  33. Murdock CJ, Leitch JW, Teo WS, Sharma AD, Yee R, Klein GJ. Characteristics of accessory pathways exhibiting decremental conduction. Am J Cardiol. Mar 1 1991;67(6):506-10. [Medline].

  34. Obel OA, Camm AJ. Supraventricular tachycardia. ECG diagnosis and anatomy. Eur Heart J. May 1997;18 Suppl C:C2-11. [Medline].

  35. Obel OA, Camm AJ. Accessory pathway reciprocating tachycardia. Eur Heart J. May 1998;19 Suppl E:E13-24, E50-1. [Medline].

  36. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. Jan 1998;31(1):150-7. [Medline].

  37. Oren JW 4th, Beckman KJ, McClelland JH, Wang X, Lazzara R, Jackman WM. A functional approach to the preexcitation syndromes. Cardiol Clin. Feb 1993;11(1):121-49. [Medline].

  38. Phillips J, Spano J, Burch G. Chaotic atrial mechanism. Am Heart J. Aug 1969;78(2):171-9. [Medline].

  39. Pieper SJ, Stanton MS. Narrow QRS complex tachycardias. Mayo Clin Proc. Apr 1995;70(4):371-5. [Medline].

  40. Reimold SC. Avoiding drug problems. The safety of drugs for supraventricular tachycardia. Eur Heart J. May 1997;18 Suppl C:C40-4. [Medline].

  41. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol. Feb 1974;33(2):291-4. [Medline].

  42. Scheinman MM. Catheter ablation for cardiac arrhythmias, personnel, and facilities. North American Society of Pacing and Electrophysiology Ad Hoc Committee on Catheter Ablation. Pacing Clin Electrophysiol. May 1992;15(5):715-21. [Medline].

  43. Scher DL, Arsura EL. Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment. Am Heart J. Sep 1989;118(3):574-80. [Medline].

  44. Siberry GK, Iannone R. The Harriet Lane Handbook: A Manual for Pediatric House Officers. 15th ed. St. Louis, Mo: Mosby-Year Book; 2000.

  45. Strickberger SA, Okishige K, Meyerovitz M, Shea J, Friedman PL. Evaluation of possible long-term adverse consequences of radiofrequency ablation of accessory pathways. Am J Cardiol. Feb 15 1993;71(5):473-5. [Medline].

  46. Sung RJ, Castellanos A, Mallon SM, Bloom MG, Gelband H, Myerburg RJ. Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome. Circulation. Sep 1977;56(3):409-16. [Medline].

  47. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide. 5th ed. New York, NY: McGraw Hill; 2000.

  48. Trohman RG. Supraventricular tachycardia: implications for the intensivist. Crit Care Med. Oct 2000;28(10 Suppl):N129-35. [Medline].

  49. Vidaillet HJ Jr, Pressley JC, Henke E, Harrell FE Jr, German LD. Familial occurrence of accessory atrioventricular pathways (preexcitation syndrome). N Engl J Med. Jul 9 1987;317(2):65-9. [Medline].

  50. Waldo AL, Wit AL. Mechanisms of cardiac arrhythmias. Lancet. May 8 1993;341(8854):1189-93. [Medline].

  51. Wellens HJ. Value and limitations of programmed electrical stimulation of the heart in the study and treatment of tachycardias. Circulation. May 1978;57(5):845-53. [Medline].

  52. Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J. 1930;5:685-704.

  53. Wood KA, Drew BJ, Scheinman MM. Frequency of disabling symptoms in supraventricular tachycardia. Am J Cardiol. Jan 15 1997;79(2):145-9. [Medline].

  54. Wu D, Denes P, Amat-Y-Leon F, Wyndham CR, Dhingra R, Rosen KM. An unusual variety of atrioventricular nodal re-entry due to retrograde dual atrioventricular nodal pathways. Circulation. Jul 1977;56(1):50-9. [Medline].

  55. Xie B, Thakur RK, Shah CP, Hoon VK. Clinical differentiation of narrow QRS complex tachycardias. Emerg Med Clin North Am. May 1998;16(2):295-330. [Medline].

  56. Fu H, Hu H, Yang Q, Cui K, Chu N, Jiang J. [A retrospective study of 4865 cases of paroxysmal supraventricular tachycardia treated with catheter ablation]. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. Jun 2009;26(3):499-503. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

paroxysmal supraventricular tachycardia, PSVT, supraventricular tachycardia, SVT, multifocal atrial tachycardia, MAT, tachyarrhythmia, atrial fibrillation, AF, conduction pathway disturbance, conduction pathway abnormality, conduction pathway anomaly, dysrhythmia, heart condition, heart rhythm problem, atrial tachyarrhythmia, atrioventricular tachyarrhythmia, AV tachyarrhythmia, sinus tachycardia, inappropriate sinus tachycardia, IST, sinusnodal reentranttachycardia, SNRT, atrial tachycardia, atrial flutter, AV tachyarrhythmias, AV nodal reentrant tachycardia, atrioventricular nodal reentrant tachycardia, AVNRT, atrioventricular reentrant tachycardia, AV reentrant tachycardia, AVRT, junctional ectopic tachycardia, JET, nonparoxysmal junctional tachycardia, NPJT, heartfailure, pulmonary edema, myocardial ischemia, myocardial infarction, syncope, sudden death, tachycardia-induced cardiomyopathy, WPW syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Monika Gugneja, MD, Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

Phillip L Kraft, MD, Director, Interventional Cardiology and Cardiac Catheterization Laboratory, William Beaumont Hospital
Phillip L Kraft, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of St Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa
Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.