Paroxysmal Supraventricular Tachycardia Medication

  • Author: Monika Gugneja, MD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Jan 23, 2012
 

Medication Summary

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

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Antiarrhythmic agents

Class Summary

Used to treat or prevent arrhythmia.

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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.

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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.

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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).

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Class IV calcium channel blockers (nondihydropyridine)

Class Summary

Decrease conduction velocity and prolong refractory period.

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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.

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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.

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Class II beta-blockers

Class Summary

Increase refractory period of AV node.

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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.

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Esmolol (Brevibloc)

 

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

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Cardiac glycosides

Class Summary

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

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Digoxin (Lanoxin)

 

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

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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.

Specialty Editor Board

Alan D Forker, MD  Professor of Medicine, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research, 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

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Amer Suleman, MD  Private Practice

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

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author James V Talano, MD to the development and writing of this article.

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Sinus tachycardia. Note that the QRS complexes are narrow and regular. The patient's heart rate is approximately 135 bpm. P waves are normal in morphology.
Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V1.
Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.
Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.
Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. Rhythm is irregularly irregular. P waves are not discernible.
Atrioventricular nodal reentrant tachycardia. The patient's heart rate is approximately 146 bpm with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.
Same patient as in Media file 6. Patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.
Image A displays the slow pathway and the fast pathway, with a regular impulse being conducted through the atrioventricular node. Image B displays a premature impulse that is conducted in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, as is seen in typical atrioventricular nodal tachycardia. Image C displays the premature impulse conducting in a retrograde manner through the pathway and the impulse reentering the pathway with anterograde conduction, which is seen commonly in patients with atypical atrioventricular nodal tachycardia.
Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.
The left image displays the atrioventricular node with the accessory pathway. The impulse is conducted in an anterograde manner in the atrioventricular node and in a retrograde manner in the accessory pathway. This circuit is known as orthodromic atrioventricular reentrant tachycardia and can occur in patients with concealed accessory tracts or Wolff-Parkinson-White syndrome. The right image displays the impulse being conducted in an anterograde manner through the accessory pathway and in a retrograde manner via the atrioventricular node. This type of circuit is known as antidromic atrioventricular reentrant tachycardia and only occurs in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.
Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.
The left panel depicts antidromic atrioventricular reentrant tachycardia. The right panel depicts sinus rhythm in a patient with antidromic atrioventricular reentrant tachycardia. Note that the QRS complex is an exaggeration of the delta wave during sinus rhythm.
Atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.
 
 
 
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