You are in: eMedicine Specialties > Cardiology > Arrhythmias Atrioventricular Nodal Reentry Tachycardia (AVNRT)Article Last Updated: Aug 9, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine Brian Olshansky 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 Coauthor(s): Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics; Mukesh Garg, MD, MRCP, Assistant Professor, Department of Internal Medicine, Section of Cardiology, Truman Medical Center, University of Missouri at Kansas City; Annette Quick, MD, Medical Director, Cardiovascular Care Unit, Associate Professor, Department of Medicine, University of Missouri at Kansas City; Marina Hannen, MD, Clinical Assistant Professor, Department of Cardiology, Section of Cardiovascular Diseases, University of Kansas Medical Center; Consulting Staff, Mid-American Cardiology Associates; Marco A Barzallo, MD, Consulting Staff, HeartCare Midwest, SC; Shamila Garg, MD Editors: Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Marschall S Runge, MD, PhD, Marion Covington Distinguished Professor of Medicine, Vice Dean for Clinical Affairs, Chairman, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital Author and Editor Disclosure Synonyms and related keywords: atrioventricular nodal reentry tachycardia, AVNRT, AV junctional tachycardia, reentrant supraventricular tachycardia, paroxysmal supraventricular tachycardia, tachyarrhythmia, arrhythmia, chronic heart disease, rhythm disorder, atrioventricular nodal reentry, AV nodal reentry, premature ventricular stimulation INTRODUCTIONSection 2 of 11
  BackgroundAtrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal SVT has been used to describe these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, more specific nomenclature based on the mechanism of reentry helps in better quantifying these arrhythmias and thus helps in choosing appropriate therapies. PathophysiologyThe substrate for AVNRT may be functional rather than anatomic. These arrhythmias occur in young, healthy patients and in those with chronic heart disease. In patients with atrioventricular (AV) nodal reentry, the AV node is functionally divided into 2 longitudinal pathways that form the reentrant circuit. In the majority of patients, during AVNRT, antegrade conduction occurs to the ventricle over the slow (alpha) pathway and retrograde conduction occurs over the fast (beta) pathway (see Image 1). The tachycardia is initiated when an appropriately timed atrial premature complex is blocked in the fast pathway (longer refractory period) and conducts in the slow pathway (shorter refractory period) (see Image 1). While the impulse conducts to the ventricle in the slow pathway (antegrade conduction), the fast pathway recovers so that the impulse can conduct retrograde up the fast pathway to the atrium and the atrial end of the slow pathway (retrograde conduction). This sets up the reentrant circuit. In approximately one third of patients, AVNRT is induced by premature ventricular stimulation. In addition to the typical mechanism of AV nodal reentry described above, atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in the fast pathway and retrograde conduction in the slow pathway. Less commonly, the reentrant circuit can be over 2 slow pathways, the so-called slow-slow AV node reentry. FrequencyUnited StatesAVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT. The prevalence of SVT in the general population is likely several cases per thousand persons. InternationalFrequency is similar to that in the United States. Mortality/MorbidityAVNRT is usually well tolerated; it often occurs in patients with no structural heart disease. In patients with coronary artery disease, AVNRT may cause angina or myocardial infarction. Prognosis for patients without heart disease is usually good. SexMore women than men have AVNRT. AgeAVNRT may occur in persons of any age. It is common in young adults. CLINICALSection 3 of 11
History
Physical
Causes
DIFFERENTIALSSection 4 of 11
Atrial Fibrillation Atrial Flutter Atrial Tachycardia Multifocal Atrial Tachycardia Paroxysmal Supraventricular Tachycardia Wolff-Parkinson-White Syndrome
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| Drug Name | Adenosine (Adenocard) |
|---|---|
| Description | Slows conduction time through AV node. Can interrupt reentry pathways through AV node and restore normal sinus rhythm in paroxysmal SVT, including PSVT associated with WPW syndrome. Has a short half-life. |
| Adult Dose | Initial dose: 6 mg rapid IV bolus over 1-2 s, followed by a fluid bolus through a widely patent IV site; if no response within 1-2 min, administer 12 mg rapid IV bolus; repeat 12-mg dose a second time prn Doses >12 mg are not generally recommended |
| Pediatric Dose | Not established |
| 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; prolonged asystole may ensue in heart transplant patients |
| Interactions | Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects; methylxanthines may antagonize effects; coadministration with digitalis or verapamil may be associated with ventricular fibrillation |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Adenosine-induced bronchoconstriction may occur in patients with asthma; asystole may occur with heart transplants |
These agents are used for AV nodal blockade.
| Drug Name | Digoxin (Lanoxin) |
|---|---|
| Description | Cardiac glycosides have direct and indirect inotropic effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased vagal activity for any given increase in mean arterial pressure. Administered IV to terminate an acute attack (but delayed onset of action and less effective than other therapies) and PO to prevent recurrence. |
| Adult Dose | IV: 0.5-1 mg IV over 10-15 min, followed by 0.25 mg q2-4h; not to exceed 1.5 mg/d PO: 1-1.5 mg PO initially, followed by 0.25-0.5 mg q6h for a total dose of 2-3 mg; follow by maintenance dose of 0.125-0.5 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity, beriberi heart disease, idiopathic hypertrophic subaortic stenosis, ventricular fibrillation, constrictive pericarditis, WPW syndrome with atrial fibrillation, and carotid sinus syndrome |
| Interactions | Medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, and procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Hypokalemia may reduce positive inotropic effect and increase risk of toxic arrhythmias; 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 second-degree AV block may progress to complete block when treated with digoxin; caution in hypothyroidism, hypoxia, neonates, premature infants, breastfeeding, hypermetabolic states, and acute myocarditis; reduce dose in renal dysfunction |
These agents are used for AV nodal blockade.
| Drug Name | Diltiazem (Dilacor, Tiamate, Cardizem) |
|---|---|
| Description | During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Administered IV to terminate an acute attack and PO to prevent recurrence. |
| Adult Dose | Initial dose: 0.25 mg/kg IV over 2 min (20-mg dose is reasonable for average patient); if tachycardia not terminated, repeat dose of 0.35 mg/kg IV over 2 min Alternatively, 120-360 mg PO qd in divided doses |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, and hypotension (<90 mm Hg systolic) |
| Interactions | May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase levels |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur |
| Drug Name | Verapamil (Calan, Covera-HS, Verelan) |
|---|---|
| Description | By interrupting reentry at AV node, can restore normal sinus rhythm in patients with paroxysmal SVTs. This is the second-line treatment for AVNRT after emergent adenosine. Causes fewer adverse effects, is less expensive, and lasts longer, but action is not as rapid and hypotension, bradycardia, and a negative inotropic effect may occur; good to use in lieu of adenosine if AVNRT recurs after termination |
| Adult Dose | 5-10 mg IV slowly, followed by a second dose 15-30 min later if patient does not satisfactorily respond to initial dose |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity, severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (<90 mm Hg systolic) |
| Interactions | May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | 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 verapamil treatment); monitor liver function periodically |
These agents are used for AV nodal blockade.
| Drug Name | Esmolol (Brevibloc) |
|---|---|
| Description | Excellent for use in patients at risk for experiencing complications from beta-blockade (particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease). Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed. |
| Adult Dose | Loading dose: 250-500 mcg/kg/min IV for 1 min, followed by a 4-min maintenance infusion of 50 mcg/kg/min If adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min); sequence may be repeated up to 4 times if needed As desired heart rate is approached, omit loading infusion and reduce incremental dose of maintenance infusion from 50 mcg/kg/min IV to 25 mcg/kg/min IV or lower; interval between titration steps may be increased from 5-10 min if needed |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, cardiogenic shock, and AV conduction abnormalities |
| Interactions | Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | 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 |
| Media file 1: Electrophysiological mechanism of atrioventricular nodal reentry tachycardia. | |
 | View Full Size Image | Media type: Photo |
| Media file 2: A 12-lead ECG in a patient with typical atrioventricular nodal reentry tachycardia. The retrograde P waves are visible only as subtle deflections at the end of the QRS complexes, called pseudo S waves in the inferior leads and pseudo R' waves in leads aVR and V1. | |
 | View Full Size Image | Media type: ECG |
Atrioventricular Nodal Reentry Tachycardia (AVNRT) excerpt
Article Last Updated: Aug 9, 2006
