AVNRT medical therapy: Difference between revisions
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==Overview== | ==Overview== | ||
Medical therapy | Medical therapy to terminate and prevent AVNRT includes drugs that slow AV nodal conduction. | ||
==First Line Therapy== | == First Line Therapy == | ||
===[[Adenosine]]=== | |||
=== [[Adenosine]] === | |||
Adenosine is generally considered first line therapy for AVNRT. | |||
Treatment of AVNRT with adenosine can be complicated by: | |||
*The development of [[shortness of breath]] due to [[bronchospasm]] | |||
*In some cases there can be [[asystole]] which is transient given the short [[half life]] of adenosine | |||
*[[Atrial fibrillation]] may be induced by [[adenosine]] administration | |||
*[[Ventricular fibrillation]] is rarely induced by adenosine. When it does occur it is due to block of the [[AV node]] with rapid antegrade conduction of [[atrial fibrillation]] down the bypass tract. It is for this reason that [[defibrillation]] equipment be available. | |||
*Adenosine should not be used in [[heart transplant]] patients | |||
*[[Dipyridamole]] may potentiate the effect of [[adenosine]] | |||
*[[Theophylline]] may reduce the effectiveness of [[adenosine]] | |||
Administration: | |||
*Place a large bore (18 gauge and larger) intravenous line | |||
*The initial dose is 6 mg and this should be followed a saline flush with elevation of the arm to assure that the drug is infused | |||
*If this is not effective, then 12 mg or 18 mg of [[adenosine]] can be admininistered | |||
===[[Beta blocker]]s=== | ===[[Beta blocker]]s=== | ||
A short acting beta-blocker such as [[esmolol]] (half life of 8 minutes) can be used to terminate an episode of AVNRT. Longer acting beta-blockers such as [[atenolol]], [[metoprolol]], and [[propranolol]] can also be used to reduce the risk of recurrent episodes. [[Atenolol]] may be preferable among patients with [[bronchospasm]] as it selectively blocks [[beta-1 receptors]] with little effect on [[beta- 2 receptors]]. | |||
==Second Line Therapy== | ==Second Line Therapy== | ||
Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include [[flecainide]] or [[amiodarone]]. Both adenosine and beta blockers may cause [[ | |||
Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include [[flecainide]] or [[amiodarone]]. Both adenosine and beta blockers may cause [[bronchoconstriction|tightening of the airways]], and are therefore used with caution in people who are known to have [[asthma]]. Calcium channel blockers should be avoided if there is a [http://www.wikidoc.org/index.php?title=Wide_complex_tacycardia&action=edit&redlink=1 wide complex tacycardia] and the diagnosis of AVNRT is not clearly established in so far as [[calcium channel blockers]] should be avoided in [[ventricular tachycardia]]. If the diagnosis of AVNRT is established, then non-dihydropyridine [[calcium channel blocker]]s (such as [[verapamil]]) may be administered to terminate the rhythm if other agents are not effective. Verapamil acts longer than adenosine and acts rapidly. Its administration can be complicated by [[hypotension]], [[bradycardia]] and [[negative inotropic effects]]. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[CME Category::Cardiology]] | |||
[[Category:Cardiology]] | [[Category:Cardiology]] |
Latest revision as of 04:33, 15 March 2016
AVNRT Microchapters |
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Treatment |
Case Studies |
AVNRT medical therapy On the Web |
American Roentgen Ray Society Images of AVNRT medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Medical therapy to terminate and prevent AVNRT includes drugs that slow AV nodal conduction.
First Line Therapy
Adenosine
Adenosine is generally considered first line therapy for AVNRT.
Treatment of AVNRT with adenosine can be complicated by:
- The development of shortness of breath due to bronchospasm
- In some cases there can be asystole which is transient given the short half life of adenosine
- Atrial fibrillation may be induced by adenosine administration
- Ventricular fibrillation is rarely induced by adenosine. When it does occur it is due to block of the AV node with rapid antegrade conduction of atrial fibrillation down the bypass tract. It is for this reason that defibrillation equipment be available.
- Adenosine should not be used in heart transplant patients
- Dipyridamole may potentiate the effect of adenosine
- Theophylline may reduce the effectiveness of adenosine
Administration:
- Place a large bore (18 gauge and larger) intravenous line
- The initial dose is 6 mg and this should be followed a saline flush with elevation of the arm to assure that the drug is infused
- If this is not effective, then 12 mg or 18 mg of adenosine can be admininistered
Beta blockers
A short acting beta-blocker such as esmolol (half life of 8 minutes) can be used to terminate an episode of AVNRT. Longer acting beta-blockers such as atenolol, metoprolol, and propranolol can also be used to reduce the risk of recurrent episodes. Atenolol may be preferable among patients with bronchospasm as it selectively blocks beta-1 receptors with little effect on beta- 2 receptors.
Second Line Therapy
Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma. Calcium channel blockers should be avoided if there is a wide complex tacycardia and the diagnosis of AVNRT is not clearly established in so far as calcium channel blockers should be avoided in ventricular tachycardia. If the diagnosis of AVNRT is established, then non-dihydropyridine calcium channel blockers (such as verapamil) may be administered to terminate the rhythm if other agents are not effective. Verapamil acts longer than adenosine and acts rapidly. Its administration can be complicated by hypotension, bradycardia and negative inotropic effects.