Usefulness of isoproterenol in facilitating atrioventricular nodal reentry tachycardia during electrophysiologic testing

Brownstein, Sheldon L.; Hopson, Rosanne; Martins, James B.; Aschoff, Ann M.; Olshansky, Brian; Constantin, Luis; Kienzle, Michael G.

doi:10.1016/0002-9149(88)90121-x

Cited by 29 publications

(6 citation statements)

References 14 publications

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“…In patients with AVNRT, β-agonists enhance both antegrade slow pathway and retrograde fast pathway conduction. 1 These agents are useful for arrhythmia induction, especially after ablation. β-Agonists are particularly important in patients who have evidence of persistent dual AV nodal pathways (ie, nonlinear A1A2-A2H2 curve or AV nodal echo beats during programmed stimulation).…”

Section: Discussionmentioning

confidence: 99%

Paradoxical reflex bradycardia after epinephrine infusion for arrhythmia induction in the electrophysiology laboratory

Larsen

Kaszala

Tan

et al. 2018

HeartRhythm Case Reports

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Section: Discussionmentioning

confidence: 99%

Paradoxical reflex bradycardia after epinephrine infusion for arrhythmia induction in the electrophysiology laboratory

Larsen

Kaszala

Tan

et al. 2018

HeartRhythm Case Reports

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“…The acceleration of AV nodal recovery and lessening of fatigue caused by 13-adrenergic receptor stimulation may account for the role of sympathetic activation in the occurrence of AV nodal reentry. 33,35,36 On the other hand, enhancement of fatigue and slowing of AV nodal recovery may contribute to the salutary effects of f-adrenergic receptor blockers in supraventricular arrhythmias.38-41…”

Section: Potential Significancementioning

confidence: 99%

“…31,32 The autonomic adjustments to upright posture facilitate the induction of sustained AV nodal reentrant tachycardia,33 and in some patients with AV nodal reentrant tachycardia, programmed stimulation fails to induce the tachycardia unless isoproterenol is infused. [34][35][36] ,-Blockade slows AV nodal conduction37 and can prevent the induction3839 and clinical occur-rence39-41 of AV nodal reentry. The sympathetic nervous system thus plays an important role in regulating AV nodal function and determining the occurrence and manifestations of supraventricular arrhythmias.…”

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confidence: 99%

Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Nayebpour

Talajic

Nattel

1992

Circulation Research

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Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.

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“…[1][2][3][4][5][6][7][8][9][10][11][12] Sympathetic stimulation is commonly used to facilitate induction of these tachycardias, [1][2][3][4][5][6] whereas enhanced vagal tone by use of pharmacological or physical maneuvers is commonly used to terminate tachycardias. [7][8][9][10][11][12] However, in some patients, the onset of AV nodal reentrant tachycardia (AVNRT) occurs at times of presumed increased vagal tone, for example, during sleep or after sudden bending forward or squatting.…”

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confidence: 99%

Effects of Continuous Enhanced Vagal Tone on Dual Atrioventricular Node and Accessory Pathways

et al. 2003

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Background-The aim of this study was to test the electrophysiological effects of continuous enhanced vagal tone on dual atrioventricular (AV) nodal and accessory pathways. Methods and Results-This study included 10 patients with typical, slow-fast AV nodal reentrant tachycardia (AVNRT) and 10 patients with AV reciprocating tachycardia. Electrophysiological data were measured before and during continuous vagal enhancement by using phenylephrine infusion (0.6 to 1.5 g/kg per min). For patients with AVNRT, during phenylephrine infusion, 1:1 conduction times over the anterograde fast and slow and retrograde fast pathways were prolonged (453Ϯ64 to 662Ϯ120 ms, PϽ0.001; 379Ϯ53 to 443Ϯ95 ms, PϽ0.05; 405Ϯ112 to 442Ϯ118 ms, PϽ0.05). The effective refractory period and functional refractory period of the anterograde fast pathway were prolonged with phenylephrine (394Ϯ73 to 544Ϯ128 ms, PϽ0.001; 454Ϯ60 to 596Ϯ118 ms, PϽ0.001). In contrast, the effective refractory period and functional refractory period of the anterograde slow and retrograde fast were not significantly changed. No significant change was observed in the conduction or refractoriness of the accessory pathways in patients with AV reciprocating tachycardia nor in atrial or ventricular refractoriness. Conclusions-Enhanced

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Usefulness of isoproterenol in facilitating atrioventricular nodal reentry tachycardia during electrophysiologic testing

Cited by 29 publications

References 14 publications

Paradoxical reflex bradycardia after epinephrine infusion for arrhythmia induction in the electrophysiology laboratory

Paradoxical reflex bradycardia after epinephrine infusion for arrhythmia induction in the electrophysiology laboratory

Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Effects of Continuous Enhanced Vagal Tone on Dual Atrioventricular Node and Accessory Pathways

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