Atrial Reciprocal Rhythm

Kistin, Albert D.

doi:10.1161/01.cir.32.5.687

Cited by 36 publications

(9 citation statements)

References 49 publications

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“…AV nodal reentry can be initiated by a properly timed premature atrial impulse which blocks in one region of the upper node but conducts through another region and eventually returns to the atrium after fibers in the region of block and fibers in the atrium recover excitability (34). A recent clinical report has indicated that verapamil is highly effective against supraventricular tachycardia (1), an arrhythmia that sometimes results from reentry within the AV node (35,36). Our studies show that verapamil prevents the initiation of tachycardia in the isolated rabbit atrium by prolonging the effective refractory period of the AV node.…”

Section: Discussionmentioning

confidence: 99%

Effect of Verapamil on the Sinoatrial and Atrioventricular Nodes of the Rabbit and the Mechanism by Which it Arrests Reentrant Atrioventricular Nodal Tachycardia

Wit

Cranefield

1974

Circulation Research

274

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The effects of verapamil, an antiarrhythmic drug that apparently blocks slow inward currents, were studied on the isolated, superfused sinoatrial (SA) and atrioventricular (AV) nodes of the rabbit heart with intracellular microelectrodes. Verapamil decreased the rate of spontaneous impulse initiation by the SA node. This effect could be overcome with epinephrine. Concomitantly, verapamil decreased the amplitude of SA node action potentials without reducing maximum diastolic potential. The peak of the action potential fell well short of reversal after exposure to the drug. Verapamil had similar effects on the action potentials of the upper and middle AV nodal regions, reducing action potential amplitude so that the overshoot vanished without significantly reducing maximum diastolic potential. Action potentials of fibers in the lower region of the AV node were not affected as greatly. Verapamil slowed conduction of atrial impulses through the AV node; such slowing increased when the atrial rate increased. Verapamil also prolonged the effective refractory period of the AV node, thus slowing or blocking conduction of premature impulses. Verapamil prevented AV nodal reentry and initiation of atrial tachycardia by causing premature impulses to block rather than to conduct with the delay needed to initiate reentry. Verapamil had no effect on the rate of depolarization, action potential amplitude, or maximum diastolic potential of atrial or His bundle fibers. The results are consistent with the hypotheses that fibers in the SA and AV nodes show slow response activity, that the slow response plays a crucial role in causing certain cardiac arrhythmias, and that drugs that block the slow response are therefore antiarrhythmic. KEY WORDSslow response cardiac antiarrhythmic drugs tachycardia overshoot calcium-dependent action potentials reentrant arrhythmias effective refractory period

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Section: Discussionmentioning

confidence: 99%

Effect of Verapamil on the Sinoatrial and Atrioventricular Nodes of the Rabbit and the Mechanism by Which it Arrests Reentrant Atrioventricular Nodal Tachycardia

Wit

Cranefield

1974

Circulation Research

274

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“…Functional longitudinal dissociation seems to be a property of the normal AV node, as is evident both from studies on experimental animals (3-5) and from clinical studies (6,7). It has often been postulated that a circus movement within the AV node was the mechanism responsible for a reciprocating tachycardia (6,(8)(9)(10)(11)(12). During a study on the conduction in the AV node of isolated 404 JANSE, VAN CAPELLE, FREUD, DURRER rabbit heart preparations, recording the transmembrane potentials of several AV nodal cells simultaneously, we observed in several experiments that a single premature atrial stimulus elicited an atrial tachycardia.…”

mentioning

confidence: 99%

Circus Movement within the AV Node as a Basis for Supraventricular Tachycardia as Shown by Multiple Microelectrode Recording in the Isolated Rabbit Heart

Janse

Capelle

Freud

et al. 1971

Circulation Research

184

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Supraventricular tachycardia in an isolated rabbit heart preparation was repeatedly initiated and terminated by carefully timed atrial premature beats. Transmembrane action potentials of AV nodal cells were recorded simultaneously by a "brush electrode" consisting of 10 microelectrodes. Surface electrograms of atrium and His bundle were also recorded. The moments of activation of 54 different AV nodal cells, both during regular driving of the atrium and during tachycardia were ascertained. Premature atrial beats introduced during tachycardia would either "reset" the tachycardia or terminate it. The sequence of activation of the AV nodal cells when initiating tachycardia, during tachycardia itself, and when premature beats were interpolated during tachycardia warrant the conclusion that a circus movement in the AV node, based on functional longitudinal dissociation of the upper AV node, was the underlying mechanism of the arrhythmia. KEY WORDS reciprocating tachycardia echo beats longitudinal dissociation transmembrane potentials atrial premature beats initiation and termination of tachycardia• On the basis of experiments on turtle hearts, Mines (1) described the basic mechanism underlying a reciprocating rhythm: "A slight difference in the rate of recovery of two divisions of the AV connexion might determine that a extrasystole of the ventricle . . . should spread up to the auricle by that part of the AV connexion having the quicker recovery process and not by the other part. In such a case, when the auricle became excited by this impulse, the other portion of the AV connexion would be ready to take up the transmission back to the ventricle. Provided the transmission in each direction was slow, the chamber at either end would be ready to respond . . . and thus the condition once

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“…Of note, there were frequent P-QRS-P' complexes interrupting the cardiac cycle. The electrocardiographic characteristics ofthese P-QRS-P' complexes fulfilled the diagnostic criteria of a 'reciprocal rhythm' (Kistin, 1965;Roelandt and Van der Hauwert, 1968) in which the P' waves were related to retrograde activation of the atria (the low septal right atrium in the vicinity of the atrioventricular node was activated 20 ms before the high right atrium) (Fig. 2).…”

Section: Electrophysiologymentioning

confidence: 87%

“…This phenomenon, when perpetuated, may produce a run of reciprocating tachycardia (Kistin, 1965). The presence of dual pathways or the development of functional longitudinal dissociation within the atrioventricular node is known to favour its occurrence (Mendez and Moe, 1966;Denes et al, 1973).…”

mentioning

confidence: 99%

Atrioventricular reciprocal rhythm and chronic reciprocating tachycardia in a newborn infant with concealed Wolff-Parkinson-White syndrome.

Sung¹,

Ferrer²,

García³

et al. 1977

Heart

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A case of atrioventricular reciprocal rhythm and chronic reciprocating tachycardia in a newborn infant is presented. Electrophysiological studies suggest that these rhythm disturbances are related to the presence of a right-sided atrioventricular accessory pathway capable only of retrograde conduction (concealed Wolff-Parkinson-White syndrome). The technique of recording the sequence of atrial activation during the tachycardia is described and its clinical importance emphasised.

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Atrial Reciprocal Rhythm

Cited by 36 publications

References 49 publications

Effect of Verapamil on the Sinoatrial and Atrioventricular Nodes of the Rabbit and the Mechanism by Which it Arrests Reentrant Atrioventricular Nodal Tachycardia

Effect of Verapamil on the Sinoatrial and Atrioventricular Nodes of the Rabbit and the Mechanism by Which it Arrests Reentrant Atrioventricular Nodal Tachycardia

Circus Movement within the AV Node as a Basis for Supraventricular Tachycardia as Shown by Multiple Microelectrode Recording in the Isolated Rabbit Heart

Atrioventricular reciprocal rhythm and chronic reciprocating tachycardia in a newborn infant with concealed Wolff-Parkinson-White syndrome.

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