Phenomenon of the Gap in Atrioventricular Conduction in the Human Heart

Wit, Andrew L.; Damato, Anthony N.; Weiss, Melvin B.; Steiner, Charles

doi:10.1161/01.res.27.5.679

Cited by 62 publications

(8 citation statements)

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“…• One type of supernormal conduction, i.e., the paradoxical propagation of closely coupled stimuli when stimuli at longer coupling intervals are blocked, reflects a gap phenomenon (1)(2)(3)(4)(5)(6). This phenomenon occurs when the refractory period of a distal conduction site limits conduction.…”

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Nature of the Gap Phenomenon in Man

Denes

Dhingra

et al. 1974

Circulation Research

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The atrioventricular (AV) gap phenomenon occurs when the effective refractory period of a distal site is longer than the functional refractory period of a proximal site and when closely coupled stimuli are delayed enough at the proximal site to allow distal site recovery. According to previous studies, in type 1 gap, the distal site of block is distal to the His bundle (ventricular specialized conduction system) and the proximal site of block is in the AV node. In type 2 gap, both the proximal and the distal sites of conduction block are within the ventricular specialized conduction system. Using His bundle recordings and atrial extra-stimulus techniques in man, we observed three previously undescribed types of gaps between (1) the AV node (distal) and the atrium (proximal), (2) the His bundle (distal) and the AV node (proximal), and (3) the ventricular specialized conduction system or a bundle branch (distal) and the His bundle (proximal). The delays at the His bundle in the second and third types of gaps seen in this study were demonstrated as splitting of His bundle potentials. Gaps between the AV node or the His bundle and the ventricular specialized conduction system were more easily demonstrated at long cycle lengths, but gaps between the atrium and the AV node were more easily demonstrated at short cycle lengths. Therefore, the previous subdivision of gaps into two types is an oversimplification, because gaps can occur between multiple sites in the conduction system. The gap phenomenon may be potentiated by both long and short cycle lengths; long cycle lengths increase the effective refractory period of a distal site, e.g., the His bundle and the ventricular specialized conduction system, and the short cycle lengths decrease the functional refractory period of a proximal site, e.g., the atrium and the AV node. KEY WORDS atrial extra stimuli functional block cycle length His bundle electrogram supernormal conduction refractory period split His bundle potentials intra-atrial conduction delay• One type of supernormal conduction, i.e., the paradoxical propagation of closely coupled stimuli when stimuli at longer coupling intervals are blocked, reflects a gap phenomenon (1-6). This phenomenon occurs when the refractory period of a distal conduction site limits conduction. With closely coupled stimuli, enough proximal delay occurs so that the impulse arrives at the distal conducting site late enough to be conducted. Gallagher and co-workers (5) have defined two types of gaps. In type 1 gap, the initial distal site of block is distal to the His bundle recording site, and the proximal site of delay is in the atrioventricular (AV) node. In type 2 gap, both the distal and the proximal site of conduction delay are distal to the His bundle recording site (5). A third kind of gap has recently been described by Agha and co-workers (6) in a patient with AV block; however, this kind of gap appears to reflect supernormal conduction, and proximal and distal sites of delay have not been defined (6).In the present st...

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confidence: 99%

Nature of the Gap Phenomenon in Man

Denes

Dhingra

et al. 1974

Circulation Research

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“…Class 1 antiarrhythmic drugs such as lidocaine and procainamide do not have comparable antifibrillatory effects (12,30,31). These drugs also differ from bretylium and bethanidine in their effects on cardiac action potential parameters (33)(34)(35)(36)(37), which further indicates that antifibrillatory and antiarrhythmic drug actions are not directly related. This report demonstrates that these differing drug actions are correlated with differences in the blockade of membrane ionic currents.…”

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confidence: 98%

“…The blockade of IK explains the most consistent electrophysiologic action of bretylium, which is to increase the action potential duration (APD) (33)(34)(35). Bethanidine and meobentine have also been reported to have similar effects on APD in rat heart (37).…”

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“…Acad. Sci failure to decrease upstroke velocity (Vmax) of the normal cardiac action potential (33)(34)(35), which suggests that bretylium is also unable to cross the cardiac membrane. The lack of effect of external bretylium and bethanidine on IK in squid axons is attributable to the lack of an external receptor for most potassium channel blockers in this preparation, in contrast to other nerve and cardiac preparations where it is present (46,47).…”

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Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

Bacaner¹,

Clay²,

Shrier³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.

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“…[2][3][4][5][6][7][8][9][10][11][12][13] In all cases, the gap phenomenon was explained in terms of different refractory or conductive properties or both of two consecutive units of the conduction system (e.g., atrium-atrioventricular [AV] node, AV node-bundle of His, bundle of His-His Purkinje system). The prerequisite for the development of the gap phenomenon in most instances was the existence of a distal unit with an effective refractory period longer than the functional refractory period of the proximal unit.…”

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A new mechanism for atrioventricular nodal gap-vagal modulation of conduction.

1989

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The well-known paradoxic behavior of atrioventricular conduction, the so-called gap phenomenon, that occurs when impulses within a certain range of coupling intervals are blocked while impulses with shorter coupling intervals are conducted is attributed to differences in properties of refractoriness in neighboring regions of the conduction system. In contrast, in the present study a model was developed showing a similar phenomenon, dependent on different electrophysiologic mechanisms and localized within the atrioventricular node in an isolated rabbit heart tissue preparation (n=11). The hearts were paced at cycle length of 400-500 msec, and atrioventricular nodal conduction times (A2H2) were measured versus atrial extrastimulus (A1A2) coupling intervals by standard extrastimulus techniques. Postganglionic vagal stimulation was applied in the atrioventricular node as short bursts of subthreshold (for myocardium) stimuli with duration of 50-150 msec, amplitude of 20-800 ,uA, and absolute phase (delay after A,) of 0-500 msec. Vagal bursts with appropriate parameters consistently produced bimodal conduction curves. Initially, gradual shortening of the A1A2 coupling interval was associated with an increasing A2H2, with an accentuated increase (or even atrioventricular block) within an intermediate A1A2 range. However, further shortening of the A1A2 coupling interval produced a decrease in A2H2, which subsequently was followed by a block at the effective refractory period. Microelectrode recordings indicated that this characteristic bimodal pattern of conduction curves, demonstrating a gap, reflected transient vagally induced hyperpolarization in the N region of the node. In those instances where conduction block occurred and gap was manifest, the most marked hyperpolarization coincided with the time of arrival of midcycle premature extrastimuli, whereas the conduction of extrastimuli with either more or less prematurity was under less-marked vagal influence. Thus, this study demonstrates a new electrophysiologic mechanism producing anomalous conduction curves and the gap phenomenon within the atrioventricular node based on vagal-induced nonuniform recovery of diastolic excitability. (Circulation 1989;79:417-430) T he term "gap in atrioventricular conduction" was originally used by Moe et all to describe a seemingly paradoxical electrophysiologic phenomenon-premature atrial stimuli with progressively decreasing coupling intervals conducted to the ventricles with increasing PR intervals until atrioventricular block occurred. However, a further decrease in the coupling interval of the atrial stimulus was unexpectedly associated with restoredFrom the cardiovascular divisions

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Phenomenon of the Gap in Atrioventricular Conduction in the Human Heart

Cited by 62 publications

References 13 publications

Nature of the Gap Phenomenon in Man

Nature of the Gap Phenomenon in Man

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

A new mechanism for atrioventricular nodal gap-vagal modulation of conduction.

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