Rate-dependent AV nodal refractoriness: a new functional framework based on concurrent effects of basic and pretest cycle length

2009 ◽  
Vol 297 (6) ◽  
pp. H2136-H2143 ◽  
Author(s):  
Rafik Tadros ◽  
Jacques Billette
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Rabbit Heart ◽  
Combined Effects ◽  
Av Node ◽  
His Bundle ◽  
Rate Dependent ◽  
Supraventricular Tachyarrhythmias ◽  
Induced Changes ◽  
Fast Rates

The atrioventricular (AV) node filters atrial impulses. Underlying rate-dependent refractory properties are assessed with the effective (ERPN; longest nonconducted atrial cycle length) and functional (FRPN; shortest His bundle cycle) refractory period determined with premature protocols at different basic rates. Fast rates prolong ERPN and shorten FRPN, but these effects vary with subjects, age, and species. We propose that these opposite and variable effects reflect the net sum of concurrent cumulative and noncumulative effects associated with basic (BCL) and pretest cycle length (PTCL), respectively. To test this hypothesis, we assessed selective and combined effects of five BCL (S1S1) and six PTCL (S1S2) on ERPN, FRPN, and their subintervals (ERPN = A2H2 + H2A3 and FRPN = H2A3 + A3H3, where A is atrium and H is His bundle) with S1S2S3 protocols in six rabbit heart preparations. At control BCL, PTCL shortenings prolonged ERPN (113 ± 12 vs. 101 ± 14 ms, P < 0.01) as a net result of prolonged A2H2 and curtailed H2A3. At control PTCL, BCL shortenings increased ERPN (127 ± 20 vs. 101 ± 14 ms, P < 0.01) by prolonging A2H2. FRPN did not vary with BCL but decreased (163 ± 6 vs. 175 ± 10 ms, P < 0.01) with PTCL that curtailed H2A3. Equal BCL and PTCL shortenings as in standard protocols prolonged ERPN but left FRPN unchanged. Notably, ERPN and FRPN significantly correlated through their H2A3 subinterval. In conclusion, BCL and PTCL are both important determinants of AV nodal refractoriness and together account for rate-induced changes in ERPN and FRPN observed during standard premature protocols. ERPN and FRPN are related variables. Similar functional rules may govern nodal refractory behavior during supraventricular tachyarrhythmias.

Modulation of AV nodal and Hisian conduction by changes in extracellular space

1999 ◽  
Vol 276 (3) ◽  
pp. H953-H960
Author(s):  
Keith G. Lurie ◽  
Atsushi Sugiyama ◽  
Scott McKnite ◽  
Paul Coffeen ◽  
Keitaro Hashimoto ◽  
...  
Keyword(s):  
Extracellular Space ◽  
Left Ventricular ◽  
Conduction Time ◽  
Av Node ◽  
Total Blood ◽  
His Bundle ◽  
Induced Changes ◽  
Total Blood Flow ◽  
Dose Dependent Increase ◽  
Dose Dependent

Previous studies have demonstrated that the extracellular space (ECS) component of the atrioventricular (AV) node and His bundle region is larger than the ECS in adjacent contractile myocardium. The potential physiological significance of this observation was examined in a canine blood-perfused AV nodal preparation. Mannitol, an ECS osmotic expander, was infused directly into either the AV node or His bundle region. This resulted in a significant dose-dependent increase in the AV nodal or His-ventricular conduction time and in the AV nodal effective refractory period. Mannitol infusion eventually resulted in Wenckebach block ( n = 6), which reversed with mannitol washout. The ratio of AV nodal to left ventricular ECS in tissue frozen immediately on the development of heart block ( n = 8) was significantly higher in the region of block (4.53 ± 0.61) compared with that in control preparations (2.23 ± 0.35, n = 6, P < 0.01) and donor dog hearts (2.45 ± 0.18, n = 11, P < 0.01) not exposed to mannitol. With lower mannitol rates (10% of total blood flow), AV nodal conduction times increased by 5–10% and the AV node became supersensitive to adenosine, acetylcholine, and carbachol, but not to norepinephrine. We conclude that mannitol-induced changes in AV node and His bundle ECS markedly alter conduction system electrophysiology and the sensitivity of conductive tissues to purinergic and cholinergic agonists.

scholarly journals Functional mathematical model of dual pathway AV nodal conduction

2011 ◽  
Vol 300 (4) ◽  
pp. H1393-H1401 ◽  
Author(s):  
A. M. Climent ◽  
M. S. Guillem ◽  
Y. Zhang ◽  
J. Millet ◽  
T. N. Mazgalev
Keyword(s):  
Atrial Fibrillation ◽  
Mathematical Model ◽  
Refractory Period ◽  
Effective Refractory Period ◽  
Atrial Pacing ◽  
Wave Fronts ◽  
Av Node ◽  
Inferior Margin ◽  
His Bundle ◽  
Av Conduction

Dual atrioventricular (AV) nodal pathway physiology is described as two different wave fronts that propagate from the atria to the His bundle: one with a longer effective refractory period [fast pathway (FP)] and a second with a shorter effective refractory period [slow pathway (SP)]. By using His electrogram alternance, we have developed a mathematical model of AV conduction that incorporates dual AV nodal pathway physiology. Experiments were performed on five rabbit atrial-AV nodal preparations to develop and test the presented model. His electrogram alternances from the inferior margin of the His bundle were used to identify fast and slow wave front propagations. The ability to predict AV conduction time and the interaction between FP and SP wave fronts have been analyzed during regular and irregular atrial rhythms (e.g., atrial fibrillation). In addition, the role of dual AV nodal pathway wave fronts in the generation of Wenckebach periodicities has been illustrated. Finally, AV node ablative modifications have been evaluated. The model accurately reproduced interactions between FP and SP during regular and irregular atrial pacing protocols. In all experiments, specificity and sensitivity higher than 85% were obtained in the prediction of the pathway responsible for conduction. It has been shown that, during atrial fibrillation, the SP ablation significantly increased the mean HH interval (204 ± 39 vs. 274 ± 50 ms, P < 0.05), whereas FP ablation did not produce significant slowing of ventricular rate. The presented mathematical model can help in understanding some of the intriguing AV node mechanisms and should be considered as a step forward in the studies of AV nodal conduction.

Differential effect of verapamil isomers on sinus node and AV junctional region

1983 ◽  
Vol 244 (1) ◽  
pp. H80-H88
Author(s):  
H. O. Gloor ◽  
F. Urthaler
Keyword(s):  
Sinus Rhythm ◽  
Sinus Node ◽  
Conduction Time ◽  
Av Node ◽  
Junctional Rhythm ◽  
His Bundle ◽  
Sinus Node Artery ◽  
Rate Dependent ◽  
Av Conduction ◽  
Differential Responsiveness

The l- and d-isomers of verapamil were selectively perfused into the sinus node artery and atrioventricular (AV) node artery of 48 dogs. Injection of l-verapamil into the sinus node artery during sinus rhythm and into the AV node artery during AV junctional rhythm depresses both sinus rhythm and AV junctional rhythm significantly more than does the d-isomer. l-Verapamil is three to four times more powerful than d-verapamil. Injection of the isomers into the AV node artery during sinus rhythm rapidly impairs AV conduction. Increments in conduction time are measured exclusively at the level of the A-H interval of the His bundle electrogram, and l-verapamil is six times more powerful than d-verapamil. Neither d- nor l-verapamil in concentrations that exert a profound negative chronotropic effect or cause AV block, has any significant effect on transatrial or His bundle conduction. Thus these concentrations of d-verapamil have little or no significant effect on the fast sodium channel, but both verapamil isomers affect the slow channel. The main difference in action between l- and d-verapamil appears to be only quantitative in nature. The sinus node is significantly more sensitive to the negative chronotropic action of verapamil than is the AV junctional pacemaker, and this differential responsiveness appears to be related to the different intrinsic rates of the two pacemakers. During sinus rhythm (either in the presence or absence of atropine) sinus node automaticity is less affected than AV conduction when verapamil is given parenterally. We propose that this greater negative dromotropic effect of verapamil is also in part due to a rate-dependent process, since during sinus rhythm AV junctional cells have to be depolarized at frequencies significantly higher than their intrinsic rates.

The Influence of Cycle Length On the Effective and Functional Refractory Period of the Human Av Node

Angiology ◽  
1976 ◽  
Vol 27 (7) ◽  
pp. 468-474 ◽  
Author(s):  
Norman A. Cagin ◽  
Dorothy Kunstadt ◽  
Barrie Levitt
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Av Node

Mechanism of atrioventricular nodal facilitation in rabbit heart: role of proximal AV node

1997 ◽  
Vol 273 (4) ◽  
pp. H1658-H1668 ◽  
Author(s):  
Todor Mazgalev ◽  
Kent Mowrey ◽  
Igor Efimov ◽  
Gerard J. Fahy ◽  
David Van Wagoner ◽  
...  
Keyword(s):  
Cellular Response ◽  
Cycle Length ◽  
Cellular Responses ◽  
Rabbit Heart ◽  
Black Box ◽  
Av Node ◽  
Functional Studies ◽  
Microelectrode Recordings ◽  
Coupling Interval

The phenomenon of atrioventricular (AV) nodal “facilitation,” described in traditional “black box”-functional studies, implies enhanced AV nodal dromotropic function. We investigated the role of atrial prematurities in the modulation of the nodal cellular responses in the mechanism of AV nodal facilitation. Atrial and His (H) bundle electrograms and microelectrode recordings from proximal AV nodal cells were analyzed in 15 superfused rabbit AV node preparations. The pacing protocol consisted of 30 basic beats (S1; coupling interval S1-S1= 300 ms) followed by a facilitating prematurity (S2; coupling intervals S1-S2of 300, 200, 150, and 130 ms) followed by the test beat (S3; coupling interval S2-S3scanned in 5-ms steps). Conduction curves (S2-H2vs. S1-S2, S3-H3vs. S2-S3, and S3-H3vs. H2-S3) were constructed. Facilitation (i.e., shortening of S3-H3when S1-S2was shortened) was demonstrated in all preparations using the H2-S3( P < 0.001) but not the S2-S3format. Microelectrode recordings revealed a causal relationship between the improved proximal AV nodal cellular responses in facilitation and the prolonged S2-S3interval. There was no evidence for enhanced nodal dromotropic function directly resulting from the introduction of the facilitating beats. Thus facilitation is based on inherent cycle-length-dependent properties of the AV node during application of a complex pacing protocol and primarily reflects the uncontrolled modulation of the proximal cellular response.

Facilitated ventriculoatrial conduction: effects of sequential pacing interval and basic cycle length

1995 ◽  
Vol 268 (1) ◽  
pp. H384-H390
Author(s):  
A. F. Kuguoglu ◽  
D. W. Wallick ◽  
P. J. Martin
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Effective Refractory Period ◽  
Conduction Time ◽  
Time Intervals ◽  
Av Node ◽  
Anesthetized Dogs ◽  
Alpha Chloralose ◽  
Retrograde Conduction ◽  
Basic Cycle Length

We studied 1) the effects of pacing interval, 2) the timing of atrioventricular sequential pacing, and 3) the effects of successive premature intervals on retrograde conduction of the atrioventricular (AV) node in open-chest alpha-chloralose-anesthetized dogs. The ventricles and atria were sequentially paced at one of three levels of basic cycle length and one of six sequential time intervals (V1-A1) for three basic cycles (V1-V1). Then a premature ventricular impulse was introduced at various V1-V2 intervals, and the resultant retrograde conduction time (V2-A2 interval) was measured. Successive V1-V2 intervals were applied in an incremental or a decremental fashion. The V1-V2 intervals ranged from V1-V1 to V1-V2, at which the retrograde conduction was blocked. For each level of the above three factors, we plotted retrograde conduction time (V2-A2) as a function of the various premature intervals (V1-V2). We found that the time between atrial and ventricular activations was the most important factor in determining V1-V2 and in decreasing the effective refractory period of the AV node during retrograde conduction.

Propofol Has No Direct Effect on Sinoatrial Node Function or on Normal Atrioventricular and Accessory Pathway Conduction in Wolff-Parkinson-White Syndrome during Alfentanil/Midazolam Anesthesia

1995 ◽  
Vol 82 (4) ◽  
pp. 888-895. ◽  
Author(s):  
Michael D. Sharpe ◽  
Wojciech B. Dobkowski ◽  
John M. Murkin ◽  
George Klein ◽  
Raymond Yee
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Accessory Pathway ◽  
Right Atrial ◽  
Conduction Time ◽  
Av Node ◽  
White Syndrome ◽  
Sa Node ◽  
The Right ◽  
Wolff Parkinson White Syndrome

Background Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA) node and on normal atrioventricular (AV) and accessory pathways in patients with Wolff-Parkinson-White syndrome are unknown. Therefore, this study examined the effects of propofol on the cardiac electrophysiologic properties in humans to determine whether propofol promotes bradyarrhythmias and its suitability as an anesthetic agent in patients undergoing ablative procedures. Methods Twelve patients with Wolff-Parkinson-White syndrome undergoing radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (50 micrograms/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 micrograms.kg-1.min-1) and midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic study was performed consisting of measurement of the effective refractory period of the right atrium, AV node, and accessory pathway and the shortest cycle length of the AV node and accessory pathway during antegrade stimulation plus the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway during retrograde stimulation. Determinants of SA node function including sinus node recovery time, corrected sinus node recovery time, and SA conduction time; intraatrial conduction time and atrial-His interval also were measured. Reciprocating tachycardia was induced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were measured. Alfentanil/midazolam was then discontinued. Propofol was administered (bolus 2 mg/kg + 120 micrograms.kg-1.min-1), and the electrophysiologic measurements were repeated. Results Propofol caused a statistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of the AV node, right ventricle, and accessory pathway, as well as the shortest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciprocating tachycardia was inducible in 8 of 12 patients, and propofol had no effect on its electrophysiologic properties. All accessory pathways were successfully identified and ablated. Conclusions Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduction system. In addition, propofol has no direct effect on SA node activity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients undergoing ablative procedures who require either a neuroleptic or general anesthetic.

Regional distribution of ECS in contractile and conductive elements of rat and rabbit heart

1992 ◽  
Vol 263 (1) ◽  
pp. H168-H176
Author(s):  
K. G. Lurie ◽  
J. Dutton ◽  
P. Wiegn
Keyword(s):  
Regional Differences ◽  
Regional Distribution ◽  
Rabbit Heart ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Ventricular Muscle ◽  
Av Node ◽  
His Bundle ◽  
Ventricular Tissue ◽  
Left And Right

By adaptation of recently developed quantitative microanalytic techniques, the size of the extracellular space (ECS) was measured regionally in the rat and rabbit cardiac conductive and contractile tissues. When inulin and sucrose were measured as extracellular markers in rabbit heart, the ECS in the atrioventricular (AV) node was found to be, respectively, 2.4 and 2.2 times larger than that of adjacent ventricular muscle. By use of inulin, the ECS in the rabbit His bundle was found to be 1.8 times larger than the adjacent ventricular tissue. Similarly, when inulin was used in rat, the ECS of the AV node, His bundle, right bundle branch, and right atrium was found to be, respectively, 2.5, 1.9, 1.8, and 1.2 times larger than that of left and right ventricular muscle. Similarly, significant regional differences in ECS were also observed in rat heart with sucrose. By use of glucose as an ECS marker, these results also revealed a 2.5-2.9 times larger ECS in rat and rabbit AV node compared with contractile elements. In contrast, ATP content, measured as an intracellular marker, was the same in both AV nodal and ventricular muscle tissue from both rat and rabbit. These data demonstrate that there are significant regional variations in ECS within the cardiac conduction system. Collectively, the data obtained with all extracellular markers indicate that the size of the ECS of the conduction system is markedly larger than the adjacent contractile muscle.

scholarly journals Integrated rate-dependent and dual pathway AV nodal functions: principles and assessment framework

2014 ◽  
Vol 306 (2) ◽  
pp. H173-H183 ◽  
Author(s):  
Jacques Billette ◽  
Rafik Tadros
Keyword(s):  
Experimental Studies ◽  
Ventricular Rate ◽  
Av Node ◽  
Functional Studies ◽  
Rate Dependent ◽  
Pathway Function ◽  
Dual Pathway ◽  
Cycle Lengths ◽  
Supraventricular Tachyarrhythmias ◽  
Reentrant Arrhythmia

The atrioventricular (AV) node conducts slowly and has a long refractory period. These features sustain the filtering of atrial impulses and hence are often modulated to optimize ventricular rate during supraventricular tachyarrhythmias. The AV node is also the site of a clinically common reentrant arrhythmia. Its function is assessed for a variety of purposes from its responses to a premature protocol (S1S2, test beats introduced at different cycle lengths) repeatedly performed at different basic rates and/or to an incremental pacing protocol (increasingly faster rates). Puzzlingly, resulting data and interpretation differ with protocols as well as with chosen recovery and refractory indexes, and are further complicated by the presence of built-in fast and slow pathways. This problem applies to endocavitary investigations of arrhythmias as well as to many experimental functional studies. This review supports an integrated framework of rate-dependent and dual pathway AV nodal function that can account for these puzzling characteristics. The framework was established from AV nodal responses to S1S2S3 protocols that, compared with standard S1S2 protocols, allow for an orderly quantitative dissociation of the different factors involved in changes in AV nodal conduction and refractory indexes under rate-dependent and dual pathway function. Although largely based on data from experimental studies, the proposed framework may well apply to the human AV node. In conclusion, the rate-dependent and dual pathway properties of the AV node can be integrated within a common functional framework the contribution of which to individual responses can be quantitatively determined with properly designed protocols and analytic tools.

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