Effect of phasic vagal stimulation and atrial pacing site on atrioventricular conduction time

1997 ◽  
Vol 272 (5) ◽  
pp. H2289-H2298 ◽  
Author(s):  
D. A. Igel ◽  
D. W. Wallick ◽  
P. J. Martin ◽  
M. N. Levy

We tested the hypothesis that the effect of phasic vagal stimulation on atrioventricular (AV) conduction time is affected by the site of atrial pacing in anesthetized dogs. We paced the right atrium at a constant cycle length from the interatrial septum (IAS), superior coronary sinus (SCS), or inferior coronary sinus (ICS) regions, and we evaluated the time-dependent effects of vagal stimulation on AV conduction at each pacing site. When we stimulated the vagi at stimulus (St)-A phases greater than 136 +/- 40 ms and less than the phase that blocked AV conduction (182 +/- 70 ms), IAS pacing prolonged A-V intervals by 8.6 +/- 8.2 ms more than ICS pacing. A change in pacing site affected the A-V intervals by up to 30 ms when we stimulated the vagus at those times that caused the A-V intervals to prolong maximally. Furthermore, the effect of atrial pacing site on A-V intervals was modulated by AV nodal recovery times during the second or third cycles after the vagal stimulus.

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.


1988 ◽  
Vol 66 (9) ◽  
pp. 1198-1205 ◽  
Author(s):  
Margaret R. Warner ◽  
Jerod M. Loeb

The beat-by-beat changes in atrioventricular (AV) conduction evoked by constant frequency and phase-coupled vagal stimulation were examined both qualitatively and quantitatively in 13 anesthetized dogs. The effects of pacing cycle length and sympathetic activity on the vagally induced phasic changes in AV conduction were also characterized. When the vagal stimulus interval was nearly equal to the pacing cycle length and the vagal stimulus moved progressively through the cardiac cycle, AV interval oscillated in a rhythmic fashion. The rhythmicity of the vagally induced AV interval oscillations was altered substantially by changes in either the vagal stimulus interval or the pacing cycle length. The vagally induced AV interval oscillations were abolished during phase-coupled vagal stimulation; however, the magnitude of the resultant steady-state AV interval depended on the time relative to the phase of the cardiac cycle that the vagal stimulus was delivered. In the presence or absence of sympathetic stimulation, a vagal stimulus falling approximately 200 ms prior to atrial depolarization evoked the greatest prolongation in AV interval, regardless of the pacing cycle length. Additionally, the effects of combined sympathetic and phase-dependent vagal stimulation on the AV interval were additive. These data confirm that the influence of a vagal stimulus on AV interval can be predicted from the phase in the cardiac cycle that the vagal stimulus is delivered. Moreover, this phase dependency of vagal effects evokes marked qualitative variations in AV interval response patterns when either the vagal stimulus interval or the pacing cycle length is altered.


1990 ◽  
Vol 258 (1) ◽  
pp. H38-H44 ◽  
Author(s):  
A. S. Pickoff ◽  
A. Stolfi

The effects of tonic right and left vagal stimulation (RVS and LVS) on electrophysiological properties of the immature myocardium and specialized conduction system were evaluated in 11 neonatal canines pretreated with propranolol (1 mg/kg iv). Electrophysiological studies were performed by recording intracardiac electrograms from multiple endocardial catheters during programmed electrical stimulation. Assessments were made of sinus node function, intra-atrial, atrioventricular (AV) nodal and His-Purkinje conduction, and atrial and ventricular refractoriness in the control state and during RVS and LVS at 4–12 Hz. Vagal stimulation prolonged the sinus cycle length; RVS produced a 38% increase and LVS a 25% increase at 8 Hz (P less than 0.01). There were no changes in the intra-atrial or His-Purkinje conduction times. Comparable increases occurred during RVS and LVS in the paced cycle length resulting in AV nodal Wenckebach, the AV nodal conduction time at a paced cycle length of 340 ms, and the effective and functional refractory periods of the AV node, suggesting symmetrical influences of the right and left vagus on neonatal AV nodal function. Right atrial effective and functional refractory periods shortened significantly during vagal stimulation (ERP, 36% RVS and 23% LVS; FRP, 27% RVS and 15% LVS), and in 5 of 11 neonates, a sustained regular atrial tachyarrhythmia was induced during atrial extra-stimulation. Small yet significant increases were observed in the right ventricular ERP and FRP during vagal stimulation. This study provides information regarding the functional integrity of the parasympathetic nervous system and its potential role as a modulator of the electrophysiological properties of the newborn heart.(ABSTRACT TRUNCATED AT 250 WORDS)


1975 ◽  
Vol 228 (5) ◽  
pp. 1440-1445 ◽  
Author(s):  
WJ Mandel ◽  
MM Laks ◽  
AI Arieff ◽  
K Obayashi ◽  
H Hayakawa ◽  
...  

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.


1999 ◽  
Vol 90 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Michael D. Sharpe ◽  
Daniel J. Cuillerier ◽  
John K. Lee ◽  
Magdi Basta ◽  
Andrew D. Krahn ◽  
...  

Background The effects of sevoflurane on the electrophysiologic properties of the human heart are unknown. This study evaluated the effects of sevoflurane on the electrophysiologic properties of the normal atrioventricular conduction system, and on the accessory pathways in patients with Wolff-Parkinson-White syndrome, to determine its suitability as an anesthetic agent for patients undergoing ablative procedures. Methods Fifteen patients with Wolff-Parkinson-White syndrome undergoing elective radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (20-50 microg/kg) and midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (0.5 to 2 microg x kg(-1) x min(-1)) and midazolam (1 or 2 mg every 10-15 min, as required). An electrophysiologic study measured the effective refractory period of the right atrium, atrioventricular node, and accessory pathway; the shortest conducted cycle length of the atrioventricular node and accessory pathway during atrial pacing; the effective refractory period of the right ventricle and accessory pathway; and the shortest retrograde conducted cycle length of the accessory pathway during ventricular pacing. Parameters of sinoatrial node function included sinus node recovery time, corrected sinus node recovery time, and sinoatrial conduction time. Intraatrial conduction time and the atrial-His interval were also measured. Characteristics of induced reciprocating tachycardia, including cycle length, atrial-His, His-ventricular, and ventriculoatrial intervals, also were measured. Sevoflurane was administered to achieve an end-tidal concentration of 2% (1 minimum alveolar concentration), and the study measurements were repeated. Results Sevoflurane had no effect on the electrophysiologic parameters of conduction in the normal atrioventricular conduction system or accessory pathway, or during reciprocating tachycardia. However, sevoflurane caused a statistically significant reduction in the sinoatrial conduction time and atrial-His interval but these changes were not clinically important. All accessory pathways were successfully identified and ablated. Conclusions Sevoflurane had no effect on the electrophysiologic nature of the normal atrioventricular or accessory pathway and no clinically important effect on sinoatrial node activity. It is therefore a suitable anesthetic agent for patients undergoing ablative procedures.


1985 ◽  
Vol 248 (1) ◽  
pp. H61-H68 ◽  
Author(s):  
W. C. Randall ◽  
J. L. Ardell

From right thoracotomy (T4-T5), the canine heart was suspended in its pericardium to expose its major venous inputs. Vagal and sympathetic trunks were prepared for electrical stimulation (10-20 Hz, 5.0 ms, 3-5 V) before and after each separate denervation procedure. Vagal stimulation was instituted with and without concurrent atrial pacing. The following surgical interventions were performed. 1) The superior vena cava was cleared of connective and nervous tissues from the pericardial reflection caudally to the level of the right pulmonary artery. 2) The azygos vein was cleared, tied, and sectioned. 3) The right pulmonary veins were isolated and cleared intrapericardially. 4) The dorsal surface of the atria was dissected between the right and left pulmonary veins and painted with phenol. Each step in the procedure elicited successive stepwise deletion of parasympathetic influences on sinoatrial tissues of the canine heart with only minor ablation of sympathetic inputs. 5) Dissection of the triangular fat pad at the junction of the inferior vena cava and inferior left atrium eliminated the remaining parasympathetic efferent input to the heart with dramatic deletion of atrioventricular block during either left or right vagal stimulation, again with preservation of most of the sympathetic innervation. These experiments clearly demonstrate differential and selective inputs of parasympathetic pathways to sinoatrial (SAN) and atrioventricular (AVN) regions of the dog heart but relatively little interference with sympathetic distributions.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 254 (4) ◽  
pp. H651-H657
Author(s):  
J. M. Loeb ◽  
J. M. deTarnowsky

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.


1991 ◽  
Vol 260 (2) ◽  
pp. H459-H464 ◽  
Author(s):  
S. Yamasaki ◽  
A. Stolfi ◽  
A. S. Pickoff

We studied the responses of sinus cycle length and atrioventricular (AV) nodal conduction to brief, critically timed vagal stimuli in 25 neonatal (9.6 +/- 3.1 days) canines. Vagal stimuli were delivered to the right or left decentralized cervical vagosympathetic trunk as either a single, brief stimulus train or a repetitive, phase-coupled train with both stimulation paradigms programmed to scan the entire cardiac cycle. The effects of brief vagal stimuli on cardiac cycle length were measured while the heart was beating spontaneously, and the vagal effects on AV nodal conduction were measured while the cycle length was held constant by atrial pacing at 300 ms. Neither changes in sinus cycle length nor AV nodal conduction demonstrated classical phase dependency, i.e., a gradual increase in the magnitude of the vagal response as stimuli are delivered progressively later in the cardiac cycle until the latency period (that point in the cardiac cycle at which vagal stimulation no longer affects the next cardiac cycle) is reached. Phase-response curves (PRCs) to single and repetitive stimuli typically exhibited either a flat response or a small decrease in magnitude as the latency period of the PRC was approached. Thus the neonatal sinus and AV node PRCs exhibit a different configuration than that reported in the adult.


1965 ◽  
Vol 208 (5) ◽  
pp. 946-953 ◽  
Author(s):  
Skoda Afonso ◽  
George G. Rowe ◽  
Jorge E. Lugo ◽  
Charles W. Crumpton

Only a part of heat produced by the left ventricle is removed by the coronary blood. During a cold saline infusion into the right ventricle, LV myocardial temperature decreases and the myocardium loses a measurable amount of heat. A part of this heat is also removed by the coronary blood. If simultaneous thermal curves are recorded from the aorta and coronary sinus during the infusion it is possible to calculate left ventricle heat production by the following formula: H = LV weight x ΔT x Δt x K x 60:A, where ΔT = myocardial temperature drop during the infusion; Δt = coronary sinus-aorta blood temperature difference prior to infusion; K = specific heat of myocardium; A = difference of areas of superimposed coronary sinus and aorta's thermal curves. Heat production estimated by the formula in 19 determinations has been compared with the heat production calculated from myocardial oxygen consumption. Measurements obtained by this method seem to be representative of left ventricle heat production.


1986 ◽  
Vol 251 (6) ◽  
pp. H1126-H1133 ◽  
Author(s):  
M. R. Warner ◽  
J. M. Loeb

We examined the integration of heart rate and neural influences at the atrioventricular (AV) node in conscious dogs. Animals were anesthetized and, under sterile conditions, instrumented to chronically record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded on a beat-by-beat basis, and heart rate and AV interval were plotted graphically as a function of time. Resting animals exhibited both respiratory sinus arrhythmia and marked oscillations in AV conduction time associated with respiration. During inspiration AV interval was shortened, and during expiration AV interval was prolonged. To obviate the effect of cyclic changes in heart rate, atrial pacing was used to increase heart rate over a wide range both abruptly and linearly. Regardless of the pattern of heart rate change, AV interval oscillated at the respiratory frequency at pacing rates 10-100 beats/min above control. Higher levels of atrial pacing resulted in AV conduction patterns that were correlated with changes in blood pressure. Thus in the conscious dog variations in AV conduction time occur on a beat-by-beat basis in conjunction with respiration; oscillatory activity of AV conduction is not dependent on simultaneous changes in heart rate; and during atrial pacing, autonomic neural activity associated with respiration and blood pressure appears to dynamically modulate AV conduction with respiratory effects predominating at low heart rates and blood pressure effects at high heart rates.


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