scholarly journals Conduction of Excitation from the Sinus Node to the Atrioventricular Node

1967 ◽  
Vol 31 (3) ◽  
pp. 373-380 ◽  
Author(s):  
MASAO TAKAYASU
Keyword(s):  
Sinus Node ◽  
Atrioventricular Node ◽  
Conduction Of Excitation

Abstract MP083: Autonomic Imbalance at the Level of Atrioventricular Node, but Not at the Level of Sinus Node, is Associated With Sudden Cardiac Death: The Atherosclerosis Risk in Community Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Srini V Mukundan ◽  
Muammar M Kabir ◽  
Jason Thomas ◽  
Golriz Sedaghat ◽  
Jonathan W Waks ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cox Regression ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Av Node ◽  
Atherosclerosis Risk In Communities ◽  
Autonomic Imbalance ◽  
Summary Effect ◽  
Atherosclerosis Risk

Introduction: Autonomic imbalance, quantified by decreased heart rate variability (HRV), is associated with increased cardiovascular mortality. It is unknown if autonomic influences on sinus and atrioventricular (AV) nodes are equally important for the risk of sudden cardiac death (SCD). Hypothesis: Autonomic influences on sinus and AV node are equally strongly associated with increased SCD, non-sudden cardiac death (non-SCD), and non-cardiac death. Methods: Baseline visit 10-second ECGs (n=14,250) of the Atherosclerosis Risk in Communities (ARIC) cohort were analyzed. Normalized variance of P-onset to P-onset intervals (PPVN) and QRS-onset to QRS-onset intervals (QQVN) was calculated to assess autonomic influence on sinus and AV node respectively. Normalized variance of Rpeak - Rpeak intervals was determined as HRV measure. Values were log-transformed to normalize distribution. SCD served as primary outcome. Secondary outcomes were non-SCD and non-cardiac death. Three Cox regression models were constructed for dichotomized at 20 th percentile predictor variables. Results: Over median follow-up of 24.4 years, there were 497 SCDs (incidence 1.66 [95%CI 1.52-1.82], 742 non-SCDs (incidence 2.48 [95%CI 2.31-2.67], and 3,753 non-cardiac deaths (incidence 12.6 [95%CI 12.1-13.0]) per 1,000 person-years. In paired analysis, LogPPVN was significantly larger than LogQQVN (-7.28±1.06 vs. -7.72±1.24; P<0.0001). There was no difference between LogQQVN and Log RRVN (-7.72±1.24 vs -7.72±1.23; P=0.364). After full adjustment, LogRRVN and LogQQVN were significantly associated with non-SCD and SCD. Association with non-SCD was stronger. LogPPVN was independently associated with non-SCD but not SCD. No value was associated with non-cardiac death. Conclusion: Autonomic imbalance at the AV node, with likely summary effect at the bundle of His, is associated with SCD and non-SCD. Autonomic imbalance at the SA node is associated with non-SCD only. Autonomic input to SA and AV node should be further studied.

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

1999 ◽  
Vol 90 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Michael D. Sharpe ◽  
Daniel J. Cuillerier ◽  
John K. Lee ◽  
Magdi Basta ◽  
Andrew D. Krahn ◽  
...  
Keyword(s):  
Cycle Length ◽  
Sinoatrial Node ◽  
Sinus Node ◽  
Accessory Pathway ◽  
Atrioventricular Node ◽  
Conduction Time ◽  
White Syndrome ◽  
The Right ◽  
Ablative Procedures ◽  
Wolff Parkinson White Syndrome

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.

Atrial premature beats

ESC CardioMed ◽  
2018 ◽  
pp. 2050-2052
Author(s):  
Tatjana Potpara
Keyword(s):  
Heart Disease ◽  
Sinus Node ◽  
Pulmonary Veins ◽  
Atrioventricular Node ◽  
Structural Heart Disease ◽  
Class Iii ◽  
P Waves ◽  
Asymptomatic Patients ◽  
Narrow Qrs Complex ◽  
Premature Beats

Atrial premature beats (APBs), also referred to as atrial or supraventricular extrasystoles, represent premature atrial depolarization occurring earlier than the next expected regular sinoatrial activation, usually from a site outside the sinus node. Premature depolarizations originating from the atrioventricular node or His bundle are termed atrioventricular junctional premature beats. In general, APBs occur in adults of any age, with or without structural heart disease. Increased atrial volume and/or pressure, or increased sympathetic tone are associated with increased frequency of APBs, while in individuals without structural heart disease APBs often originate from the pulmonary veins and may precipitate atrial fibrillation. Patients with APBs are often asymptomatic, or experience palpitations, dizziness, or even presyncope. Significant haemodynamic compromise due to APBs is uncommon. Physical examination may reveal pulse irregularity, and surface electrocardiograms (ECGs) usually show premature P waves which differ from the sinus P morphology, followed by a normal, shortened, or prolonged PR interval (depending on the APB site of origin) and narrow QRS complex. Ambulatory ECG (Holter) monitoring helps to establish the diagnosis when symptoms are sporadic or to quantify the frequency of APBs. Counselling and reassurance would suffice in most minimally symptomatic or asymptomatic patients with APBs, but any underlying cardiovascular disorder must be treated. Beta blockers or class III antiarrhythmic drugs (or class IC in patients without significant structural heart disease) can be used to attenuate symptoms or suppress the APBs facilitating other tachyarrhythmias. Catheter ablation could be considered in selected patients.

Posterior sinus node artery and accessory atrioventricular node artery arising by a common origin: A case report

1998 ◽  
Vol 11 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Shigenori Tanaka ◽  
Hye-Yeon Lee ◽  
Shigeki Mizukami ◽  
Toshio Nakatani ◽  
In-Huyk Chung
Keyword(s):  
Case Report ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Common Origin ◽  
Sinus Node Artery

Simulation analysis of conduction of excitation in the atrioventricular node

1987 ◽  
Vol 126 (3) ◽  
pp. 275-288 ◽  
Author(s):  
Seiichi Urushibara ◽  
Mitsuo Kawato ◽  
Kazuo Nakazawa ◽  
Ryoji Suzuki
Keyword(s):  
Simulation Analysis ◽  
Atrioventricular Node ◽  
Conduction Of Excitation

Vagally induced hyperpolarization in atrioventricular node

1986 ◽  
Vol 251 (3) ◽  
pp. H631-H643 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson ◽  
A. Pelleg
Keyword(s):  
Action Potentials ◽  
Cycle Length ◽  
Time Course ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Conduction Time ◽  
Sinus Cycle Length ◽  
Atrioventricular Nodal Conduction ◽  
The Moment

The effects of postganglionic vagal stimulation on atrioventricular nodal conduction were studied in 12 rabbit atrial-atrioventricular nodal preparations. Vagal stimulation was introduced in the sinus and atrioventricular nodes, separately or in combination, using single bursts of subthreshold stimuli. The sinus cycle length was scanned to identify the phasic effect of vagal stimulation. Action potentials from cells in the AN, N, and NH regions of the atrioventricular node were recorded by microelectrode techniques. Vagally induced hyperpolarization of cells in the atrioventricular node resulted in a phase-dependent prolongation of conduction time and reflected the level of residual hyperpolarization at the moment of arrival of the next atrial beat at the atrioventricular nodal input region. Vagally induced hyperpolarization was membrane potential dependent, although its overall time course was similar at different phases. Increased diastolic depolarization followed the maximal hyperpolarization. This "rebound" observed at certain phases was responsible for paradoxical shortening of the conduction time after vagal stimulation. The predominant effects of local vagal stimulation in the atrioventricular node were observed in cells in or near the N region. Slower rate of rise, shorter amplitude and duration, as well as step formations were among the changes in action potentials recorded from these cells. The effects of vagal stimulation were inhomogeneous between different regions of the atrioventricular node as well as within the N region, producing alternative pathways of conduction and the potential for reentry. The concomitant changes in sinus cycle length resulting from vagal stimulation in the sinus node region altered the phasic effects of vagal stimulation introduced in the atrioventricular node. This was related to a direct influence of the prolonged sinus cycle length on atrioventricular nodal refractoriness as well as an indirect effect on the degree of residual vagally induced hyperpolarization at the moment of arrival of the delayed atrial beat. These findings provide mechanistic explanations for the complex effects of vagal stimulation on atrioventricular nodal conduction.

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade

1984 ◽  
Vol 108 (5) ◽  
pp. 1255-1261 ◽  
Author(s):  
Paolo Alboni ◽  
Narashimhan Shantha ◽  
Laura Filippi ◽  
Roberto Pirani ◽  
Sabino Preziosi ◽  
...  
Keyword(s):  
Sinus Node ◽  
Atrioventricular Node ◽  
Clinical Effects ◽  
Autonomic Blockade

Causes, diagnosis, and therapeutic strategy in bradyarrhythmias

2016 ◽  
Author(s):  
Harminder S. Gill ◽  
Jaswinder S. Gill
Keyword(s):  
Therapeutic Strategy ◽  
Care Setting ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Underlying Disease ◽  
System Disease ◽  
Permanent Pacing ◽  
Transcutaneous Pacing ◽  
Conduction System Disease ◽  
Underlying Causes

Bradyarrhythmias (defined as a heart rate <60 beat/min) occur frequently in the critical care setting. Most are related to underlying disease processes and the multidrug therapies administered. Because of the intense monitoring of these patients, recognition is generally easy. Examination of the ECG will allow diagnosis of the type of bradycardia based on the sinus node, atrioventricular node and the infra-Hissian conducting system. The extent of conduction system disease can be estimated and this has an influence on the prognosis. Bradycardias causing haemodynamic collapse require treatment of underlying causes, resuscitation, and administration of atropine and epinephrine. If there is no response to these then either transcutaneous pacing, or temporary transvenous pacing is necessary. This can be followed by implantation of a permanent pacing system. The outcome of correctly diagnosing and treating a bradyarrhythmia is excellent as long as the causative pathology can be stabilized.

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