CHANGES IN ATRIAL RATE DURING AND FOLLOWING VENTRICULAR ARREST FROM ACETYLCHOLINE INJECTIONS INTO THE ATRIOVENTRICULAR NODE ARTERY OF THE DOG

1967 ◽  
Vol 45 (3) ◽  
pp. 375-388 ◽  
Author(s):  
R. A. Nadeau ◽  
A. K. Amir-Jahed ◽  
F. A. Roberge
Keyword(s):  
Sinus Rhythm ◽  
Closed Loop ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Relaxation Oscillator ◽  
Electronic Relaxation ◽  
Atrial Rate ◽  
Model Experiments ◽  
Relaxation Oscillators ◽  
Ventricular Activity

During ventricular arrest obtained by injections of acetylcholine into the canine atrioventricular node artery, atrial acceleration of variable magnitude was observed. Upon return of ventricular activity a marked slowing of atrial rate was usually noted, followed by a gradual return to the initial sinus rhythm. Similar phenomena were observed with a preparation in which the sinus node was destroyed and its activity simulated by an electronic relaxation oscillator coupled to the heart in a closed-loop fashion. Model experiments with two interacting relaxation oscillators suggested that atrial acceleration during ventricular arrest, and atrial slowing during the return of ventricular activity, were governed by some sort of feedback from ventricles to sinus node.

SIMULATION OF SINUS NODE ACTIVITY BY AN ELECTRONIC RELAXATION OSCILLATOR

1966 ◽  
Vol 44 (2) ◽  
pp. 301-315 ◽  
Author(s):  
F. A. Roberge ◽  
R. A. Nadeau
Keyword(s):  
Sinus Node ◽  
Relaxation Oscillator ◽  
Rhythmic Activity ◽  
Electronic Relaxation ◽  
Node Activity ◽  
Relaxation Oscillators ◽  
Ventricular Response ◽  
Sinus Node Activity ◽  
The Right ◽  
Intact Heart

After the sinus node was destroyed, its rhythmic activity was simulated by an electronic relaxation oscillator coupled to the beating heart. The output of the oscillator was used to stimulate the right atrium, and the ventricular response was returned to the input of the relaxation oscillator. By manually varying the frequency of this artificial pacemaker it was possible to produce changes in the rate of the atrio–ventricular (A–V) node similar to those obtained by perfusion of the intact sinus node with chronotropic agents. Particular attention was paid to the transitions from "oscillator" rhythm to A–V nodal rhythm, and vice versa. The results provide support for the following hypotheses relative to the intact heart: (i) some form of sinus node activity persists during A–V nodal rhythm, and (ii) the principal pacemakers of the heart, the sinus and A–V nodes, behave as a system of coupled relaxation oscillators.

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.

scholarly journals Crisis of transient chaos in an electronic relaxation oscillator

2003 ◽  
Vol 52 (5) ◽  
pp. 1079
Author(s):  
Lu Yun-Qing ◽  
Wang Wen-Xiu ◽  
He Da-Ren
Keyword(s):  
Relaxation Oscillator ◽  
Transient Chaos ◽  
Electronic Relaxation

Effect of Antiarrhythmic Drugs on Ventricular Late Potentials at Sinus Rhythm and at Constant Atrial Rate

1983 ◽  
pp. 767-772 ◽  
Author(s):  
R. A. Jauemig ◽  
J. Senges ◽  
W. Lengfelder ◽  
I. Rizos ◽  
Ellen Hoffmann ◽  
...  
Keyword(s):  
Sinus Rhythm ◽  
Antiarrhythmic Drugs ◽  
Late Potentials ◽  
Ventricular Late Potentials ◽  
Atrial Rate

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
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