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

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.

1966 ◽  
Vol 44 (2) ◽  
pp. 317-324 ◽  
Author(s):  
R. A. Nadeau ◽  
T. N. James

Direct perfusion of the canine sinus node with various pharmacological agents having negative chronotropic effects commonly leads either to abrupt sinus arrest or to a gradual transition from sinus to atrio–ventricular (A–V) nodal rhythm with progressive shortening of the P–R interval. The reappearance of sinus rhythm is usually preceded by a change in A–V nodal rate and a progressive lengthening of the P–R interval to a stable value. During A–V nodal rhythm, changes in heart rate are observed following injections into the sinus node artery. As perfusion of the sinus node is selective, these cannot be attributed to a direct pharmacological effect of the perfusates on the A–V node. Deliberate suppression of A–V nodal pacemaking dominance reveals the persistence of slow sinus node activity which is unapparent electrocardiographically during A–V nodal rhythm. It would seem that even in the absence of P waves, the sinus node may still influence the rate of the A–V node. These observations are consistent with the hypothesis that the sinus and A–V nodes behave as a system of coupled relaxation oscillators.


1967 ◽  
Vol 45 (3) ◽  
pp. 375-388 ◽  
Author(s):  
R. A. Nadeau ◽  
A. K. Amir-Jahed ◽  
F. A. Roberge

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.


1991 ◽  
Vol 2 (1) ◽  
pp. 140-149 ◽  
Author(s):  
Patricia Gonce Morton

Pacemaker technology continues to advance in the direction of restoring a normal hemodynamic response under varying physiologic conditions. Rate-responsive pacemakers meet this challenge by adjusting the pacing rate in response to a sensed physiologic variable other than sinus node activity. In an effort to design the ideal rate-responsive system, various physiologic cues have been tested. To translate shifts in the sensed physiologic indicator into an appropriate pacing rate, specialized sensor systems also have been developed and include mechanical, chemical, thermal, and electrical sensors. Although each sensor system offers advantages and disadvantages, continued research and clinical experience will determine the future of this exciting new form of cardiac pacing


1995 ◽  
Vol 05 (06) ◽  
pp. 1439-1486 ◽  
Author(s):  
TERESA REE CHAY

Heart rhythms exhibit the following interesting phenomena: First, rhythmic cells such as sinus node cells cease their rhythmic activity when a single brief current pulse of the right magnitude is given to the cell at the right time. Second, a premature pulse can initiate a tachycardia (i.e., reentrant arrhythmia) from a quiescent atrial tissue. This tachycardia can be sustained for hours until another brief current pulse is given. Third, ECG recording sometimes shows alternans in electrical activity prior to ventricular tachycardia. Some suggested that this alternans is the first bifurcation in a period doubling sequence. Fourth, a certain class of antiarrhythmic drugs may increase the chance of sudden cardiac death for patients with a history of myocardial infarction. Fifth, when an "adjustable" tricuspid ring is shortened, the conduction velocity of a reentrant wave becomes oscillatory. When the ring size is shortened further, reentry terminates after several oscillatory cycles. Sixth, sustained reentry arises in a tricuspid ring when Class IC drugs (i.e., which exclusively block the sodium channel) are added. On the other hand, Class III (which exclusively blocks the potassium channel) can terminate sustained reentry in the tricuspid ring. In this tutorial review, we explain how one can utilize a bifurcation analysis to explain all these interesting phenomena involved in heart rhythms.


1993 ◽  
Vol 7 (3) ◽  
pp. 132-137 ◽  
Author(s):  
Anna Toso ◽  
Alessandro Mezzani ◽  
Luigi Padeletti ◽  
Mohamed Bamoshmoosh ◽  
Simone Salvi ◽  
...  

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