The isolated left atrium of the rabbit, which showed no spontaneous activity, was electrically driven for 20 beats with a cycle length of 500 msec. Tachycardia could be repeatedly initiated by the application of a single adequately timed stimulus shortly after the refractory period of the last basic beat. After the termination of the tachycardia, either spontaneously or artificially by a properly timed stimulus, this procedure was repeated. The number of beats of these tachycardias varied from just one (coupled extrasystole) to many hundreds. Surface electrograms were recorded at about 300 different sites. From the moments of activation of these sites, the spread of activation during regular driving and during the premature beat and the subsequent tachycardia could be determined. In contrast to the radial spread of the activation during basic rhythm, the impulse of the premature beat was propagated in a circular pathway. This circus movement was maintained during tachycardia. These results show that even in a small area of atrial muscle containing no anatomical obstacle the impulse can be entrapped in a circus movement. This circus movement was the underlying mechanism of the arrhythmia.

Circus Movement in Rabbit Atrial Muscle as a Mechanism of Tachycardia

Since recording potentials directly from the sinoatrial node (SAN) is not yet possible, the electrophysiologic evaluation of this structure in intact human subjects must be accomplished with indirect technics. Two technics have been used to study SAN function in man: premature atrial stimulation (PAS) and rapid atrial pacing. Recent discussions of data using these technics have emphasized their role in determining SAN automaticity, but their role in evaluating conduction from atrium to SAN or SAN to atrium has not been fully explored. Using the technic of PAS, we have studied five patients with sinus bradycardia and symptoms of dizziness or syncope. Our analysis of the results obtained from these studies discloses the unique ability of this technic to evaluate conduction into and out of the SAN. An atrial premature depolarization (APD) elicited late in atrial diastole is followed by a compensatory pause (nonreset of the SAN pacemaker). An APD elicited earlier in atrial diastole is followed by a pause that is less than compensatory (SAN reset). From these responses estimates of sinoatrial conduction time were made. In one patient reset was never seen, suggesting markedly prolonged sinoatrial conduction. With these results in mind, the literature was reviewed and an alternate interpretation posed for existing data. PAS is not only a means of determining SAN automaticity, but also a very useful means of unmasking sinoatrial conduction abnormalities.

Premature Atrial Stimulation as a Key to the Understanding of Sinoatrial Conduction in Man Presentation of Data and Critical Review of the Literature

The tachycardia-bradycardia syndrome consists of paroxysmal atrial fibrillation, flutter or tachycardia followed by sinoatrial block or sinus arrest resulting in Stokes-Adams attacks. Detailed histologie findings of the conduction system of 2 patients with this entity correlated well with the clinical observation of cardiac rhythm disturbances in the sinus node, atria and atrioventricular (A-V) junction. Eight other patients with the syndrome were studied clinically. The mechanisms (as revealed by the electrocardiogram) producing the bradycardia phase include depression of pacemaker function (arrest) or of conduction (exit block) of the sinus impulse, or both, plus depression of A-V junctional impulse formation. Proper therapy usually requires electrical pacing in conjunction with administration of digitalis or propranolol, or both. Our findings suggest that the term “sick sinus syndrome” is an inaccurate and inappropriate synonym for the tachycardia-bradycardia syndrome.

Tachycardia-bradycardia syndrome (so-called “sick sinus syndrome”): Pathology, mechanisms and treatment

Twenty patients of mean age 66.2 years, with suspected sinus node dysfunction, underwent extensive electrophysiologic study. Sinus bradycardia (18), sinus pauses (3), and sinoatrial block (1) were identified in their ECGs prior to study. Also 11 patients had some abnormality of atrioventricular nodal and/or intraventricular conduction prior to study. At the time of electrophysiological study, 10/20 patients (50%) had a mean cycle length exceeding 1000 msec, and mean P-V interval exceeded 210 msec in 7/20 (35%). The estimated "sinoatrial conduction time" exceeded 215 msec in 6/16 (38%) patients. The maximum first escape cycle following pacing at six different rates exceeded a value equal 1.3 X the mean value of the control cycle length + 101 msec (slope of regression line + Y intercept + 1 SD) in 13/9 (68%) patients. Nineteen patients received 1 mg atropine intravenously and mean cycle length decreased by 19%, from 891 +/- 175.8 msec to 718 +/- 182.9 msec. Graded infusion of isoproterenol was employed in 19 patients; four patients required an infusion rate greater than 28.3 ng/kg/min to produce a 20% decrease in spontaneous sinus cycle length. These data would indicate that a variety of interventions are required to characterize the disturbance of sinus node automaticiy and sinoatrial conduction in patients with sinus node dysfunction.

Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction.

Data in 20 patients with normal sinus rhythm who, following induced premature atrial beats (PABs), manifested re-entry in the region of the sinus node are presented. PABs at coupling intervals ranging between 230-535 msec were followed by sinus node re-entry (SNR). Several criteria were applied to diagnose SNR: the temporal sequence of atrial excitation, the intra-atrial conduction time, the shape and polarity of the P waves, and manifestation of re-entry independent of atrioventricular (A-V) nodal delays. In 18 patients SNR lasting for one to several beats was observed. In the remaining two patients sustained SNR was manifested as supraventricular tachycardia (SVT), with cycle lengths ranging between 320-500 msec, which persisted for several minutes prior to its termination by properly timed atrial stimuli. In one of the latter two patients sustained SNR and SVT were produced only after atropine administration. Sinus node re-entry could be elicited at will in a specific echo zone with a duration ranging ...

Sinus node re-entry: a mechanism for supraventricular tachycardia.

In the spontaneously beating isolated right atrium of the rabbit, premature beats were elicited by electrical stimulation. When the premature beat was elicited early in the atrial cycle, the postextrasystolic pause had a short duration and the sum of the pre- and postextrasystolic pause was about the same as the duration of a normal spontaneous interval. We have tried to demonstrate, using simultaneous multiple microelectrode impalements of SA node fibers, that by such an early atrial premature beat the atrium could be activated by a reentrant mechanism. The results of our experiments led us to the conclusion that the impulse of the premature beat, elicited early in the atrial cycle, discharges the SA node only fractionally and that the fibers in the neighborhood of the activated area are influenced electrotonically. This causes a change of both the site and the moment of the spontaneous impulse formation. The SA node discharges spontaneously after such an early premature beat. Reentry activation is likely to occur when a series of atrial premature beats is observed. A supraventricular tachvcardia might be caused by repeated atrial discharges following a stimulus very shortly after the atrial refractory period.

Flex I. M. Bonke

Papers

Effect of an Early Atrial Premature Beat on Activity of the Sinoatrial Node and Atrial Rhythm in the Rabbit