Sinus Impulse Research Articles

Influence of sinus impulses on the parasystolic cycle length

Recently, it has been shown that in most clinical cases of parasystole, the parasystolic rhythm is not completely independent of the sinus rhythm. In this study, to disclose the mechanism of such “irregular” parasystole, parasystolic cycles with an intervening sinus QRS complex (XSX) were compared with their immediately adjacent pure parasystolic cycles without any intervening nonparasystolic QRS complexes (XX) in 10 cases of ventricular parasystole. In eight cases, the XSX interval was equal to or nearly equal to the adjacent pure XX interval; in one, the XSX interval was shorter than the XX interval; and in only one, the XSX interval was longer than the XX interval. In six cases in which the XSX interval was almost equal to the XX interval, calculated XSX intervals with a later intervening sinus QRS complex were obtained from the differences between the XSSX interval (ie, interectopic interval with two intervening sinus QRS complexes) and its adjacent XX interval. In five of the six cases, the calculated XSX interval was shorter than the XX interval. These observations suggest that in most cases of parasystole, early intervening sinus impulses do not change the parasystolic cycle, whereas late intervening sinus impulses shorten the parasystolic cycle. This suggests the presence of type I second-degree entrance block as the mechanism of “irregular” parasystole.

Atrioventricular Junctional Parasystole with Ventricular Fusion Beats Due to Complicating Wolff-Parkinson-White Syndrome

We present a case of atrioventricular (AV) junctional parasystole manifesting with ventricular fusion beats due to the presence of an accessory AV conduction pathway. Ventricular fusion beats are usually impossible in AV junctional parasystole. In the reported case the ventricular fusion occurs because the ectopic AV junctional impulse is conducted through the His bundle, whereas the sinus impulse is conducted to the ventricles through the Kent bundle.

Mechanisms of atypical atrioventricular Wenckebach periodicity. A theoretical model derived from the concepts of inhomogeneous excitability and electrotonically mediated conduction.

To explain the mechanisms of atypical atrioventricular (AV) Wenckebach periodicity, a model of the AV node was theoretically derived from the concepts of "inhomogeneous excitability" and "electrotonically mediated conduction." The theoretical model of the AV node has the following characteristics: (1) increased vagal tone depresses excitability in the AV node, (2) depressed excitability in the AV node is inhomogeneous in both transverse and longitudinal directions, and (3) electrotonically mediated conduction occurs across inexcitable gaps in the AV node. Many features in atypical AV Wenckebach periodicity are explained by the use of this model. Delayed AV conduction is caused mostly by electrotonically mediated conduction across a much-depressed region in the AV node, and thereafter AV conduction is blocked at the same region, resulting in the occurrence of an AV Wenckebach period with gradual lengthening of PR intervals. Occasionally, longitudinal dissociaton and concealed reentry in the AV node occur in the part below (distal to) the above depressed region, resulting in the occurrence of an AV Wenckebach period with sudden marked lengthening of a PR interval. The sinus impulse following such suddenly delayed AV conduction is usually blocked in the AV node as the result of concealed reentry of the preceding impulse.

Concealed ventricular hexageminy

The authors report a case of concealed ventricular hexageminy in which, with a few exceptions, extrasystoles were separated by sinus beats conforming to the formula 6n - 1. Whenever an exception to this formula occurs, the intervening beats are not all of sinus origin, but include also a ventricular extrasystole that is different from those occurring in hexageminal distribution. The pattern is explained by a parasystolic rhythm modulated by sinus impulses, assuming a 3:1 ratio between the parasystolic cycle and the sinus cycle. Such a ratio would have to be associated with a trigeminal or concealed trigeminal distribution. There is, however, a 2:1 ectopic-ventricular block, leading to a change of the ectopic distributional pattern from theexpected concealed trigeminy to that of the concealed hesageminy.

Vagally induced block and delayed conduction as a mechanism for circus movement tachycardia in frog atria.

Episodes of tachycardia induced by strong vagal stimulation in spontaneously beating isolated atria of frog (Rana temporaria) were studied with multielectrode mapping technique. These episodes were inducible in 19 of 39 preparations. The arrhythmia started several seconds after cessation of vagal stimulation strong enough to cause sinus arrest, without electrical stimulation of the myocardium. The arrhythmia consisted of two to 20 beats (6 +/- 4, mean +/- SD, n = 42) with a cycle length of 100-500 msec. Recording from 32 sites with spatial resolution of 1-2 mm showed that the arrhythmia was due to intra-atrial circus movement. The estimated perimeter of the reentrant circuit ranged from 6 to 20 mm. In circuits of the minimal size, the average conduction velocity along the circuit was as low as 2-3 cm/sec. Paroxysms of the tachycardia were always preceded by vagally induced nonuniform depression of conduction, with some areas of atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner, their unblocking being significantly (p less than 0.05) delayed after inhibition of tissue cholinesterase by proserine. The reentrant tachycardia was initiated when a sinus impulse arrived during certain phase of the unblocking. Unlike the well-known mechanism of reentrant excitation, which is based on inhomogeneous refractoriness and critically timed extrabeat(s), the circus movement in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.

Electrotonic inhibition of an idioventricular escape focus by nonconducted sinus impulses

Electrotonic inhibition of an idioventricular escape focus by nonconducted sinus impulses

Two-to-One Sinoatrial Block: Normalization by Carotid Massage

In a clinical case of 2:1 sinoatrial block, carotid massage, paradoxically, released the sinoatrial block and doubled the manifest sinus rate. This resulted from a deceleration of the sinus discharge rate which allowed consecutive sinus impulses to traverse the sinoatrial junction.

Concealed Ventricular Bigeminy with Exceptions due to Time-Dependent Modulation of an Ectopic Rhythm

This presentation reflects a case of atypical concealed bigeminy, where some interectopic intervals contain even numbers of sinus beats. Exceptions to the rule of concealed bigeminy only occur during slowing of the sinus node. The pattern is explained on the basis of modulated parasystole, by drawing a phase-response curve which explains all the interectopic intervals on the basis of the modulating effect exerted by the sinus impulses upon a parasystolic focus.

“Irregular” ventricular parasystole: The influence of sinus rhythm on a parasystolic focus

Fifteen cases of ventricular parasystole were analyzed to determine whether the interectopic intervals were regular, as experessed by long intervals being exact multiples of the short ones, or not. The regularity of the interectopic intervals was assessed by means of the variation index: the ratio of the maximal difference between various measurements of the parasystolic cycle length and the mean parasystolic cycle length. Three out of 15 cases had a variation index less than 5, and were classified as “regular parasystole.” Twelve cases were associated with a variation index greater than 7.5, and were classified as “irregular parasystole.” The cases of irregular parasystole were then analyzed to determine whether the variability of the interectopic intervals was casual or dependent on action of the sinus beats. A parasystolic resetting by critically timed sinus impulses (a form of intermittent parasystole) was evident in three cases. The irregularity in the remaining nine cases was due to modulation (viz., due to electrotonic influence exerted by the sinus beats on the parasystolic focus). In every case of modulated parasystole a phase-response curve was constructed, which enabled an analysis of all the interectopic intervals on the basis of a time-dependent effect exerted by the sinus impulses on an otherwise rhythmic parasystolic focus.

MECHANISM OF 2:1 ATRIOVENTRICULAR BLOCK IN INFANTS WITH CONGENITAL LONG QT SYNDROME

The mechanism of 2:1 atrioventricular block in infants with the congenital long QT syndrome has been postulated to result from a long ventricular effective refractory period interrupting conduction of successive sinus impulses. Three infants age 1-2 days exhibited bradycardia demonstrated to be 2:1 atrioventricular block by the surface electrocardiogram. Mean sinus cycle length (SCL) was 0.56 sec where as mean QT interval was 0.65 sec (QTc 0.63); this .07 sec difference between the SCL and mean QTc was sufficient to block successful capture of the ventricles by successive sinus impulses. Programmed ventricular extrastimulation in one patient demonstrated a markedly prolonged ventricular effective period (480 sec) at ventricular basic cycle length (BCL) 1000 msec shortening to 280 msec with a ventricular BCL of 400 msec. Permanent ventricular pacing shortened the ventricular effective refractory period in each infant and effectively suppressed polymorphic ventricular arrhythmias in the affected two. We conclude that the mechanism of 2:1 atrioventricular block in infants with the congenital long QT syndrome is a function of the age related SCL relative to the QT interval as well as the markedly prolonged but rate dependent ventricular effective refractory period. Ventricular pacemaker implant is effective in increasing ventricular rate, shortening ventricular effective refractory period, and suppressing complex ventricular arrhythmias.

Sinus modulation of atrial parasystole

Recognition of atrial parasystole may be difficult if the characteristic features are absent. Thus, ectopic atrial beats can be associated with fixed coupling intervals, as a manifestation of “reversed coupling,” and atrial fusion beats may be absent. 1,2 We report a patient with atrial parasystole in whom the ectopic atrial pacemaker was electronically modulated by sinus impulses. This resulted in an irregular ectopic discharge so that the characteristic mathematical relation between the interectopic intervals was distorted and not apparent.

Supernormal modulation of ventricular parasystole: The triphasic phase-response curve

Modulation of ventricular parasystole by sinus beats has been shown both in vitro and in vivo to result in a classic biphasic phase-response curve. The first clinical presentation of 3 cases of supernormal modulation of ventricular parasystole resulting in a triphasic phase response curve is reported. Supernormal modulation reflects an unexpected early enhancement expedition of the ectopic ventricular impulses. An alternative explanation for the triphasic phase-response curve is the discharge and resetting of the parasystolic focus by critically timed sinus impulses.

Mechanisms of concealed ventricular bigeminy: The concept of concealed conduction in the reentrant pathway

To clarify the presence of concealed conduction in the reentrant pathway of extrasystoles, 20 patients with ventricular extrasystoles were studied in whom two forms of interectopic periods were found in the same recording. One form is the XS1S2X period, in which two sinus QRS complexes (S1 and S2) intervene between an interpolated extrasystole (the first X) and the next extrasystole (the second X). The other is the XS2X or XS1X period, in which one sinus QRS complex intervenes between two extrasystoles. In all patients except one, the XX interval in the XS1S2X period was longer than that in the XS2X or XS1X period though shorter than twice the latter XX interval. This strongly suggests the presence of two-level block in the reentrant pathway of the extrasystoles. It appears that the sinus impulse S1 in the XS1S2X period invaded a large portion of the reentrant pathway and then was blocked at a distal site of the pathway; namely, that concealed conduction of the impulse S1 occurred in the pathway. It is suggested that such concealed conduction prolonged the conduction time of the following sinus impulse, S2, in the reentrant pathway, resulting in lengthening of the XX interval. The presence of three- or four-level block is also suggested. By the use of such multilevel block, mechanisms of concealed ventricular bigeminy are explained.

Inhibition of premature ventricular extrastimuli by subthreshold conditioning stimuli

The purpose of this study was to determine whether trains of subthreshold high frequency conditioning stimuli (333 Hz, 1 ms duration, 2 ms interval) delivered to the canine ventricle inhibited the response to a premature stimulus (S2) more effectively than did a single subthreshold conditioning stimulus. It was found that trains of conditioning stimuli (mean 1.21 mA) inhibited the response to S2 152 ms beyond expiration of the ventricular effective refractory period, whereas a single conditioning stimulus inhibited S2 only 20 ms or less beyond the ventricular effective refractory period. In late diastole, trains of conditioning stimuli failed to inhibit S2 when the train of stimuli caused ventricular depolarization or the latter occurred in response to the next sinus impulse. Trains of conditioning stimuli did not induce ventricular arrhythmias. Lidocaine or autonomic blockade did not alter the response to trains of conditioning stimuli. Trains of conditioning stimuli or a single conditioning stimulus inhibited the response to S2 only when they were delivered at the same electrode site. By lengthening the ventricular effective refractory period, trains of conditioning stimuli could prevent or terminate tachycardias, but this possibility is constrained, at present, by the spatial limitations of the technique.

Concealed atrial bigeminy: Mechanisms of disappearance and reappearance of manifest extrasystoles

ECGs taken from four patients with concealed atrial bigeminy were analyzed to find the mechanisms of disappearance and reappearance of extrasystoles. Observations in three patients showing the classic form of concealed bigeminy suggest that when the extrasystole disappeared, the first sinus impulse after the last manifest extrasystole and its subsequent alternate sinus impulses passed through the reentrant pathway and thereafter became concealed extrasystoles. The other alternate sinus impulses appear to have been blocked within the reentrant pathway but after concealed conduction. It is suggested that such concealed conduction prolonged the conduction time of the next sinus impulse in the reentrant pathway and favored reappearance of the extrasystole. On the contrary, observations in one patient showing the even-number variant suggest that the first sinus impulse after a manifest extrasystole and its subsequent alternate sinus impulses were blocked in the reentrant pathway without appreciable concealed conduction.

Periodic variation in atrioventricular conduction time: Mechanisms of initiation, maintenance and termination of periods of long PR intervals

Five patients with periodic variation in atrioventricular (AV) conduction time are reported in whom periods of comparatively short PR intervals alternated with periods of comparatively long PR intervals. In all patients, the transition from a period of long PR intervals to a period of short PR intervals usually occurred without a blocked P wave. In 3 patients, however, the period of long PR intervals was occasionally terminated by a blocked P wave. The mechanisms of initiation, maintenance and termination of periods of long PR intervals are explained by the use of dual AV pathways consisting of fast and slow pathways. It is suggested that the effective refractory period of the fast pathway was abnormally prolonged by increased vagal tone and that, during the period of long P-R intervals, sinus impulses anterogradely passed only through the slow pathway and later retrogradely excited the fast pathway. Apparently, when vagal tone was decreased, the effective refractory period of the fast pathway was shortened, resulting in abrupt improvement in atrioventricular conduction without a blocked P wave.

Second degree entrance block with supernormal conduction in intermittent ventricular parasystole

A patient with intermittent ventricular parasystole is reported in whom the presence of second degree entrance block with supernormal conduction was suggested for the first time. In this patient, ventricular extrasystoles with variable coupling frequently occurred. The QRS configuration of the extrasystoles was different from that of the parasystolic beats. When extrasystoles did not occur, the parasystolic beat was never seen because the conducted sinus impulse always reset the parasystolic rhythm. When an extrasystole occurred 0.52 sec or more after the preceding sinus beat, this extrasystolic impulse also reset the parasystolic rhythm. On the other hand, when an extrasystole occurred between 0.47 and 0.51 sec after the sinus beat, the parasystolic focus was protected from this extrasystolic impulse. When, however, an extrasystole occurred in a short terminal portion of the T wave of the preceding sinus beat, this extrasystolic impulse reset the parasystolic rhythm again, suggesting entrance block failure during the supernormal phase.

QRS normalization by ventricular fusion simulating tachycardia dependent left bundle branch block

We report an example of ventricular fusion of a sinus impulse conducted with bundle branch block with an ectopic impulse arising on the ipsilateral side of the blocked bundle branch. The manifestation simulates the normalization which occurs during the relatively slow phase of a tachycardia dependent left bundle branch block.

Pseudoatrioventricular Block

The diagnosis of Mobitz II (second-degree, atrioventricular [AV]) heart block implies a primary disorder of conduction localized to the His-Purkinje system and the potential for sudden progression to complete heart block.¹However, an ectopic focus located in the His bundle or a bundle branch may, with proper timing, partially penetrate the conduction system and collide with normal sinus impulses, causing either slowing or complete blockage of the sinus impulse. This phenomenon, a manifestation of concealed conduction, may mimic first- or second-degree AV block, including a Mobitz II pattern, resulting in what has been termed<i>pseudoatrioventricular block</i>.²Pseudoatrioventricular and true AV blocks have different therapeutic and prognostic implications. Therefore, identification of pseudoatrioventricular block is clinically important. <h3>REPORT OF A CASE</h3> A 29-year-old woman was admitted to the hospital for elective repair of an ostium primum atrial septal defect. Her admission ECG disclosed normal sinus rhythm, a left-axis deviation, and

Hemodynamics and intracardiac conduction after operative repair of tetralogy of fallot

Electrophysiologic studies were performed in 47 children aged 3 to 18 years, 15 of whom had cardiac arrhythmias 1 to 15 years after repair of tetralogy of Fallot. Six exhibited sinus or atrioventricular nodal dysfunction, 8 had ventricular extrasystoles, and 1 had supraventricular tachycardia. Hemodynamic and electrophysiologic data were obtained at postoperative catheterization. Although electrophysiologic responses were abnormal in a proportion of both the children with and those without arrhythmia, hemodynamic values were similar. Three of 6 children with impaired sinus impulse generation or atrioventricular nodal conduction had a prolonged A-H interval, and in 3 Wenckebach heart block developed at low pacing rates. Ventricular ectopic rhythm was not associated with any particular abnormality of basic intracardiac conduction intervals. Thus, arrhythmias and conduction abnormalities are not consistently related to residual right ventricular hypertension. Abnormalities in electrophysiologic function are common after repair of tetralogy of Fallot in patients with sinus rhythm and may have prognostic implications for these patients.