Pacing techniques in the management of supraventricular tachycardias. Part 2. An implanted atrial synchronous pacemaker with a short atrioventricular delay for the prevention of paroxysmal supraventricular tachycardias.

An implanted atrial synchronous pacemaker with an atrioventricular delay of 30 msec is described. This pacemaker was implanted into a patient with paroxysmal supraventricular tachycardia due to an intra AV nodal reciprocal mechanism. The pacemaker was able to trigger from atrial potentials following atrial premature beats down to a coupling time of 300 msec. Following each triggering atrial potential, a ventricular stimulus was applied 30 msec later thereby producing a ventricular premature beat in response to each sinus beat or each atrial premature beat. Retrograde conduction from this atrial premature beat blocked the re-entry mechanism within the AV node and prevented the initiation of tachycardia. A detailed discussion on all parameters of function of this pacemaker is presented.     

Chest wall stimulation in evaluation of patients with implanted ventricular-inhibited demand pacemakers.

Chest wall electrical stimuli, too weak to affect the heart, act as electrical signals to an implanted ventricular-inhibited (QRS blocking) demand pacemaker which interprets them as originating from the heart and consequently responds according to its specifications. Rapid external stimulation permits diagnostic interpretation of the spontaneous electrocardiogram by completely inactivating the implanted pacemaker. The slow random delivery of external stimuli throughout the cardiac cycle delineates the pacemaker refractory period after the emission of a pacing stimulus and after the sensing of a spontaneous beat. During apparent fixed-rate pacing the demand capability of the pacemaker may be easily seen by appropriately timed chest wall stimulation which induces the pacemaker to sense a spontaneous QRS complex. This simple technique may reveal subtle changes in pacemaker performance, and contributes to the understanding of pacemaker arrhythmias.     

Ventricular tachycardia induced by pacing algorithm designed to avoid atrial fibrillation

A patient with a dual chamber pacemaker was admitted to the emergency room after out-of-hospital cardioversion for syncopal sustained monomorphic ventricular tachycardia. Device interrogation revealed an abnormally timed ventricular spike after a ventricular premature beat at the beginning of the event, caused by a pacemaker algorithm designed to avoid atrial fibrillation, non-competitive atrial pacing. Despite the absence of significant coronary lesions, in the setting of a vulnerable substrate – a hypokinetic and hyperechogenic region of ventricular myocardium – an upgrade to a dual-chamber implantable cardioverter-defibrillator was performed, and substrate ablation was planned.     

Arrhythmia resulting from sensing malfunction in a P wave triggered pacemaker

P wave triggered pacemakers can produce complicated arrhythmias during normal function. A ventricular, R wave inhibited pacemaker and an atrial sensing pacemaker were both present and functioning normally in the patient reported here. A premature paced beat was observed every 12th beat which resulted from discharge of the atrial sensing pacemaker. This arrhythmia appeared because a “P” wave occurred during the noise sampling period of the atrial sensing pacemaker, disabling the demand function and resulting in generator discharge on or near the T wave of a preceding unsensed beat while the pacemaker was in the asynchronous mode.     

Atrial and ventricular rate response and patterns of heart rate acceleration during maternal-fetal terbutaline treatment of fetal complete heart block

Terbutaline is used to treat fetal bradycardia in the setting of complete heart block (CHB); however, little is known of its effects on atrial and ventricular beat rates or patterns of heart rate (HR) acceleration. Fetal atrial and ventricular beat rates were compared before and after transplacental terbutaline treatment (10 to 30 mg/day) by fetal echocardiography in 17 fetuses with CHB caused by immune-mediated damage to a normal conduction system (isoimmune, n = 8) or a congenitally malformed conduction system associated with left atrial isomerism (LAI, n = 9). While receiving terbutaline, 9 of the 17 fetuses underwent fetal magnetocardiography (fMCG) to assess maternal HR and rhythm, patterns of fetal HR acceleration, and correlation between fetal atrial and ventricular accelerations (i.e., AV correlation). Maternal HR and fetal atrial and ventricular beat rates increased with terbutaline. However, terbutaline's effects were greater on the atrial pacemaker(s) in fetuses with isoimmune CHB and greater on the ventricular pacemaker(s) in those with LAI-associated CHB. Patterns of fetal HR acceleration also differed between isoimmune and LAI CHB. Finally, despite increasing HR, terbutaline did not restore the normal coordinated response between atrial and ventricular accelerations in isoimmune or LAI CHB. In conclusion, the pathophysiologic heterogeneity of CHB is reflected in the differing effect of terbutaline on the atrial and ventricular pacemaker(s) and varying patterns of HR acceleration. However, regardless of the cause of CHB, terbutaline augments HR but not AV correlation, suggesting that its effects are determined by the conduction system defect rather than the autonomic control of the developing heart.     

Quantitative study of the supernormal phase of ventricular excitability in man.

The supernormal phase of excitability of the human heart was studied by means of fixed rate endocardial pacing in 11 patients with acute and chronic bradyarrhythmias. Ten of the eleven patients manifested a supernormal phase. The duration of the phase increased with increasing intensity of subthreshold stimuli and ranged from 91 to 148 percent of the Q-T interval. Subthreshold stimuli of a wide range of intensity could elicit a full response. Two types of supernormal phase, early and late in relation to the cardiac cycle, were observed. The latter was attributed to the summation of subthreshold stimuli with either spontaneous phase 4 depolarization of a ventricular ectopic pacemaker or atrial depolarization potentials. Its possible connection with Wedensky facillitation was suggested. The ventricle was less excitable after an ectopic beat than after a normally conducted beat.     

Prevention of Tachycardia Initiation by Programmed Stimulation

A 20-year-old female with a left-sided concealed atrioventricular accessory pathway was studied during programmed stimulation to investigate the mechanisms of prevention of tachycardia by timed stimulation of the ventricle after a tachycardia initiating atrial extrastimulus. After the atrial tachycardia initiation zone was determined, the prvention zone of the ventricular stimulus was determined for each initiating interval. Two different prevention mechanisms were found, one whereby the ventricular depolarization was blocked retrogradely in the accessory pathway and another whereby the ventricular depolarization was conducted over the accessory pathway to the atrium but subsequently blocked anterogradely in the AV node. The preventive zone timed from the last ventricular complex to the ventricular stimulus was always greater than 30 msec whereby the minimum preventive internal was determined by the ventricular refractory period. This could be of value when such a preventive algorithm is incorporated into a dual-chamber antitachycardia pacemaker. Knowing the exact mechanisms by which the prevention occurs allows one to predict how tachycardia can be prevented when the atrial extra beat originates from a different site and when the parameters of the heart are changed due to changes in antonomic tone or catecholamine level.     

Undesirable cardiac arrhythmias associated with rate hysteresis pacemakers

The introduction of the ventricular inhibited pulse generator with the feature of rate hysteresis has been associated with a variety of rhythm disturbances, some causing serious concern. This pulse generator has two different pacing rates: (1) the automatic rate, which is the interval between two successive paced beats (usually 860 msec or 70/min), and (2) the hysteresis interval, which results in a 1,000 msec delay between a sensed cardiac contraction and the next pacemaker discharge. The hysteresis interval after a sensed signal may result in long pauses that may predispose to the development of serious cardiac arrhythmias. Two examples of this type of complication were recently observed. One patient had bigeminal rhythm with mechanically ineffective cardiac contractions and an effective cardiac rate of 35/min; he experienced dyspnea and weakness during these prolonged episodes. Another patient had repeated episodes of ventricular fibrillation. The cardiac arrhythmias were not controlled by antiarrhythmic agents, and both patients required replacement of the pulse generator.The proposed advantages of pulse generator hysteresis are (1) prolongation of battery life, and (2) maintenance of effective atrial transport; these advantages may be outweighed by undesirable cardiac arrhythmias that may be associated with this mode of pacemaker function. Rate hysteresis cardiac pacemakers should be reserved for patients having predominantly sinus rhythm without ventricular irritability. In patients with frequent ectopic ventricular activity, atrial fibrillation or high degree atrioventricular block, the rate hysteresis pacemaker offers no advantage over the conventional demand pacemaker. For patients with frequent ectopic ventricular activity not easily controlled by antiarrhythmic agents, consideration should be given to the use of a permanent demand pacemaker with external rate control, which may provide greater flexibility in arrhythmia management.     

Alternating bundle branch block

Mechanisms postulated for alternating bundle branch block are incomplete-and cycle-length-dependent-block in both the right and left bundle branches. A patient with severe longstanding cardiac conduction disease who developed alternating bundle branch block during treatment for advanced ischemic heart disease and malignant ventricular arrhythmia is presented. In this patient alternation was induced by atrial premature beats as well as spontaneous and pacemaker induced premature ventricular beats. Right bundle branch block which followed a premature atrial beat resulted from the longer refractory period of the right bundle. The maintenance of right bundle branch block at long cycle lengths was presumed to be due to continuous retrograde reentry. This was terminated when a pause following a premature beat allowed functional recovery of the right bundle branch. This patient died suddenly at home with a functioning pacemaker, demonstrating the high risk of death from ventricular dysrhythmia in the post myocardial infarction patient with a new conduction defect.     

Sinus nodal echoes. Clinical case report and canine studies

Sinus nodal echoes are illustrated in (1) a case report, and (2) a study of the effects of atrial premature beats after atrial drive in dogs. When atrial premature beats confront the sinus node while it is still refractory, 3 types of response may be seen: (1) Complete interpolation—the subsequent sinus beat (or escape) comes precisely at the expected time; (2) incomplete interpolation—the subsequent sinus beat is delayed; and (3) sinus echoes—the sinus beat appears earlier than expected. In all 3 instances the node is entered, but the pacemaker fails to be reset. Although the echo has the form of a sinus beat, it is followed by a pause, presumably as a result of repenetration of the sinus node through pathways unused during exit. The curves characterizing the expansion by vagal stimulation of the nodal refractory period and total echo circuit time are defined, together with the latency of cholinergic effect on nodal refractoriness, sinus automaticity and exit conduction of the echo. The secondary concealment zone of a completely interpolated atrial premature beat is established. Atrial preexcitation (before the echo) sometimes evokes a second echo. The limiting factor on sustained sinoatrial reciprocation thus appears to be total echo circuit time rather than refractoriness of atrium or echo entrance pathways. The repetitive echoes seen in this study may be the basis for some clinical cases of sinus or atrial tachycardia.     

Problems of artificial pacemaker therapy

Four hundred and sixty-seven cases with implantation of an artificial pacemaker were studied. The postoperative survival rate was 63% for 15 years. Seventy-two percent of type III patients of the sick sinus syndrome were free from postoperative thromboembolism and the lowest of the three types of the sick sinus syndrome. Comparing postoperative physical activity, cardiothoracic ratio and exercise tolerance time, physiological pacing was superior to ventricular pacing in hemodynamic effects and clinical symptoms. In a hundred cases of physiological pacing, complications and problems of physiological pacing were discussed. Atrial sensing failure and over-sensing were observed in seven and two cases respectively. A low amplitude of atrial potential and use of unipolar atrial leads were considered to be the main causes of these complications. Bipolar lead should be used as the atrial lead to avoid such complications, because the atrial potential by bipolar leads is not less than that by unipolar leads. Atrial sensing may be more sensitive without electromagnetic interference. The fixed A-V delay time whenever the atrium is sensed or paced, often results in a ventricular fusion beat and hemodynamic change on every beat, according to the interval of atrial and ventricular contractions. The A-V delay time should be changed in accordance with atrial sensing or pacing.     

Sustained vortex-like waves in normal isolated ventricular muscle.

Sustained reentrant excitation may be initiated in small (20 x 20 x less than 0.6 mm) preparations of normal ventricular muscle. A single appropriately timed premature electrical stimulus applied perpendicularly to the wake of a propagating quasiplanar wavefront gives rise to circulation of self-sustaining excitation waves, which pivot at high frequency (5-7 Hz) around a relatively small "phaseless" region. Such a region develops only very low amplitude depolarizations. Once initiated, most episodes of reentrant activity last indefinitely but can be interrupted by the application of an appropriately timed electrical stimulus. The entire course of the electrical activity is visualized with high temporal and spatial resolution, as well as high signal-to-noise ratio, using voltage-sensitive dyes and optical mapping. Two- and three-dimensional graphics of the fluorescence changes recorded by a 10 x 10 photodiode array from a surface of 12 x 12 mm provide sequential images (every msec) of voltage distribution during a reentrant vortex. The results suggest that two-dimensional vortex-like reentry in cardiac muscle is analogous to spiral waves in other biological and chemical excitable media.     

Complete abolition of the reentrant supraventricular tachycardia zone using a new modality of cardiac pacing with simultaneous atrioventricular stimulation

In an attempt to prevent recurrent reentrant supraventricular tachycardia, an experimentally designed new pacemaker has been developed. The pacemaker, when connected to both atrial and ventricular electrodes, is capable of sensing either an atrial or ventricular signal and, in turn, triggers simultaneous atrioventricular (A-V) stimulation. Efficacy of this pacemaker was tested in four patients with recurrent paroxysmal A-V nodal reentrant tachycardia during electrpphysiologic studies. After connection of the electrodes to the new pacemaker, all atrial or ventricular premature stimuli elicited simultaneous A-V stimulation with resultant impulse collision in the A-V junction. Consequently, the reentrant tachycardia zone was completely abolished in all patients. This study has thus demonstrated the clinical feasibility of simultaneous A-V pacing to abolish the supraventricular tachycardia zone in man.     

The mechanisms of exercise provocation of supraventricular tachycardia

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.     

Pacemaker syndromes

The pacemaker syndrome refers to symptoms and signs in pacemaker patients caused by inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in decreased cardiac output and increased in atrial pressure which elicits a systemic hypotensive reflex response. These hemodynamic disturbances mostly occur in the presence of retrograde VA conduction is present. The incidence of pacemaker syndrome is uncertain, and varies from 7% to 20% of all ventricular paced patients. Neurologic symptoms or symptoms suggesting low cardiac output or congestive heart failure are indicative of the pacemaker syndrome. These symptoms may vary from mild to severe, they are nonspecific and very common among cardiac patients with or without pacemaker. In many patients they are not even noted until AV synchrony is restored. The pacemaker syndrome is not restricted to the VVI stimulation mode. It can be seen, though rarely, in atrial and even dual-chamber pacing (VDD, DDI, DDD). In these cases it is usually occasional and may be due to inappropriate programming or selection of the pacing mode.     

Sinoatrial pacemaker shift following atrial stimulation in man.

Indirect evidence of a sinoatrial pacemaker shift after programmed atrial stimulation in man is presented. Following electrically induced beats, time intervals and postextrasystolic morphology of atrial electrogram and P waves were scrutinized in 30 catheterization studies. Applying premature atrial stimulation, a decrease of the interval between the last basic atrial depolarization and the stimulus-produced atrial excitation (curtailed cycle) below a critical interval was followed by a sinoatrial pacemaker shift in three cases. This electrophysiologic event consisted of a concomitant change in shape of high right atrial electrogram and an increase of atrial cycle length. Simultaneous alteration of P waves could be detected in 2/3 patients. Assuming that the pacemaker shift indicates the arrival of ectopic activation in the sinus node, capture of the sinus node by the premature beat could be distinguished from failure to capture. Thus, pacemaker shift can be used for estimating sinoatrial conduction time in addition to present methods using measurement of postextrasystolic atrial intervals. The changes described could be seen both before and after atropine administration. Tracings of a pacemaker shift after cessation of rapid atrial pacing are also presented. In summary, we found a sinoatrial pacemaker shift underlying sinus node response to ectopic atrial activation in man, a phenomenon which contributes to our understanding of indirect assessment of sinoatrial conduction time by the premature stimulation technique.     

The influence of atrial systole on ventricular capture by failing artificial pacemakers. II. Experimental observations

The mechanism by which atrial systole influences the efficacy of ventricular capture by a failing pacemaker was investigated in 12 dogs with atrioventricular heart block. Atrial systole caused facilitation of ventricular capture in eight dogs, and inhibition of capture in 10 dogs. Interpolating atrial extrasystoles caused an enhancement or depression of the hemodynamic performance of the atrial systole that affected the efficacy of the pacemaker stimulus. These interpolation experiments showed that atrial systole influenced the efficacy of capture by a mechanical mechanism and not by an electrotonic mechanism. Atrial systole probably caused motion of the endocardial pacing catheter and/or ventricular myocardium. This motion increased or decreased the contact between the pacing electrode and the endocardium with subsequent changes in the efficacy of capture. In three dogs with pacing through epicardial electrodes, atrial systole had no effect on the efficacy of capture.     

Parasystole, reentry, and tachycardia: a canine preparation of cardiac arrhythmias occurring across inexcitable segments of tissue

A protected ectopic focus created in tissue excised from one heart was allowed to interact with the activity of the intact heart of another animal. The protected focus consisted of a Purkinje fiber in which a narrow central zone was rendered inexcitable. The model permitted us to study parasystole, modulated parasystole, reentry, and tachycardia in the same preparation. At moderate levels of electrotonic influence across the region of block, frequency scans revealed wide zones of pacemaker entrainment. The incidence and pattern of premature ventricular contractions generated were always a sensitive function of heart rate. Parasystolic patterns could be converted to apparent reentrant patterns by simple alteration of the atrial driving rate or the level of block. Suppression of pacemaker automaticity converted a modulated parasystole model to one of pure reentry. Reciprocation of the impulse across the inexcitable tissue segment generated a ventricular tachycardia that could be initiated and terminated by a single properly timed event. Our observations suggest that ectopic activity that behaves like parasystole and activity characteristic of what is commonly diagnosed as reentry, including tachycardia and idioventricular rhythms, may be a manifestation of a common mechanism whose arrhythmic expression differs as a continuous function of heart rate, level of block, or level of automaticity.     

Effects of stable and changing rates and premature ventricular beats on transient tachycardia-, pseudobradycardia-, and bradycardia-dependent bundle branch block alternans.

New circumstances under which bundle block (BBB) alternans may appear or disappear are described. 1) Tachycardia-dependent as well as bradycardia-dependent BBB alternans may begin after constant BBB is interrupted by a premature ventricular beat. Tachycardia- and bradycardia- dependence may be differentiated by the shape of the first beat after the pause. 2) When BBB alternans disappears during a constant ventricular rate, tachycardia-dependent BBB alternans changes to persistent normal or more normal intraventricular conduction, whereas bradycardia-dependent BBB alternans changes to a persistently greater degree of BBB. 3) BBB alternans appears to be tachycardia- or pseudobradycardia-dependent in relation to the cycle length and antegrade and retrograde refractory periods in the involved bundle branch. 4) BBB alternans may be recognized during persistent irregular ventricular action in atrial fibrillation. Here the recognition of BBB alternans depends upon the sequence of contours as well as upon the cycle lengths.     

Unique Interaction Between an Atrial Single-Chamber Pacemaker and a Ventricular Defibrillator

A well described interaction between an antibradycardia pacemaker and a ventricular defibrillator is sensing of pacemaker stimuli by the ventricular defibrillator. This report describes an interaction between an atrial demand pacemaker and a ventricular defibrillator that resulted in ventricular asystole and polymorphic ventricular tachycardia. In this case, the ventricular defibrillator sensed atrial pacing stimuli when complete atrioventricular block with a slow ventricular escape rate developed. Defibrillator-based ventricular demand pacing was inhibited, resulting in prolonged periods of ventricular asystole, polymorphic ventricular tachycardia, and multiple defibrillator shocks. Ventricular defibrillator sensing of atrial pacemaker stimuli in the setting of complete atrioventricular block and ventricular asystole cannot be simulated during defibrillator implantation when atrioventricular conduction is intact. Therefore, a pacemaker programmed to atrial demand pacing in a patient with a ventricular defibrillator can result in inappropriate inhibition of ventricular pacing in the setting of complete heart block. Furthermore, this interaction can be avoided with a dual-chamber pacing ventricular defibrillator.