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.     

The electrophysiologic demonstration of atrial ectopic tachycardia in man

Three patients with almost continuous atrial tachycardia were studied in an attempt to delineate the mechanism responsible for their cardiac arrhythmia. During cardiac catheterization intracardiac electrograms and specific atrial stimulation sequences revealed: (1) episodes of tachycardia were initiated by atrial premature depolarizations (APD's) which exhibited no increased delay in AV nodal conduction, (2) during tachycardia atrial cycle length was not a direct function of AV nodal conduction, (3) initial cycles of tachycardia showed progressive shortening in cycle length, (4) APD's introduced during tachycardia resulted in resetting of the atrial cycle, and (5) single APD's and atrial overdrive during tachycardia failed to interrupt it. The electrophysiologic behavior of the arrhythmia was consistent with the hypothesis that it was initiated and was sustained by an ectopic rapidly firing automatic atrial pacemaker.     

Successful treatment of drug-resistant atrial tachycardia and intractable congestive heart failure with permanent coupled atrial pacing

Temporary coupled atrial stimulation slowed the ventricular rate by nearly 50% in an adolescent patient with intractable congestive heart failure and focal repetitive atrial tachycardia that was resistant to drug treatment. Because of the success with the temporary pacemaker, a specially designed permanent pacemaker was implanted to provide coupled atrial stimulation. The necessary electrophysiologic conditions for ventricular slowing by coupled atrial pacing are: (1) an atrial effective refractory period shorter than that of the atrioventricular junction, and (2) depolarization of the ectopic atrial pacemaker by the responses to coupled atrial stimulation. During a 4 year follow-up period the treatment resulted in elimination of the tachycardia, followed by return of the heart size to normal and complete clinical recovery. Coupled atrial stimulation can provide effective treatment in selected patients with disabling drug-resistant atrial tachycardia in whom this mode of therapy is shown to be effective by careful electrophysiologic studies.     

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.     

The influence of atrial activity on ventricular capture by failing artificial pacemakers. I. Report of two new cases and review of the literature.

Atrial activity can influence the ability of a failing artificial pacemaker to excite the heart. An appropriately timed atrial beat may cause failure in excitation by pacemaker stimuli which are usually successful in ventricular capture. Conversely, stimuli which usually fail in excitation may be made to succeed by an appropriately timed atrial beat. Two case reports and a review of the literature are presented. Alternative mechanisms for this influence of atrial activity are electrotonic effects (Wedensky facilitation or inhibition) and mechanical effects (motion of the pacing catheter or ventricular myocardium). The authors consider the latter mechanism preferable.     

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.     

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.     

Comparative effects of overdrive on sinus and subsidiary pacemaker function.

Recent evidence has suggested a difference in response to overdrive pacing dependent on the location of the pacemaker within the A-V conduction system. To test this hypothesis, the effects of overdrive pacing were evaluated in five anesthetized dogs with experimentally induced A-V block and in seven patients with advanced A-V block. In the animals, sinoatrial node recovery times were studied over wide ranges of rates (130 to 210 beats per minute) and durations (30 to 180 seconds) of atrial pacing. All sinus node recovery times were less than 600 msec. with a mean maximum pause of 0.540+/-0.043 seconds (M.+/-S.E.M.). In contrast, after ventricular pacing (rates 90 to 150 beats per minute; durations 30 to 180 seconds), subsidiary pacemaker recovery times were significantly greater (p less than 0.025) with a mean maximum recovery time of 28.4+/-8.3 seconds. In the seven patients studied, all sinus node recovery times were less than 1,400 msecs. with a mean maximum pause of 0.954+/-0.051 seconds. As seen with the experimental animals, a significantly longer (p less than 0.025 mean maximum subsidiary pacemaker recovery time of 3.55+/-0.92 seconds was observed. The present studies in both experimental animals and in man without evidence of sinus node dysfunction showed that sinus node recovery time was independent of both rate and duration of atrial overdrive pacing. In contrast, subsidiary pacemaker recovery time was correlated with both rate and duration of ventricular overdrive pacing. In both experimental protocols, subsidiary pacemaker recovery time was shown to exceed sinus node recovery time at all rates and at all durations of pacing. Postrecovery sinus node acceleration was consistently observed after atrial overdrive pacing. In contrast, postrecovery subsidiary pacemaker "depression" characterized ventricular overdrive pacing. It is concluded that subsidiary pacemakers are significantly more susceptible to overdrive suppression than the sinoatrial node, a feature of substantial clinical significance.     

Antitachycardia pacing therapies and arrhythmia monitoring diagnostics for the treatment of atrial fibrillation

The case of a patient with frequent episodes of atrial fibrillation that organizes into atrial flutter following implantation of a dual chamber, rate adaptive pacemaker is reported. The atrial flutter was effectively pace-terminated following activation of the atrial antitachycardia pacing therapies in the pacemaker. This resulted in a decrease in atrial fibrillation burden over time. The present case also illustrates the value of diagnostic data retrieved from pacemakers for monitoring atrial fibrillation frequency over time and evaluating the efficacy of pacing and drug therapy.     

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.     

Oversensing of atrial flutter in the recipient atrium of a heart transplant patient with a permanent atrial pacemaker

Sinus node dysfunction requiring permanent pacemaker implantation is a common problem following heart transplantation. There are unique problems to consider in pacing the transplanted heart. This report describes a case of far-field sensing of atrial flutter in the recipient atrial remnanl, with resultant inhibition of the atrial pacemaker in the donor atrium, and symptomatic bradycardia. Although postulated to be a potential problem, oversensing of the recipient atrium has not been reported prior to this case. Awareness of this problem will provide for more effective pacemaker troubleshooting.     

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.     

Complete heart block as a cause of syncope in asymmetric septal hypertrophy

This case report presents a young adult with asymmetric septal hypertrophy (ASH) and syncope. Infranodal complete heart block was demonstrated as his cause for syncope. Therapy consisted of implantation of a A-V sequential pacemaker. Cardiac output determinations and systolic time intervals demonstrated the beneficial effects of properly timed atrial contractions.     

Atrial rhythms in response to an early atrial premature depolarization in man

The effect of an early atrial premature depolarization (APD) on spontaneous atrial rate was assessed in 16 patients in sinus rhythm. At close coupling intervals (range 27 to 48 per cent of the preceding sinus cycle), atrial acceleration was observed for several beats following the APD in 13 patients. On the basis of P wave configuration and the intra-atrial activation sequence, the accelerated beats appeared to originate from the sinus node. Furthermore, this “sinus” acceleration appeared regardless of the site at which the APD was introduced and was unrelated to latency or current strength. The findings are consistent with APD-induced sinus node re-entry, although sinus node pacemaker acceleration and shift is an alternative mechanism. Sinus node re-entry may explain certain instances of “interpolated” APD's and atrial tachyarrhythmias seen clinically.     

Interaction Between Atrial Pacing Lead and Epicardial Ventricular Wire Resulting in Unintended Ventricular Capture by Pacemaker Atrial Output

A 65-year-old man with a history of coronary artery disease underwent coronary artery bypass grafting in 1997 and 1998. He also received a permanent dual chamber pacemaker implantation during the second bypass surgery for complete heart block. He presented a year later to our pacemaker clinic for follow-up. Initial ECG showed ventricular capture by pacemaker atrial output (bottom tracings, left side). When the atrial output was decreased by 0.5V, normal atrial and ventricular pacemaker function was restored (bottom tracings, right side). A chest X-ray revealed an active fixation atrial lead implanted to the right atrium and a passive fixation lead to the ventricle. There was no apparent insulation failure of either lead by X-ray or by impedance measurements. An epicardial pacing lead implanted during bypass surgery for temporary postoperative pacing was not completely removed. The proximity between the retained epicardial wire and the screw of the active fixation atrial lead (arrow) support the hypothesis that the atrial output was conducted by the retained epicardial wire into the ventricles, resulting in unintended ventricular capture by the atrial output. However, we could not exclude the possibility that the atrial lead directly resulted in ventricular capture due to its proximity to the AV grove.     

Pseudo failure of sensing in patients with universal pacemakers and junctional rhythms

Ventricular fibrillation has been only rarely observed as a complication of cardiac pacing after the advent of demand pacemakers. Automatic AV sequential pacing (DDD) may provide the setting for ventricular fibrillation in patients with junctional rhythms. In this report we present two patients with implanted DDD pacemakers in whom ventricular pacemaker spikes were seen occurring on top of the T wave during episodes of junctional rhythm. This apparent lack of sensing of QRS complexes does not represent pacemaker malfunction, but rather, is the result of physiologic lack of sensing (blanking) which occurs 56 to 100 msec. following the output of the atrial and ventricular channels. During junctional rhythm when the atrial spike occurs at the beginning of a QRS complex the ventricular channel is blanked and does not sense the intrinsic ventricular activity and thus, ventricular output occurs during repolarization. Increasing the maximum pacemaker rate and decreasing the AV delay will reduce the chance occurrence of this phenomenon.     

Sinus node dysfunction. An overview with emphasis on autonomic and pharmacologic consideration.

Sinus node dysfunction is a disorder of impulse generation and impulse conduction. Previous works have emphasized that the dysfunction occurs not only within the sinus node but also within the escape pacemaker. Adrenergic and cholinergic mechanisms, as well as pulsations and pressure within the sinus node artery, play an important role in normal sinus node activity. Although perinodal fibers act as a buffer zone for sinoatrial conduction, their role in man is yet to be clarified. During normal sinus node activity, pacemaker shifts from the sinus node to the crista terminalis have been shown to occur. Following sinus node destruction, similar shifts do occur. Clinical methods of determining sinus node function, such as the sinus node recovery time and sinus atrial conduction time, are useful but have limitations. Dynamic electrocardiographic monitoring provides the best clinical method available for detecting sinus node dysfunction. Digitalis appears to improve the parameters of sinus node function by increasing the automaticity of latent atrial pacemakers. The atrial arrhythmia of sinus node dysfunction appears to be related to the characteristics of latent atrial pacemaker and "enhanced" cholinergic tone.     

Ventriculoatrial conduction in swine during cardiac pacing: animal model for retrograde conduction

Studies on cardiac conduction disorders and pacemaker tachycardias are usually conducted in patients because the phenomenon of ventriculoatrial (retrograde) conduction resulting from ectopic beats and pacing the ventricles has only been reported in humans. This study was conducted to characterize the ventriculoatrial (VA) conduction and retrograde P wave electrogram (EGM) amplitude and slew rate in 10 anesthetized pigs. Three transvenous pacemaker leads were positioned in the heart: one in the right atrial appendage, one in the sinoatrial (SA) node region, and another in the apex of the right ventricle. Ventriculoatrial conduction always occurred when the heart was paced from the right ventricle. There was a significant difference (p less than 0.05) between the amplitude and slew rate of the intrinsic P wave EGM (6.36 +/- 1.88 mV, 1.03 +/- 0.35 mV/msec) compared to the retrograde P wave EGM (3.12 +/- 1.37 mV, 0.57 +/- 0.18 mV/msec) detected at the SA node region. However, there was no significant difference between the intrinsic P wave EGM (4.81 +/- 2.01 mV, 0.40 +/- 0.26 mV/msec) and the retrograde P wave EGM (4.13 +/- 3.74 mV, 0.13 +/- 0.05 mV/msec) detected in the atrial appendage. The advantage of positioning an electrode in close proximity to the SA node for optimum atrial EGM detection and differentiation from retrograde P wave EGM is evident. The VA conduction time (178.5 +/- 8.5 msec) was significantly greater (p less than 0.01) than the antegrade conduction time (120.0 +/- 18.2 msec). The pig with its VA conduction is a useful model for pacemaker-induced tachycardias and for in vivo testing of drugs and/or pacemaker programs that can be utilized for controlling or preventing them.     

Surgical treatment of tachyarrhythmias

As a treatment for tachyarrhythmia, we have experienced 3 cases of Kent bundle division for WPW syndrome and 7 cases for implantation of atrial pacemaker. In two cases of Kent bundle division for A type and B type WPW syndrome, reappearance of premature supraventricular tachycardia was noticed but with less frequency and in number. A case of B type was cured surgically. Seven cases (including a case with elapse of 6 years) implanted with R-F atrial pacemaker termination of tachyarrhythmia resulted by rapid atrial pacing for 10 seconds.     

The effect of atropine on cardiac arrhythmias and conduction. Part 2

The effects of atropine on various components of the specialized conduction system of the heart and the myocardium itself are reviewed. These actions are sometimes unpredictable or paradoxical, depending on the component showing the dominant effect and the health of the entire system. Atropine is best known for its chronotropic effect. Improved sinoatrial conduction has been demonstrated but the effect on the refractoriness of atrial muscle is unsettled. Atropine stimulates the atrioventricular (A-V) junctional pacemaker and facilitates conduction through the A-V node. The response of the subjunctional portion of the specialized conduction system to the drug is unpredictable and controversial in some respects.Atropine is useful in the diagnosis of sinus node dysfunction, in the evaluation of coronary artery disease during atrial pacing, and in attempting to produce normal conduction in patients with the Wolff-Parkinson-White Syndrome. Its principal therapeutic application is in correcting the hypotension-bradycardia syndrome occurring during acute myocardial infarction. It also has a role in the temporary management of sinus node dysfunction. Atropine may also cause arrhythmias, including atrial fibrillation, A-V dissociation, ventricular tachycardia, and ventricular fibrillation. The clinical settings in which atropine may be arrhythmogenic are discussed.