Pacemaker-mediated Tachycardia Research Articles

Device Diagnosis of Pacemaker‐Mediated Tachycardia: True or False?

Device Diagnosis of Pacemaker‐Mediated Tachycardia: True or False?

Atrial lead malfunction presenting as new onset pacemaker-mediated tachycardia

This report describes the de novo occurrence of pacemaker-mediated tachycardia (PMT) in a patient with a dual-chamber implantable cardioverter-defibrillator and stable retrograde ventriculoatrial conduction time. The same rate-adaptive post-ventricular atrial refractory period (PVARP) duration had previously prevented PMT. Oversensing of atrial false signals from a defective lead shortened the PVARP with consequent sensing of retrograde conduction.

Pacemaker-mediated tachycardia initiated by an atrioventricular search algorithm to minimize right ventricular pacing

We report the initiation of pacemaker-mediated tachycardia by a St Jude implantable cardioverter-defibrillator with a programmed Ventricular Intrinsic Preference algorithm used for minimizing or inhibiting right ventricular pacing. This feature prolongs the atrioventricular (AV) delay periodically to determine if ventricular sensed events follow atrial events. Retrograde ventriculoatrial conduction and pacemaker-mediated tachycardia were initiated by long extended AV delays of 300 and 400 milliseconds. The 400-millisecond AV delay consisted of the programmed sensed AV delay (100 milliseconds) plus the Ventricular Intrinsic Preference increment (200 milliseconds) plus 100 milliseconds imposed by the AutoCapture algorithm when it detected loss of ventricular capture.

Termination of pacemaker-mediated tachycardia by a critically timed atrial extrasystole

Termination of pacemaker-mediated tachycardia by a critically timed atrial extrasystole

Catheter Ablation of Accessory Pathway in the Treatment of Pacemaker‐Mediated Tachycardia

Pacemaker-mediated tachycardia (PMT) remains a clinical problem in patients with dual-chamber pacemaker despite technological advances. The onset mechanism of this tachycardia is sensing of retrograde atrial activation after ventricular stimulation. Repeated retrograde conduction perpetuates tachycardia. Postventricular atrial refractory period prolongation has been used for prevention of PMT, but this is not the solution in all cases. We present a case with PMT where the retrograde limb is a left accessory pathway, which is treated with radiofrequency ablation successfully.

Common pitfalls in interpreting pacemaker electrocardiograms in the emergency department

The number of patients receiving pacemakers and defibrillators has grown substantially over the last 20 years. In addition, the complexity and sophistication of these devices have increased, making diagnosis of pacemaker problems using the electrocardiogram (ECG) more difficult for clinicians in the emergency department. This article will focus on a few of the pitfalls to be avoided when interpreting paced ECGs. Pacemaker algorithms designed to minimize right ventricular pacing may be confused with pathologic failure to output. Automatic capture threshold detection schemes may be misinterpreted as failure to capture as well as undersensing due to the extra “backup” pacemaker spikes noted on rhythm strips. Device testing done in the emergency department may produce waveforms on monitor resembling ventricular tachycardia if pacemaker-mediated tachycardia is produced accidentally. Ventricular safety pacing algorithms may also be misinterpreted as failure to sense appropriately, triggering questions about pacemaker malfunction. Certain types of true undersensing may resemble morphologies consistent with pacemaker lead dislodgment. In addition, sophisticated programming features designed to mimic normal physiology could be misconstrued as pacemaker malfunction. These include pacemaker hysteresis and sleep mode. The presence of frequent premature ventricular complexes would cause a pacemaker to inhibit ventricular pacing appropriately. However, this could produce a palpated heart rate that is substantially lower than the programmed lower rate of the device due to reduced perfusion by the premature ventricular complexes, again raising questions about the appropriate functioning of the pacemaker. All of these situations will be discussed in detail along with approaches to systematically examining the paced ECGs to minimize the risk of misinterpretation. Pacemaker timing cycles as they relate to troubleshooting of the paced ECG will also be introduced.

Cyber–Physical Modeling of Implantable Cardiac Medical Devices

The design of bug-free and safe medical device software is challenging, especially in complex implantable devices that control and actuate organs in unanticipated contexts. Safety recalls of pacemakers and implantable cardioverter defibrillators between 1990 and 2000 affected over 600 000 devices. Of these, 200 000 or 41% were due to firmware issues and their effect continues to increase in frequency. There is currently no formal methodology or open experimental platform to test and verify the correct operation of medical device software within the closed-loop context of the patient. To this effect, a real-time virtual heart model (VHM) has been developed to model the electrophysiological operation of the functioning and malfunctioning (i.e., during arrhythmia) heart. By extracting the timing properties of the heart and pacemaker device, we present a methodology to construct a timed-automata model for functional and formal testing and verification of the closed-loop system. The VHM's capability of generating clinically relevant response has been validated for a variety of common arrhythmias. Based on a set of requirements, we describe a closed-loop testing environment that allows for interactive and physiologically relevant model-based test generation for basic pacemaker device operations such as maintaining the heart rate, atrial-ventricle synchrony, and complex conditions such as pacemaker-mediated tachycardia. This system is a step toward a testing and verification approach for medical cyber-physical systems with the patient in the loop.

Differentiating pacemaker-mediated tachycardia from tachycardia due to atrial tracking: Utility of V-A-A-V versus V-A-V response after postventricular atrial refractory period extension

Dual-chamber pacemaker systems can lead to two forms of pacemaker-facilitated tachycardia: pacemaker-mediated tachycardia (PMT) and tracking of sinus or atrial tachycardia. Current pacemaker algorithms cannot always differentiate between these two tachycardias. The purpose of this study was to investigate a novel algorithm for distinguishing the two mechanisms of pacemaker-facilitated tachycardia, which is based on the specific termination response to postventricular atrial refractory period (PVARP) extension. We prospectively tested our algorithm using the Medtronic Virtual Interactive patient (VIP) II simulator (version 1.53) and a Medtronic Adapta ADDR01 dual-chamber pacemaker. Thirty-five scenarios that triggered "PMT detection" by the device were evaluated. All 12 scenarios of atrial tachycardias with intact AV conduction terminated with a Vp-Ar-Vs (V-A-V) response as a result of PVARP extension. Of the 11 scenarios of atrial tachycardia with complete heart block, all terminated with a Vp-Ar-As-Vp response. All four episodes of PMT with intact AV conduction terminated with a Vp-Ar-As-Vs (V-A-A-Vs) response. Of the eight episodes of PMT with complete heart block, all terminated with a Vp-Ar-As-Vp response. In the presence of intact AV conduction, the V-A-V response to PVARP extension is specific to atrial (or sinus) tachycardia, whereas the V-A-A-Vs response is specific to PMT. Recognizing the difference between the two forms of pacemaker-facilitated tachycardias has important implications for pacemaker programming.

Atypical pacemaker-mediated tachycardia from the atrial channel: What is the mechanism?

547-5271/$ -see front matter © 2011 Heart Rhythm Society. All rights reserved fibrillation was evaluated for an abrupt syncope. Echocardiogram showed no abnormalities, and Holter monitoring showed sinus arrhythmia with right bundle branch block (RBBB) and signs of sick sinus syndrome due to significant pauses. A dual-chamber pacemaker was implanted without complications (ventricular electrode in the right ventricular apex and atrial electrode at the high right atrial appendage). Pacemaker settings were DDDR mode, basic rate 65 bpm, maximum sensor rate 110 bpm, maximum tracking rate 150 bpm, and dynamic AV interval of maximum 280/minimum

Atypical Initiation of Endless-Loop, Pacemaker-Mediated Tachycardia

Atypical Initiation of Endless-Loop, Pacemaker-Mediated Tachycardia

Pacemaker-Mediated Tachycardia over the Upper Rate Limit in a Biventricular Pacemaker System: What is the Mechanism?

Pacemaker-Mediated Tachycardia over the Upper Rate Limit in a Biventricular Pacemaker System: What is the Mechanism?

Relatively narrow QRS complex after magnet application: what is the mechanism?

A 63-year-old man with sick sinus syndrome, who underwent dual-chamber permanent pacemaker implantation, was admitted due to frequent episodes of palpitation as a result of pacemaker-mediated tachycardia (PMT) ( Figure 1A ), which is terminated by magnet application ( Figure 1B …

Initiation of Ventricular Tachycardia by Interruption of Pacemaker‐Mediated Tachycardia in a Patient with a Dual‐Chamber Implantable Cardioverter Defibrillator

A 74-year-old man with a dual-chamber implantable cardioverter defibrillator implanted 3 years before experienced multiple ventricular tachycardias (VTs). All episodes were initiated by pacemaker-mediated tachycardia (PMT) that was either stopped by atrial undersensing or the tachycardia termination algorithm of the device. After the termination of PMT, two rapid ventricular paced beats, the first initiated by artificial triggering and the second due to retrograde conduction of the first one, initiated VT that was successfully terminated by antitachycardia pacing or a direct current shock of the device. All episodes revealed this pattern of initiation with a short-long-short ventricular sequence inducing VT.

Pacemaker-mediated tachycardia with varying cycle length: what is the mechanism?

As new algorithms are being developed to promote intrinsic atrioventricular conduction in preventing the deleterious effects of right ventricular pacing, more complex rhythm strips can be encountered. In our patient with a dual-chamber implantable cardioverter-defibrillator, such an algorithm resulted in a pacemaker-mediated tachycardia with several changes in cycle length.

Nonsustained pacemaker-mediated tachycardia during biventricular pacing: What is the mechanism?

Nonsustained pacemaker-mediated tachycardia during biventricular pacing: What is the mechanism?

Repetitive pacemaker-mediated tachycardia occurring only during left ventricular pacing: What is the mechanism?

A 54-year-old man with an artificial aortic valve and a history of hemodynamically unstable sustained ventricular tachycardia was admitted for placement of an implantable cardioverter-defibrillator (ICD). The patient had an enlarged left ventricle, low ejection fraction (35%), left bundle branch block, QRS 195 ms, and low exercise tolerance. A biventricular ICD (Kronos LV-T, Biotronik, Berlin, Germany) was implanted with the left ventricular (LV) lead in the posterolateral vein. Two days later, predischarge evaluation by chest x-ray film revealed stable positions of the right ventricular (RV), LV, and atrial leads. Detailed device checkup confirmed good thresholds and sensing in all chambers. However, immediately after the device was programmed to DDD LV pacing only (basic rate 60 bpm, upper tracking rate 130 bpm), an arrhythmia appeared (Figure 1). These episodes of tachycardia took the form of repetitive salvos that were interspersed with one to a few LV-paced beats at a rate of 70 bpm. This profile was repeated each time the pacing mode was changed from either DDD BiV or DDD RV to DDD LV. Reprogramming to DDD BiV or DDD RV pacing always abolished the arrhythmia and prevented its recurrence. Figure 2, Figure 3 show intracardiac ECGs with event markers during the arrhythmia, sinus rhythm, and RV, LV, and BiV pacing. What was the mechanism of the tachycardia? Figure 2Shown from top to bottom are event markers, surface ECG, and atrial and right ventricular (RV) intracardiac electrograms. Note that atrial oversensing artifacts (AS) appear 300 ms after left ventricular pacing (VP) but only 60 ms after the peak of the RV intracardiac deflection. View Large Image Figure Viewer Download Hi-res image Figure 3Shown from top to bottom are event markers, surface ECG, and atrial and right ventricular (RV) intracardiac electrograms. A: Left ventricular (LV) pacing. Tachycardia terminates for one beat and then resumes. Termination coincides with sensing of intrinsic atrial depolarization. B: LV pacing. As the degree of fusion becomes smaller, atrial oversensing artifacts (ARS) appear progressively further from the LV pacing artifact (VP)—60, 200, and 280 ms—with the last artifact (AS) falling outside the postventricular atrial refractory period. However, regardless of the distance from the beginning of the QRS, the oversensing artifacts always follow RV intracardiac deflection with a constant coupling of 60 ms. C: During RV pacing, atrial oversensing artifacts (ARS) appear 120 ms after the RV pacing artifact (VP). D: During conducted atrial depolarization, atrial oversensing artifacts (AS) appear 80 ms after commencement of the QRS. E: During biventricular pacing, atrial oversensing artifacts (ARS) appear 130 ms after the pacing artifact (VP). View Large Image Figure Viewer Download Hi-res image

Could C- and D-network mobile phones endanger patients with pacemakers?

To investigate prospectively the extent of potentially harmful interference of cardiac pacemakers by mobile phones in the C (analog) and D (digital) networks in use in Germany. 104 patients (54 men, 50 women; mean age 75.8 [40-100] years) with 58 different implanted pacemaker models (43 one-chamber and 15 two-chamber systems) underwent uniform tests at various functional states with three different telephones (D1 portable 8 Watt, D1 Handy model 2 Watt, C Handy model 0.5 Watt). The distances between telephone aerial and pacemaker, as well as reception sensitivity and polarity of the pacemaker were varied. All tests were done during continuous ECG monitoring. 28 different pacemaker types (48.3%) in 43 patients (41.3%) showed interference in the form of pacemaker inhibition and switching to interference frequencies as well as triggering of pacemaker-mediated tachycardias in the DDD mode, as well as in the temperature-regulated frequency-adaptive function. D portables influenced pacemaker function more often and at greater distance than the D Handy model, which was little different from the c network hand phone. Reduction in pacemaker sensitivity as well as switching to bipolar reception only partly eliminated the interference. Patients with implanted pacemakers should if possible not use mobile phones in the C and D networks. Individual testing with suitable programming of pacemaker sensitivity and polarity can reduce the risk of interference.

Etomidate Unlikely to Have Induced Pacemaker-mediated Tachycardia

University of Texas M. D. Anderson Cancer Center, Houston, Texas. mrozner@mdanderson.orgAlthough I agree that the case “Etomidate-induced Pacemaker-mediated Ventricular Tachycardia”1could represent an important contribution to our literature, I am concerned that the data presented in this article cannot justify the conclusion that myoclonus from the etomidate was actually responsible for this pacemaker-driven tachycardia (this is not actually an arrhythmia). Therefore, this article might be cited by future practitioners when, in fact, etomidate likely made little or no contribution to the ventricular pacing shown at 140 beats/min.The rate-responsive mechanism in this Medtronic Prodigy pacemaker (St. Paul, MN) is a piezo crystal attached to the case of the pacemaker.2It is activated by case deformation (pressing on the case). The rate-responsive algorithm has a number of programmable settings that determine how the pacemaker will change the pacing rate (called activity-indicated rate) due to stimulation of this crystal. These settings include the following (not specified in the article): lower pacing rate, upper activity rate, activity threshold, activity rate response, acceleration time, and deceleration time. In the default setting, the acceleration time is 0.5 min, so in 30 s, the pacemaker will achieve 90% of the difference between the current paced rate and the higher (calculated) activity-indicated rate consistent with the activity level.The default deceleration time is 5 min and is of interest here. Upon abrupt cessation of activity, the pacing rate begins decreasing almost immediately, and it will decrease over 5 min by 90% from the current (high) paced rate to the new, lower activity-indicated rate. In this case, assuming that the lower pacing and upper activity rates had been programmed to 70 and 140 beats/min, respectively, the actual pacing rate would have been approximately 122 beats/min at 30 s, 109 beats/min at 1 min, and 92 beats/min at 2 min (fig. 1). No time intervals were reported in the article, but 30 or more seconds likely elapsed from the last patient movement to the reprogramming of the pacemaker.Therefore, I believe that the continued pacing at 140 beats/min suggests that something else was affecting the pacemaker. It might have been the weight of the programming head. In fact, the Prodigy manual warns: “Clinical studies of activity rate responsive pacemakers have reported instances of … an increase in the pacing rate up to the programmed Upper Activity Rate … by pressing the programmer head over the pacemaker.”The stability of the heart rate (determined by the intervals between the QRS complexes) in the author's published figure 2 suggests that the pacemaker was sensing continuous mechanical activity. If the mechanical activity had ceased, the pacing rate would have been slowing, which would resulted in the successive lengthening of the intervals between the QRS complexes.This article is an important reminder that pacemakers (and implanted cardioverter–defibrillators) are mere computers that respond to electrical and environmental signals in a predictable fashion. The authors should have emphasized that these devices can produce unusual pacing behavior that might be misinterpreted by clinicians (likely true in this case) and, therefore, induce inappropriate treatment, which did not happen here. For example, pressure on the chest over a pacemaker or defibrillator due to instruments or surgical personnel, as well as mechanical activity over a pacemaker or defibrillator from surgical site preparation, can lead to a paced tachycardia approaching the upper activity rate. In fact, misinterpretation of pacemaker (pseudomalfunction) behavior is common,3and sometimes it leads to disastrous results with patient injury.4Finally, the comment in this article that “It is essential that the pacemaker should be programmed to an asynchronous mode” is not justified by any part of the case presentation, the discussion, any literature, or any manufacturer recommendation. Pacemaker and implantable cardioverter–defibrillator manufacturers do recommend a comprehensive interrogation of any device that has “seen” an external cardioversion or defibrillation.University of Texas M. D. Anderson Cancer Center, Houston, Texas. mrozner@mdanderson.org

Etomidate Unlikely to Have Induced Pacemaker-mediated Tachycardia

We thank Dr. Rozner for his interest in our case report, “Etomidate-induced Pacemaker-mediated Ventricular Tachycardia,”1and we appreciate the opportunity to address some of the points he raises in his letter.He first questions our use of the term pacemaker-mediated ventricular tachycardia , asserting that the rhythm we reported is not actually an arrhythmia. We agree that the rhythm we observed was indeed not a clinical arrhythmia. Perhaps a more accurate description might be his term, abnormal pacemaker-driven tachycardia .Dr. Rozner then refers to the programmable settings that affect the rate-responsive function. In our patient, the lower pacing rate and upper activity rates were 70 and 160 beats/min, activity threshold was medium, acceleration time was 0.5 min, and deceleration time was 5 min. Dr. Rozner's discussion of the rate-responsive mechanism demonstrates his well-known expertise2in the area of implantable cardiac devices, but his calculation using the deceleration time is not relevant to our case. His letter examines the situation where the stimulus activating the rate-responsive function terminates, and the pacing rate thus begins to decrease gradually as he describes. However, we have stated that the rapid rhythm (shown in fig. 2 of our case report) ceased immediately after the rate-responsive function was disabled. That is, the stimulus (myoclonus) did not stop, but instead the pacemaker was reprogrammed to stop responding to the stimulus. Once the rate-response function is disabled, a pacemaker will immediately revert to its baseline settings (VVI at the lower pacing rate of 70 beats/min, in our case) as shown in figure 2.Therefore, we agree with Dr. Rozner's statement that “the pacemaker was still sensing activity,” but we maintain that etomidate-induced myoclonus is a much more plausible explanation than the weight of the programming head without any additional pressure being applied. If the programming head were solely responsible for the rapid ventricular pacing (as Dr. Rozner suggests), we would expect to have gotten the same result each time the rate-responsive function was restored, not just the first time.We have considered other possible causes for tachycardia in this setting, such as erroneous programming of the pacemaker (e.g. , if the operator accidentally turned off the mode switch in a patient with atrial fibrillation, the device might pace at the upper activity rate) or inappropriate atrial sensing (e.g. , 1:2 sensing of an atrial rate of 280 beats/min). However, we believe that the observed myoclonic activity led to this case of pacemaker-driven tachycardia. This abnormal rate-response is clearly corroborated by the data shown in figure 2. Our hypothesis is also supported by the fact that there were no further episodes of rapid ventricular pacing with reactivation of the rate-responsive function, after waiting to ensure complete cessation of the myoclonus. Persistent myoclonic activity for this amount of time is reasonable; etomidate-induced myoclonus has been reported to last up to 8 min.3Finally, Dr. Rozner takes exception to our recommendation that the pacemaker be set to an asynchronous mode. Although we agree that this statement is not valid for a cardioversion, it remains sound advice for anesthesiologists who take patients to the operating room, where unipolar electrocautery is routinely used, and we apologize for any confusion this generalized statement may have caused.The authors thank Robert N. Goldstein, M.D. (Assistant Professor of Medicine, Director, Cardiac Device Clinic, Division of Cardiology/Electrophysiology, University Hospitals Case Medical Center, Cleveland, Ohio), for his assistance in the preparation of the manuscript.*University Hospitals Case Medical Center, Cleveland, Ohio. michaelaltose@yahoo.com

Temporary epicardial pacing after cardiac surgery: a practical review

The first part of this two-part review discussed the indications for various types of epicardial pacing systems and an overview of the routine care of a pacemaker-dependent patient. Dual chamber temporary pulse generators now feature many of the refinements developed initially for use in permanent pacemakers. Few of these are utilised in the immediate postoperative period, often solely due to lack of familiarity with all but basic functions. The second part of the review deals with the selection of pacing modes. Troubleshooting real and apparent pacemaker malfunctions, including manual adjustment of parameters such as the AV interval, post atrial refractory period and upper rate limit, to avoid over- and undersensing, cross-talk and pacemaker-mediated tachycardia will also be addressed.