Unforeseen Consequences of Device-Device Interaction TOON BUYSSENS, M.D.,* and FRANK PROVENIER, M.D., PH.D.† From the *Department of Cardiology, Ghent University Hospital, Ghent, Belgium; and †Department of Cardiology, AZ Maria Middelares, Ghent, Belgium
pacemaker, far-field, sensing, syncope, device-device interaction
Case Introduction An 88-year-old man presents to the emergency department with reports of syncope, dizziness, altered consciousness, and blurred vision. Monitoring showed a heart rhythm at 25 beats/min to 65 beats/min, with long arrests of more than 5 seconds. In 1996, a DDD-pacemaker was implanted because of complete heart block following concomitant coronary artery bypass grafting and aortic valve replacement. Later that year the aortic valve bioprosthesis was urgently replaced with an aortic root prosthesis and a mechanical valve because of aortic valve endocarditis with valve dehiscence and paravalvular regurgitation, which resulted in lung edema and cardiogenic shock. Considering the critical state of the patient, and the absence of clinical and transesophageal echocardiographic arguments for lead or pocket infection, it was decided not to explant the pacemaker system. In 2004, pacemaker lead infection necessitated explantation of the pacemaker with extraction of the pacemaker leads. This was followed by the implantation of an epicardial pacing system (Medtronic EnPulse DDDR, Medtronic Inc., Minneapolis, MN, USA) to avoid recurrence of endovascular infection.1 In order to secure longterm pacing, the two epicardial leads were placed at the right ventricle, functionally resulting in a VVI pacing system. Despite all that, poor tolerance of VVI pacing with aggravating symptoms of heart failure and increase of the pacing threshold on both epicardial leads (5.5 V at the atrial channel and 6 V at the ventricular channel) compelled the implantation of a new endocardial dual-chamber pacing system (Medtronic EnPulse,
No conflict of interest. Address for reprints: Toon Buyssens, M.D., Department of Cardiology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. Fax: +329 332 49 66; e-mail: toon_buyssens@ hotmail.com Received September 25, 2013; revised February 7, 2014; accepted February 9, 2014. doi: 10.1111/pace.12397
replaced in 2012 by Medtronic Adapta ADDR01 because of end of life, both programmed in DDDR mode).2 The epicardial pacing system (Medtronic EnPulse DDDR) was left intra-abdominally to avoid the need for general anaesthesia considering the patient’s poor general medical condition. The epicardial pacing system (Medtronic EnPulse DDDR) was programmed at a minimal rate of 30 beats/min, with a high output amplitude of 7.5 V and width of 1.5 ms to ensure capture if needed. The epicardial lead at the ventricular channel showed loss of sensing, but the epicardial lead at the atrial channel properly sensed the ventricular evoked response on endocardial stimulation, at a programmed sensitivity of 5.6 mV. Therefore, the epicardial device was programmed in AAI, functionally resulting in VVI pacing since both epicardial leads were placed at the right ventricle. At the emergency department, the presenting electrocardiogram (ECG) revealed an atrial sensed, ventricular paced rhythm at a rate of 62 beats/min with competitive ventricular unipolar pacing at 65 beats/min with noncapture in both the atrium and the ventricle (Fig. 1). Interrogation of the endocardial pacing system (Medtronic Adapta ADDR01) showed intermittent inhibition due to sensing of the ventricular unipolar pacing output pulses (Fig. 2). How can a pacing system programmed AAI at 30 beats/min pace VVI at 65 beats/min? Commentary Interrogation of the epicardial pacing system (Medtronic EnPulse DDDR) revealed the cause of the pacemaker’s sudden change in output: it was switched to elective replacement indicator (ERI) pacing mode (VVI 65 beats/min, amplitude 7.5 V with pulse width 1.5 ms and sensitivity 5.6 mV). Since there was loss of sensing, this resulted in uninterrupted pacing at a rate of 65 beats/min, seen as unipolar output pulses on the ECG and the intracardiac electrogram (EGM; Figs. 1 and 2). The unipolar ventricular output pulses of the epicardial pacing system (Medtronic EnPulse DDDR) were mislabeled as sensed events on the ventricular channel by the endocardial pacing system (Medtronic Adapta ADDR01) and resulted in ventricular pacing inhibition.
©2014 Wiley Periodicals, Inc. 526
April 2015
PACE, Vol. 38
UNFORESEEN CONSEQUENCES OF DEVICE-DEVICE INTERACTION
Figure 1. The 12-lead electrocardiogram showing atrial sensed, ventricular paced, rhythm at a rate of 62 beats/min with competitive ventricular unipolar pacing at 65 beats/min with noncapture in both atrium and ventricle. Far-field sensing is clinically most relevant when happening on the ventricular channel of the endocardial pacing system (Medtronic Adapta ADDR01), with inhibition of ventricular pacing (black arrows). Far-field sensing on the atrial channel results in tracking of ventricular pacing (white arrow).
Figure 2. Intracardiac electrogram from the endocardial pacing system (Medtronic Adapta ADDR01) shows atrial paced or sensed, ventricular paced rhythm. The ventricular unipolar pacing output pulses at 65 beats/min are labeled as ventricular sensed events, resulting in inhibition of ventricular pacing (black arrow). When the unipolar pacing pulses are sensed within the safety pacing window (110 ms after atrial sensing), they are followed by ventricular safety pacing (white arrow).
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BUYSSENS AND PROVENIER
The sensing of the endocardial pacing system was bipolar in both chambers, with atrial sensitivity programmed at 0.18 mV and ventricular sensitivity at 2 mV, both with sensing assurance activated. Moreover, since there was loss of capture through the epicardial lead, this resulted in the long arrest, causing the patient’s symptoms. The initial settings of the epicardial pacing system (Medtronic EnPulse DDDR) were AAI at a minimal rate of 30 beats/min. The choice for the atrial channel was made because of preserved sensing and still borderline capture in the lead connected with the atrial channel. The automated switch from AAI to VVI in ERI pacing mode resulted in loss of sensing in the epicardial pacing system (Medtronic EnPulse DDDR) with inappropriate pacing in the presence of ventricular activity, but also induced noncapture. Moreover, the ERI stimulation at 65 beats/min outpaced the basic rate of 60 beats/min of the endocardial pacing system (Medtronic Adapta ADDR01), resulting in long periods of pacing inhibition and thus cardiac arrests. Reprogramming the epicardial pacing system (Medtronic EnPulse DDDR) only temporarily solved the problem; new battery voltage measurements resettled the ERI conditions in the device, necessitating explantation of the epicardial pacing system to restore the normal function of the endocardial pacing system (Medtronic Adapta ADDR01). Although not observed in this patient, the same scenario of life-threatening device-device interaction could be initiated anytime during the implanted years if the device switched to a “power on reset” (POR) mode. This automated
switch to POR mode may occur when the device is exposed to strong electromagnetic fields such as electrocautery or defibrillation. The POR settings are typically the same as the device’s ERI settings (VVI 65 beats/min).1 Provocative testing for device-device interaction at the time of implantation could have anticipated the aforementioned problems and is critical in the care of patients with dual devices and pacemaker dependency. The endocardial ventricular lead should have been positioned at a distance from the epicardial leads, so that epicardial stimulation remained under the sensitivity levels of the endocardial device. If not feasible, the epicardial pacemaker should have been extracted. Conclusion We presented a case where a second pacemaker was implanted, without explanting the first. Because the latter was programmed at a minimal rate, with preserved sensing and borderline capture in AAI mode, this could be done without any overt problems of interference between the two devices. However, one should keep in mind that an automated switch to ERI mode, as the battery’s longevity declines, or POR mode, if exposed to the right conditions, can occur anytime, in this case turning a seemingly harmless combination of two pacemakers into a life-threatening situation as the unipolar output pulses of one pacemaker inhibited vital ventricular pacing of the other. Therefore, provocative testing for devicedevice interaction at the time of implantation is mandatory in dual device settings.
References 1. Medtronic ENPULSE, Pacemaker Programming Guide, downloaded from http://manuals.medtronic.com (accessed September 10, 2013).
528
2. Medtronic ADAPTA, Pacemaker Programming Guide, downloaded from http://manuals.medtronic.com (accessed September 10, 2013).
April 2015
PACE, Vol. 38
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
pacemaker, far-field, sensing, syncope, device-device interaction
Case Introduction An 88-year-old man presents to the emergency department with reports of syncope, dizziness, altered consciousness, and blurred vision. Monitoring showed a heart rhythm at 25 beats/min to 65 beats/min, with long arrests of more than 5 seconds. In 1996, a DDD-pacemaker was implanted because of complete heart block following concomitant coronary artery bypass grafting and aortic valve replacement. Later that year the aortic valve bioprosthesis was urgently replaced with an aortic root prosthesis and a mechanical valve because of aortic valve endocarditis with valve dehiscence and paravalvular regurgitation, which resulted in lung edema and cardiogenic shock. Considering the critical state of the patient, and the absence of clinical and transesophageal echocardiographic arguments for lead or pocket infection, it was decided not to explant the pacemaker system. In 2004, pacemaker lead infection necessitated explantation of the pacemaker with extraction of the pacemaker leads. This was followed by the implantation of an epicardial pacing system (Medtronic EnPulse DDDR, Medtronic Inc., Minneapolis, MN, USA) to avoid recurrence of endovascular infection.1 In order to secure longterm pacing, the two epicardial leads were placed at the right ventricle, functionally resulting in a VVI pacing system. Despite all that, poor tolerance of VVI pacing with aggravating symptoms of heart failure and increase of the pacing threshold on both epicardial leads (5.5 V at the atrial channel and 6 V at the ventricular channel) compelled the implantation of a new endocardial dual-chamber pacing system (Medtronic EnPulse,
No conflict of interest. Address for reprints: Toon Buyssens, M.D., Department of Cardiology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. Fax: +329 332 49 66; e-mail: toon_buyssens@ hotmail.com Received September 25, 2013; revised February 7, 2014; accepted February 9, 2014. doi: 10.1111/pace.12397
replaced in 2012 by Medtronic Adapta ADDR01 because of end of life, both programmed in DDDR mode).2 The epicardial pacing system (Medtronic EnPulse DDDR) was left intra-abdominally to avoid the need for general anaesthesia considering the patient’s poor general medical condition. The epicardial pacing system (Medtronic EnPulse DDDR) was programmed at a minimal rate of 30 beats/min, with a high output amplitude of 7.5 V and width of 1.5 ms to ensure capture if needed. The epicardial lead at the ventricular channel showed loss of sensing, but the epicardial lead at the atrial channel properly sensed the ventricular evoked response on endocardial stimulation, at a programmed sensitivity of 5.6 mV. Therefore, the epicardial device was programmed in AAI, functionally resulting in VVI pacing since both epicardial leads were placed at the right ventricle. At the emergency department, the presenting electrocardiogram (ECG) revealed an atrial sensed, ventricular paced rhythm at a rate of 62 beats/min with competitive ventricular unipolar pacing at 65 beats/min with noncapture in both the atrium and the ventricle (Fig. 1). Interrogation of the endocardial pacing system (Medtronic Adapta ADDR01) showed intermittent inhibition due to sensing of the ventricular unipolar pacing output pulses (Fig. 2). How can a pacing system programmed AAI at 30 beats/min pace VVI at 65 beats/min? Commentary Interrogation of the epicardial pacing system (Medtronic EnPulse DDDR) revealed the cause of the pacemaker’s sudden change in output: it was switched to elective replacement indicator (ERI) pacing mode (VVI 65 beats/min, amplitude 7.5 V with pulse width 1.5 ms and sensitivity 5.6 mV). Since there was loss of sensing, this resulted in uninterrupted pacing at a rate of 65 beats/min, seen as unipolar output pulses on the ECG and the intracardiac electrogram (EGM; Figs. 1 and 2). The unipolar ventricular output pulses of the epicardial pacing system (Medtronic EnPulse DDDR) were mislabeled as sensed events on the ventricular channel by the endocardial pacing system (Medtronic Adapta ADDR01) and resulted in ventricular pacing inhibition.
©2014 Wiley Periodicals, Inc. 526
April 2015
PACE, Vol. 38
UNFORESEEN CONSEQUENCES OF DEVICE-DEVICE INTERACTION
Figure 1. The 12-lead electrocardiogram showing atrial sensed, ventricular paced, rhythm at a rate of 62 beats/min with competitive ventricular unipolar pacing at 65 beats/min with noncapture in both atrium and ventricle. Far-field sensing is clinically most relevant when happening on the ventricular channel of the endocardial pacing system (Medtronic Adapta ADDR01), with inhibition of ventricular pacing (black arrows). Far-field sensing on the atrial channel results in tracking of ventricular pacing (white arrow).
Figure 2. Intracardiac electrogram from the endocardial pacing system (Medtronic Adapta ADDR01) shows atrial paced or sensed, ventricular paced rhythm. The ventricular unipolar pacing output pulses at 65 beats/min are labeled as ventricular sensed events, resulting in inhibition of ventricular pacing (black arrow). When the unipolar pacing pulses are sensed within the safety pacing window (110 ms after atrial sensing), they are followed by ventricular safety pacing (white arrow).
PACE, Vol. 38
April 2015
527
BUYSSENS AND PROVENIER
The sensing of the endocardial pacing system was bipolar in both chambers, with atrial sensitivity programmed at 0.18 mV and ventricular sensitivity at 2 mV, both with sensing assurance activated. Moreover, since there was loss of capture through the epicardial lead, this resulted in the long arrest, causing the patient’s symptoms. The initial settings of the epicardial pacing system (Medtronic EnPulse DDDR) were AAI at a minimal rate of 30 beats/min. The choice for the atrial channel was made because of preserved sensing and still borderline capture in the lead connected with the atrial channel. The automated switch from AAI to VVI in ERI pacing mode resulted in loss of sensing in the epicardial pacing system (Medtronic EnPulse DDDR) with inappropriate pacing in the presence of ventricular activity, but also induced noncapture. Moreover, the ERI stimulation at 65 beats/min outpaced the basic rate of 60 beats/min of the endocardial pacing system (Medtronic Adapta ADDR01), resulting in long periods of pacing inhibition and thus cardiac arrests. Reprogramming the epicardial pacing system (Medtronic EnPulse DDDR) only temporarily solved the problem; new battery voltage measurements resettled the ERI conditions in the device, necessitating explantation of the epicardial pacing system to restore the normal function of the endocardial pacing system (Medtronic Adapta ADDR01). Although not observed in this patient, the same scenario of life-threatening device-device interaction could be initiated anytime during the implanted years if the device switched to a “power on reset” (POR) mode. This automated
switch to POR mode may occur when the device is exposed to strong electromagnetic fields such as electrocautery or defibrillation. The POR settings are typically the same as the device’s ERI settings (VVI 65 beats/min).1 Provocative testing for device-device interaction at the time of implantation could have anticipated the aforementioned problems and is critical in the care of patients with dual devices and pacemaker dependency. The endocardial ventricular lead should have been positioned at a distance from the epicardial leads, so that epicardial stimulation remained under the sensitivity levels of the endocardial device. If not feasible, the epicardial pacemaker should have been extracted. Conclusion We presented a case where a second pacemaker was implanted, without explanting the first. Because the latter was programmed at a minimal rate, with preserved sensing and borderline capture in AAI mode, this could be done without any overt problems of interference between the two devices. However, one should keep in mind that an automated switch to ERI mode, as the battery’s longevity declines, or POR mode, if exposed to the right conditions, can occur anytime, in this case turning a seemingly harmless combination of two pacemakers into a life-threatening situation as the unipolar output pulses of one pacemaker inhibited vital ventricular pacing of the other. Therefore, provocative testing for devicedevice interaction at the time of implantation is mandatory in dual device settings.
References 1. Medtronic ENPULSE, Pacemaker Programming Guide, downloaded from http://manuals.medtronic.com (accessed September 10, 2013).
528
2. Medtronic ADAPTA, Pacemaker Programming Guide, downloaded from http://manuals.medtronic.com (accessed September 10, 2013).
April 2015
PACE, Vol. 38
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
