© 2004 by European Society of Cardiology
OLD ISSUE REVISITED
Adverse effects of direct current cardioversion on cardiac pacemakers and electrodes
Is external cardioversion contraindicated in patients with permanent pacing systems?
Medizinische Universitätsklinik Würzburg, Germany
Manuscript submitted 27 May 2003. Accepted after revision 9 November 2003.
*Corresponding author. Universitätsklinik Würzburg, Medizinische Klinik, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany. Tel.: +49-931-201-36904; fax: +49-931-201-36302. E-mail address: waller_c{at}medizin.uni-wuerzburg.de (C. Waller).
Abstract
Use of pacing in sick sinus syndrome and recent developments in pacemaker therapy for intermittent atrial fibrillation raise the question of whether external electrical cardioversion should be used for termination of atrial fibrillation. This paper analyzes three cases of pacemaker and/or electrode dysfunction appearing after direct current (DC) cardioversion for termination of atrial fibrillation. Despite similar conditions during cardioversion in all cases, different dysfunctions reflecting damage to the pulse generator and/or a rise of the stimulation threshold in both, atrial and ventricular leads, have been observed. The possible mechanisms for these effects are discussed and recommendations for the management of cardioversion in patients with permanent pacemaker systems are given.
Key Words: cardioversion, pacemaker dysfunction, lead dysfunction
Introduction
Direct current (DC) cardioversion is highly effective for the termination of atrial fibrillation and flutter. These rhythm disturbances are frequently seen in pacemaker patients with sick sinus syndrome. Recently, prevention of intermittent atrial fibrillation by special pacing algorithms has been introduced [1]
and may increase the number of permanently paced patients in whom electrical cardioversion is discussed in certain conditions. However, possible damage to the pacemaker and/or the leads is suspected by many physicians and induces some uncertainty.
Only a few reports [2,3] have been published describing the potential adverse interactions between cardiac pacing and electrical cardioversion. Following shocks of 200 J or lower, dysfunction of the cardiac stimulator and an acute loss of capture with complete recovery of function have been reported. In contrast, electrical defibrillation shocks of 200 J or higher may lead to a chronic increase in ventricular stimulation threshold [4–7].
Since the late 1960s, protective circuits have been introduced in pacemakers and defibrillators to shield the electronics from damage due to electrical shocks [8]. In both pacemakers and defibrillators, one or more Zener diodes are connected in series [9] to protect against electrical shocks.
Three cases are presented in which elective cardioversion was performed in patients with modern permanent dual lead pacemaker systems. External cardioversion resulted either in a persistent increase in ventricular and/or atrial stimulation threshold or in a damage to the pulse generator itself. Different potential causes for these effects are discussed and suggestions are presented for the management of the pacemaker patient who requires electrical cardioversion.
Case reports
Case 1
A 70-year-old woman had an implanted programmable DDD pacemaker (CPI Discovery DR) since August 1999 for the treatment of sick sinus syndrome with symptomatic bradycardias. The pulse generator was located in the right pectoral region. The configuration was bipolar for the atrial electrode and unipolar for the ventricular lead. The patient had a first episode of atrial fibrillation in January 1999. After drug treatment, supraventricular tachycardia converted successfully into sinus rhythm. A second episode of atrial fibrillation was diagnosed in November 2000. Therefore, external cardioversion was accomplished with an anterior–lateral paddle position using a single shock of 100 J. This resulted in sinus rhythm. Subsequent testing of the pacemaker showed normal pacing and sensing thresholds. One day later, exit block was detected on a 12 lead ECG. The problem could not be solved by reprogramming of the pulse generator. Intraoperative threshold measurements during pacemaker replacement showed a rise in ventricular stimulation threshold to 7.7 V at 0.5 ms, whereas atrial stimulation threshold was unchanged (1.55 V at 0.4 ms). The impedance of both leads was normal (Table 1a, b). Consequently, the ventricular lead had to be replaced.
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Case 2
A 50-year-old man received a DDD pacemaker (Vitatron Diamond 3) in March 1998 to treat intermittent complete atrioventricular (AV) block. The pulse generator was placed in the right pectoral region. Electrode configuration in the ventricle was unipolar and bipolar in the atrium. In July 2000, the patient was admitted with a first episode of persistent atrial fibrillation requiring cardioversion. External cardioversion was accomplished under adequate anticoagulation with an anterior–lateral paddle orientation using two shocks of 200 J. Measurements 2 h after cardioversion showed a major rise in the ventricular stimulation threshold from 1.3 V at 0.5 ms before the intervention to 3.8 V at 1 ms after intervention. The atrial stimulation threshold remained unchanged and pulse generator function was normal. The pacing impedances of both leads were in the normal range. Five days after cardioversion the rise in the stimulation threshold was persistent (Table 1a, b). Finally, the ventricular lead had to be replaced since the patient had pectoral muscle stimulation with an output of 5 V at 1 ms.
Case 3
A 50-year-old man received a DDD pacemaker (Vitatron Diamond 3) 2 years ago for sick sinus syndrome with symptomatic bradycardias. The patient suffered from intermittent atrial fibrillation with tachycardias since 1995. The pulse generator was implanted in the right pectoral region. Atrial lead configuration was bipolar, configuration of the ventricular lead was unipolar. In August 2000, the patient was admitted to the hospital with an episode of persistent atrial fibrillation requiring external cardioversion. A first attempt using 200 J converted atrial fibrillation to sinus rhythm. Two hours after intervention, ventricular and atrial stimulation thresholds were slightly increased from 1.0 V (1.0 ms) prior to cardioversion to 1.35 V (1.0 ms) in the ventricle and from 0.25 V (1.0 ms) to 1.05 V (1 ms) in the atrium. The pulse generator function and impedances of both the leads were normal. Measurements performed five weeks later revealed a further increase in ventricular and atrial stimulation thresholds to 2.5 V at 1.0 ms and 5.0 V at 1.0 ms, respectively (Table 1a, b). Finally, both atrial and ventricular lead had to be replaced.
Discussion
Three patients are presented with either a chronic increase in stimulation threshold and/or damage to the pulse generator following external cardioversion. In all cases, the pulse generator was located in the right pectoral region and cardioversion was performed as far as possible from the pulse generator by means of an anterior–lateral paddle position. One paddle was placed at the right sternal border and the second was located on the left side of the thorax. These positions were chosen to avoid a dipole of current flow parallel to the endocardial lead. Nevertheless, substantial damage of the implanted equipment requiring replacement was found in all cases. In one of our patients cardioversion resulted in a persistent increase in the atrial stimulation threshold. This finding shows that current after external cardioversion can be shunted also to bipolar leads, which indicates that a bipolar configuration does not always prevent damage caused by cardioversion.
Increasing numbers of patients with sick sinus syndrome are treated with a pacemaker and therefore, will possibly require external cardioversion for therapy of intermittent atrial fibrillation. Relatively little has been done to protect cardiac stimulators during a large energy surge. Voltage regulators such as Zener diodes protect the pacemaker circuitry by shunting the energy delivered during cardioversion through the lead to the electrode tip. However, this may result in concentration of the energy at the electrode–myocardial interface, leading to burns and electrical trauma [5,9]. Additionally, capacitive coupling of energy to the pacing lead and the heart due to a paddle orientation parallel to a portion of the lead system has been discussed as a potential cause for an increase in the stimulation threshold [2]. Malfunction of the cardiac stimulator has been described elsewhere [10,11]. Pacemaker analysis in these studies showed damage to the voltage oscillator and to the protective Zener diode. Other groups have found reprogramming defects due to damage to the software programme [3].
Our data do not allow any estimate of likelihood of occurrence but the possibility that external cardioversion may result in acute or chronic pacemaker and lead dysfunction, requiring device replacement, has to be borne in mind. Precautions are particularly necessary to be taken in pacemaker dependent patients (Table 2). Prior to external cardioversion, programming of a higher voltage output is recommended in order to avoid exit block with loss of capture. However, the amount of voltage increase may not be adequate for safety as shown in our first case. Pacemaker function, stimulation and sensing threshold should be tested immediately after cardioversion, at discharge and 4–6 weeks later. Further tests are recommended in the case of an increase in pacing or sensing threshold. In accordance with our experience, an improvement of the threshold can hardly be expected [2] and therefore, the decision for pacemaker or electrode replacement has to be correctly timed.
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It has also been recommended that the defibrillator paddles be placed 15 cm from the pulse generator and be oriented in an anterior–lateral, anterior–posterior or left pectoral–right hypochondrial (for right sided generators) positions in order to place the electric field perpendicular and not parallel to the course of the leads. Some manufacturers recommend use of VOO or AOO modes during cardioversion in order to switch off the amplifier. Additionally, the time between two successive shocks ought to be about 5 min in order to allow cooling of the diodes.
External cardioversion may result in pacemaker dysfunction, even in modern devices, and a significant increase in the stimulation threshold with potential acute or chronic loss of capture. Despite numerous precautions prior to and after cardioversion the patient has to be informed about the potential risks. Company product liability does not apply. At least, in view of a high reappearance rate of atrial fibrillation following cardioversion, indication for external cardioversion in pacemaker patients may be more restrictive than in other patients. Options such as pharmacological cardioversion or simple heart rate control may be considered. Additionally, internal electrical cardioversion using 1–10 J shocks may be considered as an alternative to external cardioversion.
References
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[3] Altamura G., Bianconi L., Lo Bianco F., et al. Transthoracic DC shock may represent a serious hazard in pacemaker dependent patients. Pacing Clin Electrophysiol 1995; 18: 194–198.[CrossRef][Medline]
[4] Das G. and Staffanson D.B. Selective dysfunction of ventricular electrode–endocardial junction following CD cardioversion in a patient with a dual chamber pacemaker. Pacing Clin Electrophysiol 1997; 20: 346–365.
[5] Guarnieri T., Datorre S.D., Bondke H., et al. Increased pacing threshold after an automatic defibrillator shock in dogs: effects of class I and class II antiarrhythmic drugs. Pacing Clin Electrophysiol 1988; 11: 1324–1330.[CrossRef][Medline]
[6] Giedwoyn J.O. Pacemaker failure following external defibrillation. Circulation 1971; 44: 293.
[7] Gould L., Patel S., Gmoes G.I., et al. Pacemaker failure following external defibrillation. Pacing Clin Electrophysiol 1981; 4: 575–577.[CrossRef][Medline]
[8] Lau F.Y.K., Bilitch M., Wintrob H.J. Protection of implanted pacemakers from excessive electrical energy of DC shock. Am J Cardiol 1969; 23: 244–249.[CrossRef][ISI][Medline]
[9] Dahl C.F., Ewy G.A., Warner E.D., Thomas E.D. Myocardial necrosis from direct current countershock: effect of paddle electrode size and time interval between discharges. Circulation 1974; 50: 956–960.
[10] Aylward P., Blood R., Tonkin A. Complications of defibrillation with permanent pacemaker in situ. Pacing Clin Electrophysiol 1979; 2: 462–464.[CrossRef][Medline]
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