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Pacemaker-driven tachycardia induced by electrocardiograph monitoring in the recovery room.


Monitoring devices are known to induce tachycardia in minute-ventilation rate-responsive pacemakers. This is because some monitoring devices measure the same parameter as do the pacemakers (change in thoracic impedance). Hence, the biological signal to the pacemaker is increased and is misconstrued as increased minute ventilation causing tachycardia which resolves when the monitoring device is removed. Whilst this could occur for all minute-volume rate responsive pacemakers, most reported interactions have been with the Telectronics META series. We present a case of an interaction between a Telectronics Tempo DR pacemaker (St. Jude Medical) and an Agilent Patient Care System (Philips). Failure to recognise the true nature and cause of such tachycardias may lead to mismanagement of the patient, including the inappropriate use of cardio-active medications.

Key Words: pacemakers, rate-responsive, arrhythmia, tachycardia, monitoring, minute ventilation


The interaction between minute-ventilation rate-responsive pacemakers (MV-RRP) and monitoring devices in common usage in the operating theatre, intensive care and recovery areas has been described previously (1-3). These pacemakers set a rate in accordance to exercise demand, using measurements of minute ventilation to evaluate this demand. They sense minute ventilation by emitting a pulsed current and detecting the changes in thoracic impedance during the respiratory cycle. However, it has been established that the current from other monitoring devices that also measure thoracic impedance (such as those monitors that display respiratory frequency) can summate with the pulsed current from MV-RRP. This increased impedance signal is perceived by the pacemaker as increased minute ventilation, which causes the ensuing tachycardia at the pre-programmed rate (3). This phenomenon has previously been reported with Telectronics META series pacemakers'. We report a case involving a Telectronics Tempo pacemaker (St. Jude Medical, St, Paul, MN, U.S.A.)and an Agilent Patient Care System: Viridia 24CT (previously Hewlett Packard, now owned by Philips Medical, Amsterdam, The Netherlands), and discuss the implications of such an interaction.


The patient was a 74 year-old woman who presented for right knee arthroscopy after swelling, pain and decreased range of movement in that knee. She had a history of known osteoarthritis, hypertension, hypercholesterolaemia, congestive cardiac failure, significant gastro-oesophageal reflux disease and a complex cardiac arrhythmia.

She had been treated for paroxysmal atrial fibrillation but developed facial flushing and sinus bradycardia when given amiodarone, requiring the implantation of a dual chamber pacemaker (Telectronics Tempo DR) in November 2001. This was followed by an attempt at atrioventricular (AV) junction ablation, performed in February 2002. For technical reasons this did not result in complete severance, but did result in first-degree atrioventricular block, which was considered sufficient. Her underlying rhythm remained that of bradycardia with first-degree atrioventricular block. However, she had ongoing episodes of palpitations which were attributed to paroxysmal atrial tachycardia/atrial fibrillation with atrioventricular conduction, rather than pacemaker-mediated tachycardia. Unfortunately, she did not tolerate sotalol to control her atrial rate. Repeat atrioventricular ablation was not deemed necessary.

Regular pacemaker checks were satisfactory, with a pacemaker interrogation three months before the procedure. Her pre-operative pacemaker setting was dual chamber sensed, dual chamber paced, dual inhibited and triggered, rate-response mode (DDDR). She was assessed in the anaesthesia preadmission clinic. No changes were recommended to the settings due to the peripheral nature of the procedure. The preoperative electrocardiogram (ECG) showed a paced rhythm of 75 beats per minute. Her medications were carvedilo1 25 mg twice daily, pravastatin 10 mg nocte, rabeprazole 20 mg daily, aspirin 100 mg daily, perindopril 4 mg daily and frusemide 40 mg mane.

The patient underwent an uneventful procedure under general anaesthesia with midazolam, fentanyl, propofol, suxamethonium and sevoflurane. Other medications given were dexamethasone and ketorolac.

In recovery, she was monitored with an Agilent Viridia 24CT monitor. She was noted to be tachycardic, but her blood pressure was not compromised. Intravenous morphine administered by the recovery room staff prior to patient review had no impact on the tachycardia. A 12-lead ECG was taken which showed similar broad-complex QRS-wave morphology compared to her preoperative ECG, but a higher rate of 120 beats per minute (Figure 1). Of note, pacing spikes were not apparent on 12-lead ECG, but were visible on the monitoring device. The provisional diagnosis of a pacemaker-induced tachycardia was soon made. As the mechanism of this occurrence was unclear, advice was sought from the pacemaker technicians at our institution. They suggested removal of the monitoring lead. This led to return to a paced rhythm of 60 beats per minute over a minute (Figure 2). There were no negative sequelae from the transient iatrogenic tachycardia.




Minute ventilation rate-responsive pacemakers (MV-PPM) use physiological monitoring to control the pacemaker output, matching heart rate to increased workload, and have the advantage of not requiring any special implantation techniques (4). They have been documented to improve well-being and exercise tolerance (1). Disturbingly however, such pacemakers can interact with certain cardiac monitoring and other equipment and this has been noted by the FDA in a warning to health professionals (5). The prevalence of the issue can be indicated by the various MV RRPs marketed and listed by the FDA in their warning: Telectronic's (St Jude Medical) META and Tempo series, Medtronic's Legend Plus and Kappa 400 series and ELA Medical's Chorus RM and Opus RM series. To date, only the Telectronic's META series has been documented to cause tachycardia secondary to monitoring equipment (1). To the authors' knowledge, this is the first report of a Telectronic's Tempo device causing this problem.

The rate-responsive mode of these pacemakers measures thoracic impedance to gauge minute ventilation, matching heart rate to this value. It does this by injecting low-amplitude pulsed currents and detecting voltage produced by this pulse. This system is susceptible to interference from externally introduced currents (3). Unfortunately, many medical devices, including the patient monitoring systems used in our recovery, also measure bioelectric impedance by injecting a small current. If these devices are used concurrently with an active MV RRP, the signals may be reinforced and incorrectly interpreted by the pacemaker as elevated minute ventilation, with the subsequent response of a higher paced rate. The potential of such an interaction can be appreciated by the list of devices using impedance measurement technology: respiratory monitoring equipment (including apnoea monitors), cardiac monitoring equipment (lead-off function), echocardiograph equipment, and external defibrillators (5,6). Management includes supportive measures for maintaining oxygenation and blood pressure stability and removal of the cause.

Our experience has highlighted other issues. The complexity of the arrhythmia history and management in our case demonstrates the difficult task of preoperative assessment, given the advances made in many areas of medicine. Our pacemaker technician and cardiology colleagues were invaluable sources of information before and after the case. Although not an issue for us, the availability of such backup at all hours must be seen as a priority. Furthermore, cardiac pacemaking is made even more complex by the possibility of manufacturers being no longer in existence despite their product being in use. There may be newer devices in the future and an increase in the number of indications for implantation (7). This complexity necessitates our close association with cardiologists and pacemaker technicians. Nevertheless, our reliance on our colleagues may come at the cost of the opportunity for anaesthetists to pursue the breadth of knowledge required for the complete care of these patients, by education and even crossspecialty training (7). Furthermore, medical colleagues can be unaware of pacemaker issues specific to theatre or recovery room environments'. The need for pacemaker manufacturers to be in dialogue with clinicians in 'real-life' setting and their ethical obligation to inform of relevant concerns are also highlighted by our case.

The American College of Cardiology and the American Heart Association have issued guidelines about the perioperative management of implantable pacemakers (8). Before the procedure, the underlying rhythm should be determined and its battery status and programmed settings evaluated, in particular deciding the appropriate upper sensor rate that would avoid haemodynamic disturbances. Consideration should be given to reprogramming the pacemaker prior to the procedure. After the procedure, the pacemaker should be checked again to detect changes from electromagnetic interference or changes in a patient's physiological status (6). A heart rate response of 120 bpm in our patient did not produce haemodynamic instability; rigorous testing three months earlier certainly helped to ensure this. Disabling the rate-responsive mode in this case may have provided a greater margin of safety and this has been suggested as the appropriate preoperative manoeuvre for all rate-responsive pacemakers (9).

This case also demonstrates the commonly observed phenomenon of pacemaker spikes from bipolar leads not always being visible on an ECG rhythm strip. This was recognised early on and hence did not result in needless delay in the diagnosis of pacemaker-induced tachycardia.

Finally, although there were no negative sequelae in our case, the potential for harm must be appreciated. Tachycardia in theatre could have been interpreted as inadequate anaesthetic depth. The broad-complex tachycardia (especially when pacing spikes are filtered out by the monitor) could have been managed as for a malignant arrhythmia, with potentially toxic anti-arrhyhmcs being inappropriately given or cardioversion attempted. Myocardial ischaemia, myocardial infarction and systemic hypotension are further potential complications that highlight the relevance of correct diagnosis and treatment (3).

Accepted for publication on December 12, 2005.


(1). Southorn PA, Kamath GS, Vasdev GM, Hayes DL. Monitoring equipment induced tachycardia in patients with minute ventilation rate-responsive pacemakers. Br J Anaesth 2000; 84:508-509.

(2). Wallden J, Gupta A, Carlsen HO. Supraventricular tachycardia induced by Datex patient monitoring system. Anesth Analg 1998; 86:1339.

(3). Chew EW, Troughear RH, Kuchar DL, Thorburn CW Inappropriate rate change in minute ventilation rate responsive pacemakers due to interference by cardiac monitors. Pacing Clin Electrophysio11997; 20:276-282.

(4). Mond H, Strathmore N, Kertes P, Hunt D, Baker G. Rate responsive pacing using a minute ventilation sensor. Pacing Clin Electrophysio11988; 11:1866-1874.

(5). (accessed July 7, 2005).

(6). Rozner MA, Nishman RJ. Pacemaker-driven tachycardia revisited. Anesth Analg 1999; 88:965.

(7). Rozner MA. Pacemaker misinformation in the perioperative period: programming around the problem. Anesth Analg 2004; 99:1582-1584.

(8). Eagle KA, Berger PB, Calkins H et al. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery. An esth Analg 2002; 94:1052-1064.

(9). Levine PA. Rate-adaptive cardiac pacing: implications of environmental noise during craniotomy. Anesthesiology 1997; 87:1261.

R. HU *, D. A. COWIE ([dagger]) Department of Anaesthesia, Austin Health, Heidelberg Victoria, Australia

* M.B., B.S., Anaesthesia HMO, Department of Anaesthesia, Austin Health, Heidelberg Victoria, Australia.

([dagger]) M.B., B.S., F.N.Z.C.A., Staff Anaesthetist, Department of Anaesthesia, Austin Health, Heidelberg, Victoria.

Address for reprints: Dr Dean A. Cowie, Department of Anaesthesia, Austin Health, Studley Rd, Heidelberg, Vic. 3084, Australia.
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Title Annotation:Case Report
Author:Hu, R.; Cowie, D.A.
Publication:Anaesthesia and Intensive Care
Date:Apr 1, 2006
Previous Article:Anaesthesia and medical student education.
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