Noncardiac surgery and pacemaker cardioverterdefibrillator management

CASE CONFERENCE F r e d e r i c k A. Hensley, Jr, M D Solomon Aronson, MD, FACC Section Editors

CASE 12-2-1998 Noncardiac Surgery and Pacemaker CardioverterDefibrillator Management Yatin Mehta, MD, DNB, FRCA, Madhav Swaminathan, MD, Rajiv Juneja, DA, MD, Anil Saxena, MD, DNB, and Naresh Trehan, MD Commentary by John L. Atlee, MD

DISCUSSION*

Case Presentation

A 58-year-old man presented for the surgical repair of a left inguinal hernia in July 1996. He gave a history of hypertension and non-insulin-dependent diabetes mellitus. He underwent coronary artery bypass surgery in 1983, after which he developed recurrent episodes of palpitation and cardiac decompensation, later diagnosed as ventricular tachycardia, which did not respond to lidocaine hydrochloride, mexiletine, or amiodarone. His left ventricular ejection fraction (LVEF) was 30%. A pacercardioverter-defibrillator (PCD) (Medtronic Active Jewel Can PCD model 7219C; Medtronic Inc, Anaheim, CA) was implanted in April 1995 at the authors' institute because of inducibility of arrhythmias despite amiodarone therapy. He was active at the time of presentation before surgery, and was in New York Heart Association (NYHA) class II functional status. His LVEF was 30% and he was receiving enalapril, digoxin, and amiodarone. Diazepam, 5 rag, was administered orally as premedication the night before and 2 hours before surgery. Monitoring included continuous two-lead electrocardiogram (ECG) (leads II and Vs), oxygen saturation by pulse oximetry, invasive arterial pressure, and central venous pressure using an 8F sheath in the right internaljugular vein. An external pulse generator and transvenous pacing leads were kept ready in the operating room (OR). External countershock paddles were checked and kept ready. An 18-G epidural catheter (Portex, Kent, UK) was inserted into the fourth lumbar interspace with the patient in the left lateral position. After a test dose with 2% plain lidocaine hydrochloride, 2 mL, 0.5% bupivacaine hydrochloride, 15 mL, was injected. A T10 sensory block was obtained. The patient was administered oxygen via nasal prongs at 4 L/min and diazepam, 5 mg, was given intravenously for sedation. An electrocautery grounding pad was placed beneath the right buttock. The PCD was disabled before the start of surgery using a noninvasive programming device (Medtronic Inc). After completion of the procedure, which lasted 1 hour, the PCD was enabled and the patient was transferred to the postoperative intensive care unit (ICU) for observation. Monitoring in the ICU included continuous ECG, arterial pressure, and pulse oximetry. Epidural buprenorphine, 0.3 rag, was administered for postoperative analgesia and the epidural catheter was removed 24 hours later. The patient was discharged from the hospital the following day. Journal of Cardiothoracic and Vascular Anesthesia,

The implantable cardioverter-defibrillator (ICD) has been shown to reduce mortality associated with malignant ventricular arrhythmias not responsive to medical therapy. 1 Since the first ICD was implanted in 1980,1 technical advances have also incorporated pacing functions in the device (pacer-cardioverterdefibrillator, PCD). The use of these devices has increased and more patients with an ICD/PCD will present for noncardiac surgical procedures. Incorporation of cardiac pacing (antitachycardia, as well as antibradycardia functions) in the same device has led to the development of the PCD. These devices are capable of monitoring cardiac rhythm for various arrhythmias, and delivering tiered therapy for ventricular arrhythmias (ie, cardiac pacing, low-energy cardioversion, and defibrillation). 2 There is little published experience to date regarding the anesthetic management of patients with a PCD device. The first PCD in India was implanted at the authors' institute in April 1995,3 and since then more patients have benefited from this device in other centers as well. To the authors' knowledge, this was the first reported case of a patient with a PCD presenting for noncardiac surgery in this country. Anesthesiologists today should be aware of the problems associated with these patients, especially in view of the growing number of PCDs being implanted. The PCD device is an implantable, multiprogrammable, automatic arrhythmia management system, designed to detect episodes of ventricular tachycardia and ventricular fibrillation. On detection of the arrhythmia, the device delivers programmed pacing, cardioversion, or defibrillation therapies. In addition, the device also has a backup antibradycardia pacing function.2 The device is contained in a hermetically sealed titanium shell

*Y. Mehta, M. Swaminathan,R. Juneja,A. Saxena, and N. Trehan From the Departments of Anesthesiology and Cardiology, Escorts Heart Institute and Research Centre, New Delhi, India. Address reprint requests to Yatin Mehta, MD, DNB, FRCA, Chief of Anesthesiology, Escorts Heart Institute and Research Centre, Okhla Rd, New Delhi - 110 025, India. Commentary by: John L. Atlee, MD, Professor of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI. Copyright © 1998 by W.B. Saunders Company 1053-0770/98/1202-002158.00/0 Key words: pacer cardioverter-defibrillato~ noncardiac surgery, cardioverter

Vo112,No 2 (April), 1998:pp 221-224

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(Active Can; Medtronic Inc, Anaheim, CA), which also acts as one pole of the defibrillator system. It is connected to a tripolar lead that has bipolar sensing and pacing at the tip and a defibrillation coil in the right ventricular portion, proximal to the tip. The charge is delivered between the active can and the defibrillation coil. A monophasic or biphasic current waveform can be chosen, and the current pathway can be set from device shell to the right ventricular coil and vice versa. Energies of 0.4 to 34 joules can be delivered. Most patients with a PCD have underlying ischemic or idiopathic dilated cardiomyopathy with poor left ventricular function. Because most have regular follow-ups, their current cardiac status should be well documented. Intraoperative monitoring must include continuous two-lead ECG monitoring because these patients may be at risk for perioperative myocardial ischemia and arrhythmias. A central line was believed to be clinically indicated in the patient presented to allow access for the possible infusion of vasoactive drugs or insertion of a transvenous pacing lead for bradycardia. However, central venous lines should be avoided with recently placed (<1 month) transvenous PCD leads to avoid dislodgment of the endocardial wires. ? A similar precaution is taken with recently implanted transvenous pacemaker leads. The guide wire used for insertion of the central venous catheter by the Seldinger technique is potentially arrhythmogenic. For these reasons, an external defibrillator must be checked, functional, and available at all times, especially after the PCD has been temporarily disabled. The requirement for an invasive arterial pressure monitor must be weighed against the underlying cardiac condition and the type and expected duration of surgery. In the absence of an arterial catheter, the plethysmographic signal of an oximeter probe provides much needed information regarding pulsatile flow should arrhythmias occur.4 The PCD device must be disabled before the start of surgery. This is essential because the electrocautery should not be used in the presence of an active PCD. 2 The use of electrocautery (within 15 cm) or direct defibrillation may result in permanent damage to the unit. The presence of a pulse generator and transvenous pacing leads must, therefore, be ensured in the OR. The tachyarrhythmia detection feature must also be switched off during electrocautery to avoid triggering automatic therapy. 2 Gaba et 3,14 report a serious complication arising from the interaction between active PCD and electrocantery. The current generated by the cautery triggered a countershock, which precipitated ventricular tachycardia. The possibility of the device giving a countershock has prompted Lee 5 to advise OR personnel to wear gloves for protection against shocks. Placement of the electrocantery grounding pad should be as far away from the field of surgery as possible. Specifically, the manufacturer recommends placement at least 15 cm (6 in) from the PCD. In the present situation, the grounding pad was placed beneath the right buttock to keep the current flow away from the PCD device. Electrocautery should be used sparingly, if at all, and when used, short bursts with low energy are recommended. If life-threatening arrhythmias necessitating external countershock occur, the PCD may be damaged or the initial countershock may fail because the current may be routed through the unit.4 The reason for this is that PCD epicardial patch electrodes

CASE 12-2--1998

"insulate" a portion of the heart tissue and therefore reduce the effectiveness of a transthoracic defibrillation. 2 Because placing the external paddles in the standard position may damage the device permanently or result in inadequate energy for defibrillation, it has been recommended that the paddles be placed at a right angle to a line joining the implanted patch electrodes to minimize this problem. 6 Interchanging paddle positions on the chest has also been reported to help. 7 The PCD will have to be interrogated postcountershocks to determine functional integrity of circuits and programmed parameters before enabling the device. The patient with a disabled PCD depends only on optimal drug therapy for control of perioperative arrhythmias. Therefore, all the necessary antiarrhythmic drugs, such as lidocaine hydrochloride, amiodarone, beta-blockers, etc, must be kept ready in the OR. The choice of anesthetic agents should be governed by the level of cardiac dysfunction (ie, reduced ejection fraction). In this case, the authors used epidural anesthesia as the technique of choice. Besides facilitating the surgery and postoperative analgesia, it has been shown to have beneficial effects on preload and transmyocardial blood flow distribution. 8 Epidural anesthesia was preferred because it would avoid potential arrhythmogenic effects of laryngoscopy, tracheal intubation, and volatile anesthetic agents. It must also be made certain that epinephrine-free lidocaine is used as the epidural test dose. Although theoretically lidocaine may be preferable to bupivacaine in view of its more beneficial cardiac electrophysiologic effects, 9 plasma levels at which bupivacaine is cardiotoxic are unlikely to be achieved with a single epidural injection.1° Moreover, conditions such as hypercarbia and acidosis conducive to bupivacaine cardiotoxicity are also improbable during a short surgical procedure. The authors used bupivacaine to achieve prolonged analgesia extending into the postoperative period. To conclude, the challenges faced by the anesthesiologist in the OR are the choice of anesthetic technique to be used, adverse interactions between an enabled PCD and electromagnetic interference (ie, electrocautery), arrhythmogenic potential of drugs, and anesthetic techniques and concerns with external countershock, if required, and avoidance of unwanted internal countershocks. For these reasons, it is preferable that these patients are managed at centers equipped to deal with the problems outlined above. An understanding of the basic working principles of these devices and the special problems associated with them will make anesthesia safer for this high-risk group. COMMENTARYI

Today more than 500,000 patients in the United States have implanted pacemakers or ICD or PCD devices, u,/2 More than 40,000 persons at risk for sudden death from malignant tachyarrhythmias have ICDs or PCDs (US). ICDs deliver R/S wave-synchronized direct current (cardioversion, DC) or nonsynchronized (defibrillation, DF) shocks to terminate tachyarrhythmias. PCD can provide one to several ("tiered") antitachy-

tJ. Atlee

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cardia pacing algorithms (eg, extra stimulation, burst pacing, ramp pacing, and overdrive pacing), determined by the results of cardiac electrophysiologic testing before delivering DC shocks for ventricular (or supraventricular) tachycardia. PCDs can also provide backup single-chamber pacing (usually ventricular ventricular inhibited) for bradycardia after tachycardia termination. Devices featuring dual-chamber and rate-adaptive pacing are in clinical trials. Other recent refinements in ICDPCD technology include: (1) miniaturization, devices can be implanted subpectorally, the same as pacemaker devices; (2) transvenous leads, today used almost exclusively in place of epicardial patch leads; and (3) event recording, stores ECG data around the electrophysiologic event that triggered ICD-PCD therapy. ICD-PCDs are interrogated or programmed with a programmer (not compatible with devices of other manufacturers, or necessarily older devices of the same manufacturer); some devices may already or soon will be capable of being interrogated or programmed transtelephonically. Obviously, ICD-PCDs are highly sophisticated and constantly (explosively) evolving technologic devices. They are implanted in patients with severe, irreversible structural heart disease (usually ischemic, dilated, or hypertrophic cardiomyopathy) that provides the electrophysiologic substrate for potentially lethal tachyarrhythmias. In addition, ICD-PCD patients usually have severe functional myocardial compromise (ejection fraction < 35%), and significant associated major organ system disease. An additional problem is the real possibility that a device will not function as intended in the highly contaminated (by electromagnetic interference, EMI) perioperative environment. EMI "noise" can have several undesirable effects: (1) Inappropriate therapy, EMI may be detected as an arrhythmia, leading to delivery of unnecessary therapy, and stimulation of dangerous tachyarrhythmias;4 (2) altered programmed parameters, EMI may be misinterpreted as radiofrequency programming information, altering detection and treatment parameters or algorithms; and (3) damage to circuitry, leads, electrodes, sufficient EMI in the vicinity of the pulse generator, circuitry, leads, or electrodes could render the device system inoperable or cause permanent myocardial damage. Because of the potential for harm, all US manufacturers of ICD-PCDs (Table 1) recommend that devices be disabled (ie, antitachycardia and other functions be suspended if patients are to be exposed to perioperative EMI (Table 2). (Strictly speaking, the device is not inactivated because it can still be enabled Table 1. Address and Tel/Fax Numbers for Current US Manufacturers of ICD-PCD

Company

Address

Contact

Guidant Corporation Cardiac Pacemakers (CPI) Medtronic, Inc

4100 Hamline Ave N, St Paul, MN 55112-5798 7000 Central Ave NE, Minneapolis, MN 55432-3576

Tel. 1-612-638-4000 (24-hour consultation service) Tel. 1-612-574-4000; 1-800-328-2518 (24-hour consultation service) Fax. 1-612-574-4879 Tel. 1-800-733-3455 Fax. 1-408-735-8750

Ventritex, Inc

709 E Evelyn Ave, Sunnyvale, CA 94086-6527

Table 2. Common Sources for Perioperative EMI

Nuclear magnetic resonance imaging equipment Surgical electrocautery, diathermy Extracorporeal shockwave lithotripsy External cardioverter-defibrillator equipment High-voltage electrical systems Radio transmitters Radiation therapy (not diagnostic x-rays)

through an external programming device.) At most US medical centers, disabling or enabling of ICD-PCDs is performed by a pacemaker-ICD-PCD clinic or technician (24-hour emergency availability). Positioning a strong magnet over the pulse generator will temporarily suspend the automatic detection and therapy capabilities of the ICD-PCD device, although the individual manufacturers should be consulted as to the specifics (ie, not just any magnet will work with all devices; tones may or may not be emitted, etc). Other recommendations for perioperative management have been outlined in the accompanying case conference by Mehta et aP 3 and elsewhere. 14 Unfortunately, this is not an ideal world, as the author found out recently when asked a question regarding perioperative ICD-PCD management at a conference in Hvar, Croatia. Apparently, on more than one occasion, an American or Continental tourist with an ICD-PCD device has come to the Adriatic Coast and required emergency anesthesia and surgery. It is not difficult to imagine a similar scenario in rural North America. Maybe it will not be possible to temporarily disable the device, or to reach the manufacturer for instructions. Possibly, the clinician will not even be able to identify the device (even with radiograph, because the codes are indecipherable). And the patient may not have the necessary identification (Medic-Alert tag, cards, etc) on his or her person. So what to do? The applicable precautions listed by Mehta et a113 should be adhered to. For example: (1) "15 cm rule," Bovie grounding plate; (2) external defibrillator pad orientation, this should not be a problem with transvenous leads (the patient will not have a thoracotomy/sternal scar), but do not place paddle/ patch electrode over the ICD-PCD pulse generator; and (3) monitor pulse waveform and ECG, this will allow the detection of malfunction (inappropriate therapy, failure to deliver therapy, etc). Certainly, there are many things that can be done to minimize the risk of ICD-PCD malfunction if a device cannot be temporarily disabled for one reason or another (eg, use ligatures v cautery, bipolar cautery, etc), and these should be discussed with the surgeon. A less desirable solution that may have to be considered to avoid potentially lethal consequences is lead disruption and temporary explantation of the pulse generator because it is more practical and far less expensive to replace or revise the leads than to replace a permanently damaged pulse generator. REFERENCES

1. Mirowski M, Reid PR, Mower MM, et al: Termination of malignant ventricular arrhythmias with an implanted automatic defibrillator in human beings. New Engl J Med 303:322-324, 1980 2. Mehta Y, Dhole S, Kler TS: PCD implantation and its implications for the anaesthesiologist. Indian Heart J 48:68-70, 1996 3. Technical Manual: Medtronic Jewel PCD 7219. Anaheim, CA, Medtronic Inc, 1995

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4. Gaba DM, Wyner J, Fish KJ: Anesthesia and the automatic implantable cardioverter/defibrillator. Anesthesiology 62:786-792, 1985 5. Lee EM: More on automatic cardioverter-defibrillators. Anaesthesia 303:322-324, 1980 6. Zaidan JR: Cardiac pacemakers, in American Society of Anesthesiologists Annual Refresher Course Lectures, Las Vegas, NV, 1990, pp 232-238 7. Mirowski M, Reid PR, Watkins L, et al: Clinical treatment of life-threatening arrhythmias with the automatic implantable defibrillator. Am Heart J 102:265-270, 1981 8. Blomberg S, Emanuellson H, Kvist H: Effects of epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease. Anesthesiology 73:840-847, 1990

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9. Moller RA, Covino BG: Cardiac electrophysiologic effects of lidocaine and bupivacaine. Anesth Analg 67:107-114, 1988 10. Reiz S, Nath S: Cardiotoxicity of local anesthetic agents. Br J Anaesth 58:736-746, 1986 11. Barold SS, Zipes DP: Cardiac pacemakers and antiarrhythrnic devices, in Braunwald E (ed): Heart Disease (ed 5). Philadelphia, PA, Saunders, 1997, pp 705-741 12. Kusumopto FM, Goldschlager N: Medical progress: Cardiac pacing. N Engl J Med 334:89, 1996 13. Mehta Y, Swaminathan M, Juneja R, et al: Case conference. J Cardiothorac Vasc Anesth 12:221-224, 1998 14. Atlee JL: Cardiac pacing and electroversion, in Kaplan JA (ed): Cardiac Anesthesia (ed 4). Philadelphia, PA, Saunders, 1998