Manual of Cardiovascular Medicine

I.INTRODUCTION

A.The modern implantable cardioverter–defibrillator (ICD) is a multifunctional, multiprogrammable electronic device designed to abort life-threatening arrhythmias. It is programmed to automatically detect and manage episodes of ventricular tachycardia (VT), ventricular fibrillation (VF), or bradycardia. Current ICDs are able to deliver multitiered therapies, which may include a combination of antitachycardia pacing (ATP), cardioversion, and defibrillation. The devices also offer bradycardic support, which may include rate-responsive single- or dual-chamber pacing and automatic mode switch function. Modern ICDs are able to deliver resynchronization therapy, a significant advancement in the management of heart failure. The devices are also able to store electrograms (EGMs), which can be easily retrieved. This function can be of immense use for follow-up management of the patient and programming of the device.

Multiple clinical trials have demonstrated the efficacy of ICDs to accurately detect and manage sudden cardiac death (SCD). ICDs are superior to conventional medical therapy in both primary and secondary prophylaxis of SCD. The majority of patients who have indications for an ICD implant are those with left ventricular (LV) dysfunction, both ischemic and nonischemic.

B.Mirowski first introduced the concept of an ICD in the 1960s, with the first human implant reported in 1980. Early ICD implantations required a thoracotomy for placement of an epicardial lead system. Subsequent advancements in device and lead technology over the last 35 years have significantly reduced the size of the pulse generator, while improving programmability and diagnostic data stored within the device. An improved understanding of VF, defibrillation, and cardiac pacing has resulted in the development of biphasic shock waveforms and transvenous pace/defibrillation lead systems that preclude the need for epicardial patches. As a result, modern ICDs are increasingly more compact, provide expansive programming capability, and offer convenience with added features such as remote interrogation.

C.To avoid complications associated with vascular access in patients who have an indication for ICD therapy but who do not require pacing, a new generation of ICD systems can be placed without transvenous access. The subcutaneous ICD (S-ICD) was developed over the last decade and allows for defibrillation therapy without venous access. The pulse generator is implanted under the skin on the lateral chest wall and connected to a defibrillation lead that is tunneled along the left lateral margin of the breastbone. In 2012, the United States Food and Drug Administration (FDA) approved the use of S-ICDs after several initial studies demonstrated comparable efficacy in cardioversion of induced and spontaneous VT and VF when compared to conventional transvenous systems. These initial studies also showed that inappropriate shocks occurred in a similar percentage of patients compared to conventional ICDs. The long-term efficacy of S-ICDs is currently being investigated in a randomized trial and prospective registries.

II.ICD COMPONENTS

A.The current-day ICD is a sophisticated and intelligent computer. It consists of a generator and leads. The ICD generator consists of a battery, capacitors, DC–DC converter using an oscillator rectifier mechanism, a microprocessor, and telemetry communication coils and their connections. The generator serves as an active electrode within the shocking configuration in most of the modern ICDs and is thus called the “hot can.” The newest generation of ICDs utilize a lithium manganese dioxide battery. These can generate approximately 3.2 V at full charge. Because most ICDs use two batteries connected in series, the full initial voltage is approximately 6.4 V. The generator has capacitors that can charge within 7 to 30 seconds to store up to 30 to 40 J of energy. This can be delivered to the heart within a 10- to 20-ms interval when therapy is required.

B.The three essential functions of the ICD—tachycardia detection, tachycardia therapy, and bradycardia pacing—are delivered through the active electrodes, which are the noninsulated segments of the leads. Most of the current-day leads have sensing and pacing electrodes at the tip and distal (right ventricle) and proximal (superior vena cava [SVC]) shocking coils. The function of ventricular sensing and pacing is achieved by a technology similar to that in pacemakers. This is done through two “dedicated bipolar” electrodes at the distal end of the right ventricular (RV) lead (tip/ring). Sometimes, it may be achieved by “integrated bipolar” electrodes, wherein the bipole is formed by the tip of the ventricular lead and the distal shocking coil (tip/coil). Ventricular pacing in biventricular ICDs is from the tip of the RV and LV leads, respectively, to either the ring (true bipolar) or the distal shocking coil (integrated bipolar). To avoid the problem of “double counting,” most newer devices restrict the ventricular sensing function to the RV lead alone.

C.For the delivery of shock therapy, most systems now incorporate either the RV coil, SVC coil, and pulse generator can or the RV coil and can without an SVC coil.

III.INDICATIONS AND CONTRAINDICATIONS

A.ACCF/AHA/HRS 2012 focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. These are the most current guidelines for the implantation of ICDs. The guidelines stratify the various indications as class I, class II (a and b), and class III on the basis of the data from clinical trials and opinion of a panel of experts.

B.Class I indications. These are conditions for which there is evidence and/or general agreement that ICD therapy is beneficial, useful, and effective.

1.Survivors of SCD secondary to VF or hemodynamically unstable VT after evaluation to define the cause of the arrhythmia and to exclude completely reversible causes

2.Syncope of unknown etiology with inducible VF or hemodynamically significant VT during electrophysiology study

3.Structural heart disease and spontaneous hemodynamically unstable or stable VT

4.Ischemic cardiomyopathy, New York Heart Association (NYHA) class I, and a left ventricular ejection fraction (LVEF) ≤30% who are at least 40 days post–myocardial infarction (MI)

5.Ischemic cardiomyopathy, NYHA class II or III with an LVEF ≤35% who are at least 40 days post-MI

6.Ischemic cardiomyopathy, ejection fraction (EF) ≤ 40%, nonsustained VT, and inducible VF or sustained VT at electrophysiology study

7.Nonischemic dilated cardiomyopathy, NYHA class II or III, and LVEF ≤ 35%

C.Class IIa indications. These are conditions for which there is evidence and/or general agreement that ICD therapy can be beneficial, useful, and effective.

1.Unexplained syncope with significant LV dysfunction and nonischemic cardiomyopathy

2.Normal or nearly normal LVEF with sustained VT

3.Patients with hypertrophic cardiomyopathy and at least one risk factor for SCD

4.Patients with arrhythmogenic RV dysplasia with at least one risk factor for SCD

5.Patients with long QT with syncope or VT while taking β-blockers

6.Patients waiting heart transplantation (nonhospitalized)

7.Patients with Brugada with a history of syncope or VT but no episodes of cardiac arrest

8.Patients with catecholaminergic polymorphic VT with syncope or sustained VT while taking β-blockers

9.Patients with cardiac sarcoid, giant cell myocarditis, or Chagas disease

D.Class IIb. These are conditions for which the usefulness/efficacy of ICD therapy is uncertain or not well established.

1.Nonischemic cardiomyopathy with an EF ≤35% and NYHA class I

2.Long QT and risk factors for SCD

3.LV noncompaction

4.Patients with familial cardiomyopathy and a predisposition to SCD

5.Patients with structural heart disease and syncope but with no identifiable etiology

E.Class III indications/contraindications. These are conditions for which there is general agreement that ICDs are not useful and possibly harmful. These include patients with a structurally normal heart and syncope without any inducible ventricular arrhythmias. ICDs should also be avoided in patients with VT and a treatable or ablatable cause (Wolff–Parkinson–White syndrome, outflow tract VTs, fascicular VTs, etc.) or a reversible cause (acute MI, myocardial ischemia, electrolyte imbalance, drug toxicity, or trauma). It is also important to avoid using ICDs in patients with severe psychiatric illnesses or in patients with terminal illnesses, where the expected life span is less than 12 months. ICDs could do more harm than good in patients with incessant ventricular arrhythmias, where it is important to control the arrhythmia before ICD implantation to avoid recurrent painful shocks. ICDs are also contraindicated in patients with NYHA class IV heart failure who are drug refractory and are not candidates for heart transplantation or cardiac resynchronization therapy (CRT).

IV.IMPLANTATION

A.Device implantation. Currently, available devices are small enough to allow implantation in the left pectoral region. Animal studies have shown that the defibrillation efficacy of the hot-can ICDs is superior in the left pectoral or axillary regions followed by the right pectoral and then the abdominal sites. A right pectoral system may be necessary in patients who have vascular access problems on the left side or who have undergone pectoral surgery (e.g., mastectomy). For patients with high defibrillation thresholds (DFTs), additional lead placement, such as a subcutaneous array or coil, an azygous coil, a coronary sinus coil, or an epicardial patch, may be necessary. Epicardial patch placement is usually reserved for patients who have failed to meet implantation criteria with a transvenous lead system or if there has been previous bilateral pectoral or tricuspid valve replacement surgery.

For pectoral implants, a single 2″ to 3″ incision is made transversely below the clavicle, about 1 cm below and parallel to the deltopectoral groove. Transvenous lead placement is achieved through a subclavian vein puncture or by cephalic vein cutdown. An “extrathoracic” subclavian vein puncture or cephalic vein cutdown for access minimizes the risk of pneumothorax and also the risk of lead failure caused by subclavian crush injury.

B.Lead placement. The lead is advanced to the RV apex under fluoroscopic guidance, where the tip is secured via an active fixation screw or embedded in the trabeculae with passive fixation tines. It is important to assess the quality of signals at the time of implant, because it is the best guide to the adequacy of long-term sensing of the lead. The DFT is optimized with the lead placed at the RV apex; therefore, this position is often preferred even if there is compromise of the sensing thresholds. If there is already a pacemaker lead in the RV apex, then septal placement of the lead tip is chosen so that the lead tips are at maximal distance from each other to avoid device–device interactions. On occasion, placing an additional pacing–sensing lead in the right ventricle may be necessary when the defibrillation efficacy and pace–sense function of the leads are optimized at different locations.

C.Threshold studies. The lead is tested for pace–sense thresholds using an external high-voltage system analyzer or pacing system analyzer. In general, an acute pacing threshold of 2 V or less, R-wave amplitude of 5 mV or more, and lead impedance within the accepted range of the manufacturer (typically 300 to 1,200 Ω) are necessary to meet the implant criteria. The lead is secured within the pocket with a suture sleeve tie-down. If the device uses an atrial and/or an LV lead, then these are implanted at this time. The leads are attached to the pulse generator, and the system is placed in either a submuscular or a subcutaneous pocket. The pulse generator should be placed with excess lead coiled posteriorly to reduce the risk of damaging the leads at the time of generator change and to maximize the ability to communicate with an external programming wand. The device is then interrogated to ensure appropriate communication. Pace–sense thresholds are again tested by telemetry to demonstrate consistency.

D.Defibrillation testing is best assessed by evaluating the DFT, which is defined as the lowest delivered shock strength required for successful defibrillation. A synchronized sinus test shock may be performed by delivery of a low-energy (<2 J) synchronized shock on the QRS complex. This low-energy test allows the assessment of sensing as well as shock impedance (typically 35 to 90 Ω). For the purpose of defibrillation testing, VF is typically induced with a shock on T wave. Alternatively, or if shock on the T wave is unsuccessful, ultrafast burst pacing (30-ms intervals) or application of an alternating current may be used. Appropriate ICD detection and effective therapy are verified. In our lab, we typically start with a 10 to 15 J therapy, with subsequent therapies escalating in steps of 5 to 15 J. Usually, a maximum of three device-based therapies are attempted before rescue with external defibrillation at maximum energy. Two successful therapies that are at least 10 J less than the maximal output of the device are generally required. In general, this approach identifies the level of energy required to achieve a 50% to 75% success rate of defibrillation. Defibrillation therapy is then programmed at a level at least 10 J over the DFT. Rarely, a patient may require the addition of a shocking coil in the SVC, azygous vein, or subcutaneous coil to achieve an adequate safety margin.

Recent studies have revealed a trend toward ICD implantation without DFT testing. Although the risk of failing defibrillation is very low, patients receiving ICDs in the current era may have more severe heart failure, comorbidities, and a higher risk of failing defibrillation. In the absence of prospective randomized trials, DFT testing is currently recommended for most patients undergoing initial ICD implantation. Reasons to avoid DFT testing include left atrial or ventricular thrombus, atrial fibrillation without therapeutic anticoagulation, hemodynamic instability, severe aortic stenosis, severe unrevascularized multivessel or left main coronary artery disease, active ischemia, recent stroke, or significant respiratory comorbidity that would inhibit the use of adequate sedation.

E.Risks and complications. The risks involved with implantation are similar to those of pacemaker insertion. Operative risks include bleeding, pneumothorax, hemothorax, infection, myocardial damage, vascular/cardiac perforation, tamponade, thromboemboli, deep venous thrombosis, acceleration of arrhythmias, air embolism, and death. A rare but dangerous complication is the occurrence of electromechanical dissociation or refractory VF during DFT testing. Because of the nature of the procedure, a separate standby external pacemaker–defibrillator should be immediately available for rescue therapy should the implanted device fail to appropriately treat an arrhythmia. The overall mortality rate is much less than 1%. Late complications include chronic nerve damage, erosion, extrusion, fluid accumulation, infection, formation of hematomas/cysts, keloids, lead migration, lead dislodgment, and venous occlusion.

V.DEVICE REPLACEMENT

A.Battery status is determined by the measured voltage, and this is retrieved with device interrogation. Generator replacement is generally recommended when the device reaches a battery voltage of around 2.6 V, termed elective replacement indicator. In such situations, the generator should be replaced within a few months. With continued depletion of the battery voltage, the generator reaches end of life, a situation that indicates a more urgent need for generator replacement as the battery voltage drops below 2.2 V. This may lead to longer charge times and incomplete or inappropriate function of the device.

B.Pulse generator replacement represents a vulnerable period for the ICD/lead system. A four fold increased risk of infection has been reported with ICD pulse generator replacement. In the past, manufacturers have had multiple-lead models of variable pin lengths and diameters. Beginning in 1991, they adopted the 3.2-mm international pace–sense standard (IS-1) and the 3.2-mm defibrillation standard (DF-1). Prior to an attempted device replacement, assessment of the lead model should be done to verify that the appropriate replacement header or adapters are available at the time of surgery.

C.Leads may be inadvertently damaged during exploration of the pocket or during the exchange of pulse generators. Intraoperative assessment of lead function is imperative prior to introducing the replacement generator to the operative field. Replacement of a pace–sense or defibrillation lead may be necessary and requires the use of a different device header.

VI.TACHYCARDIA DETECTION AND THERAPY

A.EGM and tachycardia sensing. The ICD senses the intracardiac EGM signal via the implanted ventricular sensing electrodes. Recognition of a ventricular arrhythmia depends mainly on the analysis of the R-R intervals (heart rate is determined similarly). Accuracy of the EGM depends on the health of the adjacent myocardium and appropriate contact. Accuracy also depends on far-field signals from the muscles, atrium, or other sources of electromagnetic interference. The sensed signals are passed through a band-pass filter that consists of high- and low-frequency cutoffs to represent true signal events. The accuracy of signals in newer devices has been further improved by analysis of the signal frequency, slew rate, amplitude, EGM width, autogain, and autothreshold. These variables are important in helping the device differentiate VT and VF from other events like atrial fibrillation, sinus tachycardia, and other supraventricular tachycardias (SVTs), thus reducing the incidence of spurious shocks.

Each EGM event and R-R interval is marked and detected, and there are various algorithms that attempt to identify events as either normal or abnormal. “Abnormal” events include bradycardia that requires pacing, VT requiring ATP or low-energy synchronized shocks, or VF requiring defibrillation. Most algorithms depend on the ventricular rate criterion. Other variables, such as the suddenness of onset, variation in cycle length, and change in EGM morphology, help to increase the specificity for diagnosis but at a cost of reduced sensitivity. These should be adjusted and programmed on the basis of individual requirement and clinical scenario of each patient.

B.Event detection occurs if the device reaches a specified number of intervals programmed by the physician to detect VT or VF, at which point the ICD delivers the prescribed therapy. Most devices reconfirm the ongoing episode to avoid therapy for nonsustained events. After delivery of therapy, the device either confirms termination of the episode or meets criteria for redetection, and the next programmed therapy is delivered. The ICD automatically adjusts its sensitivity thresholds following sensed and paced events through an autogain mechanism. This allows the device to automatically adjust its sensitivity during a tachycardia episode in response to the changing amplitude of the ventricular signal.

C.Atrioventricular (AV) sequential devices incorporate programmable dual-chamber supraventricular criteria that may help to exclude inappropriate management of supraventricular tachyarrhythmias.

D.Tachycardia therapy. Most devices allow for programming of several tachycardia zones. The VT zone is programmed with a lower detection cutoff that would include any clinical VT events. Ideally, the cutoff rate for the detection of tachycardia should be above the patient’s maximal heart rate to avoid therapy for sinus tachycardia. ATP schemes include burst pacing and ramp pacing. Burst pacing sequences deliver a set of ventricular pulses at a fixed rate faster than that of the VT in an attempt to terminate the reentry VT by overdriving the circuit. Ramp pacing consists of a set of ventricular pulses in which each subsequent paced interval is incrementally shorter than the preceding one. Although this is a more aggressive protocol, there is also a higher chance of the VT degenerating into VF with this therapy. Overall, some studies have shown about 90% success in termination of VT with ATP.

Following a failed ATP attempt, interburst decrement allows a more aggressive shortening of the intervals during either a burst or a ramp attempt. The first pulse of a burst or ramp sequence (S₁) is delivered at a calculated percentage of the tachycardia cycle length. The S₁ percentage cycle lengths, number of pulses, interburst decrement, and number of ATP attempts are all programmable features. In addition, cardioversion therapy (1 to 36 J) can be programmed in a VT zone. All VT zones have a programmable time limit on episode duration, at which point the device defaults to the next zone. Also, if a tachycardia is accelerated to a faster arrhythmia, then the ICD will deliver the therapy appropriate for the rate of the accelerated tachycardia.

E.Defibrillation therapy. Successful ICD management of VF can occur only with rapid defibrillation therapy. To avoid any delay to defibrillation, ICDs can now deliver ATP during the time needed for capacitor charging before shock delivery. When this ATP therapy is successful, the device will abort charging prior to shock delivery. All devices are programmed with a VF zone because of the risk of acceleration with ATP or cardioversion. Because of the hemodynamic instability seen with fast VT or VF, most devices are typically programmed to manage any sustained episode with rates higher than 180 to 200 beats/min with defibrillation therapy. The device should be programmed with at least a 10-J safety margin over the DFT observed either at implant or during follow-up testing. Up to six additional shocks may be programmed, with maximal outputs programmed at the second or third shock and onward. Several ICD programming trials have demonstrated that a longer detection delay before ICD shock delivery reduces inappropriate shocks. The Multicenter Automatic Defibrillator Implantation Trial–Reduce Inappropriate Therapy (MADIT-RIT) trial was a large, randomized study that demonstrated using a rate cutoff of 200 beats/min with a 2.5-second delay before device therapy initiation is associated with a significant reduction in unnecessary ICD therapy and all-cause mortality in patients with primary prevention ICDs.

VII.BRADYCARDIA DETECTION AND THERAPY

A.All currently available ICDs provide basic VVI pacing with separate programmable postshock lower rate limit and output. Some dual-chamber devices have been introduced with an atrial lead for diagnostic use only or for AV-synchronized pacing. These devices allow multiple programmable pacing modes, including single- and dual-chamber, fixed-rate, or rate-responsive pacing with automatic mode switch. These expanded pacing modes have obviated the need for a separate dual-chamber pacemaker. In addition, they may reduce the inappropriate shocks attributed to SVT. Such devices may also have capabilities to detect and treat atrial arrhythmias in a manner similar to that for the ventricular arrhythmias. However, in patients without any pacing indications, it may actually be detrimental to pace the right ventricle, especially in patients with preexisting LV dysfunction. This has been well demonstrated in the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial. Such patients should either be given a single-chamber ICD or, if there are indications for a dual-chamber ICD for tachycardia discrimination or atrial arrhythmias, be programmed for backup pacing in the VVI mode.

B.In AV-synchronized devices, the ICD can continue to sense tachyarrhythmias in both chambers regardless of the programmed bradycardic pacing mode. To maintain proper sensing, both atrial and ventricular sensing thresholds are adjusted with autogain. The ICD has multiple blanking periods to avoid postpacing polarization, T-wave oversensing, and cross talk between chambers. To avoid undersensing of tachyarrhythmias, short cross-chamber blanking periods after paced events and no cross-chamber blanking after sensed events are necessary. The AV synchronous devices have programmable refractory periods available for bradycardia functions, but these refractory periods do not affect tachyarrhythmia detection.

VIII.MAGNET FUNCTION

A.Confusion abounds concerning the function of a magnet with ICDs. The pulse generator contains a reed switch that is closed when a magnet is placed over the device. Closure of the reed switch prevents delivery of tachyarrhythmia therapy. Unlike pacemakers, bradycardia pacing is not affected by the use of a magnet in ICDs. Normal device therapy resumes when the magnet is removed and the reed switch opens.

IX.MANAGING AND FOLLOWING PATIENTS

A.In the United States, the government mandates patient registration and tracking. Once registered, a patient receives a permanent identification card to carry at all times. A MedicAlert is strongly encouraged. Manufacturer guidelines suggest that patients should follow up every 3 to 6 months depending on clinical status. Even if remote follow-up is available, it should be supplemented by clinic visits. Patients should be informed that they are likely to receive therapies. At the follow-up visit, a history of symptoms that might suggest tachyarrhythmias should be obtained. The diagnostic and episode data should be reviewed. Current devices also include stored-episode EGMs to allow review of aborted shocks as well as delivered therapies. Device pacing and sensing thresholds should be obtained. There are no specific guidelines for follow-up testing of ICD defibrillation function. In general, patients experiencing device activation should be evaluated shortly after an event to assess for safe and appropriate device function. When device function or concomitant antiarrhythmic therapy is modified, an evaluation of the sensing, pacing, and DFTs is often necessary. Practice patterns vary widely regarding empirical device programming and electrophysiologic testing of modified ICD programming. Some sources recommend that operating a motor vehicle should be avoided for 6 months following a symptomatic arrhythmic event.

B.In general, ICD pulse generators have a 5 to 10 year longevity depending on usage. The programmer allows evaluation of battery status. As the device approaches the elective replacement interval, follow-up visits should be intensified. In general, once the device reaches the elective replacement interval, it operates normally for at least 3 months, depending on the frequency of therapy. Capacitor deformation occurs during periods when no shocks are delivered and results in longer charge times as well as decreased battery longevity. Current ICDs perform an automatic capacitor reformation that charges the capacitors and delivers the energy to an internal test load. This function improves subsequent charge times and battery longevity.

C.Typically, 40% of patients receive a therapy within the first year after implantation and 10% per year thereafter. If multiple ICD discharges are experienced, medical attention should be sought emergently.

D.Inappropriate shocks have been estimated to occur in 10% to 15% of patients with ICDs. These inappropriate therapies contribute to significant morbidity and distress for the patient. Early studies including MADIT II and SCD HeFT demonstrated an association between inappropriate shocks and greater all-cause mortality. Importantly, these studies did not use SVT-VT discrimination algorithms. The MADIT-RIT study found that reprogramming ICD therapy to reduce inappropriate shocks brought about a reduction in all-cause mortality during an average follow-up of 1.4 years. Recently, a single-center cohort study, involving nearly 1,700 patients, investigated the association between inappropriate ICD shocks and adverse outcomes. Over a 10-year period, this study found no association between inappropriate ICD therapy and increased mortality. Failure to discriminate between ventricular and supraventricular rhythms is the most common reason for inappropriate shocks. It is important to evaluate the patients for appropriateness of therapy. The most common cause of inappropriate shocks is atrial fibrillation with a fast ventricular rate. Shocks delivered during physical exertion noted to have gradually increasing heart rates and gradually decreasing V-V intervals suggest sinus tachycardia. Therapy is likely to be inappropriate in this setting also. Ideally, the cutoff rate for the detection of tachyarrhythmias should be greater than the patient’s maximal heart rate. In many cases, the VT rate falls within the patient’s achievable sinus rate. Programmable enhancements, such as sudden onset and sustained high rate, can allow sinus tachycardia overlap into the VT zone without delivery of an inappropriate shock. Additional enhancements such as morphology discrimination of the ventricular EGM as well as the introduction of dual-chamber devices with timing intervals, marker channels, and mode-switching capabilities have improved the specificity of device therapy. The annual rate of inappropriate shocks has fallen from as high as 50% for SVT alone in early studies to as low as 1% in modern clinical trials with the use of these sophisticated SVT-VT discrimination algorithms. Patients who are likely to benefit most from these algorithms are those with slower monomorphic VT, those at risk for atrial fibrillation with rapid ventricular rates, or those capable of exercising to sinus rates in the VT zone.

E.In the event of multiple ICD discharges, a magnet can be used to inhibit ICD therapy so that the underlying rhythm can be appropriately assessed and managed. The device should be interrogated as soon as possible to assess ICD function and facilitate diagnosis. If a SVT is present, then it should be managed as medically appropriate. For patient comfort, the magnet should be left in place to inhibit ICD therapy until the device can be reprogrammed or the SVT is terminated. If VF is present, the device is assumed inoperable and cardiopulmonary resuscitation with external defibrillation should be applied.

F.Patients receiving ICDs may suffer from significant psychological and emotional disturbances. Education and psychological support are beneficial in improving these patients’ quality of life.

X.ELECTROMAGNETIC INTERFERENCE. Patients should be counseled to avoid sources of electromagnetic interference because such interference may cause the pulse generator to become inhibited and either fail to deliver appropriate therapy or deliver inappropriate therapy. Potential sources of electromagnetic interference include industrial transformers, radiofrequency transmitters such as radar, therapeutic diathermy equipment, arc welding equipment, toy radio transmitters, antitheft devices, and magnetic security wands. The safe use of medical technologies such as electrosurgery, lithotripsy, external defibrillation, and ionizing irradiation can be accomplished by deactivating the device before the event. Shielding of the device is also appropriate when possible. The device should be evaluated for appropriate operation following exposure. Magnetic resonance imaging (MRI) is contraindicated for most devices; however, some newer generation ICDs have been deemed MRI compatible by the FDA. Reports of interference created by cellular phones may be related to either a magnetic field from within the phone or the radiofrequency signal generated by the phone. It is suggested that if a patient with ICD wishes to use a cellular phone, it should be held to the ear opposite the device and should not be carried in a pocket close to the device.

XI.FUTURE. ICD implantation rates have risen tremendously over the last two decades. Multiple clinical studies have demonstrated the role of ICDs in the primary and secondary prevention of SCD. Multiple trials have also demonstrated the role of an ICD in combination with CRT in reducing mortality and hospital admissions in patients with heart failure. Improvements in electronic technology will continue to expand the programming capabilities of these devices while reducing their size. S-ICDs are now available and provide a less invasive approach for patients who have an indication for ICD therapy but do not require pacing. ICD lead technology is also expected to improve, thereby decreasing the number of lead-related complications. Leadless systems are in clinical trials and may be an option for select patients in the future.

ACKNOWLEDGMENTS: The author thanks Dr. Christopher Ingelmo for his contributions to earlier editions of this chapter.