Methods

Top Methods Author & Article Info References

We selected peer-reviewed original articles and reviews addressing aspects of implantable defibrillator therapy that are relevant to the clinician. The selected articles were chosen from a MEDLINE search and our personal files.

Current Status of Implantable Defibrillator Technology

Implantable defibrillator therapy has become increasingly complex [6]. The first devices were nonprogrammable, "shock-only" units produced by one manufacturer [7]. Currently, seven different manufacturers produce implantable defibrillator systems [8]. Advanced devices have extensive programmability, telemetric, and diagnostic capabilities. Tiered-therapy implantable defibrillators deliver high-energy defibrillation shocks plus low-energy shocks, and antitachycardia pacing to terminate ventricular tachycardia [9, 10]. They also provide back-up ventricular pacing for bradyarrhythmias. The lead systems used to interface the generator and heart have also evolved. Several different nonthoracotomy lead systems are used clinically and already are the first choice for defibrillator implantation [11, 12] (Figure 1). Although nonthoracotomy lead systems decrease implant-related morbidity, they are still susceptible to complications, including infection, lead dislodgment, and failure [13-15].

View larger version (142K): [in this window] [in a new window]   Figure 1. Radiograph of the chest showing a completely transvenous implantable defibrillator system. The passive-fixation, triple-electrode lead has been positioned in the right ventricular apex. The distal tip is used for sensing and pacing. The defibrillation shocks are delivered between the two coils located in the right ventricle and the junction of the right atrium and superior vena cava. The lead has been tunneled down to the defibrillator generator in the abdominal left upper quadrant (not shown).

Unfortunately, the availability of many different systems is not without drawbacks. Each device requires a different programmer and software [16], and no devices are compatible. This incompatibility is not expected to change in the foreseeable future. The problem is compounded because the terminology used by different manufacturers to describe similar features also varies. The days in which the function of the only available implantable defibrillator could be completely controlled by applying a magnet are long past.

Emergency Identification and Deactivation of Implantable Defibrillators

Rapid identification of the defibrillator model is important when the device must be deactivated or reprogrammed. Patients with defibrillators should carry identification cards that list manufacturer information, the model number, therapy options, the type of lead system, and a 24-hour emergency contact telephone number. However, compliance with this recommendation is not perfect. In an emergency, an overpenetrated radiograph that shows the generator permits the identification of the device because all manufacturers' pulse generators have a radiopaque identifier.

The capacity of an implantable defibrillator to recognize and treat tachyarrhythmias can be temporarily disabled by placing a magnet on top of all implantable defibrillators. However, the deactivating position of the magnet relative to the defibrillator unit may vary according to the model. The magnet overrides the automatic function of the device when the specific programmer is not available. The magnetic field closes a reed switch in the generator circuit, triggering a response that differs among models (Table 1). In obese patients, the magnetic field from a single magnet may not be strong enough, and two doughnut-shaped magnets (one on top of the other) may be needed. Defibrillators from the Ventak series (Cardiac Pacemakers, Inc., Saint Paul, Minnesota) can be completely deactivated with a magnet. In other devices, recognition and treatment of tachyarrhythmia is disabled only as long as the magnet remains close to the generator. In those cases, the magnet must be taped to the generator site so that its inactivated status is maintained. The Ventak defibrillators generate beeping tones when they are placed under a magnetic field. Intermittent tones synchronized with the heartbeat are emitted when the device is active. A continuous tone indicates that the device is inactive. With other devices (in the absence of the programmer), the disabled status cannot be confirmed until a tachycardia episode occurs.

Diagnosis and Therapy in Patients with Implantable Defibrillators

Although implantable defibrillators resist most forms of electromagnetic radiation, a conservative approach in dealing with sources of electromagnetic radiation can aid patient safety. Possible effects of strong electromagnetic fields on defibrillator systems include cessation or intermittent delivery of antibradycardia pacing; inadvertent delivery of antitachycardia therapy; resetting of programmed parameters; and damage to the pulse generator, the tissues interfacing with the electrodes, or both.

Most diagnostic and therapeutic maneuvers can be safely done in patients with implantable defibrillators if a few rules are followed. In general, the device should be deactivated before the procedure and reactivated as soon as the procedure is concluded. In patients who are not pacemaker-dependent, pacing should also be disabled. Medical personnel familiar with implantable defibrillators should be available to deactivate and activate the device and to monitor the patient's cardiac rhythm. If severe ventricular tachyarrhythmias occur while the device is inactive, knowledge of the patient's previous response to antiarrhythmic therapy can be useful. Finally, the device should be carefully reassessed after the procedure to confirm satisfactory operation.

The presence of a defibrillator is not a contraindication to required surgery. Electrocautery energy can be falsely detected as a rapid cardiac rhythm, thereby triggering inappropriate defibrillator shocks. The device must therefore be deactivated before any procedure is done in which the use of cautery is contemplated. With "noncommitted" devices, electrocautery could be used with an active defibrillator and proper programming if each episode of application is relatively short. However, this practice is not recommended because it could cause clinically inapparent aborted shocks and substantial waste of battery charge. Other possible detrimental effects of electrocautery are less common and can be reduced by positioning the electrocautery ground electrode so that the current flow through the implanted electrode system is minimized [17].

Ionizing radiation (radioactive cobalt, linear accelerators, betatrons), particularly at high doses, may adversely affect the circuitry of a defibrillator [18]. Because the effect is cumulative, total radiation dosage determines whether, and to what extent, damage will occur. The generator should always be shielded during delivery of radiation therapy. However, because shielding does not guarantee protection, the operation of the generator must be evaluated after it is exposed to radiation. If tissue near the implant site must be irradiated with high cumulative dosages, device relocation may be advisable [19].

In theory, the mechanical and electromagnetic forces generated during extracorporeal shock wave lithotripsy could damage an implantable defibrillator generator, which is generally close to the focal point of those forces. Successful lithotripsy without damage to a contralateral defibrillator generator has been described in at least one report [20]. Bench testing also suggests that contralateral lithotripsy should not be contraindicated in patients with implantable defibrillators [21]. A styrofoam shield should be placed on the patient's back directly posterior to the generator to help absorb the energy created [21]. No data are available to assess the safety of lithotripsy applied ipsilateral to an implantable defibrillator.

Short-wave diathermy consists of the therapeutic application of current directly to the skin and can be a source of high-frequency interference. Diathermy applied too close to the pulse generator may damage its circuitry by heating. Selective localized heating of the metal case of the generator may be so intense that the tissues are burned [17]. Therefore, diathermy should only be used far from defibrillator generators in which all functions have been deactivated. Patients dependent on pacemakers should not have therapeutic diathermy.

At most institutions, an implantable defibrillator is considered an absolute contraindication to magnetic resonance imaging. Magnetic resonance imaging devices contain strong magnetic fields that can exert significant mechanical force on the ferromagnetic components of the defibrillator. Such force could theoretically cause physical pain and even damage the generator. Alternating magnetic and radiofrequency fields from magnetic resonance imaging devices could also cause a pulse generator to deliver a shock to the patient or result in rapid pacing. Because not all these concerns are equally well supported, the feasibility of magnetic resonance imaging in patients with pacemakers or implantable defibrillators is being studied [22]. Until more data become available, magnetic resonance imaging should be considered contraindicated in patients with implantable defibrillators.

Patients will frequently ask about the risks of electromagnetic radiation sources they may encounter during daily life. The electrophysiology team generally adequately instructs patients on these issues. It is important to know that microwave ovens represent no hazard. When traveling, patients should notify airport security personnel that they have an implantable defibrillator. It is appropriate to walk through the security gate as instructed, although it may detect the metal device can. Hand-held wands should be avoided because they contain magnets that could eventually deactivate some devices.

Cardiopulmonary Resuscitation in Patients with Implantable Defibrillators

The presence of an implantable defibrillator should not deter standard resuscitation techniques [23, 24]. If ventricular fibrillation is documented, the implantable defibrillator should be assumed to be inoperative, and external defibrillation should be administered promptly. Epicardial defibrillation patches may increase the energy requirement for external defibrillation. Proposed mechanisms include a shielding effect of the insulation portions of the patches or a shunting of current away from the myocardium through the conducting portions of the patches. The phenomenon may be more marked with larger patches [25, 26]. If external defibrillation is initially unsuccessful, paddle positions should be changed. An anteroposterior configuration of the external defibrillation paddles has been efficacious in patients with epicardial defibrillation patches and should be considered at the beginning of the resuscitation effort [27]. No data are available on the effects of nonthoracotomy defibrillation systems on the energy requirements for external defibrillation; however, significant interactions are expected only if a chest paddle is placed directly over a subcutaneously implanted patch electrode.

Persons administering cardiopulmonary resuscitation might feel a mild electric shock on the patient's body surface from an implantable defibrillator discharge. These shocks do not pose a risk to persons or external monitoring equipment. If the patient is in a controlled environment, it may be advisable to deactivate the implantable defibrillator during cardiopulmonary resuscitation. Rapid supraventricular tachycardias with adequate perfusion are common during resuscitation maneuvers. These tachycardias could trigger internal defibrillator discharges, which may result in reinduction of ventricular tachycardia or fibrillation [24, 28]. However, inactivation should not halt resuscitation efforts because valuable seconds may be lost. To avoid inadvertent shocks to providers of postmortem examination or preparation, the defibrillator should be deactivated if resuscitative efforts are unsuccessful [28].

Rarely, external defibrillation shocks can damage the pulse generator. After external defibrillation, the pulse generator should be monitored for proper function and interrogated to confirm that the programmed parameters have not been reset. In devices with pacing capabilities, the capture threshold should be reassessed. If possible, the pulse generator should also be tested by inducing an arrhythmia and allowing the device to deliver shock therapy. This is the only way to verify that the output circuitry is functioning properly.

Multiple Defibrillator Shocks

Multiple defibrillator discharges in a relatively short period of time are detrimental in several ways and require prompt attention. Patients and their families tolerate multiple defibrillator discharges poorly. Most patients describe the experience as unpleasant, and many become anxious and agitated [29, 30]. Multiple shocks may be a manifestation of defibrillator system failure. Rapid identification of the problem could be life-saving. Multiple shocks may also cause myocardial injury and transient depression of left ventricular function. Finally, multiple shocks result in significant drainage of battery energy. An expensive defibrillator, which is supposed to last more than 3 years under normal operating conditions, can be depleted after delivering more than 150 shocks, which can occur within a few hours.

The causes of multiple defibrillator shocks are myriad, and accurate diagnosis is needed for correct management (Table 2). The defibrillator may be firing appropriately to terminate recurrent episodes of ventricular tachyarrhythmias (that is, ventricular electric storm). Several shocks may also occur in series for one episode of tachycardia that is not easily terminated. Causes of inefficient tachycardia termination include programming an inappropriately low amount of energy for the first shock, increased defibrillation thresholds (triggered, for example, by acute ischemia or a change in antiarrhythmic drug therapy) [31], and migration or dislodgment of the defibrillation lead system.

Committed defibrillators (those that do not reconfirm the persistence of the arrhythmia immediately before shock delivery) may discharge for episodes of nonsustained ventricular tachycardia that are long enough to satisfy their detection criteria. Implantable defibrillators can also discharge inappropriately for rapid supraventricular rhythms that fulfill detection criteria. Atrial fibrillation and sinus tachycardia are frequent offenders [32]. Tiered-therapy devices may recognize the supraventricular tachyarrhythmia as ventricular tachycardia. The ensuing antitachycardia pacing or low-energy cardioversion can then induce ventricular tachycardia or fibrillation [33]. Finally, an implantable defibrillator can discharge inappropriately during sinus rhythm because of oversensing signals. This most frequently occurs with sensing lead insulation or conductor breakdown [14, 34, 35]. This breakdown produces electrical "noise" that is recognized as a ventricular tachyarrhythmia. Less frequent causes of implantable defibrillator discharge during normal rhythms are oversensing of T waves, external electromagnetic interference [36], and double-counting of pacing artifacts [37].

Patients with multiple defibrillator shocks should be initially evaluated in a setting that allows electrocardiographic monitoring and advanced cardiac resuscitation. The device should be interrogated as soon as possible. Implanting institutions should provide 24-hour coverage and patient response systems with personnel experienced in managing patients with defibrillators [38]. Delays may be unavoidable at smaller hospitals. Electrocardiographic monitoring should be initiated immediately so that one spontaneous discharge can be recorded. In devices with limited diagnostic capabilities, this could be the only way to establish a diagnosis. With some newer devices, diagnosis of the rhythms that triggered the discharges can often be made by analyzing the stored electrograms [39]. The defibrillator should not be deactivated until a diagnosis is established. Frightened, anxious patients may require sedation. Because most patients with defibrillators have impaired left ventricular function, their hemodynamic status should be carefully assessed, and decompensated cardiac failure should be treated promptly.

The pattern of discharges can help in the diagnosis. Several consecutive shocks occurring within seconds of each other may result from inappropriate detection of supraventricular tachyarrhythmias, device inefficacy, or oversensing. Isolated shocks recurring every few minutes suggest that recurrent ventricular tachyarrhythmias are being appropriately terminated [40]. Shocks preceded by chest pain suggest arrhythmias induced by myocardial ischemia. Other arrhythmogenic conditions, including elec-trolyte imbalance or drug-induced proarrhythmia, should be sought and eliminated. The presence of atrial fibrillation should suggest that transient acceleration of the ventricular response above the defibrillator cut-off rate caused the shocks [41]. The 12-lead electrocardiogram should be examined for rhythm, signs of antiarrhythmic drug toxicity, and acute myocardial ischemia. Some caveats apply here. Transient ST-segment elevation Figure 2 or depression are common immediately after an internal defibrillation shock and cannot be interpreted as signs of myocardial ischemia [42, 43]. Epicardial defibrillation patches can produce an electrocardiographic pseudoinfarction pattern, more commonly in the lateral leads [44]. Multiple consecutive shocks could result in the release of myocardial isoenzymes in the absence of myocardial ischemia or necrosis [43].

View larger version (13K): [in this window] [in a new window]   Figure 2. Holter monitor recording showing a spurious shock (arrow) delivered during normal sinus rhythm in a patient with an insulation breakdown in the sensing leads. The ST segment was markedly and transiently elevated immediately after the shock. Each continuous strip represents 1 minute of recording.

A patient with multiple defibrillator shocks secondary to ventricular electric storm must be admitted to an intensive care unit. A cardiac electrophysiologist should be promptly consulted because of the possible adverse interactions between antiarrhythmic drugs and devices and the frequent need to reprogram and retest the defibrillator system. Potentially reversible causes should be treated vigorously. Thrombolysis should be considered in patients with evolving myocardial infarction. Intravenous magnesium is the treatment of choice for drug-induced torsade de pointes [45]. Intravenous antiarrhythmic drugs remain the mainstay of therapy for ventricular electric storm when reversible causes are not identified. The defibrillator should not be deactivated unless frequently recurring ventricular tachycardia is well tolerated or hemodynamic instability secondary to inefficient defibrillation develops. In patients with epicardial defibrillation patches, difficulty with transthoracic defibrillation should be anticipated. Prophylactic application of self-adhesive defibrillation pads in an anteroposterior configuration is useful [27]. The cardiac electrophysiologist may consider instituting antitachycardia pacing or catheter ablation of the arrhythmogenic focus for the patient with incessant ventricular tachycardia [46].

The defibrillator should be deactivated if spurious firing is documented. Spurious shocks can induce ventricular tachycardia or fibrillation [47], which might not be detected or terminated if the defibrillator is malfunctioning. Nonsustained ventricular arrhythmias that trigger defibrillator discharges should be approached in a manner similar to that used for more sustained ones. Careful prolongation of the number of tachycardia intervals required for detection may be useful when nonsustained arrhythmias remain hemodynamically stable. Pharmacologic control of the ventricular rate is the initial maneuver when defibrillator shocks are triggered by atrial fibrillation. Digoxin alone is generally insufficient. Combination therapy that includes calcium-channel blockers or ß-blockers is frequently required [48]. Because of its short half-life, esmolol is useful in the acute setting for patients with left ventricular dysfunction [49]. Catheter ablation of the atrioventricular junction should be considered when the above maneuvers fail [50]. Shocks during sinus rhythm or paced rhythms at rates lower than the detection rate always represent oversensing of signals. Rapid consultation with the cardiac electrophysiologist is required for definitive treatment (reprogramming or hardware revision). Patients should have continuous electrocardiographic monitoring while their device is inactive. The defibrillator should be reactivated only after the condition that triggered the spurious shocks is controlled.

Infection of Implantable Defibrillator Systems

An infection of the implantable defibrillator system is potentially life-threatening and should never be taken lightly. The incidence of this complication has ranged from 1% to 7% [51]. It is more common after generator replacement than after initial implantation [52]. As with infections of other prosthetic implants, these infections could be classified as early ( 60 days after implantation) or late (>60 days after implantation) infections that differ in microbiologic characteristics, pathogenesis, presentation, and treatment [53]. Early infections are more commonly caused by staphylococci. They may result from contamination of an intraoperative wound or device or from hematogenous seeding immediately after surgery by microorganisms that originate from indwelling catheters, drains, or respiratory or urinary tract infection. Late infections may result from transient bacteremia (probably rare), device skin erosion, or delayed onset of an infection that is acquired soon after surgery. Staphylococcus epidermidis is frequently associated with infections with indolent courses. Antibiotic prophylaxis is currently not recommended during procedures that may cause transient bacteremia in patients with implantable defibrillators.

Infection involving a defibrillator system should be suspected when local and general signs of inflammation develop. Clinical manifestations depend on the site of involvement and the time elapsed since implantation. Most defibrillator system infection involve the pulse-generator pocket and therefore initially cause local tenderness, swelling, erythema, and warmth. Frank drainage of pus or device erosion may also occur. Fluctuation developing soon after surgery is a nonspecific sign because it is observed in the first few weeks in most patients with subcutaneous pockets. Systemic symptoms and signs (such as fever and leukocytosis) may be initially absent. In rare instances, the external wounds and pocket may look normal when overt system-related septicemia is present. Defibrillator system infections should never be considered to be localized. In infections of the generator pockets, electrodes are always contaminated at the connector site. Moreover, microorganisms can migrate along the electrodes toward the heart or pocket. Computed tomographic studies are helpful in assessing the presence (and extent) of infection by showing distortion of the epicardial patches and the fluid accumulation around them [54].

The treatment of choice for an infection of an implantable defibrillator system is removal of the entire system and administration of parenteral antibiotic agents. Empiric oral antibiotic therapy should never be given to patients with signs of inflammation at the generator pocket or to patients with implanted defibrillators and unexplained fever. Because oral antimicrobial therapy can only partially suppress the infection, diagnosis and treatment are more difficult at later stages. Suspected defibrillator infection should be confirmed by culture, and antibiotic agents should be selected accordingly. Blood cultures are rarely positive. A fluctuant pocket suspected of being infected should be aspirated with an aseptic technique in which the leads are carefully avoided. Patients may be too sick at presentation for antibiotic agents to be withheld until culture results are available. Vancomycin provides good coverage against coagulase-negative staphylococci, methicillin-resistant S. aureus, Propionibacterium acnes, and diphtheroids that are common causes of defibrillator infection. Therefore, intravenous vancomycin is the empiric treatment of choice.

Removal of a defibrillator system (particularly one implanted through thoracotomy) may be risky. In patients with a limited lifespan because of another systemic illness, avoiding surgery may be desirable. In such patients, a course of parenteral antibiotic agents plus local continuous irrigation followed by long-term therapy with oral antibiotic agents may provide a reasonable clinical outcome [55].

Managing patients after removal of a defibrillator system is complex because they continue to have a high risk for sudden death [56]. Alternative effective antiarrhythmic therapy is frequently unavailable. The possibility of reimplanting a transvenous defibrillator system facilitates the decision. Several weeks should elapse between explantation and reimplantation so that the chances of recurrent infection are minimized. This could translate into a prolonged hospital stay for patients who are not well protected by antiarrhythmic drugs. The timing of this decision should be coordinated among consultants in infectious disease, cardiac arrhythmias, and possibly thoracic surgery. Every safeguard must be taken to avoid the potentially disastrous outcome associated with recurrent or repeat infection.

Psychiatric Syndromes in Patients with Implantable Defibrillators

Most patients with implantable defibrillators have coronary artery disease and therefore face the usual psychological and social adjustments that patients with this disease experience. Their lifestyle is further complicated by the presence of an implantable device that would "save" them should they experience recurrences of life-threatening arrhythmias. Little research has been done on the psychological effect of defibrillator implantation. Although a reduction in the level of anxiety in patients with implantable defibrillators has been described [57], it is clear that defibrillator implantation is not always a psychologically benign procedure [58, 59]. The development of adjustment disorders specific to the defibrillator is not uncommon. Syndromes that have been described include anxiety with secondary panic reaction; defibrillator dependence, abuse, or withdrawal; negative effect on body image; and imaginary shocks [58, 60, 61].

Group therapy provides support and education and promotes positive adjustment to the implanted defibrillator [62]. Psychotherapeutic counseling may be particularly useful in patients with maladjustment syndromes. The development of coping skills to manage fatigue, achieve maximum levels of physical and social activity, resolve interpersonal conflict, and deal with ongoing anxiety about death provides psychological benefit to patients who believe they have lost control over key parts of their lives [63]. Behavioral and cognitive approaches are available to manage anxiety, deal with catastrophic thinking, and reframe the meaning of implantation from a device on which one's life must center to a relatively neutral medical intervention designed to prolong and enhance the quality of life [58].

The need to use psychotropic agents may arise frequently. Benzodiazepines are useful when mild to moderate sedation is needed. Benzodiazepines have no known proarrhythmic effects, and, in theory, could ameliorate ventricular arrhythmias that are facilitated by high sympathetic tone. The need for therapy should be periodically reassessed when benzodiazepines are prescribed in the outpatient setting [64]. Antidepressant and antipsychotic medications can exacerbate cardiac arrhythmias. Treatment with these types of medication should be coordinated between psychiatrists and cardiac electrophysiologists. If the patient is already receiving antiarrhythmic drugs that have electrophysiologic properties similar to those of the psychotropic agent, dosages may need to be carefully adjusted to avoid toxicity resulting from potentially additive effects.

Electroconvulsive therapy is safe and effective for treating depression in the medically compromised patient, but special considerations apply to its use in patients with implanted defibrillators [58]. Methohexital is a safe anesthetic agent in these patients [65]. In patients with cardiac disease, electroconvulsive therapy frequently induces transient arrhythmias [66]. The device should be deactivated just before therapy and reactivated immediately after therapy so that unnecessary charges are avoided [67]. Continuous electrocardiographic monitoring is necessary while the device is inactivated. Grounding of the patient during application of electrical current should be carefully avoided because rerouting of the delivered current to the heart through the defibrillator electrodes can result in ventricular fibrillation.