Characteristics of AICDs

The basic components of an AICD, including sensing electrodes, defibrillation electrodes, and a pulse generator (Fig. 13-2), can be seen on a chest radiograph. Transvenous electrodes have obviated the previous need for surgical placement. They are inserted into the pectoralis muscle. Many transvenous systems consist of a single lead containing a distal sensing electrode and one or more defibrillation electrodes in the right atrium and ventricle.¹⁰ Leads are inserted through the subclavian, axillary, or cephalic vein into the right ventricular apex. The left side is preferred because of a smoother venous route to the heart and a more favorable shocking vector.¹¹ In an effort to improve the efficiency of defibrillation, an additional defibrillation coil may be used.¹¹ Various placements of AICDs are demonstrated in Figure 13-3.

The pulse generator is a sealed titanium casing that encloses a lithium–silver–vanadium oxide battery. It has voltage converters and resistors, capacitors to store charge, microprocessors and integrated circuits to control analysis of the rhythm and delivery of therapy, memory chips to store electrographic data, and a telemetry module.¹² Whereas a pacemaker can draw the voltage required for function from its component battery, the energy needed for defibrillation requires a battery that is prohibitively large.⁶ To circumvent this problem, an AICD contains a capacitor that maximizes the voltage required by transferring energy from the battery before discharge. To achieve the energy required, AICDs use capacitors that are charged over a period of 3 to 10 seconds by the battery and then release this energy rapidly for defibrillation.¹⁰ The maximal output is 30 J in most units and 45 J in higher-energy units.⁶ This energy is high enough that a discharge is very obvious and often distressing to the patient.

Most AICDs use a system in which the pulse generator is part of the shocking circuit, often described as a “can” technology, and most of them have a dual-coil lead with a proximal coil in the superior vena cava and a distal coil in the right ventricle.¹³ Current flows in a three-dimensional configuration from the distal coil to both the proximal coil and the generator.¹⁴ This dispersion of the electrical field increases the likelihood of depolarizing the entire myocardium at once, thereby leading to successful defibrillation.¹⁴

AICDs may have the same programming capabilities as pacemakers and can be single chambered, dual chambered, or used with cardiac resynchronization therapy (CRT) .¹⁵ Single-chamber devices have only a right ventricular lead. They often have difficulty identifying atrial arrhythmias, which can result in inappropriate defibrillation of atrial tachycardias. Dual-chamber AICDs have right atrial and right ventricular leads and improved ability to discriminate rhythms. In most studies, dual devices have been found to offer improved discrimination between ventricular and supraventricular arrhythmias, thus decreasing inappropriate shocks as a result of rapid supraventricular rhythms or physiologic sinus tachycardia.¹⁶ Approximately 50% of AICDs implanted in the United States are dual-chamber devices.¹⁷ CRT devices add an additional left ventricular lead that is placed in the coronary sinus or epicardium. In patients requiring both AICD and pacemaker functions, both these devices are placed together. The advent of technology has allowed placement of a single device that can perform both pacemaker and defibrillator functions.

AICDs use a combination of antitachycardia pacing, low-energy cardioversion, defibrillation, and bradycardiac pacing in a combination also known as tiered therapy. They are programmed with specific algorithms that identify and treat specific rhythms. Ventricular arrhythmias may initially be converted (or undergo attempts at conversion) with antitachycardiac pacing as opposed to immediate defibrillation. This overdrive pacing may terminate the rhythm without the need for electrical defibrillation in up to 90% of events. It is most successful for terminating monomorphic ventricular tachycardia with a rate of less than 200 beats/min.¹ Overdrive pacing is better tolerated by patients than cardioversion and reduces the risk for inducing atrial fibrillation.¹⁸ These events may be silent, not felt by the patient, and discovered only by interrogating the device.

If unsuccessful, the next intervention may be low-energy cardioversion (<5 J). The device may be programmed to very low levels of electricity that, again, are better tolerated by the patient. This works best for ventricular rates higher than 150 and lower than 240 beats/min.¹⁴ This may be followed by a high-energy defibrillation. Traditionally, the energy level of the first shock is set at least 10 J above the threshold of the last defibrillation measured.¹² If the first shock fails, a backup shock may be required, but this may induce or aggravate ventricular arrhythmias (see the later section “Pacemaker-Mediated Tachycardia”). Unlike the proarrhythmic effects of medication, these arrhythmias are almost never fatal, although they may be associated with increased morbidity.¹¹ Currently used biphasic waveforms have improved defibrillation thresholds.¹²

This tiered approach obviates the need for unnecessary energy requirements. The devices also have antibradycardiac pacing that allows these patients to have one device instead of separate units. Additional complications associated with AICDs that have antibradycardiac pacing algorithms include a tendency toward oversensing, increased current drain, potential detection problems, and an increased incidence of hardware and software design problems.¹ At the time of insertion the amount of energy required for various AICD functions, such as the defibrillation threshold, is determined for any given patient, and output and sensing functions can be adjusted by reprogramming as needed.

History

Although patients who go to the ED because of implantable pacemaker–related issues may have one or more of several complaints, those with AICD-related issues are generally seen because their device has discharged. They will often describe a sensation of being kicked or punched in the chest, and the sensation is not subtle. In fact, some patients live in fear of the shock after having experienced it previously, and this is one reason for removal of the device. Ask the patient about the number of discharges and associated symptoms, including chest pain, shortness of breath, lightheadedness, palpitations, syncope, extremity edema (raising concern for congestive heart failure or lower extremity deep vein thrombosis), or dyspnea on exertion. In addition, elicit general symptoms such as fever, chills, nausea, or vomiting, which could be indicative of infection. Inquire about medication history. Ask about the specific implanted device that they possess. Most pacemaker and AICD patients should have an identification card on their person that will identify the manufacturer, model number, lead system, and a 24-hour emergency contact number. Sophisticated information and the prior electrical events and settings of the device can be ascertained in the ED by simply placing an external interrogating device over the unit.

Physical Examination

First, assess for airway patency, adequate ventilation, and cardiovascular status. The patient’s mental status may also be an important clue to the severity of the symptoms. Perform an appropriate physical examination with emphasis on examining the heart and lung to seek murmurs, pericardial friction rubs, and evidence of pulmonary effusion or other abnormalities. Inspect the pacemaker or AICD site for erythema or edema. Palpate the skin for evidence of obvious lead abnormalities. Examine the extremities for evidence of edema or erythema.

Radiography

The imaging modality of choice, at least initially, in a patient with complaints related to an implanted pacemaker or AICD is the plain chest radiograph. If the patient’s stability is in question, obtain a portable anteroposterior film. In addition to the standard cardiac, pulmonary, vascular, and skeletal evaluation, this study will probably confirm the location of the pulse generator case, as well as the current location of any leads. Survey the radiograph for evidence of lead fracture or displacement (see Fig. 13-1E). Compare with previous chest films. If the patient does not have a device identification card in immediate possession, take an overpenetrated radiograph to look for a radiopaque marker identifying the model type.

Electrocardiography

Perform an ECG to seek evidence of pacing, ectopy, and ST-segment or T-wave abnormalities. A comparison ECG may be helpful. If an AICD shock has been delivered, the shock itself can cause transient electrocardiographic changes, and waiting for several minutes to repeat the ECG may identify whether the changes are due to the discharge or an ongoing disease process.²⁹

Cardiopulmonary Resuscitation, ACLS Interventions, and External Cardiac Defibrillation in Patients with Implanted Pacemakers or AICDs

In general, ACLS interventions may be performed safely and effectively in patients with pacemakers and AICDs when indicated. Cardiopulmonary resuscitation (CPR) can usually be performed in standard fashion. If an AICD is present, rescuers may notice mild electrical shocks while performing CPR; these shocks are harmless to the rescuer. If the AICD shocks are impeding rescuer performance of CPR or if supraventricular tachycardias are noted during resuscitation, disable the AICD by applying a magnet over the corner of the device from which the leads emerge. This location is generally found easily by palpation but may be located blindly by slowly relocating the magnet until AICD activity ceases.

External cardiac defibrillation may be performed safely in patients with pacemakers and AICDs with the standard expected efficacy; however, it is recommended that external paddles or defibrillator pads be placed at a location approximately 10 cm distant from the pulse generator if possible.³⁰ A transcutaneous cardiac pacemaker may also be used in similar fashion, again with a recommendation that the pacing pads be placed in anatomically appropriate locations but preferably at a distance of 10 cm from the pulse generator.

Placing the external defibrillation or transcutaneous pacemaker pads in an anteroposterior configuration is advised because this configuration may circumvent energy shunting and shielding.¹¹ Every attempt should be made to avoid application of the defibrillators directly over the device. Use of the lowest possible energy setting for cardioversion or defibrillation is recommended. If available, biphasic cardioverter-defibrillators are further suggested.³⁰ In the event of successful resuscitation and return of spontaneous circulation, the pacemaker or AICD should be interrogated expeditiously by a cardiologist or electrophysiologist to ensure that no damage was sustained as a result of the resuscitation effort.

Regarding pharmacologic adjuncts, amiodarone has been reported to be more effective for the treatment of potentially lethal arrhythmias in the setting of implanted devices.³¹ Antiarrhythmic medications may be required for a resistant malignant rhythm when the AICD is functioning properly but the arrhythmia persists (Fig. 13-6G).

Several additional considerations are unique to the setting of ACLS in patients with a pacemaker or AICD. In cases of acute myocardial infarction involving areas of the myocardium in contact with the pacemaker leads, the implanted pacemaker may experience operative failure. Therefore, maintain a high level of suspicion for the potential requirement for supplemental transcutaneous or transvenous cardiac pacing.

Also, in the postresuscitation setting involving a patient with an implanted pacemaker or AICD, it is important to maintain a higher index of suspicion for device lead fracture or disruption resulting from CPR. Finally, in the postresuscitation phase the clinician should closely watch for the development of pneumothorax, hemothorax, pericardial effusion, or other aforementioned pathophysiologic processes that could adversely affect the function of the implanted device.

Pacemaker Output Failure

Pacemaker generator output failure is present when no pacing “spike” is noted on the ECG despite an indication for pacing. This condition may result from battery failure, fracture or loss of insulation in the pacer leads, oversensing of extraneous signals resulting in pacer inhibition, disconnection of the leads from the pacer generator, or in the case of a dual-chamber pacer, erroneous sensing of the pacemaker’s atrial signal by a ventricular sensor.³³ The latter phenomenon is commonly referred to as crosstalk.³⁴

Given that the reason for pacemaker implantation in most cases was for the treatment of an underlying bradycardia condition, initial clinical management of patients with some degree of pacer output failure will usually focus on pharmacologic management aimed at restoring an acceptable intrinsic heart rate. Subsequently, a transcutaneous or transvenous pacemaker may be required to ensure stabilization of the patient. Once stabilization has been accomplished, further ED management should include a thorough secondary survey, 12-lead electrocardiographic and continuous cardiovascular monitoring, portable chest radiograph to assess the condition of the pacemaker leads and identify related pathology, and any other pertinent diagnostic studies. At this point the clinician should seek to identify the type and model of the pacemaker and should consult an available cardiologist or electrophysiologist. Final disposition of the patient depends on the results of the stabilization, diagnostic studies, and cardiology consultation, and admission is often required.

Failure to Capture

In the case of failure to capture, pacemaker spikes are present on the ECG. However, some or all of the spikes are not followed by atrial or ventricular complexes, as appropriate for the pacemaker model in question. Failure to capture may result from deterioration of lead insulation; fracture or dislodgment of the leads; electrolyte disturbances, including hyperkalemia or hypocalcemia; a new condition requiring an elevated pacing threshold; acid-base disturbance; direct damage to the myocardium, which is in contact with the pacer lead’s tip (such as myocardial infarction or direct trauma); or dysfunction of the microcircuitry of the pulse generator. In addition, flecainide, a class IC antiarrhythmic medication, has been identified as an acute cause of the rise in ventricular capture thresholds in patients with implanted pacemakers.³² Likewise, all class I antiarrhythmic agents (sodium channel antagonists) may affect pacer capture thresholds and should therefore be identified as potential etiologic agents in patients suffering failure to capture.

Failure to Sense

Failure of an implanted cardiac pacemaker to sense the patient’s intrinsic cardiac rhythm may be subdivided into conditions related to oversensing or undersensing. Oversensing is present when the pacemaker erroneously identifies extrinsic electrical signals, such as those from skeletal muscle potentials or electromagnetic interference (EMI), and is inhibited from delivering an appropriate pacemaker pulse. For additional information on extrinsic EMI, refer to “Electromagnetic Interference and Implantable Devices” later in this chapter.

Management of pacemaker failure to sense will be driven largely by the patient’s clinical condition. A prudent clinician will order cardiovascular monitoring, intravenous access, and a portable chest radiograph, with additional measures as dictated by the patient’s condition. In the event of symptomatic bradycardia, placement of a magnet over the pacemaker pulse generator may be indicated because this maneuver will usually place the pacemaker in an asynchronous ventricular pacing mode and thereby restore a stable and regular paced ventricular rhythm while a consulting cardiologist or electrophysiologist is summoned.

Undersensing is said to occur when the pacemaker fails to identify intrinsic cardiac depolarization and delivers a pacing signal. This condition may result from damage or dislodgment of the pacemaker leads, myocardial infarction, direct cardiac trauma, failure of the pacemaker’s power source, and even the application of a magnet. Initial ED management of this condition is similar to that performed in the case of oversensing. Magnet placement may also be appropriate in this setting because it will restore a stable, regular, and normal cardiac rhythm until the pacemaker and its leads may be more thoroughly examined.

Runaway Pacemaker Syndrome

This condition is seen almost exclusively in older pacemaker models, particularly as they approach the end of their battery life or when the pulse generator is damaged by exposure to radiation or direct impact. The hallmark of runaway pacemaker syndrome is uncontrolled tachycardia resulting in ventricular rates approaching 300 to 400 beats/min. In addition to initial attempts at stabilization, magnet placement may be attempted. However, this is often ineffective. If the patient is hemodynamically unstable in the setting of runaway pacemaker syndrome, it may be necessary to disconnect the pulse generator. To do this, identify the location of the pacer leads by physical examination or a portable chest radiograph. Dissect through the skin and subcutaneous tissue and then sever the leads with a wire cutter or similar tool.

Pacemaker-Mediated Tachycardia

In some circumstances, patients with implanted pacemakers or AICDs may be seen in the ED because of symptomatic tachycardias resulting specifically as a complication of their pacemaker devices. This condition, referred to as pacemaker-mediated tachycardia and, alternatively, as pacemaker-induced tachycardia, most often results from one of three clinical scenarios. In patients with dual-chamber pacemakers, one of the pacemaker leads may function as a pathway for either anterograde or retrograde conduction and result in what is referred to as endless loop syndrome and thus a tachycardiac arrhythmia, which may often become hemodynamically unstable. In general, patients suffering from endless loop syndrome will not have a ventricular rate greater than the maximum tracking rate of the pacemaker device. Consequently, this condition will rarely be manifested as hemodynamic instability. One caveat, however, is that patients with underlying coronary artery disease and endless loop syndrome may experience coronary ischemia. In such a case or in a patient who is hemodynamically unstable because of the increased ventricular rate, application of a magnet will terminate the syndrome in most cases. Once stabilized, this condition may be prevented or at least mitigated by reprogramming of the pacemaker’s atrial sensor lead by an electrophysiologist.

A second scenario in patients with dual-chamber pacemakers occurs under the circumstance in which the patient experiences an intrinsic atrial tachycardia, at which point the implanted pacemaker begins to continuously discharge at its maximum preprogrammed ventricular rate. This condition may continue until the underlying atrial tachycardia is terminated by intervention.

A third instance of pacemaker-mediated tachycardia occurs in patients with AICD units that have backup antibradycardia pacing capability. It appears that if this pacemaker feature is switched on in such patients and an ectopic ventricular stimulus is delivered after a sudden pause in the intrinsic ventricular depolarization cycle, a ventricular tachyarrhythmia may be triggered.2,35

Diagnosis of Acute Myocardial Infarction in the Presence of a Paced Cardiac Rhythm

Patients undergoing active ventricular pacing from an implanted pacemaker device will normally have ECGs that resemble a left bundle branch block pattern. As a result, electrocardiographic diagnosis of acute ischemic changes is equally challenging in both populations. Sgarbossa and coworkers³⁶ published a series of criteria in 1996 that offer some utility in the interpretation of ECGs in patients with active ventricular pacing in whom acute coronary syndromes are suspected. These criteria are depicted in Table 13-2.⁷

Automatic Implantable Cardioverter-Defibrillators—Unique Malfunctions

Issues with sensing problems, lead migration, and battery failure are similar to pacemaker complications, and most occur within 3 months after implantation.³⁷ A potential malfunction unique to AICDs is inappropriate or lack of defibrillation of the device. An analysis of 23,000 Medicare patients with AICDs revealed a complication rate of 11%, with lead dislodgement being the most common problem followed by hematoma or hemorrhage, infection, and pneumothorax.³⁸

The AICD may not terminate ventricular arrhythmias, which may or may not be the result of malfunction of the device. AICD malfunction may be a result of battery depletion, component failure, failure-to-sense, or lead malfunction. Failure to cardiovert or defibrillate occurring in the setting of a functioning AICD system may be caused by inappropriate cutoff rates, failure to satisfy multiple detection criteria, completed and exhaustion of therapies, and cross-inhibition by a separate pacemaker.¹¹ The advent of AV or dual-chamber AICD devices has improved the sensitivity of detecting arrhythmias and thus preventing the delivery of inappropriate shocks.

Inappropriate AICD-delivered shocks occur in 20% to 25% of patients³⁸ and are the most common adverse events observed in AICD patients.³² The main causes are atrial arrhythmias, sinus tachycardia, nonsustained ventricular tachycardia, lead fracture or EMI, or electrical storm.³⁸ By definition, this phenomenon occurs when three or more shocks are delivered in a 24-hour period, occurs in 10% to 20% of AICD patients,³⁹ and constitutes a medical emergency.⁴⁰ AICD patients who experience this phenomenon may have end-stage cardiac failure and increased long-term mortality.⁴¹ Specific causes of electrical storm are unclear, but it is associated with ventricular tachycardia in the setting of LVEF lower than 30% and occurs more frequently in patients with demonstrated coronary artery disease who have not as yet undergone revascularization procedures. Suggested initial treatment includes the administration of amiodarone and β₂-adrenergic antagonists to pharmacologically suppress the arrhythmias and urgent cardiology consultation for possible pacemaker interrogation, overdrive pacing, or even catheter ablation.^41–43

The AICD may discharge inappropriately in response to rapid supraventricular rhythms such as atrial fibrillation, supraventricular tachycardia, or even sinus tachycardia. Multiple shocks may be a manifestation of inefficient termination of tachycardia, such as inappropriately low-energy delivery at the first shock, increased defibrillation thresholds, and migration or dislodgment of the defibrillation lead system or failure of the defibrillator system. Shocks that occur every few minutes may suggest that recurring ventricular tachyarrhythmias are being terminated appropriately (see Fig. 13-6).

AICD discharges in the setting of chest pain may be a result of myocardial ischemia–induced tachyarrhythmias.²⁸ As noted earlier, any electrocardiographic abnormalities noted immediately after shocks should be interpreted with caution because ST elevation or depression can occur immediately after a shock.²⁹ If the patient receives shocks in association with chest pain, ischemia is suggested, but other causes, including hypokalemia, hypomagnesemia, drug-induced proarrhythmia, or drugs that can prolong the QT interval (such as phenothiazines), should also be considered as underlying causes.¹¹

In some settings, the AICD may fail to sense sustained ventricular tachycardia or fibrillation. Such failure may be caused by an intrinsic arrhythmia rate below the programmed detection rate, usually as a result of concurrent pharmacologic therapy. If the patient is hemodynamically stable, it may be advantageous for the cardiologist to interrogate the pacer before initiating further antiarrhythmic therapy. If unsuccessful or if the patient is experiencing a nonperfusing ventricular arrhythmia, other pharmacologic interventions include procainamide26,44 or amiodarone. Box 13-4 depicts the outcome of AICD placement in a general population.

“Twiddler’s Syndrome”

In some cases, patients with implantable pacemakers choose to “twiddle” with the device: they manipulate the pulse generator case within its physiologic pocket under the skin in the chest. Note that a generator may also be placed in the abdominal wall (Fig. 13-7). This practice of “twiddling” may result in coiling, dislodgment, or disconnection of the pacemaker leads (Fig 13-8). It may even lead to actual displacement of the pulse generator case. At a minimum it may result in physical discomfort and may, in fact, precipitate cardiac arrhythmias or other complications local to the site of pacemaker placement. After initial stabilization of the complaint, these patients may require readjustment or replacement of their pacemaker devices. As part of their care, pacemaker patients should be educated to avoid manipulating their pacemakers.⁴⁶

Mental Health Issues Related to Implanted Pacemakers and AICDs

Patients with these devices may manifest a number of anxiety-related complications, including adjustment disorder, panic attacks, depression, imaginary shock, and defibrillator dependence, abuse, or withdrawal.47,48 These patients may benefit from psychiatric referral either as an outpatient or as part of the admission evaluation if applicable. The conditions may be severe enough that the device is removed by patient request.

Implantable Pacemaker and AICD Recalls

Since 1990 there have been approximately 29 Food and Drug Administration safety alerts and recalls affecting nearly 337,000 AICDs.⁴⁹ These advisories were issued as a result of unanticipated failure of devices identified after release of the product and widespread clinical use.⁴⁹ The decision to remove the devices is complex, and there has been difficulty reaching consensus on the optimal management of patients with these recalled devices. The decision to replace them should be multifactorial and take into consideration the estimated malfunction rate of the device, anticipated consequences of failure of the device, the individual center’s procedural risk for complications resulting from generator replacement, and patient preferences and desired level of risk tolerance.⁵⁰

Electromagnetic Interference and Implantable Devices

Given the plethora of new technologies, there is always concern about the interaction of EMI with pacemakers and AICDs. The sources of EMI comprise a significant spectrum and may involve radiated and conducted sources.

The most common response of implanted devices to EMI is inappropriate inhibition or triggering of pacemaker stimuli, reversion to asynchronous pacing, and spurious detection of tachyarrhythmias by the AICD. Reprogramming of operating parameters and permanent damage to the circuitry of the device or the electrode-tissue interface can also occur but are much less frequent.³⁰ Additional adverse effects that may occur include inhibition of bradycardia pacing, inadvertent delivery of a shock, or antitachycardia pacing.

The use of hermetic shielding in metal cases, filtering, interference rejection circuits, and bipolar sensing have helped mitigate most of this interference.⁵⁰ Nonetheless, the clinician should be familiar with common sources of EMI that may affect pacemakers and AICDs.

Several caveats will help avoid the deleterious effects of EMI on implantable devices. Cell phones should not be kept in a pocket over the device. When in use, they should be held at least 6 inches away from the device. In the case of hands-free headphones, when used these devices should be placed in the ear opposite the implanted pacemaker or AICD. In addition, patients should be advised to not linger in theft detection areas or airport metal detectors. Box 13-6 identifies different devices and the corresponding potential EMI that can occur with pacemakers and AICDs.^51,52

Out-of-Hospital Discharge of AICD

Patients are told to adhere to standard advice defining an appropriate response to out-of-hospital discharges of the AICD (Box 13-7). Many, however, come to the ED for evaluation after every shock. There is no standard ED intervention mandated by historical information, and clinical decisions are made on an individual basis corresponding to the current scenario. Options include prolonged ED observation, consultation, cardiac monitoring, laboratory testing (such as electrolytes and cardiac enzymes), or interrogation.

Disposition Criteria

In the majority of cases, patients seen in the ED with pacemaker complications or malfunctions will be symptomatic. Accordingly and regardless of the clinical requirement for admission, they will probably require device interrogation and possible recalibration or replacement by a cardiologist. In most cases this will be accomplished during hospital admission.

With regard to AICD malfunctions and disposition, patients who have had a single shock and no other specific complaints or comorbidity can be discharged with follow-up in 24 to 48 hours. Patients with symptoms concerning for ischemia, potentially lethal arrhythmias, or symptomatic illness should be admitted and specialty consultation obtained expeditiously. Patients who have had multiple shocks will need admission for observation and interrogation of their AICD device. Interrogation reveals significant information about the device, such as why it fired, the rhythm history, and an accurate assessment of the underlying problem (Fig. 13-9).

1. Trohman, RG, Kim Michael, H, Pinski, SL. Cardiac pacing: the state of the art. Lancet. 2004;364:1701.

2. Vukmir, RB. Emergency cardiac pacing. Am J Emerg Med. 1993;11:166.

3. Munter, DW, DeLacey, WA. Automatic implantable cardioverter-defibrillators. Emerg Med Clin North Am. 1994;12:579.

4. Ludmer, PL, Goldschlager, N. Cardiac pacing in the 1980s. N Engl J Med. 1984;311:1671.

5. Coppola, M, Yealy, DM. Transvenous pacemakers. Emerg Med Clin North Am. 1994;12:633.

6. Stone, KR, McPherson, CA. Assessment and management of patients with pacemakers and implantable cardioverter defibrillators. Crit Care Med. 2004;32:155.

7. Munter, DW. Assessment of implanted pacemaker/AICD devices. In: Roberts JR, Hedges JR, Chanmugan AS, et al, eds. Clinical Procedures in Emergency Medicine. 4th ed. Philadelphia: Saunders; 2004:258.

8. Furman, S, Hurzeler, P, DeCaprio, V. Appraisal and reappraisal of cardiac therapy. Am Heart J. 1977;93:794.

9. Bunch, TJ, Hayes, DL, Friedman, PA. Clinically-relevant basics of pacing and defibrillation. In Hayes DL, Friedman PA, eds.: Cardiac Pacing, Defibrillation and Resynchronization: A Clinical Approach, 2nd ed, West Sussex, UK: Wiley-Blackwell, 2008.

10. Clemo, HF, Ellenbogen, KA, Belz, MK, et al. Safety of pacemaker implantation in patients with transvenous (nonthoracotomy) implantable cardioverter defibrillators. Pacing Clin Electrophysiol. 1994;17:2285.

11. Pinski, SL. Emergencies related to implantable cardioverter-defibrillators. Crit Care Med. 2000;28(10 Suppl):N174.

12. DiMarco, JP. Implantable cardioverter-defibrillators. N Engl J Med. 2003;349:1836.

13. Wilbur, SL, Marchlinski, FE. Implantable cardioverter-defibrillator follow-up: what everyone needs to know. Cardiol Rev. 1999;7:176.

14. Moses, HW, Mullin, JC. Implantable cardioverter defibrillator and antitachycardia pacing. In: Moses HW, Mullins JC, eds. A Practical Guide to Cardiac Pacing. Philadelphia: Lippincott; 2007:112.

15. Kadish, A, Mehra, M. Heart failure devices: implantable cardioverter-defibrillators and biventricular pacing therapy. Circulation. 2005;111:3327.

16. Goldberger, Z, Lampert, A. Implantable cardioverter-defibrillators: expanding indications and technologies. JAMA. 2006;295:809.

17. Goldberger, A, Elbel, B, McPherson, CA, et al. Cost advantage of dual chamber versus single chamber cardioverter-defibrillator implantation. J Am Coll Cardiol. 2005;46:850.

18. Estes, NAM, Haugh, CJ, Wang, PJ, et al. Antitachycardia pacing and low energy cardioversion: a clinical perspective. Am Heart J. 1994;127:1038.

19. Epstein, AE, DiMarco, JP, Eleenbogen, KA, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. Heart Rhythm. 2008;5(6):e1–e62.

20. Doval, HC, Nul, DR, Grancelli, HO, et al. Randomised trial of low-dose amiodarone in severe congestive heart failure. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA). Lancet. 1994;344:493–498.

21. Naccarelli, GV, Luck, JC, Wolbrette, DL, et al. Pacing therapy for congestive heart failure: is it ready for prime time? Curr Opin Cardiol. 1999;14:1–3.

22. Bristow, MR, Saxon, LA, Boehmer, J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004;350:2140–2150.

23. Bradley, DJ, Bradley, EA, Baughman, KL, et al. Cardiac resynchronization and death from progressive heart failure: a meta-analysis of randomized controlled trials. JAMA. 2003;289:730–740.

24. McAlister, FA, Ezekowitz, J, Hooten, N, et al. Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction. JAMA. 2007;297:2502–2514.

25. Kusumoto, F, Goldschlager, N. Implantable cardiac arrhythmia devices—part II: implantable cardioverter defibrillators and implantable loop recorders. Clin Cardiol. 2006;29:189.

26. Zipes, DP, Camm, AJ, Borggrefe, M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—executive summary: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for practice guidelines. J Am Coll Cardiol. 2006;48:1064.

27. McPherson, CA, Manthous, C. Permanent pacemakers and implantable defibrillators: considerations for intensivists. Am J Respir Crit Care Med. 2004;170:933.

28. Pinski, SL, Trohman, RG. Implantable cardioverter-defibrillators: implications for the nonelectrophysiologist. Ann Intern Med. 1995;122:770.

29. Eysmann, SB, Marchlinski, FE, Buxton, AE, et al. Electrocardiographic changes after cardioversion of ventricular arrhythmias. Circulation. 1986;73:73.

30. Pinski, SL, Trohman, RG. Interference in implanted cardiac devices, part II. Pacing Clin Electrophysiol. 2002;25:1496.

31. Pinter, A, Dorian, P. Approach to antiarrhythmic therapy in patients with ICDs and frequent activations. Curr Cardiol Rep. 2005;7:376.

32. Rosenqvis, M, Beyer, T, Block, M, et al. Adverse events with transvenous implantable cardioverter-defibrillators: a prospective multicenter study. Circulation. 1998;98:663.

33. Hayes, DL, Vlietstra, RE. Pacemaker malfunction. Ann Intern Med. 1993;119:828.

34. Pinski, SL, Trohman, RG. Interference in implanted cardiac devices, part I. Pacing Clin Electrophysiol. 2002;25:1367.

35. Himmrich, E, Przibille, O, Zellerhoff, A, et al. Proarrhythmic effect of pacemaker stimulation in patients with implanted cardioverter-defibrillators. Circulation. 2003;108:192.

36. Sgarbossa, E, Piniski, SL, Gates, KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. Am J Cardiol. 1996;77:423–424.

37. Becker, R, Ruf-Rickter, J, Senges-Becker, JC, et al. Patient alert in implantable cardioverter defibrillators: toy or tool? J Am Coll Cardiol. 2004;44:95.

38. Reynolds, MR, Cohen, DJ, Kugelmass, AD, et al. The frequency and incremental cost of major complications among medicare beneficiaries receiving implantable cardioverter-defibrillators. J Am Coll Cardiol. 2006;47:2493.

39. Bailey, SM, Wilkoff, BL. Complications of pacemakers and defibrillators in the elderly. Am J Geriatr Cardiol. 2006;15:102.

40. Emkanjoo, Z, Alihasani, N, Alizadeh, A, et al. Electrical storm in patients with implantable cardioverter-defibrillators: can it be forecast? Tex Heart Inst J. 2009;36:563–567.

41. Srivasta, UN, Ebrahimi, R, El-Bialy, A, et al. Electrical storm: case series and review of management. J Cardiovasc Pharmacol Ther. 2003;8:237.

42. Sesslberg, HW, Mosss, AJ, McNitt, S, et al. Ventricular arrhythmia storms in postinfarction patients with implantable defibrillators for primary prevention indications: a MADIT-II substudy. Heart Rhythm. 2007;4:1395–1402.

43. Carbucicchio, C, Santamaria, M, Trevisi, N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators: short and long term outcomes in a prospective single-center study. Circulation. 2008;117:462.

44. Gorgels, APM, van den Dool, A, Hofs, A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol. 1996;78:43.

45. Chapman, PD, Veseth-Rogers, JL, Duquette, SE. The implantable defibrillator and the emergency physician. Ann Emerg Med. 1989;18:579.

46. Nicholson, WJ, Tuohy, KA, Tilkemeier, P. Twiddler’s syndrome. N Engl J Med. 2003;348:1726–1727.

47. Vlay, SC, Olson, LC, Fricchione, GL, et al. Anxiety and anger in patients with ventricular tachyarrhythmias. Responses after automatic internal cardioverter defibrillator implantation. Pacing Clin Electrophysiol. 1993;16:186.

48. Fricchione, GL, Olson, LC, Vlay, SC. Psychiatric syndromes in patients with the automatic implantable cardioverter defibrillator: anxiety, psychological dependence, abuse and withdrawal. Am Heart J. 1989;117:1411.

49. Maisel, WH. Safety issues involving medical devices: implications of recent implantable cardioverter-defibrillator malfunctions. JAMA. 2005;294:955.

50. Amin, MS, Matchr, DB, Wood, MA, et al. Management of recalled pacemaker and implantable cardioverter-defibrillators: a decision analysis model. JAMA. 2006;296:412.

51. Pinski, SL, Trohman, RG. Interference with cardiac pacing. Cardiology Clin North Am. 2000;18:219.

52. Spencer, WH, Block, PC. What interferes with pacemakers and AICD’s? Cardiosource. Available at www.cardiosource.com.