ICD Shocks: What every physician needs to know.

Multiple clinical trials support the use of implantable cardioverter-defibrillators (ICDs) for prevention of sudden cardiac death in patients with heart failure (HF). Of the patients who have an ICD implanted for primary prevention, approximately 20% to 35% will experience an appropriate shock within 1 to 3 years of the implant. Another one third of patients will experience an inappropriate shock, defined as a shock delivered through the device for a non–life-threatening problem over the same time period.

Implantable cardioverter-defibrillators are implanted for both primary prevention of ventricular arrhythmic (VA) death in patient populations known to be at high risk for VA death or as secondary prevention for those who have already survived a VA event. Shocks delivered through these implanted devices to cardiovert ventricular tachycardia or to defibrillate ventricular fibrillation are, although lifesaving, painful, often poorly tolerated, and not without at least transient detrimental effect to the heart in terms of myocardial dysfunction.

Patients with significant left ventricular dysfunction at baseline (the vast majority of ICD patients) appear to be most at risk for developing acute myocardial dysfunction following shock. Repetitive shocks are associated with recurrent hospitalizations, anxiety, depression, and even posttraumatic stress disorder. Whether appropriate or inappropriate, an ICD shock is associated with a 2- to 5-fold increase in mortality, with the most common cause being progressive HF.

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Despite this prognosis, current guidelines do not provide a clear stepwise approach to managing patients at high risk for recurrent shock. Appropriate diagnosis and treatment are critical. To approach these patients systematically, it is important to understand that in general, there are four causes of shock.

These can be summarized as follows:

  • Device malfunction: Device malfunction has many causes, but some of the most common include fractured leads, dislodged leads, loss of capture after ICD shock, and redundant loops of endocardial leads. Recognition and management of device malfunction is critical, as it results in completely unnecessary therapies being delivered to the patient.

    In addition to the discomfort the patient experiences, battery longevity is negatively affected. In general, management of this category of shock involves fixing the implanted system, either with device reprogramming or reoperation.

  • Electromagnetic interference: Electromagnetic interference (EMI) is fortunately fairly infrequent with bipolar leads, but still occurs. There are many causes of EMI, the most common of which include magnetic resonance imaging (MRI), large magnetic fields, and arc welding.

    Specific examples these authors have encountered include: Improper copper wiring in a shower, carrying stereo speakers, working on a running car engine, and lingering in a store’s surveillance gating. EMI is not an issue with microwave, airport security, televisions/household appliances, pagers, personal computers, or radios.

    To prevent shock from EMI often involves a certain amount of detective work. Once the cause of the EMI is identified, the patient must avoid the culprit, or in some cases, the device can be reprogrammed to prevent recognition of the EMI. It is our practice for example, to have our ICD patients come to clinic after being fitted with any form of implantable stimulator so that device-device interaction can be identified, and if possible programmed around.

  • Supraventricular arrhythmias: Although the vast majority of devices have algorithms to detect and differentiate ventricular arrhythmias (VT) from supraventricular arrhythmias (SVT), the detection algorithms are not perfect, and patients still receive shocks for non–life-threatening ventricular arrhythmias.

    Management of supraventricular arrhythmias for which the patients receive a shock includes traditional management of SVT, up to and including ablation. Modern ICDs all incorporate sophisticated tachycardia detection algorithms within their programming designed to minimize detection mistakes by the device. They are often not utilized to their full benefit. Thus, careful attention should be paid the programming of the device.

    Fine tuning of the detection and differentiation algorithms is critical, and best done by a practitioner who understands the subtle differences among the different manufacturers. Placing an atrial pacing lead and upgrading a single-chamber system to a dual-chamber system for improved SVT discrimination is sometimes necessary and points out the significance of carefully screening for any history of SVT prior to initial ICD implant.

  • Ventricular arrhythmias: These arrhythmias are what the device was designed for and implanted to detect and treat. Nevertheless, most VT does not need to be shocked. Careful attention to programming is critical. Detection intervals, monitored zones and pain-free therapies such as antitachycardia pacing (ATP) should be optimized. Receiving a shock for ventricular tachycardia or fibrillation is appropriate and can be lifesaving, but still carries significant distress and psychological impact for some patients.

Diagnostic Confirmation: Are you sure your patient had an real ICD Shock?

Initial evaluation

The initial evaluation of a patient who receives an ICD shock begins with interrogation of the device. The setting in which this takes place will depend largely upon the patient’s status when the shock was delivered. Phantom shocks are a very real occurrence.

If the patient received a single isolated shock without symptoms or change in clinical status, and he or she is enrolled in one of the device-specific monitoring services, this can be performed almost immediately by having the patient transmit a remote interrogation for review. If they are not, they should be seen in clinic as soon as possible (generally within a week).

This will clarify in most cases whether the shock was appropriate (VT/VF), or inappropriate (SVT, noise/artifact, device malfunction). Multiple ICD shocks or shocks accompanied by worsening HF symptoms, syncope, or angina warrant emergency medical attention as these are poor prognostic indicators of survival. Figure 1 provides a useful algorithm for initial evaluation and management of ICD shock in the heart failure patient.

A. History Part I: Pattern Recognition:

A patient who receives multiple shocks is not difficult to identify. They will present to an emergency department with the specific complaint that their defibrillator has fired several times. At that point in time, it is critical to define the etiology of the shocks (i.e., what is the ICD “seeing” that is triggering therapy). Perform initial evaluation as above. The device needs to be fully interrogated, with careful analysis of all of the stored EGMs recorded from the recent therapies.

B. History Part 2: Prevalence:

Implantable defibrillators are implanted for two broad reasons:

  • As primary prevention in those patients that we believe to be high risk for sudden cardiac death

  • As secondary prevention in those patients who have already survived sudden death or have had sustained monomorphic ventricular tachycardia

Twenty to thirty-five percent of HF patients who receive an ICD for primary prevention will experience an appropriate shock within 1 to 3 years of implant.

C. History Part 3: Competing diagnoses that can mimic ICD Shock.

Inappropriate shocks are therapies delivered for reasons other than a true malignant ventricular arrhythmia. Up to one third of patients will experience an inappropriate shock. Phantom shocks are also a very real occurrence in device patients. Common causes of inappropriate (non-VT/VF) shocks are listed below:

Common Causes of Inappropriate Shock

  • Supraventricular tachycardia with rapid ventricular response rate

  • Device oversensing:

    QRS and T-wave double counting

    Electromagnetic interference (EMI)

    Diaphragmatic sensing

  • Mechanical malfunctions

    Lead fracture

    Insulation break

    Lead dislodgement

D. Physical Examination Findings.

A thorough history and physical examination is essential in following ICD shock and device interrogation. The vast majority of ICD patients are heart failure patients with or without underlying ischemic heart disease and thus should be assessed for a change or progression in their disease state precipitating an arrhythmic episode.

Among heart failure patients, ICD shock is associated with a 2- to 5-fold increase in mortality, generally due to progressive heart failure. Conditions, such as COPD, dehydration, anemia, infection, and electrolyte imbalances may trigger ventricular and supraventricular tachycardia.

The patient should be questioned about positional muscle twitching suggesting possible lead malfunction. If present, or if nonphysiologic noise is seen on the interrogation strips, active manipulation of the arm and device pocket should be performed while recording a rhythm strip with device channel markers through the interrogation box to determine if it is reproducible.

E. What diagnostic tests should be performed?

The single most important diagnostic test is interrogation of the patient’s device. The information stored there documents the arrhythmia, or lack thereof, for which shock therapy was delivered. In the acute setting, a 12-Lead ECG should also be obtained to assess for possible underlying myocardial ischemia or Q–T prolongation.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

There are potentially reversible causes for appropriate and inappropriate ICD shocks, such as electrolyte and thyroid hormone level abnormalities, which should be checked and corrected if abnormal. More extensive laboratory evaluation may be warranted in the setting of accompanying angina or worsening heart failure.

Many of these patients are already on some form of antiarrhythmic drug therapy with all of their potential proarrhythmic effects. Drug toxicity (digoxin, sotalol, dofetilide, etc.) should be considered especially in the setting of progressive renal and hepatic disfunction or with the recent initiation of a new drug.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In the patient who has received an appropriate shock, echocardiographic evaluation of cardiac function is frequently done to assess the patient’s left ventricular ejection fraction. Depending on the patient’s symptoms and previous evaluation, an assessment of ischemic burden is also sometimes pursued.

Chest x-rays are frequently ordered to assess proper lead placement in the cardiac chambers. In patients with suspected lead malfunction, an overexposed chest radiograph may help identify the problem, such as lead damage (Figure 2), set screw issues (Figure 3), or lead dislodgement. These are often easily identified with standard posteroanterior and lateral chest films.

Figure 2.

Atrial and ventricular pacing lead fractures resulting in pectoralis muscle twitching.

Figure 3.

Loose set screw.

III. Management.

Strategies for reducing both appropriate and inappropriate ICD shocks include optimal device programming, drug therapy, catheter ablation of the offending arrhythmia and in cases of refractory VT, sympathetic denervation of the heart.

A. Immediate management.

In general, there are four reasons for a patient to receive an ICD shock:

Device malfunction

Electromagnetic interference

Supraventricular arrhythmias

Ventricular arrhythmias

The first three are considered as “inappropriate” in that device therapy was delivered for a non–life-saving reason. As previously stated, timely interrogation of the device is usually the quickest and most effective way to determine the cause upon presentation.

Whether appropriate or not, repetitive shocks are a medical emergency. Whether a programmer is available or not, in this situation it is important to monitor the patient on telemetry and obtain a standard 12-Lead surface ECG for arrhythmia diagnosis and monitoring.

If device malfunction is suspected, therapy (antitachycardia pacing and shock) can be immediately suspended by placing a magnet over the ICD can. Unlike a pacemaker, this will not alter the device’s pacing capabilities.

Should a true ventricular arrhythmia subsequently declare itself, removing the magnet will immediately reactivate all device therapies. Subsequent treatment will depend on the determined underlying cause.

B. Long-term management.

Managing appropriate ICD shocks for ventricular arrhythmias

Strategies for reducing appropriate ICD shocks include optimal device programming; drug therapy; VT catheter ablation; and in cases of refractory VT, sympathetic denervation of the heart. Key published trials supporting each of the management strategies discussed are denoted in the text.

Antitachycardia pacing (ATP) to reduce ICD Shocks

Delivering a sequence of ventricular paced beats at prespecified coupling intervals slightly faster than the ventricular tachycardia (VT) cycle length has been proven to be a highly effective means of reducing appropriate ICD shock therapy. This comes at no increased risk to the patient in terms of higher mortality or incidence of syncope.

There is in fact a demonstrated survival benefit to ATP over shock therapy for VT termination. ATP terminates reentrant forms of VT by colliding with the leading edge of the VT wave front and reducing the excitable gap of ventricular myocardium in the VT circuit rendering the tissue refractory when the orthodromic wave front returns.

It has proven to be highly effective in termination of both slow VT as well as fast VT, which is generally considered to be VT at cycle lengths between 240 and 320 ms (188 to 250 bpm). ATP rarely accelerates even fast VT. It has not been shown to increase the likelihood of syncope, significantly prolong episode duration, or reduce the effectiveness of subsequent shock therapy should it fail (PainFREE 1 and 2).

Although there may be some instances when patient-specific programming is required by the nature of the patient’s arrhythmia, prospective randomized trials (Comparison of Empiric to Physician-Tailored Programming of Implantable Cardioverter-Defibrillators [EMPIRIC], Primary Prevention Parameters Evaluation [PREPARE]) have shown that customized programming of the ICD by the physician is not more effective than a standardized empiric therapy algorithm incorporating ATP with longer VT detection intervals.

There does not appear to be any clear advantage of shorter, more tightly coupled burst sequences or longer burst sequences over what is considered to be conventional burst pacing (eight pulses at 88% of VT cycle length). Ramp pacing has been found to be inferior to burst pacing for termination of fast VT, with a higher propensity to accelerate the VT.

There are some forms of VT which may not benefit from ATP programming, including non–reentrant ventricular arrhythmias, such as those associated with catecholaminergic VT, hypertrophic cardiomyopathy, long Q–T, and Brugada syndrome. Generally these patients come with their diagnosis before the time of ICD implantation, allowing for the programing of shorter detection windows and minimization of ATP prior to shock delivery.

Increasing detection intervals to reduce ICD Shocks

Patients randomized to ICD therapy in the early primary and secondary prevention ICD trials were found to have substantially higher rates of appropriate ICD shocks when compared to the rate of sudden cardiac death experienced by patients randomized to medical therapy. This suggests ICD recipients are receiving unnecessary device therapy for runs of what would otherwise be nonsustained VT.

Extending the number of intervals to detect (NID) prior to device therapy has proven to be highly effective in reducing the number of unnecessary ICD shocks (EMPERIC, PainFREE 1 and 2, PREPARE). The Role of Long Detection Window Programming in Patients with left Ventricular Dysfunction, Nonischemic Etiology in Primary Prevention Treated with a Biventricular ICD (RELEVANT) trial observed that 91% of VT episodes in the longest NID cohort (30 out of 40) self-terminated in the interval between 13 and 29 beats, avoiding the need for ultimately unnecessary device intervention.

In summary, extending the NID from 12 out of 16 to 18 out of 24 and even further out to 30 out of 40 intervals has been shown to substantially reduce the number of aborted capacitor charges and unnecessary shocks without an associated increase in syncope or mortality by both prospective and retrospective analysis of multiple ICD trials.

Increasing the NID is a proven effective and safe means of reducing unnecessary shock therapy in most ICD patients with the added benefit of potentially prolonging ICD battery life. It may not be ideal programming in patients with a history of rapid loss of consciousness associated with their ventricular arrhythmia or in patients with poor R wave sensing or observed R wave dropout during VT/VF, which could result in potential ventricular arrhythmia under sensing with delay of therapy.

Consider upgrade to biventricular ICD in patients who meet CRT implantation criteria

There is growing evidence that biventricular pacing in heart failure patients reduces the incidence of ventricular arrhythmias, although the effect is usually not seen immediately but rather over a prolonged period of CRT therapy suggesting that myocardial remodeling is the beneficial effect. In the Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy (MADIT CRT), high responders to CRT therapy (≥25% reduction in LVESV at 12 months) experienced a 55% reduction in risk for ventricular arrhythmia over a mean follow-up of 2.4 years.

Biventricular burst pacing has been shown to be more effective in terminating slow and fast VT than RV burst pacing in ischemic heart failure patients. However, we would be remiss in noting that biventricular pacing has also been demonstrated to be clearly proarrhythmic in a small minority of patients due to adverse changes in the sequence of ventricular depolarization, which cannot be predicted prior to LV lead placement.

Nondevice therapy to reduce ICD Shock

When programming strategies are ineffective in preventing appropriate ICD shocks, pharmacologic, catheter-based ablative therapies, and possibly cardiac sympathectomy should be considered.

Antiarrhythmic drug therapy for new-onset ventricular arrhythmias (VT/VF) in ICD patients

Review of long-term data from the original ICD trials shows that nearly 20% of these patients ultimately require some form of adjunctive therapy to prevent recurrent ventricular arrhythmias that necessitate an ICD shock to terminate. In most circumstances, this will result in at least an initial trial of antiarrhythmic drug therapy (ADD) with progression to alternative treatment modalities should drug therapy prove ineffective.

Drug therapy is often effective in reducing the incidence of ventricular and supraventricular arrhythmia and thus does play a potential role in the management of patients receiving both appropriate and inappropriate shocks. Beta-blockers have time and again been proven to reduce the risk of ventricular arrhythmias and are a mainstay in the treatment or VT storm. Uptitration of a beta-blocker should be considered if tolerated.

The class III antiarrhythmics sotalol and amiodarone are the most commonly used antiarrhythmics employed to suppress recurrent ventricular arrhythmias resulting in device shock. Sotalol has been shown to be a safe and effective drug for the suppression of VT with the added benefit of not slowing the VT CL below the programmed detection rate. The risk for torsades de pointes limits its use in the presence of baseline Q–T interval prolongation and renal impairment.

Amiodarone when used in combination with a beta-blocker has been shown to be highly efficacious for the prevention of both appropriate and inappropriate ICD shocks, as well as VT storm.

It can slow the ventricular arrhythmia cycle length (CL) and raise defibrillation thresholds (DFT) and thus non-invasive programmed stimulation (NIPS) and DFT testing through the ICD after initiation of amiodarone is recommended. It has significant side effects that need to be regularly monitored so long as the patient is maintained on the therapy.

Mexiletine is not infrequently used for the suppression of recurrent ventricular arrhythmia, generally being added to ongoing amiodarone therapy for additional arrhythmia suppression. It is a class IIb antiarrhythmic with considerable GI side effects and also raises the DFT threshold. Dofetilide, a newer class III antiarrhythmic has been recently reported to be effective in suppressing VT in ICD patients.

Class I AAD therapy is generally not felt to be safe or effective in the treatment of ventricular arrhythmia in patients with recurrent VT/VT storm. A notable exception is the use of quinidine to suppress VF in patients with Brugada syndrome. It has been successfully used to suppress electrical storm in ICD patients with Brugada syndrome.

Ranolazine is a drug with antianginal and antiischemic effects, which has also been shown in case series to be effective in reducing VT burden and ICD shocks in ischemic patients with drug-refractory VT, usually when used in combination with another class III drug, although it does not have FDA approval for this use.

Beta-blockers have not been formally studied for the treatment of ventricular arrhythmia in ICD patients however, they play an essential role in suppressing VT storm in patients with congenital long-QT syndrome and catecholaminergic polymorphic VT.

Omega-3 polyunsaturated fatty acids, statin therapy, and ACEI have also been reported to be of benefit in decreasing ICD shocks and certainly should be incorporated in any treatment strategy especially if there is another clear indication for their use in managing the patient’s underlying disease process.

Treatment of refractory ventricular arrhythmias
  • Catheter ablation of ventricular Arrhythmia

Catheter ablation is an effective first-line and adjunctive therapy for ventricular arrhythmia suppression and the prevention of recurrent ICD shocks. Most electrophysiologists use catheter ablation as “the next step” for patients with recurrent ventricular arrhythmias after inadequate suppression on antiarrhythmic drug therapy (secondary VT ablation).

Clinical trials directly comparing the strategy of first-line catheter ablation therapy vs. AAD therapy for the treatment of recurrent VT are currently ongoing. The incidence of VT storm in primary prevention ICD recipients is 4% and approaches 20% in patients receiving ICDs for secondary prevention.

Several small ablation trails have evaluated the strategy of performing VT substrate ablation prior to ICD implantation to prevent potential future VT storm and shocks. Early evidence does not demonstrate improved long-term survival with this approach over secondary ablation of refractory VT following AAD failure.

Catheter Ablation of VF Storms

Polymorphic VT and VF present as arrhythmia storm in approximately 20% of patients with ICDs. Polymorphic VT/VF is often triggered by focal ventricular ectopy often from the distal left-sided cardiac conduction system (Purkinje system) or from myocardial triggers elsewhere. Targeting these “triggers” of VF has been successfully used as a bailout procedure in patients with structural heart disease ,as well as in those with primary cardiac electrical disorders (Brugada, long Q–T, idiopathic VF).

Neuraxial Modulation for Refractory Ventricular Arrhythmias

Neuraxial modulation of the heart’s autonomic innervation has been extensively described in the pediatric literature for the treatment of adrenergically driven arrhythmias in structurally normal hearts (Long QT, catecholaminergic polymorphic VT). Growing clinical evidence shows that surgical left cardiac sympathetic denervation (LCSD) or emergent temporary thoracic epidural anesthesia (TEA) to achieve the immediate same effect can also be highly effective tools in suppressing refractory ventricular arrhythmias/VT storm in patients with structural heart disease.

The antiarrhythmic mechanism of this strategy is achieved by modulating the neuraxial efferent input to the heart thus lengthening the repolarization time and refractoriness of the sympathetically denervated myocardium. The effect is to potentially reduce automatic ventricular ectopic triggers of VT and lengthening or extinguishing reentrant VT cycle lengths by reducing the excitable gap.

Both techniques have been successfully used in patients with structural heart disease for the suppression of drug refractory VT. This technique may best be used as a temporizing measure to bridge these patients to more definitive therapies such catheter ablation, cardiac surgery, or transplantation.

Managing inappropriate shocks


The most common cause of an inappropriate ICD shock is atrial fibrillation (AF) or SVT with rapid ventricular conduction because initial device detection of VT or ventricular fibrillation (VF) is based predominantly on ventricular rate. Algorithms which use morphology, stability, and onset characteristics of the tachycardia are incorporated in most modern ICD detection platforms to reduce the incidence of inappropriate therapy.

However, these algorithms are often not turned-on, and are often limited by a “time-out” function that overrides the SVT discriminators in cases of prolonged SVT with rapid ventricular response (RVR). Pharmacologic therapy in the form of AV nodal blocking agents (calcium channel blockers, beta-blockers, digoxin) often in combination with antiarrhythmic drug therapy to provide rate control, as well as arrhythmia suppression.

Appropriate initial device selection at implantation (single chamber vs. dual chamber) is key to avoiding this problem in patients with a known history of SVT. SVT ablation, device upgrade ,and in certain situations AV node ablation are required to definitively manage this problem.

Inappropriate sensing

Oversensing occurs when the device detects more ventricular activity than is actually present. This can be caused by both intracardiac and extracardiac sources of electrical potential such as T wave oversensing, QRS complex double counting, oversensing of diaphragmatic myopotentials (more common in older integrated bipolar RV defibrillation leads).

This problem can usually be corrected by decreasing the sensitivity level of the affected lead so that only ventricular activity is sensed or prolonging the programmed refractory periods to avoid sensing and counting large T waves as QRS complexes. When reprogramming cannot achieve adequate noise reduction without compromising arrhythmia detection, new lead placement may be required.

Extracardiac sensing is usually a result of external electromagnetic interference (EMI) or lead malfunction, including fracture, dislodgement, or insulation break. Device interrogation in this situation will usually demonstrate a change in lead impedance, a failure to sense or capture appropriately, and nonphysiologic (too short) R-R intervals.

These findings can often be provoked by pocket and or limb manipulation while performing the interrogation. For electromagnetic interference (EMI), a thorough history of time, place, and activity around the time of shock is usually revealing. Device reprogramming is sometimes successful in eradicating the noise the device is acting upon; however, the patient should be educated on the need to avoid the offending source of EMI (listed above) in the future.

Device malfunction/safety alerts

With lead malfunction, tachyarrhythmia detection must be turned off to avoid inappropriate shock and the lead revised. Device safety alerts are unfortunately a reality and are more common with ICDs than pacemakers. Prophylactic removal or replacement of a generator or lead on alert is generally not recommended unless the patient is pacer dependent.

All device manufactures with products on alert have published management guidelines to physicians, which should be updated as new data is collected. The response to a safety alert must be individualized to each patient and balance the patient’s risk of death from malfunction vs. the likelihood of malfunction and the known risk associated with going back in the pocket in terms of infection, perforation, bleeding, etc.

IV. Management with Co-Morbidities

Identifying and addressing the significant detrimental effects of ICD shock

The ICD has proven to be an effective last line of defense for the prevention of SCD in patients at highest-risk for arrhythmic death whether implanted for primary or secondary indications. A discharge from the device, appropriate or not, can come at considerable cost to the patient beyond the acute physical pain.

Outcome data from the original device trials clearly demonstrates an increase in patient morbidity and mortality following both appropriate and inappropriate ICD shock. One of the intangible benefits of ICD implantation should be to provide the patient with a sense of security knowing that they are “protected” at all times.

For many, this provides the confidence to participate in an active life. Perhaps most devastating to a postshock “survivor” is a well-documented reduction in quality of life resulting from the loss of this sense of security, which has now been supplanted by a constant, sometimes crippling fear of the “next” unexpected shock.

Adjustment reactions to ICD shock. Electric shock is a feature specific to ICD technology that provides patients with a unique, aversive stimulus that may challenge psychosocial adjustment. Shock seems to be the most distressing aspect of the ICD, notable for its deleterious effects on quality of life, and for depression, and anxiety.

Patients generally rate the pain of shock as a “6” on a 0 to 10 pain scale and report that it feels like receiving a rapid punch or a swift kick in the chest from the inside-out. A closer examination of anxiety in ICD patients further clarifies the need for a conceptualization of device-specific anxiety that is distinctly related to ICD shock, as opposed to more generalized or trait anxiety.

Shock anxiety is the fear or anticipation of ICD shock that often results in increased heart-focused anxiety symptoms and hypervigilance to physical cues. Shock anxiety may be experienced in isolation or within the context of a psychological disorder, thereby exacerbating symptoms.

Shock anxiety may be present in patients who have been shocked, as they have likely experienced a fearful reaction to the device discharge, thereby increasing their anxiety about future shocks. However, shock need not be a precursor to shock anxiety. Patients who have never had a shock may be prone to overestimate the pain and negativity of the stimulus, thereby exacerbating shock anxiety beyond that of patients who have actually experienced a shock.

Shock anxiety may also be responsible for the development and maintenance of avoidance behaviors to minimize patients’ perceived risk of triggering a shock. Research has shown that approximately 55% of ICD patients engaged in regular avoidance of places, people, and activities in a perceived effort to prevent shock.

Some patients may avoid physically strenuous activities that could cause increased heart rate. Others may distance themselves from people and places due to anticipated fear of embarrassment or helplessness should a shock occur. Regardless, these reasons are often inhibiting in that they prevent the patient from reengaging in activities associated with physical, social, and psychological health.

Shock anxiety can be assessed via a short questionnaire, the Florida Shock Anxiety Survey (FSAS). The FSAS contains 10 items that have shown a two-factor structure, including a Consequence Factor (e.g., fear of creating a “scene” if the device were to fire) and a Trigger Factor (e.g., fearing physical or sexual activity).

Higher scores on the FSAS reflect patient anxieties about the ability to cope with the impact of shock, rather than confidence in the device. When used in both clinical and research settings, this questionnaire may be useful for identifying patients who may be experiencing shock anxiety and benefit from additional psychosocial care and education.

What's the Evidence for specific management and treatment recommendations?

Larsen, G, Evans, J, Lambert, W. “Shocks burden and increased mortality in implantable cardioverter-defibrillator patients”. Heart Rhythm. vol. 8. 2011. pp. 1881-6. (Excellent study shedding light on the likely detrimental effects of shocks on patient mortality not seen with appropriate ATP therapy and after correcting for baseline markers of disease.)

Mishkin, JD, Saxonhouse, SJ, Woo, GW. “Appropriate evaluation and treatment of heart failure patients after implantable cardioverter-defibrillator discharge”. JACC. vol. 54. 2009. pp. 1993-2000. (Excellent review of the morbidity and mortality implications of ICD shocks in the heart failure patient population with advice on how to evaluate and manage these very sick patients.)

Bourke, T, Vaseghi, M, Michowitz, Y. “Neuraxial modulation for refractory ventricular arrhythmias: value of thoracic epidural anesthesia and surgical left cardiac sympathetic denervation”. Circulation. vol. 121. 2010. pp. 2255-62. (Physicians managing ICD patients should keep this option in mind when all else has failed.)

Carbucicchio, C, Santamaria, M, Trevisi, N. “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. vol. 117. 2008. pp. 462-9. (Demonstrates the effectiveness of this treatment option in the management of refractory VT and raises the question as to whether this procedure should be done sooner rather than later in managing ICD patients with a history of appropriate shock.)

Gard, J, Friedman, P. “Strategies to reduce ICD shocks: the role of supraventricular tachycardia-ventricular tachycardia discriminators”. Card Electrophysiol Clin. vol. 3. 2011. pp. 373-87. (Very thorough overview of specific device programming options available to reduce ICD shocks.)

Sears, S, Todaro, J, Lewis, T. “Examining the psychosocial impact of implantable cardioverter defibrillators: a literature review”. Clin Cardiol. vol. 22. 1999. pp. 481-9. (Insight into the heavy psychological and social cost to the patient as a result of ICD shocks.)

Wathen, MS, Sweeney, MO. ” Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease”. Circulation. vol. 104. 2001. pp. 796-801.

Wathen, MS, DeGroot, PJ. ” Prospective randomized multicenter trial of empirical antitachycardia pacing versus shocks for spontaneous rapid ventricular tachycardia in patients with implantable cardioverter-defibrillators: Pacing Fast Ventricular Tachycardia Reduces Shock Therapies (PainFREE Rx II) trial results”. Circulation. vol. 110. 2004. pp. 2590-6.

Wilkoff, BL, Ousdigian, KT. “A comparison of empiric to physician-tailored programming of implantable cardioverter-defibrillators: results from the prospective randomized multicenter EMPERIC trial”. J Am Coll Cardiol. vol. 48. 2006. pp. 330-9.

Wilkoff, B, Williamson, B, Stern, R. “Strategic programming of detection and therapy parameters in implantable cardioverter-defibrillators reduces shocks in primary prevention patients: results from the PREPARE (Primary Prevention Parameters Evaluation) Study”. JACC. vol. 52. 2008. pp. 541-50.