Advanced ICD Troubleshooting: Part II - PacerICD.compacericd.com/documents/ARTICLES/Advanced ICD Troubleshooting P… · Advanced ICD Troubleshooting: Part II ... In this case, stability

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REVIEW

Advanced ICD Troubleshooting: Part IICHARLES D. SWERDLOW* and PAUL A. FRIEDMAN†From the *Cedars-Sinai Medical Center, Los Angeles, California, and †Mayo Clinic, Rochester, Minnesota, USA

Failure to Deliver Therapy or Delay of TherapyAbsent or delayed therapy may be caused

by programmed values (including human error),ICD system performance, or a combination of thetwo. The most common causes are ICD inactiva-tion, VT slower than the programmed detection in-terval, SVT-VT discriminators, undersensing, andintradevice software interactions. Pacemaker-ICDinteractions, once important, are now rare due toincorporation of dual- and triple-chamber pace-makers in ICDs.

ICD InactivationIf detection is programmed OFF for surgery

using electrocautery, reprogramming must be per-formed at the end of the procedure, a fact easily for-gotten, especially in outpatient surgery. One studyreported an unexplained 11% annual incidenceof transient suspension of detection.1 MedtronicICDs sound an audible Patient AlertTM 6 hours af-ter the ICD is programmed “off” to alert the patientto the possibility of inadvertent.2

VT Slower Than the Programmed DetectionInterval

In most ICD patients, VT with cycle lengths>400–450 ms are tolerated well, while repeatedinappropriate therapies are not. However, slow VTmay be catastrophic in patients with severe LV dys-function or ischemia.2 All SVT-VT discriminationalgorithms (except ELAs)3–5 deliver less inappro-priate therapies if the VT detection interval is pro-grammed to a shorter cycle length so that fewerSVTs are evaluated. To prevent underdetectionof irregular VT, the VT detection interval shouldbe set at least 40–50 ms longer than the slow-est predicted VT for consecutive-interval count-ing and 30–40 ms longer for X-of-Y or interval +interval-average counting.5 It should be a longercycle length if rapidly conducted SVT is unlikelyor SVT-VT discrimination is reliable at long cyclelengths (ELA ICDs). A long VT detection interval isimportant in patients with advanced heart failure,

Address for reprints: Charles D. Swerdlow, M.D., 8635 W. ThirdStreet, Ste 1190 W, Los Angeles, CA 90048. Fax: (310) 659-8387;e-mail: [email protected]

Received February 15, 2005; revised June 1, 2005; acceptedJune 6, 2005.

in whom slow VT may be catastrophic2 (see figure8 in Part I of this review). The VT detection intervalshould be increased if antiarrhythmic drug ther-apy is initiated, particularly with amiodarone or asodium-channel blocking (Type 1) drug.6,7 It maybe prudent to measure the cycle length of inducedVT at electrophysiological testing after initiationof drug therapy.6 However, spontaneous VT oftenis slower than induced VT.8

SVT-VT DiscriminatorsSVT-VT discriminators may prevent or delay

therapy if they misclassify VT or VF as SVT.9–12

Discriminators that reevaluate the rhythm diagno-sis during an ongoing tachycardia, such as stabilityand most dual-chamber algorithms, reduce the riskof underdetection of VT compared with discrimi-nators that withhold therapy if the rhythm is notclassified correctly by the initial evaluation, suchas onset or chamber of origin. The minimum cyclelength for SVT-VT discrimination should be set toprevent clinically significant delay in detection ofhemodynamically unstable VT.

Single-Chamber Discriminators

Although spontaneous VT often begins withirregular R-R intervals, stability algorithms clas-sify it as VT as soon as R-R intervals regularize,even transiently. Thus, they rarely prevent detec-tion of VT (∼0.5%) if they are programmed to nom-inal settings and the patient is not receiving anantiarrhythmic drug that decreases cycle lengthregularity in VT9,13 (see “Antiarrhythmic Drugs”).Previously, we noted that single-chamber stabilitymay be programmed in Medtronic dual-chamberICDs to reject atrial fibrillation during redetection.In this case, stability is applied before the dual-chamber algorithm. Because stability responds toirregular rhythms by resetting the VT counter tozero, the dual-chamber algorithm does not eval-uate rhythms rejected by stability. Thus, stabilitymay delay detection of VT even if the ventricularrate is greater than the atrial rate.

Morphology discriminators also reevaluaterhythm diagnosis during ongoing tachycardias.But if they misclassify monomorphic VT initially,the error usually persists and prevents detectionfor the duration of the tachycardia. The St. Judemorphology algorithm, which analyzes only therate-sensing electrode, continuously misclassifies

C©2006, The Authors. Journal compilation C©2006, Blackwell Publishing, Inc.

70 January 2006 PACE, Vol. 29

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ADVANCED ICD TROUBLESHOOTING

5–10% of monomorphic VTs as SVT. But, whenit is restricted to tachycardias with ventricularrate ≤ atrial rate in dual-chamber ICDs, only 2%of VTs are misclassified.11 The Medtronic mor-phology algorithm, which usually analyzes high-voltage electrograms, misclassifies 1–2% of VTs asSVTs.14 In contrast, the onset discriminator uni-formly misclassifies VT if it either accelerates grad-ually across the sinus-VT zone boundary or occursduring SVT with cycle length in the VT zone.

Dual-Chamber Discriminators

If the atrial lead dislodges to the ventricle, theatrial channel records a ventricular electrogram.Any VT will appear to the ICD as a tachycardiawith 1:1 AV relationship and nearly simultaneousatrial and ventricular activation. Some discrimina-tors designed to withhold therapy from SVT with1:1 AV conduction may then withhold appropri-ate VT therapy. These include the Medtronic 1:1SVT rule and the St. Jude Rate Branch Algorithmwithout additional discriminators, which shouldnot be programmed until the atrial lead is stable.

VT with 1:1 VA conduction is a difficult diag-nosis for dual-chamber algorithms. Guidant’s olderAtrial ViewTM misclassifies it as SVT unless the on-set of VT is abrupt. Medtronic’s PR LogicTM mis-classifies it as SVT in the rare cases in which theVA interval is both long and constant. Guidant’sRhythm IDTM and St. Jude’s BranchTM misclassifyit if a morphology match occurs.11,15

Duration-Based “Safety-Net” Features to OverrideDiscriminators

These programmable features deliver therapyif an arrhythmia satisfies the ventricular rate cri-terion for a sufficiently long duration even ifdiscriminators indicate SVT (Guidant Sustained-Duration OverrideTM (SRD), Medtronic High RateTimeoutTM, and St. Jude Maximum Time toDiagnosisTM (MTD)). The premise is that VT willcontinue to satisfy the rate criterion for the pro-grammed duration while the ventricular rate dur-ing transient sinus tachycardia or atrial fibrillationwill decrease below the VT rate boundary. The lim-itation is delivery of inappropriate therapy whenSVT exceeds the programmed duration, which oc-curs in ∼10% of SVTs at 1 minute and 3% of SVTsat 3 minutes.12,14 The decision to use a discrimi-nator override should be based on clinical factorsincluding the probability that discriminators willprevent detection of VT, the likely consequences offailure to detect VT, and the likelihood of sustainedSVT in the VT rate zone. For example, override fea-tures should be considered whenever a morphol-ogy algorithm is programmed without inducing VTat electrophysiologic study. The programmed du-ration in Guidant Atrial ViewTM and St. Jude algo-

rithms should be increased from the nominal valueof 30 seconds to reduce inappropriate therapies. Inmost patients, a duration of 2–5 minutes is reason-able.

UndersensingVF may be undersensed due to combinations

of programming (sensitivity, rate, or duration),low-amplitude electrograms, rapidly varying elec-trogram amplitude, drug effects, or post-shock tis-sue changes. Clinically significant undersensing ofVF is rare in modern ICD systems if the baseline R-wave amplitude is ≥5–7 mV.16 Post-shock under-sensing was an important clinical problem in olderICD systems using integrated-bipolar leads withclosely spaced electrodes.17 Currently, the mostcommon causes of VF undersensing are drug or hy-perkalemic effects that slow VF into the VT zone,ischemia, and rapidly varying electrogram ampli-tude.4,18 ICDs that adjust dynamic range based onthe amplitude of the sensed R-wave (Guidant) maybe most vulnerable to the latter, extremely rareproblem.18 Prolonged ischemia from sustained VTslower than the VT detection interval may causedeterioration of signal quality, resulting in under-sensing of VF. Lead, connector, or generator prob-lems may also present as undersensing.

Pacemaker-ICD InteractionsInteractions between ICDs and separate pace-

makers have become rare since ICDs incorpo-rated dual-chamber bradycardia pacing in the late1990s. Nevertheless, a few combined systems havenot been revised due to vascular access problemsor other reasons. The multiple potential interac-tions have been reviewed and testing protocols todetect them have been developed.19–21 The princi-pal interaction that may delay or prevent ICD ther-apy is oversensing of high-amplitude pacemakerstimulus artifacts. If this occurs during VF, repet-itive automatic adjustment of sensing thresholdand/or gain may prevent detection of VF.

Intradevice InteractionsToday, “intradevice interactions”—in which

bradycardia pacing features of dual-chamber ICDsinteract with and impair detection of VT or VF—pose a greater challenge than pacemaker-ICD inter-actions.22 During high-rate, atrial or dual-chamberpacing, sensing may be restricted to short periodsof the cardiac cycle because of the combined ef-fects of ventricular blanking after ventricular pac-ing and cross-chamber ventricular blanking afteratrial pacing, which is needed to avoid cross talk. Ifa sufficient fraction of the cardiac cycle is blanked,systematic undersensing of VT or VF may occur.When pacing and blanking events occur at in-tervals that are multiples of a VT cycle length,

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SWERDLOW AND FRIEDMAN

Figure 1. Failure to detect VT due to an intradevice interaction. The rate-smoothing algorithm in-troduced atrial and ventricular pacing complexes with associated blanking periods that preventeddetection of VT during post-implant testing. An external rescue shock was required. Shown fromtop to bottom are surface ECG, atrial electrogram, ventricular electrogram, and event markers.At top VT is induced by programmed electrical stimulation with drive cycle length 350 ms andpremature stimuli at 270, 250, and 230 ms (intervals labeled next to event markers). The firstsensed ventricular event occurs 448 ms after the pacing drive (“PVC 448”). The rate smoothingalgorithm drives pacing to prevent a pause after the “premature ventricular complex” (PVC),labeled AP↓1638. A ventricular-paced event does not follow the first AP↓ because a ventricularevent is sensed (VT 415). Subsequent rate smoothing generated atrial and ventricular pacingpulses (indicated by AP↓ and VP↓ markers, respectively). The resultant post-pacing blankingperiods are shown in the figure as horizontal bars. PAB denotes cross-chamber (post-atrial-pace)ventricular blanking period. VBP denotes same-chamber (post-ventricular-pace) blanking period.Together, they prevent approximately 4 of every 6 VT complexes from being sensed. Since the VTcounter must accumulate 8 out of 10 consecutive complexes in the VT zone for detection of VTto occur, VT is not detected.

ventricular complexes are repeatedly under-sensed, delaying or preventing detection (seeFig. 1).22–24

Although uncommon, intradevice interac-tions have been reported most frequently with theuse of the Rate SmoothingTM algorithm in GuidantICDs.22–24 This algorithm is intended to preventVT/VF initiated by sudden changes in ventricularrate.25 It prevents sudden changes in ventricularrate by pacing both the atrium and ventricle at in-tervals based on the preceding (baseline) R-R inter-val. As an unintended consequence, it may preventsensing of VT/VF in some patients because it intro-duces repetitive post-pace blanking periods. Thealgorithm applies rate-smoothing to baseline inter-vals independent of their cycle length, includingintervals in the VT or VF zones. Intradevice inter-actions that result in delayed or absent detectionof VT/VF are most common and most danger-ous when VT is fast. The parameter interrelation-ships that result in delayed or absent detection of

VT/VF are complex and difficult to predict, butthey usually elicit a programmer warning. Gen-erally, aggressive rate-smoothing (a small allow-able percentage change in R-R intervals), a highupper pacing rate, a long and fixed AV intervalfavor undersensing and should be avoided. If rate-smoothing is required, parameter settings that re-sult in warnings should be avoided by program-ming a dynamic AV delay, limiting the upper rateto less than 125 beats/min, and shortening ventric-ular blanking after atrial-paced events to maximizethe sensing window for VT/VF. This programmingreduces, but does not eliminate, the risk of under-sensing.22–24,26

Unsuccessful TherapyBecause defibrillation success is probabilistic,

occasional shocks fail, but failure of more than twomaximum-output shocks is rare if the safety mar-gin is adequate.27 If an ICD classifies a shock as un-successful, stored electrograms must be reviewed


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to determine both if the shock was delivered fortrue VT/VF and if the shock actually failed to ter-minate VT/VF. Shocks from chronic ICD systemsthat defibrillated reliably at implant may fail to ter-minate true VT or VF because of patient-related orICD system-related reasons. The problem of high-implant DFTs has been reviewed.3,4 In chronicallyimplanted systems, most patient-related causes ofunsuccessful shocks can be reversed, but mostsystem-related causes require operative interven-tion.

Misclassified TherapyICDs misclassify effective therapy as ineffec-

tive if VT/VF recurs before the ICD determines theVT/VF episode as terminated and reclassifies thepost-therapy rhythm as sinus. Decreasing the du-ration for redetection of sinus rhythm (St. Jude)might correct this classification error. However,this type of misclassification usually does not con-stitute a clinical problem, while post-shock detec-tion of nonsustained VT does. An exception oc-curs when one iteration of antitachycardia pacingis programmed for the first therapy and a shock forthe second. If antitachycardia pacing terminatesVT, but it recurs before the rhythm is classified assinus, the recurrent VT will receive a shock in-stead of potentially effective antitachycardia pac-ing. Programming multiple iterations of antitachy-cardia pacing can mitigate this problem. However,the “Smart Mode” in Medtronic ICDs (nominally“on”) disables antitachycardia pacing if it is classi-fied as unsuccessful on four consecutive episodes.Thus, if successful antitachycardia pacing is mis-classified repeatedly, Smart Mode will disable it.In this setting, Smart Mode should be programmedoff.

ICDs may also misclassify shocks as ineffec-tive if the post-shock rhythm is SVT in the VTrate zone (catecholamine-induced sinus tachycar-dia or shock-induced atrial fibrillation). Solutionsinclude applying SVT-VT discriminators to rede-tection of VT, increasing shock strength to preventshock-induced atrial fibrillation, or administeringβ-blockers to slow post-shock SVT.

Patient-Related FactorsFactors that raise DFTs reversibly at the cel-

lular level include hyperkalemia, antiarrhythmicdrugs, and ischemia. Pleural or pericardial effu-sions raise the DFT by forming parallel intratho-racic current paths that shunt current away fromthe heart. Progressive cardiac enlargement or newmyocardial infarction may also raise the DFT andare less easily reversed. Usually, defibrillation test-ing should be performed to confirm reliable de-fibrillation after the suspected cause has been re-versed.

A few patient-related causes that would oth-erwise require operative revision may be resolvedby programming shock pathway and waveformparameters. For ICDs with fixed-tilt waveforms,waveform duration depends on output capaci-tance and pathway resistance.28 ICDs with pro-grammable waveform duration or tilt (St. Jude)permit optimization of waveform parameters in-dependent of pathway resistance. Shortening theentire waveform might reduce DFT.29 Shorteningphase-two might reduce DFT after amiodaronetherapy is started.30 Migration of an active-canpulse generator low on the chest wall can increaseDFT by altering the shock vector. This may be re-solved by excluding the pulse generator from theshock circuit, which may be done noninvasivelyin Medtronic ICDs.

ICD System-Related ReasonsICD-related causes include insufficient pro-

grammed shock strength, battery depletion, gen-erator component failure, lead failure, device-lead connection failures, and lead dislodgment.In evaluating data from the ICD interrogation,attention should be paid to arrhythmia dura-tion, electrograms from the shocking electrodes,charge time, battery voltage, the relationship be-tween programmed and delivered shock strength,impedance of the high-voltage lead at the time ofshock, and trend plots of lead impedance. Pro-longed episodes may increase the shock strengthrequired to convert VT or VF. They may becaused by delayed detection and/or prolongedcharge times. Programmer software identifies somesystem-related problems and displays messages toalert the clinician.

Problems Identified at Routine Follow-UpBattery DepletionBattery Discharge Curves—Relationship toElective-Replacement and End-of-Service Indicators

ICDs use batteries composed of lithium an-odes and silver vanadium oxide (Ag2V4O11) cath-odes31 in which reduction at the cathode occurs inmultiple steps. The corresponding discharge char-acteristics and battery behavior during capacitorcharging have been a source of confusion amongclinicians familiar with the slow, constant voltagedecline typical of lithium-iodine pacemaker bat-teries. Initially, the cathodal contribution to bat-tery voltage is due to two simultaneous reactionscorresponding to reduction of V+5 (V+5 + e− →V+4) and Ag+1 (Ag+1 + e− → Ag+0). Unloaded cellvoltage falls from about 3.2 to 3.1 V at about 30%battery depletion. In most ICD batteries, voltagethen falls rapidly to about 2.6 V, where it reaches aplateau until the battery is 80–90% depleted. This


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voltage decrease is caused by a combination of fac-tors, including build-up of inert material at thecathode and depletion of the V+5 valence state ofvanadium so that the cathodal half-cell voltage re-flects reduction of V+4 (V+4 + e− → V+3). The 2.6-Vplateau is nominal performance for most (but notall) ICD batteries. End-of-service indicators corre-spond to either an unequivocal reduction in un-loaded voltage about 0.1 V below this plateau oran excessive increase in charge time.

Premature Battery Depletion

The most common cause is excessive exter-nal power drain due to pacing or capacitor charg-ing. Pacing problems include unnecessary ventric-ular pacing, high pacing outputs, and lead insula-tion failures. The most common cause of asymp-tomatic premature battery depletion related to ca-pacitor charging is repeated aborted shocks due torepetitive nonsustained VT or oversensing due tolead-connector problems. Repeated shocks due toVT storm might also rapidly deplete the battery.Some diagnostic features have high power con-sumption. In Medtronic ICDs, “prestorage” of elec-trograms prior to each VT/VF episode results incontinuous amplification of the unfiltered electro-gram, substantially reducing longevity. In contrast,prestorage in Guidant and St. Jude ICDs, whichstore only filtered electrograms, does not cause sig-nificant battery depletion. ICD component failureis a rare cause of battery depletion.

Lead ProblemsVentricular lead problems are the most com-

mon cause of ICD system malfunction.32–35 Theyusually present either as oversensing, resultingin inappropriate shocks, or as abnormal diagnos-tic measurements at routine follow-up. Presen-tation as undersensing during VF or unsuccess-ful therapy is uncommon but often fatal. Clin-ical and lead-design factors identify patients athigh risk for ventricular lead problems and meritintensified follow-up. Noninvasive assessment isusually diagnostic.36 The introduction of remoteICD monitoring,37,38 which permits transmissionof complete ICD interrogation via telephone or theinternet, may enhance noninvasive identificationof subclinical lead failure (Fig. 2). Patients withMedtronic ICDs may present with audible “PatientAlert” warnings (see below).

In ventricular ICDs, atrial lead malfunctionsmay present as failure to discriminate VT fromSVT. Atrial lead dislodgment to the ventricle re-sults in sensing of ventricular electrograms on theatrial channel, causing detection of one “atrial”event for each ventricular event. This may causedual-chamber algorithms misclassify of VT as SVTand withhold appropriate therapy. Atrial lead dis-

lodgment to the ventricle might also result in inap-propriate shocks caused by ventricular oversens-ing of noise generated by contact between the leads(Fig. 3).

Diagnosis of Lead Failure

A systematic approach to the patient with sus-pected lead failure requires evaluation of elec-trograms from all electrodes on the lead, pacingthreshold, pacing impedance, and painless high-voltage electrode impedance; system radiography;stored episode electrograms, data logs, and flash-back memory (extended recording of R-R intervalsin Medtronic ICDs).36 The yield of these tests isshown in Table I. The Sensing Integrity CounterTM

(Medtronic) displays the number of nonphysio-logic short intervals detected in the 120–140-msrange. With intact, true-bipolar leads, the countremains at zero. With intact, integrated-bipolarleads, the large proximal sensing electrode (thedistal ICD coil) permits occasional oversensing ofdiaphragmatic myopotentials, but a count >300over 3 months suggests a lead problem.39

Pacing Impedance

The normal value for pacing impedance is afunction of lead design; but for any lead (exceptY-adapted lead combinations), impedance <200� indicates an insulation defect and impedance>2,000 � suggests a conductor failure if a looseset screw or faulty adapter are excluded.40,41 Mod-ern ICDs perform serial impedance measurementsautomatically. The range of variability of pacinglead impedances has been studied for coaxial pace-maker leads,42 but corresponding data for coaxialand multi-lumen defibrillation electrodes are lim-ited. Generally, conductor failures do not presentwith moderate changes in impedance. Either theimpedance exceeds 2,000 � (continuously or in-termittently), or it is normal, and conductor failureis diagnosed by identification of a characteristicpattern of oversensing. Pacing lead impedance isinsensitive to inner insulation failure of Medtronic6936 leads.41 Isolated pacing insulation failure ofmulti-lumen leads is sufficiently rare that the sen-sitivity of pacing lead impedance is unknown.Inner insulation failure in Medtronic 6936 or6966 leads may be detected by a fall in ring-coilimpedance with normal pacing impedance.41 Re-view of ring-coil impedance may require sendingthe programmer’s “save-to-disk” file to the manu-facturer for analysis by a specialized software.

High-Voltage Impedance

Shocking-pathway impedance normally is25–75 � in transvenous systems. Values out-side this range suggest a conductor defect (highimpedance) or insulation failure/short circuit


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Figure 2. Asymptomatic malfunction in coaxial defibrillation lead (Medtronic model 6936) detected by internet-based,remote patient monitoring (Medtronic CareLinkTM). The Sensing Integrity Counter provides a cumulative count ofnonphysiologic short intervals caused by oversensing. Multiple episodes of nonsustained VT with cycle lengths 140–210 ms also suggest oversensing. In the absence of exposure to electromagnetic interference, this is highly suggestive ofan inner-insulation failure. The pacing and defibrillation lead impedances are insensitive to early insulation failure.Analysis of ring-coil impedance from the programmer “save-to-disk” file is often diagnostic. See text. Courtesy ofPhysician Assistant Sheila Reynolds and Dr. Dwight Reynolds.

(low impedance). Periodic assessment of theimpedance of the high-voltage electrodes usingweak test pulses may detect a loss of lead integritybefore inappropriate or ineffective therapies occur.In Medtronic and Guidant ICDs, painless pulsesare delivered automatically at periodic intervalsto create trend plots. In St. Jude ICDs, high-voltagelead impedance is assessed by delivering a 12-Vtest pulse using the programmer command. Pa-tients feel this pulse and may perceive it to be un-comfortable.

High-voltage impedance measured by weakpulses correlates well with values measuredby high-energy shocks.43,44 In Guidant ICDs,impedance values recorded painlessly are compa-rable to those recorded during high-voltage shock.In older Medtronic ICDs, the pulse is delivered be-tween the lead tip and the distal coil, resultingin nominal low-voltage impedance values of 11–20 �, significantly lower than the impedance of

a high-energy shock. If a proximal coil is present,its integrity is not assessed. Medtronic MarquisTM

ICDs and newer models report independent prox-imal and distal coil impedances that closely ap-proximate those of high-voltage shocks. When alead defect is suspected, a full-output shock maybe necessary to evaluate lead integrity. Partial insu-lation defects may not be identified by low-energypulses that deliver insufficient current to activatethe shorted high-output protection feature (seebelow).

Electrogram Amplitude (R-Wave, P-Wave) and PacingThreshold

The amplitude of the R-wave during sinusrhythm should be at least 5–7 mV for assurancethat the low-amplitude electrograms during VFwill be sensed reliably.16 Causes of reduced elec-trogram amplitude include antiarrhythmic drugs,myocardial infarction, shocks, fibrosis at the lead


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Figure 3. Atrial lead dislodgment causing inappropriate shock. Top right box shows the episode summary, indicatingan episode detected as VF (via the combined count), for which the first VF therapy was delivered. The intervalsummary plot (middle panel) demonstrates a regular “atrial” rate (boxes) of 640 ms, with a highly variable ventricularcycle length (black circles), leading to detection and delivery of a 34.6-J shock. The bottom panel shows the atrialelectrogram (Atip to Aring), near-field ventricular electrogram (Vtip to Vring), calculated A-A intervals, event markers,and calculated V-V intervals. Each ventricular electrogram is associated with an atrial-channel electrogram that haslarge amplitude and slope. The sensing of ventricular events on the atrial channel in the absence of sensed atrial eventssuggests atrial lead dislodgment to the ventricle. The presence of smaller deflections on the ventricular electrogram(the first is sensed as “VS 550”) is consistent with oversensing of “noise” signals caused by contract with the atriallead. This oversensing results in detection of VF and delivery of shocks during normal rhythm. AR = atrial refractorysense; VS = ventricular sense; TS = tachycardia sense (in VT zone); VF = fib sense (in VF zone).

tip, new conduction defects, and lead dislodg-ment. These same factors may also elevate thepacing threshold. The introduction of automaticcapture assessment45 in conjunction with remotemonitoring systems that permit review of devicemeasurements and trend plots between clinic vis-its37,38 may further facilitate early diagnosis of leadproblems.

Radiography

Abnormal radiographic features are identifiedin less than half of patients with ICD lead malfunc-tions.36,46 Lead dislodgment is diagnosed when thelead tip is in a different position than in the post-operative radiograph, but variability due to car-diac and respiratory motion may prevent diagnosisof minor dislodgments. Typically, RV apical leadsdislodge toward the tricuspid valve; atrial leadsdislodge into the RV; and coronary venous leads of

resynchronization ICDs dislodge proximally intothe coronary sinus or right atrium.

Subclavian crush occurs when a lead is com-pressed in the narrowly confined space betweenthe first rib and clavicle;47,48 this common site offracture requires careful examination if lead failureis suspected (Fig. 4). Radiography may also detectconductor defects, inadequate pin insertion intothe header, abandoned or incompletely removedleads, or torsion due to Twiddler’s syndrome. How-ever, some intact electrical connections in leadsand adapters appear radiographically to have con-ductor discontinuity (“pseudo fracture,” Fig. 5).Fluoroscopy of an unopened lead or adapter (ifavailable) can be used to determine the expectedradiographic appearance.

Real-Time Telemetry

Real-time display of intracardiac electrogramsis used to assess the effect of body position and


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TABLE I.

Detection of Malfunction in Transvenous ICD Leads

Test Sensitivity*

Asymptomatic Patients with All Patients withPatients Inappropriate Shocks Lead Failures(n = 11) (n = 7) (n = 18)

Individual testsStored electrograms 27% 100% 56%X-ray 27% 29% 28%Pacing threshold 36% 14% 28%R-wave amplitude 55% 0% 6%Pacing impedance 9% 0% 6%High-voltage lead impedance 29% 14% 43%Defibrillation threshold 0% 0% 0%

Combination of testsAll pacing/sensing tests 82% 14% 78%Pacing/sensing, stored electrograms and x-ray 100% 100% 100%Sensing and detection of induced VF 29% 14% 43%

Modified from Luria et al.36

maneuvers on recorded signals. The appearance ofnoise during Valsava or inspiration may be causedby myopotential oversensing49 or a structural leaddefect. Abnormalities of pacing function, R-waveamplitude, pacing and shocking impedance, andstored evidence of oversensing39 usually indicatelead defect. Simultaneous surface ECG recordingwith telemetry of the sensing signal, the far-field

Figure 4. Subclavian crush injury to defibrillation electrode. (A) Note the sharp bend on the leadat the site where it passes between the subclavian vein and the first rib (arrow). (B) Lead extractedfrom a patient with subclavian crush. Note the disrupted insulation and the disarray of the filers(the circumferentially coiled conductor) at the site of crush. Reprinted with permission from Lloydet al.46

electrogram (between shocking electrodes), andsensing/pacing markers may permit localizationof the malfunction to a specific component of thelead. Medtronic ICDs permit use of special teleme-try Holter monitors for troubleshooting.50 Theyprovide a simultaneous, 24-hour recording of a sur-face ECG lead with two intracardiac electrogramsand an extended Marker ChannelTM (Fig. 5).


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Figure 5. Oversensing identified by telemetry Holter monitor. Telemetered ECG and ventricularintegrated-bipolar and high-voltage electrograms are recorded with extended marker channelshowing usual markers (top line) and multiple other device parameters. The sixth line shows theVF counter which increments from 0 to 3 during oversensing. Saturation of the sensing electrogramand intermittent oversensing are characteristic of electrode problems, in this case intermittentconductor failure. The Holter was performed because the Short Interval Counter was abnormal.In this case, the lead impedance was normal.

Stored Episodes

Lead, adapter, or set screw malfunction oftenpresents as oversensing, resulting in inappropri-ate detection of VF and aborted or inappropriateshocks. This results from make-break contact noiseor oversensing of extracardiac signals due to insu-lation defects. The pattern of oversensing often in-cludes extremely short nonphysiological intervals(<140 ms, Fig. 6). In Medtronic ICDs, the combi-nation of a high Sensing Integrity CountTM of non-physiological intervals, nonsustained tachycardiaepisodes with nonphysiological intervals, and ab-normal lead impedance triggers a lead alert warn-ing on interrogation.39

Patient Alerts

Medtronic ICDs emit patient-alert tones forpacing or high-voltage lead impedances out ofrange, low battery voltage, long charge time, three

shocks delivered per episode, or all therapies in azone delivered. Most serious problems identifiedby alerts are lead-related40 (Fig. 6). Unfortunately,ICD recipients may not hear alert tones or may notrecognize their significance. Alerts are a useful ad-junct to, but not a substitute for, periodic deviceinterrogation and follow-up.

Risk Factors for Lead Failure

Clinical factors predictive of lead failure in-clude epicardial leads,34,51 abdominal pulse gener-ator location,36,47 coaxial defibrillation leads,36,41

subclavian venous access,48,52 and dual-chamber(as opposed to single-chamber) ICD systems.52 Inepicardial systems, sensing and defibrillation areperformed by different leads, eliminating over-sensing as an early warning for failure of defibrilla-tion leads. Thus, periodic assessment of shockinglead impedance is essential. Currently, epicardial


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Figure 6. Conductor failure identified by lead alert. Top panel shows marked, abrupt increasesin all measured impedance values triggering a lead alert on July 28, 2 days after the patient wasseen in clinic. The patient did not hear the alert tones, probably because the ICD was implantedsubmuscularly. Middle panel shows episode summaries from inappropriately detected episodesof VF during intense stationary bicycle exercise in “spinning” class (August 1). Bottom panelshows the corresponding stored electrogram from the true-bipolar sensing lead. Signals are prob-ably caused by mechanical motion at the fracture site. Saturation of rate sensing electrogram ischaracteristic of conductor failure; but persistence of oversensing throughout the cardiac cycle isnot and is probably caused by intense exercise.

systems are used only in patients with a univen-tricular heart or mechanical tricuspid valve. Sub-cutaneous patches, which have similar construc-tion to epicardial patches and have similar highfailure rates, also warrant careful observation.34,53

Abdominal pulse generator placement, indepen-dent of epicardial or transvenous approach, maycause lead stress associated with tunneling andmechanical friction of the pulse generator againstthe lead.36,54 Cardiac resynchronization leads havea higher dislodgment rate than other electrodes.55

Adapters increase the number of mechanicalconnections and stress points and may increasethe risk of system malfunction. A loose set screw(in the header or an adapter) can mimic lead frac-ture, with make-break contact noise and elevatedimpedance.

Coaxial leads have higher failure rates thanmulti-lumen leads, in which conductors are longi-tudinally arrayed along the length of the lead.56

Medtronic TransveneTM coaxial leads (models6936 and 6966) are prone to failure causedby metal ion oxidation of a middle insulation

layer.36,57 A drop in the ring-to-coil impedanceis an early marker of this failure,41 which resultsin oversensing of nonphysiological signals. Use ofring-to-coil impedance, the nonsustained episodelog, and Sensing Integrity Counter may permitidentification of early failure before oversensingcauses inappropriate shocks (Fig. 2). A “signa-ture” presentation of this type of lead failure isoversensing of electrical noise following shocks(Fig. 7).41

Protecting ICDs from High-Voltage, Short Circuits

Low impedance on the shock electrodes in-dicates an insulation failure that diverts shockcurrent from the heart. It may produce sufficientpeak current that the ICD’s output circuit fails by“electrical overstress.”58 For example, an insula-tion failure in the pocket may produce a short cir-cuit from the high-voltage coil to the can with aresistance of 8 �. A maximum-output (∼800 V)shock would result in a peak current of 100 A inthe high-voltage output circuit, causing it to failcatastrophically.59 Shorting between two active


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Figure 7. Post-shock oversensing. Panels show recordings of true-bipolar sensing and markerchannel during VF induced at replacement of an ICD pulse generator attached to a chronicallyimplanted Medtronic model 6936 TransveneTM, coaxial defibrillation electrode. Top and middlepanels are continuous. At left of top panel, T-wave shock (CD) induces VF, which is reliably sensed,detected, and terminated by a programmed 20-J shock (CD 19.6 J) in the middle of the middlepanel. Post-shock intermittent oversensing saturates electrogram signals, resulting in failure toidentify sinus rhythm and repetitive inappropriate redetection of VF, with multiple shocks abortedusing the programmer. The lower panel shows one aborted shock with detection of VF (FD). Theshort charge time between FD and CE markers is caused by high residual voltage output capacitorafter previous aborted shocks. Post-shock oversensing is the typical early sign of inner insulationfailure in this coaxial defibrillation electrode.

intracardiac electrodes of opposite polarity cancause the same effect. To prevent electrical-overstress component failure, modern ICDs protectthe output circuit by aborting the shock pulse im-mediately if the current in the defibrillation path-way is excessive. Depending on the manufacturer,this corresponds to a series lead impedance of 15–20 �. The presumption is that the short circuitdiverts current from the heart, preventing shocksfrom terminating VT/VF. In addition to preserv-ing the generator, this feature has a safety ben-efit. Simultaneous insulation failure of the rate-sensing and high-voltage components of RV leadsmay present as oversensing. Diverting the resultantinappropriate shock prevents unnecessary pain.Further, it may prevent fatal proarrhythmia froma weak shock delivered in the vulnerable period

with no effective means to rescue the patient60 (seeFig. 8).

Pulse Generator FailureImplantable ICD pulse generator failure is

rare, although the incidence is largely unknowndue to limitations in current reporting methods.61

Pulse generator failure might result from primarysemiconductor component failure caused by ex-posure to extreme voltages or currents (electri-cal overstress). It can occur due to inappropri-ate internal arcing, commonly associated with thehybrid circuit.58 In older ICDs without shortedhigh-output protection, pulse generators fail ifshocks are delivered into a short circuit resultingfrom lead insulation failure.


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Figure 8. Protection for shorted output of high-voltage circuit. Text therapy summary indicates sequence of therapiesafter induction of VF by a 0.6 J T-wave shock (T-shock) during replacement of an ICD pulse generator attached to achronically implanted Guidant Model 00125 defibrillation electrode. The measured high-voltage lead impedance is<20 �. Despite programmed shocks strengths of 15, 20, and 30 J, delivered energies are 0.2, 0.3, and 0.3 J, respectively,because of shorted output protection feature. Short charge times for second and third shocks correspond to highresidual energy on capacitors at end of previous shock. Top left panel shows interval plot. Top right panel shows thirdunsuccessful shock (followed by minimum distortion of post-shock, high-voltage electrogram due to low voltage) andexternal rescue. An insulation failure in the pocket shorted the high-voltage lead to the generator can.

Pulse generator failure may manifest as ab-sence of telemetry, emission of device tones, inap-propriate shock, premature battery depletion, dis-play of fault codes upon interrogation, inability tointerrogate or program, failure to charge the capac-itors or retain a charge, early battery depletion, orfailure to deliver therapy. Failed pulse generatorsshould be explanted and returned to the manu-facturer for analysis, and the incident should bereported to the Food and Drug Administration’sManufacturer and User Facility Device Experiencedatabase (http://www.fda.gov/cdrh/maude.html).Rigorous reporting and analysis may distinguishrandom component failure from a systemic failure,correctable by design or manufacturing modifica-tions before many patients are affected.61

Considerations for Bradycardia Pacing in ICDsTo prevent intradevice interactions (see

“Pacemaker-ICD Interactions”), dual-chamberICDs have interlocks between pacing and VT/VFdetection parameters that limit the fraction of thecardiac cycle affected by pacing-related blanking

periods. These interlocks limit combinationsof the upper rate limit and AV delay based onthe VT detection interval. Adaptive, rate-relatedshortening of the post-pacing ventricular blankingperiod permits higher pacing rates with lessventricular blanking, but might increase the riskof T-wave oversensing.62

In patients with LV dysfunction, RV apicalpacing promotes ventricular dyssynchrony, atrialfibrillation, and heart failure.63,64 Dual-chamberICDs should be programmed to minimize ventric-ular pacing in this population. One approach isto use a nontracking pacing mode (DDI) and along AV interval. However, this may introduce pa-rameter interlocks or—in conjunction with rate-smoothing—intradevice interactions resulting inundersensing of VT/VF. Specific algorithms thatpromote intrinsic conduction periodically deter-mine whether intrinsic conduction is presentduring dual-chamber pacing. They either prolongthe AV interval (Search HysteresisTM in GuidantICDs; AutoIntrinsic Conduction SearchTM in St.Jude) or change the pacing mode to a modified


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Figure 9. Algorithm for maximizing intrinsic AV conduction. (A) Hospital telemetry strip. Thefirst four complexes demonstrate atrial pacing with intrinsic ventricular conduction in a patientwith MVPTM Mode programmed in a Medtronic ICD. The fifth atrial-paced beat is not conducted,followed by AV pacing on the sixth beat. This algorithm paces in the AAI mode with ventricularsurveillance, to minimize ventricular pacing. Ventricular pacing occurs only if a nonrefractorysensed or paced atrial event is not conducted (allowing for a maximum pause of two timesthe lower rate limit plus 80 ms). Nominal performance of this algorithm may be confused withpacemaker malfunction. (B) From top to bottom: surface ECG, electrogram markers, and near-fieldventricular electrograms. The first three complexes depict DDDR pacing mode with MVPTM Modeprogrammed on. The algorithm periodically checks for the return of AV conduction to minimizeventricular pacing (seen in the fourth complex, AS-VS). AS = atrial sense; VS = ventricular sense;VP = ventricular pace.

AAI mode with ongoing assessment of AV conduc-tion (AAI+ or AAIR+ mode, Medtronic MVPTM).The AAIR+ mode eliminates interlocks betweenthe pacing upper rate limit and VT zone, permit-ting paced rates in the VT zone. In the AAIR+mode, early ventricular events reset the VA inter-val and ventricular pacing does not occur at a fixedor dynamic AV delay. The AAIR+ mode thus elim-inates interlocks to permit rate-responsive pac-ing in the VT zone without the risk of intrade-vice interactions that may prevent detection ofVT by competitive bradycardia pacing22–24 (see“Pacemaker-ICD Interactions”). Because the PR in-terval is not limited, a single nonconducted P-wave may occur (see Fig. 9). A potential risk of thispacing mode is ventricular proarrhythmia causedby pause-dependent VT.

Troubleshooting Cardiac ResynchronizationTherapy in ICDs

The vast majority of cardiac resynchroniza-tion pacing in the United States is performed us-

ing ICDs.65–67 The two widely spaced ventricularleads in resynchronization ICDs introduce novelintradevice interactions between resynchroniza-tion pacing and detection of VT/VF. We addresstheir unique troubleshooting implications. Opti-mizing pacing for hemodynamic benefit68 is be-yond the scope of this review.

Ventricular Sensing ProblemsEarly, resynchronization systems utilized

adapters that have multiple modes of pacing andsensing malfunction.68,69 The first dedicated sys-tem (Guidant Contak CDTM) sensed between theLV and RV electrodes to determine R-R inter-vals. This “extended bipolar” sensing configura-tion “merges” events sensed in the LV or RVinto a single recording channel. During pacing,RV and LV depolarizations are synchronized andrefractory periods prolonged, preventing double-counting. But during conducted rhythms or VT, R-wave double-counting occurs whenever the inter-val between local electrograms of conducted beats


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Figure 10. Multiple shocks in a patient with a cardiac resynchronization ICD with extendedbipolar sensing (Contak CTM) due to double counting initiated by a pacemaker-mediated tachy-cardia prevention algorithm. Electrograms from top to bottom are atrial, ventricular near-field,and ventricular far-field. The initial rhythm is sinus tachycardia, with P-synchronous pacing atthe maximum tracking rate (“VP-MT”). This algorithm periodically extends the post-ventricularatrial refractory period during upper-rate limit pacing to abort a pacemaker-mediated tachycardia(indicated by “PMT-B”). The following atrial-sensed event falls in the extended post ventricularatrial refractory period (indicated by the parenthesis, “(AS)”) and is therefore not tracked. Cessa-tion of ventricular pacing permits double counting of the intrinsic-wide QRS complex by extendedbipolar sensing, leading to inappropriate detection of VF. VS = ventricular sense in sinus zone.Other abbreviations as in Figure 11.

at the RV and LV electrodes is greater than the ven-tricular blanking period, leading to double sens-ing of a single ventricular depolarization.70 Anyevent that inhibits ventricular pacing even tran-siently and thus permits AV conduction (e.g., pre-mature complex, conducted sinus tachycardia, orSVT) may cause R-wave double-counting and in-appropriate therapy (Fig. 10 [and fig. 4 in Part I ofthis review]).

R-wave double-counting may result in shocksfor SVT slower than the programmed VT detectioninterval because alternate device-detected inter-vals correspond to (1) the interval between the twosensed components of the ventricular electrogramand (2) the difference between the true ventricu-lar cycle length and the double-counting interval.See Figure 6 for details. Because alternate “R-R”intervals in any conducted rhythm increment theVF counter, all detected VT or SVT episodes areclassified as VF and treated with shocks, regard-less of cycle length. Because there are two detectedintervals for each ventricular electrogram, tran-sient nonsustained tachycardias may satisfy theVF detection criterion, resulting in aborted shocks.Pacemaker algorithms—such as those designed toterminate pacemaker-mediated tachycardia—may

promote inappropriate shocks by temporarily sus-pending ventricular pacing and permitting double-counting (Fig. 10).

Extended bipolar ventricular sensing also in-creases the risk of oversensing P-waves, mostcommonly when the LV lead dislodges into thecoronary sinus. This may inhibit pacing, prevent-ing resynchronization therapy for heart failure, orcause ventricular asystole in patients with com-plete heart block. Oversensing of atrial arrhyth-mias may cause inappropriate shocks despite aslow ventricular rate.69 Oversensed events mayhave complex and unanticipated interactions withdetection enhancements (Fig. 11).

LV Threshold and RV Anodal CaptureEven if they use RV sensing, most ICDs

use dual-cathodal (“extended bipolar”) pacing inwhich the LV and RV tip electrodes serve as thecombined cathode. The common anode may be ei-ther the RV coil (integrated-bipolar pacing config-uration) or the RV ring (true-bipolar pacing con-figuration). Some ICDs permit simultaneous (ortemporally offset) true-bipolar pacing in both theLV and RV (Fig. 11).


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Figure 11. Extended and true bipolar left LV pacing configurations (available in the Contak Renewal 3TM ICD). The toptwo panels depict extended bipolar pacing, in which pacing occurs between LV and RV electrodes. This configurationhas the advantage of requiring only a single LV electrode, but the disadvantage of permitting anodal capture (Fig. 13).The ability to select either the distal or proximal LV electrode as cathode for pacing functionally permits “moving” theLV lead via noninvasive reprogramming. This can be advantageous postoperatively if the pacing threshold increasesor phrenic-nerve stimulation occurs. The bottom two panels depict true-bipolar LV pacing, which eliminates thepossibility of anodal RV capture, but requires a bipolar LV lead.

Determining whether the LV lead is captur-ing can be difficult. At least seven possible statesof ventricular pacing can occur in cardiac resyn-chronization systems that use an extended bipolarpacing configuration. These are no capture (intrin-sic conduction) and capture from six specific pac-ing configurations: RV cathodal + LV cathodal (theintended state); LV (cathodal) only; RV cathodalonly; RV anodal only; RV anodal + LV cathodal;and RV (cathodal + anodal) + LV (“triple site” pac-ing). Most of these can be distinguished by anal-ysis of intracardiac electrograms combined with a12-lead ECG, which is invaluable for follow-up ofresynchronization pacing systems.

In early cardiac resynchronization systems,dual-cathodal pacing applies the same voltage tothe commonly wired LV and RV cathodes. Sincethe local LV and RV thresholds usually differ,

the pacing pulse may be supra-threshold in onechamber and subthreshold in the other, leading toloss of resynchronization. In these ICDs, a changeof ventricular-electrogram morphology during athreshold test indicates loss of capture at one elec-trode; the corresponding change in the surfaceECG usually indicates which pacing configura-tion is capturing (see below). Current systems per-mit independent programming of RV and LV out-puts, facilitating determination of the RV and LVthreshold.

ECG changes associated with biventricularpacing have been reviewed.68 During determina-tion of the LV pacing threshold, the QRS complexusually widens with loss of LV capture. It becomesless negative in lead I and more negative in leadIII as ventricular excitation originates from the in-ferior RV as opposed to the lateral LV (Fig. 12).


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Figure 12. QRS morphology during biventricular pacing. The morphology of the paced QRScomplex depends on lead positions and the distribution and properties of diseased myocardium.Left panel: LV capture is suggested by a markedly negative QRS in lead I. Middle panel: Loss ofLV capture is associated with a positive QRS compels in lead I and a more negative deflection inlead III. Right panel: With loss of capture, intrinsic conduction returns. In this case, the intrinsicQRS is narrow.

During dual-cathodal pacing, a ventricular electro-gram that follows the pacing stimulus by 50–200ms may assist in determining the site of capture. Itoccurs when one ventricular electrode senses thewavefront propagating from the site of capture inother ventricle, giving rise to the second event.

“Anodal capture” occurs when the deliveredvoltage captures at the RV anode either in isola-tion or in conjunction with the LV cathode. Whenanodal capture results in “triple-site” pacing (LVcathode, RV cathode, and RV anode), the QRS du-ration may decrease by 10–20 ms and QRS ampli-tude of leads I and aVL may increase.71 If anodalRV capture is mistaken for LV capture, the pac-ing output may be programmed to a subthresholdvalue in the LV, resulting in loss of cardiac resyn-chronization (Figs. 13 and 14). It is much morecommon if the RV anode is a ring electrode (true-bipolar pacing), which has a small surface area(high current density) and may be in direct contactwith endocardium than if the RV anode is a de-

fibrillation coil (integrated-bipolar pacing), whichhas a large surface area (low current density). Thus,anodal capture is extremely rare in Medtronic andGuidant ICDs, which use integrated-bipolar pac-ing. St. Jude ICDs use true-bipolar pacing if the LVlead is unipolar and the RV lead is true-bipolar.Anodal capture is more common in this pacingconfiguration.

Ensuring Delivery of Effective ResynchronizationIn order to provide effective cardiac resyn-

chronization, a high frequency of biventricularpacing must be delivered. A practical goal is toresynchronize 90% of R-R intervals. Figure 15shows a systematic approach to confirming resyn-chronization. Loss of resynchronization occurs ifLV capture fails. Kay provides a comprehensive re-view of the differential diagnosis of loss of resyn-chronization for reasons other than loss of LVcapture.72 The most common causes are intrin-sic AV conduction due to a long programmed AV


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Figure 13. Possible modes of anodal capture duringbiventricular pacing. In all examples, an extendedbipole paces between LV and RV leads. The top left paneldemonstrates biventricular pacing using an integrated-bipolar RV lead, in which the common anode is the dis-tal defibrillation coil. Since the RV coil has a large sur-face area and thus a low current density, anodal captureis rare. The remaining panels depict biventricular pac-ing between a LV electrode and a true-bipolar RV lead, inwhich the common anode is the RV ring electrode. Thetop right panel depicts normal function, with captureonly at the LV tip during LV-only pacing. The bottomleft panel depicts capture only at the anode. This oc-curs if the anodal RV-ring threshold is lower than the LVthreshold and the pacing output is between the RV an-odal threshold and LV cathodal thresholds. The bottomright panel depicts anodal and cathodal capture. Thismay confound the determination of LV pacing threshold.See Figure 14.

delay and loss of atrial tracking at fast atrial rates.Others include frequent premature ventricularcomplexes, sensing malfunction (see above), pro-gramming considerations and/or specific pacingalgorithms (see below). Interruption of cardiacresynchronization pacing is common, but it canusually be restored by noninvasive or invasive in-tervention.73

ICD Programming and Resynchronization Algorithms

Any parameter setting that minimizes ventric-ular pacing or permits ventricular fusion will ad-versely affect cardiac resynchronization. Such set-tings include a long AV delay, a prolonged post-ventricular atrial refractory period or extension ofthe post-ventricular atrial refractory period aftera premature ventricular complex, a low maximal-tracking rate, AV search hysteresis, rate-smoothingup or down, or use of a DDI pacing mode. Atrial un-

dersensing and ventricular oversensing may simi-larly minimize ventricular pacing and limit resyn-chronization.

Resynchronization ICDs have features de-signed to maintain LV stimulation. To prevent LVT-wave oversensing, Guidant RenewalTM ICDsincorporate an LV refractory period, which mayinhibit LV pacing. Additionally, they include anLV protection period after a sensed or paced eventduring which pacing will not occur. Although de-signed to prevent pacing in the LV vulnerable pe-riod, this parameter reduces the maximum LV pac-ing rate and may inhibit cardiac resynchronization(Fig. 16).

Resynchronization ICDs also employ algo-rithms designed to maximize ventricular pac-ing during potentially disruptive events such aspremature ventricular complexes or rapidly con-ducted atrial arrhythmias. In Medtronic resyn-chronization ICDs, the Ventricular Sense Res-ponseTM feature triggers pacing in one or bothventricles after each RV-sensed event.74 BothMedtronic and Guidant systems include al-gorithms that temporarily shorten the post-ventricular atrial refractory period to regain atrialtracking and restore resynchronization after pre-mature ventricular complexes or during sinustachycardia faster than the nominal upper ratelimit. Medtronic’s Conducted AF ResponseTM

resynchronizes conducted beats in atrial fibrilla-tion up to a minimum R-R interval without increas-ing ventricular rate. Guidant’s Ventricular RateRegularizationTM algorithm is intended to restoreresynchronization and ventricular regularity bypacing the ventricle during irregular conductionof atrial fibrillation. Concealed conduction into theAV node from the paced events may slow AV nodalconduction, thereby limiting the pacing-inducedincrease in ventricular rate. These and other algo-rithms designed to maximize cardiac resynchro-nization therapy may result in pacing after QRSonset on surface ECGs and pacing at “unexpected”times (Fig. 17).

Phrenic-Nerve StimulationLeft phrenic-nerve stimulation by an LV elec-

trode may make cardiac resynchronization intol-erable. It may become manifest only after im-plantation due to postural changes or minor leadmigration. In Guidant ICDs, daily impedancemeasurements performed to assess lead integritytemporarily increase the pacing amplitude. Theymay need to be programmed “off” in patients whohave phrenic stimulation at the higher output. De-creasing the pacing output noninvasively elimi-nates phrenic stimulation if there is a sufficientsafety margin between the LV and phrenic-nervethresholds. Data are insufficient to determine how


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Figure 14. Anodal capture during testing of LV capture threshold. LV pacing occurs between a LV cathode and aRV ring anode. (A) Upper left panel: From top to bottom: surface ECG, electrogram markers and intervals, atrialelectrogram, and ventricular near-field electrogram. At left, pacing output is 2.5 V and anodal capture is present,with capture occurring at both the LV electrode and the RV ring. No electrograms are visible on the LV channeldue to the simultaneous RV and LV capture. With a decrement in pacing output to 2.25 V, the QRS morphologychanges on the ECG (circled complex); and electrograms appear on the ventricular channel, representing local RVdepolarization. Inset at lower right shows that the time between the pacing stimulus and the RV electrogram representsthe interventricular conduction time during LV pacing. (B) With further decrement in LV pacing output from 0.75 to0.5 V, true loss of LV capture occurs, with widening of the surface ECG due to left bundle branch block. The local RVdepolarizations are similar during LV pacing (in A) and intrinsic AV conduction (panel B).

often phrenic-nerve stimulation can be eliminatedby reprogramming from unipolar to bipolar LV pac-ing or changing the LV pacing vector on a multi-polar LV lead (Guidant EZTRAK 2†TM). The alter-native is repositioning the LV lead.

Troubleshooting Interactions with ICDsAntiarrhythmic Drugs

Antiarrhythmic drugs are prescribed com-monly to ICD patients.75–78 Serious drug-ICD inter-actions associated predominantly with the use ofsodium- or potassium-channel blocking (Vaughn-Williams class IA, IC, or III) drugs have been re-viewed7,76,79 and are summarized in Table II. Theseinteractions must be considered when antiarrhyth-mic drug treatment is initiated or the dose is al-tered.7

Sensing, Detection, and Pacing

Drug effects on the amplitude and slew rateof local electrograms may impair sensing. Thismay delay or prevent detection of VT/VF. Antiar-rhythmic drugs that slow the rate of VT belowthe programmed VT rate cutoff can prevent ini-tial detection of VT2 or divert appropriate ther-apy during reconfirmation (Fig. 18). Class ICdrugs bind sodium channels in the open state,resulting in greater drug effect during tachy-cardias. They may alter ventricular-electrogrammorphology sufficiently in SVT to invalidatea morphology-algorithm template acquired at anormal sinus rate. Because VT displays increasedcycle length variability in patients taking ClassIC drugs,9,13 interval-stability detection enhance-ments may misclassify VT as atrial fibrillation.The effect of Class IC drugs to increase pacing


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Figure 15. Systematic approach to insuring delivery of cardiac resynchronization therapy. CRT =cardiac resynchronization therapy; PVC = premature ventricular complex; VTns = nonsustainedVT; AVN = AV node.

Figure 16. Inhibition of LV pacing by the programmable LV protection period in a Contak Re-newal 3TM. Shown from top to bottom are ECG lead II, RV electrogram, and LV electrogram. Aprogrammer command for LV pacing was issued during atrial fibrillation. Since the LV protec-tion period prevented pacing at the selected rate, markers indicating inhibition of pacing appear(“inh-LVP”). Programming the protection period off permitted assessment of the LV threshold.RVS = right ventricular sense.


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Figure 17. Algorithms designed to maintain a high percent of cardiac resynchronization pacing during atrial fibrilla-tion may be confused with inappropriate pacing. (A) Hospital telemetry shows ventricular pacing occurring after theQRS onset due to the Medtronic Ventricular Sense ResponseTM algorithm, which introduces a triggered biventricularpacing pulse after each RV-sensed event. (B) Surface ECG lead II, event markers, and the RV tip to LV tip electrogramare displayed during atrial fibrillation. The first three complexes represent biventricular pacing (“BV”). The last com-plex represents a conducted complex that was sensed (“VS”). The split marker associated with the “VS” indicatesthat a triggered pace pulse resulted. (C) Hospital telemetry shows pacing during rapidly conducted atrial fibrillationdue to an algorithm designed to maximize cardiac resynchronization pacing. This pacing, with the patient at rest, isdistinct from rapid, rate-responsive pacing that is triggered by a sensor.

thresholds is greatest at rapid rates, so that an-titachycardia pacing could be subthreshold evenif bradycardia pacing is supra-threshold at slowerrates.80 This rarely presents a clinical problem be-cause the pulse amplitude for antitachycardia pac-ing nominally is higher than that for bradycardiapacing. When Class IA, IC, or III antiarrhythmicdrugs are started in an ICD patient, the slowestVT zone detection interval should be increased by≥40 ms, SVT-VT discriminators should be activeto prevent inappropriate therapy of SVT with rateoverlapping that of drug-slowed VT, the interval-stability discriminator should be programmed toa less specific value, a new morphology tem-plate should be acquired during atrial pacing ata rapid rate, and a sustained-duration overrideshould be considered. Noninvasive programmedstimulation may be appropriate to determine ifVT/VF is detected accurately and terminatedpromptly.

Defibrillation

Antiarrhythmic drugs may cause potentiallylife-threatening rises in DFTs. Drug-defibrillationinteractions are complex. Studies are confoundedby anesthetic effects, heterogeneity in ICD leadsand waveforms, and inter-species variability (e.g.,human vs canine vs porcine). Drugs that block thefast inward sodium current (such as lidocaine) el-evate the DFT, whereas agents those that block re-polarizing potassium currents (such as sotalol anddofetilide) lower the DFT slightly.7 Improved de-fibrillation safety margins have mitigated these ad-verse pharmacologic effects, and potent sodium-channel blocking drugs are rarely prescribed forchronic oral therapy in ICD patients. However,chronic oral amiodarone increase DFTs to a clin-ically relevant degree in some patients.81 Whentreatment is initiated with amiodarone or anotherdrug that often elevates the DFT, the defibrillationsafety margin should be confirmed if it is both


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TABLE II.

Adverse Interactions Between Antiarrhythmic and ICDs

ICD Function Effect Drugs

Undersensing (rare) Diminished electrogram slew rate/amplitude 1A, 1CUnderdetection of VT VT slowed to rate < detection rate IA, IC, III

Increase in cycle length variability of VT results inmisclassification of VT as SVT by stability enhancement

Inappropriate detection of SVT Organization of atrial fibrillation into atrial flutter with 1:1AV conduction

1C

Use-dependent altered morphology of ventricularelectrogram causes misclassification of SVT as VT

1C

Increase in pacing threshold Baseline Amiodarone, 1CRapid pacing rates for antitachycardia 1C

Bradyarrhythmias Battery depletion from more bradycardia pacing Amiodarone, β-blockers,calcium antagonists

Pacing-induced dyssynchronyIncrease in defibrillation threshold Unsuccessful shocks/death Amiodarone, 1BMore aborted or delivered shocks Proarrhythmia IA, IC, III

marginal (e.g., safety margin <10 J) and if an in-sufficient safety margin would result in a changein therapy (revision of the defibrillation system ordiscontinuation of the drug). Similar considera-tions apply to substantial increases in amiodaronedose.

Metabolic EffectsHyperkalemia is the metabolic abnormality

with the greatest clinical effect on ICD func-tion. In addition to increase in pacing thresh-old,7,82,83 it can present as T-wave oversensing,83,84

R-wave double-counting, or failure to detect VT orVF (Fig. 19). Hypokalemia and hypomagnesemia

Figure 18. Underdetection of VF caused by antiarrhythmic drugs (amiodarone and mexiletine).Displayed from top to bottom are the atrial, ventricular near-field and ventricular far-field elec-trograms, and event markers. VT degenerates to VF. The left panel shows detection of VF. Despitepersistence of VF (seen in far-field ventricular electrograms), slowing in local near-field electro-gram results in four events at cycle length 378–388 ms, slower than the VT detection interval(“VS”) resulting in diversion of therapy (“Dvrt Chrg”). Detection occurred eventually, and theresultant ICD shock terminated VF. Atrial asystole occurs during VT/VF.

may contribute to repetitive episodes of VT (“VTstorm”).85

Electromagnetic InterferenceUbiquitous environmental electromagnetic

energy can generate electrical potentials on ICDsensing electrodes. Such electromagnetic interfer-ence (EMI) can result in inappropriate detectionof VT/VF, failure to sense VT/VF, and inappro-priate pacing or inhibition of pacing. A staticmagnetic field causes reversion to magnet mode,which usually disables detection of VT/VF butdoes not alter pacing. Electromagnetic interfer-ence with frequencies less than ∼2 Hz may be


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Figure 19. Underdetection of VF caused by hyperkalemia (potassium 6.7) in the setting of chronicamiodarone therapy. (A) Near-field and far-field ventricular electrograms and a Marker Channel ofa Guidant Prizm VRTM ICD are shown. The top panel shows a sine-wave VT in the far-field channel,which is detected as VF because local electrograms on the near-field channel are double-counted.At right of upper panel, four intervals greater than the programmed VF detection interval of 316ms (190 bpm) result in an aborted shock. Lower panel shows persistence of VF after the shock isaborted. Too few intervals are sensed in the VF zone to permit detection of VF. The patient wasresuscitated by external shock. (B) ICD system testing after correction of hyperkalemia. InducedVF is sensed reliably and terminated by an ICD shock. The near-field electrogram is narrow,indicating that the double electrograms present during the clinical arrhythmia were caused byfunctional conduction block. Courtesy of Dr. Felix Schnoell.

detected as R-waves and prevent automatic ad-justment of sensitivity from sensing VT/VF. Over-sensing of higher frequency electromagnetic in-terference may cause inappropriate detection ofVT/VF. Pacemaker function may respond as track-ing (atrial channel) or inhibition (ventricular chan-nel). These effects have been reviewed.86,87 Withthe exception of industrial and military sources,clinically significant interference by nonmedicalsources is rare.88,89 Interference from sources inthe medical environment has been studied specif-ically, including magnetic resonance imaging90,91

radiofrequency catheter ablation92 and surgicalelectrocautery.93 We address limited issues rele-vant to troubleshooting.

Electromagnetic interference is a lesser prob-lem for true-bipolar sensing than for integrated-bipolar sensing. It is diagnosed based on history ofexposure and characteristic high-frequency, non-physiological signals that are larger in far-fieldthan near-field electrograms (fig. 3 in part I of thisreview). Diminishing programmed sensitivity maymitigate interference. VT/VF detection may be dis-abled during planned, unavoidable exposure (e.g.,surgical electrocautery) if an external defibrillatorand trained personnel are present. Field strengthin the patient’s environment may be measured ifexternal electromagnetic interference is suspected.Static magnetic fields >5 G should be avoided. ICDdetection of time-varying, external magnetic fields


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depend on their frequency and orientation as wellas the size and number of inductive loops in thelead. Reasonable field intensity limits are 6000V/m for 60 Hz alternating current, 70 V/m forhigh-frequency fields (>150 kHz), 80 Gauss formodulated magnetic fields with frequency <10MHz, and 1 G for those with frequency >10MHz.94

Given the variable response to time-varying fields,one approach to assessing electromagnetic safetyof an environment is to place an identical andidentically programmed ICD in a saline bath orconductive gel and expose it to the environment.The ICD should be connected to the same leadwith several loops to assess the effect of inducedcurrents. Electrograms and telemetered markersshould be recorded. Alternatively, the patient’sICD electrogram and marker channels may berecorded while the patient is operating equip-ment, preferably with the ICD in a “monitor-only” mode and a contingency plan for promptdefibrillation.

Post-Implant Programming to Optimize TherapyThe medieval jurist Henry de Bracton ap-

plied the phrase “An ounce of prevention is wortha pound of cure” to philosophy of law. But itis equally applicable to ICDs: Appropriate pro-gramming minimizes the need for troubleshoot-ing. In clinical studies, better programming ofSVT-VT discriminators would have prevented ap-proximately one-quarter of inappropriate therapyfor SVT.11,95 In practice, this fraction probably ishigher. Further, reports continue to include fatalproarrhythmia and sudden deaths due to ICD pro-gramming errors.4,60,96

SensingIf the amplitude of the sinus-rhythm R-wave at

implant is ≥7 mV, nominal sensitivity near 0.3 mVprovides adequate sensing of VF.16 More sensitivesettings may be selected if the R-wave is ≤3 mV.Less sensitive settings decrease the risk of T-waveoversensing in Medtronic ICD, but may increasethe risk of undersensing VF.

Detection Zones and Zone BoundariesTypical values for these rate boundaries are

360–500 ms for slower VT, 340–300 ms for fasterVT, and 280–240 ms for VF. Some experts (includ-ing the authors) recommend three-zone program-ming in most patients implanted for secondaryprevention—even those whose only clinical ar-rhythmia is VF—because most spontaneous VFbegins with rapid VT and most rapid VT can beterminated by antitachycardia pacing.97,98 Threezones permit different antitachycardia pacing for

two distinct rates of VT and antitachycardia pac-ing for monomorphic VT that overlaps in rate withpolymorphic VT. Other experts recommend tworate zones with the slowest at cycle length 340–320ms for patients whose only spontaneous arrhyth-mia is VF. This approach lowers the risk of inap-propriate therapy but increases the risk of not treat-ing VT. In the largest primary-prevention trial,99

ICDs were programmed to a single detection zoneat cycle length 320 ms, without SVT-VT discrim-inators. Approximately half of shocks were inap-propriate; the incidence of sudden death from un-detected VT has not been reported.

The sinus-VT rate boundary should be slowenough to ensure detection of all hemodynami-cally compromising VT. The boundary betweenthe two VT zones should be based on the cy-cle length at which different types or fewer tri-als of antitachycardia pacing are preferred. TheVT-VF rate boundary is based on the cycle lengthbelow which antitachycardia pacing should notbe delivered. In Medtronic ICDs, which useconsecutive-interval counting above the VF Inter-val and X-of-Y counting below it,62 this bound-ary should be set to prevent underdetection of ir-regular, polymorphic VT by consecutive-intervalcounting.

Duration for Detection and RedetectionDetection duration prior to antitachycardia

pacing should not be decreased from nominalvalues because therapy is immediate after detec-tion and undersensing of monomorphic VT israre. It should be increased in patients who havelong episodes of nonsustained VT. Substantial in-creases in duration for detection of VT proba-bly are safe in St. Jude and Guidant ICDs, whichuse counting methods that are insensitive to occa-sional long ventricular intervals or undersensing:Guidant ICDs use X-of-Y counting, and St. JudeICDs count based on the interval and average of theprevious three intervals. In contrast, consecutive-interval counting used by Medtronic ICDs in theVT zone may underdetect VT if occasional longventricular intervals or undersensing occur.9 Un-less VT is known to be highly regular, the num-ber of intervals to detect VT usually should notbe more than 50% greater than the nominal valuein Medtronic ICDs. Duration for detection of VFmay be reduced from nominal only if there isno alternative method to ensure reliable detec-tion. Redetection time for VT should be increasedfrom nominal if VT is well-tolerated, but anti-tachycardia pacing is not. Redetection time for VFshould be decreased if post-shock undersensingoccurs.


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SVT-VT DiscriminationSome SVT discriminators should be pro-

grammed at implant in all patients with intact AVconduction. See Section III D.

Programmed TherapyAntitachycardia pacing should be pro-

grammed in all patients unless it is known tobe ineffective or proarrhythmic. See Section IVC The first shock strength for VF should be seteither in relation to an established implant safetymargin or to maximum.16,27 In modern ICDs withshort charge times, we recommend that shocks forhemodynamically stable VT be programmed tothe same strength as those for VF, rather than to alow energy. This maximizes the likelihood that aventricular shock will terminate (inappropriatelydetected) rapidly conducted, atrial fibrillation. Italso minimizes both the risk that a ventricularshock will accelerate VT and the risk that itwill be weaker than the atrial upper limit ofvulnerability (and thus initiate atrial fibrillation ifit is delivered during the atrial vulnerable period).But we recognize that practice differs with regardto this issue.

Evolving TrendsThe ICD has expanded from a single-purpose

“shock box” to a multi-purpose platform for elec-trical cardiac therapies; ICDs under developmentinclude sensors for monitoring heart failure andother comorbidities. This increasing functionalityand complexity is likely to expand the domain oftroubleshooting and to result in yet unknown, un-intended consequences, including novel intrade-vice interactions.

Present ICDs have approximately 500 pro-grammable features. Despite simplified user in-terfaces that might reduce operator errors, bothnonlethal100,101 and lethal4,96 programming errorsoccur. The automatic, self-checking, and self-adjusting functions in today’s ICDs are a wel-come addition, given the time pressures of presentclinical practice and the fact that troubleshootingis both time consuming and poorly reimbursed.However, automated features should be disabledin some conditions. Examples discussed in thisreview include the need to disable automatic up-dating of morphology-algorithm templates in pa-tients with rate-related aberrancy and the need todisable Medtronic Smart Mode when VT recursrapidly after effective antitachycardia pacing. Fu-ture automated features may also introduce un-foreseen consequences that require novel forms oftroubleshooting.

A potential risk of simplifying the user inter-face is loss of programming flexibility and trou-bleshooting tools. ICDs are required to performmultiple functions based on input signals and clin-ical conditions that vary widely from patient topatient. Features optimized for one condition donot perform optimally for another condition. Con-sider familiar clinical trade-offs: The preferred so-lution to rejection of far-field R-waves depends onthe relative sizes and timing of the P-wave and far-field R-wave as well as the likelihood that the pa-tient will develop atrial fibrillation or flutter. Thepreferred solution to discriminating SVT from VTwith a 1:1 AV relationship depends on various fea-tures such as the reliability of morphology discrim-ination with available electrograms, the differencebetween VA and AV times during VT and SVT, andthe specific responses of VT and SVT to antitachy-cardia pacing. Prophylactic implantation of ICDswithout prior electrophysiological evaluation in-creases the conflicting requirements for reliabledetection of all VTs while rejecting unanticipatedSVTs.

ICD manufacturers are working to provide asimplified user interface that provides sufficientoptions for common clinical situations. At thesame time, they seek to maintain and increasethe wide range of flexible options that permit op-timal programming for outlier patients or clini-cal conditions. Manufacturers must also providephysicians with adequate technical references fortroubleshooting. Reference manuals are no longerpackaged with ICDs, although some manufacturersprovide online manuals.

Present ICDs provide troubleshooting alerts tothe patient and physician for specific risk condi-tions.40 Most relate simply to a parameter “out-of-range,” but at least one lead-integrity alert that in-tegrates multiple parameters has been verified andreleased.39,102 The capability to download ICD dataremotely over the Internet37,38 permits develop-ment of automated troubleshooting algorithms thatrequire computing power beyond that available toimplanted ICDs or even ICD programmers. One ap-plication would be high-level, automated analysisof stored arrhythmia episodes to evaluate the ac-curacy of SVT-VT discrimination and recommendprogramming changes. Physician-initiated or au-tomated ICD reprogramming via internet couldboth simplify troubleshooting and introduce novelproblems.

Acknowledgments: We wish to thank Jim Gilkerson,Ph.D. (Guidant), Walter Olson, Ph.D., and Jeff Gillberg, M.S.(Medtronic), and Tami Shipman, B.S. (St. Jude Medical) fortheir diligent reviews of this article.


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