Sensing and Detection With Cardiac Implantable Electronic Devices

Amplification and Sampling

Modern CIEDs use digital circuitry because they use less power than their analog counterparts. Sampling is the process of converting an analog EGM signal into a digital sequence of sampled voltages. It must be performed at ≥2 times the source's signal frequency to reproduce the source's information content completely (Nyquist theorem). The fidelity of the sampled signal depends on sampling rate, sampling precision (voltage increment of the least significant bit), and dynamic range of the amplifier. The filtered signal is then amplified. For the true sampling precision to equal the number of bits stored, amplifier noise must be less than the sampling precision. Otherwise, the least significant bits of the sampled signal will be altered by amplifier noise, and the true sampling precision will be less than implied by the number of bits stored. Higher sampling rates (>400 Hz), precision (<10 µV) and dynamic range (>12 bits) may require more power, which is at a premium in implantable devices. Efficient circuit design can mitigate higher current requirements, but compromises in performance are still required to maintain battery longevity. To date, no CIED has successfully used EGM characteristics to discriminate far-field R waves or antegrade versus retrograde atrial EGMs, in part because sufficient sampling rate, precision, and amplifier dynamic range are not practical.

ICD sampling circuitry reproduces cardiac signals faithfully because the low pass filter is at a high enough frequency to include almost all the signal content (39-80 Hz, see Table 4-2 ) and sample above the Nyquist rate (128-400 Hz per channel). However, 128-Hz sampling superimposes a periodic 8-Hz distortion (beat frequency) on 60-Hz signals such as electromagnetic interference (EMI) because the signal is sampled only slightly faster than the Nyquist rate, and provides only slightly more than two samples per cycle ( Fig. E4-4 ). This 8-Hz “signature” uniquely identifies 60-Hz EMI in devices with 128-Hz sampling.

Filtering and Rectification

Once the signal is in the digital domain, it is band-pass filtered to remove baseline wander and select certain ranges of frequencies depending on the application (see Table 4-2 ). For sensing, the key is to filter in such a way as to reduce unwanted signals such as T waves, while retaining as much of the desired signal, the R wave. In ventricular fibrillation (VF), R waves have amplitude and frequency characteristics that overlap with those of T waves ( Fig. 4-7 ). It is essential not to filter out too much of the VF signal, even though the result is occasional T-wave oversensing. When band-pass filtering alone cannot isolate the signal of interest, additional processing such as morphology matching or time-frequency pattern recognition can be applied successfully as described below.

After the filtered EGM signal has been amplified, it is rectified so that all signals are represented by their absolute magnitudes. This removes polarity information but allows sensing to be accomplished with a single-sided comparison. Sensing occurs when the amplitude of the rectified EGM exceeds the threshold voltage (see Fig. 4-6 ).

Electrogram Amplitude: Effect of Measuring Methods and Signal Processing

It is important to understand how differences in measurement processes can affect measured amplitude to distinguish these from biological changes caused by progression of disease. Figure 4-8 illustrates the primary variables: base-peak versus peak-to-peak, signal filtering, and measurement point. Historically, operators measured peak-peak amplitude “manually” at the intrinsic deflection of unfiltered signals. Usually automated CIED measurements are performed differently. Typically CIEDs measure the base-peak filtered and rectified signal. They measure the maximum amplitude in a short time window (50-120 msec) after the sensed event. Thus if there is a long period of low amplitude signal at the onset the EGM, changing the sensing threshold can alter the measured amplitude. Traditional operator-measured EGM amplitude usually exceeds device-measured EGM amplitude, but automatic measurements usually provide a better indicator of device sensing performance.

Blanking Periods

Blanking periods ( Fig. 4-9 ) are designed to ensure that a single event is sensed only once rather than multiple times, by inhibiting sensing after sensed depolarizations, pacing pulses, or shocks. In early CIEDs, blanking was a hardware feature that turned off (“blanked”) the sense amplifier. In modern CIEDs, most blanking is performed using software. Blanking must be longer after paced events than sensed events because there is an activation delay from the paced event to onset of global cardiac depolarization; in contrast, cardiac depolarization begins before sensed events. Some CIEDs have partial blanking periods on the atrial channel, an interval following the blanking period in which the sensing threshold is increased. See subsequent discussion of atrial sensing and blanking.

Multichamber CIEDs have cross-chamber blanking periods. The ventricular blanking period after atrial-paced events is designed to prevent oversensing that causes crosstalk inhibition of ventricular bradycardia pacing (see Chapter 36 ) and may cause inappropriate detection of ventricular tachycardia/ventricular fibrillation (VT/VF). The postventricular atrial blanking period (PVAB) after ventricular paced or sensed events is designed to prevent cyclical oversensing of far-field R waves that results in inappropriate mode switching and incorrect classification of the atrial rhythm as atrial tachycardia or atrial fibrillation (AF). Unlike same-chamber blanking periods that correspond to physiologic refractory periods, cross-chamber blanking periods have no physiologic correlate. As described below, they may cause functional undersensing of cardiac EGMs in the blanked chamber.

Refractory Periods

Some manufacturers use the term “refractory period” instead of blanking period. Others reserve “refractory period” for an interval following the blanking period in which the sense amplifier is enabled but bradycardia pacemaker functions do not respond to sensed events as they do during typical alert periods (see Fig. 4-9 ).

Refractory-sensed events are not used for basic pacemaker timing cycles (see Chapter 36 ), but they are used for atrial tachyarrhythmia detection and some advanced pacemaker functions. Marker channels denote events sensed during refractory periods. Software blanking may blur the traditional distinction between blanking and refractory periods because software-blanked atrial events are also used for atrial tachyarrhythmia sensing. Software blanking may blur the traditional distinction between blanking and refractory periods as software-blanked and refractory atrial events are both used for atrial tachyarrhythmia detection, but not for pacemaker timing. Marker channels apply different designations to distinguish events during sensing alert periods, refractory periods, and atrial software blanking periods.

Considerations for Different Cardiac Implantable Electronic Devices

Early pacemakers had long same-chamber blanking periods to prevent oversensing from inhibiting pacing. However, CIEDs require short blanking periods to sense all activations during tachyarrhythmias. ICDs have short ventricular blanking periods to sense R-R intervals reliably in VF and modern multichamber pacemakers, and ICDs have short atrial blanking periods to sense short A-A intervals in AF. Some ICDs have longer partial blanking periods in the atrium to prevent far-field ventricular EGMs from interrupting normal pacemaker function. Special considerations that apply to cardiac resynchronization therapy-defibrillators/pacemakers (CRT-D/Ps) are covered in Chapters 18 and 36 .

Fixed Sensing Thresholds

Early pacemakers used “fixed” sensing thresholds programmable to a constant value. Typically, fixed ventricular sensing thresholds are set higher (less sensitive) than atrial thresholds because of the differences in R-wave versus P-wave amplitude; unipolar sensing thresholds are set higher than bipolar sensing thresholds to reduce oversensing of far-field cardiac and extracardiac signals. Some pacemakers automatically adjust fixed sensing thresholds periodically to adapt to changes in EGM amplitude over time.

Dynamic Sensing Thresholds

High sensitivity is required to ensure reliable sensing of low-amplitude ventricular EGMs in VF and atrial EGMs in VF. Because continuous high sensitivity results in undesirable oversensing, CIEDs that sense AF or VF use feedback mechanisms based on P- or R-wave amplitude that adjust the sensing threshold dynamically ( Fig. 4-10 ). This is referred to by various terms, including automatic adjustment of sensitivity, autoadjusting sensitivity, and automatic sensitivity control. Some early ICDs used automatic step adjustments of sensing-amplifier gain (automatic gain control) as a primary means for avoiding T-wave oversensing and ensuring detection of low-amplitude VF EGMs. This resulted in sensing errors when EGM amplitude changed abruptly and has been abandoned.

Presently, all ICDs and many pacemakers adjust sensitivity “dynamically” in relation to the amplitude of each sensed intrinsic depolarization or pacing pulse. At the end of the blanking period after each sensed event, the sensing threshold is set to a high value. It then decreases with time until a minimum value is reached. In comparison with a fixed sensing threshold, automatic adjustment of sensitivity increases the likelihood of sensing low-amplitude and varying EGMs during AF or VF, while reducing the likelihood of far-field R-wave oversensing in the atrium or T-wave oversensing in the ventricle. After either sensing or pacing, ICDs are most vulnerable to oversensing of low-amplitude signals late in the diastole of bradycardia, when the amplifier sensitivity is maximal for an extended period.

This section considers dynamic sensing in the ventricle. The same considerations apply to dynamic sensing in the atrium, except that in the atrium minimum values of sensitivity are lower and the rate at which the sensing threshold decreases over time is faster.

Postsensing automatic adjustment of ventricular sensitivity.

Details differ among manufacturers (see Table 4-3 ) ( Fig. E4-5 , Fig. E4-6 ), but they all have these common features: (1) ICDs blank the sense amplifier postsense (nominal values 110-135 msec) to prevent R-wave double-counting. (2) The sensing threshold is highest at the end of blanking period (minimum sensitivity). In general, the highest value of the sensing threshold is greater if the R-wave amplitude is greater; some manufacturers limit this value to reduce the likelihood of undersensing VF with highly variable amplitude ( Fig. E4-5 ). No manufacturer displays this value on the programmer. (3) The sensing threshold decreases to a minimum value that determines the smallest EGM amplitude that can be sensed, corresponding to the programmed value of sensitivity (nominal values 0.3-0.8 mV). Depending on the manufacturer, this threshold decrease may occur as a series of step functions, a linear decay, or an exponential decay. (4) The minimum value of the sensing threshold is programmable; in contemporary ICDs, it remains fixed, independent of R-wave amplitude.

Programmable and nonprogrammable differences among manufacturers affect the trade-off between preventing T-wave oversensing and ensuring sensing of VF. A combination of a high value for high-pass filter and high starting point for dynamic sensitivity can reduce T-wave oversensing, but rare cases of serious VF undersensing have been reported caused by failure of sensitivity to adjust when rapid changes in EGM amplitude occur. Figure 4-11 shows a clinical example. It is prudent to test sensing of induced VF after programming that increases the risk of VF undersensing if a sensing safety margin was not determined at implant.

Postshock Sensing

Postshock sensing is critical for redetection of VF after unsuccessful shocks and for accurate detection of episode termination. Postshock polarization may take seconds to minutes to decay off the electrodes and thus interfere with postshock sensing. Furthermore, the strong electric fields of shocks cause electroporation, the creation of microscopic holes in the cardiac cell membranes. This has been proposed as an additional mechanism for postshock distortion of EGMs recorded from high-voltage electrodes. Because EGMs of dedicated bipolar sensing electrodes are minimally affected by shocks, they became standard for early epicardial ICDs. For transvenous ICDs, postshock sensing recovers more rapidly with dedicated bipolar sensing configurations than with integrated bipolar sensing. This is a minor issue for present integrated bipolar leads with a pacing tip electrode to distal coil spacing of about 12 mm or greater. However, it has reemerged as a potential problem for subcutaneous ICDs that sense using shock electrodes (see below). Transvenous ICDs use the shock EGM to discriminate VT from supraventricular tachycardia (SVT) by ventricular EGM morphology. These morphology discrimination algorithms can be distorted for several minutes postshock.

Recognition

Oversensing is diagnosed if more than one ventricular sensing marker occurs within one true cardiac cycle. Oversensing of noncardiac signals is diagnosed by the superimposition of these signals on true ventricular EGMs. The diagnosis is most certain when independent, true ventricular EGMs are identified. However, in patients without an intrinsic ventricular rhythm, oversensing inhibits bradycardia pacing, so the absence of true ventricular EGMs or pacing markers complicates the diagnosis. In these patients, oversensing may be confirmed if the oversensed signal is not recorded on the shock channel, even if analysis of the sensing channel alone does not permit definitive differentiation of VF from oversensing.

Classification: Cyclical Versus Noncyclical Oversensing

Oversensing can be classified by EGM morphology, temporal pattern (cyclical versus noncyclical), source type (physiologic versus nonphysiologic), and source location (intracardiac versus extracardiac) ( Fig. 4-12 ). Specific sources generate oversensed signals with characteristic morphological features that differ from true cardiac EGMs in frequency content and amplitude.

It is useful to classify the temporal pattern of oversensed signals as varying consistently with the ventricular cycle (cyclical) or independent of the ventricular cycle (noncyclical). A cyclical pattern indicates an intracardiac source of oversensing, but a noncyclical pattern may occur with extracardiac or intracardiac sources. Oversensing of intracardiac physiologic signals (R-wave double-counting or P/T-wave oversensing) usually produces a characteristic pattern of one oversensed event for each true ventricular cycle. Cyclical nonphysiologic, intracardiac signals may present as multiple oversensed events in each ventricular cycle.

In contrast, extracardiac signals (physiologic or nonphysiologic) always produce noncyclical oversensing, with superposed extraneous signals that are dissociated from true ventricular EGMs, analogous to the relationship between ECG artifacts and the cardiac rhythm.

P-Wave Oversensing

Recording an atrial EGM facilitates recognition of P-wave oversensing. During a stable, 1 : 1 rhythm, the device-detected “R-R” pattern consists of alternating sensed P-R and R-P intervals ( Fig. 4-13 ). If first-degree AV block is present, these intervals may be approximately equal. In AF, ventricular oversensing of atrial EGMs may result in multiple oversensed physiologic signals for each true cardiac cycle, producing an interval plot with short, irregular intervals, characteristic of nonphysiologic oversensing.

Oversensing of spontaneous P waves is rare in adults because the ventricular sensing bipole is usually far from the atrium. Thus early after implant, P-wave oversensing usually indicates RV lead dislodgement to a position closer to the atrium/tricuspid valve. However, P-wave oversensing may occur in children with small right ventricles and in adults with integrated-bipolar sensing. It must be distinguished from atypical, end-diastolic cyclical oversensing in fractures of the cable to the ring electrode (see below).

P-wave oversensing may result in inappropriate detection of VT if the atrial rhythm is a tachycardia and in inappropriate detection of VF if the atrial rhythm is AF (see Fig. 4-13 ). The first approach to significant P-wave oversensing is to reduce the programmed ventricular sensitivity. If this is unsuccessful or sensing of VF is not reliable at the reduced sensitivity, the ventricular lead should be revised. As a temporary measure, P-wave oversensing in sinus rhythm may be mitigated by forced atrial pacing.

Ventricular oversensing of atrial paced events (crosstalk) is addressed in Chapter 36 .

R-Wave Double-Counting

R-wave double-counting occurs if the duration of the sensed EGM exceeds the ventricular blanking period. Consistent double counting results in an alternation of ventricular cycle lengths ( Fig. 4-14 ). The expected sensed event early in the R wave is followed by a second event as soon as the ventricular blanking period ends. The interval between these two events is always short enough to be in the VF zone. The duration of the device-detected interval that begins with the second event approximates the difference between the spontaneous ventricular cycle length and the blanking period of the ICD. This produces a characteristic “railroad track” pattern on a plot of stored ventricular intervals. Of course, any cause of alternating cycle lengths also produces this pattern ( Fig. 4-15 ).

R-wave double-counting often results from local ventricular conduction delay. It is most common when ICDs with short ventricular blanking periods ≤120 msec (Biotronik and Medtronic) are connected to integrated-bipolar leads. For integrated-bipolar sensing we suggest increasing programmable blanking periods to >120 msec. R-wave double-counting may be precipitated by reversible conduction block caused by hyperkalemia or sodium channel blocking antiarrhythmic drugs. Conduction delays during PVCs or VT/VF may facilitate R-wave double-counting (see Fig. 4-14 ). Most such double counting does not require intervention because it is infrequent (PVCs), occurs only intermittently during VT, or occurs during VF. Rarely, slow or self-terminating tachycardias may receive unnecessary therapy. The primary troubleshooting intervention is to increase the ventricular blanking period. In CRT-Ds, loss of RV capture may present as R-wave double-counting (see Fig. 4-14 ). The ICD counts both the paced ventricular event and the wavefront conducted from LV capture to the RV sensing bipole, if the conduction delay exceeds the ventricular blanking period.

T-Wave Oversensing in Conducted Rhythms

The root cause of T-wave oversensing is the requirement that ICDs reliably sense VF, which is characterized by R-R intervals shorter than the typical Q-T interval in addition to some EGMs with low amplitudes and slew rates. In contrast to the alternating device-measured “R-R” intervals typical of double-counted R waves, the hallmark of T-wave oversensing is alternating sensing EGM morphologies caused by alternation of EGM frequency content ( Fig. 4-16 ). Higher-frequency R waves alternate with the lower-frequency T waves. This may be easier to appreciate on wide-band EGMs than narrow-band EGMs (see Fig. 4-5 ). Device-detected “R-R” interval alternation (R-T versus T-R) is subtle if the Q-T interval is short or the sinus rate is fast; occasionally, it is absent. A simultaneous shock EGM confirms that alternate low-frequency EGMs represent T waves. Bigeminal PVCs during sinus tachycardia or bidirectional catecholaminergic VT may produce a similar pattern on the filtered sensing EGM, but each R wave has a corresponding T wave on the shock EGM. Alternation of EGM amplitude without alternation in morphology is rare and suggests true tachycardia.

Oversensing of spontaneous T waves may be dichotomized by the amplitude of the corresponding R waves (see Fig. 4-16 ) because the therapeutic approaches often differ : If the R wave is large and T wave just above the sensing threshold, some T-wave oversensing can be resolved by reducing programmed sensitivity; with small R waves, resolution usually requires one of the alternative approaches discussed below. T-wave oversensing with large R waves is caused by an absolute increase in T-wave amplitude. Clinical correlates include pediatric patients, hypertrophic cardiomyopathy, long QT syndrome, short QT syndrome, hyperkalemia, and rarely, other drug and metabolic abnormalities. In contrast, in the setting of small R waves, oversensed T waves usually have normal amplitude, such as in Brugada syndrome, or advanced myocardial disease. The root cause relates to a fundamental limitation of automatically adjusted sensitivity, which links the initial value of sensitivity to the amplitude of the preceding R wave (see Fig. E4-5A ). Exercise-induced T-wave oversensing may be caused by increase in absolute T-wave amplitude, decrease in R-wave amplitude, or both.

A limitation of dichotomizing T-wave oversensing by R-wave amplitude is that large variations in R-wave amplitude are common in dedicated-bipolar leads. These variations are often abrupt and transient, rather than gradual and progressive. Presently, most cases have no identifiable clinical correlate and thus cannot be predicted, although one case report attributed temporal variation to an inflammatory process (sarcoidosis).

T-Wave Oversensing: Prevention and Remediation

Because T-wave oversensing usually is unpredictable, features that mitigate it should be enabled proactively at implant and operate continuously, providing they do not cause undersensing in VF. Some mitigations may increase undersensing in VF. These should be implemented reactively, after T-wave oversensing has occurred.

Device-based options.

Other approaches ( Fig. 4-17 ) described in a recent review may reduce T-wave oversensing. Biotronik offers programmable rectification options. A higher, nominal high-pass filter (e.g., 20 Hz versus 10 to 15 Hz, St. Jude Medical, and Boston Scientific) reduces T-wave oversensing. Theoretically, a higher high-pass filter might increase undersensing in VF; we are not aware of published data on time to detect VF with different high-pass filters.

If the sensing bipole is programmable, changing from dedicated to integrated-bipolar may prevent T-wave oversensing. SVT morphology discriminators or algorithms that withhold shocks for oversensing related to lead failure do not prevent T-wave oversensing, but they may withhold inappropriate therapies. Algorithms that identify T waves based on frequency content or morphology are discussed under “Enhanced Sensing” below.

A new ICD or pace-sense lead should be inserted if R-wave amplitude is low and T-wave oversensing cannot be prevented without programming that compromises sensing of VF.

Postpacing T-Wave Oversensing

T-wave oversensing is a lesser problem after paced than sensed beats because ICD blanking periods are longer after pacing and because postpacing T-wave oversensing resets the pacing timing cycle, preventing inappropriate detection of VT/VF in pacemaker-dependent patients. In these patients, it is not a clinical problem unless it causes bradycardia pacing or antitachycardia pacing (ATP) at the wrong rate. If AV conduction is intact (e.g., CRT-D patients), consistent postpacing T-wave oversensing causes a repeating sequence of three intervals in which the first two are in the VT or VF zones: pacing stimulus to oversensed T, oversensed T to spontaneous R, and spontaneous R to pacing stimulus. Inappropriate therapy is unusual, but it may occur with a probabilistic counting detection algorithm if only two thirds of intervals are required to be in the VT zone (e.g., 8/12 with fast first and last intervals ) or a few spontaneous premature (PVC) beats. Solutions include adjusting sensitivity and increasing the postpacing blanking period. In CRT-D/Ps, programming V-V pacing delay or LV-only pacing may also resolve T-wave oversensing that inhibits biventricular pacing.

Diaphragmatic Myopotentials

These low-amplitude, high-frequency signals are more prominent on the sensing EGM than the shock EGM because the sensing bipole is closer to the source. Their amplitude varies with respiration, but not the cardiac cycle ( Fig. 4-18 ). Oversensing is most common with integrated-bipolar sensing at the RV apex. It usually begins when sensitivity is maximal, after long diastolic intervals or ventricular paced events, and often ends with a sensed R wave, which reduces sensitivity abruptly. Thus it commonly occurs in pacemaker-dependent patients in whom inhibition of pacing maintains high ventricular sensitivity, resulting in persistent oversensing and inappropriate detection of VF. With chronically implanted leads, oversensing may first occur after the dominant rhythm changes from ventricular sensed to ventricular paced, such as “upgrade” to CRT or AV junction ablation. Oversensing may be reproduced by monitoring real-time EGMs during deep breathing or straining in different positions, after programming VF detection OFF.

To minimize the risk of oversensing proactively in pacemaker-dependent patients, it may be prudent to program a sensitivity of 0.45 to 0.60 mV if this sensitivity is not nominal, especially if integrated-bipolar sensing is used. The nonprogrammable Boston Scientific “noise rejection” algorithm operates continuously and may reduce oversensing. Occasionally, correction requires inserting a new sensing or defibrillation lead away from the diaphragm.

Pectoral Myopotentials

These high-frequency, variable amplitude signals are prominent on EGMs that include the ICD Can, including shock EGMs and leadless ECG. They may be reproduced by pectoral muscle exercise. Because ICDs do not use these signals as primary sensing channels, pectoral myopotentials do not cause oversensing if the lead is intact. However, they may cause misclassification of exercise-induced sinus tachycardia as VT because algorithms that discriminate VT from SVT based on ventricular EGM morphology usually use the RV coil-Can vector. Pectoral myopotentials might also interfere with algorithms that evaluate lead integrity by comparing near-field and far-field signals (see below).

The diagnosis may be confirmed by monitoring the real-time sensing EGM during pectoral muscle exercise. Oversensing of pectoral myopotentials on sensing EGMs typically indicates an in-pocket insulation breach ( Fig. 4-19 and Case Study 4-1 ). Rarely, pectoral myopotentials may be oversensed in pacemaker-dependent patients with intact integrated-bipolar leads. Additionally, reversal of high-voltage connections on DF-1 dual-coil, integrated-bipolar leads may present as myopotential oversensing caused by change of the sensing vector to a far-field signal that includes the SVC coil and Can as electrodes ( Fig. E4-7 ).

Case Study 4-1

Implantable Cardioverter-Defibrillator Shock during Exercise

Clinical Summary

Medical History

In 2006, a 48-year-old man had a sustained wide complex tachycardia at a rate of 185 bpm (cycle length 324 msec) while working as an electrician repairing railroad cars for Amtrak. He was hypotensive and required cardioversion. Ten years previously, he had been diagnosed with supraventricular tachycardia (SVT) in his country of origin (Armenia). In 2006, evaluation for structural heart disease identified arrhythmogenic right ventricular cardiomyopathy (ARVC). He underwent electrophysiological study and ablation of monomorphic induced VT with morphology identical to the clinical arrhythmia and a rate of 200 bpm (cycle length 300 msec). He was treated with metoprolol 50 mg twice daily, and a dual-chamber implantable cardioverter-defibrillator (ICD) (Medtronic EnTrust Model D153ATG) was implanted with a dedicated-bipolar lead (Medtronic Sprint Fidelis Model 6949).

In 2009, he received a shock after 30 minutes of vigorous exercise on a rowing machine. In clinic, pacing and sensing thresholds were nominal. Lead impedances were stable on multiple repeat measurements (typical values: atrial 456 ohms, RV Tip-Ring 660 ohms, right ventricular (RV) Coil-Can 54 Ω). A good quality chest x-ray showed no abnormality of the leads or generator. A spot film of the pocket confirmed complete insertion of all lead pins into the header.

Diagnosis and Treatment of Device-Detected Ventricular Tachycardia

Electrogram Analysis and Troubleshooting

Tables E4-1 and E4-2 show programmed detection zones and SVT-VT discrimination criteria. This older ICD lacked a morphology discrimination algorithm. It discriminated VT from SVT by the pattern and cycle lengths of dual-chamber intervals (PR Logic, see Fig. E4-27 ).

TABLE E4-1

Programmed Detection Zones

	Detection Interval	NID
VF	300 msec	30/40
FVT via VF	220 msec	(30/40)
VT	350 msec	24

FVT, Fast ventricular tachycardia; NID, number of intervals to detect ventricular fibrillation; VF, ventricular fibrillation; VT, ventricular tachycardia.

TABLE E4-2

Supraventricular Tachycardia-Ventricular Tachycardia Discrimination Criteria

PR Logic Discriminators	SVT Limit 280 msec
Sinus tachycardia ON
Atrial fibrillation ON	Stability OFF
Other 1 : 1 SVT ON	Onset OFF

SVT, Supraventricular tachycardia.

Figure E4-37 shows the interval plot with events identified by numeric markers. The plot begins with a 1 : 1 tachycardia slightly slower than the VT detection interval of 350 msec (1). The tachycardia accelerates gradually across the detection boundary (2). Simultaneously, atrial intervals become rapid and irregular (3). The ICD identifies a regular ventricular rhythm in the VT zone with dissociated, rapid, irregular atrial rhythm. Based on this analysis of intervals, the ICD classifies the rhythm (Detection) as a dual tachycardia (VT + atrial fibrillation). It delivers three sequences of successively faster burst antitachycardia pacing (ATP), (4)-(6). When tachycardia persists, the ICD charges the shock capacitors.

Figure E4-38 displays dual-chamber electrograms (EGMs) recorded from the right atrium (RA) and far-field ventricular EGM (RV Coil-Can). The upper panel shows the real-time, sinus-rhythm EGMs recorded in clinic, and the lower panel shows the stored EGM during redetection of VT after the third trial of ATP (TD marker, VT RX 2 CV). By visual inspection, ventricular EGM morphology is identical in the two panels. The combination of EGM morphology match and gradual acceleration (see Fig. E4-37 ) is diagnostic of sinus tachycardia. Although far-field R waves (FFRW) can be identified on the atrial channel, sensing of atrial and ventricular EGMs is accurate in each panel. Nevertheless, intermittent FFRW oversensing is a potential reason for misclassification of sinus tachycardia as dual-tachycardia.

Figure E4-39 shows the stored EGM at initial detection of VT. Upper and lower panels are continuous. The ventricular markers change from TS to TD as sinus tachycardia accelerates gradually across the sinus-VT rate boundary (1). The marker channels show erratic atrial oversensing. Both EGMs show high-frequency signals that do not represent cardiac EGMs. The differential diagnosis includes electromagnetic interference (EMI) from a poorly grounded rowing machine, pectoral myopotentials, and lead-related oversensing.

The RV Coil-Can EGM includes a large electrode in close proximity to the pectoral muscle. It commonly records pectoral myopotentials and is not used for rate sensing. The consistent ventricular markers indicate that the dedicated RV tip-ring bipole senses the ventricular EGMs accurately. However, an undamaged closely spaced, intracardiac bipole should not record pectoral myopotentials. Further, myopotentials have approximately constant amplitude on the ventricular channel before ATP (VT Rx 1 Burst in lower panel), but they are absent in sections of the atrial channel (2) and their amplitude varies markedly in others (3). External EMI rarely causes the combination of continuous, constant-amplitude extracardiac signals on the shock channel with intermittent, variable-amplitude signals on the atrial channel. However, this combination is characteristic of an in-pocket insulation breach of the atrial lead.

Figure E4-40 shows real-time EGMs recorded in clinic. The upper panel shows surface ECG lead II and the right atrial (RA) EGM during pocket manipulation. The lower panel shows the right atrial and RV sensing EGMs during isometric arm exercises. Both panels show intermittent, variable amplitude, high-frequency extracardiac signals consistent with pectoral myopotentials (1). Additionally, the upper panel shows a progressive decrease in amplitude of the RA EGM from baseline at left, through an intermediate amplitude in the center (2), to a low amplitude at the right. This reduction in amplitude may reflect the reduced potential difference between the two conductors as each is partially grounded to the potential of extracellular fluid.

Returning to Figure E4-37 , atrial oversensing stops and the ICD senses a 1 : 1 tachycardia reliably as the shock capacitors charge after the third ATP sequence (6). Further, the sinus tachycardia rate slows below the sinus-VT detection boundary (7). Nevertheless, the ICD delivers a shock (35 J). This behavior highlights two limitations of this detection algorithm. First, SVT-VT discriminators do not apply in redetection. Second, in this ICD, shock confirmation requires a cycle length within 60 msec of the VT interval to compensate for potential undersensing in ventricular fibrillation. Newer Medtronic ICDs correct the second limitation and will not synchronize on an interval that exceeds the VT interval. The episode ends after eight consecutive postshock intervals are slower than the VT interval (Term.). Additionally, it is likely that the EGM morphology discriminator would prevent initial inappropriate detection in similar cases.

Clinical Management

At surgery, the atrial lead had a visible, pinhole-sized, outer insulation breach from a coil-can abrasion. It was extracted and replaced. The recalled Fidelis lead was also extracted and replaced.

In some cases of atrial oversensing, it may be preferable to retain the atrial lead (e.g., intermittent FFRW oversensing) or to delay lead revision or replacement. In such cases, single-chamber discriminators may be substituted for dual-chamber discriminators. In present Medtronic dual-chamber ICDs, ventricular EGM morphology is the most useful single-chamber discriminator. In this older model, Onset (sudden onset) would have classified this patient's sinus tachycardia correctly. In other patients, the single-chamber Stability criterion may be used in conjunction with consecutive interval counting to reject rapidly conducted atrial fibrillation, but only in the VT zone.

Summary of Key Points

Oversensing on the atrial channel caused dual-chamber pattern and rate analysis to misclassify sinus tachycardia as a regular VT with coexisting atrial fibrillation. This type of misclassification is unlikely in ICDs with morphology discriminators. Although oversensing stopped before the last redetection, VT was redetected because the ICD does not apply SVT-VT discriminators in redetection. The “conservative” confirmation algorithm delivered the shock despite slowing of sinus tachycardia from the VT zone to the sinus zone. Analysis of the stored atrial and RV Coil-Can EGMs indicated that the atrial rhythm was misclassified because the atrial channel oversensed pectoral myopotentials. In contrast to the RV Coil-Can EGM, atrial EGMs recorded from normally functioning, closely spaced bipoles do not record pectoral myopotentials. Intermittent and variable pectoral myopotentials on a dedicated-bipolar channel are typical of in-pocket insulation failure. This diagnosis was confirmed by real-time maneuvers, despite a normal chest x-ray and normal atrial lead impedance. Lead impedance is measured only a few times per day, and it may not be measured at the moment an intermittent insulation breach opens.

Reference

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  Swerdlow CD, Ellenbogen KA: Implantable cardioverter-defibrillator leads: design, diagnostics, and management. Circulation 128:2062–2071, 2061–2069, 2013.