Surface Electrocardiogram vs. Intracardiac Electrogram

An electrogram (EGM) is a graphic display of the potential difference between two points in space over time. During the upstroke of a myocardial action potential, the inside of the cell abruptly changes from its resting negative potential (with respect to the outside of the cell) to a neutral or slightly positive potential. After about 250 to 400 milliseconds (msec), the cell membrane is then repolarized, with the inside of the cell returning to its resting, negatively charged state. Figure 3-1 illustrates how an EGM is recorded between two electrodes in contact with the myocardium.

Figure 3-1 An electrogram (EGM) is recorded between two electrodes in contact with the myocardium.

A, At rest, both electrodes record a similar charge, with no potential difference between them. B and C, As a wavefront of depolarization moves under electrode 1, a difference in electrical charge is generated such that electrode 1 becomes electrically negative with respect to electrode 2. D, As the wavefront propagates under electrode 2, no potential difference between the two electrodes is recorded. E, The depolarization wavefront is followed by a wavefront of repolarization, during which a potential difference of opposite polarity is recorded. Because the EGM is determined by the instantaneous potential difference between the electrodes, the amplitude and shape of the recorded signal are determined by the direction from which the wavefront approaches the electrodes. For example, if a wavefront of depolarization reached both electrodes at the same time, there would be no potential difference between the electrodes, and an EGM would not be inscribed.

The electrocardiogram (ECG) is recorded from two electrodes on the surface of the body at some distance from the heart. The typical amplitude of its QRS complex is about 1 millivolt (mV). The locations of the two electrodes determine the vectorial “viewpoint” from which the electrical activity of the entire heart is observed from the body surface. In contrast, the ventricular endocardial unipolar EGM typically is 5 to 20 mV in amplitude when recorded from a small electrode on the tip of a lead placed in direct contact with the apex of the right ventricle (Fig. 3-2). The second electrode needed to record this unipolar EGM is the pacemaker or ICD metal “can,” which is located some distance from the heart. The location of this distant second electrode, sometimes called the “indifferent electrode,” has a much smaller effect on the signal’s properties, although it may record noncardiac electric potentials (e.g., from pectoral muscle). The ECG records electrical activity from the entire heart, whereas the EGM records only local wavefronts of depolarization and repolarization. The EGM depends on the viability of approximately 1 or 2 cm³ of myocardium immediately under the tip electrode,^1,2 as depicted in Figure 3-2.

Figure 3-2 Concept drawing of spatial and temporal relationships for unipolar endocardial EGM.

Upper panel, Anatomic drawing. Lower panel, EGM recorded from a small-surface-area electrode at the tip of a pacemaker or defibrillator lead that makes direct contact with the endocardium in the right ventricular (RV) apex. The second electrode required to record an EGM is not shown, because it is a distant and “indifferent” electrode, usually the metal can of the pulse generator, and its location is not important provided that it is a substantial distance from the tip electrode. During a ventricular depolarization, the depolarization wavefront propagates from the septum, around the RV apex, and up the RV free wall (arrows). When the wavefront of depolarization arrives at location 1, just as it approaches the electrode, the initial positive deflection of the EGM occurs, at time 1. When the wavefront passes closest to the tip electrode at location 2, the major negative deflection on the EGM occurs, labeled as time 2. As the wavefront recedes from the electrode at location 3, the final portion of the EGM is inscribed at time 3. This local EGM is not affected by the depolarization wavefront as it travels farther from the electrode. Therefore, the local EGM is shorter in duration than the surface electrocardiographic QRS complex.

Electrode Systems

Figure 3-3 contrasts endocardial unipolar (tip-to-can), bipolar (tip-to-ring), and integrated bipolar (tip-to-coil) electrode systems, and Figure 3-4 shows representative examples. Epicardial electrode systems may be either unipolar (tip-to-can) or bipolar (tip-to-tip). These different electrode configurations have EGMs with similar R-wave amplitudes and slew rates, provided that the interelectrode spacing is at least 10 mm, as is true of almost all commercial pacemaker and defibrillator leads. Because they are more likely to oversense than bipolar EGMs, unipolar electrode systems are contraindicated for ICDs and are used infrequently for modern pacemakers. ICD integrated bipolar electrodes sense between the right ventricular tip electrode and right ventricular high-voltage coil, with sensing characteristics closer to the bipolar than the unipolar configuration. Compared with true bipolar electrodes, integrated ICD bipolar electrodes are more likely to oversense myopotentials and electromagnetic interference (EMI).^3,4 In one study, oversensing occurred in 40% of patients with integrated bipolar sensing, compared with 8% of patients with true bipolar systems.⁴

Figure 3-3 The three practical endocardial electrode configurations used by most pacemakers and ICDs.

The distant and indifferent or “can” electrode is not shown because it is out of the field of view. The unipolar configuration used in Figure 3-1 to explain EGM formation simply records the signal between the tip electrode and the can. The tip electrode can be an active-fixation screw or a small-surface-area tip electrode with various geometries. This unipolar configuration is subject to considerable noise and interference signals and is not suitable for ICDs. The bipolar configuration uses the Tip and Ring electrodes shown in this figure. The interelectrode spacing is typically 12 to 15 mm, and the ring electrode may or may not make contact with the endocardium. The integrated bipolar configuration uses the Tip and RV-Coil electrodes shown in the figure. EGMs recorded from bipolar and integrated bipolar configurations are very similar, and one less conductor is needed for the integrated bipolar configuration. The main disadvantages of the integrated bipolar configuration are susceptibility to diaphragmatic myopotentials, undesired atrial EGMs in small hearts, and slower postshock recovery times caused by electrode polarization. RV, Right ventricular.

Figure 3-4 Ventricular electrocardiograms (ECGs) recorded from different electrode configurations in the same patient.

The central panel shows a left anterior oblique radiograph of a cardiac resynchronization ICD system. Each of the four tracings shows surface ECG lead II, EGM markers, and one ventricular EGM during atrial pacing at a rate of 75 bpm. Top left, Far-field EGM recorded between the right ventricular (RV) coil electrode and the electrically active ICD housing (CAN). Lower left, Integrated bipolar EGM recorded between RV tip and RV coil electrodes. Lower right, True bipolar EGM recorded between the RV tip and ring electrodes. Top right, Left ventricular (LV) unipolar EGM recorded between the LV tip electrode and can. EGM scale is 0.5 mV/mm, except for the LV unipolar EGM, which has a scale of 2 mV/mm. The downward EGM ventricular sense (VS) markers correspond to the time at which the true bipolar RV tip-ring EGM crosses the sensing threshold. Because the “field of view” of this EGM is local, its duration is short. It occurs early in the QRS complex of this patient with left bundle branch block. The integrated bipolar tip-coil EGM has a peak-to-peak amplitude and slew rate similar to those of the true bipolar EGM. However, its field of view is larger due to the size of the RV coil, and therefore the T wave is larger. Low-amplitude atrial EGMs are visible because of the proximity of the coil to the tricuspid anulus. Both the RV coil-CAN and the LV unipolar EGM are widely spaced, between an intracardiac electrode and the extracardiac can. Their duration is closer to that of the QRS complex. The intrinsic deflection of the LV unipolar electrode is late in the QRS complex, corresponding to late activation of the lateral left ventricle. The greater amplitude of the LV unipolar EGM reflects the greater muscle mass of the left ventricle. EGMs recorded from the superior vena cava (SVC) coil and from the atrial bipole (right atrium, RA) are not shown. Radiograph and EGMs are from different patients. Radiograph is for illustrative purposes only.

Amplitude, Slew Rate, and Waveshape

The largest and steepest deflection on the local EGM, called the intrinsic deflection, occurs when the wavefront of depolarization passes the small-tip electrode. The EGM amplitude traditionally is defined as the peak-to-peak amplitude of the intrinsic deflection (measured in mV), as shown in Figure 3-5. The duration of a ventricular EGM usually is less than that of the QRS of the surface ECG, because the EGM is a local signal. The amplitude of an atrial electrogram (AEGM) or ventricular electrogram (VEGM) is determined primarily by the excitable tissue near the tip electrode and therefore is usually similar for unipolar and bipolar signals. Typical amplitudes are 5 to 30 mV for VEGMs and 1.5 to 6 mV for AEGMs.^1,2,5

Figure 3-5 Major clinical descriptors of electrogram.

The peak-to-peak amplitude of the EGM is the difference in voltage recorded between two electrodes and is measured in millivolts (mV). The slew rate is equal to the first derivative of the EGM (dV/dt) and is a measure of the sharpness of the EGM and therefore its frequency content. Slew rate is measured in volts per second (V/sec). Usually, the amplitude of the EGM should be greater than 1.5 to 2.0 mV in the atrium and at least 5 to 6 mV in the ventricle at the time of lead implantation, to ensure adequate sensing. The slew rate should be at least 0.3 V/sec in the atrium and at least 1 V/sec in the ventricle.

The maximum slope of the intrinsic deflection is the slew rate, measured in volts per second, which represents the maximum rate of change of EGM voltage. Mathematically, it is the first derivative of the voltage, dV/dt, so it depends on both the amplitude and the duration of the EGM, and it provides a crude representation of the frequency content. The frequency content of ventricular and atrial EGMs is similar and in the range of 5 to 50 Hz. T waves and far-field R waves have lower frequency content, whereas most myopotentials and EMI have higher frequency content (Fig. 3-6). Typical values for slew rates are 2 to 3 V/sec for VEGMs and 1 to 2 V/sec for AEGMs.^3,4 Usually, an EGM with acceptable amplitude also has an acceptable minimum slew rate (>1 V/sec for VEGMs, >0.3 V/sec for AEGMs). EGMs with very low amplitude will not be sensed, regardless of the slew rate.

Figure 3-6 Signal amplitude versus frequency.

This plot shows the approximate characteristics of the P and R waves that pacemakers and ICDs are intended to sense and the approximate characteristics of the electromagnetic interference (EMI, muscle potentials), T waves, and far-field R waves that they are intended not to sense. The sense amplifier’s filters are designed to sense signals that are above the U-shaped amplifier threshold curve and to reject signals that are below the curve. P waves and R waves have similar frequency characteristics, but usually R waves have higher dominant frequency than P waves. Muscle potentials usually have higher-frequency components than intracardiac signals. T waves and far-field R waves have lower frequencies. As shown, there are some overlaps in these amplitude-frequency characteristics that cause oversensing or undersensing in particular situations. The ellipses representing the amplitude-frequency characteristics in this figure are conceptual and are not based on quantitative measurements.

Increasing the size of the tip electrode in the range of 2 to 10 millimeters (mm) has minimal effect on atrial EGM amplitude but increases EGM duration (Fig. 3-7). For short ventricular bipolar interelectrode spacing of 5 mm or less, the R-wave amplitude decreases, because the difference between the two unipolar EGMs from each electrode causes cancellation in the net bipolar signal. The slew rate increases, because the time between arrival of the wavefront at the two electrodes decreases more than the EGM amplitude. When two electrodes are widely separated, as in early Y-adapted cardiac resynchronization electrode systems, two distinct intrinsic deflections may be recorded on the EGM—one representing right ventricular (RV) activation and the other left ventricular (LV) activation. The interval between these deflections is determined by the conduction delay between the ventricles near the two electrodes.

Figure 3-7 Effects of electrode configurations on atrial endocardial electrogram.

The EGMs were obtained from a single patient with two catheters placed simultaneously in the right atrial appendage. One catheter had 2-mm ring electrodes (top three tracings), and the other catheter had 1-mm orthogonal electrodes. The surface electrocardiogram tracing is shown at the top of the figure. Time and voltage amplitude scales are shown. For each electrode configuration (right), the corresponding EGM is shown (left), with the peak-to-peak amplitude and EGM duration labeled. “Contact” refers to electrodes in contact with the atrial tissue. “Floating” refers to noncontact electrodes in the atrial chamber. Note that greater ring electrode spacing, from 2 to 10 mm, prolongs EGM duration without altering the amplitude. The unipolar EGM shows a wider and diminished atrial EGM and a prominent far-field ventricular EGM as well. The orthogonal electrode configurations provide EGMs of lesser amplitude and shorter duration, compared with the ring electrodes.

The waveshapes of EGMs are quite variable (Fig. 3-8), probably because geometry of the trabecular endocardium adjacent to the tip electrode is complex. In one study at pacemaker lead implantation, 58% of unipolar EGMs were biphasic, with an initial upstroke followed by a roughly equal downstroke; 30% were predominantly monophasic negative, and 12% were predominantly monophasic positive.¹

Figure 3-8 Similarities of unipolar and bipolar electrograms.

Examples recorded from a lead placed in the right atrial appendage in 10 patients. Note that the amplitudes of unipolar and bipolar EGMs are similar for each patient. The waveshapes of unipolar and bipolar EGMs for a given patient may be quite similar (patient 3) or quite different (patient 8), although these differences can be attributed to the relative size of the major inflections. Some of these differences may depend on whether the ring electrode for the bipolar recording makes contact with the myocardium. On the whole, intrapatient differences between unipolar and bipolar recordings appear to be less than interpatient differences.

The ventricular depolarization recorded on the atrial electrode is referred to as the far-field R wave (FFRW). Oversensing of the FFRW confounds interpretation of the atrial rhythm. The amplitude of the FFRW depends on the location of the atrial electrode. It is greatest near the septum, intermediate in the right atrial appendage, and least on the right atrial free wall. Even if the FFRW has comparable amplitude to the P wave, its slew rate usually is much lower. In one series, the mean slew rate was 1.2 V/sec for AEGMs and 0.13 V/sec for FFRWs.¹

If an active-fixation, screw-in tip electrode is successfully attached to the myocardium, the acute VEGM has a current of injury, with an elevated ST segment (Fig. 3-9) that is usually greatly reduced within 10 minutes after electrode fixation. During this 10-minute period, the EGM amplitude and slew rate usually do not change despite changes in waveshape, but the pacing threshold decreases by an average of 40%.²

Figure 3-9 Acute current of injury at implantation.

Top panel, High-resolution recording shows marked ST-segment elevation, indicating the current of injury when an active fixation screw-in tip electrode is extended into the endocardium. Middle panel, After only 10 minutes, most of the ST-segment elevation in the signal has disappeared. Bottom panel, The EGM is not appreciably different at 1 hour after implantation.

Acute to Chronic Changes and Fixation

The amplitude and slew rate of intracardiac EGMs typically decline during the first several days to weeks after lead implantation and then increase to chronic values that are slightly lower than those measured at implantation.⁶ The initial decrease in EGM amplitude is caused by the inflammatory response and edema at the electrode-tissue interface. This gradually resolves and is followed by development of a small, inexcitable fibrotic zone surrounding the electrode tip (Fig. 3-10). This inflammation and fibrotic tissue effectively increases the distance between the surface of the electrode and excitable myocardium that generates the EGM signal. Although chronic EGM amplitudes usually are reduced by less than 10% compared with acute amplitudes, chronic slew rates are reduced by 30% to 40%.⁷

Figure 3-10 Gross microscopic slide specimen shows myocardium remaining after removal of endocardial active-fixation screw lead.

The large dotted line shows where the lead body was located, and the colored staining shows a thin, fibrotic sheath around the lead body. The approximate location of the helical screw-tip electrode is shown by the solid coiled line. The oval shape (dotted line) shows the size of the fibrotic capsule that formed around the helical extended-tip electrode. Most of the tissue outside the dotted lines stained red, indicating that it was active myocardium capable of conducting depolarizations. The tip region of this electrode is similar to that of the tip electrode in Figure 3-1, so propagation of depolarization wavefronts must travel around the tip electrode, in tissue largely out of the field of view on the right side of this figure.

The acute reduction in EGM amplitude is often greater with active-fixation leads than with passive fixation leads. Atrial undersensing can occur during the acute phase despite adequate EGM amplitudes at implantation. To account for these time-related changes in EGM amplitude, the filtered EGM recorded at lead implantation should be at least twice the sensitivity threshold that will be programmed in the pulse generator. Greater sensing safety margins are preferred for active-fixation leads.

The method of lead tip stabilization, active screw-in or passive tines, has had no significant effect on sensing characteristics in most studies.^8,9 Steroid-eluting electrodes reduce chronic pacing thresholds substantially, but also have no significant effects on sensing.^10–13

Ventricular Electrograms during Premature Ventricular Complexes, Ventricular Tachycardia, and Ventricular Fibrillation

Premature ventricular complexes (PVCs) may have lower-amplitude R waves than sinus-rhythm R waves, as shown in Figure 3-11, but the reverse may also be true. For monomorphic ventricular tachycardia (VT), mean amplitude decreased only slightly from values in sinus rhythm—14% for epicardial EGMs and 5% for endocardial EGMs.²⁷ In contrast, EGM amplitudes during ventricular fibrillation (VF) decreased by 25% for epicardial and 41% for endocardial EGMs. More importantly, EGMs in VF often have low, highly variable, and rapidly changing amplitudes and slew rates. Figure 3-12 shows endocardial spontaneous VF EGMs from different patients, illustrating variability in intrinsic deflections, amplitudes, slew rates, and morphologies. In a study of induced VF reproducibility, 50% of the variability was caused by interpatient differences and the other 50% occurred among repeated episodes in the same patient.²⁸ In another study, the VEGM amplitude in VF was 1 mV or less in at least one VF episode in 29% of patients.²⁷ If VF lasts for minutes, the amplitude and slew rate of the EGMs decrease.

Figure 3-11 Surface electrocardiogram (ECG) lead II, bipolar right ventricular electrogram, and event markers with downward pulses that show when sensing occurred.

The QRS amplitude on the ECG is about 1 mV, which is typical. The peak-to-peak amplitude of the sinus R waves is about 10 to 12 mV, which is also typical. The slew rate is the maximum slope (dV/dt) of the EGM intrinsic deflection; it is difficult to measure with a paper speed this slow. The two premature ventricular complexes (PVCs) (fourth and sixth) have different amplitudes and shapes on both the ECG and the EGM. The sinus beat in the center, between the two PVCs, has its main intrinsic deflection during the last part of the ECG QRS complex. The left edge of the sense marker indicates the instant that sensing by the ICD occurred. Therefore, EGM morphology and timing of the sense marker may not correspond to the start of the QRS on the ECG as electrocardiographers expect. Each R wave was sensed only once because sensing is blanked by the ICD for 120 msec after each ventricular sense (VS).

Figure 3-12 Variability in electrograms during spontaneous ventricular fibrillation (VF).

Bipolar EGMs recorded during VF detection and charging by Medtronic Gem ICDs are shown for nine patients. The 1-mV calibration markers are the same except for the bottom tracing, where the calibration pulse is about three times larger, meaning that the ventricular EGM for this patient was three times smaller than for the other eight patients. Also note that rapid intrinsic deflections are visible on all tracings, although some substantial beat-to-beat variations in amplitude occurred. The abbreviated sense markers are shown at the bottom edge of each stored EGM strip. The sense amplifier blanking period was 120 msec, and the programmed sensitivity in each case was 0.3 mV, except in the sixth tracing from the top, which had 0.6 mV sensitivity. Note that there was slight VF undersensing on the bottom tracing when large EGMs were followed by smaller EGMs.

Subcutaneous Electrocardiography

The subcutaneous ECG is similar to the surface ECG because the two subcutaneous electrodes are sufficiently distant from the heart that they record electrical activity from the entire heart. As with the surface ECG, the amplitude of subcutaneous ECG signals usually is 1 mV or less. Simultaneous recordings of subcutaneous ECG signals and surface ECG signals from electrodes placed directly over the subcutaneous locations have similar amplitude and signal-to-noise ratio.⁴¹ Practical implantation considerations usually limit the subcutaneous electrode separation distance to 4 to 8 cm, compared with the typical surface ECG limb lead electrode separation of 40 to 60 cm.

The orientation of the two subcutaneous electrodes relative to the heart can affect the amplitude of the signal recorded.⁴² Mapping studies on the chest skin with 4-cm electrode spacing in the range used by implantable loop recorders (ILRs) show larger intrinsic QRS amplitudes of 0.5 ± 0.1 mV for vertical orientation in the left parasternal zone and for horizontal orientation near the apex of the heart. Subcutaneous ECGs are used to detect arrhythmias in ILRs, to obviate the need for surface ECG electrodes during follow-up of pacemakers and ICDs, and to detect VT/VF in an ICD without intravascular electrodes.

General Concepts

Figure 3-13 shows the primary functional operations of sensing systems used by pacemakers and ICDs. The raw signal passes from the leads to the connector, through hermetic feedthroughs with high-frequency filters and high-voltage protection circuitry, before reaching the sensing amplifier. After the signal is amplified, a band-pass filter processes it to reduce T waves, myopotentials, and EMI (filtering). Then, it is rectified to nullify effects of signal polarity (rectification). Finally, it is compared with the sensing-threshold voltage. At the instant the processed signal exceeds the sensing-threshold voltage, a sensed event is declared to the timing circuits and indicated by a marker pulse on the programmer marker channel. The sense amplifier in the same chamber is turned off or “blanked” for a short blanking period (20-250 msec) after each spontaneous depolarization or pacing stimulus, to prevent a single depolarization resulting in multiple sensed events. In the refractory period that follows the blanking period, the sense amplifier remains enabled. Sensed events occurring in refractory periods do not alter pacemaker timing cycles but may be sensed for tachyarrhythmia detection algorithms.

Figure 3-13 Functional block diagram for pacemaker or implantable cardioverter-defibrillator (ICD) sense amplifier.

The EGM signal from the two implanted electrodes is first amplified for subsequent processing. Band-pass filtering reduces the amplitude of lower-frequency signals such as T waves and far-field R waves and higher-frequency signals such as myopotentials and electromagnetic interference. After band-pass filtering, the signal is rectified to make polarity unimportant. The thresholding operation compares the amplified, filtered, and rectified signals with the sensing threshold voltage. At the instant the processed signal exceeds the sensing threshold voltage, the sense amplifier is blanked (turned off) for 20 to 120 msec, so each depolarization is sensed only once, and a sensed event is declared to pacemaker or ICD timing circuits. For pacemakers, the programmed sensitivity controls the constant sensing threshold voltage. For ICDs, the amplifier gain may be controlled by the input EGM amplitude. The programmable sensing threshold for ICDs controls the high and low limits on the sensing threshold, which automatically adjusts on a beat-by-beat basis (see text discussion). In actual circuits, some functions (e.g., amplification, filtering) may be integrated.

Blanking and Refractory Periods

Blanking periods and refractory periods are used to prevent undesirable behavior caused by oversensing or double-counting of cardiac activity (Figs. 3-14 and 3-15). The specifications of blanking/refractory periods have substantial impact on ICD sensing and pacing functions (Fig. 3-16). Same-chamber blanking/refractory periods after sensed events reduce double-counting of intrinsic cardiac depolarizations that may result in escape pacing at a rate slower than the programmed lower rate in pacemakers or inappropriate detection of VF in ICDs. After paced events, the same-chamber blanking/refractory periods are typically longer and prevent oversensing of the pacing artifact and evoked response. The blanking/refractory periods in the ventricle after atrial sensed or paced events and in the atrium after ventricular sensed or paced events are called cross-chamber blanking/refractory periods. Cross-chamber blanking periods help to prevent oversensing of the pacing artifact after a paced event in the opposite chamber.

Figure 3-14 Loss of atrial sensing with apparent ventricular undersensing and ventricular pacing.

In the second complex, an atrial pacing stimulus follows the P wave because of undersensing in the atrium. The atrial pacing stimulus occurs at the start of the ventricular QRS complex. The ventricular EGM is not sensed because of blanking in the ventricular sensing amplifier immediately after the atrial pacing stimulus. This sequence is repeated in the fourth, sixth, and eighth complexes. Atrial undersensing may lead to apparent ventricular undersensing because the ventricular blanking period does not permit sensing of electrical signals for 10 to 40 msec after an atrial output pulse.

Figure 3-15 Oversensing of T waves causing interruptions in VVI pacemaker timing.

The surface electrocardiogram (top tracing) and pacemaker marker channel (bottom tracing) show ventricular oversensing of T waves. The first three complexes show ventricular pacing (VP) with capture. The pauses after the third and fourth complexes result from T-wave oversensing (VS), demonstrated by the marker channel.

Figure 3-16 Basic blanking and refractory periods for DDDR mode (Medtronic Marquis DR ICD and EnPulse DR pacemakers).

The top tracings show the surface electrocardiogram (ECG), atrial electrogram (AEGM), and ventricular electrogram (VEGM) signals. The bottom two marker diagrams illustrate atrial or ventricular pacing (AP, VP), atrial or ventricular sensing (AS, VS), blanking periods (purple), and refractory periods (blue). Blanking periods in ICDs are usually of fixed duration, whereas same-chamber blanking in pacemakers is generally adaptive, with short (30-50 msec) blanking periods that “retrigger” when suprathreshold signals are present during the blanking period. Adaptive blanking periods can extend indefinitely, resulting in activation of noise-reversion asynchronous pacing. Note the considerably shorter blanking periods on the atrial channel in the ICD; this allows more accurate sensing of atrial depolarizations during high ventricular rates, which is critical for tachyarrhythmia detection and discrimination algorithms. Also note the lack of ventricular refractory periods in ICDs; this allows inhibition of pacing when high rates are sensed. Ventricular blanking periods in pacemakers may be shorter than in ICDs because of the approximately 10-fold less sensitive sensing threshold in pacemakers compared with ICDs.

The atrial blanking period after ventricular events, postventricular atrial blanking (PVAB), is designed to avoid oversensing of ventricular pacing stimuli and FFRWs. Longer postventricular atrial refractory periods (PVARPs) prevent retrogradely conducted atrial activation from resetting atrial timing cycles for dual-chamber pacing. Cross-chamber blanking in the atrium after a ventricular event must be minimized in ICDs with tachyarrhythmia detection (ICDs or atrial therapy ICDs) to avoid undersensing the atrial rhythm, particularly during high ventricular rates. Long PVAB periods prevent reliable sensing of AF and atrial flutter/atrial tachycardia (AT). However, short PVAB periods may result in atrial sensing of FFRWs.

Implantable cardioverter-defibrillators that require tachyarrhythmia detection typically have shorter blanking and refractory periods than standard pacemakers, so that short cardiac cycles can be sensed reliably. As shown in the bottom marker diagrams of Figure 3-16, blanking periods may be adaptively extended based on noise-sampling windows (30-60 msec) if suprathreshold activity (due to cardiac or extracardiac sources such as EMI) is identified on the EGM immediately after a sensed event. If noise is seen in consecutive windows after a sensed event, the blanking period is “retriggered” for that beat to avoid double-counting or continuous oversensing. This operation may result in paradoxical undersensing of the cardiac rhythm when more sensitive sensing levels are programmed if noise is oversensed.^43,44

The duration of the total atrial refractory period (TARP), equal to the atrioventricular (AV) delay plus the PVARP, in DDD pacing modes limits atrial tracking of the atrium at high sinus rates without affecting atrial sensing, as shown in Figure 3-17. Because the AV delay of most dual-chamber pacemakers shortens in response to increasing atrial rates or sensor input, the TARP also shortens. Several manufacturers now offer dual-chamber pacemakers that shorten the PVARP with increasing atrial or sensor-indicated rates, further reducing the TARP during exercise. The result of these newer algorithms is that the programmed upper tracking rate can be safely increased while providing protection at lower heart rates from initiation of pacemaker-mediated tachycardia caused by retrograde conduction.

Figure 3-17 Intracardiac marker channels.

In a patient with a DDD pacemaker, channels identify atrial events within postventricular atrial refractory periods (PVARPs) that are sensed but not tracked. The surface electrocardiogram (top tracing) demonstrates ventricular pacing at the upper rate limit during atrial flutter. The atrial marker channel demonstrates atrial events that were sensed within PVARP (AS) and atrial events sensed outside PVARP (AS). After a ventricular pacing stimulus (VP), some atrial EGMs are not sensed, resulting in apparent EGM dropout because the atrium is blanked for a period after delivery of a VP. Only atrial signals recorded outside PVARP (AS) are tracked.

Sensing Thresholds in Pacemakers

Sensing thresholds in most pacemakers are programmable to a constant value. Ventricular sensing channels in conventional pacemakers typically operate at sensing thresholds of 2.5 to 3.5 mV, about 10 times less sensitive than those in ICDs. Therefore, pacemakers may undersense VF. Atrial sensitivity thresholds are typically 0.3 to 0.6 mV, to allow sensing of small-amplitude atrial EGMs during AF and to improve the accuracy of AF diagnostics.

Unipolar sensing thresholds typically are set higher (less sensitive) than bipolar sensing thresholds to reduce oversensing of far-field cardiac and extracardiac signals that can lead to inappropriate pacemaker inhibition or tracking. Newer pacemakers automatically adjust the sensitivity setting to adapt to changes in EGM amplitude over time. Typically, these functions operate to modify sensing thresholds based on a series of 10 to 20 ventricular beats. One such algorithm employs two simultaneous sensing levels: the programmed sensitivity (inner target) and a value twice the programmed value (outer target) (Fig. 3-18).⁴⁵ Sensed EGMs exceeding both target values decrease the sensitivity. Signals exceeding only the inner target increase the sensitivity. In this manner, a 2 : 1 sensing margin is maintained. Rapid, automated sensitivity adjustments may be desired when EGM amplitudes can be expected to change over a brief period, such as beat-to-beat variations from respiration, body position changes, or fluctuating EGM morphologies during AF.⁴⁶

Figure 3-18 Autosensing algorithm to maintain a 2 : 1 sensing safety margin.

See text for details.

(From Castro A, Liebold A, Vincente J, et al: Evaluation of autosensing as an automatic means of maintaining a 2:1 sensing safety margin in an implanted pacemaker. Autosensing Investigation Team. Pacing Clin Electrophysiol 19:1708-1713, 1996.)

Far-field R-wave oversensing can be minimized by (1) selecting an atrial lead with a closely spaced bipolar electrode pair (≤10 mm), (2) choosing an implantation location that yields an FFRW/P-wave ratio of less than 0.5,⁴⁷ (3) titrating programmed sensitivity to reject FFRWs without undersensing P waves and low-amplitude AF, and (4) using PVAB.

Ventricular Sensing in Ventricular ICDs

The guiding design principle is that sensing of VF and polymorphic VT should be sufficiently reliable that clinically significant delays in detection do not occur. Although high sensitivity is required to ensure reliable sensing during VF, continuous high sensitivity results in oversensing of cardiac or extracardiac signals during regular rhythm, which may cause inappropriate detection of VT or VF. To minimize both undersensing during VF and oversensing during regular rhythms, ICDs use feedback mechanisms based on R-wave amplitude that adjust the sensing threshold dynamically. To maximize the likelihood of detecting VF, blanking periods are kept short.

Automatic Adjustment of Sensitivity

Adjustment of Sensitivity in Normal Rhythm

All ICDs automatically adjust sensitivity in relation to the amplitude of each sensed R wave (Fig. 3-19). At the end of the blanking period after each sensed ventricular event, the sensing threshold is set to a high value. It then decreases with time until a minimum value is reached. Compared with a fixed sensing threshold, automatic adjustment of sensitivity increases the likelihood of sensing low-amplitude and varying EGMs, while minimizing the likelihood of T-wave oversensing.

Figure 3-19 Automatic adjustment of sensitivity.

ICDs adjust sensitivity in relation to the amplitude of each sensed R wave. The goal of this feature is to permit sensing of low-amplitude and varying-amplitude EGMs while minimizing T-wave oversensing. The figure shows two sinus beats followed by the onset of ventricular fibrillation (VF). The upper panel shows the unfiltered ventricular EGM. The lower panel shows the corresponding filtered and rectified EGM. After each sensed ventricular event, the sensing threshold is set to a predetermined fraction of the R-wave amplitude. For large R waves, the initial sensing threshold may have a maximum value. The threshold then decreases with time until it reaches a minimum value equal to the programmed sensitivity, which is nominally about 0.3 mV. For sinus beats, the threshold is larger than the T waves, preventing oversensing. When VF begins, the smaller R waves keep the threshold at a lower value, which allows sensing of R waves that are even smaller than the T waves in sinus rhythm.

The methods of the different manufacturers for automatic adjustment of sensitivity perform similarly after small R waves but differently after large R waves. Figure 3-20 shows that after large R waves, the Boston Scientific ICDs increase the sensing floor. In the Cognis/Teligen family, the sensing floor is set to one-eighth the amplitude of the measured R wave if that value is greater than the programmed sensitivity. This prevents T-wave oversensing in the setting of large R waves and reduces oversensing of low-amplitude noncardiac signals (e.g., diaphragmatic myopotentials, EMI). However, it may increase the risk of undersensing during rare episodes of VF with highly variable EGM amplitude.⁴⁸

Figure 3-20 Comparison of automatically adjusted sensitivity after sensed ventricular events for three manufacturers of ICDs after large (10 mV) R wave.

The programmed sensing threshold is approximately 0.3 mV. After sensed ventricular events, Medtronic ICDs reset the sensing threshold to 8 to 10 times the programmed sensitivity, up to a maximum of 75% of the sensed R wave. The value of Auto-Adjusting Sensitivity then decays exponentially from the end of the (sense) blanking period, with a time constant of 450 msec, until it reaches the programmed (maximum) sensitivity. At the nominal sensitivity of 0.3 mV, there is little difference between the sensitivity curves of Medtronic ICDs after large and small spontaneous R waves. If the R wave is large, the entire Auto-Adjusting Sensitivity curve can be altered substantially by changing the programmed value of maximum sensitivity (see Fig. 3-19). At nominal settings, the St. Jude Threshold Start begins at 62.5% of the measured R wave for values between 3 and 6 mV. If the R-wave amplitude is greater than 6 mV or less than 3 mV, the Threshold Start is set to 62.5% of these values (3.75 mV and 1.875 mV, respectively). The sensing threshold remains constant for a Decay Delay period of 60 msec and then decays linearly with a slope of 3 mV/sec. Both the Threshold Start percent and the Decay Delay are programmable, over the range of 50% to 75% and 0 to 220 msec, respectively (see Fig. 3-21). Boston Scientific Cognis-Telegin ICDs set the starting threshold to 75% of sensed R waves with a maximum limit of 3/2 · Peak Running Average. Sensitivity then decays using digital steps, each seven-eighths the amplitude of the previous step. For sensed events, the duration of the first step is 65 msec, and the duration of subsequent steps is 35 msec. This results in a sensitivity of one-half the peak R wave in about 170 msec. (See text for further details.) After a paced ventricular event, all ICDs also adjust sensitivity dynamically, starting at the end of the (pace) blanking period, but the threshold starts at a more sensitive setting.

(Modified from Swerdlow C, Friedman P: Advanced ICD troubleshooting. Part I. Pacing Clin Electrophysiol 28:1322-1346, 2005.)

Postpacing Automatic Adjustment of Sensitivity

After ventricular pacing, all ICDs set ventricular sensitivity to a highly sensitive value to prevent pacing during VF. The sensitivity threshold then decays to the programmed sensitivity level (Fig. 3-21). Thus ICDs are especially vulnerable to oversensing of low-amplitude signals late in diastole during pacing, when the amplifier sensitivity or gain is maximal. Clinically, the most important manifestation is the oversensing of diaphragmatic myopotentials.³

Figure 3-21 Comparison of automatic adjustment of sensitivity after paced and sensed ventricular events.

The filtered and rectified ventricular EGM, the corresponding sensing threshold, and ventricular (V) event markers are shown. Horizontal bars denote postpacing blanking periods. The blanking periods after paced events are longer than those after sensed events (250-350 vs. 120-140 msec), and the initial values of sensitivity are less. In this Medtronic ICD example, the initial sensing threshold after sensed events is 8 times the minimum programmed sensitivity of 0.3 mV, whereas the initial threshold after paced events is 4.5 times that value. The goal of a lower initial postpacing threshold is to prevent pacing into ventricular fibrillation. It compensates in part for the longer postpacing blanking period.

Automatic Gain Control

Early Ventritex ICDs (St. Jude Medical) used automatic step adjustments of gain 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.^49–51

In Boston Scientific ICDs before the Cognis/Teligen models, “slow” Automatic Gain Control adjusts the dynamic gain of the sensing amplifier slowly in response to temporal changes in R-wave amplitude. This ensures that the peak of the sensed R wave reaches about 75% of the amplifier gain, and that the sensing EGM is not truncated or “clipped.” The minimum value of amplifier range is one eighth of the maximum value, so the minimum sensitivity decreases as R-wave amplitude increases. In Cognis/Teligen models, the range sense amplifier is sufficient (0 to 32 mV) that “slow” Automatic Gain Control is not used. In these Boston Scientific ICDs, “Automatic Gain Control” refers to automatic adjustment of sensitivity. In older Boston Scientific ICDs, “fast” Automatic Gain Control refers to automatic adjustment of sensitivity.

Thus, whatever the name applied, automatic control of sensitivity, rather than gain, has become the primary method of beat-to-beat sensing adjustment in all ICDs.

Ventricular Blanking Periods

Ventricular blanking periods prevent ventricular oversensing of same-chamber signals (R-wave double-counting) and cross-chamber signals (atrial pacing pulses and P waves) in regular rhythms. Because reliable sensing in VF requires minimizing blanking periods, blanking periods in ICDs are short and may occasionally be insufficient to prevent oversensing.

Short Same-Chamber Blanking Periods and R-wave Double-Counting

In adults who are not taking antiarrhythmic drugs, inter-EGM intervals for filtered EGMs in VF vary from about 130 to 300 msec, with a peak near 200 msec (Fig. 3-22). Therefore, fixed or nominal blanking ICD periods after ventricular sensed events range from 120 to 135 msec. R-wave double-counting occurs if the duration of the sensing EGM exceeds the ventricular blanking period.

Figure 3-22 Sensed cycle lengths of human ventricular fibrillation (VF) EGMs by ICD sensing system compared with manual cycle-length measurements of same signals from many patients.

Two histograms are superimposed. The red and orange vertical bars show the manually measured cycle lengths during VF (786 intervals); the blue bars show the intervals sensed by the ICD (772 intervals). Intervals of less than 120 msec, the blanking period, were not permitted. Note that there was some oversensing for intervals shorter than 180 msec, a slight amount of undersensing for intervals between 180 and 280 msec, and a small number of long intervals greater than 280 msec, which represent undersensing during VF. The peak in the histograms occurs at about 220 msec.

Cross-Chamber Blanking Periods and Undersensing of VT/VF

Under most conditions, ICDs apply only the minimum cross-chamber ventricular blanking required to prevent “crosstalk” resulting from an atrial pacing stimulus. During high-rate atrial or dual-chamber pacing, ventricular sensing may be restricted to short periods of the cardiac cycle because of the combined effects of ventricular blanking after ventricular events and cross-chamber ventricular blanking after atrial pacing. If a sufficient fraction of the cardiac cycle is blanked, systematic undersensing of VT or VF may occur. When pacing and blanking events occur at intervals that are multiples of a VT cycle length, ventricular complexes may be repeatedly undersensed, delaying or preventing detection.^52–54 This occurs most often with rate-smoothing algorithms.

“Sensing” Other Ventricular Electrograms

Implantable cardioverter-defibrillator may use information derived from other VEGMs (shock-channel EGM, LV EGM in resynchronization systems) to enhance their functionality. The EGM from the shock channel (far-field EGM) is not used by transvenous ICDs for rate counting because bipolar or integrated bipolar EGMs are less susceptible to extracardiac signals. However, some manufacturers (Boston Scientific, Medtronic) use morphologic characteristics of far-field EGMs for discrimination of supraventricular tachycardia (SVT) from VT.

Automatic analysis of the far-field EGM has also been proposed as a method to identify oversensing in ICDs resulting from lead fracture or sensing-lead connection problem. In one approach, the peak-peak far-field EGM amplitude is measured in a small window centered around each sensed event (on near-field channel) to discriminate rapid oversensing from true VT/VF. Oversensing is identified when sensed events on the near-field channel correspond to isoelectric periods on the far-field channel.^55,56 In true VF, isoelectric periods are rare on the far-field channel (Fig. 3-23).

Figure 3-23 Algorithm to discriminate pace-sense conductor failure of true bipolar ICD leads from ventricular fibrillation using far-field EGM (Medtronic Protecta ICDs, currently investigational).

In pace-sense conductor failures, the far-field EGM has long isoelectric segments, which are not present in true VF. Stored EGM tracings during lead noise oversensing (left) and spontaneous VF (right) are shown; top tracings are the near-field (RVtip-RVring) EGM, middle tracings are the far-field EGM (RV coil-can), and the sensing markers are the lower tracing. Oversensing is identified by analyzing the peak-peak amplitudes of the far-field EGM in a 200-msec window centered at each of 12 sense markers (sensing derived from near-field EGM), as shown by the red arrows and boxes. Oversensing is identified when there are at least two far-field EGM analysis windows with isoelectric (<1 mV) amplitudes and at least one analysis window with peak-peak amplitude at least six times greater than the average of the two smallest amplitudes. Lead noise oversensing would have been properly discriminated from VF in these two examples.

Atrial Sensing in Dual-Chamber ICDs and Atrial ICDs

Accurate sensing of atrial EGMs is essential for accurate discrimination between VT/VF and rapidly conducted SVTs that satisfy ventricular rate criteria in dual- or triple-chamber ICDs. Rapid discrimination is essential to ensure prompt delivery of ventricular therapy while minimizing inappropriate shocks. Historically, some inappropriate detection of AT/AF has been considered an acceptable consequence of maintaining high sensitivity for detecting VT/VF.

The atrial lead should be positioned at implantation to minimize FFRWs. Leads with an interelectrode spacing of 10 mm or less reduce oversensing of FFRWs. Atrial lead dislodgement, oversensing of FFRWs, or undersensing from low-amplitude AEGMs or atrial blanking periods can cause inaccurate identification of AEGMs. These errors in sensing may result in misclassification of VT as SVT, or vice versa.

Postventricular Atrial Blanking and Rejection of Far-Field R Waves

To prevent oversensing of FFRWs, older dual-chamber ICDs had fixed PVAB periods, similar to those in pacemakers (Fig. 3-24). With a fixed blanking period, the blanked proportion of the cardiac cycle increases with the ventricular rate. Atrial undersensing caused by PVAB causes underestimation of the atrial rate during rapidly conducted atrial flutter or AF, resulting in inappropriate detection of VT⁶⁷ (Fig. 3-24, lower panel). Without PVAB, however, atrial oversensing of FFRWs could cause overestimation of the atrial rate during tachycardias with a 1 : 1 AV relationship.⁶⁸ This may result in either inappropriate rejection of VT as SVT, if FFRWs are counted consistently as atrial EGMs, or inappropriate detection of SVT as VT, if FFRWs are counted inconsistently.⁶⁹

Figure 3-24 Effect of postventricular atrial blanking (PVAB) on atrial sensing.

Upper panel shows the surface electrocardiogram (ECG), atrial electrogram (AEGM), and event markers during atrial sensed (As)–ventricular paced (Vp) rhythm. The first segment of each upper horizontal bar denotes the period of PVAB; the second segment denotes the postventricular atrial refractory period (PVARP); FFRW, far-field R wave on the atrial channel. The lower horizontal bars denote the postpacing ventricular blanking periods. With a short PVAB (left), the FFRWs are oversensed. A longer PVABP (right) prevents oversensing of FFRWs. Lower panel shows the ECG, AEGM, and ventricular electrogram (VEGM) tracings from a patient with atrial flutter with 2 : 1 atrioventricular (AV) conduction. The thin horizontal bars on the ventricular channel denote the periods of PVAB, which resulted in atrial undersensing of alternate atrial flutter EGMs (in boxes). The resultant incorrect calculation of atrial rate resulted in inappropriate ventricular therapy for atrial flutter (not shown), because the ICD did not classify the ventricular rate as less than the atrial rate.

Medtronic ICDs also reject FFRWs algorithmically by identifying a specific pattern of atrial and ventricular events that fulfill specific criteria (Fig. 3-25). Intermittent sensing of FFRWs or frequent premature atrial events may disrupt this pattern, resulting in misclassification of a tachycardia. Therefore, it is preferable to reject FFRWs after sensed ventricular events by decreasing atrial sensitivity, if this can be done without undersensing of AF. Atrial sensitivity can be reduced to 0.45 mV with a low risk of undersensing AF. Less sensitive values should be programmed only if the likelihood of rapidly conducted AF is low. FFRW oversensing that occurs only after paced ventricular events (when auto-adjusting atrial sensitivity is maximal) does not cause inappropriate detection of SVT as VT, but it may cause inappropriate mode switching and can contribute to inappropriate detection of AF or atrial flutter.

Figure 3-25 Algorithmic rejection of far-field R waves (FFRW) by pattern analysis.

ICDs with minimum cross-chamber blanking (Medtronic) reject FFRWs by the timing pattern of atrial and ventricular intervals. Atrial events are classified as FFRWs if all the following criteria are met: (1) there are exactly two atrial events for each V-V interval; (2) timing of one P wave is consistent with a FFRW (R-P interval <160 msec); (3) there is a stable interval between the FFRW and the ventricular electrogram (VEGM); (4) there is a short-long pattern of P-P intervals (to distinguish FFRW oversensing from atrial flutter); and (5) the pattern occurs frequently (4 of 12 intervals). A, Atrial electrogram (AEGM), VEGM, and dual-chamber event markers are shown. All five criteria for FFRWs are fulfilled. Horizontal double-ended arrows below event markers denote alternation of long (L) and short (S) atrial intervals. AR, Atrial refractory event; P, P wave; TS, ventricular event in ventricular tachycardia zone. B, Interval plot (left) and stored EGM (right) from episode of sinus tachycardia with consistent FFRW oversensing that is classified correctly. On the interval plot, open squares denote A-A interval and closed circles denote V-V interval. Horizontal lines denote ventricular tachycardia (VT) and ventricular fibrillation (VF) detection intervals of 400 and 320 msec, respectively. Alternating A-A intervals whose sum equals that of the VV intervals produce a characteristic “railroad track” appearance (arrow). The algorithm rejects FFRWs despite that FFRW oversensing does not occur for one V-V interval between seconds 9 and 10. C, Interval plot (left) and stored EGM (right) from episode of sinus tachycardia with consistent FFRW oversensing that was detected inappropriately as VT. Intermittent oversensing of FFRWs occurs as sinus tachycardia accelerates gradually across the VT detection interval of 480 msec (arrow), resulting in inappropriate therapy (“Burst” antitachycardia pacing marker on interval plot, VT marker on EGM event markers).

Medtronic ICDs (starting with Entrust) and Boston Scientific ICDs (starting with Vitality) may use brief atrial blanking or a period of reduced, automatically-adjusting sensitivity (or both) to reject FFRWs without preventing detection of AF (Fig. 3-26). St. Jude ICDs and Medtronic ICDs starting with Entrust provide programmable atrial blanking after sensed ventricular events to individualize the trade-off between oversensing of FFRWs and undersensing of AEGMs in AF. St. Jude ICDs also provide programmable atrial sensing Threshold Start and Decay Delay, corresponding to the same features in the ventricular channel.

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