Timing Cycles of Implantable Devices

Chapter 23

Timing Cycles of Implantable Devices PAUL J. WANG • HENRY CHEN • HIDEO OKAMURA • AMIN AL-AHMAD • HENRY H. HSIA

T o better understand device behaviors and to optimize management, physicians must be familiar with the timing cycles of implantable pacemakers and their constant interactions with the patient’s intrinsic rhythm.1 Timing cycles refer to the beat-by-beat behavior of implantable devices in response to changes in intrinsic and paced behavior. Although some of the parameters involved in timing cycles are programmable, others are unalterable within the device itself. Each type of device uses timing cycles in a somewhat different way. The purpose of this review is to provide a detailed discussion of the various parameters that affect timing cycles in pacemakers, implantable cardioverter-defibrillators (ICDs), and resynchronization therapy devices. Revised Pacing System Code It is necessary to have a basic understanding of the operational modes of the pacemakers. The pacing systems may be single-chamber systems, limited to either atrium or ventricle, or they may be dual-chamber systems. They may sense in one chamber and pace the other, sense one and pace both, or sense and pace both chambers. Their functionality can vary from beat to beat depending on the programmed mode and the underlying rhythm. As a result of a joint approach of the North American Society of Pacing and Electrophysiology (NSAPE) and the British Pacing and Electrophysiology Group (BPEG), a NASPE/BPEG Generic

(NBG) Pacemaker Code was developed (Table 23-1). The latest revision, in 2002, incorporated multisite pacing.2 This is a three- to five-position code used to designate the programmed mode of the device. The first letter designates the chamber or chambers paced. A stands for atrium, V for ventricle, and D for pacing capability in both the atrium and ventricle; O is used if the unit is deactivated without pacing. The letter in position II designates the chamber or chambers sensed. O stands for asynchronous operation without sensing. The third letter describes the unit’s response to a sensed signal. I indicates that the pacemaker pacing is inhibited by a sensed event; T indicates that a pacing stimulus is triggered by a sensed event; and D represents an operating mode in which a stimulus may be triggered by a sensed event in one chamber and inhibited by a sensed event in the other. For example, a DDD pacemaker senses an atrial signal that triggers a ventricular pacing output; however, a sensed ventricular signal will inhibit the pacing stimulus in the ventricle. The fourth letter describes the rate-modulation capability. Position V of the revised NBG code is used to denote multisite pacing. Position V represents a change in the NBG code and is represented in Table 23-1 in bold type to emphasize this change. O indicates no more than one site in each chamber paced. A indicates that more than one pacing site is present in the atrium. V indicates that more than one pacing site is present in the ventricle. D indicates that more than one pacing site is present in the atrium and ventricle. In the DDDRO mode, there are sensing and pacing at single 969

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The Revised NASPE/BPEG Generic (NBG) Code for Antibradycardia Pacing* TABLE 23-1.

Position

I

II

III

IV

V

Category

Chamber paced O = None A = Atrium V = Ventricle D = Dual (A + V)

Chamber sensed O = None A = Atrium V = Ventricle D = Dual (A + V)

Response to sensing O = None T = Triggered I = Inhibited D = Dual (T + I)

Rate modulation O = None R = Rate adaptive

Multisite pacing O = None A = Atrium V = Ventricle D = Dual (A + V)

Manufacturer’s designation only

S = Single (A or V)

S = Single (A or V)

*The Code was modified in 2002 and includes multisite pacing. BPEG, British Pacing and Electrophysiology Group; NASPE, North American Society of Pacing and Electrophysiology. From Bernstein A, Daubert J, Fletcher R, et al.: The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. PACE 23:260-264, 2002.

sites within the atrium and the ventricle, along with atrial tracking, ventricular inhibition, and rate adaptive pacing. In DDDRV mode, all of the same features are available as in DDDRO, but in addition there is pacing at two sites in the ventricles, such as in the right ventricle (RV) and the left ventricle (LV). Dual-site atrial pacing for atrial fibrillation prevention would be represented as the DDDRA mode.

As described earlier, the pacing mode describes the set of basic pacemaker functions. Associated with each pacing mode is a set of rules that govern the timing of events. The beat-to-beat intervals that define when paced events occur in that mode are called timing cycles. The physicians must be familiar with the nomenclature and definition of the timing cycles, as well as the basic rules that govern their behaviors.

pacing. In the VVI mode, after a sensed intrinsic ventricular activation (R wave) or a paced event (V), the pacemaker waits for the next intrinsic beat. However, if the escape interval elapses before a ventricular signal is sensed, the pacemaker delivers a ventricular pacing stimulus. Any sensed or paced ventricular event initiates the ventricular escape interval. Intrinsic events may occur at intervals shorter than the escape interval, but the longest time between any two ventricular events is the ventricular escape interval (Figs. 23-1 and 23-2). The escape interval defines the LRL (usually expressed in pulses per minute), which may also be called the minimum, basic, or base pacing rate. The timing of ventricular sensed events is initiated when the intrinsic signal reaches the necessary sensing threshold after passing through specific amplifiers and filters. The point in the intrinsic signal that is sensed may be delayed compared with the onset of the ventricular activation of the surface electrocardiogram (ECG). The largest amount of delay in sensing of the intrinsic signal from a right ventricular apical lead occurs in the setting of right bundle branch block.

Single-Chamber Pacing Modes

Refractory Periods/Blanking Periods

SSI Mode

To sense and pace within the same chamber, “samechamber” refractory periods must be included to avoid inappropriate oversensing of the intrinsic event or

Single-Chamber Pacing Modes and Timing Cycles

The AAI and VVI modes act in a comparable manner, with pacing and sensing in the same chamber (atrium or ventricle) and the pacing output inhibited by a sensed event in that chamber. For practical purposes, AAI and VVI modes may be considered to be a common SSI mode. In each mode, a pacing output is delivered at the end of the escape interval that corresponds to the programmed lower rate limit (LRL) of the device. If a sensed event (S) occurs, the pacing output is inhibited and the escape interval is reset. VVI Mode In the VVI mode, the ventricular inhibited pacing mode, the pacemaker senses and paces in the ventricle. This mode is most appropriate for patients in chronic atrial fibrillation for whom atrial sensing or pacing is not needed. The VVI mode may sometimes be programmed for patients who require infrequent

Figure 23-1. VVI mode. The ventricular rate in this example is 1000 msec and is indicated by the V-V interval. The intrinsic R wave comes 760 msec after the second ventricular paced event. The next ventricular paced event occurs 1000 msec after the intrinsic ventricular event. R, ventricular sensed event; V, ventricular paced event.

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Figure 23-2. Diagrammatic representation of the VVI mode of pacing (rate = 80 pulses per minute). The QRS marked 1 is sensed. Beats 2 and 3 are paced complexes. A ventricular extrasystole (beat 4) and a normal conducted QRS (beat 5) are sensed. The sixth and seventh beats are paced. The pacemaker ventricular refractory period (300 msec) is shown by a rectangle. Complexes 4 and 5 reset and start the lower rate counter before the zero level has been reached—that is, before completion of the escape or automatic interval. The pacemaker emits its stimulus only from the zero level. ECG, electrocardiogram. (From Lendermans FW: Diagrammatic representation of pacemaker function. In Barold SS [ed]: Modern Cardiac Pacing. Mt. Kisco, NY, Futura, 1985, pp 323-353.)

Figure 23-3. VVI ventricular refractory periods. The black bar indicates the ventricular blanking period, during which events are not sensed. The gray bar indicates the ventricular refractory period, during which ventricular sensed events are not used to reset timing cycles.

Figure 23-4. VVI ventricular oversensing. The T wave of the first beat, indicated by the asterisk, is sensed outside the ventricular refractory period. The ventricular escape interval is 1000 msec. Because the T wave of the first beat is sensed, the R-V interval is 1200 msec instead of 1000 msec. The following V-V interval is the expected 1000 msec.

pacing (Fig. 23-3).3,4 Immediately after a ventricular paced event, during a ventricular blanking period (VBP) or time interval (ranging from 50 to 100 msec), all ventricular events are “blanked” or not sensed. The VBP is designed to prevent oversensing of the afterpotentials from pacing stimuli. After this period of absolute lack of sensing, there is a ventricular refractory period (VRP), a programmable time window (usually expressed in milliseconds) during which the pacemaker sensing amplifier is active but does not use the ventricular sensed event to reset the timing cycle. Noise sampling may occur during the VRP, and the VRP is used to prevent oversensing due to the paced evoked potentials, the intrinsic ventricular electrogram, or repolarization signals (T wave).

event that does not represent ventricular depolarization. Parts of the QRS complex, the T wave,5 afterdepolarizations,6 atrial activity,7,8 noise from lead abnormalities,9 myopotentials, and electromagnetic interference are possible causes of ventricular oversensing.10,11 In ventricular oversensing, the additional sensed event resets the ventricular escape interval, resulting in a longer interval than the programmed pacing cycle length (Fig. 23-4). In ventricular undersensing, the pacemaker does not sense an intrinsic ventricular depolarization (R wave). The ventricular escape interval is not reset by this R wave. Instead, the ventricular escape interval is created by the previous sensed or paced event. The pacing interval therefore is shorter than the pacing cycle length (Fig. 23-5).

Ventricular Oversensing and Ventricular Undersensing

Hysteresis Rate

Ventricular sensing may result in abnormalities in the ventricular timing cycles. The pacemaker senses an

Hysteresis provides for a longer escape interval from the last ventricular sensed event to the first ventricular paced event (R-V, called the hysteresis interval) but no

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Figure 23-5. VVI ventricular undersensing. The second R wave, indicated by the asterisk, is not sensed. The next event is a ventricular paced event after a ventricular escape interval of 1000 msec. The subsequent V-V interval is also 1000 msec.

Figure 23-6. VVI ventricular hysteresis. The first and second ventricular events are paced with a V-V interval of 1000 msec. The third event is a ventricular sensed event. The fourth event is a ventricular paced event (indicated by the asterisk) after an R-V interval of 1200 msec. The hysteresis interval is 1200 msec, and the pacing interval is 1000 msec.

change in the time from the last ventricular paced event (Fig. 23-6).12 Hysteresis allows the intrinsic heart rate to be lower before pacing occurs, but if pacing does occur, it will occur at a faster rate. For example, if the hysteresis pacing rate is 50 beats per minute (bpm) and the base pacing rate is 60 bpm, pacing will not occur if the patient continues to maintain rates faster than 50 bpm. If the heart rate falls below 50 bpm, however, pacing will occur at 60 bpm. This feature favors intrinsic activation and facilitates conduction in the patient with atrial fibrillation or atrioventricular (AV) synchrony in the patient in sinus rhythm. When hysteresis is programmed ON, the maximum V-to-V interval (defined by the lower rate interval) is shorter than the maximum R-to-V interval (defined by the hysteresis interval). Hysteresis is often expressed as an absolute rate (beats per minute) or as an interval (in milliseconds) from the intrinsic R wave to the first ventricular paced event (V). Hysteresis may also be expressed as the difference between the hysteresis rate and the pacing rate or the difference between the hysteresis escape interval (R-V) and the pacing escape interval (VV). The hysteresis rate may sometimes be expressed as a percentage subtracted from the lower rate. The hysteresis often results in a decreased frequency of pacing, because it allows more time to expire after an intrinsic event. Commonly, the lower rate interval is set to the

Figure 23-7. VOO mode. In the VOO mode, there are ventricular paced events and no sensing. The first two ventricular events are paced at a V-V interval of 1000 msec. The third event is an intrinsic ventricular event, but it is not sensed in the VOO mode. The next V event, indicated by the asterisk, occurs during the physiologic refractory period of the preceding ventricular event. The final V event, also noted by an asterisk, is also in the physiologic refractory period.

Figure 23-8. AAI mode. The atrial pacing rate in the AAI mode in this example is 1000 msec; it represents the time from either an atrial paced event (A) or an atrial sensed event (P) to the next atrial paced event. Each of the P-A intervals occurs at 1000 msec, whereas the ventricular sensed events may occur earlier than the atrial pacing rate.

slowest rate that is desirable hemodynamically. Once pacing occurs, it will continue until the intrinsic ventricular rate exceeds the pacing rate. VOO Mode In the VOO mode, ventricular pacing without ventricular sensing is present (Fig. 23-7). No intrinsic events are sensed, and therefore ventricular pacing occurs independently of the intrinsic rhythm. VOO is programmed ON to prevent electromagnetic interference from resulting in ventricular inhibition in the pacemaker-dependent patient. AAI Mode In the AAI mode, the atrial inhibited pacing mode, the pacemaker will deliver an atrial pacing stimulus at the end of the atrial LRL, measured from the previous paced or sensed atrial event. If the atrial channel does not sense an intrinsic atrial event and the programmed LRL has expired, the pacemaker will deliver an atrial impulse (Fig. 23-8). Timing is based on sensed intrinsic atrial events (P) or atrial paced events (A). The intervals used in timing can be described as P-P, P-A, A-A, and A-P. Conceptually, the timing intervals in the AAI pacing mode are similar to those of the VVI pacing mode. However, in the AAI mode, only atrial but not ventricular events result in resetting of the timing cycle (Fig. 23-9).

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Figure 23-9. AAI pacing. In this example, the pacemaker rate is 70 pulses per minute (ppm), the interval is 857 msec, and the refractory period is 250 msec. There is intermittent prolongation of the interstimulus interval, because the atrial lead senses the far-field QRS complex just beyond the 250-msec pacemaker refractory period. When the refractory period was programmed to 400 msec, the irregularity disappeared, and regular atrial pacing at a rate of 70 ppm was restored. Stars indicate intervals with oversensing. (From Barold SS, Zipes DP: Cardiac pacemakers and antiarrhythmia devices. In Braunwald E [ed]: Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1992, pp 726-755.)

Figure 23-10. AAI mode atrial refractory periods. The atrial pacing rate in the AAI mode in this example is 1000 msec and represents the time from either an atrial paced event (A) or an atrial sensed event (P) to the next atrial paced event. Each of the P-A intervals occurs at 1000 msec, whereas the ventricular sensed events may occur earlier than the atrial pacing rate. The black bar indicates the atrial blanking period, during which events are not sensed. The gray bar indicates the atrial refractory period, during which atrial sensed events are not used to reset timing cycles.

Although individual physician and regional practice variations exist, in general the candidates most suited for the AAI mode are those who are in sinus rhythm and have intact AV conduction. Because this mode does not pace the ventricle, it is not appropriate if compromised AV conduction is suspected.13 The ability to maintain 1:1 AV conduction during atrial pacing at rates of 120 or 130 bpm or faster during the pacemaker implant procedure is frequently used to determine the absence of significant AV conduction abnormalities. Recent concern about the possible deleterious impact of ventricular pacing has increased the interest in atrial pacing.14 The atrial refractory period (ARP) is similar to the VRP and constitutes a time interval after a paced or sensed atrial event in which the pacemaker is refractory to spontaneous atrial signals (Fig. 23-10). It is divided into an atrial blanking period (ABP), often programmable, followed by a refractory period during which noise sampling occurs (Fig. 23-11). The ABP is used primarily to prevent sensing of the afterpotential of the pacing stimulus. The ARP, which ranges from 150 to 500 msec, is used to prevent the atrial lead from oversensing the afterpotential of a paced stimulus, the local evoked potential produced by an atrial pacing stimulus, or “far-field” sensing of the ventricular depolarization. Atrial hysteresis may also be used in the AAI mode. The P-A interval, called the atrial escape interval (AEI), is longer than the A-A interval (the atrial pacing interval). Atrial hysteresis, similar to ventricular hysteresis, may be used to minimize atrial pacing (Fig. 23-12).

Figure 23-11. AAI blanking period. The black bar indicates the atrial blanking period, during which events are not sensed. The gray bar indicates the atrial refractory period.

Bradycardia Timing Cycles Dual-Chamber Timing Cycles Dual-chamber devices in the DDD mode provide a mechanism to combine pacing and/or sensing in either or both chambers.15-17 These functions include pacing in both the atrium and ventricle, inhibition of pacing by sensed events in the respective chamber, and AV coordinated pacing (Fig. 23-13). A sensed intrinsic atrial event inhibits atrial pacing, and a sensed intrinsic ventricular event inhibits ventricular pacing. An atrial sensed event that occurs before the AEI has “timed out” is “tracked,” or followed by a ventricular paced output (see Fig. 23-13). Timing is based on atrial sensed events (P), atrial paced events (A), ventricular sensed events (R), and ventricular paced events (V). Intervals between atrial and ventricular events can be described as A-R, A-V, P-R, and P-V (Fig. 23-14). Atrioventricular Interval The atrioventricular interval (AVI) is a programmable parameter that determines the maximum time after an

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atrial event in which an intrinsic ventricular event can occur before delivery of a ventricular pacing stimulus (see Fig. 23-13). It is initiated after a sensed or a paced atrial event. The AVI is similar to the native P-R interval and hence is programmed to optimize the hemodynamic benefit of AV coordination. The AVI permits atrial contraction, resulting in ventricular filling in end-diastole. The AVI is programmed at rest to maintain coordinated timing of atrial and ventricular contractions, permit intrinsic AV conduction when possible, and conserve generator energy. For patients who do not have coordinated AV contractions due to P-R prolongation, this may result in impaired left ventricular filling, because atrial contraction occurs so much

Figure 23-12. AAI atrial hysteresis. The atrial pacing interval in this example is 1000 msec. The atrial hysteresis interval is 1200 msec. The first event is an atrial paced event (A), followed by the second event that is also an atrial paced event 1000 msec later. The third event is an intrinsic atrial event (P) at an interval of 800 msec. The fourth atrial event is a paced event at a hysteresis interval of 1200 msec. The hysteresis interval begins with an intrinsic atrial event and ends with an atrial paced event.

earlier than the ventricular contraction. Recent trials involving patients with both preserved and depressed ventricular function suggest that maintaining intrinsic AV conduction and minimizing right ventricular pacing are also desirable hemodynamically, because improved ventricular contraction and cardiac output are seen with normal ventricular activation. Therefore, a balance must be achieved between permitting a short enough AVI to optimize coordination of atrial contraction and ventricular contraction and prolonging

Figure 23-13. DDD mode. The lower rate in this example is 60 beats per minute or 1000 msec. This is an example of ventricular-based timing. The atrial escape interval, or the time from the R-A or V-A, is 800 msec, equal to 1000 msec minus the A-V interval of 200 msec. A, paced atrial event; P, sensed atrial event; R, sensed ventricular event; V, paced ventricular event.

Figure 23-14. Diagrammatic representation of the function of a DDD pacemaker. Hatching indicates refractory periods. Lower rate timing is ventricular based and is controlled by ventricular events (paced or sensed). The four fundamental intervals are as follows: LRI, lower rate interval; VRP, ventricular refractory period; AV, atrioventricular delay; PVARP, postventricular atrial refractory period. The two derived intervals are atrial escape (pacemaker VA) interval, which is equal to LRI − AV, and the total atrial refractory period (TARP), which is equal to AV + PVARP. Reset refers to the termination and reinitiation of a timing cycle before it has “timed out” to its completion according to its programmed duration. Premature termination of the programmed AV delay by Vs is indicated by its abbreviation. The upper rate interval (URI) is equal to TARP. The As (beat 3) initiates an AV interval terminating with Vp; As also aborts the atrial escape interval (AEI) initiated by the second Vp. The third Vp resets the LRI and starts the PVARP, VRP, and URI. The fourth beat consists of an Ap, which terminates the AEI initiated by the third Vp, followed by a sensed conducted QRS (Vs). The AV interval is therefore abbreviated. Vs initiates the AEI, LRI, PVARP, VRP, and URI. Beat 5 is a ventricular extrasystole (ventricular premature contraction), that initiates AIE, PVARP, and VRP and resets the LRI and the URI. The last beat is followed by an atrial extrasystole that is unsensed because it occurs within the PVARP. APC, atrial premature contraction; Ap, atrial paced beat; As, atrial sensed beat; Vp, ventricular paced beat; Vs, ventricular sensed beat. (From Barold SS, Zipes DP: Cardiac pacemakers and antiarrhythmic devices. In Braunwald E [ed]: Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1992, pp 725-755.)

Chapter 23: Timing Cycles of Implantable Devices

A-V conduction for enough time to result in intrinsic ventricular activation. The programmed AVI that results in optimal hemodynamics may vary considerably and may be difficult to predict accurately. Many clinicians select the programmed AVI that permits the P-R interval to be as much as 280 to 300 msec. There may be a role for assessment of interatrial conduction delay in setting the optimal AVI, but data are currently limited.18 There may be a differential time of ventricular activation, depending on whether the atrium is paced or is activated intrinsically. Usually, the time for a paced electrical impulse to result in atrial activation is longer than the time required for intrinsic atrial activation. A differential AVI may be programmed and is discussed later in this chapter. Finally, to conserve battery energy, the AVI may be extended in patients without AV block, in order to reduce pacing. Atrioventricular Interval, Crosstalk, and Ventricular Safety Pacing Crosstalk is the inappropriate sensing of far-field signals from the opposite chamber, causing pacing inhibition or oversensing. One of the most serious manifestations of crosstalk in a dual-chamber pacing system is oversensing of far-field atrial stimuli resulting in ventricular inhibition and asystole in the “pacemakerdependent” patient. The AVI therefore encompasses multiple refractory and blanking timing intervals on each atrial/ventricular channel, as well as on the “opposite” channel, to prevent crosstalk (Figs. 23-15; see Fig. 23-14).

Figure 23-15. DDD refractory periods. The lower rate is 60 beats per minute or 1000 msec. This is an example of ventricular-based timing. The atrial escape interval, or the time from the R-A or V-A, is 800 msec, equal to 1000 msec minus the A-V interval of 200 msec. The refractory periods and sensing windows are given on the atrial and ventricular sensing channels. On the atrial channel, the atrial blanking period occurs after an atrial paced or (usually) an atrial sensed event. After a sensed or paced ventricular event, there may be, on the atrial channel, a postventricular atrial blanking period followed by a postventricular atrial refractory period. On the ventricular channel, the ventricular sensed or paced event creates a ventricular refractory period. On the ventricular channel after an atrial paced event, there is a cross-channel ventricular blanking period, which is usually followed by a crosstalk safety pacing window and an alert period. A, paced atrial event; P, sensed atrial event; R, sensed ventricular event; V, paced ventricular event.

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An atrial pacing output also initiates multiple timing windows on the ventricular channel. Atrial pacing output triggers a VBP at the beginning of the AVI in an attempt to avoid oversensing the atrial stimulus artifact on the ventricular lead (Fig. 23-16). This absolute VBP is usually short, ranging from 20 to 44 msec, and is programmable in certain pacemaker models. Immediately after the VBP, the ventricular sensing amplifier becomes active during the ventricular safety pacing (or crosstalk sensing) window in the second portion of the AVI (up to 80 to 120 msec). Signals sensed during the crosstalk sensing window (<120 msec from the atrial pacing output) are considered “nonphysiologic” due to the close coupling interval and may be caused by oversensing of atrial pacing afterpotentials, spontaneous premature ventricular depolarizations (PVCs), or noise (see Fig. 23-16). Ventricular safety pacing (VSP) is a feature that is designed to prevent inappropriate inhibition of the ventricular pacing caused by crosstalk (Figs. 23-17 and 23-18). After an atrial paced depolarization, if a sensed event occurs during the safety pacing window, the pacemaker, instead of inhibiting ventricular pacing, will deliver a ventricular pacing stimulus at a shortened AVI, typically ranging from 80 to 130 msec. The shortened AVI makes the identification of safety pacing apparent. It also decreases the likelihood of a ventricular paced event occurring during ventricular repolarization, particularly if the baseline AVI is relatively long; this minimizes the risk of ventricular proarrhythmia. Crosstalk in this situation is

Figure 23-16. DDD safety pacing windows. On the ventricular channel after an atrial paced event, there is a crosschannel ventricular blanking period followed by a crosstalk safety pacing window and an alert period. During the crosschannel ventricular blanking period, no sensing occurs on the ventricular channel. This blanking period prevents the atrial stimulus from inhibiting ventricular output. During the crosstalk safety pacing window, a ventricular sensed event will result in a ventricular paced event at a shorter than usual atrioventricular (A-V) interval, usually 80 to 130 msec. During the sensing window, a sensed ventricular event will result in inhibition of the next ventricular paced event. After the ventricular paced or sensed event, there will be a ventricular refractory period.

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prevent the sensing of ventricular paced events or far-field ventricular sensed events on the atrial channel. After a paced or sensed ventricular event, a postventricular atrial refractory period (PVARP) is created (see Fig. 23-20). During the PVARP, atrial events are refractory sensed events and do not affect the timing of events. Differential Atrioventricular Interval

Figure 23-17. Ventricular safety pacing. On the left, there is an atrial paced event (A) and a ventricular paced event (V) separated by an A-V interval of 200 msec. On the right, there is an atrial paced event followed by a ventricular paced event after 110 msec. This represents safety pacing caused by a ventricular sensed event’s occurring in the crosstalk safety pacing window

most likely to occur in the presence of high atrial pacing output (e.g., 6 V at 1 msec) along with high ventricular sensitivity (e.g., 2 mV). Safety pacing may also be seen when atrial undersensing occurs and the conducted intrinsic ventricular beat is sensed in the crosstalk safety pacing window (Fig. 23-19). On the atrial channel, a paced event may result in an absolute atrial blanking period (ABP), preventing sensing of the afterpotential of the pacing stimulus (Fig. 23-20). In some devices, a sensed atrial event also initiates an ABP. After the ABP, sensed atrial events may be used for detection of pathologic atrial tachyarrhythmia for mode-switching, overdrive suppression algorithm, or noise reversion. After a ventricular sensed or paced event, there may be a postventricular ABP (see Fig. 23-20), to

In some devices, the AVI initiated after a sensed atrial event (SAV) can be different from the AVI initiated after a paced atrial event (PAV). This difference is called a differential AVI. The optimal AVI achieves coordination of the atria and ventricles, particularly the left atrium and the LV. Usually, impulse formation starts first in the sinus node and then travels to the right atrial lead and is on its way to the AV node By the time the event is sensed on the atrial channel, contraction of the atria has already begun, necessitating only relatively short delay until the time that ventricular excitation occurs. There is time that elapses between the initiation of an intrinsic atrial depolarization and the point at which most of the atria are depolarized. This delay is determined by the distance between the initiation point and the location of the lead, as well as the conductive properties of the atrial tissue. In effect, by the time the atrial lead has sensed the intrinsic depolarization, the impulse has already gotten a “head start” to the AV node, compared with an atrial paced event. Programming the AVI after a sensed atrial depolarization (PV) to be shorter than after a PAV (Fig. 23-21) makes the time to ventricular pacing after a PAV similar to that after an SAV. This is an attempt to provide a more physiologic AV synchrony. The SAV may be expressed as a percentage of the PAV or as an absolute difference (up to 100 msec) between the two differential AVIs.

Figure 23-18. Ventricular safety pacing. The top channel is the surface electrocardiogram (ECG). The bottom channel is the marker channel, with the atrial channel on top and the ventricular channel on the bottom. In the absence of crosstalk, the first, fourth, and last atrioventricular (AV) intervals are equal to the programmed value of 200 msec. Intermittent crosstalk (solid black circles) leads to activation of the ventricular safety pacing mechanism, so that the A-V interval of the second, third, fifth, and seventh beats is abbreviated to 110 msec. The marker channel below the ECG confirms the presence of crosstalk with ventricular sensing (Vs) of the atrial stimulus (Ap) within the ventricular safety pacing period but beyond the short ventricular blanking period initiated by Ap. The arrows point to Vp triggered at the end of the ventricular safety pacing period (110 msec after the release of Ap). In a DDD pulse generator with ventricular-based lower rate timing, activation of the ventricular safety pacing mechanism by continual crosstalk leads to an increase in the pacing rate even though the atrial escape interval remains constant. (From Barold SS, Zipes DP: Cardiac pacemakers and antiarrhythmic devices. In Braunwald E [ed]: Heart Disease, 5th ed. Philadelphia, WB Saunders, 1997, pp 705-741.)

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-19. Ventricular safety pacing due to atrial undersensing. On the left, there is an atrial paced event and a ventricular paced event, separated by an atrioventricular (A-V) interval of 200 msec. On the right, there is an undersensed intrinsic atrial event, occurring after an atrial pacing stimulus, that is not captured due to physiologic refractoriness. The atrial event conducts to the ventricle. The sensed intrinsic ventricular event falls exactly within the crosstalk safety pacing window, resulting in a ventricular safety pacing.

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Figure 23-21. Differential atrioventricular interval (AVI). A differential AVI permits a shorter AVI for a sensed atrial event than for a paced atrial event. In the first complex, the sensed atrial event initiates an AVI of 160 msec, but AV conduction occurs within 140 msec. Similarly, in the second complex, the paced atrial event initiates an AVI of 200 msec, but AV conduction is faster than that. In the third complex, the P wave is sensed and initiates a shorter A-V interval of 160 msec, compared with the AVI of 200 msec. In the last complex, the sensed P wave also starts an A-V interval of 160 msec, but AV conduction occurs.

rate or on the sensor-driven rate, and they are programmed from a baseline AVI to a so-called minimum AVI. Atrioventricular Interval Hysteresis

Figure 23-20. DDD mode, atrial blanking period. After an paced or sensed atrial event, there is a blanking period on the atrial channel. After a sensed or paced ventricular event, there may be a postventricular atrial blanking period (PAVB) on the atrial channel, followed by a postventricular atrial refractory period (PVARP). During the PVARP, an atrial sensed event will not be tracked or used to inhibit atrial pacing at the atrial escape interval.

Rate-Adaptive or Dynamic Atrioventricular Delay The shortening of AVI with exercise provides optimal AV synchrony and is designed to mimic the normal physiologic shortening of the P-R interval. The programmable parameter called rate-adaptive or dynamic AVI permits the modulation of sensed or paced AVIs based on the ventricular rate, either intrinsic or sensor driven. In addition to the hemodynamic benefits of shortening of the AVI, rate-related shortening of AVI decreases the total atrial refractory period (TARP) (see later discussion), permitting a corresponding a higher 2:1 atrial tracking rate. The changes in dynamic AVI may be linear or nonlinear, based on the sensed atrial

The AVI can also be modulated based on the presence or absence of AV conduction with a sensed ventricular event during the AVI, a feature called positive or negative AV/PV hysteresis. The term AV hysteresis is generally used to describe adaptations of either paced or sensed AVIs relative to the patient’s intrinsic P-R interval. Similar to heart rate hysteresis, AVI hysteresis is a prolongation of the AVI in response to a ventricular paced event (V), so-called positive AV/PV hysteresis. The longer-than-programmed AVI permits intrinsic AV conduction and minimizes unnecessary ventricular pacing. Positive AV/PV hysteresis is most beneficial to patients who have variable AV conduction. If the intrinsic AV conduction exceeds the AVI hysteresis and no spontaneous R wave is sensed at the end of the AVI (e.g., in AV block), the AVI is shortened to the original programmed value. There is a search function that extends the AVI periodically from the programmed baseline value to the longer AVI hysteresis interval, to promote intrinsic AV conduction and ventricular activation (Figs. 23-22 and 23-23). This function may be termed “search positive AV hysteresis.” Alternatively, a negative AV/PV hysteresis is programmed to promote and maintain ventricular pacing and avoid fusion. After an atrial event, if native ventricular conduction is sensed (R wave), then the next AVI will be shortened to promote ventricular pacing and capture (Fig. 23-24). This function may be used to promote ventricular capture, when this is desirable hemodynamically. Such conditions might include pacing for hypertrophic cardiomyopathy or biventricular pacing.

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Postventricular Atrial Refractory Period

Figure 23-22. Positive atrioventricular (AV) hysteresis. In positive AV hysteresis, the AV interval (AVI) is increased to permit intrinsic AV conduction. If conduction is present, the extended AVI persists. If AV conduction is absent, the AVI is shortened to its previous length.

After a sensed or paced ventricular event, atrial sensed events do not result in a corresponding AVI for a programmable period of time. This interval, known as the PVARP (Fig. 23-25), is used to prevent sensing of retrograde P waves occurring after a paced or sensed ventricular event. The atrial channel may sense a retrograde atrial signal as an intrinsic event and trigger ventricular pacing, resulting in another ventricular paced event, which also conducts retrograde. This repetitive sequence is known as pacemaker-mediated tachycardia (PMT) (Figs. 23-26 and 23-27), and it may continue in the absence of intervention. PMT may occur at or below the maximum tracking rate (MTR; see later discussion) and is often induced by spontaneous PVCs or loss of atrial capture. The rate of the

Figure 23-23. Positive atrioventricular (AV) hysteresis. After a period of pacing, a search mechanism is initiated in which the system automatically extends the paced or sensed AV delay. If a native R wave occurs within the extended AV delay, the longer AV delay is maintained, restoring intact AV conduction and allowing for a normal ventricular activation sequence. Although the P-R interval is longer than the P-V interval, there is intact AV conduction. When the AV delay is extended on the 256th cycle, a sensed R wave is seen by the pacemaker, inhibiting the ventricular output and re-establishing the longer AV/PV delay engendered by adding the positive hysteresis interval to the programmed intervals. This results in functional AAI pacing or inhibited pacing, except in the presence of AV block. Although the same result could be accomplished with a fixed long AV or PV delay, if AV block developed, the pacing system would be functioning in a hemodynamically deleterious long AV/PV delay until intact conduction resumed. P, atrial sensed beat; R, ventricular sensed beat; V, ventricular paced beat. (Courtesy of St. Jude Cardiac Rhythm Management Division, Sylmar, Calif.)

Figure 23-24. Negative AV/PV hysteresis. Stable PV pacing is interrupted by one cycle (110 msec) at a shorter A-Vs interval than the P-V interval (150 msec). This causes shortening of the As-Vp (P-V) interval by the programmed value, restoring PV pacing with full ventricular capture. P, atrial sensed beat (As); R, ventricular sensed beat (Vs); V, ventricular paced beat (Vp). (Courtesy of St. Jude Cardiac Rhythm Management Division, Sylmar, Calif.)

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-25. Postventricular atrial refractory period (PVARP). A premature ventricular contraction (PVC) results in retrograde conduction, indicated by the asterisk. Because the P wave occurs within the PVARP, it is not tracked and does not initiate a ventricular paced event. Instead, the next atrial paced event occurs after the atrial escape interval has been completed.

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Figure 23-26. Pacemaker-mediated tachycardia (PMT). A premature ventricular contraction (PVC) results in retrograde conduction. Because the retrograde P wave occurs after the postventricular atrial refractory period (PVARP), the P wave is tracked and initiates a ventricular paced event. This ventricular paced event results in another retrograde P wave, which is tracked, resulting in PMT.

Figure 23-27. Pacemaker-mediated tachycardia terminated and initiated by ventricular extrasystole. The three electrocardiogram (ECG) leads were recorded simultaneously. The upper rate interval (URI) is 500 msec (120 pulses per minute [ppm]); the lower rate interval (LRI) is 857 msec (70 ppm); and the atrioventricular (AV) delay is 150 msec. The cycle length of the tachycardia is longer than the URI. (From Barold SS, Falkoff MD, Ong LS, et al.: Electrocardiography of contemporary DDD pacemakers: A. Basic concepts, upper rate response, retrograde ventriculoatrial conduction, and differential diagnosis of pacemaker tachycardias. In Saksena S, Goldschlager N [eds]: Electrical Therapy for Cardiac Arrhythmias: Pacing, Antitachycardia Devices, Catheter Ablation. Philadelphia, WB Saunders, 1990, pp 225-264.)

PMT depends on the retrograde conduction time, the programmed AVI, and the MTR. Commonly, PMT occurs at the MTR. However, the retrograde conduction time may be long enough to permit tracking of the atrial event with the programmed AVI, so that the rate of the PMT may be less than the MTR. To avoid PMT, the PVARP is usually programmed to be longer than the retrograde conduction time; however, if it is programmed excessively long, the sum of the PVARP and the AVI (the TARP) will determine the rate at which

one ventricular paced event occurs for two atrial sensed events, the 2:1 atrial tracking rate (see later discussion). Extension of the PVARP in response to a PVC, the socalled PVC PVARP extension or response, is available in many devices. This algorithm is designed to lengthen the PVARP and to avoid sensing of a retrograde P wave occurring after a PVC that may cause initiation of PMT. Of note, a “PVC” is usually defined by the pacemaker as a spontaneous ventricular depolarization without a preceding atrial paced or sensed event. In some cases,

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Figure 23-28. Lack of P wave tracking due to a long postventricular atrial refractory period (PVARP), 400 msec. The sinus rate is about 85 beats per minute, and there is a first-degree atrioventricular (AV) block. The P waves fall within the PVARP initiated by the preceding sensed QRS complex. Shortening the PVARP to 375 msec (bottom) restores 1:1 atrial tracking with the programmed AV interval (150 msec). VRP, ventricular refractory period. (From Barold SS, Falkoff MD, Ong LS, et al.: Timing cycles of DDD pacemakers. In Barold SS, Mugica J [eds]: New Prospectives in Cardiac Pacing. Mt. Kisco, NY, Futura, 1988, pp 69-119.)

a long PVARP may lead to absence of atrial tracking (Fig. 23-28). Similarly, oversensing of a T wave and programming on the PVC PVARP extension may cause perpetuation of absence of atrial tracking at rates below the LRL (Fig. 23-29). Repetitive functional atrial undersensing may occur in the absence of PVC PVARP extension, particularly if the AV conduction is prolonged and the intrinsic AVI plus the PVARP is longer than the sinus cycle length.19 Features such as autointrinsic search that cause prolongation of AV conduction may result in PMT by permitting retrograde conduction.20

Figure 23-29. Perpetuation of failure to track due to postventricular atrial refractory period (PVARP) extension. T wave oversensing is classified as a premature ventricular complex (PVC). The PVC PVARP extension feature results in the PVARP being extended, which places the subsequent sinus P wave within the PVARP. Because atrioventricular (AV) conduction is present, the next QRS complex is considered a PVC, which again causes PVARP extension.

Upper Rate Behavior In patients using the DDD, DDDR, VDD, or VDDR modes, one-to-one ventricular tracking of the intrinsic atrial activity is hemodynamically desirable. However, tracking of atrial arrhythmias may result in rapid ventricular pacing and lead to unfavorable hemodynamics. Therefore, these tracking modes have a parameter to limit the fastest rate at which the atrium can be tracked. The fastest rate at which atrial activity can be tracked 1:1 to the ventricle is known as the upper rate or MTR, with a corresponding upper rate interval or maximum tracking interval (Fig. 23-30). In a DDD mode of operation, whether it is atrial based or ventricular based, when the intrinsic atrial activity is faster than the programmed upper rate limit, upper rate behavior will be seen. Atrial rates faster than the MTR can still be sensed and tracked. However, delays in subsequent ventricular-paced beats occur, so the ventricular rate does not exceed the programmed MTR (Fig. 23-31). This effectively prolongs the AVI. The AVI is further extended on repeated cycles, and eventually a subsequent atrial depolarization falls within the PVARP. Because the atrial event occurs within the PVARP, it is not sensed by the atrial channel and does not lead to ventricular pacing. The next atrial event, however, can be tracked and causes ventricular pacing. The pattern that emerges is increasing time between an intrinsic atrial-sensed event and a subsequent ventricularpaced event until an atrial event is not followed by a ventricular-paced beat. Such behavior looks like a Wenckebach pattern during AV conduction and is called pseudo-Wenckebach AV response. The AVI extension is greatest when the P wave occurs just after

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Figure 23-30. Upper rate behavior. A, Apparent loss of atrial tracking related to upper rate limitation. The lower rate interval (LRI) is 1000 msec; the upper rate interval is 500 msec; and the atrioventricular interval (AVI) is 75 msec. The electrocardiogram (ECG) was recorded during a treadmill stress test. The P waves on the right are sensed (documented later by markers during repeated exercise, not shown) but the pacemaker does not emit a ventricular paced beat because a QRS complex occurs before the termination of the 75-msec AVI, thereby producing a sensed repetitive preempted Wenckebach upper rate response. B, Same patient as A. During the recovery portion of the stress test, as the sinus rate slows, the AVI gradually shortens in a few cycles until it reaches 75 msec. This produces a “reverse Wenckebach” response, with gradually more ventricular captures (fusion beats) until full ventricular capture is reestablished, preceded by a sensed atrial-topaced ventricular interval of 75 msec. (From Douard H, Barold SS, Broustet JP: Too much protection may be a nuisance. Stimucoeur 25:183-187, 1997.)

the completion of the preceding PVARP (Fig. 23-32). AVI extension may be seen at constant atrial rates during atrial or sinus tachycardias as well as during atrial premature beats (Fig. 23-33). If the intrinsic atrial rate continues to increase above the MTR, it will eventually reach the 2:1 AV tracking rate, defined by the TARP, which is the sum of the PVARP and the AVI (Fig. 23-34). The TARP defines the period during which sensing may occur and limits the MTR. TARP determines the rate at which atrial tracking occurs in a 2:1 ratio. At this atrial rate, every other P wave falls into the PVARP and is not sensed. If the intrinsic atrial rate is fast enough, one P wave can fall within the TARP while the next P wave falls outside the TARP and is tracked. If the atrial rate is just a little faster, the first P wave will be tracked and the second P wave will fall just within the PVARP and will not be tracked. As a result, for every two intrinsic atrial events,

there is one ventricular-paced beat. Such a phenomenon occurs when the intrinsic atrial rate is faster than the 2:1 AV block rate. The 2:1 AV block rate can be calculated in milliseconds as 60,000 divided by TARP. For example, for an AVI of 150 msec and a PVARP of 250 msec, ventricular pacing may follow atrial sensing 1:1 at a rate of up to 149 bpm. At a sinus rate of 150 bpm, 2:1 atrial tracking occurs and the ventricular rate abruptly drops to 75 bpm. If a patient has intrinsic AV conduction, the upper rate limit is not needed to permit tracking of rapid sinus rates during exertion. Therefore the upper rate limit, when intrinsic AV conduction is present, may be programmed at a relatively low rate. In patients with complete AV conduction block, however, it is important to permit tracking as the atrial rate rises during exertion. The upper rate limit (MTR) should be programmed high enough to allow 1:1 tracking through maximum

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Figure 23-31. DDD mode upper rate response with pacemaker Wenckebach atrioventricular (AV) block. The upper rate interval (URI) is longer than the programmed total atrial refractory period (TARP). The P-P interval (As-As) is shorter than the URI but longer than the programmed TARP. The As-Vp interval lengthens by a varying period (W) to conform to the URI. During Wenckebach response, the pacemaker synchronizes Vp to As, and because the pacemaker cannot violate its (ventricular) URI, Vp can be released only at the completion of the URI. The AV delay (As-Vp) becomes progressively longer as the ventricular channel waits to deliver its Vp until the URI has timed out. The maximum prolongation of the AV interval represents the difference between the URI and the TARP. The As-Vp interval continues to lengthen as long as the As-As interval (P-P) is longer than the TARP. The sixth P wave falls within the postventricular atrial refractory period (PVARP); therefore, it is unsensed and is not followed by Vp. A pause occurs, and the cycle restarts. In the first four pacing cycles, the intervals between ventricular stimuli (Vp-Vp) are constant and equal to the URI. When the P-P interval becomes shorter than the programmed TARP, Wenckebach pacemaker AV block cannot occur, and fixed-ratio pacemaker AV block (e.g., 2:1) supervenes. AEI, atrial escape interval; As, sensed atrial beat; Vp, paced ventricular beat. (From Barold SS, Falkoff MD, Ong LS, et al.: All dual chamber pacemakers function in the DDD mode. Am Heart J 115:1353, 1988.)

physiologic atrial rates. However, a 2:1 atrial tracking rate faster than the maximum atrial tracking rate permits a zone of pseudo-Wenckebach behavior before the development of 2:1 block. To accomplish this effect, the TARP (PVARP + AVI) is programmed shorter than the upper rate limit interval. There may be limitations to minimizing the TARP if retrograde conduction necessitates programming the PVARP to be longer than the retrograde conduction time. To avoid precipitous falls in heart rate, it is preferable to have the 2:1 AV block rate set higher than the MTR, to accommodate high intrinsic sinus rates without sudden AV block. This is achieved by minimizing TARP. There are several common ways to reduce the TARP and thereby raise the 2:1 block rate. The PVARP can be shortened (with consideration of the

greater potential for PMT), and the AVI can be programmed to be rate-adaptive and shorten with faster ventricular rates. Rate-adaptive or dynamic PVARP is also available in some models; this shortens PVARP at a faster rate, thereby reducing TARP and raising the 2:1 AV block rate. Caution should be used with rateadaptive PVARP to confirm that retrograde conduction will not occur at rapid ventricular rates, so that the conduction time does not exceed the PVARP and result in PMT. Alternatively, the pacemaker can be programmed to DDDR mode, relying on the sensor to drive pacing during exertion. If sensor-driven ventricular pacing occurs close to the sinus rate, the ventricular pacing rate will closely follow the sinus rate even though the ventricular pacing rate exceeds the maximum atrial tracking rate. This phenomenon has been termed

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Figure 23-32. Diagrammatic representation of the mechanism of atrioventricular (AV) interval prolongation in a pulse generator with a separately programmable total atrial refractory period (TARP) and upper rate interval (URI). Lower rate timing is ventricular based. The maximum AV extension, or waiting period (W), is equal to the URI minus the sum of the AV interval and the postventricular atrial refractory period (PVARP), or URI − TARP. A P wave (P1) occurring immediately after the termination of the PVARP exhibits the longest AV interval (i.e., AV + W). A P wave just beyond the W period (P4) initiates an AV interval equal to the programmed value. P waves occurring during the W period (P2 and P3) exhibit varying degrees of AV prolongation to conform to the URI depicted as the shortest interval between two consecutive ventricular paced beats (Vp). If the pacemaker is programmed with As-Vp shorter than Ap-Vp, W becomes URI − (As-Vp) − PVARP; that is, the AV extension becomes longer if the basic As-Vp is shorter than Ap-Vp. However, the maximum As-Vp duration is URI − PVARP, regardless of the programmed AV interval. AEI, atrial escape interval; LRI, lower rate interval: Ap, atrial-paced beat; As, atrial sensed beat. (From Barold SS, Falkoff MD, Ong LS, et al.: Electrocardiography of contemporary DDD pacemakers: A. Basic concepts, upper rate response, retrograde ventriculoatrial conduction, and differential diagnosis of pacemaker tachycardias. In Saksena S, Goldschlager N [eds]: Electrical Therapy for Cardiac Arrhythmias: Pacing, Antitachycardia Devices, Catheter Ablation. Philadelphia, WB Saunders, 1990, pp 225-264.)

Figure 23-33. Two-lead electrocardiogram showing DDD pacing (ventricular-based lower rate timing) with sensed atrial premature contractions (APC). The lower rate interval (LRI) is 1000 msec; the atrioventricular interval (AVI) is 200 msec; the upper rate interval (URI) is 600 msec; and the postventricular atrial refractory period (PVARP) is 155 msec. Note the extended AVI generated by the APCs to conform to the URI. This response with single beats should not be called a Wenckebach upper rate response; rather, it is best called an AV extension upper rate response.

Figure 23-34. Total atrial refractory period (TARP). The TARP represents the sum of the postventricular atrial refractory period (PVARP) and the atrioventricular interval (AVI). In this case TARP = 360 + 200 = 560 msec. Therefore, 2:1 atrial tracking would occur at an atrial cycle length of 560 msec.

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A

B

Figure 23-35. Sensor-driven appearance of atrial tracking. The diagram shows that a P wave may inhibit the sensordriven atrial stimulus and can resemble P-wave tracking above the maximum tracking rate (MTR) of 100 beats per minute (600 msec). The second and third ventricular complexes are preceded by intrinsic P waves that appear within the atrial sensing window (ASW). Sensing of atrial activity in this window results in inhibition of the atrial stimulus or Pwave tracking above the MTR. The fourth ventricular complex was preceded by an atrial paced event because the intrinsic P wave was within the atrial refractory period. ARP, atrial refractory period; AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; VP, ventricular paced event. (From Higano ST, Hayes DL: P wave tracking above the maximum tracking rate in a DDDR pacemaker. PACE 12:10441048, 1989.)

sensor-driven rate smoothing (Fig. 23-35), and it resembles tracking above the MTR.21 Upper rate behavior may also result in triggering of an apparent failure to sense P waves, because the P wave that falls within the PVARP and the subsequent QRS complex are categorized as a premature ventricular beat. Use of an algorithm to increase the PVARP after a PVC may result in a prolonged period of absence of atrial tracking (Figs. 23-36 and 23-37).22 Upper rate behavior may also be characterized by intrinsically conducted beats that may preempt the ventricular paced beats at the upper rate. Barold and colleagues23 reported that a relatively short programmed AVI, a sinus rate faster than the programmed upper rate, a relatively slow programmed upper rate, and relatively normal AV conduction are most likely to be associated with this phenomenon.

C Figure 23-36. Apparent P wave undersensing. The lower rate is 60 pulses per minute (ppm); the upper rate is 140 ppm; the atrioventricular (AV) delay after P wave sensing is 135 msec (adaptive AV delay with minimum AV delay of 75 msec); the postventricular atrial refractory period (PVARP) is 320 msec; and the automatic PVARP extension is 100 msec. A, At rest, the atrial rate is 112 beats per minute, causing atrial sensing and ventricular pacing with an AV interval of about 100 msec. B, After 1 minute of exercise, Wenckebach upper rate response occurs, and the pacemaker does not sense a P wave (arrow) in the PVARP. The P wave in the PVARP allows spontaneous AV conduction with a PR interval of about 260 msec. The pacemaker interprets the spontaneous QRS as a ventricular premature contraction (VPC) and therefore automatically lengthens the PVARP to 320 + 100 = 420 msec. Subsequent events all are spontaneous; that is, the P wave and conducted QRS complex have a P-R interval longer than the programmed As-Vp interval at that particular atrial rate (apparent lack of atrial tracking). The spontaneous QRS complex continually activates the PVARP extension as the P waves continually fall within the extended PVARP. C, In the recovery phase, the electrocardiogram shows sinus rhythm (P-R interval of 200 msec) and conversion to an atrial synchronous ventricular-paced rhythm with an AV interval of 100 msec. The P-R interval preceding ventricular pacing shows an abrupt shortening of about 40 msec without a change in P-P interval. This results in earlier detection of the conducted QRS complex. The next P wave then falls outside the extended PVARP of 420 msec. As, atrial sensed beat; Vp, ventricular paced beat. (From Van Gelder BM, Van Mechelen R, Den Dulk K, et al.: Apparent P wave undersensing in a DDD pacemaker after exercise. PACE 15:1651, 1992.)

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Figure 23-37. Loss of P wave tracking due to long postventricular atrial refractory period (PVARP), 400 msec. The sinus rate is about 85 beats per minute (bpm), and there is first-degree atrioventricular (AV) block. The P waves fall within the PVARP initiated by the preceding sensed QRS complex. Shortening the PVARP to 373 msec (bottom) restores 1:1 atrial tracking with the programmed AV interval (150 msec). VRP, ventricular refractory period. (From Barold SS, Falkoff MD, Ong LS et al: Timing cycles of DDD pacemakers. In Barold SS, Mugica J [eds]: New Perspectives in Cardiac Pacing. Mt. Kisco, NY, Futura, 1988, pp 69-119.)

Lower Rate Behavior: Atrial-Based versus Ventricular-Based Timing LRL timing has already been discussed. The use of atrial- versus24 ventricular-based timing cycles determines when atrial-paced events occur. With ventricularbased timing, in the DDD mode, an AEI is initiated after a sensed or paced ventricular event (R-A, or V-A) (Fig. 23-38). In ventricular-based timing, the AEI is “fixed.” The LRL is the maximum time interval allowed between a ventricular event (either sensed or paced) and the subsequent ventricular pacing stimulus (V-V, or R-V) The LRL is therefore equal to the AEI plus the AVI until the subsequent ventricular pace (R-A-V or VA-V). The length of the AEI can be determined by subtracting the AVI from the cycle length of the LRL (in microseconds). If another ventricular-sensed event occurs during the AEI, it will reset and initiate a new AEI. If an atrial-sensed event occurs during the AEI (after the PVARP), it will initiate the AVI, with a subsequent ventricular-sensed or paced event within the constraints of the upper rate limit. If the AEI expires sensing any atrial or ventricular event is sensed, the pacemaker will provide an atrial-paced beat. In ventricular-based timing, it is possible for the effective ventricular rate to be faster than the programmed LRL. This occurs in patients with intact AV conduction and is mainly caused by the difference between the paced AVI and the shorter intrinsic AV conduction (Fig. 23-39). For example, in a pacemaker programmed to an LRL of 60 bpm (1000 msec) that has a programmed AVI of 200 msec, the AEI is 800 msec (LRL − AVI = AEI). If AV conduction is present at 150 msec, the sensed R wave

will reset the timing cycle, whereas the AEI is “fixed” at 800 msec. The effective interval between consecutive atrial pacing beats is therefore 950 msec (AEI + A-R), which is approximately 63 bpm (see Figs. 23-38 and 23-39). In patients with intact AV conduction, the effective ventricular rate can be faster than the programmed LRL in a ventricular-based timing system. Whereas the AEI is fixed in a ventricular-based timing system, the atrial interval (A-A) is fixed in an atrial-based timing system. A sensed R wave occurring during AVI inhibits ventricular output but does not reset the basic A-A interval; therefore, the LRL is not altered. When a R wave is sensed during AEI, the A-A interval is reset, but not the AEI. This results in a longer atrial-to-atrial interval that simulates a physiologic “compensatory” pause. Some pacemaker models deploy a “modified” atrial-based algorithm, such that routine atrial sensed or paced events reset the A-A timing cycle but PVCs reset the AEI or the V-A interval (Fig. 23-40). Early sensing of the ventricular complex on the atrial channel (crosstalk) in a pacemaker with atrial-based timing has been shown to result in prolonged AEIs (Figs. 23-41 and 23-42).25 In Figure 23-41, at a more sensitive ventricular sensitivity (left panel), there is no evidence of a prolonged AEI, whereas at a less sensitive ventricular sensitivity (right panel), there is significant prolongation of the AEI. Figure 23-42 reveals that the first PVC may be sensed first on the atrial channel, resulting in prolongation of the AEI. In this device, when PVCs are sensed first on the ventricular channel, ventricular-based timing is used to set the AEI. The second PVC in this figure is sensed as a PVC and therefore does not result in prolongation of the AEI.

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Figure 23-38. DDD mode with ventricular-based lower rate timing. Diagrammatic representation of timing cycles. The second Vs is a sensed ventricular extrasystole. The fourth atrioventricular interval (AVI), initiated by an As, is abbreviated because the Vs occurs before the AVI has timed out. The postventricular atrial refractory period (PVARP) generated by the ventricular extrasystole is automatically extended by the atrial refractory period extension. This design is based on the concept that most episodes of endless-loop tachycardia (pacemaker macroreentrant tachycardia caused by repetitive sensing of retrograde atrial depolarization) are initiated by ventricular extrasystoles with retrograde ventriculoatrial conduction. Whenever possible, the AVI and the atrial escape (pacemaker V-A) interval (AEI) are depicted in their entirety for the sake of clarity. The arrow pointing down within the AEI indicates that an As has taken place. The As inhibits the release of the atrial stimulus expected at the completion of the AEI. As, atrial sensed event; REF, refractory; ventricular triggering period, ventricular-ventricular safety period; Vs, ventricular sensed event. (From Barold SS, Falkoff MD, Ong LS, et al.: All dual-chamber pacemakers function in the DDD mode. Am Heart J 115:1353, 1988.)

Figure 23-39. Ventricular-based timing cycles. The lower rate limit is 1000 msec; the atrioventricular (AV) delay is 200 msec; and the atrial escape interval is 800 msec. The R-R intervals are given. Note that the R-R interval is 1000 msec between the first and second beats. Between the second and third beats, the R-R interval is also 1000 msec. Between the third and fourth beats, it is 960 msec because the AV conduction time is less than 200 msec. A, atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event.

Figure 23-40. Atrial-based timing cycles. The lower rate limit is 1000 msec; the atrioventricular (AV) delay is 200 msec; and the atrial escape interval is 800 msec. The R-R intervals are given. Note that the R-R interval is 1000 msec between the first and second beats. Between the second and third beats, the R-R interval is 1040 msec. Between the third and fourth beats, it is 960 msec because the AV conduction time is less than 200 msec. A, atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event.

Chapter 23: Timing Cycles of Implantable Devices

A

B

Figure 23-41. Prolongation of the atrial escape interval (AEI) in an atrial-based timing pacemaker. In the left panel (A), the atrial sensitivity was programmed to 0.5 mV and the ventricular sensitivity was 1 mV. The premature ventricular contraction (PVC) resulted in an AEI of 660 msec, corresponding to the programmed AEI of 600 msec. In the right panel (B), the atrial sensitivity was still programmed at 0.5 mV, but the ventricular sensitivity was decreased to 4 mV. The PVC (arrow) resulted in prolongation of the AEI to 800 msec, corresponding to the programmed lower rate interval of 750 msec. (From Barold SS: Far-field R wave sensing causing prolongation of the atrial escape interval of DDD pacemakers with atrialbased lower rate timing. PACE 26:2188-2191, 2003.)

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functions. The pacemakers have developed from VOO to DDDR systems. In response to enhanced sympathetic drive during exercise, heart rate (HR) and stroke volume (SV) increase, leading to greater cardiac output (CO = HR × SV). Unlike people who can raise their heart rate considerably during exercise, patients with sinus node or conduction system dysfunction are unable to raise their heart rate adequately. Because heart rate is the predominant determinant of cardiac output compared with stroke volume, the pacemaker must provide rate-adaptive pacing to optimize physiologic response. Impaired heart rate response to increased metabolic demand is known as “chronotropic incompetence.” Its definition varies and is sometimes described as inability to achieve 75% of the maximum predicted heart rate for age. Individuals with chronotropic incompetence include patients who have sinus bradycardia with sinus node dysfunction and those in atrial fibrillation with a slow ventricular rate response. Both populations may exhibit blunted heart rate response to stress. Algorithms have been developed to estimate an individual’s expected maximum heart rate, as during vigorous exercise. One of the most common estimations is based on patient age (220 − age [years] = maximum heart rate). Rate-Adaptive Pacing In order to provide a greater heart rate response with exertion in efforts to support the metabolic demands during exercise, rate-adaptive pacing is essential for patients with chronotropic incompetence. For example, a patient in sinus bradycardia who has sinus node dysfunction could benefit from either an atrial- or a dualchamber–rate responsive pacemaker in order to achieve a higher heart rate response during exertion than their sinus node can provide. Similarly, patients who have chronic atrial fibrillation and a slow ventricular rate may benefit from a VVIR pacemaker that increases the rate of ventricular pacing with exertion.

Figure 23-42. Prolongation of the atrial escape interval (AEI) in an atrial-based timing pacemaker caused by far-field Rwave sensing on the atrial channel. The lower rate limit is 800 msec in an atrial-based timing system, except after premature ventricular contractions (PVCs), when ventricular-based timing is present. After the first PVC, the As marker precedes the Vs marker, suggesting early sensing of the R wave on the atrial channel. Early atrial sensing results in prolongation of the AEI, because it is an atrial-based timing system. The second PVC is not sensed first on the atrial channel and therefore is considered to be a PVC, resulting in ventricular-based timing and no prolongation of the AEI. As, atrial sensed event; Vs, ventricular sensed event. (From Barold SS: Far-field R wave sensing causing prolongation of the atrial escape interval of DDD pacemakers with atrial-based lower rate timing. PACE 26:2188-2191, 2003.)

Sensor-Driven or Rate-Adaptive Pacing Hemodynamics of Exercise and Rate Since the development of pacemakers in the early 1960s, the goals of pacing therapy have evolved from basic pacing for life support to optimizing physiologic

Timing Cycles of Sensor-Driven Pacing Sensor-driven pacing preserves the timing cycles of the basic non–rate-adaptive mode. In the VVIR mode, there is a sensor-indicated rate that serves as the LRL; the ventricular escape interval varies based on the sensorindicated rate. Similarly, in the DDDR mode, the sensor-indicated rate serves as the LRL. The timing cycles in DDDR are based on the sensor-indicated interval serving as the lower rate interval. The escape interval in a ventricular-based timing device is calculated by subtracting the paced AVI from the sensorindicated interval. Rate-Adaptive Algorithms There are algorithms that attempt to permit more physiologic response to exertion by modulating programmable intervals as rate changes. For example, in some systems the AVI can be shortened when an increased atrial rate is sensed or when the sensor-driven rate

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increases (rate-adaptive AV delay). This feature attempts to simulate the physiologic narrowing of the AV conduction time (P-R interval) that occurs with exercise. When it is responding to increased intrinsic atrial rates, it also permits a higher MTR. Because the AVI is shortened, the TARP (PVARP + AVI) also shortens, allowing for a higher 2:1 atrial tracking rate (60,000 ÷ TARP in beats per minute). A high 2:1 AV block rate affords a higher MTR to maintain 1:1 AV synchrony. For individuals who cannot tolerate a shortened PVARP because of persistent retrograde conduction, who have impaired A-V conduction, rate-modulation of the AVI can be particularly useful. The AVI also may shorten as the sensor-driven rate increases. This permits the hemodynamic effects of sensor-driven pacing to be optimized with an AVI that shortens with exertion. The PVARP may also be rate-modulated. The rate adaptation is based on the physiologic observation of decreased retrograde conduction time with increased activity seen in normal subjects. When a rate-adaptive PVARP is programmed, the PVARP shortens as the sensor-determined rate increases, which also shortens the TARP (similar to rate-adaptive AVI) and allows for a higher 2:1 tracking rate. However, shortening of the PVARP rests on the assumption that retrograde conduction time will shorten with exertion. Individuals who have retrograde conduction that is slower than that assumed by the algorithms may be at risk for development of PMT. Noise Response To minimize electromagnetic interference from lead problems, myopotentials, and environmental noise, noise response algorithms have been developed. Positioned after the VRP, the noise sampling period (usually having a duration of 60 to 200 msec) interprets any sensed events as nonphysiologic noise. This detection results in extension of the VRP or noise sampling period. If the noise is intermittent, inappropriate sensing may result and pacing may be inhibited. With more continuous noise, the pacing can become asynchronous. Depending on the nature of the extrinsic electromagnetic source, the device may “revert” to one of several nominal settings, such as a reset mode, an emergency VVI mode, or the elective replacement indicator settings. Pacemaker-Mediated Tachycardia Algorithms Algorithms have been designed to prevent or terminate the phenomenon of PMT in dual-chamber pacemakers. PMT, or endless loop tachycardia (ELT), results from retrograde conduction to the atrium after a ventricular depolarization, which can be sensed and “tracked” by the atrial lead, triggering another ventricular pacing event. The retrograde limb of the PMT is the native conduction system, and the anterograde limb is atrial tracking in the dual-chamber mode. Each ventricular-paced beat results in retrograde conduction and perpetuation of the PMT. PMT is often triggered by a PVC. The uncoupling of AV synchrony, as with failure of atrial capture or a programmed AVI that is excessively long,

Figure 23-43. Pacemaker-mediated tachycardia (PMT) intervention using extension of the postventricular atrial refractory period (PVARP). PMT is initiated with a premature ventricular beat at the left side of the panel. After eight VpAs intervals occur in less than 400 msec, the PMT intervention is initiated. The ninth ventricular paced event extends the PVARP to 400 msec for one cycle. Because the next atrial event is not tracked, the PMT terminates. As, atrial sensed event; Vp, ventricular paced event. (From Medtronic Enpulse Device Manual 5-13).

may result in PMT. Some algorithms are designed to prevent the initiation of PMT. The most common PMTprevention algorithm is PVC-PVARP extension. Without a preceding atrial activation, individuals are especially vulnerable to PMT after a PVC, because retrograde VA conduction occurs relatively easily as the native conduction system is not yet refractory. When the pacemaker senses a ventricular event without a preceding atrial event, it identifies it as a PVC and automatically lengthens the PVARP to protect against potential retrograde conduction. Such a parameter does not require that the PVARP be extended at all times, which would result in an increase in the TARP and a decrease in the 2:1 atrial tracking rate. Algorithms also may detect retrograde conduction when it is present in a sensing window (e.g., the window of atrial rate acceleration detection [WARAD]). Many algorithms have been developed to detect, terminate, or prevent PMT. Some algorithms may classify an atrial sensed and ventricular paced rhythm as PMT if atrial tracking occurs at a specific rate. The PMT detection rate may be the upper tracking rate or a rate greater than the upper tracking rate. Other algorithms detect PMT if repetitive atrial sensing follows ventricular pacing with a consistent V-to-A interval of less than 400 msec (compatible with retrograde VA conduction). When PMT is detected, different responses can occur. Some devices extend the PVARP, whereas others suspend atrial tracking for one cycle, causing PMT to terminate (Fig. 23-43). Mode Switching Automatic mode switching refers to the ability of the pacemaker to automatically switch from one mode of operation to another in response to a sensed atrial tachyarrhythmia26-29 (Fig. 23-44). When atrial tachyarrhythmias occur, atrial tracking modes such as DDD(R) or VDD(R) can result in rapid ventricular pacing with resultant hemodynamic compromise. Mode-switching algorithms have been developed to detect the presence of atrial tachyarrhythmias and convert the pacemaker to a non–atrial tracking mode such as VVI(R) or DDI(R) (see Fig. 23-44). In some cases, mode switching in DDD

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Figure 23-45. Dependence of ability to switch modes based on atrial sensitivity. Atrial undersensing increases as the device is made less sensitive. A, At atrial sensitivities greater than 1 mV, atrial undersensing becomes apparent. B, As the atrial sensitivity approaches 2 mV, the degree of oversensing of noise becomes minimal. (From Lau CP, Leung SK, Tse HF, Barold SS: Automatic mode switching of implantable pacemakers: I. Principles of instrumentation, clinical, and hemodynamic considerations. PACE 25:967-985, 2002.) Figure 23-44. Activation of the mode-switching function from DDDR to DDIR. Activation of the mode-switching function results in conversion to the DDIR mode at 60 beats per minute. Mode-switching is seen in the bottom panel. AEGM, atrial electrogram; ECG, surface electrocardiogram; MC, marker channel. (From Lau CP, Leung SK, Tse HF, Barold SS: Automatic mode switching of implantable pacemakers: I. Principles of instrumentation, clinical, and hemodynamic considerations. PACE 25:967-985, 2002.)

may result in either DDI or DDIR. An alternative modeswitching mode is VDI or VDIR. Before mode switching, there may a period of atrial tracking resulting in short paced intervals. Once mode switching is confirmed, the mode changes to the non–atrial tracking mode and the rate gradually decreases to the LRL. Mode-switching functions are often programmable. The algorithms vary but may be triggered by a specific atrial rate threshold, either an absolute or an averaged atrial rate (in beats per minute). There is usually a requirement for a sustained duration of the high rate (a number of beats or a time duration) before mode switching occurs. Other devices deploy a “running counter” that increases when the atrial rate is faster and decreases when it is slower than a specified rate limit. The pacemaker switches modes only after the counter has reached a predetermined number. This prevents inappropriate mode switching in response to frequent isolated atrial ectopic beats. Some algorithms permit detection of premature atrial beats on a beat-tobeat basis. Lau and colleagues26 described the perfect mode-switching system as having (1) rapid onset to avoid rapid ventricular pacing during initial detection of atrial tachyarrhythmias, (2) absence of fluctuation in rate or inappropriate response, (3) ability to restore AV synchrony rapidly after termination of atrial tachyarrhythmia, (4) ability to sense atrial tachyarrhythmias at a variety of rates and signal amplitudes, and (5) ability to avoid response to crosstalk, sinus tachycardia, and extraneous noise. Nonetheless, detection of atrial arrhythmias remains the greatest challenge for mode-switching algorithms.30-32 Undersensing is possible, because the amplitude of the atrial electrogram may decrease significantly during atrial tachyarrhythmia, compared with sinus rhythm. As the atrial channel becomes more sensitive, fewer undersensed events will occur, but there may be an

increase in oversensing of noise or extraneous signals (Fig. 23-45). The ABP does not usually play a significant role in atrial undersensing during atrial fibrillation.33 Oversensing can also be problematic, as with far-field signals (crosstalk) from ventricular depolarizations, T waves, myopotentials, or environmental noise. In the case of undersensing, mode switching may fail to occur, whereas in oversensing, mode switching may occur inappropriately. Symptoms are usually minimized during mode switching because of the relative rapidity of the onset of mode switching. Even when mode switching occurs swiftly, however, some patients may remain symptomatic because of the abrupt change in rate. A comparison of three different mode-switching algorithms downloaded into an implanted pacemaker was made34 (Fig. 23-46). The mean atrial interval was compared with “4 of 7” intervals and with a “1 of 1” interval as a criterion for mode switching. The shorter the criterion, the greater the number of episodes observed. The duration of mode switching decreased with shorter criteria, as expected. The symptoms did not vary significantly. Atrial Flutter Response Because atrial flutter may be associated with every other atrial electrogram falling into a blanking period, mode switching during atrial flutter may not reliably occur.35 A special response may occur when atrial flutter is detected, leading to mode switching and preventing pacing during the atrial vulnerable period.36 If an atrial event is detected within the PVARP, a programmable interval is created. Subsequent atrial events sensed within this programmable interval are not tracked, and each such event creates another programmable interval. This algorithm permits atrial tracking to be withheld even before mode switching occurs. In addition, atrial pacing does not occur until the programmable interval or PVARP expires. Once this happens, atrial pacing may occur if there are at least 50 msec and no more than the AV delay before the next ventricular paced beat. A related algorithm permits atrial flutter to trigger mode switching. If atrial cycles are sensed at an interval shorter than twice the AV delay plus the postventricular atrial blanking period

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Figure 23-46. Effect of mode-switching criterion on mode switching criteria and frequency. Three different mode switching algorithms were downloaded into an implanted pacemaker. The mean atrial interval (MAI) was compared with 4 of 7 intervals (4/7) and with 1 of 1 interval (1/1) as a criterion for mode switching. The shorter the criterion, the greater the number of episodes observed. The duration of mode switching decreased with shorter criteria, as expected. The symptoms did not vary significantly. (From Marshall HJ, Kay GN, Hess M, et al.: Mode switching in dual chamber pacemakers: Effect of onset criteria on arrhythmia-related symptoms. Europace 1:49-54, 1999.)

Figure 23-47. Atrial flutter algorithm to trigger mode switching. If atrial cycles are sensed at an interval shorter than twice the atrioventricular (AV) delay plus the postventricular atrial blanking period (PVABP) for eight consecutive cycles (asterisk), the algorithm extends the PVARP to 400 msec for one cycle (arrow). AEGM, atrial electrogram; AMS, automatic mode switching; AR, atrial refractory; AS, atrial sensed; MD, marker diagram; VP, ventricular paced. (From Israel CW, Barold SS: Failure of atrial flutter detection by a pacemaker with a dedicated atrial flutter detection algorithm. PACE 25:1274-1277, 2002.)

(PVAB) for eight consecutive cycles, the algorithm extends the PVARP to 400 msec for one cycle (Fig. 23-47). The atrial signal that had been tracked is now refractory and may activate mode switching. Figure 23-48 presents an example of atrial flutter with an atrial cycle that places an atrial signal within the PVAB, so that the atrial flutter response never occurs. Rate Smoothing Rate-smoothing algorithms are designed to “smooth” and prevent sudden changes in heart rates accompanied by hemodynamic compromise or symptoms. Sinus arrest may result in an abrupt decrease in heart rate to the escape rate, for example from 80 to 50 bpm. Rate smoothing results in a more gradual decrease in heart rate. The rate of decrease or increase in rate is constrained, respectively, by the programmed ratesmoothing “down” or “up” percentage, usually between 3% and 24%. A rate-smoothing atrial or ventricular window is created, which determines when the next atrial-paced or ventricular-paced event will occur (figure rate smoothing). The ventricular window is created by calculating the previous V-V interval and multiplying it by the rate-smoothing percentage. For example, if the previous cycle length was 1000 msec, the rate-smoothing up percentage was 12%, and the rate smoothing down percentage was 8%, the width of the rate smoothing up window would be 120 msec and that of the rate smoothing down window would be 80 msec. The atrial rate-smoothing window is calculated by subtracting the AV delay from the boundaries of the ventricular rate-smoothing window (Fig. 23-49). Sudden changes in ventricular rate can also occur in patients with intermittent atrial arrhythmias or atrial fibrillation.37 Tracking of an atrial arrhythmia that may be too transient or too slow to trigger mode switching can result in palpitations or other symptoms caused by the abrupt increase in heart rate. Rate smoothing up

Figure 23-48. Failure of atrial flutter detection algorithm. Atrial flutter has an atrial cycle that places an atrial signal within the postventricular atrial blanking period (PVAB), so that the atrial flutter response never occurs. AEGM, atrial electrogram; MC, marker channel. (From Israel CW, Barold SS: Failure of atrial flutter detection by a pacemaker with a dedicated atrial flutter detection algorithm. PACE 25:1274-1277, 2002.)

Figure 23-49. Rate-smoothing algorithm. The rate-smoothing algorithm adjusts the intervals of the successive atrial and ventricular events based on the previous cycle length rather than just the programmed atrial escape interval or the upper rate tracking interval. When rates are decreasing, the rate of slowing is constrained by the rate smoothing “down” percentage. In contrast, with increases in rate, such as with rapid atrial tracking, the rate smoothing “up” percentage constrains the rate. In the example, the atrial and ventricular events must occur within the atrial and ventricular smoothing windows.

may limit the ventricular rate to reduce the suddenness of the heart rate increase. Mode switching may interact with a variety of other programmed parameters. Ventricular tachycardia prevention algorithms may become inactivated by mode switching.38

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-50. Rate drop response. The rate drop response results in pacing at a faster rate (intervention rate) when an abrupt drop in the ventricular rate occurs, defined as a minimum drop in heart rate over a range of detection intervals. A minimum rate for a specific number of intervals alone may be used to trigger this response. The intervention rate is the pacing rate for the programmed period of time. (From Medtronic Enpulse device manual 5-22.)

Fall Back The fall back response provides a response very similar to rate smoothing by limiting the rate of the heart rate change.39 Fall back may occur when the rate decreases from the upper rate limit to the LRL during mode switching or other rate drop response. Rate Drop Response Patients who experience neurocardiogenic or vasovagal syncope become symptomatic when the heart rate falls precipitously. The rate drop response (RDR) algorithm is designed to recognize a rapid decline in heart rate using a heart rate–time duration detection window. The degree of rate drop (in beats per minute) within the specified duration (in number of beats) is programmable. The newer algorithm uses an averaged ventricular baseline rate as the reference. Once the RDR is triggered, dual-chamber pacing is initiated at a relatively fast rate, either an absolute rate (100 to 120 bpm) or a relative rate (70% or 80% of the maximum heart rate) (Fig. 23-50). The sudden bradycardia response (SBR) is another example of this type of rate algorithm. This response is initiated by a decline in the atrial rate by more than 10 bpm for a programmed number of beats (1 to 8 beats), with a weighted average serving as the baseline rate. The SBR response consists of pacing at a rate that is 5 to 40 bpm faster than the previous rate. Prevention of Atrial Fibrillation There has been considerable interest in using atrial pacing for prevention of atrial fibrillation(AF).40-44 The Pacemaker Selection Trial for the Elderly (PASE) study and the Canadian Trial of Physiological Pacing (CTOPP)45 showed that atrial pacing or dual-chamber pacing is associated with a lower occurrence of atrial fibrillation compared with ventricular pacing alone.40,46,47 Pacing from sites other than the right atrium, such as the atrial septum or Bachman’s bundle, has been shown to decrease the incidence of atrial fibrillation. Atrial

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Figure 23-51. Atrial fibrillation pacing suppression algorithm. Atrial fibrillation pacing parameters may be set to stimulate the atrium at rates faster than the intrinsic atrial rate in order to suppress the triggers of atrial fibrillation. When two P waves are detected within a 16-cycle window, the atrial pacing algorithm is initiated. The pacing occurs for a programmable number of pacing cycles. In this example, atrial pacing is already at 84 beats per minute. Because two sinus beats occur, the pacing rate increases. The pacing occurs for a programmable number of intervals, and then the interval is gradually decreased. (From St. Jude Identity device manual.)

pacing at two sites, such as the right atrium and the coronary sinus ostium, has also been examined for its effect on atrial fibrillation. Multisite atrial pacing has also shown varying efficacy in prevention of atrial fibrillation. There are specific atrial pacing algorithms that have been studied as possible methods of decreasing atrial fibrillation. Prospective randomized trials, such as the Atrial Dynamic Overdrive Pacing Trial (ADOPT) and the Overdrive Atrial Septum Stimulation (OASIS) trial, demonstrated significant reductions in atrial fibrillation burden using the Dynamic Atrial Overdrive (DAO) algorithm (St. Jude Medical, St. Paul, Minn.). Continuous atrial overdrive pacing is maintained by setting the atrial lower rate higher than the intrinsic sinus rate. The atrial pacing rate is adjusted in response to the mean atrial rate or the occurrence of premature atrial beats, or both. Atrial fibrillation pacing parameters may be set to stimulate the atrium at rates faster than the intrinsic atrial rate in order to suppress the triggers of atrial fibrillation (Fig. 23-51). When two P waves are detected within a 16-cycle window, the atrial pacing algorithm is initiated. The pacing occurs for a programmable number of pacing cycles, and then the interval is gradually decreased. Atrial pacing preference (APP) system paces in response to the atrial rate but not to premature atrial beats. In contrast, atrial pacing may specifically respond to atrial sensing in a specific interval. The atrial overdrive in a DDD(R) mode is triggered whenever two spontaneous P waves are sensed in a 16-beat window. The extent of atrial overdrive is a nonprogrammable parameter, determined by the instantaneous atrial rate. Other algorithms that increase atrial pacing include the continuous atrial pacing algorithm, which paces at 30 msec shorter than the intrinsic atrial cycle length, and a double-algorithm

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Figure 23-52. Noncompetitive atrial pacing algorithm. Pacing after a premature atrial beat that occurs during the postventricular atrial refractory period (PVARP) may cause atrial arrhythmias. To prevent so-called competitive pacing, algorithms have been developed. If an atrial event occurs within the PVARP, an additional window, called the noncompetitive atrial pacing (NCAP) period, is created. Atrial pacing is delayed until the end of this period, allowing the atrium additional time to repolarize. (From Medtronic Enpulse device manual 5-10.)

approach, which alters pacing in response to atrial premature beats (used by the Medtronic AT 500, Medtronic, Minneapolis, Minn.). However, such highrate overdrive pacing may result in undersensing due to a short atrial sensing window. Rare cases of proarrhythmia have been reported. Algorithms have also been used to prevent induction of atrial fibrillation caused by atrial pacing after an intrinsic P wave. To prevent so-called competitive pacing, if an atrial event occurs within the PVARP, an additional window, called the noncompetitive atrial pacing (NCAP) period, is created. Atrial pacing is delayed until the end of this period, allowing the atrium additional time to repolarize (Fig. 23-52). In addition, the AV interval may be shortened to a minimum of 30 msec, to stabilize the ventricular rate (Fig. 23-53). There is a need for greater understanding of the efficacy, technique, and physiology of atrial pacing compared with dual-chamber pacing. In addition to prevention of atrial fibrillation, there is some evidence that atrial overdrive pacing may terminate some atrial arrhythmias that lead to atrial fibrillation. Noncompetitive Atrial Pacing In order to prevent atrial pacing after an intrinsic atrial event has occurred during an ARP, or competitive atrial pacing, a noncompetitive atrial pacing feature may be programmed ON. This programmable parameter delays the time at which the atrial pacing stimulus occurs. Atrial sensed events may occur in the PVARP during upper rate behavior, and competitive pacing is most likely to occur when there is sensor-driven atrial pacing (see Fig. 23-52). Shortening the PVARP is another method of preventing competitive pacing, but retrograde conduction may limit this option (see Fig. 23-53). Managed Ventricular Pacing Growing evidence in the literature suggests that right ventricular pacing is detrimental to hemodynamics in a number of patient populations. The AAIsafeR algorithm functions in the AAI mode with a conversion to

Figure 23-53. Noncompetitive atrial pacing algorithm and ventricular timing. If an atrial event is sensed during the postventricular atrial refractory period (PVARP), the atrial pacing impulse will be delayed. In order to stabilize the ventricular rate, the atrioventricular (AV) interval may be shortened to a minimum of 30 msec. NCAP, noncompetitive atrial pacing period; PAV, paced A-V interval. (From Medtronic Enpulse device manual 5-10.)

DDD in the event of high-grade AV block.48 A managed ventricular pacing (MVP) algorithm is designed to minimize unnecessary right ventricular pacing. The MVP algorithm operates in an AAI(R) mode to minimize ventricular pacing; however, ventricular backup pacing is available in a VVI mode if heart block occurs. Backup ventricular pacing is triggered by any A-A interval that occurs without a sensed ventricular event and is delivered at an interval equal to the A-A interval plus 80 msec. MVP automatic switches from an AAI(R) to a DDD(R) mode if no ventricular sensed event occurs in 2 of 4 preceding A-A intervals (multiple heart blocks occur in a 4-beat window) (Fig. 23-54). MVP maintains the dual-chamber DDD(R) mode for 1 minute and then performs an “AV conduction check.” The device monitors AV conduction by temporarily switching back to AAI(R) timing during one A-A cycle. The AV conduction check is scheduled at 2 minutes, 4 minutes, 8 minutes, and so on, up to 16 hours after a transition to DDD(R) has occurred. If spontaneous R waves are sensed, the device reverts back to the AAI(R) operation (Fig. 23-55). Significant reduction of ventricular pacing has been demonstrated with the MVP algorithm. A “dynamic atrial refractory period” has been developed to avoid inappropriate switch to DDD(R) mode caused by nonconducted premature atrial ectopy or far-field Rwave oversensing. The net result of MVP is a reduction in the frequency of ventricular pacing.49 Ventricular Rate Regularization Because irregularity of the ventricular rate during atrial fibrillation may be responsible for many of the symp-

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-54. AAIR-to-DDDR mode switching. The managed ventricular pacing algorithm permits the pacemaker to automatically switch from AAIR to DDDR mode and from DDDR to AAIR mode. If transient loss of conduction occurs in the AAIR mode, after an A-A interval without a ventricular sensed event, a ventricular paced event will occur 80 msec after the escape interval. If two of the four most recent A-A intervals are missing a ventricular event, the device will switch from AAIR to DDDR or from AAI to DDD. (1), AAIR mode; (2) AV block results in ventricular backup paced beat; (3) switch to DDDR mode. (From Medtronic Intrinsic 30 7288/7287 reference manual p 169.)

Figure 23-55. DDDR-to-AAIR mode switching. The managed ventricular pacing algorithm permits the pacemaker to automatically switch from AAIR to DDDR mode and from DDDR to AAIR mode. In the DDDR mode (1), the device periodically checks for atrioventricular (AV) conduction. If AV conduction is present (2), the device switches to the DDDR mode (3). (From Medtronic Intrinsic 30 7288/7287 reference manual, p 169.)

toms that occur during atrial fibrillation, algorithms may attempt to pace in an effort to regularize the rhythm. These algorithms adjust the presence of pacing in response to the presence of ventricular sensed beats. Algorithms called ventricular response pacing (Fig. 23-56) or ventricular rate regulation (VRR) pace in response to sensed ventricular events.50 If a ventricular sensed event occurs, the ventricular pacing rate is increased, and if a ventricular paced event occurs, the ventricular pacing rate is decreased. Clinical studies have demonstrated that the variability in ventricular intervals in atrial fibrillation is markedly decreased by this approach (Fig. 23-57). DDD Hysteresis and Search Hysteresis Dual-chamber devices are capable of exhibiting hysteresis analogous to ventricular or atrial hysteresis. In dual-chamber hysteresis, the escape interval timed from an intrinsic ventricular event is longer than the escape interval after a paced ventricular event. In search hysteresis, the LRL is lowered periodically to promote intrinsic activity. After a programmed

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Figure 23-56. Ventricular response pacing. In response to a ventricular sensed event, the ventricular pacing rate is increased by 0 to 1 beats per minute; in response to a ventricular paced event, the ventricular pacing rate is decreased. VRP, ventricular response pacing. (From Tse HF, Newman D, Ellenbogen KA, et al.: Effects of ventricular rate regularization pacing on quality of life and symptoms in patients with atrial fibrillation. Atrial Fibrillation Symptoms Mediated by Pacing to Mean Rates [AF Symptoms Study]. Am J Cardiol 94:938-941, 2004.)

Figure 23-57. Ventricular response pacing. At rest and during exercise, during VRR (VVIR mode with ventricular response pacing ON), a lower proportion of patients have fast ventricular rates, compared with VVIR only (with ventricular response pacing OFF). VRP, ventricular response pacing; VRR, ventricular response rate. (From Tse HF, Newman D, Ellenbogen KA, et al.: Effects of ventricular rate regularization pacing on quality of life and symptoms in patients with atrial fibrillation. Atrial Fibrillation Symptoms Mediated by Pacing to Mean Rates [AF Symptoms Study]. Am J Cardiol 94:938-941, 2004.)

number of intervals, the device looks for intrinsic activity. During this period, if there is no intrinsic activity, pacing will occur at a rate that is a programmed amount (hysteresis offset) less than the LRL for a specified duration (e.g., eight cycles). If no intrinsic atrial activity is sensed, pacing will resume at the LRL or sensor-indicated rate. Search hysteresis helps to promote intrinsic impulse formation. Repetitive Ventriculoatrial Synchrony Competitive atrial pacing may also occur after a premature ventricular complex that conducts retrograde. Unlike in PMT, the P wave falls within the PVARP. However, the next atrial pacing stimulus comes soon

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Figure 23-58. VDD mode. In the VDD mode, atrial sensed events are tracked, initiating an atrioventricular (AV) delay. If the AV delay is not followed by a sensed ventricular event within the programmed AV delay, a ventricular paced event will occur unless the upper rate limit has been reached. In this example, the lower rate is 60 beats per minute (bpm), and the upper rate limit is 120 bpm, with an AV delay of 200 msec. In beat 1, the P wave starts an AV delay, but AV conduction occurs, so that the timing cycle is reset by the ventricular sensed event, the ventricular complex of beat 2. Before the lower rate limit can time out from beat 2 to beat 3, an intrinsic P wave again occurs. In this case, there is no ventricular sensed event by the time the AV interval expires, and so another ventricular paced event occurs in beat 3. The ventricular paced event in beat 3 resets the timing cycle, and a new V-V interval is created. From beat 3 to beat 4, there is no intrinsic P wave or R wave. Therefore, a ventricular paced event at the lower rate limit of 60 bpm (1000 msec) occurs. A new ventricular escape interval is created. Between beat 4 and beat 5, a P wave occurs, which is again tracked, creating a new AV delay. As in beat 1, intrinsic conduction occurs before the new AV delay is completed. A, atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event.

after the P wave and is not captured due to tissue refractoriness. The next ventricular event is paced and conducts retrograde. As a result, the pattern of VA conduction and competitive atrial pacing perpetuates itself. This phenomenon, sometimes been called repetitive non-reentrant VA synchrony, may result in impaired hemodynamics. Timing Cycles in Other Dual-Chamber Modes VDD Mode The VDD mode offers both atrial and ventricular sensing with only ventricular pacing (Fig. 23-58). Tracking of atrial activity occurs similar to the DDD mode. When an atrial event is sensed, the AVI is initiated, and, if a ventricular intrinsic event is not sensed by the end of the interval, a ventricular paced event is triggered. Sensing also occurs in the ventricle, which inhibits ventricular pacing. The VDD mode is not appropriate for individuals who have impaired sinus node function, because there is no atrial pacing. This mode is mostly employed in pacemaker systems in which there is a single lead that paces and senses the ventricle and senses the atrium using a specially designed “floating” atrial electrode.

Figure 23-59. DDI mode. In the DDI mode, atrial sensed events are not tracked but inhibit atrial pacing. If the atrioventricular (AV) delay is not followed by a sensed ventricular event within the programmed AV delay, a ventricular paced event will occur unless the upper rate limit has been reached. In this example, the lower rate is 60 beats per minute (bpm) with an AV delay of 200 msec. In beat 1, the P wave inhibits atrial pacing and the R wave occurs before the lower rate limit times out. In beat 2, atrial pacing occurs at the end of the atrial escape interval, because no spontaneous P wave occurs. The R wave occurs before the lower rate interval of 1000 msec expires. In beat 3, a P wave occurs and results in inhibition of atrial pacing. Atrial pacing occurs at the end of the atrial escape interval of 800 msec, because no atrial sensed event has occurred. Because no sensed ventricular event occurs, a ventricular paced event also occurs. A, atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event.

DDI Mode AV sequential pacing with dual-chamber sensing, non–P-synchronous DDI mode provides sensing and pacing in the atrium and ventricle but does not track. When atrial events are sensed, atrial pacing is inhibited, but, unlike in the DDD mode, the AVI is not initiated (Fig. 23-59). Ventricular paced events after atrial sensed events will occur at the LRL rather than after the AV delay. Ventricular sensed events result in inhibition of ventricular pacing and resetting of the AEI. Absence of intrinsic atrial events or ventricular events by the end of the LRL results in pacing in the atrium or ventricle, respectively. This mode is best suited for patients who are at risk for atrial tachyarrhythmias, because there is no atrial tracking, resulting in rapid ventricular pacing during atrial tachyarrhythmia. This mode can be useful in cases in which the modeswitching feature is unavailable or does not accurately function. In this mode, the absence of tracking results in the inability of faster intrinsic sinus rates to be followed by ventricular paced beats as the sinus rate increases in response to greater metabolic demands with exertion or exercise. In addition, AV synchrony is lost when the intrinsic sinus rate exceeds the LRL and AV conduction is absent or impaired. The use of DDIR pacing programmed so that sensor-driven pacing predominates will result in maintenance of AV synchrony. Other Modes A host of other modes are used less frequently as permanent settings or only in particular circumstances. The asynchronous modes AOO, VOO, and DOO, which pace constantly in the atrium, ventricle, or both chambers, respectively, have been discussed. These modes

Chapter 23: Timing Cycles of Implantable Devices

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Timing Cycles in Biventricular Pacing Goals of Biventricular Pacing

Figure 23-60. DVI mode. In the DVI mode, the atrium and the ventricle are paced, but only the ventricle is sensed. As a result, it is possible that atrial pacing may occur after an intrinsic atrial event. In beat 1, the R wave is sensed and creates a new atrial escape interval of 800 msec. In beat 2, atrial pacing occurs because a ventricular event has not occurred since the last ventricular event. Because there is conduction of the R wave, a ventricular paced event does not occur. In beat 3, a spontaneous P wave occurs, followed by atrial and ventricular pacing. It is possible that the atrial pacing after a spontaneous P wave could result in atrial arrhythmias. In beat 4, atrial and ventricular pacing occurs because no ventricular sensed event has occurred.

are generally used to prevent potential oversensing, such as electromagnetic interferences from electrocautery during surgery. Other sources of possible interference include transcutaneous electric stimulation (TENS), diathermy, and lithotripsy in pacemakerdependent patients. There are also triggered modes, VVT and AAT, which deliver an impulse immediately when an event in the respective chamber is sensed. These modes historically were used diagnostically to mark sensed events (in evaluating undersensing or oversensing problems), before the availability of intracardiac electrograms and marker channels. However, triggered modes are not used commonly in current practice. The VDI mode is used similarly to the VVI mode, in which pacing in the ventricle will occur unless an intrinsic ventricular depolarization is sensed within the LRL. However, atrial sensed events are also sensed, but they do not result in ventricular tracking. Instead, they are recorded for later evaluation, such as evaluation of atrial arrhythmias. Sometimes mode-switching algorithms will initiate the VDI mode if an atrial tachyarrhythmia is sensed. In the DVI mode (AV sequential, ventricular inhibited), which is the least used mode, the pacemaker provides pacing in both the atrium and ventricle (D), but only events in the ventricle (V) inhibit pacing. An AEI is reset after a sensed or paced ventricular event followed by an asynchronous atrial pacing output. However, a sensed spontaneous ventricular event within the AEI inhibits and resets both atrial and ventricular pacing stimuli. The atrial pacing stimulus is followed by the AVI, and a spontaneous R wave will inhibit the ventricular output. The difference between DVI and DDI is that no atrial sensing is incorporated in the DVI mode, in which constant, competitive atrial pacing may occur (Fig. 23-60). The absence of atrial sensing may result in a paced atrial impulse immediately after an intrinsic atrial event, potentially triggering atrial tachyarrhythmia.

The primary goal of bradycardia pacing is to achieve heart rates that are adequate to prevent symptoms and meet metabolic demand.51,52 To achieve this goal, bradycardia pacing timing cycles are designed to keep the heart rates from being too slow and to maintain appropriate AV synchrony. Heart failure may be associated with abnormal electrical delay and/or mechanical dyssynchrony. Such depressed and uncoordinated interventricular and intraventricular contraction delays are responsible for the reduced pumping effectiveness. Resynchronization therapy has been shown to improve the functional capacity of patients with wide QRS complexes, left ventricular dysfunction, left ventricular dilatation, and heart failure. Indices such as quality of life, 6-minute walk time, and heart failure class have also been shown to improve with biventricular pacing resynchronization therapy. In addition, randomized studies have demonstrated a decreased mortality rate and improved left ventricular dimensions and function. However, the benefits of resynchronization therapy are based on improved hemodynamics achieved by stimulating the heart in a more coordinated manner and minimizing interventricular and intraventricular dyssynchrony (resynchronization). Therefore, resynchronization requires that consistent pacing be maintained despite the absence of bradycardia. These distinct goals demand a new set of timing cycle rules for biventricular devices. Timing Cycles: Differences from Dual-Chamber Timing Cycles Pacing Modes Pacing modes for resynchronization therapy are similar to those for standard pacemakers, and the general criteria for mode selection are similar. In patients with chronic atrial fibrillation, VVIR pacing is the most commonly used mode, in order to achieve rate responsiveness and to maintain as close as possible to 100% ventricular pacing. In patients without atrial fibrillation, VDI, DDD, and DDDR are the most commonly used modes. VDI is appropriate for patients with normal sinus node function and intact AV conduction. DDDR should be selected for patients with chronotropic incompetence due to relative sinus bradycardia. VDI, DDD, or DDDR mode provides the capability of atrial tracking with AV coordination. The optimal hemodynamics of resynchronization therapy require maintenance of AV synchrony with maximum biventricular pacing and capture. There is no role, therefore, for AAI or other algorithms that promote intrinsic AV conduction. The basic timing cycle during resynchronization therapy relies on an AVI that maintains ventricular capture. The timing cycles for biventricular pacemakers are potentially complex, depending on which chamber or

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Section Four: Device Electrocardiography

Figure 23-61. Biventricular pacing with right ventricle (RV)–based timing may occur after a sensed or paced atrial event. AP, atrial paced event; AS, atrial sensed event; LVP, paced left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; RV-RV, interval between RV events; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

chambers are sensed, which ventricle or ventricles are paced, the interventricular delay, and the chamber or chambers that reset the escape intervals.52-56 For most commercially available biventricular devices, the sensing chamber is usually the RV and occasionally both ventricles (for older devices with ventricles connected via a Y-connection). Biventricular pacing activates both ventricular chambers, either simultaneously or sequentially (Fig. 23-61). Atrioventricular Interval in Biventricular Pacing For biventricular pacing to result in the desired hemodynamic effect, it is necessary for appropriately timed biventricular paced beats to occur after paced or sensed atrial events.57 Therefore, the AVI must be sufficiently short to ensure biventricular capture and minimize fusion, yet long enough to allow adequate diastolic filling during the atrial contraction. Because the degree of native P-R shortening during exercise may be significant, this can be a particularly challenging task. Similarly, programming an extremely short fixed AV delay that applies to all rates and physiologic conditions is unlikely to be optimal, with ventricular depolarization and contraction occurring too early. In almost all cases, therefore, a form of rate-adaptive AV delay is used in resynchronization devices. Several algorithms have been designed to maintain biventricular pacing and activation. When there is sensed ventricular activity on one pacing cycle, the AVI is shortened on the next timing cycle. This function is called AV hysteresis. If an atrial event is followed by a sensed right ventricular event, which is then followed by a left ventricular paced event, a right ventricular paced event and a left ventricular paced event may occur on the next cycle by shortening the time from the atrial sensed event to the right ventricular paced event (Fig. 23-62). In addition, if the left ventricular paced event occurs before the right ventricular sensed event, it is possible to shorten the LV-RV timing on subsequent cycles (Fig. 23-63). However, such “negative” AV hysteresis function is often ineffective, because permitting even one cycle with intrinsic conduction can have

Figure 23-62. Biventricular pacing with right ventricular sensed event (RVS) before left ventricular paced event (LVP). An atrial paced event (AP) starts the atrioventricular (AV) delay. The RVS occurs before the LVP (positive RV-LV interval) in the first cycle. In the next cycle, the AV delay has been shortened so that the right ventricular paced event (RVP) may preempt the RVS. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:6275, 2002.)

Figure 23-63. Biventricular pacing with left ventricular paced event (LVP) before right ventricular sensed event (RVS). In the first cycle, an LVP occurs before an RVS. In the next cycle, an LVP is followed by a right ventricular paced event (RVP), which may be achieved by shortening the LV-RV interval in response to the sensed RV event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

deleterious consequences. Perpetuation of native AV conduction and absence of biventricular pacing can result, as discussed later. If an intrinsic ventricular event is sensed within the AVI, one option might be to trigger a ventricular paced stimulus from the opposite ventricle, a so-called ventricular sensed response. For example, if a sensed event is detected by the right ventricular lead, a left ventricular pacing output is delivered immediately to maximize left ventricular capture and biventricular activation (Fig. 23-64). However, it is unclear whether there are limits to the benefit of this strategy, particularly with closely timed ventricular premature beats. Interventricular Timing Delay Analogous to the AVI in AV delay, there may be delay between pacing in the RV and LV (interventricular delay). There are several permutations of the relationship between the right and left ventricular timing based on the role of biventricular or unipolar sensing. With right ventricular sensing alone, which is predominantly the case in most devices today, the RV-LV interval may be positive, negative, or zero (Fig. 23-65). Several studies have demonstrated clinical or hemodynamic benefits of adjusting interventricular delay in patients who were classified as “nonresponders” to conventional resynchronization therapy. Various echocardio-

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-64. Biventricular sense response. If a right ventricular sensed event occurs, one option is for a left ventricular paced event (LVP) to occur almost immediately, to promote biventricular pacing. AS, atrial sensed event; AP, atrial paced event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-65. Biventricular RV-LV interval. The RV-LV interval may be positive, negative, or zero. AS, atrial sensed event; LVP, paced left ventricular event; RVP, paced right ventricular event;. RVS, sensed right ventricular event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

graphic Doppler parameters and timing intervals have been used to assess interventricular dyssynchrony, and tissue Doppler imaging (TDI) has been used to determine interventricular dyssynchrony for V-V optimization. The interduction of delay raises several theoretical issues. As discussed further in the context of univentricular sensing and biventricular pacing, an interventricular delay may increase the likelihood of induction of ventricular tachycardia due to an unsensed, improperly timed ventricular depolarization. Lower Rate Behavior As in dual-chamber pacing, a LRL is established. Atrial pacing will occur if an intrinsic atrial event does not occur at the LRL. There is a combination of events that may initiate ventricular events. In currently available devices, both ventricles may be paced, but timing is based on the RV only. One can theorize that a much larger range of combinations is possible: it is possible to pace both ventricles but to use the RV, LV, or both for ventricular timing. Univentricular Sensing and Biventricular Pacing Sensing may occur in one ventricle, as it does in dualchamber pacing. There is not usually a particular risk of induction of ventricular tachycardia due to competitive pacing. For example, if left ventricular activation occurs before left ventricular pacing would occur, it is unlikely that the left ventricular pacing stimulus would

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Figure 23-66. Right ventricular sensing only with positive RV-LV intervals. The right ventricle may be the only ventricular chamber sensed. There may be an intrinsic left ventricular event (LVS) that follows the right ventricular paced event (RVP). Because the left ventricular event is not sensed, the left ventricular pacing stimulus (LVP) will still be delivered. Because the LVP occurs after the LVS, the LVP is unlikely to be captured. AP, atrial paced event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-67. Right ventricular sensing only with premature left ventricular extrasystoles. The right ventricle may be the only ventricular chamber sensed. A spontaneous premature ventricular contraction originating in the left ventricle (LVS) will not be sensed if there is a significantly prolonged and negative RV-LV interval. As a consequence, it is possible that the left ventricular pacing stimulus (LVP) combined with the spontaneous LVS may result in ventricular proarrhythmia. There maybe an intrinsic LVS that follows a right ventricular paced event (RVP). Because the LVS is not sensed, the LVP will still be delivered. Because the LVP occurs after the intrinsic LVS, the LVP is unlikely to be captured. AP, atrial paced event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

be captured (Fig. 23-66). However, there may be a set of circumstances that increase the risk of competitive pacing. For example, if the intrinsic LV-RV conduction time is long and a long RV-LV delay is programmed, there are several scenarios that may result in a greater risk of competitive pacing. In one situation, a left ventricular sensed event occurs before right ventricular and left ventricular pacing occurs. Because there may be a considerable interval between the intrinsic left ventricular event and the left ventricular pacing stimulus, the LV may no longer be refractory, resulting in left ventricular stimulation at a short coupling interval (Fig. 23-67). In another example, an unsensed premature beat that originates in the LV may be followed by an right ventricular paced event and then a left ventricular paced event. In such a case, the right ventricular paced event occurred before conduction from the spontaneous left ventricular PVC to the RV. Biventricular Sensing and Biventricular Pacing There are a variety of rules that might be created to determine how, for example, both ventricles could be

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Section Four: Device Electrocardiography

Figure 23-68. Right ventricular sensing only with inhibition of pacing. The right ventricle may be the only ventricular chamber sensed. When a right ventricular event is sensed, the timing cycles may be reset, resulting in inhibition of pacing. AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; LVP, paced left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-70. Biventricular sensing and pacing. Triggering may be present in devices that sense and pace in both the right ventricle and the left ventricle. If a right ventricular event is sensed, a left ventricular stimulus will be delivered immediately. AS, atrial sensed event; LVP, paced left ventricular event; LVS, sensed left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

A

B Figure 23-69. A, Biventricular sensing and pacing. The right ventricular sensed event (RVS) is used to start the ventriculoatrial interval (VAI). B, The right ventricular pacing interval that would have occurred at the end of the atrioventricular interval (AVI) is used to start the VAI. Parentheses indicated the timing of the paced events that would have occurred if an intrinsic sensed event had not occurred. LVS**, left ventricular sensed event; LVP*, left ventricular paced event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

used for timing. These rules might depend on when the ventricular sensed event occurred. If the sensed event occurred in the AVI, as described earlier, a new V-A interval and timing cycle might be created with no pacing (Fig. 23-68). A variation on this function might be to permit a ventricular paced event from the opposite ventricle to occur (Fig. 23-69). This might be administered immediately after the sensed ventricular event within the AVI (Fig. 23-70) or after the programmed RV-LV delay. The V-A interval might be reset at the point of the right ventricular sensed event within the AVI (see Fig. 23-69A) or at the end of the programmed AVI (see Fig. 23-69B). A right ventricular sensed event may be followed by a left ventricular paced event, after an RV-LV interval of 0 (Fig. 23-70) or after an RV-LV interval that is positive (Fig. 23-71). It is also possible for a ventricular sensed event in the

Figure 23-71. Biventricular sensing and pacing. Triggering may be present in devices that sense and pace in both the right ventricle and the left ventricle. If a right ventricular event is sensed, a left ventricular stimulus will be delivered after an RV-LV interval that is positive in value. AS, atrial sensed event; LVP, paced left ventricular event; LVS, sensed left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

AVI not to trigger a ventricular paced beat from the opposite chamber but to have the AVI time out, with the ventricular paced event occurring at the end of the AVI. In biventricular sensing and pacing, a left ventricular sensed event in the AVI might be followed by a right ventricular sensed event within the programmed AVI (Fig. 23-72). Alternatively, the left ventricular sensed event in the AVI might trigger a right ventricular paced event that would be used to reset the V-A timing cycle (Fig. 23-73). Safety pacing with biventricular pacing might be performed using either both ventricles or only one used as backup pacing. For sensed events outside the AVI and after the VRP, there are also a variety of responses. A sensed event in the LV or RV might be used interchangeably or might result in a specific pacing response. For example, sensing in either chamber first might be used to trigger a ventricular paced event in the opposite chamber. Alternately, a sensed event in the LV or RV might inhibit pacing in either channel to prevent pacing within the vulnerable period. A left ventricular sensed event, for example, might inhibit left ventricular pacing, but a right ventricular paced event would occur unless a right ventricular sensed event occurred within the programmed LV-RV delay. If a negative RV-LV were programmed, the right ventricular

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-72. Biventricular sensing and pacing. If a left ventricular event is sensed, left ventricular pacing is inhibited. However, a right ventricular stimulus will be delivered. If a right ventricular event is sensed after the left ventricular sensed event, the timing cycles are reset. AS, atrial sensed event; AVI, atrioventricular interval; LVP, paced left ventricular event; LVS, sensed left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-73. Biventricular sensing and pacing. Triggering may be present in devices that sense and pace in both the right ventricle and the left ventricle. If a left ventricular event is sensed, a right ventricular stimulus will be delivered immediately. AP, atrial paced event; AS, atrial sensed event; LVP, paced left ventricular event; LVS, sensed left ventricular event; RVP, paced right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

sensed event could result in resetting the timing cycles or in an immediate left ventricular paced event. Univentricular Pacing It is possible for a device to be programmed to have univentricular or biventricular sensing but to pace from only one ventricle, such as the LV. In the case of univentricular pacing and sensing, a sensed left ventricular event might result in inhibition of left ventricular pacing and resetting of the V-A timing cycle (Fig. 2374). If a right ventricular sensed event occurred first, the left ventricular paced event might be inhibited, resetting the timing cycle (Fig. 23-75), or the result might be an immediate left ventricular paced event, to minimize the delay after the right ventricular sensed event (Fig. 23-76). Biventricular Pacing and Sensing and Premature Beats Biventricular pacing and sensing may create a particular problem if premature ventricular beats are present. A premature ventricular beat may occur in the A-V interval, resetting the timing cycle. The right ventricular sensed event may inhibit left ventricular pacing (Fig. 23-77) or may trigger a left ventricular paced event.

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Figure 23-74. Univentricular sensing and pacing. Sensed events in the left ventricle result in inhibition, and reset the timing cycle. AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; LVP, paced left ventricular event; LVS, sensed left ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-75. Biventricular sensing and univentricular pacing. Left ventricular paced and sensed events reset the timing cycles. Right ventricular sensed events also reset the timing cycle but do not trigger left ventricular pacing. AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; LVP, inhibited paced left ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Upper Rate Behavior in Biventricular Pacing The primary purpose of upper rate behavior in traditional dual-chamber DDD pacing is to prevent rapid atrial tracking during atrial tachycardia. The MTR is a programmable parameter, whereas the 2:1 AV block rate is determined by the TARP (60,000 ÷ TARP). When the MTR is slower than the 2:1 AV block rate, a pseudoWenckebach response occurs as the atrial rate increases and exceeds the MTR before the 2:1 AV block develops. When the 2:1 AV block rate is slower than the MTR, a sudden 50% drop in heart rate occurs as the atrial rate exceeds the 2:1 AV block limit. For biventricular pacemakers, a thorough understanding of the upper rate behavior is crucial in maintaining biventricular pacing. Most patients who need resynchronization therapy have intact AV conduction, so pacemaker-Wenckebach behavior is to be avoided, because extension of the AVI allows sensing inhibition and prevents biventricular pacing. Episodes of high atrial rate are frequently observed in this population, during heart failure exacerbation, exercise with deconditioning, or recurrent atrial arrhythmias. To maintain 100% biventricular pacing, the TARP should be sufficiently short and the MTR should be sufficiently high. Premature Beats and Biventricular Timing Cycles A premature ventricular beat (PVC) is defined as a ventricular sensed event without a preceding paced or

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Figure 23-76. Biventricular sensing and univentricular pacing. Left ventricular paced and sensed events reset the timing cycles. Right ventricular sensed events result in triggering. AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; LVP, paced left ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

sensed atrial event. In dual-chamber timing cycles, a PVC occurring in the V-A interval would reset the AEI in ventricular-based timing devices. The presence of PVCs provides special challenges in a biventricular system. The PVC-PVARP extension algorithm automatically lengthens the PVARP to protect against potential PMT. However, such PVARP extension can cause subsequent functional atrial undersensing and loss of biventricular pacing. Therefore, the PVC-PVARP extension function should be deactivated in a biventricular system. In addition, because of the interventricular (RV-LV) conduction delay, which could be considerable in patients with dyssynchrony, a PVC creates ambiguity for the timing cycles. Several possible approaches to this timing issue include a system that uses singlechamber sensing only, a cross-chamber (RV-LV) refractory period after the first ventricular sense, and a ventricular triggering mode in the opposite chamber. In an RV-sense–LV-refractory system, a PVC could have RV sensing occurring in the V-A interval that resets the AEI; the subsequent ventricular pacing (AEI + AVI) can occur “asynchronously” shortly after the delayed, nonsensed LV activation. Such improperly timed pacing stimuli may induce ventricular arrhythmia. A crosschamber trigger mode on PVC would require an upper rate limit to avoid tightly coupled stimulation that could induce ventricular arrhythmia. Refractory Periods and Biventricular Pacing Refractory periods are present after sensed or paced events. In early biventricular devices with RV and LV leads connected in parallel via a Y-connection, a single ventricular depolarization may be sensed by both RV and LV leads. With biventricular sensing, the PVARP could be reset by the second component of the ventricular sensed signal (usually from the LV). In such cases of late left ventricular sensing, the PVARP and TARP are effectively extended by an interval that equals the interventricular sensing delay (RV-LV). Such a prolonged TARP could markedly reduce the atrial sensing window for atrial tracking. The newer biventricular devices use dedicated right ventricular sensing only with pacing from both the RV and LV. After right or left ventricular pacing, a cross-

Figure 23-77. Biventricular pacing and sensing and premature beats. A premature ventricular beat occurs within the AVI, with right ventricular sensing first. The left ventricular paced beat is inhibited and left ventricular sensed event results from conduction. Right ventricular–based timing cycles. AP, atrial paced event; AS, atrial sensed event; AVI, atrioventricular interval; LVP, paced left ventricular event; LVS, sensed left ventricular event; RVP, paced right ventricular event; RVS, sensed right ventricular event; VAI, ventriculoatrial interval. (From Wang P, Kramer A, Estes NA 3rd, Hayes DC: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

chamber refractory period may be created. If there is a delay in the LV-RV interval, the total sensed refractory period may be extended. If the device is programmed to a positive LV-RV delay and a new refractory period is created after the RV pacing stimulus, the total VRP may be quite long. This prolonged sensing refractoriness can compromise detection of ventricular tachyarrhythmias. Loss of Biventricular Pacing Because the hemodynamic consequences of loss of biventricular pacing can be quite significant, it is important to identify possible causes of loss of biventricular pacing.58 Biventricular pacing may be lost if the atrial rate increases so that the P wave falls within the PVARP of the preceding ventricular beat. This occurs when the atrial cycle length is equal to the sum of the PVARP and the sensed AV delay (TARP = AVI + PVARP) or greater than the maximum atrial tracking interval. Because the P wave will not be tracked, conduction will occur. Because the resultant QRS complex will initiate a PVARP, the next P wave will fall within the PVARP (Fig. 23-78). In this situation, the programmed AVI is less than the intrinsic P-R interval, so the onset of loss of biventricular pacing requires a faster atrial rate compared with the rate at which biventricular pacing will be restored. Biventricular pacing will not be restored until the atrial cycle length is greater than the sum of the PVARP and the P-R interval, which is called the intrinsic total atrial refractory period (ITARP). In patients with a prolonged P-R interval, ITARP may be significantly longer than TARP. Once atrial undersensing in PVARP occurs during atrial tachycardia, loss of biventricular pacing is perpetuated and may be restored only at much slower atrial rates. Restoration of biventricular pacing will occur when the P wave occurring after the last conducted QRS falls outside the PVARP. Diagrammatically, the relationship between the atrial rate and loss of biventricular pacing may be seen in Figure 23-79. Atrial premature beats with conduction can produce a similar phenomenon by causing atrial undersensing and loss of biventricular pacing.59 At rapid rates, 2:1 biventricular pacing

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-78. Loss of biventricular pacing with 2:1 biventricular pacing. At rapid atrial rates, every other beat may have biventricular pacing, despite shortening of PVARP. AS, atrial sensed event; LVP, paced left ventricular event; LVS, sensed left ventricular event; PVARP, postventricular atrial refractory period; PVARP, shortening of PVARP after RVS; RVP, paced right ventricular event; RVS, sensed right ventricular event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62–75, 2002.)

Figure 23-79. Relationship between atrial rate and the loss of biventricular pacing. As the atrial rate reaches the total atrial refractory period, or TARP (PVARP + A-V interval), biventricular pacing will stop. When the atrial rate falls to the intrinsic total atrial refractory period, or ITARP (PVARP + P-R interval), biventricular pacing resumes. LRL, lower rate limit; MTR, maximum tracking rate; PVARP, postventricular atrial refractory period; x-axis, atrial rate; y-axis, biventricular rate. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

may occur, even if the PVARP is shortened in response to a right ventricular sensed event (see Fig. 23-79). Competitive Ventricular Pacing Biventricular pacing, as described earlier, has introduced a new cause of competitive ventricular pacing, a left ventricular stimulus occurring after left ventricular activation. This occurs because left ventricular sensed events are not used to inhibit ventricular pacing. For example, a conducted ventricular beat with a positive RV sense–LV sense interval due to left bundle branch block may occur and be followed by pacing, with LV pacing occur before RV pacing (Fig. 23-80) because the LV is no longer refractory, potentially inducing a ventricular arrhythmia. A feature called left ventricular pacing protection (LVPP) has been introduced to prevent left ventricular competitive pacing. After a left ventricular paced or sensed event has occurred, a left ventricular paced

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Figure 23-80. Biventricular pacing with right ventricular– based timing and competitive pacing. The left ventricular paced event (LVP) may occur when the left ventricle is no longer refractory. AP, atrial paced event; LVS, left ventricular sensed event; RVP, right ventricular paced event; RVS, right ventricular sensed event. (From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002.)

Figure 23-81. Biventricular pacing with right ventricular– based timing and left ventricular refractory extension. To prevent the possibility of left ventricular pacing (LVP) when the left ventricle is no longer refractory, the LVP may be inhibited if it is occurring too soon after an intrinsic left ventricular event (LVS). AP, atrial paced event; LVPP, left ventricular protection period; RVP, paced right ventricular event; RVS, sensed right ventricular event.

event will not occur for the duration of the programmed LVPP (Fig. 23-81). Another circumstance for competitive ventricular pacing is the occurrence of a left ventricular premature event before conduction can occur to the RV. Particularly if the RV-LV interval is positive, the left ventricular stimulus may find the LV. Conclusions As resynchronization therapy has become an important part of the therapy of patients with left ventricular failure and ventricular dyssynchrony, there has been in an increasing recognition of the importance of pacing timing cycles in biventricular pacing. Because biventricular pacing is effective only with constant pacing, the implications of timing cycles for maintenance of biventricular pacing is particularly important. There are unique implications for lower rate and upper rate behavior.

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Section Four: Device Electrocardiography

Timing Cycles of Implantable Cardioverter-Defibrillators

such as atrial oversensing with tracking in the DDD mode may lead to failure to detect ventricular tachycardia. Cases of prolonged undersensing of ventricular tachycardia have been reported during rate smoothing. Cooper and associates60 observed that ventricular tachycardia remained undetected because the ventricular tachycardia beats occurred within the VBP after atrial paced events. Atrial pacing occurred because rate smoothing had been turned on. Such an interaction is promoted by a slow ventricular tachycardia and rate smoothing algorithm. Shivkumar and colleagues61 reported a similar case of failure to detect an episode of ventricular tachycardia. Glikson and coworkers62 conducted a prospective study to examine the role of rate smoothing in preventing ventricular tachycardia detection. During ICD testing in 54 episodes of induced ventricular fibrillation/polymorphic ventricular tachycardia, 3 episodes (5%) of a minimal delay in detection were observed. However, among the 10 monomorphic ventricular tachycardia episodes, 4 had absent detection and 2 had delayed detection. Based on these observations and simulator-based modifications of programmable parameters, these authors observed that long AV delay, high upper rate, and more aggressive rate smoothing increase the risk of ventricular tachycardia underdetection. Figure 23-82 illustrates an

Pacing Algorithms in Implantable Cardioverter-Defibrillators One of the most serious issues involving timing cycles is the interaction between pacing and arrhythmia detection. The basic timing cycles in most ICDs are similar to those of comparable pacemaker devices. Many devices have a number of the following refractory or blanking periods: atrial blanking after ventricular sensed and paced events, ventricular sensed refractory period, ventricular refractory period, postventricular atrial sensed refractory period, atrial blanking after atrial pacing, and ventricular blanking after atrial paced events. Circumstances in which the MTRs and the sensor-driven rates are close to the ventricular tachycardia detection rate are most likely to result in abnormalities in arrhythmia detection. Examples of cases in which the pacing rates are likely to be particularly fast include sensor-driven pacing, tracking at or near the upper rate limit, rate smoothing, rate drop or sudden bradycardia response, ventricular rate regularization, and atrial pacing prevention algorithms. Abnormalities

A

C

B Figure 23-82. Rate smoothing leading to pacing during ventricular tachycardia. Rate smoothing led to atrioventricular (AV) pacing during ventricular tachycardia and the resultant underdetection. A and B, Two segments of a recording of sustained monomorphic ventricular tachycardia (VT). VT rate cutoff was 430 ms. Recording channels include surface ECG (top), atrial electrogram (middle), ventricular electrogram (bottom), and event markers. VT beats fall into postatrial pacing (AP) blanking period, resulting in delay in VT detection. C, Diagram demonstrating failure of detection of VT at 280 ms cycle length. The VT beats fall into blanking period after atrial paced beats. VF, ventricular fibrillation. (From Glikson M, Beeman AL, Luria DM, et al.: Impaired detection of ventricular tachyarrhythmias by a rate-smoothing algorithm in dual-chamber implantable defibrillators: Intradevice interactions. J Cardiovasc Electrophysiol 13:312-318, 2002.)

Chapter 23: Timing Cycles of Implantable Devices

Figure 23-83. Ventricular rate stabilization leading to pacing during ventricular tachycardia. The ventricular rate stabilization algorithm led to pacing during ventricular tachycardia, which led to underdetection. (From Barold SS: Ventricular rate stabilization algorithm of ICD causing dual chamber pacing during ventricular tachycardia. J Interv cardiac Electrophysiol 9:397-400, 2003.)

example of ventricular tachycardia that is underdetected due to a rate-smoothing algorithm. A similar case has been described for the ventricular rate stabilization algorithm (Fig. 23-83). Rate smoothing has also been proposed as a mechanism for preventing ventricular tachycardia by minimizing abrupt variations in cycle lengths in a short-long-short pattern. Wietholt and colleagues63 conducted the PREVENT study by randomizing patients in a 3-month crossover design to periods of rate smoothing versus no rate smoothing. Fifty seven (38%) of the 153 patients had 358 ventricular tachycardia episodes with rate smoothing OFF, compared with 145 episodes with rate smoothing ON. Ventricular sensed events, even ones at a tachyarrhythmic cycle length, are considered sensed for the purpose of bradycardia timing cycles. Therefore, such events result in inhibition of ventricular pacing. Once ventricular tachyarrhythmia detection has occurred, the pacing mode may stay the same or may be altered. In the ventricular tachycardia response (VTR), once ventricular tachycardia detection has occurred, the mode switches to VDI at the ATR/VTR fallback LRL. In some older generators, there is suspension of bradycardia pacing immediately before shock delivery to prevent underdetection of ventricular tachycardia caused by pacing-related refractory periods. In some other generators, the mode may switch from DDD(R) to VVI after charging has ended and during defibrillation therapies. During shock therapy, there may be specific changes to sensing. After shock therapy and in some devices after charging, there may be a refractory period. After ventricular tachycardia detection and before shock delivery, a number of ICDs nominally suspend pacing for at least 1 to 2 seconds after the shock. After a shock, it is typical that there are changes in the bradycardia parameters. Frequently, the outputs and LRL may be increased for a programmable period of time. REFERENCES 1. Barold SS: Modern concepts of cardiac pacing. Heart Lung 2:238252, 1973.

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2. Bernstein A, Daubert J, Fletcher R, et al.: The revised NASPE/ BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. PACE 23:260-264, 2002. 3. Barold SS: Clinical significance of pacemaker refractory periods. Am J Cardiol 28:237-239, 1971. 4. Barold SS, Gaidula JJ: Pacemaker refractory periods. N Engl J Med 284:220-221, 1971. 5. Yokoyama M, Wada J, Barold SS: Transient early T wave sensing by implanted programmable demand pulse generator. PACE 4:6874, 1981. 6. Okreglicki A, Akiyama T, Ocampo C, Flynn D: Polarization potentials causing pacemaker oversensing. Jpn Circ J 62:868-870, 1998. 7. Paraskevaidis S, Mochlas S, Hadjimiltiadis S, Louridas G: Intermittent P wave sensing in a patient with DDD pacemaker. PACE 22(4 Pt 1):689-690, 1999. 8. Frohlig G, Helwani Z, Kusch O, et al.: Bipolar ventricular far-field signals in the atrium. PACE 22:1604-1613, 1999. 9. Rosenheck S, Sharon Z, Leibowitz D: Artifacts recorded through failing bipolar polyurethane insulated permanent pacing leads. Europace 2:60-65, 2000. 10. Barold SS, Falkoff MD, Ong LS, Heinle RA: Oversensing by singlechamber pacemakers: Mechanisms, diagnosis, and treatment. Cardiol Clin 3:565-585, 1985. 11. Tse HF, Lau CP: The current status of single lead dual chamber sensing and pacing. J Interv Card Electrophysiol 2:255-267, 1998. 12. Friedberg HD, Barold SS: On hysteresis in pacing. J Electrocardiol 6:1-2, 1973. 13. Barold SS: Prolonged atrioventricular block during AAI pacing for sick sinus syndrome. J Cardiovasc Electrophysiol 11:1422, 2000. 14. Tripp IG, Armstrong GP, Stewart JT, et al.: Atrial pacing should be used more frequently in sinus node disease. PACE 28:291-294, 2005. 15. Barold SS, Falkoff MD, Ong LS, Heinle RA: Programmability in DDD pacing. PACE 7(6 Pt 2):1159-1164, 1984. 16. Barold SS, Belott PH: Behavior of the ventricular triggering period of DDD pacemakers. PACE 10:1237-1252, 1987. 17. Barold SS, Falkoff MD, Ong LS, Heinle RA: All dual-chamber pacemakers function in the DDD mode. Am Heart J 115:13531362, 1988. 18. Parravicini U, Mezzani A, Bielli M, et al.: DDD pacing and interatrial conduction block: Importance of optimal AV interval setting. PACE 23:1448-1450, 2000. 19. Bode F, Wiegand U, Katus HA, Potratz J: Inhibition of ventricular stimulation in patients with dual chamber pacemakers and prolonged AV conduction.[see comment]. PACE 22:1425-1431, 1999. 20. Dennis MJ, Sparks PB: Pacemaker mediated tachycardia as a complication of the autointrinsic conduction search function.[see comment]. PACE 27(6 Pt 1):824-826, 2004. 21. Higans ST, Hayes DL: P wave tracking above the maximum tracking rate in a pacemaker. PACE 12:1044-1048, 1989. 22. Van Gelder BM, Van Mechelen R, Den Dulk K, et al.: Apparent P wave undersensing in a DDD pacemaker after exercise. PACE 15:1651, 1992. 23. Barold SS, Gallardo I, Sayad D: Wenckebach upper rate response of pacemakers implanted for nontraditional indications: The other side of the coin. PACE 25:1283-1284, 2002. 24. Barold SS, Falk off MD, Ong LS, et al.: All dual-chamber procedures function in the DDD mode. Am Heart J 115:1353, 1988. 25. Barold SS: Far-field R wave sensing causing prolongation of the atrial escape interval of DDD pacemakers with atrial-based lower rate timing. PACE 26:2188-2191, 2003. 26. Lau CP, Leung SK, Tse HF, Barold SS: Automatic mode switching of implantable pacemakers: I. Principles of instrumentation, clinical, and hemodynamic considerations. PACE 25:967-983, 2002.

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27. Estes NA 3rd: Atrial tachyarrhythmias detected by automatic mode switching: Quo vadis? [comment]. J Cardiovasc Electrophysiol 15:778-779, 2004. 28. Israel CW: Analysis of mode switching algorithms in dual chamber pacemakers. PACE 25:380-393, 2002. 29. Leung SK, Lau CP, Lam CT, et al.: Is automatic mode switching effective for atrial arrhythmias occurring at different rates? A study of the efficacy of automatic mode and rate switching to simulated atrial arrhythmias by chest wall stimulation. PACE 23:824-831, 2000. 30. Passman RS, Weinberg KM, Freher M, et al.: Accuracy of mode switch algorithms for detection of atrial tachyarrhythmias.[see comment]. J Cardiovasc Electrophysiol 15:773-777, 2004. 31. Wood MA, Ellenbogen KA, Dinsmoor D, et al.: Influence of autothreshold sensing and sinus rate on mode switching algorithm behavior [see comment]. PACE 23(10 Pt 1):1473-1478, 2000. 32. Walfridsson H, Aunes M, Capocci M, Edvardsson N: Sensing of atrial fibrillation by a dual chamber pacemaker: How should atrial sensing be programmed to ensure adequate mode shifting? PACE 23:1089-1093, 2000. 33. Nowak B, Kracker S, Rippin G, et al.: Effect of the atrial blanking time on the detection of atrial fibrillation in dual chamber pacing. PACE 24(4 Pt 1):496-499, 2001. 34. Marshall HS, Kay GN, Hess M, et al.: Mode switching in dual chamber procedures: Effects of onset criteria on arrhythmiarelated symptoms. Europace 1:49-54, 1999. 35. Irrael CW, Barold SS: Failure of atrial flutter detection by a pacemaker with a dedicated atrial flutter detection algorithm. PACE 25:1274-1277, 2002. 36. Goethals M, Timmermans W, Geelen P, et al.: Mode switching failure during atrial flutter: The “2:1 lock-in” phenomenon. Europace 5:95-102, 2003. 37. Simpson CS, Yee R, Lee JK, et al.: Safety and feasibility of a novel rate-smoothed ventricular pacing algorithm for atrial fibrillation. Am Heart J 142:294-300, 2001. 38. Eguia LE, Pinski SL: Inactivation of a ventricular tachycardia preventive algorithm during automatic mode switching for atrial tachyarrhythmia. PACE 24:252-253, 2001. 39. Barold SS, Mond HG: Fallback responses of dual chamber (DDD and DDDR) pacemakers: A proposed classification. PACE 17: 1160-1165, 1994. 40. Ward KJ, Willett JE, Bucknall C, et al.: Atrial arrhythmia suppression by atrial overdrive pacing: Pacemaker Holter assessment. Europace 3:108-114, 2001. 41. Blommaert D, Gonzalez M, Mucumbitsi J, et al.: Effective prevention of atrial fibrillation by continuous atrial overdrive pacing after coronary artery bypass surgery [see comment]. J Am Coll Cardiol 35:1411-1415, 2000. 42. Levy T, Walker S, Rex S, Paul V: Does atrial overdrive pacing prevent paroxysmal atrial fibrillation in paced patients? Int J Cardiol 75:91-97, 2000. 43. Lam CT, Lau CP, Leung SK, et al.: Efficacy and tolerability of continuous overdrive atrial pacing in atrial fibrillation. Europace 2:286-291, 2000. 44. Attuel P, Danilovic D, Konz KH, et al.: Relationship between selected overdrive parameters and the therapeutic outcome and tolerance of atrial overdrive pacing. PACE 26(1 Pt 2):257-263, 2003. 45. Connolley SJ, Kerr CR, Gent M, et al.: Effects of physiological pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes: Canadian Trial of Physiological Pacing Investigators. N Engl J Med 342:1385-1391, 2000. 46. Israel CW, Gronefeld G, Ehrlich JR, et al.: Prevention of immediate reinitiation of atrial tachyarrhythmias by high-rate over-

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53. 54.

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56. 57.

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drive pacing: Results from a prospective randomized trial. J Cardiovasc Electrophysiol 14:954-959, 2003. Hakala T, Valtola AJ, Turpeinen AK, et al.: Right atrial overdrive pacing does not prevent atrial fibrillation after coronary artery bypass surgery. Europace 7:170-174, 2005. Savoure A, Frohlig G, Galley D, et al.: A new dual-chamber pacing mode to minimize ventricular pacing. PACE 28(Suppl 1):S43-S46, 2005. Sweeney M, Ellenbogen KA, Casavant D, et al.: Multicenter, prospective, randomized safety and efficacy study of a new atrialbased managed ventricular pacing mode (MVP) in dual chamber ICDs. J Cardiovasc Electrophysiol 16:811-817, 2005. Tse HF, Newman D, Ellenbogen KA, et al.: Atrial Fibrillation SYMPTOMS Investigators: Effects of ventricular rate regularization pacing on quality of life and symptoms in patients with atrial fibrillation (atrial fibrillation symptoms mediated by pacing to mean rates). Am J Cardiol 94:938-941, 2004. Abraham WT: Cardiac resynchronization therapy for the management of chronic heart failure. Am Heart Hosp J 1:55-61, 2003. Barold SS, Herweg B, Giudici M: Electrocardiographic follow-up of biventricular pacemakers. Ann Noninvasive Electrocardiol 10:231-255, 2005. Barold SS, Herweg B: Upper rate response of biventricular pacing devices. J Interv Card Electrophysiol 12:129-136, 2005. Chang KC, Chen JY, Lin JJ, Hung JS: Unexpected loss of atrial tracking caused by interaction between temporary and permanent right ventricular leads during implantation of a biventricular pacemaker. PACE 27:998-1001, 2004. Akiyama M, Kaneko Y, Taniguchi Y, Kurabayashi M: Pacemaker syndrome associated with a biventricular pacing system. J Cardiovasc Electrophysiol 13:1061-1062, 2002. Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. PACE 25:62-75, 2002. Riedlbauchova L, Kautzner J, Fridl P: Influence of different atrioventricular and interventricular delays on cardiac output during cardiac resynchronization therapy. PACE 28(Suppl 1):S19-S23, 2005. Taieb J, Benchaa T, Foltzer E, et al.: Atrioventricular cross-talk in biventricular pacing: A potential cause of ventricular standstill. PACE 25:929-935, 2002. Lipchenca I, Garrigue S, Glikson M, et al.: Inhibition of biventricular pacemakers by oversensing of far-field atrial depolarization. PACE 25:365-367, 2002. Cooper JM, Sauer WH, Verdino RJ: Absent ventricular tachycardia detection in a biventricular implantable cardioverterdefibrillator due to intradevice interaction with a rate smoothing pacing algorithm. Heart Rhythm 1:728-731, 2004. Shivkumar K, Feliciano Z, Boyle NG, Wiener I: Intradevice interaction in a dual chamber implantable cardioverter-defibrillator preventing ventricular tachyarrhythmia detection [see comment]. J Cardiovasc Electrophysiol 11:1285-1288, 2000. Glikson M, Beeman AL, Luria DM, et al.: Impaired detection of ventricular tachyarrhythmias by a rate-smoothing algorithm in dual-chamber implantable defibrillators: Intradevice interactions. J Cardiovasc Electrophysiol 13:312-318, 2002. Wietholt D, Kuehlkamp V, Meisel E, et al.: Prevention of sustained ventricular tachyarrhythmias in patients with implantable cardioverter-defibrillators: The PREVENT study. J Interv Card Electrophysiol 9:383-389, 2003. Barold SS: Ventricular rate stabilization algorithm of ICD causing dual chamber pacing during ventricular tachycardia. J Interv Card Electrophysiol 9:397-400, 2003.