Ventricular Blanking and Refractory Periods

To sense and pace within the same chamber, “same chamber” refractory periods must be included to avoid inappropriate oversensing of the intrinsic event or pacing^3,4 (Fig. 28-3). Immediately following a ventricular paced event, during a ventricular blanking period (VBP) or time interval (ranges from 50-100 msec), all ventricular sensed 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, which is used to prevent oversensing caused by the paced evoked potentials, the intrinsic ventricular electrogram (VEGM), or repolarization signals (T wave).

Figure 28-3 VVI ventricular refractory periods.

The solid blue squares in the open bar indicate the ventricular blanking periods, during which events are not sensed. The shaded blue rectangles in the bar indicate the ventricular refractory periods, during which ventricular sensed events are not used to reset timing cycles.

Ventricular Oversensing and Undersensing

Ventricular sensing may result in abnormalities in the ventricular timing cycles. The pacemaker senses an 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 (EMI) are possible causes of ventricular oversensing.^10,11 In ventricular oversensing the additional sensed event will reset the ventricular escape interval, resulting in longer intervals than the programmed pacing cycle length (Fig. 28-4). 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, but instead is created by the previous sensed or paced event. The pacing interval will be shorter than the pacing cycle length (Fig. 28-5).

Figure 28-4 VVI ventricular oversensing.

The T wave of the first beat (indicated by asterisk) is sensed outside the ventricular refractory period. The ventricular escape interval is 1000 msec. Because of 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.

Figure 28-5 VVI ventricular undersensing.

The second R wave (indicated by 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.

Hysteresis Rate

Hysteresis provides for a longer ventricular escape interval from the last ventricular sensed event to the first ventricular paced event (R-V, hysteresis interval) but no change in the time from the last ventricular paced event¹² (Fig. 28-6). Hysteresis allows the intrinsic heart rate to be lower before pacing occurs, but when pacing occurs, 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 above 50 bpm. When 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 AF 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 interval (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 (V-V). The hysteresis rate is sometimes expressed as a percentage subtracted from the lower rate. The hysteresis often results in a decreased frequency of pacing by allowing more time to expire after an intrinsic event. Typically, the lower rate interval is set to the slowest rate that is desirable hemodynamically. Once pacing occurs, however, it will continue until the intrinsic ventricular rate exceeds the pacing rate.

Figure 28-6 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 asterisk) after an R-V interval of 1200 msec. The hysteresis interval is 1200 msec and the pacing interval is 1000 msec.

Atrial Periods and Hysteresis

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. 28-10). It is also divided into an atrial blanking period (ABP), often programmable, followed by a refractory period during which noise sampling occurs (Fig. 28-11). The ABP is used primarily to prevent sensing of afterpotential of the pacing stimulus. The ARP (ranges from 150-500 msec) is used to prevent the atrial lead from oversensing the afterpotential of a paced stimulus, the local evoked potential produced by atrial pacing stimulus, or “far-field” sensing of the ventricular depolarization.

Figure 28-10 AAI mode atrial refractory periods.

Atrial paced events are noted by A and atrial sensed events by P. The solid blue part of bar indicates the atrial blanking period, during which events are not sensed. The shaded blue part of bar indicates the atrial refractory period, during which atrial sensed events are not used to reset timing cycles. The atrial pacing rate in the AAI mode in this example is 1000 msec and represents the time from either an atrial paced or an atrial sensed event to the next atrial paced event. Each of the P-A intervals occurs at 1000 msec while the ventricular sensed events may occur earlier than the atrial pacing rate.

Figure 28-11 AAI mode blanking period.

The blue area of bar indicates the atrial blanking period, during which events are not sensed. The purple bar indicates the atrial refractory period.

Atrial hysteresis may also be used in the AAI mode. The P-A interval, the atrial escape interval, 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. 28-12).

Figure 28-12 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, which is also an atrial paced event 1000 msec later. The third event is an intrinsic atrial event (P) at an 800-msec interval. 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.

Atrioventricular Interval

The atrioventricular interval (A-V interval, AVI) is a programmable parameter that determines the maximum time after an atrial event during which an intrinsic ventricular event can occur before delivery of a ventricular pacing stimulus (see Fig. 28-13). It is initiated after a sensed or a paced atrial event. AVI is similar to the native P-R interval and thus is programmed to optimize the hemodynamic benefit of AV coordination. AVI permits atrial contraction resulting in ventricular filling in end-diastole. AVI is programmed at rest to maintain coordinated timing of atrial and ventricular contractions, allowing intrinsic AV conduction when possible, and conserve generator energy. Patients who do not have coordinated AV contractions from PR prolongation may have impaired left ventricular filling, because atrial contraction occurs much earlier than the ventricular contraction. Recent trials involving patients with both preserved and depressed ventricular function suggest maintaining intrinsic AV conduction and minimizing right ventricular pacing is also desirable hemodynamically, because improved ventricular contraction and cardiac output are seen with normal ventricular activation.

Therefore the clinician balances permitting a short enough A-V interval to optimize coordination of AV contraction with permitting sufficient time for conduction to result in intrinsic ventricular activation. The programmed A-V interval that results in optimal hemodynamics may vary considerably and may be difficult to predict accurately. Many clinicians select the programmed A-V interval that allows a P-R interval of up to 280 to 300 msec. Assessment of interatrial conduction delay may have a role in setting the optimal A-V interval, but data are still limited.¹⁸ There may be a time differential with atrial 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 A-V interval may be programmed, as discussed later. Also, to conserve battery energy, the clinician may extend the AVI in patients without AV block to reduce pacing.

Crosstalk and Ventricular Safety Pacing

Crosstalk is the inappropriate sensing of far-field signals from the opposite cardiac 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 “pacemaker-dependent” patient. The AVI thus encompasses multiple refractory and blanking intervals on each atrial/ventricular channel, as well as on the “opposite” channel to prevent crosstalk (Figs. 28-14 and 28-15).

Figure 28-15 DDD refractory periods.

The lower rate is 60 beats per minute or 1000 ms in this example of ventricular-based timing. The atrial escape interval, 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. The refractory periods and sensing windows are given on the atrial and ventricular sensing channels. On the atrial channel, the atrial blanking period is after an atrial paced or sensed (usually) event. After a sensed or paced ventricular event, on the atrial channel, there may be 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, usually followed by a crosstalk safety pacing window and an alert period.

An atrial pacing output also initiates multiple timing windows on the ventricular channel. Atrial pacing output triggers a VBP at the beginning of the A-V interval in an attempt to avoid oversensing the atrial stimulus artifact on the ventricular lead (Fig. 28-16). This absolute VBP is usually short, ranging from 20 to 44 msec, and may be programmable in certain pacemaker models. Immediately after the VBP, the ventricular sensing amplifier becomes active during the ventricular safety pacing (VSP, or crosstalk sensing) window in the second portion of the AVI (up to 80-120 msec). Signals sensed during the “crosstalk sensing window” (<120 msec from the atrial pacing output) are considered “nonphysiologic” because of the close coupling interval and may be caused by oversensing of atrial pacing afterpotentials, spontaneous premature ventricular depolarizations, or noise (see Fig. 28-16). VSP is designed to prevent inappropriate inhibition of the ventricular pacing caused by crosstalk (Figs. 28-17 and 28-18). After an atrial paced depolarization, if there is a sensed event occurring during the VSP window, instead of inhibiting ventricular pacing, the pacemaker will deliver a ventricular pacing stimulus at a shortened A-V interval, typically 80 to 130 msec. The shortened A-V interval makes the identification of VSP apparent and decreases the likelihood of a ventricular paced event occurring during ventricular repolarization, particularly if the baseline A-V interval is relatively long, minimizing the risk of ventricular proarrhythmia. Crosstalk in this situation is 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). VSP may also be seen when atrial undersensing occurs and the conducted intrinsic ventricular beat is sensed in the crosstalk safety pacing window (Fig. 28-19).

Figure 28-16 DDD safety pacing windows.

On the ventricular channel after an atrial paced event, there is a cross-channel ventricular blanking period followed by a crosstalk safety pacing window and an alert period. During the cross-channel 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.

Figure 28-17 Ventricular safety pacing.

Left side, An atrial paced event and a ventricular paced event are separated by the A-V interval of 200 msec. Right side, An atrial paced event is followed by a ventricular paced event after 110 msec. This represents safety pacing resulting from a ventricular sensed event in the crosstalk safety pacing window.

Figure 28-18 Ventricular safety pacing.

Top channel is the surface electrocardiogram (ECG). Lower marker channel has the atrial channel on top and the ventricular channel on bottom. In the absence of crosstalk, the first, fourth, and last atrioventricular (A-V) intervals are equal to the programmed value of 200 msec. Intermittent crosstalk (solid blue circles) leads to activation of the ventricular safety pacing mechanism so that the A-V interval of the second, third, fifth, and seventh beats (black circles) is abbreviated to 110 msec. The marker channel 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 ventricular pacing (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 from continual crosstalk leads to an increase in the pacing rate, although the atrial escape interval remains constant.

(From Barold S, Zipes D: Cardiac pacemakers and antiarrhythmia devices. In Braunwald E, editor: Heart disease: a textbook of cardiovascular medicine, ed 5, Philadelphia, 1997, Saunders, pp 705-741.)

Figure 28-19 Ventricular safety pacing resulting from atrial undersensing.

Left side, An atrial paced event and a ventricular paced event are separated by the A-V interval of 200 msec. Right side, An undersensed intrinsic atrial event is followed by an atrial pacing stimulus that does not capture because of 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.

On the atrial channel, a paced event may result in an absolute ABP, preventing sensing of afterpotential of the pacing stimulus (Fig. 28-20). In some devices, a sensed atrial event also initiates an ABP. After the APB, atrial sensed 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 atrial blanking period, to prevent the sensing of ventricular paced events or far-field ventricular sensed events on the atrial channel. After a ventricular paced or sensed event, a postventricular atrial refractory period (PVARP) is created (see Fig. 28-20). During PVARP, atrial events are refractory sensed events and do not affect timing of events (see later).

Figure 28-20 DDD atrial blanking period.

After an atrial paced or sensed event, there is a blanking period on the atrial channel. After a sensed or paced ventricular event, a postventricular atrial blanking period may be followed by a postventricular atrial refractory period. During the latter, an atrial sensed event will not be tracked or used to inhibit atrial pacing at the atrial escape interval.

Differential AVI

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 in the SAV and PAV is called a differential AVI. The optimal A-V interval achieves coordination of the atria and ventricles, particularly left atrium and left ventricle. Usually, impulse formation starts in the sinus node and travels to the right atrial lead on its way to the AV node. Thus, by the time the event is sensed on the atrial channel, contraction of the atria has already begun, necessitating only relatively short delay to the time that ventricular excitation occurs. Time elapses between the initiation of an intrinsic atrial depolarization and the point that most of the atria are depolarized. This delay is determined by the distance from initiation to the location of the lead, as well as conductive properties of the atrial tissue. By the time the atrial lead has sensed the intrinsic depolarization, it has already gotten a “head start” to the AV node compared to an atrial paced event. By programming the AVI of a sensed atrial depolarization (PV) to be shorter than that after an atrial paced event (AV), the time to ventricular pacing after a paced atrial beat will be similar to that after a sensed atrial event (Fig. 28-21). 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 A-V intervals.

Figure 28-21 Differential atrioventricular (A-V) interval.

A differential A-V interval (AVI) permits a shorter AVI for a sensed atrial event compared to the interval for a paced atrial event. In the first complex here, 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. In the third complex, the P wave is sensed and initiates a shorter AVI of 160 msec compared to the AVI of 200 msec. In the last complex, the sensed P wave also starts an AVI of 160 msec, but AV conduction occurs.

Atrioventricular Interval Hysteresis

The AVI can also be modulated based on the presence or absence of AV conduction, with a sensed ventricular event during 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 AVI relative to patient’s intrinsic P-R interval. Similar to heart rate hysteresis, AVI hysteresis is a prolongation of AVI in response to a ventricular sensed event (R), called “positive AV/PV hysteresis.” The longer-than-programmed A-V interval permits intrinsic AV conduction and minimizes unnecessary ventricular pacing. Positive AV/PV hysteresis is most beneficial to patients who have variable AV conduction. However, if the intrinsic AV conduction exceeds the AVI hysteresis and no spontaneous R wave was sensed at the end of the AVI (as in AV block), A-V interval is shortened to the original programmed value. A search function extends the A-V interval periodically from the programmed baseline value to the longer AVI hysteresis interval to promote intrinsic AV conduction and ventricular activation (Figs. 28-22 and 28-23). This function may be called “search positive AV hysteresis”; alternatively, “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), the next AVI will be shortened to promote ventricular pacing and capture (Fig. 28-24). This function may be used to promote ventricular capture, when this is hemodynamically desirable. Such conditions might include pacing for hypertrophic cardiomyopathy or biventricular pacing.

Figure 28-22 Positive atrioventricular (A-V) interval hysteresis.

In positive AVI hysteresis, the A-V interval is increased to permit intrinsic AV conduction. If conduction is present, the extended A-V interval persists. If AV conduction is absent, the A-V interval will be shortened to its previous length.

Figure 28-23 Positive AVI hysteresis.

After a period of pacing, a search mechanism is initiated, and 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, thus inhibiting the ventricular output and reestablishing 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 this could be accomplished with a fixed, long AV or PV delay, when and if AV block develops, the pacing system will be functioning in a hemodynamically deleterious, long AV/PV delay until intact conduction resumes. P, Atrial sensed; R, ventricular sensed; V, ventricular paced event.

(Courtesy St. Jude Cardiac Rhythm Management Division, Sylmar, Calif).

Figure 28-24 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. After a period of pacing, the system extends the AV/PV interval to determine whether intact conduction is still present or will allow the longer interval to remain in effect. P, Atrial sensed; R, ventricular sensed; V, ventricular paced event.

(Courtesy St. Jude Cardiac Rhythm Management Division, Sylmar, Calif.)

Postventricular Atrial Refractory Period

After a sensed or paced ventricular event, atrial sensed events do not result in a corresponding A-V interval for a programmable period of time. The PVARP is used to prevent sensing of retrograde P waves following a paced or sensed ventricular event usually not preceded by an atrial or paced event (Fig. 28-25). 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), which may continue without intervention (Figs. 28-26 and 28-27). PMT may occur at or below the maximum tracking rate and is often induced by spontaneous premature ventricular beats or loss of atrial capture. The rate of PMT depends on the retrograde conduction time, the programmed A-V interval, and the maximum tracking rate. PMT usually occurs at the maximum tracking rate. However, the retrograde conduction time may be long enough to permit tracking of the atrial event with the programmed A-V interval so that the PMT rate may be less than the maximum tracking rate. To avoid PMT, the PVARP is usually programmed longer than the retrograde conduction time; however, if it is programmed excessively long, the sum of the PVARP and the A-V interval, the total atrial refractory period will determine the rate at which one ventricular paced event occurs for two atrial sensed events, the 2 : 1 atrial tracking rate (see next).

Figure 28-25 Postventricular atrial refractory period (PVARP).

A premature ventricular contraction (complex) (PVC) results in retrograde conduction indicated by the asterisk. Because the P wave occurs within the PVARP, the P wave 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.

Figure 28-26 Pacemaker-mediated tachycardia.

A premature ventricular complex (contraction) (PVC) results in retrograde conduction. Since the retrograde P wave occurs after the postventricular atrial refractory period, the P wave is tracked and initiates a ventricular paced event. This ventricular paced event results in another retrograde P wave that is tracked, resulting in pacemaker-mediated tachycardia.

Figure 28-27 Pacemaker-mediated tachycardia terminated and initiated by ventricular extrasystole.

The three ECG leads were recorded simultaneously. Upper rate interval (URI) = 500 msec (120 ppm); lower rate interval (LRI) = 857 msec (70 ppm); AV delay = 150 msec. The cycle length of the tachycardia is longer than the URI.

(From Barold SS, Falkoff MD, Ong LS, Heinle RA: Basic concepts, upper rate response, retrograde ventriculoatrial conduction, and differential diagnosis of pacemaker tachycardias. In Saksena S, Goldschlager N, editors: Electrical therapy for cardiac arrhythmias: pacing, antitachycardia devices, catheter ablation, Philadelphia, 1990, Saunders, pp 225-264.)

Extension of PVARP in response to a premature ventricular complex (PVC), called the “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 following a premature ventricular beat, which 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, a long PVARP may lead to absence of atrial tracking (Fig. 28-28). 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 lower rate limit (Fig. 28-29). Repetitive functional atrial undersensing may occur in the absence of PVC PVARP extension, particularly when the AV conduction is prolonged and the intrinsic A-V interval plus 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 28-28 Lack of P-wave tracking caused by long PVARP (400 msec).

Top tracing, Sinus rate is about 85 beats per minute, and there is a first-degree AV block. The P waves fall within the postventricular atrial refractory period (PVARP) initiated by the preceding sensed QRS complex. VRP, Ventricular refractory period. Bottom tracing, Shortening the PVARP to 375 msec restores 1 : 1 atrial tracking with the programmed A-V interval (150 msec).

(From Barold SS, Falkoff MD, Ong LS, Heinle RA: Timing cycles of DDD pacemakers. In Barold S, Mugica J, editors: New perspectives in cardiac pacing, Mt Kisco, NY, 1988, Futura.)

Figure 28-29 Perpetuation of failure to track caused by PVARP extension.

T-wave oversensing is classified as a premature ventricular complex (PVC). The PVC postventricular atrial refractory period (PVARP) extension feature results in PVARP being extended, placing the subsequent sinus P wave within PVARP. Because AV conduction is present, the next QRS complex is considered a PVC, which again causes PVARP extension.

Upper Rate Behavior

In patients in the DDD, DDDR, VDD, or VDDR modes, one-to-one (1 : 1) ventricular tracking of the intrinsic atrial activity is hemodynamically desirable. However, tracking of atrial arrhythmias may result in rapid ventricular pacing and result in unfavorable hemodynamics. Therefore, these tracking modes have a parameter to limit the fastest rate that 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, also called the maximum tracking rate (MTR), with a corresponding upper rate interval or maximum tracking interval (Fig. 28-30). In DDD mode, whether atrial or ventricular based, when the intrinsic atrial activity is faster than the programmed upper rate limit, “upper rate behavior” will be seen. Atrial rates above the MTR can still be sensed and tracked. However, delays in subsequent ventricular paced beats occur so that the ventricular rate does not exceed the programmed MTR (Fig. 28-31). This effectively prolongs the AVI. The A-V interval is further extended on repeated cycles, and the subsequent atrial depolarization eventually falls within the PVARP. Because the atrial event occurs within the PVARP, it is not sensed by the atrial channel and thus does not lead to ventricular pacing. The next atrial event, however, can be tracked and can cause ventricular pacing. The pattern that emerges is increasing duration between intrinsic atrial sensed events and ventricular paced events until an atrial event is not followed by a ventricular paced beat. Such behavior is similar to a Wenckebach period during AV conduction and is called “pseudo-AV Wenckebach.” The A-V interval extension is greatest when the P wave occurs just after the completion of the preceding PVARP (Fig. 28-32). A-V interval extension may be seen at constant atrial rates during atrial or sinus tachycardias as well as during atrial premature beats (Fig. 28-33).

Figure 28-30 Upper rate behavior.

A, Apparent loss of atrial tracking related to upper rate limitation. Lower rate interval (LRI) = 1000 msec; upper rate interval (URI) = 500 msec; atrioventricular (A-V) interval (AVI) = 75 msec. The ECG was recorded during a treadmill stress test. The P waves on the right were 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 in A. During recovery 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 capture (fusion beats) until full ventricular capture is reestablished, preceded by an atrial sensed–ventricular paced interval of 75 msec.

(From Douard H, Barold SS, Broustet JP: Too much protection may be a nuisance. Stimucoeur 25:183-187, 1997).

Figure 28-31 DDD mode upper rate response with Wenckebach pacemaker AV block.

The upper rate interval (URI) is longer than the programmed total atrial refractory period (TARP); AEI, atrial escape interval. 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 A-V interval represents the difference between the URI and the TARP. The As-Vp interval lengthens as long as the As-As interval (PP) is longer than the TARP. The sixth P wave falls within the postventricular atrial refractory period (PVARP) and is unsensed and 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 PP interval becomes shorter than the programmed TARP, Wenckebach pacemaker AV block cannot occur, and fixed-ratio pacemaker AV block (e.g., 2 : 1) supervenes.

(From Barold SS, Falkoff MD, Ong LS, Heinle RA: All dual-chamber pacemakers function in the DDD mode. Am Heart J 115:1353-1362, 1988.)

Figure 28-32 Diagrammatic representation of the mechanism of A-V interval prolongation.

The pulse generator has a separately programmable total atrial refractory period (TARP) and upper rate interval (URI); lower rate timing is ventricular based. The maximum A-V interval (AV) extension, or waiting period (W), = URI − (AV + postventricular atrial refractory period [PVARP]) = URI − TARP. A P wave (P₁) occurring immediately after termination of the PVARP exhibits the longest A-V interval, that is, AV + W. A P wave just beyond the W period (P₄) initiates an A-V 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. If the pacemaker is programmed with As-Vp shorter than Ap-Vp, W becomes URI − (As-Vp) − PVARP; that is, AV extension becomes longer if basic As-Vp is shorter than Ap-Vp. However, the maximum As-Vp duration is URI − PVARP, regardless of programmed A-V interval. AEI, Atrial escape interval; LRI, lower rate interval; Ap, atrial paced beat; Vp, ventricular paced beat.

(In Barold SS, Falkoff MD, Ong LS, Heinle RA: Basic concepts, upper rate response, retrograde ventriculoatrial conduction, and differential diagnosis of pacemaker tachycardias. In Saksena S, Goldschlager N, editors: Electrical therapy for cardiac arrhythmias: pacing, antitachycardia devices, catheter ablation. Philadelphia, 1990, Saunders, pp 225-264.)

Figure 28-33 Two-lead electrocardiogram showing DDD pacing.

Ventricular-based lower rate timing with sensed atrial premature contractions (APC). Lower rate interval (LRI) = 1000 msec; AV = 200 msec; upper rate interval (URI) = 600 msec; postventricular atrial refractory period (PVARP) = 155 msec. Note the extended A-V interval 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.

If the intrinsic atrial rate continues to increase above the MTR, it will eventually reach the 2 : 1 AV tracking rate, defined by the total atrial refractory period (TARP), which is the sum of the PVARP and the AVI (Fig. 28-34). 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 slightly faster, the first P wave will be tracked and the second P wave fall just within the PVARP and is not 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 as 60,000 (in msec) divided by TARP (in msec). For example, for an AVI of 150 msec and PVARP of 250 msec, ventricular pacing may follow atrial sensing at a 1 : 1 rate 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.

Figure 28-34 Total atrial refractory period (TARP).

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

When patients have intrinsic A-V conduction, the upper rate limit (URL) is not needed to permit tracking of rapid sinus rates during exertion. Therefore, when intrinsic A-V conduction is present, the URL may be programmed at a relatively low rate. When patients have complete AV conduction block, however, it is important to permit tracking as the atrial rate rises during exertion. The URL (MTR) should be programmed high enough to allow 1 : 1 tracking through maximum physiologic atrial rates. However, having the 2 : 1 atrial tracking rate faster than the atrial MTR permits a zone of pseudo-Wenckebach behavior before development of 2 : 1 block. To accomplish this effect, the TARP (PVARP + AVI) is programmed shorter than the URL interval.

There may be limitations to minimizing TARP because of retrograde conduction necessitating a PVARP to be programmed 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 above the MTR to accommodate high intrinsic sinus rates without sudden AV block. This is achieved by minimizing TARP, with several common ways to reduce TARP and raise the 2 : 1 block rate. The PVARP can be shortened (with increased risk of PMT), and the AVI can be programmed to be rate adaptive and to shorten with faster ventricular rates. Rate-adaptive or dynamic PVARP is also available in some models, which shortens PVARP at a faster rate and thus reduces TARP and increases the 2 : 1 AV block rate. Caution should be used with rate-adaptive PVARP to confirm that retrograde conduction will not occur at rapid ventricular rate, so that the conduction time does not exceed the PVARP, resulting in PMT. Alternatively, the pacemaker can be programmed to DDDR mode and can rely 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 rates, even though the ventricular pacing rate exceeds the atrial MTR. This phenomenon has been termed sensor-driven rate smoothing and resembles tracking above the MTR (Fig. 28-35).

Figure 28-35 Sensor-driven appearance of atrial tracking.

Diagram shows that a P wave may inhibit the sensor-driven atrial stimulus and can resemble P –wave tracking above the maximum tracking rate (MTR) of 100 bpm or 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 P-wave 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. AP, Atrial paced; AS, atrial sensed; AVI, atrioventricular interval; VP, ventricular paced event.

(From Higano ST, Hayes DL: P wave tracking above the maximum tracking rate in a DDDR pacemaker. Pacing Clin Electrophysiol 12:1044-1048, 1989.)

Upper rate behavior may also result in triggering an apparent failure to sense P waves because the P wave falls within PVARP, and the subsequent QRS complexes are categorized as premature ventricular beats. An algorithm to increase the PVARP following a PVC may result in prolonged absence of atrial tracking (Figs. 28-36 and 28-37). Upper rate behavior may also be characterized by intrinsically conducted beats that may preempt the ventricular paced beats at the upper rate. Barold et al.²¹ describe a relatively short programmed A-V interval, a sinus rate faster than the programmed upper rate, a relatively slow programmed upper rate, and relatively normal AV conduction as most likely to be associated with this phenomenon.

Figure 28-36 Apparent P-wave undersensing.

Lower rate = 60 pulses per minute (ppm); upper rate (UR) = 140 ppm; AV delay after P-wave sensing = 135 msec (adaptive AV delay with minimum AV delay of 75 msec); postventricular atrial refractory period (PVARP) = 320 msec; automatic PVARP extension = 100 msec. A, At rest, the atrial rate is 112 beats per minute (bpm), causing atrial sensing and ventricular pacing with 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 P-R interval of about 260 msec. The pacemaker interprets the spontaneous QRS complex as a premature ventricular contraction (complex) and therefore automatically lengthens the PVARP to 320 + 100 = 420 msec. Subsequent events all are spontaneous, that is, P wave and conducted QRS complex with 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, ECG shows sinus rhythm (P-R = 200 msec) and conversion to an atrial synchronous ventricular paced rhythm with an A-V 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 and subsequently the next P wave falls outside the extended PVARP of 420 msec.

(From van Gelder BM, van Mechelen R, den Dulk K, el Gamal M: Apparent P wave undersensing in a DDD pacemaker after exercise. Pacing Clin Electrophysiol 15:1651, 1992.)

Figure 28-37 Loss of P-wave tracking caused by long PVARP (400 msec).

The sinus rate is about 85 ppm, and there is first-degree 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 A-V interval (150 msec). VRP, Ventricular refractory period.

(From Barold SS, Falkoff MD, Ong LS, Heinle RA: Timing cycles of DDD pacemakers. In Barold S, Mugica J, editors: New perspectives in cardiac pacing, Mt Kisco, NY, 1988, Futura.)

Lower Rate Behavior: Atrial- versus Ventricular-Based Timing

The use of atrial-based versus ventricular-based timing cycles determines when atrial paced events occur. In ventricular-based timing in the DDD mode, an atrial escape interval (AEI) is initiated after a sensed or paced ventricular event (R-A or V-A). In ventricular-based timing, AEI is “fixed.” The lower rate limit (LRL) is the maximum time allowed between a ventricular event (either sensed or paced) and the subsequent ventricular pacing stimulus (V-V or R-V). The LRL is thus the AEI plus the AVI to the subsequent ventricular pacing (R-A-V or V-A-V). The length of the AEI can be determined by subtracting the AVI from the cycle length of LRL (in msec). 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 URL constraints. However, if the AEI expires before sensing any atrial or ventricular event, the pacemaker will provide an atrial paced beat.

In ventricular-based timing, the effective ventricular rate can 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. 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 is thus 950 msec (AEI + A-R), which is approximately 63 bpm (Figs. 28-38 and 28-39). In patients with intact AV conduction, the effective ventricular rate can be faster than the programmed LRL in a ventricular-based timing system.

Figure 28-38 DDD mode with ventricular-based lower rate timing.

Diagrammatic representation of timing cycles; REF, refractory; ventricular triggering period, ventricular ventricular safety period. The second ventricular sensed event (Vs) is a sensed ventricular extrasystole. The fourth A-V interval initiated by an atrial sensed event (As) is abbreviated because Vs occurs before the A-V interval has timed out. The 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 macro-reentrant tachycardia caused by repetitive sensing of retrograde atrial depolarization) are initiated by ventricular extrasystoles with retrograde ventriculoatrial (VA) conduction. Whenever possible, the A-V interval and atrial escape (pacemaker VA) interval (AEI) are depicted in their entirety for the sake of clarity. The arrow pointing down within the AEI indicates that As has taken place. The As inhibits the release of the atrial stimulus expected at the completion of AEI.

(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 28-39 Ventricular-based timing cycles.

The lower rate limit is 1000 msec, and the AV delay is 200 msec. 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.

Compared to a ventricular-based timing in which the AEI is fixed, the atrial interval (A-A) is fixed in atrial-based timing. A sensed R wave occurring during AVI inhibits ventricular output but does not reset the basic A-A interval, and thus LRL is not altered. When an 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, which 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, whereas premature ventricular beats reset the AEI or the V-A interval (Fig. 28-40). Early sensing of the ventricular complex on the atrial channel (crosstalk) in a pacemaker with atrial-based timing may result in prolonged AEIs²² (Figs. 28-41 and 28-42). In Figure 28-41, A, at greater ventricular sensitivity there is no evidence of a prolonged AEI, while at less ventricular sensitivity (B), AIE is significantly prolonged. Figure 28-42 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 AEI. The second PVC in the figure is sensed as a PVC and thus does not result in AEI prolongation.

Figure 28-40 Atrial-based timing cycles.

The lower rate limit is 1000 msec, and the AV delay is 200 msec. The atrial escape interval is 800 msec. The R-R intervals are given; note that the R-R interval is 1000 msec between first and second beats. Between the second and third beats, the R-R interval is 1040 msec; between the third and the 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 28-41 Prolongation of atrial escape interval in atrial-based timing pacemaker.

A, In the left panels, atrial sensitivity was programmed to 0.5 millivolt (mV) and the ventricular sensitivity was 1 mV. The premature ventricular complex (PVC) resulted in an atrial escape interval (AEI) of 660 msec, corresponding to the programmed AEI of 600 msec. B, In the right panels, 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 of 800 msec, which corresponds 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 atrial-based lower rate timing. Pacing Clin Electrophysiol 26:2188-2191, 2003.)

Figure 28-42 Prolongation of atrial escape interval in atrial-based timing pacemaker.

AEI prolongation is caused by far-field R-wave sensing on the atrial channel. Lower rate limit is 800 msec in an atrial-based timing system, except for after premature ventricular complexes (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 AEI prolongation 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 AEI prolongation.

(From Barold SS: Far-field R-wave sensing causing prolongation of the atrial escape interval of DDD pacemakers with atrial-based lower rate timing. Pacing Clin Electrophysiol 26:2188-2191, 2003.)

The response to a PVC varies based on the individual manufacturer’s timing cycles. A PVC may result in initiation of the entire lower rate interval in milliseconds (60,000 divided by lower rate in beats per minute) before initiating an atrial paced event, resulting in an R-R interval that is longer than the lower rate interval (Biotronik). On the other hand, the interval from the PVC to the atrial paced event is equal to PVARP plus 330 msec in another timing cycle schema (St. Jude). If an atrial event is sensed within the PVARP, the interval to the atrial paced event is 330 msec (St. Jude). In remaining cases, AEI is equal to the lower rate interval minus the programmed A-V interval (Medtronic, Boston Scientific, ELA/Sorin).²³

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 function. The pacemakers have developed from VOO to DDDR systems. In response to enhanced sympathetic drive during exercise, the heart rate and stroke volume 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 so adequately. Heart rate is the predominant determinant of cardiac output compared with stroke volume, so 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, sometimes described as inability to achieve 75% of the maximum predicted heart rate for age. Individuals with chronotropic incompetence include patients who are in sinus bradycardia with sinus node dysfunction or those in AF 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 = maximum heart rate).

Rate-Adaptive Pacing

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, patients in sinus bradycardia with sinus node dysfunction could benefit from either an atrial or a dual-chamber rate-responsive pacemaker to achieve a higher heart rate response during exertion than their sinus node can provide. Similarly, patients who have chronic AF and slow ventricular rate may benefit from a VVIR pacemaker, which increases rate of ventricular pacing with exertion.

Timing Cycles of Sensor-Driven Pacing

The timing cycles in sensor-driven pacing preserve 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 will vary based on the sensor-indicated 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 A-V interval from the sensor-indicated interval.

Rate-Adaptive Algorithms

Special algorithms 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 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 responding to increased intrinsic atrial rates, it also permits a higher MTR. Since 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 that maintains 1 : 1 AV synchrony. For individuals who cannot tolerate a shortened PVARP because of persistent retrograde conduction, who have impaired AV conduction, rate-modulation of the AVI can be particularly useful. The A-V interval also may shorten as the sensor-driven rate increases. This permits the hemodynamic effects of sensor-driven pacing to be optimized with an A-V interval that shortens with exertion. The PVARP may also be rate modulated. The rate adaptation is based on the physiologic observation of decreased retrograde conduction with increased activity seen in normal subjects. When rate-adaptive PVARP is programmed, as the sensor-determined rate increases, the PVARP shortens, which also shortens TARP (similar to rate-adaptive AVI) and allows for a higher 2 : 1 tracking rate. However, shortening the PVARP rests on the assumption that retrograde conduction 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.

VDD Mode

The VDD mode offers both atrial and ventricular sensing with only ventricular pacing (Fig. 28-58). 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 with a single lead that paces and senses the ventricle and that senses the atrium using a specially designed “floating” atrial electrode.

Figure 28-58 VDD mode.

In the VDD mode, atrial sensed events are tracked, initiating an 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 bpm, and the upper rate limit is 120 bpm, with an AV delay of 200 msec. A, Atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event. 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, in beat 3, there is no ventricular sensed event by the time the A-V interval expires, 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.

DDI Mode

Atrioventricular 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 the DDD mode, the AVI is not initiated (Fig. 28-59). Ventricular paced events following atrial sensed events will occur at the LRL rather than after the AV delay. Ventricular sensed events result in inhibition of ventricular pacing and reset the AEI. Absence of intrinsic atrial events or ventricular events by the end of the LRL results in pacing in the atrium and the ventricle, respectively. This mode is best suited for patients at risk for atrial tachyarrhythmias because there is no atrial tracking resulting in rapid ventricular pacing during atrial tachyarrhythmia. This mode can be useful when the mode-switching feature is unavailable or does not accurately function. In DDI mode the absence of tracking results in the inability of faster intrinsic sinus rates to be followed by ventricular paced beats as the sinus rates increase in response to greater metabolic demands with exertion and 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.

Figure 28-59 DDI mode.

In the DDI mode, atrial sensed events are not tracked, but they inhibit atrial pacing. 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 bpm, with an AV delay of 200 msec. A, Atrial paced event; P, atrial sensed event; R, ventricular sensed event; V, ventricular paced event. 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 since 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 atrial escape interval of 800 msec since no atrial sensed event has occurred. Because no sensed ventricular event occurs, a ventricular paced event also occurs.

Other Modes

Many other modes are used less frequently as permanent settings and are used only in particular circumstances. As discussed, the asynchronous modes AOO, VOO, and DOO pace constantly in the atrium, ventricle, or both chambers, respectively. These modes are generally used to prevent potential oversensing, such as EMI from electrocautery during surgery. Other sources of possible interference include transcutaneous electrical stimulation (TENS), diathermy, and lithotripsy in pacemaker-dependent patients.

The triggered modes VVT and AAT 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) before the availability of intracardiac electrograms and marker channels. However, triggered modes are infrequently used in current practice.

The VDI mode is used similar 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 do not result in ventricular tracking, and instead are recorded for later evaluation, such as evaluation of atrial arrhythmias. In some devices, mode-switching algorithms will initiate the VDI mode when atrial tachyarrhythmia is sensed.

In the DVI (AV sequential, ventricular inhibited) mode, which is the least used, the pacemaker will provide pacing in both atrium and ventricle (D), but only events in the ventricle (V) inhibit pacing. An atrial escape interval will be reset after a sensed or paced ventricular event, followed by an asynchronous atrial pacing output. However, a sensed spontaneous ventricular event within the AEI will inhibit and reset both atrial and ventricular pacing stimuli. The atrial pacing stimulus is followed by the A-V interval, 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. 28-60). The absence of atrial sensing may result in a paced atrial impulse immediately after an intrinsic atrial event, potentially triggering atrial tachyarrhythmia.

Figure 28-60 DVI mode.

In the DVI mode, the atrium and the ventricle are paced, but only the ventricle is sensed. As a result, 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 since 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. The atrial pacing after a spontaneous P wave could result in atrial arrhythmias. In beat 4, atrial and ventricular pacing occurs because no ventricular sense event has occurred.

Pacing Modes

Pacing modes for CRT pacemakers and general criteria for mode selection are similar to standard pacing. In patients with chronic atrial fibrillation, VVIR pacing is the most common mode, to achieve rate responsiveness and to maintain as close as possible to 100% ventricular pacing. In patients without AF, the most common mode is VDI, DDD, or DDDR. VDI is appropriate for patients with normal sinus node function and intact AV conduction. DDDR should be selected in patients with chronotropic incompetence from relative sinus bradycardia. VDI, DDD, or DDDR mode allows atrial tracking with AV coordination. The optimal hemodynamics of CRT requires maintenance of AV synchrony with maximum BiV pacing and capture. There is no role, therefore, for AAI or other algorithms that promote intrinsic AV conduction. The basic timing cycle during CRT relies on an A-V interval that maintains ventricular capture.

The timing cycles for BiV pacemakers are potentially complex, depending on which chamber(s) is sensed, which ventricle(s) is paced, the inter-ventricular delay, and the chamber(s) that resets the escape intervals.^52–56 For most commercially available BiV devices, the sensing chamber(s) is usually the right ventricle and occasionally both ventricles (for older devices with Y connection). BiV pacing activates both ventricular chambers either simultaneously or sequentially (Fig. 28-61).

Figure 28-61 Biventricular pacing with right ventricular (RV)–based timing may occur after atrial event.

A premature ventricular beat PVS creates a new VAI. AP, Atrial paced event; AS, atrial sensed event; LVP, left ventricular paced event; RVP, RV paced event; RVS, RV sensed event; VAI, ventriculoatrial interval; RV-RV, interval between RV events.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Atrioventricular Interval

For biventricular pacing to result in the desired hemodynamic effect, it is necessary for appropriately timed BiV paced beats to occur after paced or sensed atrial events.⁵⁷ Therefore, AVI must be sufficiently short to ensure BiV capture and minimize fusion, yet long enough to allow adequate diastolic filling during the atrial contraction. Because the degree of native PR shortening during exercise may be significant, this may 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 CRT devices.

Several algorithms have been designed to maintain BiV pacing and activation. When a ventricular event is sensed on one pacing cycle, the A-V interval is shortened on the next timing cycle (AV hysteresis). If an atrial event is followed by a sensed right ventricular (RV) event, which is then followed by an LV paced event, on the next cycle, an RV paced event and an LV paced event may occur by shortening the time from the atrial sensed event to the RV paced event (Fig. 28-62). In addition, if the LV paced event occurs before the RV sensed event, it is possible to shorten the LV-RV timing on subsequent cycles (Fig. 28-63). However, such “negative” AV hysteresis function is often ineffective; permitting even one cycle with intrinsic conduction may have deleterious consequences. Perpetuation of native AV conduction and the absence of BiV pacing can result, as discussed later. If an intrinsic ventricular event is sensed within the A-V interval, one option might be to trigger a ventricular paced stimulus from the opposite ventricle, so-called ventricular sensed response. For example, if a sensed event is detected by the RV lead, an LV pacing output is delivered immediately to maximize LV capture and BiV activation (Fig. 28-64). However, it is unclear if the benefit of this strategy has limits, particularly with closely timed ventricular premature beats.

Figure 28-62 Biventricular pacing with RV sensed event before LV paced event.

An atrial paced event (Ap) starts the AV delay. The right ventricular sensed event (RVS) occurs before the left ventricular paced event (LVP) (positive RV-LV interval) in the first cycle. On the subsequent 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. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-63 Biventricular pacing with LV paced event before RV sensed event.

In the first cycle, there is a left ventricular paced event (LVP) before the right ventricular sensed event (RVS). In the subsequent 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 RVS. AP is an atrial paced event.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-64 Biventricular sense response.

If a right ventricular sensed event (RVS) occurs, one option is for a left ventricular event to occur almost immediately to promote biventricular pacing; AS, atrial sensed event; AP, atrial paced event; LVP, left ventricular paced event; RVP, right ventricular paced event; VAI, ventriculoatrial interval.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Interventricular Timing Delay

Analogous to the A-V interval in atrioventricular delay, there may be delay between pacing in the right and left ventricles (interventricular delay). Several permutations of the relationship exist between the RV and LV timing based on the role of BiV or unipolar sensing. With RV sensing alone, which is predominantly the case in most current devices, the RV-LV interval may be positive, negative, or zero (Fig. 28-65) Several studies have demonstrated clinical or hemodynamic benefits of adjusting interventricular delay in patients who were classified as “nonresponders” to conventional CRT. Various echocardiographic Doppler parameters and timing intervals have been used to assess interventricular dyssynchrony, and tissue Doppler imaging (TDI) has been used to determine intraventricular dyssynchrony for V-V optimization. The introduction of delay raises several theoretical issues. As discussed further in the context of univentricular sensing and biventricular pacing, an interventricular delay may increase the risk of ventricular tachycardia from an unsensed, improperly timed ventricular depolarization.

Figure 28-65 Biventricular RV-LV interval.

The RV-LV interval may be positive, negative, or zero; AS, atrial sensed event; LVP, paced left ventricular 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. Pacing Clin Electrophysiol 25:62-75, 2002.)

Lower Rate Behavior

As in dual-chamber pacing, a lower rate limit is established. Atrial pacing will occur if an intrinsic atrial event does not occur at the LRL. A combination of events may initiate ventricular events. In current devices, both ventricles may be paced, but timing is based on the right ventricle only. One can theorize that more combinations are possible, such as pacing both ventricles but using the right ventricle, left ventricle, or both ventricles for ventricular timing.

Univentricular Sensing and Biventricular Pacing

Sensing may occur in one ventricle as it does in dual-chamber pacing. Usually, ventricular tachycardia is not a risk from competitive pacing. For example, if LV activation occurs before LV pacing, the LV pacing stimulus would unlikely be captured (Fig. 28-66). However, a set of circumstances may 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, several scenarios may result in a greater risk of competitive pacing. In one situation an LV sensed event occurs before RV and LV pacing occurs. Because there may be a considerable interval between the intrinsic LV event and the LV pacing stimulus, the left ventricle may no longer be refractory, resulting in LV stimulation at a short coupling interval (Fig. 28-67). In another example, an unsensed premature beat that originates in the left ventricle may be followed by an RV paced event and then an LV paced event. In such a case, the RV paced event occurred before conduction from the spontaneous LV PVC to the right ventricle.

Figure 28-66 Right ventricular sensing only with positive RV-LV interval.

The right ventricle may be the only ventricular chamber sensed. There may be an intrinsic LV event that follows the RV paced event. Since the LV event is not sensed, the LV pacing stimulus will still be delivered. Because the LV stimulus occurs after the intrinsic LV events, the LV stimuli are unlikely to capture. AP, Atrial paced event; LVP, left ventricular 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. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-67 Right ventricular sensing only with premature left ventricular extrasystoles.

The right ventricle may be the only ventricular chamber sensed. A spontaneous premature ventricular complex (PVC) originating in the left ventricle will not be sensed if there is a significantly prolonged and negative RV-LV interval. Therefore the left ventricular pacing combined with the spontaneous LV sensed event may result in ventricular proarrhythmia. AS, Atrial sensed event; LVP, left ventricular 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. Pacing Clin Electrophysiol 25:62-75, 2002.)

Biventricular Sensing with Univentricular Pacing

It is possible for a device to be programmed to have BiV sensing but only to pace from one ventricle, such as the left ventricle. In this case a sensed LV event might result in inhibition of LV pacing and resetting of the VA timing cycle (Fig. 28-74). If an RV sensed event occurred first, the LV paced event might be inhibited, resetting the timing cycle (Fig. 28-75), or might result in an LV paced event immediately, to minimize the delay after the RV sensed event (Fig. 28-76).

Figure 28-74 Biventricular sensing and unipolar pacing.

Sensed events in the left ventricle result in inhibition and reset the timing cycle. AS, atrial sensed event. AP, atrial paced event; AVI, atrioventricular interval; LVP, left ventricular paced event; LVS, left ventricular sensed event; VAI, escape interval. Parentheses indicate that pacing is not delivered because of refractoriness.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-75 Biventricular sensing and unipolar pacing.

Left ventricular paced events reset the timing cycles. Right ventricular sensed events also reset the cycle, inhibiting left ventricular pacing. AS, atrial sensed event; AVI, atrioventricular interval; RVP, right ventricular paced event; RVS, right ventricular sensed event; VAI, escape interval. Parentheses indicate that pacing is not delivered because of refractoriness.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-76 Biventricular sensing and unipolar pacing.

Left ventricular paced events reset the timing cycles. Right ventricular sensed events result in triggering a left ventricular paced event. AS, atrial sensed event; AVI, atrioventricular interval; LVP, left ventricular paced event; RVP, right ventricular paced event; RVS, right ventricular sensed event; VAI, escape interval.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Upper Rate Behavior

The primary purpose of upper rate behavior in traditional dual-chamber pacing is to prevent rapid atrial tracking during atrial tachycardia. The maximum tracking rate 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, pseudo-Wenckebach behavior occurs as the atrial rate increases and exceeds the MTR before 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 BiV pacing. Most patients who need CRT have intact AV conduction, so pacemaker-Wenckebach behavior should be avoided because extension of AVI allows sensing inhibition and prevents BiV 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% BiV pacing, TARP should be sufficiently short and the MTR should be sufficiently high.

Premature Beats and Biventricular Timing Cycles

A premature ventricular beat is defined as a ventricular sensed event without a preceding paced or sensed atrial event. In dual-chamber timing cycles, a premature ventricular beat (complex, contraction, PVC) occurring in the V-A interval (VAI) would reset the atrial escape interval (AEI) in ventricular-based timing devices. The presence of PVC provides special challenges in a BiV system. The PVC PVARP extension algorithm automatically lengthens PVARP to protect against potential PMT. However, such PVARP extension can cause subsequent functional atrial undersensing and loss of BiV pacing. Thus, the PVC PVARP extension function should be deactivated in a BiV 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. Approaches include a system that uses single-chamber sensing only, a cross-chamber (RV-LV) refractory period after the first ventricular sense, or a ventricular triggering mode in the opposite chamber. In a RV sense, LV refractory system, a PVC could have RV sensing in the VAI that resets the AEI; the subsequent ventricular pacing (AEI + AVI) can occur “asynchronously” shortly after the delayed, nonsensed LV activation. Such improperly timed pacing stimulus may induce ventricular arrhythmia. A cross-chamber trigger mode on PVC would require an upper rate limit to avoid tightly coupled stimulation that may induce ventricular arrhythmia.

Refractory Periods and Biventricular Pacing

Refractory periods are present after sensed or paced events. In early BiV devices with RV and LV leads in parallel via a Y-connection, a single ventricular depolarization may be sensed by both RV and LV leads. With BiV sensing, the PVARP could be reset by the second component of the ventricular sensed (usually LV) signal. In such cases of late LV sensing, the PVARP and TARP are effectively extended by an interval that equals the interventricular sensing delay (RV-LV). Such prolonged TARP could greatly reduce the atrial sensing window for atrial tracking.

The newer BiV devices use dedicated RV sensing only, with pacing from both right and left ventricles. After RV or LV pacing, a cross-chamber refractory period may be created. If there is a delay in the LV-RV interval, the total sensed refractory period may be prolonged. 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 ventricular refractory period may be quite long. This prolonged sensing refractoriness can compromise detection of ventricular tachyarrhythmias.

Loss of Biventricular Pacing

Because the hemodynamic consequences may be significant, it is important to identify possible causes of loss of BiV pacing.⁵⁸ BiV pacing may be lost when A-V conduction becomes more rapid and the RV sensed event occurs within the A-V interval (Fig. 28-77). BiV pacing may be lost when 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 sensed A-V delay (TARP = AVI + PVARP) or above the maximum atrial tracking interval. The P wave will not be tracked, so conduction will occur. Because the resultant QRS complex will initiate a PVARP, the next P wave will fall within the PVARP. In this situation the programmed A-V interval is less than the intrinsic P-R interval, and thus the onset of loss of BiV pacing requires a faster atrial rate than the rate at which BiV pacing will be restored. BiV pacing will not be restored until the atrial cycle length is greater than the sum of the PVARP and the PR interval, called the intrinsic total atrial refractory period (ITARP). In patients with prolonged P-R interval, ITARP may be significantly longer than TARP. Once atrial undersensing in PVARP occurs during atrial tachycardia, loss of BiV pacing is perpetuated and may be restored only at much slower atrial rates. Restoration of BiV pacing will occur when the P wave following the last conducted QRS complex falls outside the PVARP. The relationship between atrial rate and loss of BiV pacing is shown diagrammatically in Figure 28-78. The ability to shorten the PVARP (indicated by PVARP’) may restore tracking of atrial sensed events and may restore BiV pacing (Fig. 28-79). Atrial premature beats with conduction may cause a similar phenomenon by causing atrial undersensing and loss of BiV pacing.⁵⁹

Figure 28-77 Biventricular pacing and sensing.

More rapid AV conduction results in a right ventricular sensed event. AS, Atrial sensed event; AP, atrial paced event; AVI, atrioventricular interval; LVP, left ventricular paced event; LVS, left ventricular sensed event; RVP, right ventricular paced event; RVS, right ventricular sensed event, VAI, escape interval.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-78 Relationship between atrial rate and presence of biventricular pacing.

As the atrial rate reaches the total atrial refractory period (TARP) (PVARP + PV), BiV pacing will stop. When the atrial rate falls to intrinsic TARP (ITARP = PVARP + P-R interval), BiV pacing resumes. LRL, Lower rate limit, x-axis, atrial rate; y-axis, biventricular rate; MTR, Maximum tracking rate.

(From Wang P, Kramer A, Estes NA 3rd, Hayes DL: Timing cycles for biventricular pacing. Pacing Clin Electrophysiol 25:62-75, 2002.)

Figure 28-79 Biventricular pacing is lost when sinus rates exceed the maximum tracking rate and is restored when the PVARP is shortened. AS, atrial sensed event; LVP, left ventricular paced event; LVS, left ventricular sensed event; PVARP, postventricular atrial refractory period; PVARP’, PVARP shortened in response to loss of biventricular pacing; 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. Pacing Clin Electrophysiol 25:62-75, 2002.)