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

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