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Unexpected rhythms with normally functioning dual-chamber pacing systems

Unexpected rhythms with normally functioning dual-chamber pacing systems
Literature review current through: Jan 2024.
This topic last updated: Jul 22, 2022.

INTRODUCTION — A variety of electrocardiographic findings and rhythms may be encountered in which the pacing system is functioning normally. These include crosstalk, pacemaker-mediated or endless loop tachycardias, and repetitive nonreentrant ventriculoatrial synchronous rhythms. These might be considered functional system malfunctions since the resulting arrhythmia may be deleterious to the patient, although the device is functioning normally and in accord with its programmed specifications.

A comprehensive discussion of the normal function and programming of permanent pacemakers is presented separately. (See "Permanent cardiac pacing: Overview of devices and indications" and "Modes of cardiac pacing: Nomenclature and selection".)

CROSSTALK

Basic concepts — In a DDD pacemaker, a paced or sensed event in one channel initiates one or more timing circuits in the opposite channel. As a result, the release of an atrial output pulse will initiate an atrioventricular (AV) delay, which will permit a ventricular output pulse at the end of this interval if an R wave is not sensed. Concepts related to the AV interval are easiest to understand if the AV interval is not considered as a single interval but as having three distinct portions (figure 1 and figure 2 and figure 3):

The portion that begins immediately with the atrial output pulse is the "postatrial ventricular blanking period" during which the ventricular sensing channel is disabled and anything occurring in this relatively short interval will not be seen.

The second portion of the AV interval is called the "crosstalk sensing window" or "safety pacing window" and if an event is sensed during this portion of the AV interval, a foreshortened AV interval will occur if safety pacing is turned "on."

The final or third portion of the AV interval is the "alert period" and if an event is sensed on the ventricular sensing channel during this period, ventricular pacing output will be inhibited.

Current pacing systems, however, are incapable of recognizing morphologic characteristics of a complex. Any intrinsic complex, output decay, or artifact of electromagnetic interference of sufficient amplitude and frequency response that it is not filtered out by the sense amplifier is treated as a true signal. Although bipolar sensing configuration is believed to minimize far-field sensing, crosstalk can be seen with any sensing configuration. If any signal is interpreted as an R wave, and inhibits the ventricular output and resets the escape interval, the phenomenon is termed crosstalk-mediated ventricular output inhibition.

When AV nodal conduction is otherwise intact, crosstalk is asymptomatic. If there is first degree AV block, the effective paced rate may be slower than the programmed base rate, because the conducted R wave will occur after completion of the ventricular refractory period initiated by the oversensing of the atrial stimulus. The conducted R wave will be sensed, thereby resetting the atrial escape interval yet again. A clinical catastrophe may occur in the presence of complete AV block combined with crosstalk (in the absence of safety-pacing), as the system will effectively pace the atrium, but the ventricular output may be repeatedly inhibited, leaving the patient asystolic.

Predisposing factors — Factors that predispose to crosstalk associated with the atrial output include a high atrial output (either pulse amplitude, pulse duration, or both), the ventricular sensing channel programmed to a very sensitive setting, and a short post-atrial ventricular blanking period. The post-atrial ventricular blanking period is a short interval of absolute refractoriness initiated in the ventricular sense amplifier upon completion of the atrial escape interval. It is designed to coincide with the atrial output pulse and initial decay of this output. The intent of the blanking period is to prevent sensing of the atrial stimulus and, hence, prevent crosstalk. Ventricular blanking periods are usually programmable. Lengthening the ventricular blanking period may avoid crosstalk.

Prevention — An effective method to prevent crosstalk is to lengthen the post-atrial ventricular blanking period. However, a premature ventricular complex/contraction (PVC; also referred to as premature ventricular beats or premature ventricular depolarizations) that occurs within the ventricular blanking period may not be sensed if the intrinsic deflection of the PVC occurs during the blanking period. Events that are not sensed during the blanking period are a form of functional undersensing. This has the potential for inducing an adverse rhythm triggered by competition. Upon termination of the blanking period, the AV interval timer is allowed to complete, because nothing was sensed by the pacemaker, and a ventricular output pulse will be released. Depending upon the AV interval, this may place a ventricular stimulus on the apex of the T wave (ie, the vulnerable period) and may induce pathologic ventricular tachyarrhythmias in the electrically unstable patient. Thus, the extended blanking period could have an adverse effect, even though the pacing system is functioning in accord with its design and programmed parameters and the occurrence of crosstalk has been effectively prevented. Periods of forced inability to sense or inability to react to a sensed event (ie, refractory periods and blanking periods) should generally be kept as short as possible.

Since the blanking periods for dealing with crosstalk may be associated with potential problems, a special detection or sensing window on the ventricular channel that immediately follows the blanking period has been incorporated into dual-chamber pacing systems. If an event is sensed during this crosstalk detection window, the logic incorporated in the pacemaker will treat this as if it were true crosstalk. The event sensed during this special detection window causes the ventricular circuit to trigger a ventricular output pulse at the end of an abbreviated AV interval (approximately 110 milliseconds) rather than inhibiting its output. This abbreviated AV interval will result in nonphysiologic AV sequential pacing, but will protect the patient from asystole in the presence of crosstalk combined with complete heart block.

If the sensed event were a true R wave, particularly a PVC, the pacing stimulus occurring at a short AV interval would likely occur when the ventricular myocardium is physiologically refractory and would neither capture nor induce any dangerous arrhythmias. The overall phenomenon is generically called "safety pacing." In many pacing systems, this is a programmable parameter that can be enabled or disabled.

INAPPROPRIATE MODE SWITCH — Dual-chamber pacemakers capable of "tracking" the atrial rhythm recognize very rapid atrial rates and initiate mode switch to a nontracking mode when specific criteria are met. If the pacemaker senses nonphysiologic activity on the atrial channel (eg, noise) or inappropriately senses ventricular activity on the atrial sensing channel, (termed far field R wave [FFRW] sensing) [1], the detected atrial rate may not represent a true atrial tachyarrhythmia. If this artificially detected atrial rate meets criteria for the mode switch algorithm, inappropriate mode switching will occur.

PACEMAKER-INITIATED TACHYCARDIA — Pacemaker-initiated tachycardia can occur when competition, due to undersensing, functional or otherwise, triggers a native tachycardia [2]. Once the tachycardia is initiated, the pacemaker becomes an innocent bystander, being inhibited by the native arrhythmia.

PACEMAKER-MEDIATED TACHYCARDIA — A pacemaker-mediated tachycardia (PMT) is a tachycardia that can only be sustained by the continued active participation of the pacemaker.

Pacemaker-mediated tachycardia — The classic form of pacemaker-mediated tachycardia requires retrograde conduction from the ventricle to the atrium via the AV node and sensing of the retrograde P waves during the atrial alert period. When all of these events occur in succession, the atrial sensing event triggers another ventricular pacing event, which perpetuates the cycle of "endless loop tachycardia" [3].

Most individuals with a normal heart are capable of demonstrating retrograde conduction in the appropriate circumstances. It does not occur during the normal synchronization between the atrium and ventricle, because atrial and AV nodal depolarization renders these tissues physiologically refractory.

PMT is commonly initiated by premature ventricular complexes (PVCs) that occur prior to the anticipated P wave. PVCs that occur in this interval can cause retrograde conduction if the AV node and atrial tissue have recovered sufficiently to allow for conduction. Other events that may initiate PMT include atrial undersensing or oversensing and loss of atrial capture.

There are two manifestations of PMT that are most commonly seen:

The classic form, which results in ventricular pacing at the programmed maximum tracking rate. The sensed P wave is tracked, but the programmed AV interval is extended to delay release of the ventricular output pulse until the maximum tracking rate interval times out. This allows the atrial and AV nodal tissue to physiologically recover, enabling them to be depolarized by the next paced ventricular beat.

A "balanced" PMT. If retrograde conduction is sufficiently slow and the combination of the retrograde ventricular paced beat to P wave and anterograde intervals exceeds the maximum tracking rate, a PMT can result that is slower than the maximum tracking rate.

Management of PMT — Although there are a number of management options to prevent or terminate a PMT, the one way to prevent an PMT is to program the postventricular atrial refractory period (PVARP) sufficiently long to prevent the pacemaker from sensing and hence tracking the retrograde P wave. Extending the PVARP does not prevent retrograde conduction. A longer PVARP effectively lengthens the total atrial refractory period (TARP), thereby limiting the maximum atrial rate that can be sensed and tracked. If the reduction in the maximum paced atrial rate is not a clinical concern for the patient, increasing the length of the PVARP is often a definitive solution.

However, many clinicians want the pacemaker to have a mean tracking rate that is higher than that allowed by programming a long PVARP. Since PMT is frequently initiated by PVCs, manufacturers have incorporated automatic PVARP extensions following a PVC. For a pacemaker, a PVC is defined as a sensed ventricular event (R wave) that is not preceded by any paced or sensed atrial activity. The various automatic PVARP extensions, while often effective, may simply postpone the PMT for one cycle or, result in sustained pacemaker inhibition when the P wave is able to conduct with a first-degree AV block. The P wave is not seen by the pacemaker because it coincides with the PVARP. The resultant native ventricular depolarization, which is due to anterograde conduction, is called a PVC by the pacing system, reinitiating the longer PVARP for that cycle and sustaining the pacemaker inhibition. However, since PVCs are not the only trigger for an PMT, this automatic post-PVC PVARP extension algorithm is usually only a partial solution.

If permanently increasing the PVARP to a sufficient degree to prevent sensing of the retrograde P wave is not an option for prevention of PMT, a variety of tachycardia termination algorithms have been developed. As an example, when the device senses possible PMT, it can algorithmically inhibit ventricular pacing for a single beat, temporarily extend the PVARP, temporarily alter other timing intervals, or combine such maneuvers in an attempt to terminate PMT.

REPETITIVE NONREENTRANT VENTRICULOATRIAL SYNCHRONOUS RHYTHMS (AV DESYNCHRONIZATION ARRHYTHMIA) — Dual-chamber AV sequential pacing at relatively rapid rates, whether driven by the rate-adaptive sensor or associated with a relatively high programmed base rate, sets the stage for an AV desynchronization arrhythmia, also called repetitive nonreentrant ventriculoatrial synchronous rhythms (RNRVAS), that may be hemodynamically deleterious and cause symptomatic palpitations [4]. The occurrence of this arrhythmia requires intact retrograde ventricular paced conduction [5]. The pacing system is functioning normally in accord with its programmed parameters.

Mechanism — At the onset of RNRVAS, an event occurs that triggers one cycle of AV dissociation, resulting in retrograde conduction. The retrograde P wave coincides with the postventricular atrial refractory period (PVARP), precluding it from being sensed. This is intentional and functional undersensing. Hence, a PMT does not occur. However, the atrial depolarization renders the atrial myocardium physiologically refractory. As a result, there may be failure to capture with the next atrial stimulus, which occurs at the end of a relatively short atrial escape interval since the pacing rate is high and in close proximity to the intrinsic atrial depolarization. This is functional atrial noncapture. The time from the atrial depolarization to the ensuing ventricular stimulus occurring at the end of the AV interval provides sufficient time for the atrial myocardium to recover, thereby allowing retrograde conduction to occur. This can result in a rhythm in which there is sustained retrograde conduction, followed each time by an ineffective atrial stimulus.

The patient may experience palpitations from the retrograde conduction as the atrium contracts against a closed mitral and tricuspid valve, inducing cannon A waves. In addition, there may be hypotension and hemodynamic compromise due to the loss of optimal AV synchrony. This is, by definition, pacemaker syndrome.

Prevention — Prevention of an RNRVAS requires minimizing the duration of the refractory periods, allowing all native events to be sensed. If this results in a PMT, then a tachycardia termination algorithm should be used to terminate the PMT. If AV desynchronization arrhythmia is consistently enabled by a true premature ventricular complex (PVC), then a more specific post-PVC PVARP extension algorithm will prevent it. Most PVARP extensions lengthen the PVARP but do not alter the basic pacing interval that will simply sustain this problem because the atrial output pulse will still occur at a time when the atrial myocardium is physiologically refractory.

A "+PVARP on PVC" algorithm lengthens the PVARP and adds an obligatory atrial alert period following the end of the extended PVARP. As a result, despite the programmed or sensor-driven AV pacing rate, the pacemaker is disabled in favor of an atrial escape interval defined by the "+PVARP on PVC" algorithm for this one cycle. When an atrial stimulus occurs at the end of this atrial escape interval, the atrial myocardium will have physiologically recovered, assuring atrial capture and preventing this arrhythmia. If a native P wave occurs during the atrial alert period, it is sensed and tracked. Either a paced or sensed atrial event will terminate this algorithm and return the pacing system to its previous functional state.

FUNCTIONAL SINGLE-CHAMBER ATRIAL PACING — Many patients who require a pacemaker have AV conduction that is prolonged but intact. Such patients may pace their right ventricle a high percentage of the time. It is well recognized that unnecessary ventricular pacing may increase the incidence of both atrial fibrillation and congestive heart failure [6-10].

When AV nodal conduction is prolonged, but intact, and the QRS width is normal, programming the pacemaker to minimize ventricular pacing (ie, functional single-chamber atrial pacing) is recommended. A number of techniques are used to achieve this end, and these may produce unexpected rhythms.

Long programmed AV delay — One can achieve functional single-chamber atrial pacing by simply programming a very long AV delay (ie, the amount of time after an atrial beat that the pacemaker will wait to sense an intrinsically conducted QRS before pacing the RV). This is a simple approach that can be limited by the pacemaker sensing the intrinsic RV activation late in the QRS. Thus, even if the PR interval is only slightly prolonged, the RV lead may not sense the QRS until more than 300 msec after the P wave. In such cases, it may be difficult or impossible to program a long enough AV delay to avoid ventricular pacing.

Many patients with mild or moderate PR prolongation would do well most of the time with native conduction, and markedly reduced frequency of RV pacing.

Ventricular hysteresis — With this feature, a basic AV delay is set, but periodically the system extends the AV delay by a programmed amount [11-13]. If a native QRS is sensed during this extended interval, the pacemaker will continue to function with this longer AV delay, allowing native conduction and minimizing ventricular pacing. If AV block worsens, and ventricular pacing is again required, the pacemaker will return to the original, shorter AV delay for a period of time, then it will repeat the test with the longer AV delay.

AAI/DDD pacing — AAI/DDD pacing is the most commonly used technique to minimize ventricular pacing. There are subtle differences among the algorithms available [14,15], but the basic design is similar. These devices will initially function as a single-chamber, AAI pacemaker, but with continuous ventricular sensing. The system will not attempt to pace the ventricle unless sustained AV block develops (ie, it will allow long PR intervals, the maximum length being programmable or defined by the algorithm, and even one or two nonconducted P waves [dependent on algorithm]). If loss of AV conduction is sensed, the pacemaker will switch to DDD pacing for some period of time until the algorithm once again looks for intrinsic AV conduction. The rationale for this approach is that most patients will tolerate isolated pauses, and that it is more important to minimize ventricular pacing than it is to ensure that every P wave is followed by a sensed or paced QRS. (See "Modes of cardiac pacing: Nomenclature and selection", section on 'Modes to minimize ventricular pacing'.)

An example of a ventricular pacing avoidance algorithm in the setting of AV block is shown based on recordings from a Holter monitor (waveform 1). Intermittent AV block was present that was not associated with ventricular pacing, but this is consistent with the normal behavior of this algorithm. On the atrial paced beat following a cycle of AV block, ventricular pacing occurs at a foreshortened AV delay of 80 ms despite the programmed AV delay. Sustained AV block will result in a reversion to the DDD mode.

As a result of the AV dissociation that may occur as the result of a ventricular pacing avoidance algorithm, pacemaker syndrome may occur [16].

Similarly, algorithms that promote atrial pacing by AV interval extension have also resulted in the occurrence of pacemaker-mediated tachycardia [12,17].

VENTRICULAR ARRHYTHMIAS — Ventricular tachycardia (VT) and ventricular fibrillation (VF) are often preceded by abrupt changes in ventricular cycle lengths (ie, the interval between successive ventricular beats). These events are referred to as short-long-short (SLS) sequences. A common example of an SLS sequence involves premature ventricular complexes (PVCs). The "short" interval between a normal beat and a PVC is followed by a "long" interval before the next normal beat. A SLS sequence occurs if a second PVC occurs after this "long" interval. Such events produce changes in both the activation sequences and refractory periods of ventricular myocardium and the His-Purkinje system, and these alterations increase vulnerability to the onset of VT and VF.

Normal single- and dual-chamber pacing can create SLS sequences that have the potential to trigger VT or VF [18,19]. Such events can occur in a variety of settings, usually due to the response of pacemaker algorithms to atrial and/or ventricular ectopy. The incidence of SLS induced VT or VF in pacemaker patients is unknown, but is rarely recognized clinically. In the cohort of implantable cardioverter-defibrillator (ICD) patients discussed below, pacemaker facilitated ventricular arrhythmias occurred in 1 to 4 percent of patients [19]. Because these patients were already known to be at high risk for such arrhythmias, the incidence in the general population of pacemaker patients is probably substantially lower.

Pacing algorithms that maximize native conduction and minimize ventricular pacing can allow relatively long ventricular pauses. Thus, it can be theorized that these pacing modalities may increase the risk of ventricular arrhythmias [20]. However, such an increased risk was not shown in a retrospective analysis of 1055 patients from two large ICD trials [19]. Among patients whose devices were programmed DDD, VVI, and managed ventricular pacing modes, VT and VF episodes associated with pacemaker-facilitated SLS sequences occurred in 5.2, 3.3, and 2.6 percent, respectively. (See 'Functional single-chamber atrial pacing' above and "Modes of cardiac pacing: Nomenclature and selection", section on 'Modes to minimize ventricular pacing'.)

Because a ventricular pause is central to the SLS sequence, pacing strategies that minimize such pauses have been proposed as a method for reducing the risk of ventricular arrhythmias. However, such approaches have not proven successful [18,21]. This failure appears to be due to the relatively short pauses (eg, <1 second), and small changes in cycle length (eg, 40 to 200 msec) that are required to trigger ventricular arrhythmias [19,22].

SUMMARY AND RECOMMENDATIONS

When an unexpected rhythm is observed in a patient with a dual-chamber pacing system, applying the following questions should provide a basis to understanding and managing unexpected rhythms:

Is the pacing system functioning normally or not?

Is the unexpected rhythm initiated by the pacemaker, mediated by the pacemaker, or a result of a specific pacing algorithm?

To fully appreciate the variations that can occur as a result of company specific algorithms, is the provider aware of any algorithms that are programmed "on" and thoroughly understand how these algorithms function?

Detailed discussion of identification and management of specific unexpected rhythms with dual-chamber pacing occurs in the body of the topic.

Crosstalk. (See 'Crosstalk' above.)

Inappropriate mode switch. (See 'Inappropriate mode switch' above.)

Pacemaker-initiated tachycardia. (See 'Pacemaker-initiated tachycardia' above.)

Pacemaker-mediated tachycardia (PMT). (See 'Pacemaker-mediated tachycardia' above.)

Repetitive nonreentrant ventriculoatrial synchronous rhythms (RNRVAS). (See 'Repetitive nonreentrant ventriculoatrial synchronous rhythms (AV desynchronization arrhythmia)' above.)

Functional single-chamber atrial pacing. (See 'Functional single-chamber atrial pacing' above.)

Ventricular arrhythmias. (See 'Ventricular arrhythmias' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges David L Hayes, MD, who contributed to earlier versions of this topic review.

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