Pacemaker-Mediated Tachycardia

Updated: Apr 15, 2022
Author: Brian Olshansky, MD, FESC, FAHA, FACC, FHRS; Chief Editor: Jose M Dizon, MD 



A pacemaker-mediated tachycardia (PMT) can be defined as any condition in which a pacemaker paces the ventricles at rates that are inappropriately fast.[1] This can be due to (1) a rate response setting that is too sensitive, (2) tracking of atrial noise (such as what may occur with electromagnetic interference), (3) inappropriate pacemaker manipulation with rate response turned on, or (4) tracking of an atrial tachyarrhythmia related to upper rate settings.

Traditionally, however, the term pacemaker-mediated tachycardia, also called endless-loop tachycardia, is used to refer to a form of a reentrant tachycardia and can occur in patients who have dual-chamber pacemakers. The pacemaker forms the anterograde (atrium to ventricle [A → V]) limb of the circuit and the atrioventricular (AV) node is the retrograde limb (ventricle to atrium [V → A]) of the circuit.[2] This classic form is referred to and discussed as PMT for the rest of this article.

See the electrocardiograms (ECG) below.

Pacemaker-Mediated Tachycardia. Telemetered ECG tr Pacemaker-Mediated Tachycardia. Telemetered ECG tracing with surface lead II (top) and intracardiac electrograms (atrial electrogram [center] and ventricular electrogram [lower]) and marker channel (bottom) showing pacemaker-mediated tachycardia (PMT). The intracardiac markers indicate that the retrograde P waves, labeled AS for atrial-sensed event, occur 280 milliseconds after the ventricular-paced beats, labeled VP.
Pacemaker-Mediated Tachycardia. Telemetered ECG tr Pacemaker-Mediated Tachycardia. Telemetered ECG tracing showing atrioventricular (AV)–paced rhythm at 60/min after termination of the pacemaker-mediated tachycardia (PMT). The tracing, from top to bottom, shows lead II, atrial electrogram, ventricular electrogram, and marker channels. The intracardiac markers indicate the rhythm is atrial paced (AP) and ventricular paced (VP). Note that the VP beats are ventricular pseudofusion beats.
Pacemaker-Mediated Tachycardia. This is a typical Pacemaker-Mediated Tachycardia. This is a typical example of PMT with ventricular pacing at maximum tracking rate (VP-MT) and then termination of the tachycardia as the atrial sensing (AS) is in the postventricular atrial refractory period (PVARP). This is due to PVARP extension, which is a feature of this particular pacemaker. The solid line indicates where PMT is detected and this is the point at which PVARP extension occurs. As this electrogram was detected, but not sensed to be acted upon, the ventricular tracking stopped and the tachycardia terminated. In some cases, pacemakers have a program to lengthen the PVARP after PMT detection to potentially stop the tachycardia. Alternatively, prevention of one ventricular paced beat can also stop the tachycardia. Some pacemakers use this algorithm.

Repetitive nonreentrant ventriculoatrial synchrony (RNRVAS) is a ventriculoatrial synchrony pacemaker-mediated arrhythmia that only occurs in the presence of retrograde VA conduction and dual-chamber or cardiac resynchronization devices with tracking (eg, DDD, DDDR) or nontracking pacing modes that allow AV-sequential pacing (eg, DDI, DDIR).[3]

Gjermeni et al recently reported a novel pacemaker-mediated arrhythmia that closely mimics RNRVAS but exhibits a different mechanism and was independent of VA conduction (pseudo-RNRVAS).[4] The investigators interrogated 840 dual-chamber or biventricular devices and identified 9 patients with this arrhythmia. The authors conclude that pseudo-RNRVAS is underrecognized because there are no specific device algorithms to detect and store them.[4]


The following is the most common scenario causing pacemaker-mediated tachycardia (PMT). A dual-chamber pacemaker programmed DDD or VAT, but not DDI, is implanted. The patient must have retrograde (V→A) conduction with an atrial activation time that is longer than the programmed postventricular atrial refractory period (PVARP). A ventricular-paced beat or a properly timed premature ventricular contraction (PVC) conducts retrograde via the AV node (or an accessory pathway, if present) to the atrium. If the atrial depolarization occurs after the set PVARP, but before the next timed atrial-paced beat, ventricular pacing will be triggered at the programmed AV interval.

PMT tends to occur at or near the programmed upper rate limit and depend upon the programmed AV delay and the PVARP. This generates an incessant reentrant arrhythmia circuit that persists as long as there is continuous VA conduction with atrial activation outside the PVARP. The pacemaker forms the antegrade limb of the circuit and VA conduction forms the retrograde limb as the essential critical components.[2] In many instances, the PVARP varies so that it shortens with rate. This can make PMT more likely. The AV interval can be programmed to change with the rate. This tends to reduce the risk of PMT. Depending on the pacemaker programming and the VA conduction, the rate of the PMT may vary, but it is bounded by (and generally occurs near or at) the programmed upper rate limit.

Although PMT is commonly initiated by an isolated ventricular ectopic beat, it can also be initiated by failure to capture the atrium with a paced beat followed by a ventricular paced beat. If this occurs, the atrium is then amenable to depolarization by the impulse conducted retrograde from the ventricle. The tachycardia continues until retrograde conduction ends or the atrium becomes refractory. Specific pacemaker algorithms may also terminate PMT if tracked rates persist at the upper rate limit. The pacemaker can be programmed to lengthen the PVARP after a PVC or with an incessant tachycardia at the upper rate limit or prevent one atrial sensed event from being tracked. Up to one third of patients with antegrade complete AV block have intact (or intermittent) retrograde (V→A) conduction. It has been recommended that testing for retrograde conduction be performed in all patients with AV block in order to optimize device programming and prevent PMTs.[5]

Other situations that can result in PMT include intermittent atrial undersensing. An atrial premature beat with a long A sense-V pace interval (due to a long programmed AV interval) in a patient with heart block can also initiate PMT as any antegrade concealed depolarization otherwise present cannot prevent VA conduction in this instance.[6]


Prognosis is not directly altered by an episode of pacemaker-mediated tachycardia (PMT) and is defined by the patient's underlying cardiac or medical condition.

Indirectly, in a rare event such as PMT-induced syncope, a patient could sustain injury as a result of the syncope.

Persistent PMT can cause hypotension and heart failure symptoms.


Patients may experience palpitations, rapid heart rates, lightheadedness, syncope, or chest discomfort.


PMT rarely is associated with any serious complications such as presyncope or syncope.

In many patients, the condition may be asymptomatic and is noted only with ECG or Holter monitoring.

With the appropriate programming interventions described above, the problem usually is resolved, and, in most modern pacemakers, it can be detected and treated by the device itself.

In patients who develop chest pain (angina pectoris) associated with the rapid pacing rate, consider a stress test to evaluate for coronary artery disease.



History and Physical Examination


Consider pacemaker-mediated tachycardia (PMT) in patients with a dual-chamber pacemaker (programmed DDD or VAT) who experience palpitations, rapid heart rates, lightheadedness, syncope, or chest discomfort. However, the majority of patients are asymptomatic.

Physical examination

The examination findings may confirm tachycardia and may be otherwise unremarkable, except for presence of a pacemaker.[7]

Findings on ECG demonstrate intermittent or continuous ventricular-paced rhythm at or near the upper rate limit, which typically is set at 120-130 bpm.

There may be cannon A waves, hypotension, or heart failure (if episodes are prolonged and incessant).



Diagnostic Considerations

Any rapid atrial rhythm, such as atrial tachycardia, atrial flutter, or atrial fibrillation, sensed by the atrial lead, can then be tracked by the pacemaker to the upper rate limit.[8] This is confirmed when intracardiac electrograms are examined or by evaluation of the underlying rhythm. In unipolar pacemakers, myopotentials from the chest wall muscles or electromechanical signals from an electrocautery device in the operating room may be oversensed and also may drive the pacemaker to the upper rate limit.[9]

Extremely rare, but of concern, in older pacemakers, the pacemaker circuitry may malfunction, resulting in a runaway pacemaker in which the pacemaker paces the heart at a very rapid rate and this cannot be programmed off.[10] All the above problems require active involvement of the pacemaker to maintain the tachycardia but are not reentrant in nature and so not considered classic pacemaker-mediated tachycardia.



Other Tests

Ventricular pacing at or near the upper rate limit of the pacemaker is evident on electrocardiography (ECG). The presence of a paced rhythm exactly at the upper rate limit with atrial sensing and exact A-V association warrants evaluation for pacemaker-mediated tachycardia (PMT).

A Holter monitor or event recorder also shows ventricular pacing at or near the upper rate limit and the initiation of the episodes. In the differential diagnosis of PMT, sinus and tracked atrial tachyarrhythmias must be considered. Monitoring of episodes, their initiation, and termination will help arrive at a diagnosis.

Telemetered intracardiac electrograms obtained through the pacemaker programmer generally indicate the diagnosis.



Medical Care

Treatment, prevention, and termination of pacemaker-mediated tachycardia (PMT) typically involves altering the pacemaker programming to prevent sensing of the retrograde P wave. This is most easily done by prolonging the postventricular atrial refractory period (PVARP). During the PVARP, the atrial lead does not sense any atrial activity; hence, ventricular pacing is not triggered. Note that prolonging PVARP may affect the upper tracking rate of the pacemaker, which is defined by the total atrial refractory period (TARP), ie, TARP = AV delay + PVARP. For example, if the AV delay is 180 milliseconds (ms) and the PVARP is increased from 320 to 420 ms, the TARP then changes from 500 ms (120 bpm) to 600 ms, which corresponds to an upper rate of 100 bpm (rate = 60,000/cycle length [ms]). This means that the pacemaker will not track atrial rates above 100 bpm and could lead to 2:1 block at rates ≥100 bpm in patients with heart block. In some pacemakers, the upper tracking rate can be programmed independently from the upper rate based on rate response.

In acute situations, when a patient is very symptomatic, regardless of the pacemaker model or when a programmer is unavailable, applying a magnet over the pacemaker inhibits sensing and makes the pacemaker pace asynchronously in the atrium and ventricle, thus terminating the PMT by blocking the antegrade limb of the circuit (by prevention of atrial tracking).[7] Carotid sinus massage or AV nodal blocking drugs such as adenosine, verapamil, or beta-blockers can block VA conduction (ie, retrograde conduction) directly and can terminate PMT.

Reprogramming a dual-chamber, dual-mode, dual pacing, dual-sensing (DDD) pacemaker to AAI, VVI, or DVI (DDI) abolishes the PMT reentrant circuit, thereby prohibiting PMT from occurring. These other programming modalities can lead to serious problems as DDD pacing may be necessary (consider the difficulty of AAI pacing in a patient with complete heart block).

Atrial sensitivity may be programmed so that sinus P waves are detected but not retrograde P waves (which can be smaller).[11] The downside of this approach is that intrinsic P-wave amplitude can be lower at higher rates, which could potentially result in atrial undersensing.[12] Making sure that atrial capture is adequate is also important. Attempting to adjust sensitivity is generally impractical.

Most modern dual-chamber pacemakers are capable of detecting PMT and initiating PMT intervention by automatically prolonging the PVARP for the beat after a ventricular-sensed event that is not preceded by atrial pacing, ie, a PVC (PVARP extension). This problem also can be minimized by the use of adaptive PVARP in rate-responsive (DDDR) pacemakers; the PVARP is long when the patient is at rest and shortens when the sensor indicates activity, allowing the pacemaker to track higher atrial rates with minimal risk of PMT.

Other pacemaker algorithms include dropping a ventricular-paced beat when the pacemaker is pacing at the maximum tracking rate for a specific period of time or shortening the AV interval for a single beat to induce retrograde AV block and terminate the tachycardia. Finally, the nonatrial sensing modes (DDI, VAT) can address both PMT and rapid ventricular rates in association with atrial arrhythmias. However, these modes do not allow AV synchrony in association with sinus rates greater than the programmed (usually lower) rate. These modes may be most useful when the sinus rate is known to be slower than the planned ventricular rate under most conditions.

Once adequate measures are taken to eliminate PMT, inpatient care is not necessary.



Medication Summary

Pacemaker-mediated tachycardia (PMT) is treated by reprogramming the pacemaker. If this is not possible, in some instances, medication to block retrograde conduction may be needed. In rare circumstances, ablation of retrograde conduction pathway (AV node or accessory pathway) is necessary.