Continuing Education Activity

Pacemaker mediated tachycardia is a type of arrhythmia that happens in patients with dual-chamber pacemakers due to reentry. Patients who develop this arrhythmia can develop palpitations, dizziness, or even syncope. The cornerstone of management involves reprogramming of the pacemaker to increase the atrial refractory period. This activity describes the pathophysiology, evaluation, and management of pacemaker mediated tachycardia and highlights the role of the interprofessional team in the care of patients with this condition.

Objectives:

• Identify the etiology and epidemiology of pacemaker mediated tachycardia.
• Describe the pathophysiology of pacemaker mediated tachycardia.
• Outline the typical management options for patients with pacemaker mediated tachycardia.
• Summarize the importance of collaboration and communication amongst the interprofessional team to promptly diagnose and manage patients with pacemaker mediated tachycardia.

Introduction

Pacemaker mediated tachycardia (PMT) generally refers to all tachyarrhythmias in which the pacing device plays a major role. There are various conditions that can lead to the development of this type of arrhythmia, including tracking of an atrial tachyarrhythmia (atrial tachycardia or sinus tachycardia) or tracking of electromagnetic interference. However, classically PMT or endless loop tachycardia (ELT) usually denotes a form of reentrant tachycardia that is encountered in patients with dual-chamber pacemakers, in which the pacemaker forms the antegrade limb, and the AV node (or an accessory pathway) forms the retrograde limb of the reentrant circuit.

Etiology

There are several factors that are integral to the initiation and maintenance of pacemaker mediated tachycardia: 

• The pacemaker has to be in a pacing configuration where it senses the atrium and paces the ventricle (DDD or VAT mode). This is why this form of tachyarrhythmia does not happen in single-chamber pacemakers or with other pacing modes like VVI or AAI.

• There needs to be an event that dissociates the P wave from the QRS complex and triggers the tachycardia. In most instances, this is a premature ventricular contraction or premature atrial contractions, but it can also occur when there is an intermittent loss of atrial sensing or loss of atrial capture.

• There has to be retrograde conduction through either the AV node or an accessory pathway.

• The ventriculoatrial (VA) conduction needs to be long enough that it is able to be sensed by the atrial lead, meaning that it lasts beyond the atrial refractory period.

Epidemiology

The cornerstone mechanism of pacemaker mediated tachycardia, which is retrograde VA conduction, is observed in about 30-80% of patients with pacemakers. It is more common in patients with sick sinus syndrome and AV block, among other indications for pacemaker implantation.

One study reported that around 20% of patients where VA conduction is present and 6% of all patients with pacemakers had at least one documented episode of pacemaker mediated tachycardia.[1][2]

Pathophysiology

The majority of dual-chamber pacemakers are programmed to allow AV sequential pacing (i.e., physiologic pacing), as this has many advantages over other pacing modes; including maintaining AV synchrony, and subsequently improving hemodynamics, reducing the risk of stroke, as well as lower incidence of pacemaker syndrome.[3][4][5]

The way DDD programming works is that when the atrial lead senses an electrical activation in the atrium (P wave), it inhibits the pacemaker and allows for normal conduction to happen. If no P wave is sensed, the pacemaker will then pace the atrium at a set lower rate. After an atrial activation is sensed or paced, a period of AV delay starts, during which if there is no ventricular activation (R wave), the pacemaker will pace the ventricle, and this restarts the whole cycle again. It is important to note that after an R wave is either sensed (from spontaneous ventricular activation) or paced (by the device), the atrial lead cannot sense any electrical activation in the atrium for a prespecified period of time. This is called the post ventricular atrial refractory period (PVARP).

PMT results from retrograde conduction of a ventricular beat through the AV node (or if present, an accessory pathway). This typically happens when there is a premature ventricular beat that disrupts the normal cycle and separates the P wave from the QRS complex, thus serving as a triggering event for the tachycardia. When retrograde conduction of this ventricular beat takes place, the resulting earlier than normal atrial activation is sensed by the atrial lead, specifically if the atrial refractory period (PVARP) is passed. This earlier sensing of the P wave subsequently leads to ventricular activation with subsequent ventricular pacing after the set period of AV delay. If the retrograde conduction persists, a reentrant circuit will form with continuous ventricular activation.

PMT or endless loop tachycardia refers to this scenario where the antegrade limb of the reentrant tachyarrhythmia is the pacemaker, and the retrograde limb is the VA conduction through the AV node. Since the pacemaker constitutes the antegrade limb of the reentrant circuit, and each beat requires the presence of atrial sensing and ventricular pacing, the persistence of the tachyarrhythmia is dependent on the normal function of the pacemaker. The rate at which PMT happens is dependent on the AV delay and the VA conduction times. If, for example, a certain pacemaker is programmed to allow an AV delay of 160 milliseconds before pacing the ventricle, and the VA conduction time was 240 milliseconds, if PMT happens, the cycle length will be 400 milliseconds or 150 beats per minute. The rate of PMT is always equal to or less than the programmed upper tracking limit.[6]

History and Physical

Presentation

Patients with PMT can present with different symptoms related to the rate of the tachycardia or to the hemodynamic consequences of it.

Symptoms may include palpitations, chest pain, dizziness, syncope, or even worsening of heart failure symptoms. In many cases, however, patients are asymptomatic.

Physical Examination

The examination may be normal and only show tachycardia. In cases where the arrhythmia persists for prolonged times, hypotension or signs of heart failure may be evident.

Evaluation

PMT should be considered in any patient with a dual-chamber pacemaker presenting with tachycardia. EKG done during the episodes shows ventricular pacing at or slightly below the upper rate limit, with atrial sensing and A-V association.

Definitive diagnosis is achieved by performing device interrogation and examining the telemetered intracardiac electrograms. This will show retrograde conduction with atrial sensed beats following ventricular paced beats, whereas in normal situations, the atrial sensed beats should precede ventricular pacing.

Treatment / Management

Acute termination of PMT is achieved by applying a magnet to the pacemaker pocket. Pacemakers are, in general, programmed to respond to magnet application by switching to asynchronous pacing mode, meaning that the pacemaker will only pace at a set rate and will not track atrial activity. This will terminate the tachycardia by removing the antegrade limb of the reentrant circuit.

Other temporizing measures include carotid massage or medications that act as AV nodal blockers (digoxin, beta-blockers, and non-dihydropyridine calcium channel blockers), which can prevent the tachycardia by slowing VA conduction and thus blocking the retrograde limb of the circuit.

However, the most definitive management is the reprogramming of the pacemaker to prevent the recurrence of PMT. One easy way of doing so is to lengthen the PVARP since, as discussed earlier, a retrogradely conducted ventricular beat can only be sensed by the atrial lead if the PVARP has passed. By increasing the duration of PVARP, there is less likelihood that retrograde conduction will be sensed, and PMT will be triggered. Another option would be changing the sensitivity of the atrial lead, so that sinus P waves are sensed, but not retrograde P waves.[7]

Modern pacemakers have certain manufacturer-specific algorithms that allow detection and early termination of PMT. Including the use of adaptive PVARP in pacemakers with rate response, automatically prolonging the PVARP after an earlier than normal ventricular activation (PVC) is sensed, or dropping a ventricular paced beat after the pacemaker had been pacing at the maximum tracking rate for a specific period of time.[8]

Differential Diagnosis

Any rapid atrial rhythm, including atrial tachycardia, atrial fibrillation, or atrial flutter, can be sensed by the atrial lead and then result in ventricular pacing at the upper rate limit. This is distinguished from classic PMT by examining the underlying rhythm on the intracardiac electrograms.

Electromagnetic interferences and myopotentials from chest wall muscles can also be sensed by the pacemaker and cause pacing at the upper rate limit.

In pacemakers with rate response function, the sensor may be oversensitive or the slope of response too steep, which may result in increased pacing rates in response to low-level activities or even physiologic events.

Prognosis

Long term prognosis is typically not affected by PMT, and with the appropriate interventions mentioned above, it is easily treatable, and recurrence can be prevented. However, it is important to note that long-standing episodes can cause a worsening of heart failure due to the hemodynamic effects of tachycardia in reducing diastolic filling time.

Complications

PMT is typically not associated with long term complications. Dizziness or syncope may occur in some patients, and this may lead to head injury.

Deterrence and Patient Education

Patients with permanent pacemakers should be educated that pacing devices can be the source of a variety of abnormal rhythms, which may result in deterioration of the patient's condition. As a result, patients should be advised to follow up regularly with their electrophysiologist to have routine device checks, which can identify any abnormal events and reprogram the device accordingly. Patients should also be advised that a fast heart rate that is higher than their usual, or that is associated with symptoms like lightheadedness or chest pain needs to be taken seriously, and they should seek medical care promptly.

Enhancing Healthcare Team Outcomes

Newer pacemakers have made it possible that patients can be monitored remotely, and malfunctioning or arrhythmic episodes are identified in real-time. In the case of pacemaker mediated tachycardia, it is important that an interprofessional team consisting of the cardiac electrophysiologist, cardiac nurses, and the device company all work together in identifying this arrhythmia and informing the responsible clinician. The fact that it is easily treatable and can be prevented with simple device programming makes it more important to be identified early.

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References

1.

Barold SS. Repetitive reentrant and non-reentrant ventriculoatrial synchrony in dual chamber pacing. Clin Cardiol. 1991 Sep;14(9):754-63. [PubMed: 1720713]

2.

Richter S, Muessigbrodt A, Salmas J, Doering M, Wetzel U, Arya A, Hindricks G, Brugada P, Israel CW. Ventriculoatrial conduction and related pacemaker-mediated arrhythmias in patients implanted for atrioventricular block: an old problem revisited. Int J Cardiol. 2013 Oct 09;168(4):3300-8. [PubMed: 23639463]

3.

Rediker DE, Eagle KA, Homma S, Gillam LD, Harthorne JW. Clinical and hemodynamic comparison of VVI versus DDD pacing in patients with DDD pacemakers. Am J Cardiol. 1988 Feb 01;61(4):323-9. [PubMed: 3341209]

4.

Ausubel K, Furman S. The pacemaker syndrome. Ann Intern Med. 1985 Sep;103(3):420-9. [PubMed: 3896087]

5.

Healey JS, Toff WD, Lamas GA, Andersen HR, Thorpe KE, Ellenbogen KA, Lee KL, Skene AM, Schron EB, Skehan JD, Goldman L, Roberts RS, Camm AJ, Yusuf S, Connolly SJ. Cardiovascular outcomes with atrial-based pacing compared with ventricular pacing: meta-analysis of randomized trials, using individual patient data. Circulation. 2006 Jul 04;114(1):11-7. [PubMed: 16801463]

6.

Frumin H, Furman S. Endless loop tachycardia started by an atrial premature complex in a patient with a dual chamber pacemaker. J Am Coll Cardiol. 1985 Mar;5(3):707-10. [PubMed: 3838323]

7.

Klementowicz PT, Furman S. Selective atrial sensing in dual chamber pacemakers eliminates endless loop tachycardia. J Am Coll Cardiol. 1986 Mar;7(3):590-4. [PubMed: 3753992]

8.

Nitzsché R, Gueunoun M, Lamaison D, Lascault G, Pioger G, Richard M, Malherbe O, Limousin M. Endless-loop tachycardias: description and first clinical results of a new fully automatic protection algorithm. Pacing Clin Electrophysiol. 1990 Dec;13(12 Pt 2):1711-8. [PubMed: 1704528]

Disclosure: Ahmed Abu-haniyeh declares no relevant financial relationships with ineligible companies.

Disclosure: Said Hajouli declares no relevant financial relationships with ineligible companies.