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Pacemaker-Mediated Tachycardia Treatment & Management

  • Author: Brian Olshansky, MD; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Aug 04, 2016

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 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). 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).[9] The downside of this approach is that intrinsic P-wave amplitude can be lower at higher rates, which could potentially result in atrial undersensing.[10] 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.

Contributor Information and Disclosures

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society

Disclosure: Speaker, consultant, DSMB for: Lundbeck; Daiichi Sankyo, Amarin, On-X, Biotronik.


Noel G Boyle, MB, BCh, MD, PhD Professor of Medicine, UCLA Cardiac Arrhythmia Center, Ronald Reagan UCLA Medical Center

Noel G Boyle, MB, BCh, MD, PhD is a member of the following medical societies: American College of Cardiology, European Society of Cardiology, Heart Rhythm Society, American College of Physicians

Disclosure: Nothing to disclose.

Chirag M Sandesara, MD Virginia Cardiovascular Associates, Cardiac Rhythm Care

Chirag M Sandesara, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Rakesh Gopinathannair, MD, MA Director of Cardiac Electrophysiology, University of Louisville; Assistant Professor of Medicine, Division of Cardiovascular Medicine, University of Louisville School of Medicine

Rakesh Gopinathannair, MD, MA is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society

Disclosure: Received consulting fee from St. Jude Medical for consulting; Received honoraria from Boston Scientific for speaking and teaching.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marschall S Runge, MD, PhD Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine

Marschall S Runge, MD, PhD is a member of the following medical societies: American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Texas Medical Association, Southern Society for Clinical Investigation, American Federation for Clinical Research, Association of Professors of Medicine, Association of Professors of Cardiology, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association

Disclosure: Received honoraria from Pfizer for speaking and teaching; Received honoraria from Merck for speaking and teaching; Received consulting fee from Orthoclinica Diagnostica for consulting.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Additional Contributors

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Chair of Institutional Review Board, University of California, Los Angeles, David Geffen School of Medicine

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, International Society for Magnetic Resonance in Medicine, American College of Physicians, American Federation for Medical Research, Radiological Society of North America

Disclosure: Nothing to disclose.

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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.
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.
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 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.
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