Pacemaker-Mediated Tachycardia Treatment & Management

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

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.