Abstract
Programming maximum right ventricular output in a patient with a biventricular implanted cardioverter defibrillator resulted in ventricular oversensing and ventricular safety pacing in the same cardiac cycle.
Introduction
Ventricular oversensing in pacemakers and implanted cardioverter defibrillators (ICD) is frequently encountered with a large variety of sources for oversensing. 1 Less frequent a combination of parameter selections in dual chamber pacemakers may lead to oversensing, such as crosstalk where the atrial impulse or its afterpotential is sensed by the ventricular channel. 2 , 3 For crosstalk prevention, dual chamber devices are equipped with a ventricular safety pacing option, which warrants ventricular stimulation when ventricular sensing is detected within the ventricular safety pace (VSP) interval. 4 We report on a patient in whom the afterpotential of the ventricular impulse is leading to ventricular oversensing with inhibition but also creates ventricular safety pacing.
Case report
An 83-year-old male had his biventricular ICD replaced by a St Jude Medical Atlas II + HF V-367, (St Jude Medical, Sylmar, CA, USA), because of battery depletion. During follow-up, he presented with a gradual increase of the right ventricular (RV) stimulation threshold up to 4.25 V at 1.5 ms pulse width, which was not associated with significant changes in lead impedance. Changes in R-wave amplitude could not be evaluated due to a lack of underlying intrinsic rhythm during follow-up. To overcome loss of capture from the RV lead, ventricular output was programmed to its maximum of 7.5 V at 1.5 ms, which resulted in the following observations.
Atrial pacing was followed by ventricular pacing with shortening of the AV interval from 191 to 121 ms annotated with ‘VSP’ ( Figure 1 ).
At the end of the ventricular refractory period annotation showed ‘VS’, with prolongation of the pacing interval to 1031 ms ( Figure 1 ).
Programmer strip recording showing two surface ECG leads, RA electrogram, annotation and timing channel, and RV electrogram. The diagram explains the effect of the atrial afterpotential, ventricular afterpotential, ventricular blanking period (B), and ventricular refractory period. Atrial afterpotentials and ventricular afterpotentials are started with atrial and ventricular pacing, respectively. For clarity reasons, the afterpotential curves are represented as a straight line with a linear decay, which will be an exponential decay in practice. Both afterpotentials are superimposed on each other at the ventricular electrode, as illustrated by the line demonstrating summation of atrial and ventricular afterpotentials. When the level of this line indicating the summed afterpotentials at ventricular electrode is above the ventricular sensitivity level oversensing will occur (arrows). These sense events are giving rise to ventricular safety pace (VSP) and ventricular oversense (VS), the latter results in prolongation of the pacing interval.
After ∼12 s normal pacing was restored ( Figure 2 ). Repeating the same manoeuvre after shortening the ventricular refractory period to 150 ms, ventricular oversensing was now observed at the end of the newly programmed refractory period.
Continuation of the recording presented in Figure 1 showing spontaneous restoration of normal function 12 s after programming maximal ventricular output due to dissipation of the electrode-interface charge overload. First ventricular oversensing at the end of the ventricular refractory period disappears, followed by disappearance of ventricular safety pace. The disappearance of VSP has no effect on the Apace–Apace interval during normal function, because the pacing system functions in atrial based timing. In this timing sequence changes in the paced AV interval (121–191 ms) are not affecting the Apace–Apace interval.
Discussion
In our patient, two incidences of ventricular oversensing occurred during the same cardiac cycle. First, ventricular oversensing was present at the start of the ventricular alert period after termination of the refractory period. Because ventricular oversensing was directly related to shortening of the refractory period, T-wave oversensing could be ruled out as explanation. 5 The most likely explanation is oversensing of the afterpotential of the extreme high-output ventricular stimulus, because oversensing changes accordingly when modification of the refractory period.
The simultaneous occurrence of ventricular oversensing during the AV interval is indicated by ventricular safety pacing, is more difficult to associate with ventricular output. The most likely explanation for the relation between VSP and ventricular output is that the afterpotential which is diminishing in time still is present at initiation of the following safety pace interval in the next cardiac cycle. The summation of the afterpotential of the preceding ventricular stimulus and the afterpotential of the following atrial stimulus are giving rise to ventricular sensing after the blanking period thus initiating VSP. At a ventricular output setting of 4.25 V at 1.5 ms, no crosstalk was present. The explanation is shown schematically in the diagram added to the ECG recording in Figure 1 .
After programming maximum ventricular output, there is a gradual dissipation of this electrical charge through the capacitive elements in the ventricular electrode-myocardial interface, which first result in the correction of ventricular oversensing and subsequently disappearance of ventricular safety pacing ( Figure 2 ).
Oversensing at the end of the refractory period can be explained by the presence of a high residual electrical charge at the input of the ventricular channel, which creates a voltage drop that is detected at the transition from refractory to alert period. This implies that the timing of oversensing is directly related to the programmed refractory period, as illustrated in our patient. The observed phenomena have no relation to extreme values of lead impedance, which showed no significant changes in the follow-up. Implantation of a new pace/sense lead was mandatory regardless of our observations thus enabling nominal ventricular output settings and prevention of further malfunction.
Conclusion
High ventricular output settings may induce ventricular oversensing leading to ventricular inhibition by afterpotentials at the start of the ventricular alert period, but may also induce atrio-ventricular crosstalk leading to VSP by summation of the afterpotentials of atrial and preceding ventricular stimulation.
Conflicts of interest: BMvG is clinical advisor for Medtronic NL BV, Heerlen, the Netherlands.
