These tracings show the various possibilities for programming the amplitude of the electric shocks in the VT zone.

For the first episode initially diagnosed in the VT2 zone, the therapies are triggered in consecutive manner which end as soon as the rhythm is once again deemed as slow, or after because all therapies were exhausted. Six bursts did not terminate the arrhythmia. A first shock of 10J was subsequently delivered. This patient presented episodes of VT arising from the left ventricle (LV EGM preceding the RV). The electric shock is synchronized to RV sensing (30 ms later). On this type of arrhythmia, the EGM suggests that the shock was delivered during the onset of the left ventricular repolarization phase. The delivery of a moderate amplitude shock in the left ventricular vulnerable period explains the arrhythmogenic nature of the shock and the degradation of the arrhythmia into ventricular fibrillation. For the second patient, a maximum amplitude shock was directly programmed as a result of antitachycardia pacing.

In the absence of an optimal universal programming, the results of large-scale studies concur on the need to reduce the number of inappropriate or unnecessary therapies without jeopardizing patient safety and prioritize antitachycardia pacing in lieu of electric shocks. It is customary to program increasing aggressive therapies with antitachycardia pacing representing the first-line treatment for monomorphic tachycardia. In the VT zone (<200 beats/minute), a series of bursts rather than ramps (Class I indication) is therefore usually programmed. Indeed, the ratio between termination and acceleration of the arrhythmia appears to favor burst therapy (identical efficacy but less prominent pro-arrhythmogenic feature) compared to the ramp. If the bursts prove unsuccessful, it is then possible to program a series of ramps to promote a non-painful therapy followed by a series of electric shocks or proceed to the electric shocks directly. Various parameters influence the choice of the amplitude of the first shock in the VT zone, which can be programmed at maximum energy or at a lower amplitude (in the order of 10J). A certain number of advantages can be found in programming a first moderate amplitude shock (10J):

1. this amplitude is very often sufficient to terminate a VT episode;
2. the charge time for this amplitude is very short even though the few seconds difference with a maximum amplitude are not clinically determinant when the shock occurs after 3 burst sequences plus or minus 3 ramp sequences (more than one minute of arrhythmia);
3. battery consumption is less for a shock of 10J versus 35J despite having little impact on the wear of the batteries if the number of shocks delivered is limited;
4. despite the fact that most of the time during a VT episode, the electric shock is delivered while the patient is still conscious, the painful nature of the shock has little bearing on the decision regarding the amplitude of the first shock, given the difficulty in demonstrating a direct link between the amplitude of the shock delivered and the amplitude of the pain incurred;
5. various studies have demonstrated the deleterious nature of an electric shock and its association with an altered prognosis; it thus appears logical to assume that a shock of 10J will have fewer negative consequences than a shock of 35J and would thus favor choosing the least traumatic therapy possible.

The first tracing, however, shows the main limitation of programming a shock of 10J in the VT zone and the resulting pro-arrhythmogenic risk (concept of upper limit of vulnerability). Below a certain variable value depending on the patient and directly related to the defibrillation “threshold”, not only can a shock be ineffective in reducing an arrhythmia but can also accelerate and disorganize a monomorphic VT into a polymorphic arrhythmia compromising the patient’s prognosis in the short term. This tracing shows a rapid, polymorphic, low voltage and very worrisome arrhythmia induced by the first shock. The induced arrhythmias are often associated with very short ventricular intervals of limited amplitude, increasing the risk of undersensing and inappropriate interruption of capacitor charge. Sensing during this VF episode was very poor: namely, a moderate delay in diagnosis but especially a false diagnosis of return to sinus rhythm and temporary interruption of the charge. Sensing improves in a second step allowing the termination by electric shock. RV sensing was programmed to enhanced T wave suppression without prior oversensing of the T wave. LV sensing was set to Standard. In this patient, it would appear essential to reprogram a standard RV sensing or even an enhanced VF sensing. This new programming can subsequently be validated by induction and verification of accurate sensing of VF.

This type of adverse effect is relatively rare although constitutes a major limitation of the programming of moderate amplitude shocks. Another alternative is therefore to program a first shock of maximum amplitude so as to increase the probability of terminating a VT on the very first attempt, to reduce as much as possible the number of shocks delivered and to be above the upper limit of ventricular vulnerability.