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Third generation implantable cardioverter defibrillators are capable of complex arrhythmia detection using sensing algorithms with automatic adjustable gain settings. We report a unique case where inappropriate sensing of atrial tachycardia in a patient with a His bundle ablation lead to satisfaction of ventricular fibrillation detection criteria.

The AICD uses an automatic gain control amplifier for detecting the small electrograms during ventricular fibrillation. The latest generation of the AICD appears to have a more sensitive lock on gain amplifier, as 6 of 76 patients implanted with the new AICD had double counting of the QRS-T wave complex resulting in asymptomatic discharges. Solutions to the problem of limiting these asymptomatic discharges are difficult and include slowing of the heart rate with beta blockers, changing the lead system, or replacement of the device. One of the six patients was treated with beta blockers. Three patients had their device changed, two patients requested the inactivation of their device until a rate programmable unit was available. The potential for T wave sensing in a lock on gain amplifier represents the unique dilemma between detecting small electrograms of ventricular fibrillation, and detecting diastolic events which occur shortly after the QRS complex.

Clinical and animal investigations have pointed out that high energy electrical shocks are associated with the development of cardiac arrhythmias and with variable success in permanent ablation. The effects of electrode configuration and location on the size of the recorded electrogram was investigated to help explain variable catheter ablation results. We analyzed the cellular effects of catheter ablation shocks and found depression of resting potential, action potential amplitude, dV/dt and action potential duration. The most severe effects were noted with high current densities in tissues located between the cathode and anode. Damage was worse nearest the cathode. Similar cellular studies were completed using argon laser photoablation. Again, there was a decrease in resting potential, action potential amplitude and dV/dt. Laser energy led to a more focal region of myocardium void of action potentials and the border zone of injury was smaller. We also investigated the effects of lower energy shocks (1 to 10 joule) on cardiac tissues. Using microelectrodes, we observed that the membrane potential can "hang up" at the depolarized levels for varying periods of time and that conduction is altered during this membrane "hang-up" period. The duration and membrane hang-up level correlated with shock intensity and shock duration. Sequential shocks resulted in additive membrane "hang-up". We believe that membrane hang-up may be associated with brief arrhythmias observed following catheter ablation since conduction, refractoriness and excitability are all altered.

We set out to determine in a prospective fashion the characteristics of energy delivery related to defibrillation in a population of patients receiving the AICD. Specifically, we examined the characteristics of the delivered current, transmyocardial voltage, and transmyocardial impedance. Secondly, we determined the relationship between the energy delivered, the impedance encountered and the defibrillation threshold. Since the AICD will deliver a succession of shocks if the initial shock does not cardiovert, the effects of consecutive shocks at different energy levels on the transmyocardial impedance were also assessed.

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)

A 78-year-old man treated with amiodarone for recurrent ventricular tachycardia, had sequential placement of a bipolar VVI pacemaker and an automatic implantable cardioverter defibrillator (AICD). During defibrillation threshold testing, there was failure to capture of the pacer in the post-shock period. The time of failure to capture appeared energy-related: the greater the energy delivered, the longer the failure to capture. Careful attention will be necessary in constructing combined AICD/pacemaker units.