AIM: To find out whether it is possible to anaesthetize patients safely without analgesia and sedation, using burst pacing prolonged until the patient becomes unconscious. METHODS:One hundred and four patients undergoing implantation or reimplantation of a cardioverter-defibrillator were included. Patients randomized into Group B underwent prolonged burst pacing without analgesia and sedation. Patients in Group T underwent a T-wave shock under analgesia and sedation. Blood samples for measurement of serum neuron-specific enolase were taken before surgery and 6, 24, and 48 h after the procedure. RESULTS: From the 104 patients, 51 were randomly assigned to Group B and 53 to Group T. Four patients from Group B were switched to Group T (ventricular fibrillation not induced by burst pacing). The clinical characteristics of both groups were similar. The mean total time of cardiac arrest was significantly longer in Group B (23.0 ± 4.4 s, median 22.7) vs. Group T (10.3 ± 3.0 s, median 10.0), P < 0.0001 (Mann-Whitney U-test). The effectiveness of both induction methods was similar (92.1% in Group B and 100% in Group T). The mean neuron-specific enolase levels after 6, 24, and 48 h were similar in Groups B and T (13.1 ± 6.3 and 11.6 ± 5.8 mg/L, 14.5 ± 7.5 and 13.4 ± 6.0 mg/L, and 14.9 ± 5.9 and 12.2 ± 6.0 mg/L, respectively) as were these levels compared with baseline neuron-specificenolase levels (14.0 ± 5.9 and 13.4 ± 4.0 mg/L, respectively), P = NS for all. CONCLUSION: Despite a longer time of total cardiac arrest, prolonged burst pacing appears to be a safe and effective method for induction of ventricular fibrillation during cardioverter-defibrillator testing, which enables omission of analgesia and sedation or general anaesthesia.
RCT Entities:
AIM: To find out whether it is possible to anaesthetize patients safely without analgesia and sedation, using burst pacing prolonged until the patient becomes unconscious. METHODS: One hundred and four patients undergoing implantation or reimplantation of a cardioverter-defibrillator were included. Patients randomized into Group B underwent prolonged burst pacing without analgesia and sedation. Patients in Group T underwent a T-wave shock under analgesia and sedation. Blood samples for measurement of serum neuron-specific enolase were taken before surgery and 6, 24, and 48 h after the procedure. RESULTS: From the 104 patients, 51 were randomly assigned to Group B and 53 to Group T. Four patients from Group B were switched to Group T (ventricular fibrillation not induced by burst pacing). The clinical characteristics of both groups were similar. The mean total time of cardiac arrest was significantly longer in Group B (23.0 ± 4.4 s, median 22.7) vs. Group T (10.3 ± 3.0 s, median 10.0), P < 0.0001 (Mann-Whitney U-test). The effectiveness of both induction methods was similar (92.1% in Group B and 100% in Group T). The mean neuron-specific enolase levels after 6, 24, and 48 h were similar in Groups B and T (13.1 ± 6.3 and 11.6 ± 5.8 mg/L, 14.5 ± 7.5 and 13.4 ± 6.0 mg/L, and 14.9 ± 5.9 and 12.2 ± 6.0 mg/L, respectively) as were these levels compared with baseline neuron-specificenolase levels (14.0 ± 5.9 and 13.4 ± 4.0 mg/L, respectively), P = NS for all. CONCLUSION: Despite a longer time of total cardiac arrest, prolonged burst pacing appears to be a safe and effective method for induction of ventricular fibrillation during cardioverter-defibrillator testing, which enables omission of analgesia and sedation or general anaesthesia.