OBJECTIVE: During ICD-implantation it is necessary to prove the function and to determine the optimal threshold by means of induced ventricular fibrillation (VF). Provoked cardiac arrests cause a circulator stop of the cerebral perfusion. Our aim was to examine the changes of cerebral blood flow velocity (CBFV(MCA)) after induced VF depending on the duration of fibrillation and prior values of CBFV(MCA). PATIENTS AND METHODS: Sixty induced episodes of VF in 9 patients (mean age +/- SD 53.5 +/- 8 years) were examined during ICD-implantation. Beside the standardized anaesthesiological monitoring, transcranial Doppler sonography was used to record the cerebral blood flow velocity in the middle cerebri artery CBFV(MCA). The duration of the fibrillation-period and the range and duration of the CBFV increase during the post defibrillation-period were correlated. Additionally, we examined whether systematic differences existed between the episodes of each patient (time-trend) by means of 5 following episodes of a patient. RESULTS: During all episodes of VF and hyperperfusion was present, that means a time interval showing increased values of CBFV(MCA), compared to the values present before VF. The duration of hyperperfusion depended significantly on the fibrillation time (r = 0.57; p < 0.001). The equation of regression is: hyperperfusion time = 11.1 + 1.22 x fibrillation time. The amount of hyperperfusion, that means the maximal CBFV after defibrillation, increase significantly with CBFV(MCA) before VF (correlation = 0.88; p < 0.001). The equations of regression is hyperperfusion height = 6.11 + 1.22 x CBFV(MCA) before VF. The duration of hyperperfusion is not influenced by the maximal CBFV(MCA) after defibrillation (r = 0.08; p = 0.52). In the examined patients no significant differences in the hyperperfusion time maximal CBFV(MCA) after defibrillation between the episodes were found. CONCLUSION: After induced VF you always have to expect a reactive cerebral hyperperfusion. The amount of increase of CBFV after defibrillation depends on the prior values of CBFV before fibrillation and shows a nearly proportional relation to these. The duration of hyperperfusion shows a linear dependency on VF-times. This may show that we had VF-times, in which the cerebral autoregulation and other cerebral physiological reactions compensate the drop of the CBFV(MCA) during VF in the postfibrillation time. In further studies will be examined if there are similar changes in the cerebral metabolism as in CBFV(MCA).
OBJECTIVE: During ICD-implantation it is necessary to prove the function and to determine the optimal threshold by means of induced ventricular fibrillation (VF). Provoked cardiac arrests cause a circulator stop of the cerebral perfusion. Our aim was to examine the changes of cerebral blood flow velocity (CBFV(MCA)) after induced VF depending on the duration of fibrillation and prior values of CBFV(MCA). PATIENTS AND METHODS: Sixty induced episodes of VF in 9 patients (mean age +/- SD 53.5 +/- 8 years) were examined during ICD-implantation. Beside the standardized anaesthesiological monitoring, transcranial Doppler sonography was used to record the cerebral blood flow velocity in the middle cerebri artery CBFV(MCA). The duration of the fibrillation-period and the range and duration of the CBFV increase during the post defibrillation-period were correlated. Additionally, we examined whether systematic differences existed between the episodes of each patient (time-trend) by means of 5 following episodes of a patient. RESULTS: During all episodes of VF and hyperperfusion was present, that means a time interval showing increased values of CBFV(MCA), compared to the values present before VF. The duration of hyperperfusion depended significantly on the fibrillation time (r = 0.57; p < 0.001). The equation of regression is: hyperperfusion time = 11.1 + 1.22 x fibrillation time. The amount of hyperperfusion, that means the maximal CBFV after defibrillation, increase significantly with CBFV(MCA) before VF (correlation = 0.88; p < 0.001). The equations of regression is hyperperfusion height = 6.11 + 1.22 x CBFV(MCA) before VF. The duration of hyperperfusion is not influenced by the maximal CBFV(MCA) after defibrillation (r = 0.08; p = 0.52). In the examined patients no significant differences in the hyperperfusion time maximal CBFV(MCA) after defibrillation between the episodes were found. CONCLUSION: After induced VF you always have to expect a reactive cerebral hyperperfusion. The amount of increase of CBFV after defibrillation depends on the prior values of CBFV before fibrillation and shows a nearly proportional relation to these. The duration of hyperperfusion shows a linear dependency on VF-times. This may show that we had VF-times, in which the cerebral autoregulation and other cerebral physiological reactions compensate the drop of the CBFV(MCA) during VF in the postfibrillation time. In further studies will be examined if there are similar changes in the cerebral metabolism as in CBFV(MCA).
Authors: H J Trappe; H G Fieguth; P Pfitzner; J Heintze; P Wenzlaff; B Kielblock Journal: Pacing Clin Electrophysiol Date: 1995-01 Impact factor: 1.976
Authors: A Hagendorff; C Dettmers; P Danos; L Pizzulli; H Omran; M Manz; A Hartmann; B Lüderitz Journal: Circulation Date: 1994-07 Impact factor: 29.690