Abstract

Physiology of brain death is characterized by major disturbances of autonomic nervous system (ANS) activity which can lead to graft dysfunction. These findings exhibit the importance of early diagnosis of brain death to improve transplantation outcome. The aim of this prospective study was to assess whether heart rate variability (HRV) analysis, a noninvasive method to investigate ANS activity in comatose patients, could achieve this goal. A total of 14 brain-injured patients were included in the study as soon as they exhibited the clinical signs of imminent brain death. The electrocardiogram was then recorded from two leads with a Holter digital monitor. The clinical diagnosis of brain death was considered after an autonomic storm had occurred. HRV was assessed from 6 h before to 6 h after brain death in both time domain and spectral analysis, estimating either global ANS activity (index of variability, total power), parasympathetic activity (percentage of delta of R-R interval >50 ms, root mean square for successive interval differences, LnHF) or sympathetic activity (LnLF). Hourly averages of these variables were compared by using one-way analysis of variance. To assess whether HRV could per se diagnose brain death, receiver operating characteristic curves were generated for total power, root mean square for successive interval differences, and LnHF. We observed, for 6 h before brain death, a progressive extinction of the influence of the ANS on cardiovascular regulation. There was no activity in the two components of the ANS as soon as brain death occurred. HRV analysis appeared to be a very sensitive but a less specific method of diagnosing brain death. A total of 14 brain-injured patients with the clinical criteria of imminent brain death were enrolled for electrocardiogram recording and heart rate variability analysis (a noninvasive method to investigate autonomic nervous system activity). For 6 h before brain death, we observed a progressive extinction of autonomic nervous system activity which was not present as soon as brain death was clinically evoked.

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