No abstract

We tested if microcomputer-based measurements of heart rate variability and respiratory sinus arrhythmia (RSA) could be used as the basis of an objective sedation score. Measurements were obtained in eight ICU patients before, during and after physiotherapy. Patients were sedated with propofol and alfentanil and paralysed with atracurium. Mean ECG R-R interval showed little variation, changing from 646.15 (SD 203.15) ms to 596.08 (181.75) ms and 633.98 (184.53) ms before, during and after physiotherapy, respectively (not significant). However, the degree of respiratory sinus arrhythmia, determined using circular statistical analysis, increased significantly, from 0.14 (0.11) to 0.24 (0.15), during physiotherapy and returned to control after physiotherapy (P < 0.05). Changes in respiratory sinus arrhythmia may provide an objective measurement of sedation in ICU patients and could form the basis of a simple sedation scoring system.

No abstract

Respiratory sinus arrhythmia (RSA) is a cyclical variation in heart rate during breathing, where the heart rate increases during inspiration and decreases during expiration. RSA and the electroencephalogram (EEG) were monitored in 10 patients undergoing elective surgery with isoflurane and nitrous oxide in oxygen anaesthesia after induction with propofol. All patients were subject to controlled ventilation and recovery from competitive neuromuscular block was facilitated by neostigmine and glycopyrronium (seven patients) or atropine (three patients). Median and spectral edge (95%) frequencies of the raw EEG were derived off-line. RSA and EEG indices were obtained during preinduction (baseline), induction, incision, 0.65 and 1.2 MAC of isoflurane maintenance during surgery and recovery. Significant decreases in the level of RSA, median and spectral edge frequencies were observed during induction and significant increases in all indices were observed at recovery in all patients. Significant decreases in the median and spectral edge EEG frequencies occurred in patients treated with atropine both to counteract bradycardia after propofol induction and at antagonism of neuromuscular block (n = 3), compared with patients treated with glycopyrronium (n = 7). In contrast, the level of RSA did not decrease significantly with atropine. It is concluded that measurements of RSA could form the basis of a useful index of anaesthetic depth during isoflurane anaesthesia, even during the use of pharmacologically appropriate doses of atropine. However, any effects of atropine on the raw EEG and on indices derived from the EEG, should be characterized further so that these effects are not confused with changes in anaesthetic depth.