EEG-based indices of anaesthesia: correlation between bispectral index and patient state index?

BACKGROUND AND OBJECTIVE: Both the bispectral and the patient state indices are derived from the electroencephalogram and have been proposed as a measure of the same clinical target, the hypnotic component of anaesthesia. The present study evaluated whether there is concordance between the bispectral and the patient state indices with regard to end-points measured simultaneously in patients undergoing surgery under general anaesthesia. METHODS: Fifty-seven patients scheduled for elective abdominal, orthopaedic (Groups 1 and 2) or cardiac surgery (Group 3) under general anaesthesia were enrolled in the study. Anaesthesia was performed using remifentanil/ sevoflurane (Group 1, 19 patients), remifentanil/propofol (Group 2, 19 patients) or sufentanil/propofol/isoflurane (Group 3, 19 patients). The bispectral and the patient state indices were simultaneously recorded. Pearson's correlation between these two indices was calculated for the complete data and each group. The percentage of bispectral index values in the recommended range for general anaesthesia (45-60) that were confirmed by levels of patient state index (25-50) was calculated and vice versa. RESULTS: Overall correlation between the bispectral and the patient state indices was 0.667, 0.671 in Group 1, 0.650 in Group 2 and 0.675 in Group 3 (P < 0.01). For values of the bispectral index between 45 and 60, only 40% of corresponding patient state index values were between 25 and 50. For patient state index values of 25-50, only 50% of the corresponding bispectral index values were in the range of 45-60. CONCLUSIONS: Concordance between the bispectral and patient state indices is relatively weak, whereas both are thought to reflect the same clinical target, the hypnotic component of anaesthesia. As a consequence, further studies are required to compare reliability of both indices as indicators of different levels of hypnosis.

Dexmedetomidine decreases thiopental dose requirement and alters distribution pharmacokinetics.

BACKGROUND: alpha 2-Adrenergic agonists such as dexmedetomidine can be used to reduce the dose requirement of intravenous and volatile anesthetics. Whereas dexmedetomidine and volatile anesthetics interact pharmacodynamically (reduction of MAC), the mechanism of interaction between dexmedetomidine and intravenous anesthetics is not known. METHODS: Fourteen male ASA physical status 1 patients were randomly assigned to serve as control subjects (n = 7) or to be treated with dexmedetomidine (n = 7; 100, 30, and 6 ng.kg-1.min-1 for 10 min, 15 min, and thereafter, respectively). After 35 min, in all patients, thiopental (100 mg/min) was infused until burst suppression appeared in the raw tracing of the electroencephalogram. By using concentrations of thiopental in plasma and the electroencephalogram as a continuous pharmacologic effect measure, the apparent effect site concentrations for thiopental were estimated in both groups. Three-compartment pharmacokinetics were calculated for thiopental. RESULTS: Dexmedetomidine reduced the thiopental dose requirement for electroencephalographic burst suppression by 30%. There was no difference in estimated thiopental effect site concentrations between dexmedetomidine and control patients, suggesting the absence of a major pharmacodynamic interaction. Dexmedetomidine significantly decreased distribution volumes (V2, V3, and Vdss) and distribution clearances (Cl12 and Cl13) of thiopental. CONCLUSIONS: The thiopental dose-sparing effect of dexmedetomidine on the electroencephalogram is not the result of a pharmacodynamic interaction but rather can be explained by a dexmedetomidine-induced decrease in thiopental distribution volume and distribution clearances. Dexmedetomidine reduces thiopental distribution, most probably by decreasing cardiac output and regional blood flow.

Accidental injection of ether into the epidural space.

Five ml diethyl ether was accidentally injected into the epidural space via an epidural catheter at the end of a Caesarean section. Immediately the patient felt a hot and burning pain in her legs that led to paraparesis, with a sensory level to T8. The patient showed bilateral recovery of both motor and sensory functions 4 hours after the accident.

Effect of Wy-45,727 on 24 h intragastric acidity in twenty normal volunteers.

1. The effects of single daily doses of 20, 50 and 150 mg of WY-45,727, a novel H2-receptor antagonist, and placebo were compared using long term pH-monitoring in 20 male volunteers. 2. Intragastric acidity was measured using combined Ingold glass electrodes. Subjects underwent four studies each under identical dietary conditions. Medication was taken after the evening meal. 3. Median 24 h pH rose from 1.3 (1.2-1.4 interquartile range) on placebo to 1.9 (1.6-2.8) on 20 mg WY-45,727, to 3.1 (2.3-3.7) on 50 mg WY-45,727 and to 4.5 (3.7-4.7) on 150 mg WY-45,727. All three doses increased 24 h and night-time pH significantly compared with placebo (P less than 0.0001). 4. The PAGE test for order effects confirmed clear dose dependent inhibition of acidity (P less than 0.0001). 5. Highly consistent individual responses were found during the night following 150 mg WY-45,727.

Day-to-day variation of 24-hour intragastric acidity.

Twenty-four-hour intragastric acidity was measured continuously using an intragastric electrode in 13 normal volunteers studied four times. Subjects were studied twice in the hospital and twice as outpatients. The dietary conditions were strictly controlled and the replicate studies were compared to assess the variability of such recordings of acidity. The accuracy of the technique was assessed, and a detection limit for differences was calculated for commonly used time periods. Over 24 h, during the night, during the day, and during the evening the technique is able to detect consistent changes of pH of greater than 0.1 units. During separate 5-min periods the limits of detection were considerably greater. This study demonstrates the variability of 24-h intragastric acidity and confirms that continuous monitoring is able to detect important changes of acidity under both hospitalized and ambulant conditions.

Double blind comparison of the effects of cimetidine, ranitidine, famotidine, and placebo on intragastric acidity in 30 normal volunteers.

Continuous measurement of 24 hour intragastric acidity was carried out in 30 normal volunteers during treatment with placebo, cimetidine 800 mg, ranitidine 300 mg, and famotidine 40 mg in a double blind study. Medication was taken after the evening meal (post cenam nocte, PCN). Median 24 hour acidity decreased with all H2-receptor antagonists from 25.1 mmol/l on placebo to 10 mmol/l (-60.1%) during cimetidine, to 3.2 mmol/l (-87.25%) during ranitidine and to 2.5 mmol/l (-90.0%) during famotidine treatment (p less than 0.0005). All drugs significantly inhibited night time acidity but only famotidine decreased acidity during the late morning compared with placebo. Significantly greater acid reduction was seen with famotidine and ranitidine compared with cimetidine but no difference was found between famotidine and ranitidine.

Comparison of ranitidine 300 mg twice daily, 300 mg at night and placebo on 24-hour intragastric acidity of duodenal ulcer patients.

Continuous measurement of 24-hour intragastric acidity was performed in 12 duodenal ulcer patients in remission during treatment with placebo, ranitidine 300 mg nocte and ranitidine 300 mg b.d. Median 24-hour acidity was 79.4 mmol litre-1 during placebo treatment; it decreased to 28.2 mmol litre-1 during treatment with ranitidine 300 mg nocte and to 3.6 mmol litre-1 during treatment with ranitidine 300 mg b.d. The two regimens decreased intragastric acidity to a similar degree during the night, but significantly greater inhibition of daytime and 24-hour acidity followed use of ranitidine 300 mg b.d.