Postoperative delirium (POD) occurs frequently after cardiac surgery and is associated with increased morbidity and mortality. We analysed whether perioperative bilateral BIS monitoring may detect abnormalities before the onset of POD in cardiac surgery patients. In a prospective observational study, 81 patients undergoing cardiac surgery were included. Bilateral Bispectral Index (BIS)-monitoring was applied during the pre-, intra- and postoperative period, and BIS, EEG Asymmetry (ASYM), and Burst Suppression Ratio (BSR) were recorded. POD was diagnosed according to the Confusion Assessment Method for the Intensive Care Unit, and patients were divided into a delirium and non-delirium group. POD was detected in 26 patients (32%). A trend towards a lower ASYM was observed in the delirium group as compared to the non-delirium group on the preoperative day (ASYM = 48.2 ± 3.6% versus 50.0 ± 4.7%, mean ± sd, p = 0.087) as well as before induction of anaesthesia, with oral midazolam anxiolysis (median ASYM = 49.5%, IQR [47.4;51.5] versus 50.6%, IQR [49.1;54.2], p = 0.081). Delirious patients remained significantly (p = 0.018) longer in a burst suppression state intraoperatively (107 minutes, IQR [47;170] versus 44 minutes, IQR [11;120]) than non-delirious patients. Receiver operating analysis revealed burst suppression duration (area under the curve = 0.73, p = 0.001) and BSR (AUC = 0.68, p = 0.009) as predictors of POD. Intraoperative assessment of BSR may identify patients at risk of POD and should be investigated in further studies. So far it remains unknown whether there is a causal relationship or rather an association between intraoperative burst suppression and the development of POD. clinicaltrials.gov NCT01048775

Cerebral vasospasm remains a leading cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Cerebral ischemia may ensue when autoregulation fails to compensate for spasm. We examined how autoregulation is affected by vasospasm by using transcranial Doppler. The moving correlation coef

Background: The Bispectral Index (BIS) and the Patient State Index (PSI) quantify depth of anesthesia by analyzing the electroencephalogram. The authors examined the response of BIS and PSI to sevoflurane anesthesia. Methods: In 22 patients, sevoflurane anesthesia was induced by inhalation with a tight-fitting facemask and was maintained via a laryngeal mask. Sevoflurane concentrations were increased until burst suppression occurred and subsequently decreased until BIS recovered to values above 60. This procedure was repeated twice until patients underwent intubation for subsequent surgery. End-tidal sevoflurane concentrations, BIS, and PSI were recorded simultaneously. The performance of PSI and BIS to predict the estimated sevoflurane effect site concentration, as derived from simultaneous pharmacokinetic and pharmacodynamic modeling, was compared by determination coefficients (rho(2)) and prediction probabilities (P(K)). Results: A significant (P < 0.001) correlation between BIS and PSI was found (r(2) = 0.75), and a close sigmoid relation between sevoflurane effect site concentration and both BIS (rho(2) = 0.84 +/- 0.09) and PSI (rho(2) = 0.85 +/- 0.15) was observed. The maximum sevoflurane electroencephalographic effect resulted in PSI values (1.3 +/- 4.3) that were significantly (P = 0.019) lower than BIS values (7.9 +/- 12.1), and the effect site efflux constant k(e0) was significantly smaller (P = 0.001) for PSI (0.13 +/- 0.08 min(-1)) than for BIS (0.24 +/- 0.15 min(-1)). The probability of BIS (P(K) = 0.80 +/- 0.11) to predict sevoflurane effect site concentration did not differ (P = 0.76) from that of PSI (P(K) = 0.79 +/- 0.09). Conclusions: The BIS reacted faster to changes in sevoflurane concentrations, whereas the PSI made better use of the predefined index range. However, despite major differences in their algorithms and minor differences in their dose-response relations, both PSI and BIS predicted depth of sevoflurane anesthesia equally well.

The patient state index (PSI) and the bispectral index (BIS) quantify anaesthetic depth based on the EEG using different algorithms. We compared both indices with regard to the prediction of the depth of propofol anaesthesia. In 17 patients, propofol was infused until burst suppression occurred and stopped thereafter until BIS recovered to values above 60. This was repeated; afterwards, patients were intubated, for subsequent surgery. Without surgical stimulus, PSI and BIS were measured simultaneously and compared with the estimated effect-site concentrations of propofol. These were derived from simultaneous pharmacokinetic and -dynamic modelling in an individual two-stage and a population-based NONMEM approach. A close sigmoid relationship was observed between the propofol effect-site concentration and both PSI [coefficient of determination ρ²=0.91 (sd 0.05)] and BIS [ρ²=0.92 (0.03)], which was significantly steeper for PSI [γ=2.2 (0.6)] than for BIS [γ=1.8 (0.4)], and reached significantly lower values for PSI [E_max=0.3 (1.1)] than for BIS [E_max=5.3 (6.7)] at maximal propofol concentrations. A significantly smaller k_e0 was obtained for PSI [0.09 (0.03) min⁻¹] compared with BIS [0.10 (0.02) min⁻¹]. PSI and BIS correlated significantly with each other (ρ²=0.866) and predicted propofol effect-site concentration with a comparable probability [P_K=0.87 (0.05) and 0.86 (0.05), respectively]. NONMEM revealed E₀=89.3 and 92.3, E_max=1.9 and 8.6, C_e50=1.38 and 1.92 µg ml⁻¹, γ=1.6 and 1.48, and k_e0=0.103 and 0.131 min⁻¹ as typical values for PSI and BIS, respectively. The PSI and the BIS monitors performed equally well in predicting depth of propofol anaesthesia. However, PSI was lower than BIS by ∼10–15 points at high propofol concentrations.

Background and Purpose— Critical closing pressure (CCP) is thought to be jointly influenced by intracranial pressure and cerebrovascular tone. We examined how CCP is affected by cerebral vasospasm after subarachnoid hemorrhage (SAH). Methods— In 15 patients with vasospasm of the middle cerebral artery, CCP was calculated using 2 methods previously reported (ad modem Aaslid and Michel, indexed CCP _Aaslid and CCP _Michel , respectively) based on data of arterial blood pressure and flow velocity (FV) as assessed by transcranial Doppler. Results— CCP decreased significantly ( P <0.05) during vasospasm (CCP _Aaslid =6.3±22.9 mm Hg, CCP _Michel =14.9±16.5 mm Hg, mean±SD) as compared with baseline (CCP _Aaslid =24.4±20.3 mm Hg, CCP _Michel =27.8±19.4 mm Hg). This was not attributable to ICP, which remained unaffected by vasospasm. In addition, CCP was significantly lower on the side of vasospasm (CCP _Aaslid =11.9±24.2 mm Hg, CCP _Michel =18.4±19.6 mm Hg) as compared with the contralateral nonvasospastic side (CCP _Aaslid =24.7±22.3 mm Hg, CCP _Michel =28.2±18.0 mm Hg). Conclusions— Assuming that autoregulation-related distal vasodilatation outweighs proximal vasospasm, CCP should decrease. Alternatively, CCP might have increased during vasospasm as the tension of big vessels increase, but the turbulence occurring during vasospasm may have impaired the linear relationship between pressure and FV, thus leading to a marked underestimation of CCP. In conclusion, interpretation of CCP in vasospasm is difficult and may be overshadowed by nonlinear hemodynamic effects.