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This paper presents the application of predictive control to drug dosing during anesthesia in patients undergoing surgery. The performance of a generic predictive control strategy in drug dosing control, with a previously reported anesthesia-specific control algorithm, has been evaluated. The robustness properties of the predictive controller are evaluated with respect to inter- and intrapatient variability. A single-input (propofol) single-output (bispectral index, BIS) model of the patient has been assumed for prediction as well as for simulation. A set of 12 patient models were studied and interpatient variability and disturbances are used to assess robustness of the controller. Furthermore, the controller guarantees the stability in a desired range. The applicability of the predictive controller in a real-life environment via simulation studies has been assessed. Index Terms--Anesthesia, constraints, drug dosing control, model-based predictive control, nonlinear model, robustness.

For several decades, a number of methods have been developed for the noninvasive assessment of the level of consciousness during general anesthesia. In this paper, detrended fluctuation analysis is used to study the scaling behavior of the electroencephalogram as a measure of the level of consciousness. Three indexes are proposed in order to characterize the patient state. Statistical analysis demonstrates that they allow significant discrimination between the awake, sedated and anesthetized states. Two of them present a good correlation with established indexes of depth of anesthesia. The scaling behavior has been found related to the depth of anesthesia and the methodology allows real-time implementation, which enables its application in monitoring devices. Index Terms--Anesthesia, detrended fluctuation analysis, electroencephalography, monitoring.

Background: The adverse haemodynamic effects of the intravenous anaesthetic propofol are well known, yet few empirical models have explored the dose-response relationship. Evidence suggests that hypotension during general anaesthesia is associated with postoperative mortality. We developed a mechanism-based model that quantitatively characterises the magnitude of propofol-induced haemodynamic effects during general anaesthesia.Methods: Mean arterial pressure (MAP), heart rate (HR) and pulse pressure (PP) measurements were available from 36 healthy volunteers who received propofol in a step-up and step-down fashion by target-controlled infusion using the Schnider pharmacokinetic model. A mechanistic pharmacodynamic model was explored based on the Snelder model. To benchmark the performance of this model, we developed empirical models for MAP, HR, and PP.Results: The mechanistic model consisted of three turnover equations representing total peripheral resistance (TPR), stroke volume (SV), and HR. Propofol-induced changes were implemented by Emax models on the zero-order production rates of the turnover equations for TPR and SV. The estimated 50% effective concentrations for propofol-induced changes in TPR and SV were 2.96 and 0.34 μg ml-1, respectively. The goodness-of-fit for the mechanism-based model was indistinguishable from the empirical models. Simulations showed that predictions from the mechanism-based model were similar to previously published MAP and HR observations.Conclusions: We developed a mechanism-based pharmacodynamic model for propofol-induced changes in MAP, TPR, SV, and HR as a potential approach for predicting haemodynamic alterations.Clinical Trial Registration: NCT02043938. [ABSTRACT FROM AUTHOR]