Depth of anaesthesia monitors might help to individualize anaesthesia by permitting accurate drug administration against the measured state of arousal of the patient. In addition, the avoidance of awareness or excessive anaesthetic depth might result in improved patient outcomes. Various depth of anaesthesia monitors based on processed analysis of the EEG or mid-latency auditory-evoked potentials are commercially available as surrogate measures of anaesthetic drug effect. However, not all of them are validated to the same extent.

Given the fast development and increasing clinical relevance of ultrasound guidance for thoracic paravertebral blockade, this review article strives (1) to provide comprehensive information on thoracic paravertebral space anatomy, tailored to the needs of a regional anesthesia practitioner, (2) to interpret ultrasound images of the thoracic paravertebral space using cross-sectional anatomical images that are matched in location and plane, and (3) to briefly describe and discuss different ultrasound-guided approaches to thoracic paravertebral blockade. To illustrate the pertinent anatomy, high-resolution photographs of anatomical cross-sections are used. By using voxel anatomy, it is possible to visualize the needle pathway of different approaches in the same human specimen. This offers a unique presentation of this complex anatomical region and is inherently more realistic than anatomical drawings.

No abstract

Background The C50 of remifentanil for ventilatory depression has been previously determined using inspired carbon dioxide and stimulated ventilation, which may not describe the clinically relevant situation in which ventilatory depression occurs in the absence of inspired carbon dioxide. The authors applied indirect effect modeling to non-steady state Paco2 data in the absence of inspired carbon dioxide during and after administration of remifentanil. Methods Ten volunteers underwent determination of carbon dioxide responsiveness using a rebreathing design, and a model was fit to the end-expiratory carbon dioxide and minute ventilation. Afterwards, the volunteers received remifentanil in a stepwise ascending pattern using a computer-controlled infusion pump until significant ventilatory depression occurred (end-tidal carbon dioxide [Peco2] > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 ng/ml. Remifentanil pharmacokinetics and Paco2 were determined from frequent arterial blood samples. An indirect response model was used to describe the Paco2 time course as a function of remifentanil concentration. Results The time course of hypercarbia after administration of remifentanil was well described by the following pharmacodynamic parameters: F (gain of the carbon dioxide response), 4.30; ke0 carbon dioxide, 0.92 min-1; baseline Paco2, 42.4 mmHg; baseline minute ventilation, 7.06 l/min; kel,CO2, 0.08 min-1; C50 for ventilatory depression, 0.92 ng/ml; Hill coefficient, 1.25. Conclusion Remifentanil is a potent ventilatory depressant. Simulations demonstrated that remifentanil concentrations well tolerated in the steady state will cause a clinically significant hypoventilation following bolus administration, confirming the acute risk of bolus administration of fast-acting opioids in spontaneously breathing patients.

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.