Journal of Veterinary Anaesthesia最新文献

One hundred and fifty years after the first general anaesthetic in 1846 our knowledge about the mechanisms of general anaesthetics is still very sparse. The concept ‘depth of anaesthesia’ was introduced by John Snow (1847). He described ‘5° of narcotism’. Because one single agent had to provide all the components of general anaesthesia, the main problem for the anaesthetist was to avoid morbidity and mortality associated with excessively deep anaesthesia. The introduction of curare in 1942 allowed muscle relaxation required for surgery during a lighter level of anaesthesia, but also changed the emphasis from the problem of too deep anaesthesia and death, to too light anaesthesia and litigation. The problem of awareness during general anaesthesia with muscle relaxants provided the main impetus for monitoring depth of anaesthesia.

During daily clinical practice the anaesthesiologist relies on clinical signs to evaluate anaesthetic depth, although several studies have shown a poor correlation between the 2 (Cullen et al. 1972; Evans and Davies 1984; Russell 1993). Different methods have been used in attempts to measure anaesthetic depth (Evans and Davies 1984; Stanski 1994), but none have been developed to a state where they can be used routinely in the operating theatre. This review will cover some of the parameters used to evaluate anaesthetic depth.

The pharmacodynamics and pharmacokinetics of ketamine, when administered by infusion as an adjunct to halothane anaesthesia in horses, were investigated in 5 equine patients presented for routine castration. Anaesthesia was induced with detomidine, 20 μg/kg, followed by ketamine, 2.2 mg/kg bwt, the trachea intubated and the horses allowed to breathe halothane in oxygen. Five minutes later, a constant rate infusion of ketamine, 40 μg/kg min, was commenced and the halothane vaporiser concentration adjusted to maintain a light plane of anaesthesia. The mean infusion duration was 62 min (range 40–103). The ketamine was switched off approximately 15 min before the halothane. Plasma ketamine and norketamine levels, determined by high performance liquid chromatography, ranged from 0.74–2.04 μg/ml and 0.15–0.75 μg/ml, respectively, during the infusion period.

The harmonic mean elimination half-life of ketamine was 46.1 min, mean volume of distribution at steady state (Vdss) was 1365 (271) ml/kg, mean body clearance (Cl) was 32.3 (9.1) ml/min.kg, and average mean residence time for the infusion (MRTinf) was 105.9 (20.4) min, respectively.

Following termination of halothane, mean times to sternal recumbency and standing were 21.1 (6.9) and 41.6 (17.0) min, respectively. Surgical conditions were considered highly satisfactory, and physiological parameters were well preserved in most animals.

Some metabolic and endocrine responses to anaesthesia in sheep were studied. Adult sheep were anaesthetised with thiopentone and halothane (n=9), acepromazine, thiopentone and halothane (n=8) and pentobarbitone (n=10) on separate occasions. Routine cardiovascular monitoring was carried out and blood samples were taken for assay of cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Halothane anaesthesia induced hypotension, hypercapnia and respiratory acidosis. Sheep anaesthetised with pentobarbitone were also hypercapnic and acidotic but did not develop hypotension. Plasma cortisol, ACTH and AVP (mean maximum values: cortisol: 83 ng/ml, ACTH 278 ng/ml, AVP 135 pg/ml), increased during halothane anaesthesia but did not change significantly from control values during pentobarbitone anaesthesia (mean maximum values: cortisol: 30 ng/ml, ACTH 71 ng/ml, AVP 7.8 pg/ml). Glucose tended to increase during both halothane and pentobarbitone anaesthesia but lactate decreased. It is not clear what facet of halothane anaesthesia evokes the stress response but it may be associated with cardiovascular depression.

Medetomidine (200 μg/kg) was administered orally and, on a seperate occasion, im to 7 cats. Peak serum drug concentrations were reached more slowly after oral (43.6 ± 14.3 min) than after im administration (21.6 ± 10.0 min). The onset of sedation and recumbency lagged after oral administration. There were no statistically significant differences between the 2 routes of administration in peak serum concentrations, systemic drug availability or extent of sedation. However, there was considerable variation in these parameters between individuals after oral administration. The extent of salivation correlated negatively with systemic drug availability after oral administration. Where excessive salivation did not occur, systemic drug availability and the depth of sedation were comparable to, or even higher than, were obtained after the corresponding im administrations. In conclusion, oral administration of medetomidine induced a clinical sedation but, when accurate dosing is a necessity, the oral route may not be very reliable due to possible drug losses through salivation.

The partitioning of propofol within the blood, when administered in its usual emulsion carrier, has been determined in vitro in sheep. The blood:plasma ratio was found to be 1.13 and the blood-cell:plasma ratio 1.42. When oxalate was used as the anticoagulant, the plasma protein binding was calculated to be 92.6% - slightly lower than reported for dog, rat, rabbit and man. However, when heparin was the anticoagulant, the binding was significantly less, 83.0%. Differences from some results in the literature may be attributable to other workers using propofol without the lipid emulsion carrier. From the results of this study it is argued that anaemia and plasma levels of protein and lipid may affect propofol requirements.