The objective of the study was to determine the analgesic and sedative effects of epidural ketamine in the cow. Eight healthy cows weighing 350–450 kg were used. One of 3 doses of ketamine (0.5, 1 and 2.0 mg/kg) or a saline control were injected into the epidural space at the first intercoccygeal interspace in random sequence at one-week intervals. Ketamine was diluted in saline (0.9%) before the experiment, and the volume adjusted according to animal size. Analgesia was tested by applying a standard stimulus (needle insertion into the skin and deep muscle) and scored using a 3-point scale. A second voltage-based stimulus was also applied and the responses scored. Another scale was used for scoring the degree of sedation. The response and the degree of sedation were assessed before drug administration and at 2, 5, 10, 15 min, and every 15 min until 120 min after ketamine or saline administration. Ketamine produced dose-related analgesia of the tail, anus, perineum and vulva but not of the hindlimb area. The effect was dose-dependent in terms of intensity and duration. None of the doses produced analgesia when 70 or 80 volts were applied. Minimal side effects were observed. Epidural ketamine produces caudal analgesia in the cow. Further studies are required to determine whether this is sufficient for surgery.
A new inhalant anaesthetic, sevoflurane, was used to maintain anaesthesia in 40 animals (2 mules and 38 horses of 9 breeds) presented for various surgical procedures. Eighteen mares, 11 stallions and 11 geldings underwent 6 orthopaedic and 34 soft tissue operations. Induction of anaesthesia was achieved with combinations of xylazine (0.5–1.1 mg/kg), diazepam (0.03–0.1 mg/kg), butorphanol (0.02 mg/kg), guaifenesin (50–84 mg/kg) and ketamine (1.1 mg/kg). Following tracheal intubation, a surgical plane of anaesthesia was maintained with sevoflurane in oxygen delivered from a precision vaporiser. Temperature, ECG, arterial blood pressure and expired gas composition were monitored. Mechanical ventilation was used in most animals (n=37) because of hypoventilation (PaCO2 > 7.31 kPa [55 mmHg]). Following surgery, horses were moved to a recovery room and allowed to recover alone (n=36) or with assistance (n=4). Time to sternal recumbency, standing, the time when satisfactory coordination was present (after standing) and the number of attempts to stand were recorded. The quality of recovery was scored on a 1 (best) to 6 (worst) scale. Mean blood pressures at 30, 60, 90, 120 and 150 min of anaesthesia were 72, 73, 74, 75 and 72 mmHg, respectively. Systolic and diastolic pressures at 30, 60, 90, 120 and 150 min of anaesthesia were 97, 97, 94, 96, 93 and 59, 63, 64, 68, 67 mmHg, respectively. Dobutamine was used in 23 horses to maintain mean arterial blood pressure > 60 mmHg. Mean heart and respiratory rates at 30, 60, 90, 120 and 150 min of anaesthesia were 36, 38, 39, 38 and 38 beats/min, and 9, 8, 8, 8 and 8 breaths/min. Mean duration of anaesthesia was 121 rnin (sd: 56 min), mean time to sternal recumbency was 27 min (sd: 13 min), average time to standing (all horses) was 33 min (sd: 12 min) and time to satisfactory coordination was 44 min (sd: 13 min). Most horses (n=37) received xylazine during recovery (mean dose 0.18 mg/kg iv). The median number of attempts to sternal recumbency and standing were 1.0 (range; 1–7) and 2.0 (range; 1–20), respectively, while the median recovery score was 1.5 (range; 14). The ‘depth’ of anaesthesia was easy to control and recoveries were generally very satisfactory.
The objective of the study was to examine the relationship between the ‘depth’ of anaesthesia - as determined by clinical signs - and the bispectral index (BIS). Electroencephalograms (EEG)s were recorded in 8 female and 8 castrated male, healthy Norwegian landrace pigs undergoing isoflurane anaesthesia, from which the bispectral index (BIS) was calculated. Isoflurane was delivered in pure oxygen at end-tidal concentrations of 1.6, 1.9, 2.2 and 2.5%, in randomised order, for 30 min after which the EEG was recorded over a 5 min period. Anaesthetic depth was evaluated on a visual analogue scale (VAS) by an experienced anaesthetist. The 95% confidence interval for the mean correlation coefficient between BIS and VAS was calculated to be -0.52–0.30. Confidence intervals (95%) for the mean change in the BIS obtained during the conscious state and that obtained during anaesthesia at different isoflurane concentrations was also calculated. There was a significant decrease in the BIS recorded during consciousness and after 1.6% isoflurane anaesthesia, and between readings after inhalation of 2.2% and 2.5% isoflurane. This indicates that BIS does not accurately reflect ‘depth’ at surgical levels of isoflurane anaesthesia in the pig, and is of no use for this purpose.
The study aimed to investigate the stimulus to adrenocortical activity that is induced by halothane anaesthesia. Groups of 7 sheep were anaesthetised with thiopentone and halothane (TH) or acepromazine, thiopentone and halothane (ATH). During 120 min of anaesthesia hypotension was prevented (mean arterial blood pressure kept at pre-anaesthetic level) by infusion of a modified gelatine plasma replacer given to effect (0.34–1.1 litres with TH and 1.1–3.1 litres with ATH). Pulse rate, arterial blood pressure and gases were measured and sequential samples withdrawn for analysis of plasma cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Heart rate increased in the ATH but not the TH group. All sheep were well oxygenated but developed hypercapnia and respiratory acidosis. In both groups, cortisol increased more than 2-fold 20 min after the end of anaesthesia but there were no significant changes in ACTH. AVP was measured in the TH group only and increased 3-fold at the end of anaesthesia. Glucose and lactate remained stable except for lactate in the TH group which decreased during anaesthesia. These data indicate that hypotension is a major component of the stimulus inducing adrenocortical activity during halothane anaesthesia. However, maintenance of normotension did not entirely depress the response; halothane itself or decreased perfusion may also contribute.
The effects of medetomidine and atipamezole were examined in rainbow trout. Medetomidine proved to be an effective sedative but not an anaesthetic; its effects were antagonised by atipamezole. The clinical signs of medetomidine sedation were rapid settling to the bottom of the tank followed by progressive ataxia. The sedative effect was dose-dependent: at 1 mg/l, one of 6 fish rested on its side after 10 min, whereas at 20 mg/l all 6 rested on their sides. No loss of consciousness occurred.
The cardiopulmonary effects of an intravenous (iv) medetomidine injection (5 μg/kg) followed 5 min later by its infusion at 3.5 μg/kg/h for 115 rnin were studied in 9 horses and ponies. Five minutes after the end of infusion 60 μg/kg atipamezole were given. Physiological data during infusion were compared with pre-sedation values. Stroke volume was reduced significantly 5 min after initial medetomidine injection. Cardiac index was reduced significantly and systemic vascular resistance increased significantly for the first 20 min, but returned towards pre-sedation values after this time. Arterial blood pressures were reduced significantly from 30 min until the end of the procedure (minimum MAP was 102.4 ± 9.61 mmHg). Mixed venous oxygen tension was reduced significantly during the infusion. Respiratory rate fell and PaCO2- rose significantly from 40 min onward. Other variables showed no significant changes. The horses recovered rapidly after atipamezole was injected. Arterial blood pressures remained significantly lowered, but other cardiovascular variables returned towards pre-sedation values. It is concluded that the infusion of medetomidine at 3.5 μg/kg/h causes minimum cardiopulmonary depression once the effects of an initial 5 μg/kg injection have waned, and so could prove suitable as part of an anaesthetic technique in equidae.
To use American College of Veterinary Internal Medicine (ACVIM) criteria to evaluate a high-definition oscillometric (HDO) blood pressure monitoring device versus invasive blood pressure (IBP) measurement in normotensive rabbits anaesthetized with two different anaesthetic protocols.Prospective experimental study.A group of 20 healthy adult New Zealand White rabbits weighing 4.36 ± 0.37 kg (mean ± standard deviation).Rabbits were premedicated with butorphanol 0.5 mg kg–1 and midazolam 0.5 mg kg–1 subcutaneously (SC, group BMA) or ketamine 25 mg kg–1 and medetomidine 0.4 mg kg–1 SC (group KM). Anaesthesia was induced with alfaxalone administered intravenously (group BMA) or isoflurane by face mask (group KM) and maintained with isoflurane in oxygen. IBP was measured from the central auricular artery. The cuff for the HDO monitor was placed distal to the left elbow and distal to the left tarsus. Agreement between invasive and HDO measurements was evaluated using Bland–Altman method.In group KM there was better agreement between the HDO device and IBP when the cuff was placed on the thoracic limb, with 100% and 91% of the readings for mean (MAP) and diastolic arterial pressure (DAP), respectively, within 10 mmHg of the IBP measurements. The agreement, although worse, also met the ACVIM criteria for systolic arterial pressure (SAP; 53% of the readings within 10 mmHg). In group BMA, the device met the criteria with the cuff on the thoracic limb only, and only for MAP and DAP (73% and 75% of the measurements within 10 mmHg of the IBP, respectively) but not for SAP (12%).The HDO device met most of the ACVIM criteria for noninvasive blood pressure measurement in anaesthetized rabbits, specifically when the cuff was placed distal to the elbow and the anaesthetic protocol included ketamine and medetomidine.
The purpose of this study was to investigate the effect of a single dose (50 mg/kg) of guaiphenesin on recumbency time, surgical conditions and the ‘quality’ of anaesthesia in ponies anaesthetised for castration. Sixteen ponies were sedated with romifidine 100 μg/kg and anaesthetised with ketamine (2.2 mg/kg). Ponies allocated to Group A received no treatment and those in Group B were given 50 mg/kg of a 15% guaiphenesin solution. Guaiphenesin was given as a rapid iv injection immediately after induction of anaesthesia. All ponies were subsequently castrated. The mean (± se) time of recumbency in Group A was 20.9 ± 1.37 min and in Group B 27.2 ± 2.1 min to (P<0.05). Subjective assessment scores for the quality of surgical conditions and anaesthesia itself were significantly greater (indicating better conditions) in ponies receiving guaiphenesin, although there was no difference between groups in the quality of recovery.
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.
SUMMARY A study comparing invasive versus oscillometric techniques for the measurement of arterial blood pressure was carried out in 4 anaesthetised sows undergoing laparoscopy. Regression analysis was used to determine the correlation coefficient. Bias was 19.2 for systolic, 20.6 for mean and 18.8 for diastolic. Both bias and precision showed a consistent underestimation of blood pressure values recorded by oscillometry. These results do not support the use of the oscillometric method when accurate figures for blood pressure are required in sows.
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.
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.
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.
This study was undertaken to evaluate the effect of 3 different doses of epidurally administered morphine sulphate on the minimum alveolar concentration (MAC) of isoflurane in healthy cats. Five 4-year-old, spayed female cats weighing 4.7 ± 0.8 kg were allocated randomly to receive one of 3 doses of morphine on each study day. The 3 doses of morphine were 0.05, 0.1 and 0.2 mg/kg bwt and each cat was studied 3 times so that each cat received all doses. On each study day, cats were anaesthetised with isoflurane and instrumented. The MAC of isoflurane was determined in triplicate and morphine sulphate was administered via an epidural catheter chronically implanted prior to the study. Maximum MAC reduction was determined over the following 2 h. At the end of the study cats were allowed to recover. There was a significant reduction in MAC of isoflurane, with all doses of epidural morphine (P<0.05). The maximum reduction in MAC of isoflurane after 0.05 mg/kg bwt, 0.10 mg/kg bwt and 0.20 mg/kg bwt morphine was 21.4 ± 9.796, 30.8 ± 9.696, and 30.2 ± 6.8%, respectively, with no significant difference between doses. Systolic, mean and diastolic blood pressure, heart rate, respiratory rate and arterial pH decreased significantly whereas arterial carbon dioxide tension increased significantly after morphine administration (P<0.05). The means for all variables returned to pre-morphine values when the end-tidal isoflurane concentration was reduced to the new MAC point. In conclusion, epidural morphine decreased the concentration of isoflurane required to prevent movement in response to noxious mechanical stimulation to the tail base. A similar effect may be seen clinically allowing lower doses of isoflurane to be used to provide surgical anaesthesia for procedures involving the hind limbs, pelvis and tail.
Nine horses were each anaesthetised for 40 min using SufentaniVhalothane. No surgery was performed. After premedication (detomidine 5 pgkg bwt iv) induction of anaesthesia was achieved by a combination of guaiphenesinlthiopentone. Anaesthesia was maintained by inhalation of halothane (0.8%) in oxygen. Six horses (Group 1) received 1 pgkg bwt sufentanil followed by a second injection (1 pg/kg bwt) after 20 min. Three horses (Group 2) received 2 pg/kg bwt sufentanil also followed by a second injection (2 pg/kg bwt) after 20 min. Each sufentanil injection produced a slight decrease in mean arterial blood pressure with a gradual return to the initial pressure. Bradycardia was also observed. Sufentanil injection induced apnoea needing artificial ventilation. Arterial blood was sampled for analysis during the anaesthetic procedure. At the end of anaesthesia, 1 h and 24 h after rising, venous blood was sampled to determine concentrations of lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and creatine phosphokinase (CPK). Values obtained were compared with values in blood taken before premedication. Plasma glucose and lactate concentrations just before sufentanil administration, at the end of anaesthesia and 1 h after rising were compared to control values. Plasma glucose concentration increased significantly during anaesthesia but returned to normal values 1 h after rising. All other parameters stayed within physiological ranges. In both groups spontaneous respiration returned 20–25 min after the second sufentanil injection. Recovery was uneventful.
The dissociative anaesthetic ketamine is reported to provide potent analgesia after administration of subanaesthetic doses in human beings. To evaluate the analgesic effects of ketamine as an adjunct to inhalation anaesthesia in horses, haemodynamic and electroencephalographic changes were recorded for 10 min after injection of ketamine (0.5 mg/kg iv; n=7) or equal volumes of 0.9% NaCl solution (n=5) in surgically stimulated horses anaesthetised at approximately 1.3% end-tidal concentration of isoflurane. Neither the haemodynamic variables (mean arterial blood pressure and heart rate) nor the quantitated EEG variables (theta/delta ratio, alpha/delta ratio, beta/delta ratio, median power frequency) and 80% spectral edge frequency were affected significantly by the ketamine dose used. Comparing data obtained from both groups of horses, our results suggest that iv administration of 0.5 mg/kg bwt of ketamine was ineffective in suppressing haemodynamic and electroencephalographic responses to surgical stimulation.
The reversal of detomidine-induced sedation with iv atipamezole was studied in 6 horses. All horses were injected iv with 10 μg and 20 μg/kg bwt detomidine and 15 min later this was followed by 6-, 8- and 10-fold doses of iv atipamezole. Atipamezole caused a quick arousal in all horses with minor side effects. Bradycardia, rhythm disturbances and head ptosis caused by detomidine were not abolished completely at the end of the 15 min observation period, even with the highest atipamezole doses. All horses remained slightly sedated but without ataxia. There were no significant differences in head height, heart rate and sedation score between the different doses of atipamezole for either dose of detomidine. According to the degree of sedation, doses of 100 μg to 160 μg/kg bwt atipamezole are adequate to antagonise detomidine-induced sedation in the horse.
The cardiovascular effects of doxacurium were studied in 6 isoflurane-anaesthetised dogs. Each dog was anaesthetised twice, receiving doxacurium (0.008 mg/kg bwt) or placebo iv. Dogs were ventilated to normocapnia. Heart rate, cardiac index, systolic, diastolic, and mean arterial blood pressures, stroke volume, pulmonary vascular resistance, pulmonary artery wedge pressure, systemic vascular resistance, and pulmonary arterial pressure were determined. Neuromuscular blockade was assessed using the train-of-four technique. After recording baseline values, dogs randomly received either doxacurium or placebo iv, and data were recorded at 5, 10, 15, 30, 45, 60, 75, 90, 105 and 120 min. At 120 min, dogs treated with doxacurium received edrophonìum (0.5 mg/kg bwt iv) to antagonise neuromuscular blockade; dogs treated with placebos received saline iv. No statistically significant differences were detected after doxacurium compared to placebo. In both the doxacurium and placebo groups, significant increases in systolic arterial blood pressure, cardiac index, and stroke volume and a significant decrease in systemic vascular resistance occurred with time. Doxacurium depressed twitch tension 100% in all dogs (time to maximal twitch depression, 11 ± 7 min). First twitch tension was less than 10% of baseline values in all dogs at the time (120 min) of edrophonium administration. Additional edrophonium (1.0 ± 0.4 mg/kg iv) was required to obtain a fourth twitch to first twitch ratio of greater than 0.70. In conclusion, doxacurium is a long-acting neuromuscular blocking agent with no significant cardiovascular effects in isoflurane-anesthetised dogs. In dogs, doxacurium is indicated primarily for long surgical procedures requiring neuromuscular blockade and cardiovascular stability.
