Effects of thiopentone on the equine electroencephalogram during anaesthesia with halothane in oxygen

Objective To characterise the effects of thiopentone on the equine electroencephalogram during halothane anaesthesia. Study design Prospective controlled study. Animals Eight healthy Welsh mountain pony geldings between 5 and 9 years old and weighing between 270 and 330 kg (mean 301 kg). Methods Anaesthesia was induced with thiopentone and maintained using halothane in oxygen. End tidal halothane was maintained above 0.75 and below 0.85%. EEG was recorded continuously and a binaural broad band click stimulus was provided throughout the experiment at 6.1224 Hz. An infusion of 500 mg thiopentone was given over 5 minutes. Samples were taken for blood gas analysis and plasma thiopentone assay (HPLC) 5 minutes prior to the start of the infusion and at 3, 5, 7, 10, 15, 20, 30, 45 and 60 minutes. The median and 95th percentile of the EEG were calculated using standard statistical techniques and the mid‐latency of the auditory evoked response was generated. The values of EEG variables at each time point were compared to the average value for the 15 minute period before the infusion was started. Arterial blood gas values and plasma thiopentone concentration were compared to the baseline sample taken prior to the start of the infusion. Comparisons were made using analysis of variance for repeated measures followed by Dunnett's test if a significant difference was detected. Results The peak serum plasma concentration was 14.5 ± 2.4 µg mL^?1 (mean ± SD) occurring 5 minutes after the start of the infusion. The 95% spectral edge frequency of the EEG decreased by a maximum of 27.4 ± 18.4% 7 minutes after the start of the thiopentone infusion. No changes were seen in median frequency of the EEG or the second differential of the middle latency auditory evoked response. Conclusions These results, coupled with the lack of antinociceptive action of thiopentone, support the hypothesis that median frequency of the EEG may be a useful indicator of nociception in anaesthetized animals. Clinical relevance If the EEG is to become a useful monitoring technique then it is important to understand the relative contribution of changing plasma concentrations of the agents used in anaesthesia.     

Effects of guaiphenesin on the equine electroencephalogram during anaesthesia with halothane in oxygen

Objective To identify and characterize the effects of guaiphenesin (GGE) on the electroencephalogram during halothane anaesthesia. Study design Prospective controlled study. Animals Eight healthy Welsh mountain pony geldings between 5 and 9 years old and weighing between 270 and 330 kg (mean 301 kg). Methods Anaesthesia was induced with thiopentone and maintained using halothane in oxygen. End tidal halothane was maintained above 0.75 and below 0.85%. The EEG was recorded continuously and a binaural broad band click stimulus was provided throughout the experiment at 6.1224 Hz. An infusion of 1500 mg GGE was given over 5 minutes. Samples were taken for blood gas analysis and plasma GGE assay (HPLC) 5 minutes prior to the start of the infusion and at 3, 5, 7, 10, 15, 20, 30, 45 and 60 minutes thereafter. The median and 95th percentile of the EEG were calculated using standard statistical techniques and the mid‐latency of the auditory evoked response was generated. The values of EEG variables at each time point were compared to the average value for the 15 minute period before the infusion was started. Arterial blood gas values and plasma GGE concentration were compared to the baseline sample taken prior to the start of the infusion. Comparisons were made using analysis of variance for repeated measures followed by Dunnett's test if a significant difference was detected. Results The peak serum plasma concentration was 49.6 ± 7.8 μg mL^?1 (mean ± SD) occurring five minutes after the start of the infusion. The 95% spectral edge frequency (F95) of the EEG decreased by a maximum of 5.2 ± 14.3% 5 minutes after the start of the GGE infusion. This change did not reach statistical significance (p= 0.07). When three nonresponders were excluded, the depression in F95 at 5 minutes in the remaining five animals became 13.0 ± 12.0% and was statistically significant (p= 0.02). No changes were seen in median frequency of the EEG or the second differential of the middle latency auditory evoked potential. Conclusions These results did not demonstrate any statistically significant GGE‐induced changes in the EEG. However, there was some visible depression of F95 in five of the animals studied even though the dose of GGE used was considerably less than that used in most clinical circumstances. Clinical relevance The EEG effects seen in this study concur with the commonly held view that while GGE has some sedative effects, it is not a reliable anaesthetic agent.     

Analysis of the frequency spectrum of the equine electroencephalogram during halothane anaesthesia

The electroencephalogram (EEG) has been used in human clinical anaesthesia as an indicator of cortical activity and as an indicator of the depth of anaesthesia. It would be useful if it provided a reliable indication of the depth of anaesthesia of horses. In this study anaesthesia was induced with thiopentone and maintained with halothane in nine ponies. The end tidal halothane concentration (P_E-Hal) was monitored and 20 seconds of EEG were recorded at 0·8 per cent, 1·0 per cent and 1·2 per cent halothane, equivalent to the minimum alveolar concentration (mac), 1·25 mac and 1.5 mac. Each 20 second block of data was divided into one second segments and averaged to give one second of averaged EEG from which a frequency spectrum was obtained by using a fast Fourier transformation. The power of the waveform at low frequency (1 to 3 Hz) was compared with that at higher frequency (9 to 11 Hz). The median frequency and 95th percentile (spectral edge) were also calculated. The spectral edge frequency had the best correlation with P_E-Hal     

Comparison of electroencephalogram activity and auditory evoked responses during isoflurane and halothane anaesthesia in the rat

Objectives To compare the second differential index (SDI) calculated from the auditory evoked potential (AEP) and electroencephalogram (EEG) parameters: median frequency (MF), spectral edge frequency (SEF) and burst suppression rate (BSR) determined at four equivalent minimum alveolar concentrations (MAC) of isoflurane or halothane. Animals Twelve male Wistar rats weighing 418 g (SD ± 18.4 g). Methods Auditory evoked potentials and EEG responses were recorded in animals implanted with electrodes at established anaesthetic concentrations. Depth of anaesthesia was assessed using the strength of the pedal withdrawal reflex (PWR), and data were analysed using repeated measures anova and paired t‐tests. Results The SEF tended to decrease with increasing depth of halothane anaesthesia (F = 4.198, p = 0.05), but not with isoflurane. The MF and SDI were significantly higher during halothane than with isoflurane (F = 5.82, p = 0.036 and F = 5.263, p = 0.045, respectively) at equivalent depths of anaesthesia, and EEG burst suppression occurred at deeper planes of isoflurane but not halothane anaesthesia. Conclusions The study demonstrated that EEG and AEP characteristics recorded at MAC equivalent concentrations were suppressed to a greater degree by isoflurane than by halothane. These findings have strong implications for research projects where EEG recordings are collected, and also cast more general doubts upon the value of such parameters for evaluating depth of isoflurane anaesthesia in rats.     

Effects of peri-operative morphine administration during halothane anaesthesia in horses

OBJECTIVE: To study the effects of morphine on haemodynamic variables, blood gas values and the requirement for additional anaesthetic drugs in horses undergoing surgery. STUDY DESIGN: Prospective randomized study. METHODS: Thirty-eight client-owned horses, ASA(American Society of Anesthesiologists) category I or II, undergoing elective surgical procedures, were studied. Horses were divided between two groups, and were paired according to operation, anaesthetist, body position during surgery, mass and breed. Group M+ received morphine by intravenous (IV) injection (0.15 mg kg(-1)) before induction of anaesthesia and then by infusion (0.1 mg kg(-1) hour(-1)) throughout anaesthesia. Group M- received the same anaesthetic technique (pre-anaesthetic medication with romifidine (100 microg kg(-1)) IV; induction with ketamine (2.2 mg kg(-1)) and diazepam (50 microg kg(-1)) IV; maintenance with halothane), except that morphine was excluded. Both groups received flunixin IV (1.1 mg kg(-1)) before surgery. Both groups also received 50% nitrous oxide for the first 10 minutes of anaesthesia. During anaesthesia, end-tidal halothane was maintained at 0.9% (+/-0.1%) in both groups. Heart rate (HR) and respiratory rate (fr), systolic, mean and diastolic arterial pressures were recorded every 5 minutes. Arterial blood samples were analysed every 20 minutes. Additional anaesthetics (ketamine and midazolam) were administered whenever the horse moved. Dobutamine was infused to maintain mean arterial pressure (MAP) > 58 mm Hg, but was discontinued when MAP reached 68 mm Hg. Mechanical ventilation was imposed when PaCO(2) exceeded 9.3 kPa (70 mm Hg). RESULTS: Haemodynamic data (HR and MAP) and blood gas measurements were analysed using repeated measure analysis using a mixed covariance pattern model (SAS version 8.2). A Student's t-test was used to investigate differences between groups in the doses of additional anaesthetics required. There were no significant differences between M+ or M- groups in MAP (p = 0.65), HR (p = 0.74), PaO2 (p = 0.40) or PaCO2 (p = 0.20). Fewer horses in the M+ group received additional anaesthetics (15.8% compared to 21.1% in M- group), and the mean dose of ketamine required was higher in the M- group (mean +/- SD: M-, 0.93 +/- 0.70; M+, 0.45 +/- 0.17). These differences were not statistically significant (p = 0.28). CONCLUSIONS: Pre-anaesthetic and peri-operative morphine administration is not associated with significant haemodynamic or ventilatory changes. Horses receiving morphine tended to receive fewer and lower doses of additional anaesthetic drugs, although this was not statistically significant.     

Doxapram infusion during halothane anaesthesia in ponies

Doxapram, 0.05 mg/kg bodyweight/min, was infused during the second hour of 2 h halothane anaesthesia in six ponies. Two of the ponies were anaesthetised on a second occasion as controls and given 5 per cent dextrose in place of the doxapram. Respiratory depression typical of halothane anaesthesia in ponies developed in the first hour of anaesthesia and continued during the second hour in the control animals. During doxapram infusion arterial carbon dioxide tension decreased and pH increased. Arterial blood pressure increased but there was no change in pulse rate, the electrocardiogram or arterial oxygen tension. Anaesthesia lightened during doxapram infusion necessitating an increase in the vapouriser setting in order to prevent arousal. Recovery from anaesthesia appeared unaffected by the doxapram infusion.     

Effects of halothane anesthesia on equine liver function

Effects of halothane anesthesia were investigated in ponies prepared surgically with chronic external biliary fistulas (T tubes) to determine the effects on liver function and biliary excretion during 2 hours of anesthesia. Four studies were performed on 2 ponies, 2 to 6 months after surgery with the enterohepatic circulation held intact between studies. Intravenous bile acid infusion was used to maintain steady-state bile flow, bilirubin, and bile acid excretion during each study. Compared with the immediate 2-hour preanesthesia values (base line), halothane caused a 138% increase in bilirubin excretion, a 60% increase in biliary bilirubin concentration, and a 43% increase in PCV. Halothane anesthesia also caused a 16% reduction in plasma bilirubin, a 46% reduction in biliary bile acid concentration, and a 27% reduction in bile acid excretion. The bile acid independent fraction of bile flow appeared to increase. Plasma aspartate transaminase concentration did not change during anesthesia. The ratio of conjugated bilirubin fractions in bile [82% to 83% disconjugates of glucuronide and glucoside (2 forms) and 17% to 18% monoconjugates of glucoside, glucuronide, and xyloside] did not change during anesthesia and less than 1% was excreted unconjugated. Halothane anesthesia did not appear to affect adversely the activity of the transferase-conjugating enzymes in the presence of an increased bilirubin load. Seemingly, greatly increased conjugated bilirubin excretion observed during halothane anesthesia was most likely the result of a combination of increased hepatic clearance from plasma and increased hepatic bilirubin production from turnover of free hepatic heme or heme from the induced cytochrome P-450 system.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of posture and intraruminal pressure on the bronchial calibre of cattle during xylazine/halothane anaesthesia

The effects of changes in body position and intraruminal pressure on the bronchial calibre of anaesthetised, paralysed adult cattle were investigated using a computer-aided forced airflow oscillation technique which enabled the measurement of specific lower airways conductance (sGlaw), expiratory reserve volume (ERV) and residual resistance (RA). sGlaw and RA were highest in dorsal and lowest in sternal recumbency, but ERV was very much greater in sternal recumbency than in other positions. Turning the animals from right to left lateral recumbency resulted in a marked reduction in sGlaw and increase in ERV, providing further evidence of functional impairment of the dependent areas of the lungs of large animals. Changes in intraruminal pressure had little effect on bronchial calibre, suggesting that the respiratory dysfunction resulting from ruminal tympany is primarily caused by a reduction in compliance rather than an increase in airway resistance.     

Effects of altering the sequence of midazolam and propofol during co‐induction of anaesthesia

ObjectiveTo assess the effects of varying the sequence of midazolam and propofol administration on the quality of induction, cardiorespiratory parameters and propofol requirements in dogs.Study designRandomized, controlled, clinical study.AnimalsThirty‐three client owned dogs (ASA I‐III, 0.5–10 years, 5–30 kg).MethodsDogs were premedicated with acepromazine (0.02 mg kg^?1) and morphine (0.4 mg kg^?1) intramuscularly. After 30 minutes, group midazolam‐propofol (MP) received midazolam (0.25 mg kg^?1) intravenously (IV) before propofol (1 mg kg^?1) IV, group propofol‐midazolam (PM) received propofol before midazolam IV at the same doses, and control group (CP) received saline IV, instead of midazolam, before propofol. Supplementary boluses of propofol (0.5 mg kg^?1) were administered to effect to all groups until orotracheal intubation was completed. Behaviour after midazolam administration, quality of sedation and induction, and ease of intubation were scored. Heart rate (HR), respiratory rate, and systolic arterial blood pressure were recorded before premedication, post‐premedication, after midazolam or saline administration, and at 0, 2, 5, and 10 minutes post‐intubation. End‐tidal CO₂ and arterial oxygen haemoglobin saturation were recorded at 2, 5 and 10 minutes post‐intubation.ResultsQuality of sedation and induction, and ease of intubation were similar in all groups. Incidence of excitement was higher in the MP compared to CP (p = 0.014) and PM (p = 0.026) groups. Propofol requirements were decreased in MP and PM groups with respect to CP (p < 0.001), and in PM compared to MP (p = 0.022). The HR decreased after premedication in all groups, and increased after midazolam and subsequent times in MP (p = 0.019) and PM (p = 0.001) groups. Incidence of apnoea and paddling was higher in CP (p = 0.005) and MP (p = 0.031) groups than in PM.Conclusions and clinical relevanceAdministration of midazolam before propofol reduced propofol requirements although caused mild excitement in some dogs. Administration of propofol before midazolam resulted in less excitatory phenomena and greater reduction of propofol requirements.     

Motility of the oesophagus and gastro-oesophageal junction during halothane anaesthesia in sheep

Electromanometry and electromyography were used to study gastro-oesophageal motility in two planes of halothane anaesthesia in sheep. Gastro-oesophageal motility when present was greater in light than in deep anaesthesia. The caudal thoracic oesophagus contracted more frequently and for longer than the rostral thoracic oesophagus. In light anaesthesia oesophageal movements were peristaltic in direction with a propagation velocity of 26–29 cm sec^-1. Rumen pressures increased throughout anaesthesia and the rate of increase was greatest when the plane of anaesthesia was deep at the start. Gastro-oesophageal reflux (GOR) occurred in both planes of anaesthesia and must occur by passive mechanisms during deep anaesthesia because gastro-oesophageal motility was inhibited.A high pressure zone (HPZ) was demonstrated for a length of 2.9 cm at the gastro-oesophageal junction with a balloon-tipped catheter and a pull through technique. Open-tipped catheters could detect the HPZ but were less sensitive. The pressure in the HPZ was not significantly influenced by the depth of anaesthesia used. In 80% of cases of light anaesthesia an increase in HPZ pressure preceeded the contraction of the cranial sac of the rumen. In deep anaesthesia the HPZ continued to have rhythmic changes in tone. Spontaneous GOR coincided with a maximum gastro-oesophageal pressure gradient in 24% of cases. Rumen insufflation with oxygen provoked GOR at a rumen pressure above 33 mmHg compared with 7.2 mmHg during spontaneous reflux.The study demonstrates that a gastro-oesophageal pressure gradient was not primarily responsible for the initiation of GOR during anaesthesia and that the HPZ at the gastro-oesophageal junction of sheep had some of the properties of a lower oesophageal sphincter and played an important role in the initiation of GOR during anaesthesia.     

Effect of alfaxalone infusion on the electroencephalogram of dogs anaesthetized with halothane

ObjectiveTo describe the effects of alfaxalone on the canine electroencephalogram (EEG).Study designExperimental study.AnimalsEight healthy adult Huntaway dogs.MethodsAnaesthesia was induced with propofol and maintained with halothane (0.85-0.95 end-tidal volume %) in oxygen. Animals were ventilated to maintain stable end-tidal CO₂ and halothane concentrations. Following a 30 minute stabilisation period, alfaxalone (0.5 mg kg^?1) was infused intravenously over a 5 minute period. The electroencephalogram was recorded from the beginning of the stabilisation period until 60 minutes following the start of alfaxalone treatment. Data were subjected to fast Fourier transformation, and median frequency, 95% spectral edge frequency and total EEG power were calculated. Two-factorial repeated measures anova (time and EEG channels were factors) was used for statistical analysis (p<0.05).ResultsA shift in the dominant frequency band from beta to delta after alfaxalone treatment and occasional burst suppression were observed. Median frequency decreased significantly below baseline (9.2 ± 1.4 Hz) (mean ± SD) during alfaxalone infusion. The lowest value (4.8 ± 1.2 Hz) was recorded 5 minutes after the start of infusion. Spectral edge frequency also decreased below baseline (26.2 ± 1.5 Hz) and the lowest value (22.6 ± 1.5 Hz) also was detected at 5 minutes after the start of infusion. Total EEG power did not change significantly. In some frequencies EEG power increased soon after the start of alfaxalone infusion, then decreased below baseline later (biphasic pattern).Conclusions and clinical relevanceAlfaxalone induced biphasic changes on EEG and decreased F₅₀ and F₉₅ in halothane anaesthetized dogs.     

Effects of plasma expansion on the pituitary-adrenocortical response to halothane anaesthesia in sheep

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.     

Endocrine and metabolic responses in sheep during halothane and pentobarbitone anaesthesia with dobutamine infusion

The study investigated the stimulus to pituitary-adrenocortical activity (PACA) during halothane anaesthesia. Groups of six sheep were anaesthetized with thiopentone/halothane (TH group), acepromazine/thiopentone/halothane (ATH group) or pentobarbitone (P group). Dobutamine was infused in the TH and ATH groups to prevent hypotension (0.3–1.4 μg/kg/min) and in the P group at 0.05 μg/kg/min. Pulse rate, arterial blood gases and pressure (ABP) were measured and sequential blood samples taken for assay of cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Pulse rate increased in all groups. Arterial blood pressure decreased by 13% in TH, by 24% in ATH and remained stable in P. All three groups developed hypercapnia and acidosis but were well oxygenated. Cortisol increased in all groups; with ATH the sevenfold rise occurred earlier than with either TH (sixfold rise) or P (fivefold rise). Adrenocorticotrophic hormone changes were as for cortisol but AVP increases were not consistent. Glucose and lactate were stable, but lactate was lowest with ATH. Dobutamine infusion failed to prevent hypotension during halothane anaesthesia and PACA appeared proportional to the hypotension. Dobutamine may have stimulated ACTH and cortisol release after 120 min. Halothane-induced hypotension may cause adrenocortical activity but a direct effect of halothane cannot be ruled out.     

Effects of premedication with fentanyl and midazolam on mask induction of anaesthesia of dogs with sevoflurane

Fourteen beagles were used to determine the effects of fentanyl and midazolam as a premedicant for mask induction of anaesthesia with sevoflurane. The drugs were administered to each dog in a randomised cross-over design with a seven-day washout period between experiments. After a 15-minute equilibration period, a treatment consisting of fentanyl (10 mug/kg bodyweight) and midazolam (0.2 mg/kg) was given either intravenously or intramuscularly. Anaesthesia was then induced by the use of a facemask with sevoflurane in 100 per cent oxygen at a flow rate of 4 l/minute. Vaporiser settings were increased by 0.8 per cent at 15-second intervals until the value corresponding to 4.8 per cent sevoflurane was achieved. The time to the onset and cessation of involuntary movements, loss of the palpebral reflex, negative response to tail-clamp stimulation, and endotracheal intubation and cardiopulmonary variables were measured. Both the treatments with tentanyl and midazolam resulted in a shorter and smoother induction of anaesthesia than treatment with saline, and the cardiopulmonary changes were smaller and milder.     

Investigation of the EEG effects of intravenous lidocaine during halothane anaesthesia in ponies

OBJECTIVE: To record the electroencephalographic changes during castration in ponies anaesthetized with halothane and given intravenous (IV) lidocaine by infusion. The hypothesis tested was that in ponies, IV lidocaine is antinociceptive and would therefore obtund EEG changes during castration. ANIMALS: Ten Welsh mountain ponies referred to the Department of Clinical Veterinary Medicine, Cambridge for castration under general anaesthesia. MATERIALS AND METHODS: Following pre-anaesthetic medication with intramuscular acepromazine (0.02 mg kg(-1)) anaesthesia was induced with IV guaiphenesin (60 mg kg(-1)) and thiopental (9 mg kg(-1)) and maintained with halothane at an end-tidal concentration (FE'HAL) of 1.2%. A constant rate infusion of IV lidocaine (100 microg kg(-1) minute(-1)) was administered throughout anaesthesia. The electroencephalogram (EEG) was recorded continuously using subcutaneous needle electrodes. All animals were castrated using a closed technique. The raw EEG signal was analysed after completion of each investigation, and the mean values of EEG variables (median frequency, spectral edge frequency, total amplitude) recorded during a baseline period (before surgery began) and the removal of each testicle were compared using anova for repeated measures. RESULTS: Spectral edge frequency (SEF) 95% decreased during removal of the second testicle compared with baseline recordings. No other significant EEG changes during castration were measured. CONCLUSIONS: Lidocaine obtunded the EEG changes identified during castration in a previous control study, providing indirect evidence that lidocaine administered peri-operatively was antinociceptive and contributed to anaesthesia during castration. CLINICAL RELEVANCE: The antinociceptive effect of lidocaine combined with its minimal cardiovascular effects indicate a potential use for systemic lidocaine in clinical anaesthetic techniques.     

The bispectral index during recovery from halothane and sevoflurane anaesthesia in horses

ObjectiveTo record the bispectral index (BIS) when horses moved during either halothane or sevoflurane anaesthesia and when they made volitional movements during recovery from these anaesthetics.Study designRandomized prospective clinical study.AnimalsTwenty-five client-owned horses undergoing surgery aged 8.8 (± 5.3; 1–19) years (mean ± SD; range).MethodsBaseline BIS values were recorded before pre-anaesthetic medication (BIS_B) and during anaesthesia (BIS_A) maintained with halothane (group H; n = 12) or sevoflurane (group S; n =13) at approximately 0.8–0.9 × minimum alveolar concentrations (MAC). Bispectral indices were recorded during the surgery when unexpected movement occurred (BIS_MA), during recovery when the first movement convincingly associated with consciousness was observed (BIS_M1) and once sternal recumbency was achieved (BIS_ST).ResultsNo significant difference in BIS_M1 was found between halothane- (85 ± 7; 75–93) and sevoflurane- (87 ± 10; 70–98) anaesthetized horses although BIS_A was significantly (p = 0.0002) lower in group S (62 ± 7; 53–72) than group H (74 ± 7; 60–84). Differences between BIS_M1 and BIS_A were significant in sevoflurane (p = 0.00001) and halothane recipients (p = 0.002) but were greater in group S (25 ± 9; 4–38) compared with group H (12 ± 10; ?9–25). In six of eight horses, BIS_MA values ranged between those recorded during anaesthesia and at first movement.Conclusions and clinical relevanceBispectral indices appear to approximate levels of unconsciousness, suggesting that monitoring the BIS may assist equine anaesthesia. However, it does not predict intra-operative movement.