Hemodynamic effects of sevoflurane in spontaneously breathing cats

Sevoflurane has recently been introduced in feline anesthesia. However, its cardiovascular effects have not, to our knowledge, been reported in this species. Six healthy cats, aged 1.81 ± 0.31 years (mean ± SEM) and weighing 3.47 ± 0.11 kg, were studied. Anesthesia was induced and maintained with sevoflurane in oxygen. Body temperature was maintained between 38.5 and 39.55 °C. After instrumentation, end‐tidal sevoflurane concentration was randomly set at 1.25, 1.5, and 1.75 times the individual minimum alveolar concentration (MAC), determined in a previous study, according to a Latin Square Design. Thirty minutes of stabilization was allowed after each change of concentration. ECG and heart rate, systemic and pulmonary arterial pressures, central venous pressure (CVP), and core body temperature were continuously monitored and recorded. Inspired and end‐tidal oxygen, carbon dioxide, and sevoflurane concentrations were measured using a Raman spectrometer, calibrated every 80 minutes with three calibration gases of known sevoflurane concentration (1, 2, and 5%). Moreover, at selected times, pulmonary artery occlusion pressure and cardiac output (thermodilution) were measured, and arterial and mixed venous blood samples were collected for pH and blood gas analysis, hemoglobin concentration, hemoglobin oxygen saturation, packed cell volume (PCV) and total protein determination, and lactate concentration measurement. Cardiac index (CI), stroke index (SI), systemic and pulmonary vascular resistance indices, rate‐pressure product, left and right ventricular stroke work indices (LVSWI and RVSWI, respectively), arterial and mixed venous oxygen contents, oxygen delivery, oxygen consumption, and oxygen utilization ratio were calculated. Data were analyzed by a Repeated Measure Latin Square Design followed by a Tukey's test for 2 × 2 comparisons. Arterial pH significantly decreased from 7.40 ± 0.05 to 7.29 ± 0.07 with the administration of increasing concentrations of sevoflurane. Similarly, LVSWI decreased from 3.72 ± 0.60 to 2.60 ± 0.46 g m^?2. Mean arterial pressure, PaO₂, mixed venous pH, CI, SI, and oxygen delivery tended to decrease dose‐dependently, whereas CVP, PaCO₂, Pv CO₂, PCV, and arterial and mixed venous hemoglobin concentrations tended to increase dose‐dependently with the administration of sevoflurane. However, these trends did not reach statistical significance, possibly because of the limited number of animals studied. Sevoflurane seemed to induce dose‐dependent cardiovascular depression in cats.     

Time-related responses of spontaneously breathing, laterally recumbent horses to prolonged anesthesia with halothane

Cardiovascular and respiratory functions were serially evaluated in ten healthy, fasting, spontaneously breathing, laterally recumbent adult horses during five hours of constant 1.06% alveolar halothane (equivalent to 1.2 times the minimum alveolar concentration for horses). Mean carotid arterial pressure was about 25% higher after one hour of constant-dose halothane than after 30 minutes of constant-dose (P less than 0.05), and remained increased throughout the study. Mean carotid arterial pressure peaked after 90 minutes, and was about 30% higher than at 30 minutes. Total peripheral vascular resistance initially increased (20% at one hour), then gradually returned to the 0.5-hour value over the next four hours. Cardiac output progressively increased with time (P less than 0.05; 20% by two hours; nearly 40% by five hours) because of an increase in stroke volume. An increase (P less than 0.05) in mixed venous PO2 accompanied the increase in cardiac output. Heart rate did not change significantly (P greater than 0.05). Some measures of ventilation changed significantly with time (P less than 0.05). After four and five hours of constant alveolar halothane, the PaCO2, inspired gas flow, and ratio of inspired vs expired gas flow were significantly higher than the 0.5-hour values. Inspiratory time significantly decreased, beginning at three hours. All horses recovered from anesthesia and recumbency without complications.     

Respiratory reflexes in spontaneously breathing anesthetized dogs in response to nasal administration of sevoflurane, isoflurane, or halothane

OBJECTIVE: To characterize respiratory reflexes elicited by nasal administration of sevoflurane (Sevo), isoflurane (Iso), or halothane (Hal) in anesthetized dogs. ANIMALS: 8 healthy Beagles. PROCEDURE: A permanent tracheostomy was created in each dog. Two to 3 weeks later, dogs were anesthetized by IV administration of thiopental and alpha-chloralose. Nasal passages were isolated such that inhalant anesthetics could be administered to the nasal passages while the dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of each anesthetic at 1.2 and 2.4 times the minimum alveolar concentration (MAC) and the full vaporizer setting (5%) were recorded. Reflexes in response to administration of 5% of each anesthetic also were recorded following administration of lidocaine to the nasal passages. RESULTS: Nasal administration of Sevo, Iso, and Hal induced an immediate ventilatory response characterized by a dose-dependent increase in expiratory time and a resulting decrease in expired volume per unit of time. All anesthetics had a significant effect, but for Sevo, the changes were smaller in magnitude. Responses to administration of each anesthetic were attenuated by administration of lidocaine to the nasal passages. CONCLUSIONS AND CLINICAL RELEVANCE: Nasal administration of Sevo at concentrations generally used for mask induction of anesthesia induced milder reflex inhibition of breathing, presumably via afferent neurons in the nasal passages, than that of Iso or Hal. Respiratory reflexes attributable to stimulation of the nasal passages may contribute to speed of onset and could promote a smoother induction with Sevo, compared with Iso or Hal.     

Minimum alveolar concentration of sevoflurane in spontaneously breathing llamas and alpacas

OBJECTIVE: To determine the minimum alveolar concentration (MAC) of sevoflurane in spontaneously breathing llamas and alpacas. DESIGN: Prospective study. ANIMALS: 6 healthy adult llamas and 6 healthy adult alpacas. PROCEDURE: Anesthesia was induced with sevoflurane delivered with oxygen through a mask. An endotracheal tube was inserted, and a port for continuous measurement of end-tidal and inspired sevoflurane concentrations was placed between the endotracheal tube and the breathing circuit. After equilibration at an end-tidal-to-inspired sevoflurane concentration ratio > 0.90 for 15 minutes, a 50-Hz, 80-mA electrical stimulus was applied to the antebrachium until a response was obtained (ie, gross purposeful movement) or for up to 1 minute. The vaporizer setting was increased or decreased to effect a 10 to 20% change in end-tidal sevoflurane concentration, and equilibration and stimulus were repeated. The MAC was defined as the mean of the lowest end-tidal sevoflurane concentration that prevented a positive response and the highest concentration that allowed a positive response. RESULTS: Mean +/- SD MAC of sevoflurane was 2.29 +/- 0.14% in llamas and 2.33 +/- 0.09% in alpacas. CONCLUSIONS AND CLINICAL RELEVANCE: The MAC of sevoflurane in llamas and alpacas was similar to that reported for other species.     

Cardiopulmonary and acid-base effects of desflurane and sevoflurane in spontaneously breathing cats

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO2), arterial blood pH (pH), arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. Anesthesia was induced with propofol (8+/-2.3mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test (P<0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO2 increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20-T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously.     

The effect of hyoscine on dobutamine requirement in spontaneously breathing horses anaesthetized with halothane

OBJECTIVE: To determine whether hyoscine has a sparing effect on the volume of dobutamine required to maintain mean arterial pressure (MAP) at 70 mmHg in horses anaesthetized with halothane. STUDY DESIGN: Prospective, randomized, controlled clinical trial. ANIMALS: Twenty adult horses weighing 507 +/- 97 kg (mean +/- SD), aged 10 +/- 5 years. MATERIALS AND METHODS: Pre-anaesthetic medication in all horses was intramuscular (IM) acepromazine (40 mug kg(-1)) and intravenous (IV) detomidine (0.02 mg kg(-1)). Anaesthesia was induced with ketamine (2.2 mg kg(-1) IV) and diazepam (0.02 mg kg(-1) IV), and maintained with halothane in oxygen. Horses breathed spontaneously. Flunixin (1.1 mg kg(-1) IV) was given to provide analgesia. Heart rate, ECG, invasive arterial pressure, respiratory rate, percentage end-tidal carbon dioxide, percentage end-tidal halothane and partial pressure of oxygen and carbon dioxide in arterial blood and blood pH were monitored. Dobutamine was infused by an infusion pump to maintain MAP at 70 mmHg. Horses were randomly assigned to receive saline or hyoscine (0.1 mg kg(-1)) IV 30 minutes after induction. The heart rate, MAP and volume of dobutamine infused over 30-minute periods were measured and analysed statistically using a one-way anova. RESULTS: After administration of hyoscine, heart rate increased for 10 minutes (p < 0.01) and MAP for 5 minutes (p < 0.01). There was no difference in the volume of dobutamine infused over 30 minutes between horses given hyoscine or saline, although there was a wide individual variation in dobutamine requirements. No side effects of hyoscine were seen. CONCLUSIONS: The increase in heart rate and blood pressure that occurs after 0.1 mg kg(-1) hyoscine is given IV in anaesthetized horses, is of short duration and does not significantly alter the amount of dobutamine required to maintain arterial pressure over the next 30 minutes. Clinical relevance The short duration of action of 0.1 mg kg(-1) hyoscine IV may limit its usefulness for correction of hypotension in horses anaesthetized with halothane. Further work is necessary to investigate the effects of higher or repeated doses or constant rate infusions of hyoscine.     

Influence of halothane, isoflurane, and sevoflurane on gastroesophageal reflux during anesthesia in dogs

OBJECTIVE: To determine whether maintenance of anesthesia with halothane or sevoflurane is associated with a lower incidence of gastroesophageal reflux (GER) than the use of isoflurane in dogs undergoing orthopedic surgery. ANIMALS: 90 dogs. PROCEDURES: Dogs were evaluated during elective orthopedic surgery. Dogs with a history of vomiting or that had received any drugs that would alter gastrointestinal tract function were excluded from the study. The anesthetic protocol used was standardized to include administration of acepromazine maleate and morphine prior to induction of anesthesia with thiopental. Dogs were allocated to receive halothane, isoflurane, or sevoflurane to maintain anesthesia. A sensor-tipped catheter was placed to measure esophageal pH during anesthesia. Gastroesophageal reflux was defined as an esophageal pH < 4 or > 7.5. RESULTS: 51 dogs had 1 or more episodes of acidic GER during anesthesia. Reflux was detected in 14 dogs receiving isoflurane, 19 dogs receiving halothane, and 18 dogs receiving sevoflurane. In dogs with GER, mean +/- SD time from probe placement to onset of GER was 36 +/- 65 minutes and esophageal pH remained < 4 for a mean of 64% of the measurement period. There was no significant association between GER and start of surgery or moving a dog on or off the surgery table. Dogs that developed GER soon after induction of anesthesia were more likely to regurgitate. CONCLUSIONS AND CLINICAL RELEVANCE: Maintenance of anesthesia with any of the 3 commonly used inhalant agents is associated with a similar risk for development of GER in dogs.     

Respiratory reflexes in response to nasal administration of halothane to anesthetized, spontaneously breathing dogs

OBJECTIVE: To characterize and determine the sensory innervation of respiratory reflexes elicited by nasal administration of halothane to dogs. ANIMALS: 10 healthy Beagles. PROCEDURE: Dogs underwent permanent tracheostomy and, 2 to 3 weeks later, were anesthetized with thiopental and alpha-chloralose administered IV. The nasal passages were functionally isolated so that halothane could be administered to the nasal passages while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of halothane at concentrations of 1.25, 1.75, and 2.5 times the minimum alveolar concentration (MAC), and 5% (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of 5% halothane were also recorded following transection of the infraorbital nerve, transection of the caudal nasal nerve, and nasal administration of lidocaine. RESULTS: Nasal administration of halothane induced an inhibition of breathing characterized by a dose-dependent increase in expiratory time and a resultant decrease in expired volume per unit time. Effects were noticeable immediately after the onset of halothane administration and lasted until its cessation. Reflex responses to halothane administration were attenuated by transection of the caudal nasal nerve and by nasal administration of lidocaine, but transection of the infraorbital nerve had no effect. CONCLUSIONS AND CLINICAL RELEVANCE: Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration.     

Respiratory reflexes in response to upper-airway administration of sevoflurane and isoflurane in anesthetized, spontaneously breathing dogs

OBJECTIVE: To evaluate the respiratory effects occurring during administration of sevoflurane or isoflurane to the upper airway in dogs. STUDY DESIGN: A prospective, randomized study. ANIMALS: Twelve healthy adult beagles (6 males, 6 females). METHODS: At least 2 weeks after undergoing permanent tracheostomy, dogs were premedicated with acepromazine-buprenorphine, and anesthesia was induced with thiopental and maintained with alpha-chloralose. The upper airway was functionally isolated so that the inhalant could be administered to the upper airway while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to the administration of sevoflurane or isoflurane at concentrations of 1.2, 1.8, and 2.4 times the minimal alveolar concentration (MAC) (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of each anesthetic were also recorded following upper-airway administration of lidocaine. RESULTS: Respiratory reflexes elicited by upper-airway administration of each anesthetic were characterized by a dose-dependent increase in expiration time, with a resultant decrease in respiratory minute ventilation and increase in end-tidal PCO2. The magnitude of these responses was greater with isoflurane than with sevoflurane at 1.8 and 2.4 MAC. These reflexes were abolished after lidocaine nebulization into the upper airway. CONCLUSION: Isoflurane induces greater reflex inhibition of breathing than does sevoflurane when the anesthetic is inhaled into the upper airway at concentrations used for mask induction.     

Effects of five hours of constant 1.2 MAC halothane in sternally recumbent, spontaneously breathing horses

Circulatory and respiratory effects of five h of constant 1.06 per cent alveolar halothane in oxygen were identified in eight healthy horses, which breathed spontaneously, were otherwise unmedicated and positioned in sternal recumbency. Only a few important significant (P less than 0.05) changes occurred with time. Total peripheral resistance was about 15 per cent lower after two hours of constant dose halothane than after 30 mins of constant dose (P less than 0.05) and accounted for the significant 10 per cent reduction in mean carotid arterial blood pressure. By 5 h, the reduction in resistance and arterial blood pressure was 20 and 25 per cent respectively. Heart rate increased progressively with time and the increase became significant at 5 h (15 per cent increase). However, the heart rate change was not large enough to alter cardiac output. There were no major time-related changes in PaO2 or PaCO2. Three of four horses recovered from anaesthesia had markedly elevated serum creatine kinase levels and clinical signs of severe post anaesthetic myopathy.     

Assessment of isoflurane-induced anesthesia in ferrets and rats

OBJECTIVE: To characterize isoflurane (ISO)-induced anesthesia in ferrets and rats. ANIMALS: 8 ferrets (Mustela putorius furo) and 8 Sprague-Dawley rats. PROCEDURE: Ferrets and rats were anesthetized in a similar manner, using ISO in oxygen. Minimum alveolar concentration (MAC) was determined, using the tail-clamp method. Immediately thereafter, assessments were recorded for 0.8, 1.0, 1.5, and 2.0 MAC (order randomized) of ISO. RESULTS: MAC of ISO was (mean +/- SEM) 1.74 +/- 0.03 and 1.58 +/- 0.05% for ferrets and rats, respectively. Mean arterial blood pressure (MAP) was 75.0 +/- 4.3 and 107.9 +/- 2.7 mm Hg at 0.8 MAC for ferrets and rats, respectively, and decreased in a parallel dose-dependent manner. Respiratory frequency decreased in rats as ISO dose increased; however, respiratory frequency increased in ferrets as ISO dose increased from 0.8 to 1.5 MAC but then decreased at 2.0 MAC. At 0.8 MAC, hypoventilation was much greater in ferrets (PaCO2 = 71.4 +/- 3.5 mm Hg), compared with rats (PaCO2 = 57.7 +/- 1.9 mm Hg). In both species, PaCO2 progressively increased as anesthetic dose increased. Eyelid aperture of ferrets increased in a dose-dependent manner. Pupil diameter in ferrets and rats increased as ISO dose increased. CONCLUSIONS AND CLINICAL RELEVANCE: The MAP and PaCO2 in ferrets and rats and eyelid aperture in ferrets consistently and predictably changed in response to changes in anesthetic dose of ISO. Magnitude of respiratory depression was greater in ferrets than rats. Changes in MAP and PaCO2 in ferrets and rats and eyelid aperture in ferrets are consistent guides to changes in depth of ISO-induced anesthesia.     

Cardiopulmonary effects of halothane anesthesia in cats

The cardiopulmonary effects of 2 planes of halothane anesthesia (halothane end-tidal concentrations of 1.78% [light anesthesia] and 2.75% [deep anesthesia]) and 2 ventilatory modes (spontaneous ventilation [SV] or mechanically controlled ventilation [CV]) were studied in 8 cats. Anesthesia was induced and maintained with halothane in O2 only, and each cat was administered each treatment according to a Latin square design. Cardiac output, arterial blood pressure, pulmonary arterial pressure, heart rate, respiratory frequency, and PaO2, PaCO2, and pH were measured during each treatment. Stroke volume, cardiac index, and total peripheral resistance were calculated. A probability value of less than 5% was accepted as significant. In the cats, cardiac output, cardiac index, and stroke volume were reduced by deep anesthesia and CV, although only the reduction attributable to CV was significant. Systemic arterial pressure was significantly reduced by use of deep anesthesia and CV. Respiratory frequency was significantly lower during CV than during SV. Arterial PO2 was significantly decreased at the deeper plan of anesthesia, compared with the lighter plane. At the deeper plane of anesthesia, arterial PCO2 and pulmonary arterial pressure were significantly lower during CV than during SV. The deeper plane of halothane anesthesia depressed cardiopulmonary function in these cats, resulting in hypotension and considerable hypercapnia. Compared with SV, CV significantly reduced circulatory variables and should be used with care in cats. Arterial blood pressure was judged to be more useful for assessing anesthetic depth than was heart rate or respiratory frequency.     

Hepatic necrosis following halothane anesthesia in goats

One goat anesthetized with thiamylal sodium, xylazine, and halothane for repair of an abominal hernia, and 7 of 29 goats similarly anesthetized for an experiment unrelated to considerations of anesthesia, developed signs of hepatic failure within 24 hours of anesthesia. Affected goats had high values for serum aspartate transaminase and serum total bilirubin by 12 to 24 hours after induction of anesthesia. Necropsy of the 8 affected goats revealed centrilobular to massive hepatic necrosis (8 of 8), brain lesions consistent with hepatic encephalopathy (3 of 4), and acute renal tubular necrosis (6 of 6). Two unaffected goats had no hepatic necrosis. Causes of hepatic necrosis other than those related to anesthesia (eg, infectious agents, toxins) were ruled out by lack of supporting necropsy findings or were considered unlikely because of lack of opportunity for exposure. Hepatic lesions in these goats closely resembled those described in human beings with halothane-associated hepatic injury, although in both species these lesions are nonspecific at the gross and light microscopic levels. The pathogenesis of halothane-associated hepatic injury in goats, as in human beings, remains to be determined.     

Hepatic effects of halothane and isoflurane anesthesia in goats

OBJECTIVE: To determine hepatic effects of halothane and isoflurane anesthesia in young healthy goats. DESIGN: Randomized prospective clinical trial. ANIMALS: 24 healthy 9-month-old female goats. PROCEDURE: Goats were sedated with xylazine hydrochloride and ketamine hydrochloride and anesthetized with halothane (n = 12) or isoflurane (12) while undergoing tendon surgery. End-tidal halothane and isoflurane concentrations were maintained at 0.9 and 1.2 times the minimal alveolar concentrations, respectively, and ventilation was controlled. Venous blood samples were collected approximately 15 minutes after xylazine was administered and 24 and 48 hours after anesthesia, and serum aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT) activities and bilirubin concentration were measured. Goats were euthanatized 25 or 62 days after anesthesia, and postmortem liver specimens were submitted for histologic examination. RESULTS: All goats recovered from anesthesia and survived until euthanasia. Serum SDH, GGT, and ALP activities and bilirubin concentration did not increase after anesthesia, but serum AST activity was significantly increased. However, serum hepatic enzyme activities were within reference limits at all times in all except 1 goat in which serum AST activity was high 24 and 48 hours after anesthesia. This goat had been anesthetized with halothane and had the longest duration of anesthesia. No clinically important abnormalities were seen on histologic examination of liver specimens. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that use of halothane or isoflurane for anesthesia in young healthy goats is unlikely to cause hepatic injury.     

The effect of a 50% inspired mixture of nitrous oxide on arterial oxygen tension in spontaneously breathing horses anaesthetised with halothane

The effect of nitrous oxide (N₂O) on arterial partial pressure of oxygen (P_aO₂) was evaluated in 20 adult horses anaesthetised with halothane. A fresh gas flow rate of 20ml/kg/min, comprising a 1:1 N₂O/oxygen (O₂) mixture, was supplied via the rotameter flowmeters of an anaesthetic machine to a large animal breathing system. The horses breathed spontaneously from the circuit immediately after endotracheal intubation. Ten horses were subsequently positioned in lateral recumbency and ten in dorsal recumbency. A further twenty adult horses were anaesthetised with halothane and acted as controls; halothane in 20mls/kg/min of O₂ being supplied to the same breathing system. Fifty percent NO caused significant decreases in P_aO₂ for horses in lateral and dorsal recumbency. However when administered to horses in lateral recumbency it did not promote arterial hypoxaemia. There was a higher risk of intraopera- tive arterial hypoxaemia (P_aO₂ < 8.6kPa) associated with its use in spontaneously breathing horses in dorsal recumbency. Arterial hypoxaemia occurred in all horses during the first fifteen minutes of recovery but when N₂O was discontinued, halothane in oxygen supplied to the breathing circuit for five minutes at a flow rate of 20ml/kg/minute was sufficient to ensure that diffusion hypoxia did not occur. The magnitude of the hypoxaemia was not signficantly different between the groups. The time taken to adopt sternal recumbency was significantly shorter in the horses that had received N₂O.     

Clinical evaluation of a valveless non-absorber breathing system in spontaneously breathing canine patients

A valveless non-absorber breathing system novel to veterinary anaesthesia is described. The performance of this system was evaluated in 35 anaesthetised spontaneously breathing dogs weighing between 2.1 and 56 kg. Fresh gas flows were reduced incrementally until rebreathing (defined as an increase in end-inspired carbon dioxide tension above 0.2 per cent) started to occur, as measured by capnography. A significant relationship (P < 0.0001) between critical fresh gas flow and bodyweight was determined, and a mean critical fresh gas flow rate of 145 +/- 21 ml/kg/minute was derived for 15 dogs weighing 10 kg or less (mean 6.7 +/- 2.6 kg) and one of 98 +/- 16 ml/kg/minute for the remaining 20 dogs weighing 11 kg or greater (mean 30.2 +/- 13.9 kg). The fresh gas requirements for each group were found to differ significantly (P < 0.0001), although the correlation between critical fresh gas flow and bodyweight was not significant (P = 0.054) in the dogs weighing 10 kg or less. It is suggested that the system may prove an economical and useful addition to the breathing systems currently used in canine anaesthesia.     

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.     

Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs

The effects of halothane, isoflurane and sevoflurane anaesthesia on hepatic function and hepatocellular damage were investigated in dogs, comparing the activity of hepatic enzymes and bilirubin concentration in serum. An experimental study was designed. Twenty-one clinically normal mongrel dogs were divided into three groups and accordingly anaesthetized with halothane (n = 7), isoflurane (n = 7) and sevoflurane (n = 7). The dogs were 1-4 years old, and weighed between 13.5 and 27 kg (18.4 +/- 3.9). Xylazine HCI (1-2 mg/kg) i.m. was used as pre-anaesthetic medication. Anaesthesia was induced with propofol 2 mg/kg i.v. The trachea was intubated and anaesthesia maintained with halothane, isoflurane or sevoflurane in oxygen at concentrations of 1.35, 2 and 3%, respectively. Intermittent positive pressure ventilation (tidal volume, 15 ml/kg; respiration rate, 12-14/min) was started immediately after intubation and the anaesthesia lasted for 60 min. Venous blood samples were collected before pre-medication, 24 and 48 h, and 7 and 14 days after anaesthesia. Serum level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH GGT) activities and bilirubin concentration were measured. Serum AST, ALT and GGT activities increased after anaesthesia in all groups. In the halothane group, serum AST and ALT activities significantly increased all the time after anaesthesia compared with baseline activities. But in the isoflurane group AST and ALT activities increased only between 2 and 7 days, and in the sevoflurane group 7 days after anaesthesia. GGT activity was increased in the halothane group between 2 and 7 days, and in the isoflurane and sevoflurane groups 7 days after anaesthesia. All dogs recovered from anaesthesia without complications and none developed clinical signs of hepatic damage within 14 days. The results suggest that the use of halothane anaesthesia induces an elevation of serum activities of liver enzymes more frequently than isoflurane or sevoflurane from 2 to 14 days after anaesthesia in dogs. The effects of isoflurane or sevoflurane anaesthesia on the liver in dogs is safer than halothane anaesthesia in dogs.