Hypoxaemia during anaesthesia in seven horses with colic

Anaesthetic records of horses with colic anaesthetised between June 1987 and May 1989 were reviewed. pH and blood gas analyses were performed during 157 operations from which the horses were allowed to recover. A PaO₂ of 8.0 kPa or less was measured during anaesthesia in seven of these horses. The horses were of different breeds, ages and sexes. Anaesthesia was induced with xylazine, guaifenesin and ketamine in four horses and with xylazine, guaifenesin and thiobarbiturate in three horses. Anaesthesia was maintained with inhalation anaesthetic agent and oxygen: isoflurane in five horses, halothane in one horse, and initially halothane but later isoflurane in one horse. Systolic arterial pressures during anaesthesia ranged from 80 to 150 mmHg, diastolic arterial pressures were between 60 and 128 mmHg, and heart rates were between 28 and 44 beats /min. Controlled ventilation was initiated at the start of anaesthesia. PaCO₂ exceeded 6.7 kPa in three horses but was subsequently decreased by adjustment of the ventilator. PaO₂ of 8.0 kPa or less was measured during early anaesthesia, with one exception, and persisted for the duration of anaesthesia. The horses' inspired air was supplemented with oxygen during recovery from anaesthesia, at which time measurement of blood gases in three horses revealed no increase in PaO₂. Recovery from anaesthesia was uneventful. The surgical problems involved primarily the large intestine in five horses and the small intestine in two horses. Six horses were discharged from the hospital alive; one horse was reanaesthetised later the same day and destroyed without regaining consciousness. We concluded that none of the objective values recorded during the pre-anaesthetic evaluation could have been used to predict the complication of intraoperative hypoxaemia. We observed that once hypoxaemia developed it persisted for the duration of anaesthesia and even into the recovery period when the horses were in lateral recumbency and regaining consciousness. We assume that the altered metabolism from anaesthetic agents and hypothermia combined with adequate peripheral perfusion contributed to the lack of adverse consequences in six of the horses. The contribution of hypoxaemia to the deteriorating condition of the seventh horse is speculative.     

Effects of high and low inspired fractions of oxygen on horse erythrocyte membrane properties, blood viscosity and muscle oxygenation during anaesthesia

ObjectivesTo evaluate whether a period of hyperoxia or after a period of hypoxia produced changes attributable to reactive oxygen species in anaesthetized horses.Study designProspective randomized experimental study.AnimalsSix healthy (ASA I) geldings, aged 4.5–9.5 years and weighing 510–640 kg^?1.MethodsAfter 30 minutes breathing air as carrier gas for isoflurane, horses were assigned randomly to breathe air as carrier gas (CG0.21) or oxygen as carrier gas (CG1.00) for a further 90 minutes. After an interval of 1 month each horse was re-anaesthetized with the other carrier gas for the 90 minute test period. Ventilation was controlled throughout anaesthesia. Arterial blood was sampled to measure gas tensions, lactate, cholesterol, vitamin E, 4-hydroxy-alkenals, 8-epi-PGF_2α, half haemolysis time, half erythrolysis time, and erythrocyte membrane fluidity. Muscle blood flow and oxygenation were evaluated by near infrared spectroscopy and coloured Doppler.ResultsAfter the first 30 minutes horses were hypoxemic. Subsequently the CG1.00 group became hyperoxaemic (PaO₂～240 mmHg) whereas the CG0.21 group remained hypoxaemic (PaO₂～60 mmHg) and had increased lactate concentration. No significant changes in vitamin E, 4-hydroxy-alkenals, or 8-epi-PGF_2α concentrations were detected. During the 90 minute test period the CG0.21 group had increased resistance to free-radical-mediated lysis in erythrocytes, whereas the CG1.00 group had slightly decreased resistance of whole blood to haemolysis. CG0.21 induced a progressive muscle deoxygenation whereas CG1.00 induced an increase in muscle oxygen saturation followed by progressive deoxygenation towards baseline.Conclusions and clinical relevanceDuring isoflurane anaesthesia in horses, the hyperoxia induced by changing from air to oxygen induced minimal damage from reactive oxygen species. Using air as the carrier gas decreased skeletal muscle oxygenation compared with using oxygen.     

Effect of reducing inspired oxygen concentration on oxygenation parameters during general anaesthesia in horses in lateral or dorsal recumbency

Objective

To compare the effects of two concentrations of oxygen delivered to the anaesthetic breathing circuit on oxygenation in mechanically ventilated horses anaesthetised with isoflurane and positioned in dorsal or lateral recumbency.

Methods

Selected respiratory parameters and blood lactate were measured and oxygenation indices calculated, before and during general anaesthesia, in 24 laterally or dorsally recumbent horses. Horses were randomly assigned to receive 100% or 60% oxygen during anaesthesia. All horses were anaesthetised using the same protocol and intermittent positive pressure ventilation (IPPV) was commenced immediately following anaesthetic induction and endotracheal intubation. Arterial blood gas analysis was performed and oxygenation indices calculated before premedication, immediately after induction, at 10 and 45 min after the commencement of mechanical ventilation, and in recovery.

Results

During anaesthesia, the arterial partial pressure of oxygen was adequate in all horses, regardless of position of recumbency or the concentration of oxygen provided. At 10 and 45 min after commencing IPPV, the arterial partial pressure of oxygen was lower in horses in dorsal recumbency compared with those in lateral recumbency, irrespective of the concentration of oxygen supplied. Based on oxygenation indices, pulmonary function during general anaesthesia in horses placed in dorsal recumbency was more compromised than in horses in lateral recumbency, irrespective of the concentration of oxygen provided.

Conclusion

During general anaesthesia, using oxygen at a concentration of 60% instead of 100% maintains adequate arterial oxygenation in horses in dorsal or lateral recumbency. However, it will not reduce pulmonary function abnormalities induced by anaesthesia and recumbency.     

Muscle metabolic changes associated with long-term inhalation anaesthesia in the horse analysed by muscle biopsy and microdialysis techniques

During anaesthesia in the horse, muscle blood flow has been found to be reduced, possibly leading to hypoxia or ischaemia in the muscle. The aim of this study was to use the muscle biopsy and microdialysis techniques to determine whether long-term inhalation anaesthesia in laterally recumbent horses induces metabolic changes in gluteal muscle indicative of anaerobic metabolism. Muscle biopsies and plasma samples were taken from seven horses at the start and end of halothane anaesthesia. In six isoflurane-anaesthetised horses, given three pharmacological provocations (dobutamine, detomidine, acepromazine), repeated blood samples and microdialysis was performed during anaesthesia and muscle biopsies were taken before and at the end of anaesthesia. Adenosine triphosphate (ATP), adenosine diphosphate, adenosine monophosphate, inosine monophosphate (IMP) creatine phosphate and lactate concentrations did not differ between dependent and non-dependent muscles at either sampling time. Creatine phosphate decreased in both the halothane (-38%) and isoflurane (-28%) group. In the halothane group, ATP was decreased (-15%) at the end of anaesthesia, while IMP was increased (+32%). Lactate in muscle and plasma increased in both groups. Lactate in dialysate increased after induction and remained elevated above plasma concentrations. These results show that long-term inhalation anaesthesia in horses is associated with an anaerobic metabolic response within the muscle and that microdialysis can be used to detect metabolic changes within the muscle during equine anaesthesia.     

Review of hypoxaemia in anaesthetized horses: predisposing factors,consequences and management

Objective

To discuss how hypoxaemia might be harmful and why horses are particularly predisposed to developing it, to review the strategies that are used to manage hypoxaemia in anaesthetized horses, and to describe how successful these strategies are and the adverse effects associated with them.

Propofol compared with propofoVguaiphenesin after detornidine premedication for equine surgery

Anaesthesia using propofol alone and in combination with guaiphenesin, after detomidine premedication, was evaluated for performance of minor surgical procedures (castration and tenotomy) in horses. Twelve male horses were premedicated with 0.015 mg/kg of detomidine intravenously (iv) and divided into two groups of six. One group of horses received 2 mg/kg of propofol iv and the other group received 0.5 mg/kg of propofol mixed with 100 mg/kg of a 7.5% solution of guaiphenesin in saline iv. Induction of anaesthesia was fast and smooth in both groups. All horses were easily intubated immediately afterwards but intubation was easier in the horses which received propofol and guaiphenesin. Heart rate fell by 20% in both groups after detomidine injection, stabilising between 45 and 53 beats/minute during anaesthesia with no difference between the groups. Respiratory depression developed after detomidine injection and was slightly intensified after induction of anaesthesia. Respiratory rate was significantly lower in the propofol group (14 ± 3 breaths/minute) than with propofol/guaiphenesin (19 ± 4 breaths/minute) at five minutes after induction. Anaesthesia induced respiratory acidosis in both groups and hypoxaemia also occurred, but once the horses stood up the arterial blood oxygen partial pressure returned to basal values. Surgical time ranged between 8 and 16 minutes and with the exception of one horse in the propofol/guaiphenesin group the horses did not show signs of pain or discomfort during surgery. Recovery to standing was fast and took 26 ± 2 minutes in the propofol and 29 ± 5 minutes in the propofol/ guaiphenesin group. Most horses stood up at the first attempt with minimal ataxia. These two anaesthetic techniques appear to be useful for minor surgical procedures performed within 16 minutes of induction of anaesthesia.     

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.     

Dynamic baroreflex sensitivity in anesthetized horses, maintained at 1.25 to 1.3 minimal alveolar concentration of halothane.

Dynamic baroreflex sensitivity for increasing arterial pressure (DBSI) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (less than or equal to 2 minutes) pressure changes in the horse. Anesthesia was induced with IV administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (SAP) was increased a minimum of 30 mm of Hg in response to an IV bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the R-R interval/SAP relationship. During dynamic increases in SAP, a significant correlation between R-R interval and SAP was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between R-R interval and SAP were greater than 0.80 in 5 of 8 horses. Mean (+/- SD) DBSI was 4.8 +/- 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between R-R interval and SAP was observed in only 3 of 6 awake horses during dynamic increases in SAP. Lack of correlation between R-R interval and SAP in 3 of 6 awake horses indicated that rapidly increasing SAP with an IV phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (+/- SD) DBSI (3 horses) was 7.3 +/- 3.3 ms/mm of Hg in awake horses.     

Effects of intravenous administration of dimethyl sulfoxide on cardiopulmonary and clinicopathologic variables in awake or halothane-anesthetized horses

OBJECTIVE: To evaluate the cardiopulmonary and clinicopathologic effects of rapid IV administration of dimethyl sulfoxide (DMSO) in awake and halothane-anesthetized horses. DESIGN: Prospective study. ANIMALS: 6 adult horses. PROCEDURES: Horses received IV infusion of 5 L of a balanced electrolyte solution with and without 1 g/kg (0.45 g/lb) of 10% DMSO solution when they were awake and anesthetized with halothane (4 treatments/horse). Arterial and venous blood samples were collected immediately before and at intervals during or after fluid administration and analyzed for blood gases and hematologic and serum biochemical variables, respectively. Heart rate, respiratory rate, and arterial blood pressure variables were recorded prior to, during, and after fluid administration. RESULTS: After administration of fluid with or without DMSO, changes in measured variables were detected immediately, but most variables returned to baseline values within 4 hours. One awake control horse had signs of anxiety; agitation and tachycardia were detected in 2 awake horses administered DMSO. These clinical signs disappeared when the rate of infusion was reduced. In anesthetized horses, increased concentrations of WBCs and plasma fibrinogen and serum creatine kinase activity persisted for 24 hours, which was related to the stress of anesthesia more than the effects of fluid administration. CONCLUSIONS AND CLINICAL RELEVANCE: Infusion of 5 L of balanced electrolyte solution with or without 10% DMSO induced minimal changes in cardiopulmonary function and clinicopathologic variables in either awake or halothane-anesthetized horses. Stress associated with anesthesia and recovery had a greater influence on measured variables in anesthetized horses than fluid administration.     

Pulmonary oedema associated with anaesthesia for colic surgery in a horse

A 506 kg Warmblood horse with colic was anaesthetized for exploratory celiotomy. Anaesthesia was complicated by arterial hypoxaemia which persisted throughout surgery from the induction of anaesthesia. After endotracheal extubation in the recovery box, a degree of airway obstruction probably occurred during a brief delay in naso-tracheal intubation. Signs of pulmonary oedema were seen shortly afterwards. Furosemide and oxygen were given. Arterial hypoxaemia was present [PaO2: 6.5 kPa (49 mmHg)] when FIO2 was an estimated 0.3. The horse recovered and stood after 45 minutes. It was re-anaesthetized 3 days later when arterial blood gas analysis did not reveal hypoxaemia. The horse was killed on this occasion; post-mortem examination revealed the presence of pulmonary oedema, which probably resulted from multiple causes.     

Anaesthetic and cardiorespiratory effects of propofol at 10% for induction and 1% for maintenance of anaesthesia in horses

Reasons for performing study: Studies have demonstrated the clinical usefulness of propofol for anaesthesia in horses but the use of a concentrated solution requires further investigation. Objectives: To determine the anaesthetic and cardiorespiratory responses to a bolus injection of 10% propofol solution in mature horses. Methods: Three randomised crossover experimental trials were completed. Trial 1: 6 horses were selected randomly to receive 10% propofol (2, 4 or 8 mg/kg bwt i.v.). Trial 2: 6 horses received 1.1 mg/kg bwt i.v. xylazine before being assigned at random to receive one of 5 different doses (1–5 mg/kg bwt) of 10% propofol. Trial 3: 6 horses were sedated with xylazine (0.5 mg/kg bwt, i.v.) and assigned randomly to receive 10% propofol (3, 4 or 5 mg/kg bwt, i.v.); anaesthesia was maintained for 60 min using an infusion of 1% propofol (0.2‐0.4 mg/kg bwt/min). Cardiorespiratory data, the quality of anaesthesia, and times for induction, maintenance and recovery from anaesthesia and the number of attempts to stand were recorded. Results: Trial 1 was terminated after 2 horses had received each dose of 10% propofol. The quality of induction, anaesthesia and recovery from anaesthesia was judged to be unsatisfactory. Trial 2: 3 horses administered 1 mg/kg bwt and one administered 2 mg/kg bwt were not considered to be anaesthetised. Horses administered 3–5 mg/kg bwt i.v. propofol were anaesthetised for periods ranging from approximately 10–25 min. The PaO₂ was significantly decreased in horses administered 3–5 mg/kg bwt i.v. propofol. Trial 3: The quality of induction and recovery from anaesthesia were judged to be acceptable in all horses. Heart rate and rhythm, and arterial blood pressure were unchanged or decreased slightly during propofol infusion period. Conclusions: Anaesthesia can be induced with a 10% propofol solution and maintained with a 1% propofol solution in horses administered xylazine as preanaesthetic medication. Hypoventilation and hypoxaemia may occur following administration to mature horses. Potential relevance: Adequate preanaesthetic sedation and oxygen supplementation are required in horses anaesthetised with propofol.     

A comparison of xylazine-ketamine and detomidine-ketamine anaesthesia in horses

Anaesthesia produced by xylazine (1.1 mg/kg IV) followed in 3–5 minutes by ketamine (2.2 mg/ kg IV) (X / K) was compared to anaesthesia produced by detomidine (0.02 mg/kg IV) followed in 15–25 minutes by ketamine (2.2 mg/kg IV) (D/K) in the same six horses. Quality of induction, recovery, muscle relaxation, coordination (before and after anaesthesia) and response to stimulus were subjectively evaluated. Heart rate, respiratory rate, mean blood pressure, hemoglobin saturation, arterial pH, CO₂ and O₂ were monitored. Recumbency time and number of attempts required to stand were recorded. Recumbency time was longer in all horses with X/K (median recumbency time of 27 min) than with D/K (median recumbency time of 22 min). No significant differences between treatments were seen for any other variable measured, although 2 horses did not appear to reach a surgical plane of anaesthesia with D/K.     

Effects of acepromazine on pulmonary gas exchange and circulation during sedation and dissociative anaesthesia in horses

OBJECTIVE: To study pulmonary gas exchange and cardiovascular responses to sedation achieved with romifidine and butorphanol (RB) alone, or combined with acepromazine, and during subsequent tiletamine-zolazepam anaesthesia in horses. ANIMALS: Six (four males and two females) healthy Standardbred trotters aged 3-12 years; mass 423-520 kg. STUDY DESIGN: Randomized, cross-over, experimental study. MATERIALS AND METHODS: Horses were anaesthetized on two occasions (with a minimum interval of 1 week) with intravenous (IV) tiletamine-zolazepam (Z; 1.4 mg kg(-1)) after pre-anaesthetic medication with IV romifidine (R; 0.1 mg kg(-1)) and butorphanol (B; 25 microg kg(-1) IV). At the first trial, horses were randomly allocated to receive (protocol ARBZ) or not to receive (protocol RBZ) acepromazine (A; 35 microg kg(-1)) intramuscularly (IM) 35 minutes before induction of anaesthesia. Each horse was placed in left lateral recumbency and, after tracheal intubation, allowed to breathe room air spontaneously. Respiratory and haemodynamic variables and ventilation-perfusion (; multiple inert gas elimination technique) ratios were determined in the conscious horse, after sedation and during anaesthesia. One- and two-way repeated-measures anova were used to identify within- and between-technique differences, respectively. RESULTS: During sedation with RB, arterial oxygen tension (PaO(2)) decreased compared to baseline and increased mismatch was evident; there was no O(2) diffusion limitation or increase in intrapulmonary shunt fraction identified. With ARB, PaO(2) and remained unaffected. During anaesthesia, intrapulmonary shunt occurred to the same extent in both protocols, and mismatching increased. This was less in the ARBZ group. Arterial O(2) tension decreased in both protocols, but was lower at 25 and 35 minutes of anaesthesia in RBZ than in ARBZ. During sedation, heart rate (HR) and cardiac output (Qt) were lower while arterial-mixed venous oxygen content differences and haemoglobin concentrations were higher in RBZ compared with ARBZ. Total systemic vascular resistance, mean systemic, and mean pulmonary arterial pressures were higher during anaesthesia with RBZ compared to ARBZ. CONCLUSIONS AND CLINICAL RELEVANCE: Acepromazine added to RB generally improved haemodynamic variables and arterial oxygenation during sedation and anaesthesia. Arterial oxygenation was impaired as a result of increased shunt and mismatch during anaesthesia, although acepromazine treatment reduced disturbances and falls in PaO(2) to some extent. Haemodynamic variables were closer to baseline during sedation and anaesthesia when horses received acepromazine. Acepromazine may confer advantages in healthy normovolaemic horses.     

Prolonging dissociative anaesthesia in horses with a repeated bolus injection

The effects of prolonging romifidine/ketamine anaesthesia in horses with a second injection of ketamine alone or both romifidine/ketamine compared with only induction injection of romifidine and tiletamine/zolazepam were studied in 6 horses anaesthetised in lateral recumbency on 3 random occasions. All horses were sedated with romifidine 0.1 mg/kg bwt iv and, on 2 occasions, anaesthesia was induced by iv injection of ketamine 2.2 mg/kg bwt. To prolong the ketamine-induced anaesthesia, either ketamine (I.1 mg/kg bwt iv) or ketamine and romifidine (I.1 mg/kg bwt and 0.04 mg/kg bwt iv, respectively) were given 18–20 min after the start of the ketamine injection for induction. On the third occasion, anaesthesia was induced by iv injection of 1.4 mg/kg bwt Zoletil (0.7 mg/kg bwt tiletamhe + 0.7 mg/kg bwt zolazepam). No statistically significant differences in the measured cardiorespiratory function were found between the 3 groups. Heart rate was decreased significantly after sedation but increased during anaesthesia. Arterial blood pressure increased after sedation and remained high during anaesthesia. A significant decrease in arterial oxygen tension was observed in all groups during anaesthesia. The muscle relaxation induced by romifidine was, in most cases, not sufficient to abolish the catalepsy following a repeated injection of ketamine alone. Zoletil or a repeated injection of ketaminehornifidine resulted in smoother anaesthesia. When additional time is required to complete surgery during field anaesthesia, it is advisable to prolong romifidine/ketamine anaesthesia with an injection of both romifidine and ketamine in healthy horses. When a longer procedure is anticipated from the start Zoletil is an alternative for induction of anaesthesia. The mean time to response to noxious stimuli and mean time spent in lateral recumbency was 28 and 38 min for the anaesthesia prolonged with ketamine, 3.5 and 43 rnin for the anaesthesia prolonged with ketaminehornifidine and 33 and 45 min for the anaesthesia with Zoletil. All horses reached a standing position at the first attempt.     

Oxygenation and plasma endothelin‐1 concentrations in healthy horses recovering from isoflurane anaesthesia administered with or without pulse‐delivered inhaled nitric oxide

ObjectiveTo assess oxygenation, ventilation‐perfusion (V/Q) matching and plasma endothelin (ET‐1) concentrations in healthy horses recovering from isoflurane anaesthesia administered with or without pulse‐delivered inhaled nitric oxide (iNO).Study DesignProspective experimental trial.AnimalsHealthy adult Standardbred horses.MethodsHorses were anaesthetized with isoflurane in oxygen and placed in lateral recumbency. Six control (C group) horses were anaesthetized without iNO delivery and six horses received pulse‐delivered iNO (NO group). After 2.5 hours of anaesthesia isoflurane and iNO were abruptly discontinued, inhaled oxygen was reduced from 100% to approximately 30%, and the horses were moved to the recovery stall. At intervals during a 30‐minute period following the discontinuation of anaesthesia, arterial and mixed venous blood gas values, shunt fraction (Qs/Qt), plasma ET‐1 concentration, pulse rate and respiratory rate were measured or calculated. Repeated measures anova and a Bonferroni post hoc test was used to analyze data with significance set at p <0.05.ResultsAt all time points in the recovery period, NO horses maintained better arterial oxygenation (oxygen partial pressure: NO 13.2 ± 2.7–11.1 ± 2.7 versus C 6.7 ± 1.1–7.1 ± 1.1 kPa) and better V/Q matching (Qs/Qt NO 0.23 ± 0.05–0.14 ± 0.06 versus C 0.48 ± 0.03–0.32 ± 0.08%) than C horses. Mixed venous oxygenation was higher in NO for 25 minutes following the discontinuation of anaesthesia (NO 6.3 ± 0.2–4.5 ± 0.07 versus C 4.7 ± 0.6–3.7 ± 0.3 kPa). In both groups of horses arterial oxygenation remained fairly stable; venous oxygenation declined over this time period in the NO group but still remained higher than venous oxygen in the C group. ET‐1 concentrations were higher at most time points in C than NO. Changes in other parameters were either minor or absent.Conclusions and Clinical RelevanceDelivery of iNO to healthy horses during anaesthesia results in better arterial and venous oxygenation and V/Q matching (as determined by lower Qs/Qt) and lower ET‐1 concentrations throughout a 30‐minute anaesthetic recovery period.     

Clinical anaesthesia in the horse: comparison of enflurane and halothane

Anaesthesia was induced in 24 horses with xylazine and ketamine and maintained with halothane (12 cases) or enflurane (12 cases) in oxygen. Pulse rate, arterial blood pressure, arterial blood gas values, respiratory rate and tidal volume were measured at regular intervals during anaesthesia. Serial venous blood samples were taken for assay of glucose, urea, haemoglobin, packed cell volume, gamma glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase and creatine kinase. Operating conditions and the horses' behaviour in the recovery period were also recorded. In the case of the group of horses receiving enflurane, difficulty was experienced maintaining anaesthesia deep enough for surgery. This group also displayed greater respiratory depression. There were no significant differences between arterial blood pressure values, or any of the haematological or biochemical parameters recorded in each group. Recovery from anaesthesia was significantly faster in horses receiving enflurane but less smooth. It was concluded that, although enflurane appeared to be safe in the horse, the respiratory depression and the unpleasant recovery did not make it a desirable alternative to halothane.     

Influence of general anaesthesia on the pharmacokinetics of intravenous fentanyl and its primary metabolite in horses

REASONS FOR PERFORMING STUDY: In order to evaluate its potential as an adjunct to inhalant anaesthesia in horses, the pharmacokinetics of fentanyl must first be determined. OBJECTIVES: To describe the pharmacokinetics of fentanyl and its metabolite, N-[1-(2-phenethyl-4-piperidinyl)maloanilinic acid (PMA), after i.v. administration of a single dose to horses that were awake in Treatment 1 and anaesthetised with isoflurane in Treatment 2. METHODS: A balanced crossover design was used (n = 4/group). During Treatment 1, horses received a single dose of fentanyl (4 microg/kg bwt, i.v.) and during Treatment 2, they were anaesthetised with isoflurane and maintained at 1.2 x minimum alveolar anaesthetic concentration. After a 30 min equilibration period, a single dose of fentanyl (4 microg/kg bwt, i.v.) was administered to each horse. Plasma fentanyl and PMA concentrations were measured at various time points using liquid chromatography-mass spectrometry. RESULTS: Anaesthesia with isoflurane significantly decreased mean fentanyl clearance (P < 0.05). The fentanyl elimination half-life, in awake and anaesthetised horses, was 1 h and volume of distribution at steady state was 0.37 and 0.26 l/kg bwt, respectively. Anaesthesia with isoflurane also significantly decreased PMA apparent clearance and volume of distribution. The elimination half-life of PMA was 2 and 1.5 h in awake and anaesthetised horses, respectively. CONCLUSIONS AND POTENTIAL RELEVANCE: Pharmacokinetics of fentanyl and PMA in horses were substantially altered in horses anaesthetised with isoflurane. These pharmacokinetic parameters provide information necessary for determination of suitable fentanyl loading and infusion doses in awake and isoflurane-anaesthetised horses.     

Atelectasis causes gas exchange impairment in the anaesthetised horse

The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the 'normal' regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.     

High inspired oxygen concentrations increase intrapulmonary shunt in anaesthetized horses

OBJECTIVES: To compare pulmonary function and gas exchange in anaesthetized horses during and after breathing either O2-rich gas mixtures or air. ANIMALS: Six healthy standard bred trotters (age range 3-12 years; mass range 423-520 kg), four geldings and two mares. Study design Randomized, cross-over experimental study. METHODS: Horses were anaesthetized on two occasions with tiletamine-zolazepam after pre-anaesthetic medication with acepromazine, romifidine and butorphanol. After endotracheal intubation and positioning in left lateral recumbency, animals were allowed to breathe spontaneously. One of two, randomly allocated inspired gas treatments was provided: either i) room air (fractional concentration of inspired O2 [FIO2] = 0.21) provided throughout anaesthesia; or ii) an O2-rich gas mixture (FIO2 = >0.95) for 15 minutes, followed by room air. The alternative treatment was delivered at the second anaesthetic. Respiratory and haemodynamic variables and the distribution of ventilation-perfusion (VA/Q) ratios (using the multiple inert gas elimination technique) were determined in the standing conscious horse (baseline) after sedation and during anaesthesia. RESULTS: Breathing O2-rich gas was associated with a decreased respiratory rate (p = 0.015) increased PaCO2 (p < 0.001) and increased PaO2 (p = 0.004) compared with breathing air. All horses developed intrapulmonary shunt during anaesthesia, but shunt was significantly greater (13 +/- 5%) when O2-rich gas was delivered compared with air breathing (5 +/- 2%; p = 0.013). Ten minutes after O2-rich gas was replaced by air, shunt remained larger in horses that had initially received oxygen compared with those breathing air (p = 0.042). Mixed venous oxygen tensions were significantly lower during sedation than at baseline (p < 0.001) and during anaesthesia (p < 0.001). CONCLUSIONS: During dissociative anaesthesia, arterial oxygenation was greater when horses breathed gas containing more than 95% oxygen, compared with when they breathed air. However, breathing O2-rich gas increased intrapulmonary shunt and caused hypoventilation. The intrapulmonary shunt created during anaesthesia by high inspired O2 concentrations remained larger when FIO2 was reduced to 0.21, indicating that absorption atelectasis produced during O2-rich gas breathing persisted throughout anaesthesia. CLINICAL RELEVANCE: In healthy horses undergoing short-term dissociative anaesthesia, air breathing ensures a level of oxygen delivery that meets tissue demand. There is no benefit to horses in breathing O2-rich gas after the gas supply is discontinued. On the contrary, the degree of shunt induced by breathing O2-rich gas persists. The clinical relevance of this during recovery requires investigation.     

Effects of alpha-2 adrenoceptor agonists during recovery from isoflurane anaesthesia in horses

REASONS FOR PERFORMING STUDY: Recovery from inhalant anaesthesia in the horse is a critical and difficult period to manage; however, several factors could help to obtain a calm recovery period including choice of anaesthetic and analgesic procedure used and the conditions under which anaesthetic maintenance and recovery occur. OBJECTIVES: The objective of this study was to evaluate and compare the quality of recovery in horses administered saline, xylazine, detomidine or romifidine during recovery from isoflurane anaesthesia. METHODS: Six mature and healthy horses were premedicated with i.v. xylazine and butorphanol, and anaesthesia induced using ketamine. After 2 h of inhalant anaesthesia with isoflurane vaporised in oxygen, saline solution, xylazine (0.1 mg/kg bwt), detomidine (2 microg/kg bwt) or romifidine (8 pg/kg bwt) were administered. The quality of recovery of each horse and the degree of sedation and ataxia were evaluated. Cardiovascular and respiratory parameters were recorded, and arterial blood samples obtained and analysed for pH, PO2 and PCO2 during recovery. RESULTS: Quality of recovery was better in groups treated with alpha-2 adrenergic receptors agonists, showing less ataxia. Degree of sedation was greater in the romifidine group. CONCLUSIONS: We concluded that the administration of alpha-2 adrenoceptor agonists during recovery from isoflurane anaesthesia in horses prolonged and improved the quality of recovery without producing significant cardiorespiratory effects. POTENTIAL CLINICAL RELEVANCE: Administration of alpha-2 adrenoceptor agonists after inhalent anaesthesia could prevent complications during the recovery period.