Heart rate,arterial pressure and propofol-sparing effects of guaifenesin in dogs

ObjectiveTo evaluate the heart rate (HR) and systemic arterial pressure (sAP) effects, and propofol induction dose requirements in healthy dogs administered propofol with or without guaifenesin for the induction of anesthesia.Study designProspective blinded crossover experimental study.AnimalsA total of 10 healthy adult female Beagle dogs.MethodsDogs were premedicated with intravenous (IV) butorphanol (0.4 mg kg^–1) and administered guaifenesin 5% at 50 mg kg^–1 (treatment G50), 100 mg kg^–1 (treatment G100) or saline (treatment saline) IV prior to anesthetic induction with propofol. HR, invasive sAP and respiratory rate (f_R) were recorded after butorphanol administration, after guaifenesin administration and after propofol and endotracheal intubation. Propofol doses for intubation were recorded. Repeated measures analysis of variance (anova) was used to determine differences in propofol dose requirements among treatments, and differences in cardiopulmonary values over time and among treatments with p < 0.05 considered statistically significant.ResultsPropofol doses (mean ± standard deviation) for treatments saline, G50 and G100 were 3.3 ± 1.0, 2.7 ± 0.7 and 2.1 ± 0.8 mg kg^–1, respectively. Propofol administered was significantly lower in treatment G100 than in treatment saline (p = 0.04). In treatments G50 and G100, HR increased following induction of anesthesia and intubation compared with baseline measurements. HR was higher in treatment G100 than in treatments G50 and saline following induction of anesthesia. In all treatments, sAP decreased following intubation compared with baseline values. There were no significant differences in sAP among treatments. f_R was lower following intubation than baseline and post co-induction values and did not differ significantly among treatments.Conclusions and clinical relevanceWhen administered as a co-induction agent in dogs, guaifenesin reduced propofol requirements for tracheal intubation. HR increased and sAP and f_R decreased, but mean values remained clinically acceptable.     

The effects of diazepam or midazolam on the dose of propofol required to induce anaesthesia in cats

ObjectivesAssess effects of benzodiazepine administration on the propofol dose required to induce anaesthesia in healthy cats, investigate differences between midazolam and diazepam, and determine an optimal benzodiazepine dose for co-induction.Study designProspective, randomised, blinded, placebo-controlled clinical trial.AnimalsNinety client-owned cats (ASA I and II) with a median (interquartile range) body mass of 4.0 (3.4–4.9) kg.MethodsAll cats received 0.01 mg kg⁻¹ acepromazine and 0.2 mg kg⁻¹ methadone intravenously (IV). Fifteen minutes later, sedation was scored on a scale of 1–5, with 5 indicating greatest sedation. Propofol, 2 mg kg⁻¹, administered IV, was followed by either midazolam or diazepam at 0.2, 0.3, 0.4 or 0.5 mg kg⁻¹ or saline 0.1 mL kg⁻¹. Further propofol was administered until endotracheal intubation was possible. Patient signalment, sedation score, propofol dosage and adverse reactions were recorded.ResultsMidazolam and diazepam (all doses) significantly reduced the propofol dose required compared with saline (p < 0.001). There was no difference between midazolam and diazepam in propofol dose reduction (p = 0.488). All individual doses of midazolam reduced propofol requirement compared with saline (0.2 mg kg⁻¹, p = 0.028; 0.3 mg kg⁻¹, p = 0.006; 0.4 mg kg⁻¹, p < 0.001; 0.5 mg kg⁻¹, p = 0.009). Diazepam 0.2 mg kg⁻¹ did not reduce the propofol dose compared with saline (p = 0.087), but the remaining doses did (0.3 mg kg⁻¹, p = 0.001; 0.4 mg kg⁻¹, p = 0.032; 0.5 mg kg⁻¹, p = 0.041). Cats with sedation scores of 3 required less propofol than cats with scores of 2 (p = 0.008). There was no difference between groups in adverse events.Conclusions and clinical relevanceMidazolam (0.2–0.5 mg kg⁻¹) and diazepam (0.3–0.5 mg kg⁻¹) administered IV after 2 mg kg⁻¹ propofol significantly reduced the propofol dose required for tracheal intubation.     

Fentanyl or midazolam for co-induction of anaesthesia with propofol in dogs

ObjectivePropofol may cause adverse effects (e.g. apnoea, hypotension) at induction of anaesthesia. Co-induction of anaesthesia may reduce propofol requirements. The effect of fentanyl or midazolam on propofol dose requirements and cardiorespiratory parameters was studied.Study designRandomized, controlled, blinded clinical study.AnimalsSixty-six client owned dogs (35 male, 31 female, ASA I-II, age 6–120 months, body mass 4.7–48.0 kg) were selected.MethodsPre-medication with acepromazine (0.025 mg kg⁻¹) and morphine (0.25 mg kg⁻¹) was administered by intramuscular injection. After 30 minutes group fentanyl-propofol (FP) received fentanyl (2 μg kg⁻¹), group midazolam-propofol (MP) midazolam (0.2 mg kg⁻¹) injected over 30 seconds via a cephalic catheter and in a third group, control-propofol (CP), the IV catheter was flushed with an equivalent volume of heparinized saline. Anaesthesia was induced 2 minutes later, with propofol (4 mg kg⁻¹minute⁻¹) administered to effect. After endotracheal intubation anaesthesia was maintained with a standardized anaesthetic protocol. Pulse rate, respiratory rate (RR) and mean arterial pressure (MAP) were recorded before the co-induction agent, before induction, and 0, 2 and 5 minutes after intubation. Apnoea ≥30 seconds was recorded and treated. Sedation after pre-medication, activity after the co-induction agent, quality of anaesthetic induction and endotracheal intubation were scored.ResultsPropofol dose requirement was significantly reduced in FP [2.90 mg kg⁻¹(0.57)] compared to CP [3.51 mg kg⁻¹ (0.74)] and MP [3.58 mg kg⁻¹(0.49)]. Mean pulse rate was higher in MP than in CP or FP (p = 0.003). No statistically significant difference was found between groups in mean RR, MAP or incidence of apnoea. Activity score was significantly higher (i.e. more excited) (p = 0.0001), and quality of induction score was significantly poorer (p = 0.0001) in MP compared to CP or FP. Intubation score was similar in all groups.Conclusions and clinical relevanceFentanyl decreased propofol requirement but did not significantly alter cardiovascular parameters. Midazolam did not reduce propofol requirements and caused excitement in some animals.     

Midazolam,as a co‐induction agent,has propofol sparing effects but also decreases systolic blood pressure in healthy dogs

ObjectiveTo evaluate the effects of the co-administration of midazolam on the dose requirement for propofol anesthesia induction, heart rate (HR), systolic arterial pressure (SAP) and the incidence of excitement.Study designProspective, randomized, controlled and blinded clinical study, with owner consent.AnimalsSeventeen healthy, client owned dogs weighing 28 ± 18 kg and aged 4.9 ± 3.9 years old.MethodsDogs were sedated with acepromazine 0.025 mg kg^?1 and morphine 0.25 mg kg^?1 intramuscularly (IM), 30 minutes prior to induction of anesthesia. Patients were randomly allocated to receive midazolam (MP; 0.2 mg kg^?1) or sterile normal saline (CP; 0.04 mL kg^?1) intravenously (IV) over 15 seconds. Propofol was administered IV immediately following test drug and delivered at 3 mg kg^?1 minute^?1 until intubation was possible. Scoring of pre-induction sedation, ease of intubation, quality of induction, and presence or absence of excitement following co-induction agent, was recorded. HR, SAP and respiratory rate (f_R) were obtained immediately prior to, immediately following, and 5 minutes following induction of anesthesia.ResultsThere were no significant differences between groups with regard to weight, age, gender, or sedation. Excitement occurred in 5/9 dogs following midazolam administration, with none noted in the control group. The dose of propofol administered to the midazolam group was significantly less than in the control group. Differences in HR were not significant between groups. SAP was significantly lower in the midazolam group compared with baseline values 5 minutes after its administration. However, values remained clinically acceptable.Conclusions and clinical relevanceThe co-administration of midazolam with propofol decreased the total dose of propofol needed for induction of anesthesia in sedated healthy dogs, caused some excitement and a clinically unimportant decrease in SAP.     

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.     

Effects of medetomidine and xylazine on intraocular pressure and pupil size in healthy Beagle dogs

ObjectiveTo determine the effects of intramuscular (IM) administration of medetomidine and xylazine on intraocular pressure (IOP) and pupil size in normal dogs.Study designProspective, randomized, experimental, crossover trial.AnimalsFive healthy, purpose-bred Beagle dogs.MethodsEach dog was administered 11 IM injections of, respectively: physiological saline; medetomidine at doses of 5, 10, 20, 40 and 80 μg kg⁻¹, and xylazine at doses of 0.5, 1.0, 2.0, 4.0 and 8.0 mg kg⁻¹. Injections were administered at least 1 week apart. IOP and pupil size were measured at baseline (before treatment) and at 0.25, 0.50, 0.75, 1, 2, 3, 4, 5, 6, 7, 8 and 24 hours post-injection.ResultsA significant decrease in IOP was observed at 6 hours after 80 μg kg⁻¹ medetomidine compared with values at 0.25 and 0.50 hours, although there were no significant changes in IOP from baseline. In dogs treated with 8.0 mg kg⁻¹ xylazine, significant reductions in IOP were observed at 4 and 5 hours compared with that at 0.25 hours after administration. In dogs treated with 5, 10, 20 and 40 μg kg⁻¹ medetomidine and 0.5, 1.0 and 2.0 mg kg⁻¹ xylazine, there were no significant changes in IOP. Pupil size did not change significantly after any of the medetomidine or xylazine treatments compared with the baseline value.Conclusions and clinical relevanceLow or moderate doses of medetomidine or xylazine did not induce significant changes in IOP or pupil size. In contrast, high doses of medetomidine or xylazine induced significant changes up to 8 hours after treatment, but values remained within the normal canine physiological range. The results of this study suggest a lack of significant change in IOP and pupil size in healthy dogs administered low or moderate doses of xylazine or medetomidine.     

Dose and cardiopulmonary effects of propofol alone or with midazolam for induction of anesthesia in critically ill dogs

ObjectiveTo determine the dose and cardiopulmonary effects of propofol alone or with midazolam for induction of anesthesia in American Society of Anesthesiologists status ≥III dogs requiring emergency abdominal surgery.Study designProspective, randomized, blinded, clinical trial.AnimalsA total of 19 client-owned dogs.MethodsDogs were sedated with fentanyl (2 μg kg^–1) intravenously (IV) for instrumentation for measurement of heart rate, arterial blood pressure, cardiac index, systemic vascular resistance index, arterial blood gases, respiratory rate and rectal temperature. After additional IV fentanyl (3 μg kg^–1), the quality of sedation was scored and cardiopulmonary variables recorded. Induction of anesthesia was with IV propofol (1 mg kg^–1) and saline (0.06 mL kg^–1; group PS; nine dogs) or midazolam (0.3 mg kg^–1; group PM; 10 dogs), with additional propofol (0.25 mg kg^–1) IV every 6 seconds until endotracheal intubation. Induction/intubation quality was scored, and anesthesia was maintained with isoflurane. Variables were recorded for 5 minutes with the dog in lateral recumbency, breathing spontaneously, and then in dorsal recumbency with mechanical ventilation for the next 15 minutes. A general linear mixed model was used with post hoc analysis for multiple comparisons between groups (p < 0.05).ResultsThere were no differences in group demographics, temperature and cardiopulmonary variables between groups or within groups before or after induction. The propofol doses for induction of anesthesia were significantly different between groups, 1.9 ± 0.5 and 1.1 ± 0.5 mg kg^–1 for groups PS and PM, respectively, and the induction/intubation score was significantly better for group PM.Conclusions and clinical relevanceMidazolam co-induction reduced the propofol induction dose and improved the quality of induction in critically ill dogs without an improvement in cardiopulmonary variables, when compared with a higher dose of propofol alone.     

Cardiovascular effects of a continuous rate infusion of lidocaine in calves anesthetized with xylazine,midazolam, ketamine and isoflurane

ObjectiveTo assess the cardiovascular changes of a continuous rate infusion of lidocaine in calves anesthetized with xylazine, midazolam, ketamine and isoflurane during mechanical ventilation.Study designProspective, randomized, cross-over, experimental trial.AnimalsA total of eight, healthy, male Holstein calves, aged 10 ± 1 months and weighing 114 ± 11 kg were included in the study.MethodsCalves were administered xylazine followed by ketamine and midazolam, orotracheal intubation and maintenance on isoflurane (1.3%) using mechanical ventilation. Forty minutes after induction, lidocaine (2 mg kg^?1 bolus) or an equivalent volume of saline (0.9%) was administered IV followed by a continuous rate infusion (100 μg kg^?1 minute^?1) of lidocaine (treatment L) or saline (treatment C). Heart rate (HR), systolic, diastolic and mean arterial pressures (SAP, DAP and MAP), central venous pressure (CVP), mean pulmonary arterial pressure (mPAP), pulmonary arterial occlusion pressure (PAOP), cardiac output, end-tidal carbon dioxide (Pe’CO₂) and core temperature (CT) were recorded before lidocaine or saline administration (Baseline) and at 20-minute intervals (T20-T80). Plasma concentrations of lidocaine were measured in treatment L.ResultsThe HR was significantly lower in treatment L compared with treatment C. There was no difference between the treatments with regards to SAP, DAP, MAP and SVRI. CI was significantly lower at T60 in treatment L when compared with treatment C. PAOP and CVP increased significantly at all times compared with Baseline in treatment L. There was no significant difference between times within each treatment and between treatments with regards to other measured variables. Plasma concentrations of lidocaine ranged from 1.85 to 2.06 μg mL^?1 during the CRI.Conclusion and clinical relevanceAt the studied rate, lidocaine causes a decrease in heart rate which is unlikely to be of clinical significance in healthy animals, but could be a concern in compromised animals.     

A dose titration study into the effects of diazepam or midazolam on the propofol dose requirements for induction of general anaesthesia in client owned dogs,premedicated with methadone and acepromazine

ObjectiveTo assess the effect of a benzodiazepine co–induction on propofol dose requirement for induction of anaesthesia in healthy dogs, to describe any differences between midazolam and diazepam and to determine an optimal benzodiazepine dose for co–induction.Study designProspective, randomised, blinded placebo controlled clinical trial.AnimalsNinety client owned dogs (ASA I–III, median body mass 21.5kg (IQR 10–33)) presented for anaesthesia for a variety of procedures.MethodsDogs were randomised to receive saline 0.1 mL kg^?1, midazolam or diazepam at 0.2, 0.3, 0.4 or 0.5 mg kg^?1. All dogs received 0.01 mg kg^?1 acepromazine and 0.2 mg kg^?1 methadone intravenously (IV). Fifteen minutes later, sedation was assessed and scored prior to anaesthetic induction. Propofol, 1 mg kg^?1, was administered IV, followed by the treatment drug. Further propofol was administered until endotracheal intubation was possible. Recorded data included patient signalment, sedation score, propofol dosage and any adverse reactions.ResultsMidazolam (all groups combined) significantly reduced propofol dose requirement compared to saline (p < 0.001) and diazepam (p = 0.008). Midazolam (0.4 mg kg^?1) significantly reduced propofol dose requirement (p = 0.014) compared to saline, however other doses failed to reach statistical significance. Diazepam did not significantly reduce propofol dose requirement compared to saline (p = 0.089). Dogs weighing <5 kg, regardless of treatment group, required a greater propofol dose than those weighing 5–40 kg (p = 0.002) and those >40 kg (p = 0.008). Dogs which were profoundly sedated required less propofol than those which were mildly sedated (p < 0.001) and adequately sedated (p = 0.003).Conclusions and clinical relevanceMidazolam (0.4 mg kg^?1) given IV after 1 mg kg^?1 of propofol significantly reduced the further propofol dose required for intubation compared to saline. At the investigated doses, diazepam did not have significant propofol dose sparing effects.     

S‐ketamine versus racemic ketamine in dogs: their relative potency as induction agents

ObjectiveTo determine the potency ratio between S-ketamine and racemic ketamine as inductive agents for achieving tracheal intubation in dogs.Study designProspective, randomized, ‘blinded’, clinical trial conducted in two consecutive phases.Animals112 client-owned dogs (ASA I or II).MethodsAll animals were premedicated with intramuscular acepromazine (0.02 mg kg⁻¹) and methadone (0.2 mg kg⁻¹). In phase 1, midazolam (0.2 mg kg⁻¹) with either 3 mg kg⁻¹ of racemic ketamine (group K) or 1.5 mg kg⁻¹ of S-ketamine (group S) was administered IV, for induction of anaesthesia and intubation. Up to two additional doses of racemic (1.5 mg kg⁻¹) or S-ketamine (0.75 mg kg⁻¹) were administered if required. In phase 2, midazolam (0.2 mg kg⁻¹) with 1 mg kg⁻¹ of either racemic ketamine (group K) or S-ketamine (group S) was injected and followed by a continuous infusion (1 mg kg minute⁻¹) of each respective drug. Differences between groups were statistically analyzed via t-test, Fisher exact test and ANOVA for repeated measures.ResultsDemographics and quality and duration of premedication, induction and intubation were comparable among groups. During phase 1 it was possible to achieve tracheal intubation after a single dose in more dogs in group K (n = 25) than in group S (n = 16) (p = 0.046). A dose of 3 mg kg⁻¹ S-ketamine allowed tracheal intubation in the same number of dogs as 4.5 mg kg⁻¹ of racemic ketamine. The estimated potency ratio was 1.5:1. During phase 2, the total dose (mean ± SD) of S-ketamine (4.02 ±1.56 mg kg⁻¹) and racemic ketamine (4.01 ± 1.42) required for tracheal intubation was similar.Conclusion and clinical relevanceRacemic and S-ketamine provide a similar quality of anaesthetic induction and intubation. S-ketamine is not twice as potent as racemic ketamine and, if infused, the potency ratio is 1:1.     

Cardiovascular tolerance of intravenous lidocaine in broiler chickens (Gallus gallus domesticus) anesthetized with isoflurane

ObjectiveTo determine the cardiovascular effects of lidocaine infused intravenously (IV) in broiler chickens.Study designTwo phase study: Phase 1, randomized up-and-down study to determine effective dose 50 (ED₅₀) for lidocaine; Phase 2, prospective randomized study to determine the cardiovascular effects of lidocaine.AnimalsSeventeen Ross-708 broiler chickens (Gallus gallus domesticus) [11 chickens (Phase 1) and 6 chickens (Phase 2)], weighing 2.6–4.3 kg.MethodsAfter induction of anesthesia with isoflurane and placement of monitoring equipment including invasive blood pressure, chickens were administered lidocaine IV. During Phase 1, using an up-and-down design, each animal received a variable dose selected based on the response of the previous animal. During Phase 2, each animal was administered 6 mg kg⁻¹ of lidocaine IV over 2 minutes. Clinically irrelevant cardiovascular effects were defined as a relative decrease of heart rate (HR) and mean blood pressure (MAP) <30% subsequent to IV lidocaine administration. The ED₅₀ was defined as the dose rate that would cause clinically irrelevant cardiovascular depression in 50% of the population.ResultsDuring Phase 1, using an up-and-down study design (n = 11), the ED₅₀ of lidocaine was determined to be 6.30 mg kg⁻¹ and 6.22 mg kg⁻¹ (95% confidence interval, 5.30–7.13 mg kg⁻¹), when calculated by Dixon's up-and-down method, and logistic regression, respectively. During Phase 2, following infusion of lidocaine (6 mg kg⁻¹), no clinically relevant effects on HR or MAP were detected in any animal.Conclusions and clinical relevancePrevious reports state that the dose of lidocaine used in birds should be =4 mg kg⁻¹. In this study, 6 mg kg⁻¹ of lidocaine injected IV was not associated with adverse cardiovascular effects. These results suggest that the dose of 4 mg kg⁻¹ can be exceeded, at least in chickens, and opens the possibility of other therapeutic uses for lidocaine in birds.     

Comparison of the effects of butorphanol–midazolam–medetomidine and butorphanol–azaperone–medetomidine in wild common palm civets (Paradoxurus musangus)

ObjectiveTo assess the efficacy of butorphanol–azaperone–medetomidine (BAM) and butorphanol–midazolam–medetomidine (BMM) protocols for immobilization of wild common palm civets (Paradoxurus musangus) with subsequent antagonization with atipamezole.Study designProspective, randomized, blinded clinical trial.AnimalsA total of 40 adult wild common palm civets, 24 female and 16 male, weighing 1.5–3.4 kg.MethodsThe civets were randomly assigned for anesthesia with butorphanol, azaperone and medetomidine (0.6, 0.6 and 0.2 mg kg^–1, respectively; group BAM) or with butorphanol, midazolam and medetomidine (0.3, 0.4 and 0.1 mg kg^–1, respectively; group BMM) intramuscularly (IM) in a squeeze cage. When adequately relaxed, the trachea was intubated for oxygen administration. Physiological variables were recorded every 5 minutes after intubation. Following morphometric measurements, sampling, microchipping and parasite treatment, medetomidine was reversed with atipamezole at 1.0 or 0.5 mg kg^–1 IM to groups BAM and BMM, respectively. Physiological variables and times to reach the different stages of anesthesia were compared between groups.ResultsOnset time of sedation and recumbency was similar in both groups; time to achieve complete relaxation and tracheal intubation was longer in group BAM. Supplementation with isoflurane was required to enable intubation in five civets in group BAM and one civet in group BMM. All civets in group BAM required topical lidocaine to facilitate intubation. End-tidal carbon dioxide partial pressure was lower in group BAM, but heart rate, respiratory rate, rectal temperature, peripheral hemoglobin oxygen saturation and mean arterial blood pressure were not different. All civets in both groups recovered well following administration of atipamezole.Conclusions and clinical relevanceBoth BAM and BMM combinations were effective for immobilizing wild common palm civets. The BMM combination had the advantage of producing complete relaxation that allowed intubation more rapidly.     

Prophylactic use of a lidocaine constant rate infusion versus saline in dogs undergoing balloon valvuloplasty for management of pulmonic stenosis: A randomized control trial

ObjectiveTo evaluate the effect of a prophylactic lidocaine constant rate infusion (CRI) on the incidence and malignancy of catheter-induced ventricular ectopic complexes (VECs) during balloon valvuloplasty for management of pulmonic stenosis in dogs.Study designSingle-centre, prospective, randomized study.AnimalsClient-owned dogs (n = 70) with pulmonic stenosis.MethodsDogs were randomly assigned to one of two anaesthetic protocols: administration of lidocaine 2 mg kg^–1 bolus followed by a CRI (50 μg kg^–1 minute^–1; group LD) or a saline placebo (group SL) during balloon valvuloplasty. All dogs were premedicated with methadone (0.3 mg kg^–1) intramuscularly and a digital three-lead Holter monitor was applied. Anaesthetic co-induction was performed with administration of alfaxalone (2 mg kg^–1) and diazepam (0.4 mg kg^–1), and anaesthesia was maintained with isoflurane vaporised in 100% oxygen. CRIs were started on positioning of the dog in theatre and discontinued as the last vascular catheter was removed from the heart. All dogs recovered well and were discharged 24 hours postoperatively. Blinded Holter analysis was performed by an external veterinary cardiologist using commercially available dedicated analysis software; p < 0.05.ResultsOf the 70 dogs enrolled in the study, 61 were included in the final analysis: 31 in group LD and 30 in group SL.There was no significant difference between sinus beats (p = 0.227) or VECs (p = 0.519) between groups. In group LD, 19/31 (61.3%) dogs had a maximum ventricular rate ≥250 units and 20/30 (66.7%) dogs in group SL (p = 0.791).Conclusion and clinical relevanceIn this study, the use of a prophylactic lidocaine bolus followed by CRI in dogs undergoing balloon valvuloplasty for management of pulmonic stenosis did not significantly decrease the incidence nor the malignancy of VECs during right heart catheterization compared with a saline CRI.     

Effects of dexmedetomidine alone or in combination with opioids on intraocular pressure in healthy Beagle dogs

ObjectiveTo evaluate the effects of dexmedetomidine alone or in combination with different opioids on intraocular pressure (IOP) in dogs.Study designExperimental, prospective, crossover, randomized, blinded study.AnimalsA total of six Beagle dogs (two males and four females) aged 2 years and weighing 15.9 ± 2.9 kg (mean ± standard deviation).MethodsDogs were distributed randomly into seven treatments (n = 6 per treatment) and were administered dexmedetomidine alone (10 μg kg^–1; Dex) or in combination with butorphanol (0.15 mg kg^–1; DexBut), meperidine (5 mg kg^–1; DexMep), methadone (0.5 mg kg^–1; DexMet), morphine (0.5 mg kg^–1; DexMor), nalbuphine (0.5 mg kg^–1; DexNal) or tramadol (5 mg kg^–1; DexTra). All drugs were administered intramuscularly. IOP was measured before drug injection (time 0, baseline) and every 15 minutes thereafter for 120 minutes (T15–T120).ResultsThere were significant reductions in IOP compared with baseline in treatments Dex and DexMep at times T30–T120, and in treatment DexMet at T15–T90. IOP decreased compared with baseline in treatments DexBut, DexNal and DexTra at all evaluation times. No changes in IOP were seen in treatment DexMor. The mean IOP values in treatment DexMet at T105–T120 were higher than those for other treatments.Conclusions and clinical relevanceDexmedetomidine alone or in combination with butorphanol, meperidine, methadone, nalbuphine or tramadol resulted in decreased IOP for 120 minutes in dogs. The magnitude of the reduction was small and lacked clinical significance.     

Ketamine–propofol for total intravenous anaesthesia in rabbits: a comparison of premedication with acepromazine–medetomidine,acepromazine–midazolam or acepromazine–morphine

ObjectiveTo describe ketamine–propofol total intravenous anaesthesia (TIVA) following premedication with acepromazine and either medetomidine, midazolam or morphine in rabbits.Study designRandomized, crossover experimental study.AnimalsA total of six healthy female New Zealand White rabbits (2.2 ± 0.3 kg).MethodsRabbits were anaesthetized on four occasions, each separated by 7 days: an intramuscular injection of saline alone (treatment Saline) or acepromazine (0.5 mg kg^–1) in combination with medetomidine (0.1 mg kg^–1), midazolam (1 mg kg^–1) or morphine (1 mg kg^–1), treatments AME, AMI or AMO, respectively, in random order. Anaesthesia was induced and maintained with a mixture containing ketamine (5 mg mL^–1) and propofol (5 mg mL^–1) (ketofol). Each trachea was intubated and the rabbit administered oxygen during spontaneous ventilation. Ketofol infusion rate was initially 0.4 mg kg^–1 minute^–1 (0.2 mg kg^–1 minute^–1 of each drug) and was adjusted to maintain adequate anaesthetic depth based on clinical assessment. Ketofol dose and physiological variables were recorded every 5 minutes. Quality of sedation, intubation and recovery times were recorded.ResultsKetofol induction doses decreased significantly in treatments AME (7.9 ± 2.3) and AMI (8.9 ± 4.0) compared with treatment Saline (16.8 ± 3.2 mg kg^–1) (p < 0.05). The total ketofol dose to maintain anaesthesia was significantly lower in treatments AME, AMI and AMO (0.6 ± 0.1, 0.6 ± 0.2 and 0.6 ± 0.1 mg kg^–1 minute^–1, respectively) than in treatment Saline (1.2 ± 0.2 mg kg^–1 minute^–1) (p < 0.05). Cardiovascular variables remained at clinically acceptable values, but all treatments caused some degree of hypoventilation.Conclusions and clinical relevancePremedication with AME, AMI and AMO, at the doses studied, significantly decreased the maintenance dose of ketofol infusion in rabbits. Ketofol was determined to be a clinically acceptable combination for TIVA in premedicated rabbits.     

Comparison of intraperitoneal ropivacaine and ropivacaine–dexmedetomidine for postoperative analgesia in cats undergoing ovariohysterectomy

ObjectiveTo investigate the intraperitoneal (IP) administration of ropivacaine or ropivacaine–dexmedetomidine for postoperative analgesia in cats undergoing ovariohysterectomy.Study designProspective, randomized, blinded, positively controlled clinical study.AnimalsA total of 45 client-owned cats were enrolled.MethodsThe cats were administered intramuscular (IM) meperidine (6 mg kg⁻¹) and acepromazine (0.05 mg kg⁻¹). Anesthesia was induced with propofol and maintained with isoflurane. Meloxicam (0.2 mg kg⁻¹) was administered subcutaneously in all cats after intubation. After the abdominal incision, the cats were administered one of three treatments (15 cats in each treatment): IP instillation of 0.9% saline solution (group Control), 0.25% ropivacaine (1 mg kg⁻¹, group ROP) or ropivacaine and dexmedetomidine (4 μg kg⁻¹, group ROP–DEX). During anesthesia, heart rate (HR), electrocardiography, noninvasive systolic arterial pressure (SAP) and respiratory variables were monitored. Sedation and pain were assessed preoperatively and at various time points up to 24 hours after extubation using sedation scoring, an interactive visual analog scale, the UNESP-Botucatu multidimensional composite pain scale (MCPS) and mechanical nociceptive thresholds (MNT; von Frey anesthesiometer). Rescue analgesia (morphine, 0.1 mg kg⁻¹) IM was administered if the MCPS ≥6. Data were analyzed using the chi-square test, Tukey test, Kruskal–Wallis test and Friedman test (p < 0.05).ResultsHR was significantly lower in ROP–DEX compared with Control (p = 0.002). The pain scores, MNT, sedation scores and the postoperative rescue analgesia did not differ statistically among groups.Conclusions and clinical relevanceAs part of a multimodal pain therapy, IP ropivacaine–dexmedetomidine was associated with decreased HR intraoperatively; however, SAP remained within normal limits. Using the stated anesthetic protocol, neither IP ropivacaine nor ropivacaine–dexmedetomidine significantly improved analgesia compared with IP saline in cats undergoing ovariohysterectomy.     

Effects of midazolam before or after alfaxalone for co-induction of anaesthesia in healthy dogs

Objective

To study the effect of alternating the order of midazolam and alfaxalone administration on the incidence of behavioural changes, alfaxalone induction dose and some cardiorespiratory variables in healthy dogs.

Evaluation of analgesic,sympathetic and motor effects of 1% and 2% lidocaine administered epidurally in dogs undergoing ovariohysterectomy

ObjectiveTo compare, versus a control, the sensory, sympathetic and motor blockade of lidocaine 1% and 2% administered epidurally in bitches undergoing ovariohysterectomy.Study designRandomized, blinded, controlled clinical trial.AnimalsA total of 24 mixed-breed intact female dogs.MethodsAll dogs were administered dexmedetomidine, tramadol and meloxicam prior to general anesthesia with midazolam–propofol and isoflurane. Animals were randomly assigned for an epidural injection of lidocaine 1% (0.4 mL kg⁻¹; group L1), lidocaine 2% (0.4 mL kg⁻¹; group L2) or no injection (group CONTROL). Heart rate (HR), respiratory rate (f_R), end-tidal partial pressure of carbon dioxide (Pe′CO₂), and invasive systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures were recorded every 5 minutes. Increases in physiological variables were treated with fentanyl (3 μg kg⁻¹) intravenously (IV). Phenylephrine (1 μg kg⁻¹) was administered IV when MAP was <60 mmHg. Postoperative pain [Glasgow Composite Pain Score – Short Form (GCPS–SF)] and return of normal ambulation were recorded at 1, 2, 3, 4 and 6 hours after extubation.ResultsThere were no differences over time or among groups for HR, f_R, Pe′CO₂ and SAP. MAP and DAP were lower in epidural groups than in CONTROL (p = 0.0146 and 0.0047, respectively). There was no difference in the use of phenylephrine boluses. More fentanyl was administered in CONTROL than in L1 and L2 (p = 0.011). GCPS–SF was lower for L2 than for CONTROL, and lower in L1 than in both other groups (p = 0.001). Time to ambulation was 2 (1–2) hours in L1 and 3 (2–4) hours in L2 (p = 0.004).Conclusions and clinical relevanceEpidural administration of lidocaine (0.4 mL kg⁻¹) reduced fentanyl requirements and lowered MAP and DAP. Time to ambulation decreased and postoperative pain scores were improved by use of 1% lidocaine compared with 2% lidocaine.     

Effect of phentolamine mesylate on regression of lidocaine–epinephrine epidural anaesthesia in sheep

ObjectiveTo determine the impact of epidural phentolamine on the duration of anaesthesia following epidural injection of lidocaine–epinephrine.Study designBlinded randomized experimental study.AnimalsA group of 12 adult ewes weighing 25.7 ± 2.3 kg and aged 8–9 months.MethodsAll sheep were administered epidural lidocaine (approximately 4 mg kg^–1) and epinephrine (5 μg mL^–1). Of these, six sheep were randomized into three epidural treatments, separated by 1 week, administered 30 minutes after lidocaine–epinephrine: SAL: normal saline, PHE1: phentolamine (1 mg) and PHE2: phentolamine (2 mg). The other six sheep were administered only epidural lidocaine–epinephrine: treatment LIDEP. Each injection was corrected to 5 mL using 0.9% saline. Noxious stimuli were pinpricks with a hypodermic needle and skin pinch with haemostatic forceps to determine the onset and duration of sensory and motor block. Heart rate, noninvasive mean arterial pressure (MAP), respiratory rate and rectal temperature were recorded.ResultsThe onset times were not different among treatments. Duration of sensory block was significantly shorter in SAL (57.5 ± 6.2 minutes), PHE1 (60.7 ± 9.0 minutes) and PHE2 (62.0 ± 6.7 minutes) than in LIDEP (81.7 ± 13.4 minutes) (p < 0.05). Duration of motor blockade was significantly shorter in PHE1 (59.4 ± 5.4 minutes) and PHE2 (54.3 ± 4.0 minutes) than in SAL (84.8 ± 7.0 minutes) and LIDEP (91.5 ± 18.2 minutes) (p < 0.01). MAP in PHE2 was decreased at 10 minutes after administration of phentolamine (p < 0.05).Conclusion and clinical relevanceEpidural administration of 5 mL normal saline after epidural injection of lidocaine–epinephrine reduced the duration of sensory but not motor block in sheep. Epidural administration of phentolamine diluted to the final volume of 5 mL diminished both the duration of sensory and motor block in sheep administered epidural lidocaine–epinephrine.     

Evaluation of a dexmedetomidine–midazolam–ketamine combination administered intramuscularly in captive ornate box turtles (Terrapene ornata ornata)

ObjectiveTo characterize the effects of a combination protocol of dexmedetomidine–midazolam–ketamine (DMK) administered intramuscularly (IM) in ornate box turtles (Terrapene ornata ornata).Study designProspective experimental trial.AnimalsA total of 16 apparently clinically healthy adult ornate box turtles (eight male, eight female).MethodsEach turtle was treated with dexmedetomidine (0.1 mg kg⁻¹), midazolam (1 mg kg⁻¹) and ketamine (10 mg kg⁻¹) administered IM. Time to first response, time to maximal effect, the plateau phase and time to recovery from reversal administration were recorded. Physiologic variables, muscle tone, reflexes and the ability to perform endotracheal intubation were recorded at 5 minute intervals. Movement in response to an IM injection of 0.1 mL sterile 0.9% NaCl administered in the left pelvic limb, using a 25 gauge needle to a depth of just past the bevel of the needle, was assessed every 15 minutes. Atipamezole (0.5 mg kg⁻¹) IM and flumazenil (0.05 mg kg⁻¹) SC were administered 60 minutes after the initial DMK injections.ResultsThe mean time to first response, time to maximal effect, the plateau phase and time to recovery were 2.1, 14.9, 38.7 and 7.8 minutes, respectively. A respiratory rate was not observed in most turtles. The body temperature significantly increased over time. The palpebral reflex was persistent in 43% of turtles and the tail pinch reflex remained intact in 13% of turtles. All turtles recovered with no observed adverse effects.Conclusions and clinical relevanceIn this study, this DMK protocol administered to ornate box turtles resulted in a rapid-onset, light anesthesia lasting approximately 40 minutes and a smooth recovery with no adverse effects noted.