The influence of hypoxaemia, hypotension and hypercapnia (among other factors) on quality of recovery from general anaesthesia in horses.

OBJECTIVE: To investigate the effect of hypoxaemia, hypotension and hypercapnia, among others, on quality of recovery from general anaesthesia in horses. STUDY DESIGN: Retrospective, single-centre study. ANIMALS: A sample of 1226 horses that underwent general anaesthesia between June 2017 and June 2021. METHODS: Horses and ponies weighing > 200 kg, aged > 6 months, anaesthetized using a xylazine- or medetomidine-isoflurane balanced anaesthesia protocol and presenting a complete anaesthetic record were included. Data were extracted from the clinic record system and from the original anaesthesia records. Recoveries were divided into 'good' and 'bad' based on the available recovery scores. Influence of hypoxaemia [PaO2 < 60 mmHg (7.99 kPa)], hypotension (mean arterial pressure < 70 mmHg for at least 15 minutes) and hypercapnia [PaCO2 > 60 mmHg (7.99 kPa)], anaesthesia protocol, body weight, age, breed, sex, American Society of Anesthesiologists status, type of procedure, emergency or nonemergency, duration of anaesthesia, positioning, times spent in lateral and sternal recumbency during recovery, time until standing and nonassisted or assisted recovery on the assigned recovery score (good/bad) were investigated using generalized linear regression analysis (p < 0.05). RESULTS: Hypoxaemia and prolonged duration of anaesthesia were significantly associated with a bad recovery score. No other factors had a significant influence on recovery quality. CONCLUSION AND CLINICAL RELEVANCE: Hypoxaemia and prolonged anaesthesia duration have a negative effect on quality of anaesthetic recovery in horses. Clinically, this highlights the importance of keeping anaesthetic time as short as possible and to monitor oxygenation and treat hypoxaemia as soon as possible.

Delivery of non-viral naked DNA vectors to liver in small weaned pigs by hydrodynamic retrograde intrabiliary injection.

Hepatic gene therapy by delivering non-integrating therapeutic vectors in newborns remains challenging due to the risk of dilution and loss of efficacy in the growing liver. Previously we reported on hepatocyte transfection in piglets by intraportal injection of naked DNA vectors. Here, we established delivery of naked DNA vectors to target periportal hepatocytes in weaned pigs by hydrodynamic retrograde intrabiliary injection (HRII). The surgical procedure involved laparotomy and transient isolation of the liver. For vector delivery, a catheter was placed within the common bile duct by enterotomy. Under optimal conditions, no histological abnormalities were observed in liver tissue upon pressurized injections. The transfection of hepatocytes in all tested liver samples was observed with vectors expressing luciferase from a liver-specific promoter. However, vector copy number and luciferase expression were low compared to hydrodynamic intraportal injection. A 10-fold higher number of vector genomes and luciferase expression was observed in pigs using a non-integrating naked DNA vector with the potential for replication. In summary, the HRII application was less efficient (i.e., lower luciferase activity and vector copy numbers) than the intraportal delivery method but was significantly less distressful for the piglets and has the potential for injection (or re-injection) of vector DNA by endoscopic retrograde cholangiopancreatography.

Comparison of Recovery Quality Following Medetomidine versus Xylazine Balanced Isoflurane Anaesthesia in Horses: A Retrospective Analysis.

Medetomidine partial intravenous anaesthesia (PIVA) has not been compared to xylazine PIVA regarding quality of recovery. This clinical retrospective study compared recoveries following isoflurane anaesthesia balanced with medetomidine or xylazine. The following standard protocol was used: sedation with 7 µg·kg-1 medetomidine or 1.1 mg·kg-1 xylazine, anaesthesia induction with ketamine/diazepam, maintenance with isoflurane and 3.5 µg·kg-1·h-1 medetomidine or 0.7 mg·kg-1·h-1 xylazine, and sedation after anaesthesia with 2 µg·kg-1 medetomidine or 0.3 mg·kg-1 xylazine. Recovery was timed and, using video recordings, numerically scored by two blinded observers. Influence of demographics, procedure, peri-anaesthetic drugs, and intraoperative complications (hypotension, hypoxemia, and tachycardia) on recovery were analysed using regression analysis (p < 0.05). A total of 470 recoveries (medetomidine 279, xylazine 191) were finally included. Following medetomidine, recoveries were significantly longer (median (interquartile range): 57 (43-71) min) than xylazine (43 (32-59) min) (p < 0.001). However, the number of attempts to stand was similar (medetomidine and xylazine: 2 (1-3)). Poorer scores were seen with increased pre-anaesthetic dose of xylazine, intraoperative tetrastarch, or salbutamol. However, use of medetomidine or xylazine did not influence recovery score, concluding that, following medetomidine-isoflurane PIVA, recovery is longer, but of similar quality compared to xylazine.

Clinical Randomized Comparison of Medetomidine and Xylazine for Isoflurane Balanced Anesthesia in Horses.

Introduction: To assess drug plasma levels, preanesthetic sedation, cardiopulmonary effects during anesthesia and recovery in horses anesthetized with isoflurane combined with medetomidine or xylazine. Study design: Prospective blinded randomized clinical study. Animals: Sixty horses undergoing elective surgery. Methods: Thirty minutes after administration of antibiotics, flunixine meglumine or phenylbutazone and acepromazine horses received medetomidine 7 µg kg-1 (group MED) or xylazine 1.1 mg kg-1 (group XYL) slowly intravenously (IV) and sedation was assessed 3 min later. Anesthesia was induced with ketamine/diazepam and maintained with isoflurane in oxygen/air and medetomidine 3.5 µg kg-1 h-1 or xylazine 0.69 mg kg-1 h-1. Ringer's acetate 10 mL kg-1 h-1 and dobutamine were administered to maintain normotension. All horses were mechanically ventilated to maintain end-tidal carbon dioxide pressures at 45 ± 5 mmHg (5.3-6.7 kPa). Heart rate (HR), invasive arterial blood pressures, inspired and expired gas compositions, pH, arterial blood gases, electrolytes, lactate and glucose were measured. For recovery all horses received intramuscular morphine 0.1 mg kg-1 and medetomidine 2 µg kg-1 or xylazine 0.3 mg kg-1 IV. Recovery was timed and scored using three different scoring systems. Plasma samples to measure medetomidine and xylazine concentrations were collected at predetermined timepoints. Repeatedly measured parameters were analyzed using a two-way repeated-measures analysis of variance for differences between groups and over time; p < 0.05 was considered statistically significant. Results: Mean arterial blood pressures (MAP) stayed within normal ranges but were higher (p = 0.011) in group XYL despite significant lower dobutamine doses (p = 0.0003). Other measured parameters were within clinically acceptable ranges. Plasma levels were at steady state during anesthesia (MED 2.194 ± 0.073; XYL 708 ± 18.791 ng mL-1). During recovery lateral recumbency (MED 42.7 ± 2.51; XYL 34.3 ± 2.63 min; p = 0.027) and time to standing (MED 62.0 ± 2.86; XYL 48.8 ± 3.01 min; p = 0.002) were significantly shorter in group XYL compared to group MED. Recovery scores did not differ significantly between groups. Conclusion and Clinical Relevance: In horses anesthetized with isoflurane and medetomidine or xylazine, xylazine maintained higher MAP, reduced the dobutamine consumption and recovery time, whilst overall recovery quality was unaffected.

Effects of hypothermia and hypothermia combined with hypocapnia on cerebral tissue oxygenation in piglets.

BACKGROUND: Hypothermia and its combination with hypocapnia are frequently associated with anesthesia. AIMS: The goal was to investigate the effects of hypothermia and hypothermia combined with hypocapnia (hypothermia-hypocapnia) on cerebral tissue oxygenation in anesthetized piglets. METHODS: Twenty anesthetized piglets were randomly allocated to hypothermia (n = 10) or hypothermia-hypocapnia (n = 10). Cerebral monitoring comprised a tissue oxygen partial pressure (PtO2 ), a laser Doppler probe, and a near-infrared spectroscopy sensor, measuring regional oxygen saturation (rSO2 ). After baseline recordings, hypothermia (35.5-36.0°C) with or without hypocapnia (target PaCO2 : 28-30 mm Hg) was induced. Once treatment goals were achieved (Tr0), they were maintained for 30 minutes (Tr30). RESULTS: No changes in PtO2 but a significant increase in rSO2 (Tr0 (mean difference 8.9[95% CI for difference3.99 to 13.81], P < .001); Tr30 (10.8[6.20 to 15.40], P < .001)) were detected during hypothermia. With hypothermia-hypocapnia, a decrease in PtO2 (Tr0 (-3.2[-6.01 to -0.39], P = .021; Tr30 (-3.3[-5.8 to -0.80], P = .006)) and no significant changes in rSO2 occurred. Cerebral blood flow decreased significantly from baseline to Tr0 independently of treatment (-0.89[-0.18 to -0.002], P = .042), but this was more consistently observed with hypothermia-hypocapnia. CONCLUSIONS: The hypothermia-induced reduction in oxygen delivery was compensated by lowered metabolic demand. However, hypothermia was not able to compensate for an additional reduction in oxygen delivery caused by simultaneous hypocapnia. This resulted in a PtO2 drop, which was not reflected by a downshift in rSO2 .

Hypotension and Hypocapnia During General Anesthesia in Piglets: Study of S100b as an Acute Biomarker for Cerebral Tissue Injury.

BACKGROUND: Hypotension and/or hypocapnia might increase general anesthesia (GA)-related neuromorbidity in infants, but safe levels of perioperative blood pressure are poorly defined. Serum protein S100b has been used as screening, monitoring, and prediction tool in the management of patients with traumatic brain injury. Using an animal model, we investigated serum S100b as an acute biomarker of cerebral hypoperfusion and cerebral cell dysfunction during hypotension, hypocapnia, or combined hypotension/hypocapnia during GA. METHODS: Fifty-seven sevoflurane-midazolam anesthetized piglets aged 4 to 6 weeks were randomly allocated to control (n=9), hypotension (n=18), hypocapnia (n=20), or combined hypotension and hypocapnia (n=10). Hypotension (target mean arterial blood pressure: 35 to 38 or 27 to 30 mm Hg) was induced by blood withdrawal and nitroprusside infusion, and hypocapnia by hyperventilation (target PaCO2: 28 to 30 and 23 to 25 mm Hg). Serum S100b and albumin were measured at baseline, before and 60 minutes after the interventions, and following 60-minute recovery. RESULTS: Serum S100b concentrations decreased over time (P=0.001), but there was no difference in S100b between control piglets and those exposed to hypotension, hypocapnea, or a combination of the both (P=0.105). Albumin decreased in all 4 groups (P=0.001). CONCLUSION: S100b did not increase following 60 minutes of systemic hypotension and/or hypocapnia during GA in piglets. In this setting, the use of S100b as a biomarker of cerebral cell tissue dysfunction cannot be supported.

Effects of moderate and severe hypocapnia on intracerebral perfusion and brain tissue oxygenation in piglets.

BACKGROUND: Hypocapnia is a common alteration during anesthesia in neonates. AIM: To investigate the effects of hypocapnia and hypocapnia combined with hypotension (HCT) on cerebral perfusion and tissue oxygenation in anesthetized piglets. METHOD: Thirty anesthetized piglets were randomly allocated to groups: moderate hypocapnia (mHC), severe hypocapnia (sHC), and HCT. Cerebral monitoring comprised a tissue oxygen partial pressure and a laser Doppler probe inserted into the brain tissue as well as a near-infrared spectroscopy (NIRS) sensor placed on the skin, measuring regional oxygen saturation. Hypocapnia was induced by hyperventilation (target PaCO2 mHC: 3.7-4; sHC: 3.1-3.3 kPa) and hypotension by blood withdrawal and nitroprusside infusion (mean blood pressure: 35-38 mm Hg). Data were analyzed at baseline, during (Tr20, Tr40, Tr60) and after (Post20, Post40, Post60) treatment. RESULTS: Compared to baseline, tissue oxygen partial pressure decreased significantly and equally during all treatments (mean [SD] at baseline: mHC 35.7 [32.45]; sHC: 28.1 [20.24]; HCT 25.4 [10.3] and at Tr60: mHC: 29.9 [27.36]; sHC: 22.2 [18.37]; HCT: 18.4 [9.5] mm Hg). Decreased laser Doppler flow was detected with all treatments at Tr20 (mHC: 0.9 [0.18]; sHC: 0.88 [0.15]; HCT: 0.97 [0.13] proportion from baseline). Independently of group, regional oxygen saturation varied only after reverting and not during treatment. Blood lactate, pH, HCO3- , and PaO2 increased during treatment with no differences between groups. CONCLUSION: This animal model revealed reduced cerebral blood flow and brain tissue oxygenation during hypocapnia without detectable changes in regional oxygen saturation as measured by NIRS. Changes occurred as early as during moderate hypocapnia.

Conventional and functional magnetic resonance imaging features of late subacute cortical laminar necrosis in a dog.

Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1-weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3-year-old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three-Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2-weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W-hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion-weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia-related brain hypoxia. Three-Tesla MRI enabled identification of the laminar pattern of the cortical lesions.

Cardiovascular effects of two adenosine constant rate infusions in anaesthetized dogs.

OBJECTIVE: Adenosine induces vasodilatation. The aim of this study was to investigate cardiovascular effects of two adenosine constant rate infusion (CRI) doses in dogs. STUDY DESIGN: Experimental, longitudinal repeated measure design. ANIMALS: Ten healthy purpose-bred Beagle dogs. METHODS: Each dog was sedated with butorphanol. Anaesthesia was induced with propofol intravenously and maintained with sevoflurane (inspired oxygen fraction = 47-55%). Controlled mechanical ventilation was used to maintain normocapnia. Two doses of adenosine were administered as CRIs to each dog: 140 µg kg-1 minute-1 (A140) followed by 280 µg kg-1 minute-1 (A280). Pulse rate, invasive arterial pressure and stroke volume (by magnetic resonance phase contrast angiography) were measured at baseline, 3 minutes after starting adenosine and 3 and 10 minutes after discontinuing adenosine. Cardiac output, cardiac index and approximated systemic vascular resistances (approximate SVR) were calculated. Additionally, arterial blood gases, co-oximetry, electrolytes, glucose and lactate were measured and oxygen content and delivery calculated. One-way repeated measures analysis of variance (p < 0.05) was used for data analysis. RESULTS: A140 and A280 resulted in a significant decrease in arterial blood pressure [systolic (p = 0.008), mean (p = 0.003), and diastolic arterial pressure (p = 0.004)] and approximate SVR (p = 0.008) compared with baseline. No significant changes were detected for the other variables. All values returned to baseline within 3 minutes after adenosine discontinuation. CONCLUSIONS AND CLINICAL RELEVANCE: Adenosine CRI decreases arterial pressure by vasodilatation in healthy dogs. No additional effects were observed with the higher dose. The effects in compromised dogs remain to be investigated.

Comparison of three continuous positive airway pressure (CPAP) interfaces in healthy Beagle dogs during medetomidine-propofol constant rate infusions.

OBJECTIVE: To compare the efficacy of three continuous positive airway pressure (CPAP) interfaces in dogs on gas exchange, lung volumes, amount of leak during CPAP and rebreathing in case of equipment failure or disconnection. STUDY DESIGN: Randomized, prospective, crossover, experimental trial. ANIMALS: Ten purpose-bred Beagle dogs. METHODS: Dogs were in dorsal recumbency during medetomidine-propofol constant rate infusions, breathing room air. Three interfaces were tested in each dog in a consecutive random order: custom-made mask (M), conical face mask (FM) and helmet (H). End-expiratory lung impedance (EELI) measured by electrical impedance tomography was assessed with no interface (baseline), with the interface only (No-CPAP for 3 minutes) and at 15 minutes of 7 cmH2O CPAP (CPAP-delivery). PaO2 was assessed at No-CPAP and CPAP-delivery, partial pressure of inspired carbon dioxide (PICO2; rebreathing assessment) at No-CPAP and the interface leak (ΔPleak) at CPAP-delivery. Mixed-effects linear regression models were used for statistical analysis (p<0.05). RESULTS: During CPAP-delivery, all interfaces increased EELI by 7% (p<0.001). Higher ΔPleak was observed with M and H (9 cmH2O) in comparison with FM (1 cmH2O) (p<0.001). At No-CPAP, less rebreathing occurred with M (0.5 kPa, 4 mmHg) than with FM (1.8 kPa, 14 mmHg) and with H (1.4 kPa, 11 mmHg), but also lower PaO2 was measured with M (9.3 kPa, 70 mmHg) than with H (11.9 kPa, 90 mmHg) and FM (10.8 kPa, 81 mmHg). CONCLUSIONS AND CLINICAL RELEVANCE: All three interfaces can be used to provide adequate CPAP in dogs. The leak during CPAP-delivery and the risk of rebreathing and hypoxaemia, when CPAP is not maintained, can be significant. Therefore, animals should always be supervised during administration of CPAP with any of the three interfaces. The performance of the custom-made M was not superior to the other interfaces.

Clinical comparison of dexmedetomidine and medetomidine for isoflurane balanced anaesthesia in horses.

OBJECTIVE: To compare the effects of two balanced anaesthetic protocols (isoflurane-dexmedetomidine versus medetomidine) on sedation, cardiopulmonary function and recovery in horses. STUDY DESIGN: Prospective, blinded, randomized clinical study. ANIMALS: Sixty healthy adult warm blood horses undergoing elective surgery. METHODS: Thirty horses each were sedated with dexmedetomidine 3.5 µg kg-1 (group DEX) or medetomidine 7 µg kg-1 (group MED) intravenously. After assessing and supplementing sedation if necessary, anaesthesia was induced with ketamine/diazepam and maintained with isoflurane in oxygen/air and dexmedetomidine 1.75 µg kg-1 hour-1 or medetomidine 3.5 µg kg-1 hour-1. Ringer's lactate (7-10 mL kg-1 hour-1) and dobutamine were administered to maintain normotension. Controlled mechanical ventilation maintained end-tidal expired carbon dioxide pressures at 40-50 mmHg (5.3-6.7 kPa). Heart rate, invasive arterial blood pressure, inspired and expired gas composition and arterial blood gases were measured. Dexmedetomidine 1 µg kg-1 or medetomidine 2 µg kg-1 was administered for timed and scored recovery phase. Data were analysed using two-way repeated-measures analysis of variance and chi-square test. Significance was considered when p≤0.05. RESULTS: In group DEX, significantly more horses (n=18) did not fulfil the sedation criteria prior to induction and received one or more supplemental doses, whereas in group MED only two horses needed one additional bolus. Median (range) total sedation doses were dexmedetomidine 4 (4-9) µg kg-1 or medetomidine 7 (7-9) µg kg-1. During general anaesthesia, cardiopulmonary parameters did not differ significantly between groups. Recovery scores in group DEX were significantly better than in group MED. CONCLUSIONS AND CLINICAL RELEVANCE: Horses administered dexmedetomidine required more than 50% of the medetomidine dose to reach equivalent sedation. During isoflurane anaesthesia, cardiopulmonary function was comparable between the two groups. Recovery scores following dexmedetomidine were better compared to medetomidine.

Assessment of method reliability and determination of reference intervals for rotational thromboelastometry in horses.

OBJECTIVES: To assess the measurement reliability of rotational thromboelastometry (ROTEM) measurements in horses, establish reference intervals for healthy horses, and evaluate the relationship between ROTEM variables, hematologic variables, and standard coagulation tests. DESIGN: Prospective observational study. SETTING: University teaching hospital. ANIMALS: Fifty healthy and 10 diseased adult horses. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Blood was sampled from 10 healthy and 10 diseased horses and samples were repeatedly analyzed to evaluate measurement reliability of various ROTEM variables. Four different ROTEM assays (ie, EXTEM, INTEM, FIBTEM, and APTEM) were run simultaneously under standardized conditions. The device-related, operator-related, and day-to-day variability for the majority of ROTEM variables was very low to low, as indicated by a coefficient of variation (CV) of < 15%. Most of test-retest variability of ROTEM variables appeared to be device-related. Blood samples from 50 clinically healthy horses were used to establish reference intervals for ROTEM variables. Multiple stepwise regression analyses identified associations of different ROTEM variables with hematocrit, total protein concentration, fibrinogen concentration, platelet count, prothrombin time, activated partial thromboplastin time, and thrombin time. CONCLUSIONS: ROTEM is a feasible method to evaluate coagulation in horses. Its measurement reliability is acceptable, but device-related measurement variability has to be considered. Reference intervals are presented, but the influence of hematocrit, platelet count, and fibrinogen concentration may need to be taken into account when interpreting individual test results.

Effects of hypotension and/or hypocapnia during sevoflurane anesthesia on perfusion and metabolites in the developing brain of piglets-a blinded randomized study.

BACKGROUND: Hypotension (HT) and/or hypocapnia (HC) are frequent complications occurring during pediatric anesthesia and may cause cerebral injury in the developing brain. AIM: The aim of this study is to investigate the effects of HT and/or HC on perfusion and metabolism in the developing brain. METHODS: Twenty-eight piglets were randomly allocated to four groups: control (C), HT, HC, and hypotension and hyocapnia (HTC). Anesthesia was induced and maintained using sevoflurane. Fentanyl was added for instrumentation. Piglets were fully monitored and their lungs were artificially ventilated. Before treatment, conventional magnetic resonance imaging (MRI), dynamic susceptibility-contrast-enhanced T2*-weighted MRI (DSC-MRI), and single voxel proton MR spectroscopy ((1) H MRS) were performed. Hypotension (mean arterial blood pressure: 30 ± 3 mmHg) was induced by blood withdrawal and nitroprusside infusion, and hyperventilation was used to induce HC (PaCO2 : 2.7-3.3 kPa). (1) H MRS and DSC-MRI were repeated immediately once treatment goals were achieved and 120 min later. Radiologists were blinded to the groups. DSCI-MRI and (1) H MRS analyses were performed in the thalamus, occipital and parietal lobe, hippocampus, and watershed areas. RESULTS: In comparison to C, mean time to peak (TTP) increased with HTC in all brain areas as assessed with DSC-MRI (n = 26). Using (1) H MRS, a significant decrease in N-acetyl aspartate, choline, and myoinositol, as well as an increase in glutamine-glutamate complex (Glx) were detected independent of group. Compared to C, changes were more pronounced for Glx (due to an increase in glutamate) and myoinositol with HTC, for N-acetyl aspartate with HT, and for Glx with HC. No lactate signal was present. CONCLUSIONS: The combination of HT and HC during sevoflurane anesthesia resulted in alteration of cerebral perfusion with signs of neuronal dysfunction and early neuronal ischemia. HT and HC alone also resulted in signs of metabolic disturbances despite the absence of detectable cerebral perfusion alterations.

Cardiopulmonary effects and anaesthesia recovery quality in horses anaesthetized with isoflurane and low-dose S-ketamine or medetomidine infusions.

OBJECTIVES: To evaluate cardiopulmonary effects and anaesthesia recovery quality in horses anaesthetized with isoflurane receiving medetomidine or S-ketamine infusions. STUDY DESIGN: Randomized, blinded, prospective clinical trial. ANIMALS: Fifty horses undergoing elective surgery. METHODS: After acepromazine and flunixin meglumine premedication, horses received medetomidine (7 µg kg-1 ) intravenously (IV). Anaesthesia was induced with midazolam and racemic ketamine (Med treatment group; 2.2 mg kg-1 ; n = 25) or S-ketamine (S-ket treatment group; 1.1 mg kg-1 ; n = 25) IV and maintained with isoflurane in oxygen/air and medetomidine (Med; 3.5 µg kg-1 hour-1 ) or S-ketamine (S-ket; 0.5 mg kg-1 hour-1 ). All horses were mechanically ventilated. Cardiopulmonary variables were evaluated. Isoflurane end-tidal concentrations (Fe'Iso), dobutamine requirements and thiopental boli were recorded. Plasma samples were collected in six horses to evaluate S-ketamine and S-norketamine concentrations. After surgery, medetomidine 2 µg kg-1 was administered IV. Four independent observers scored recovery using a visual analogue scale and a numerical rating scale. RESULTS: Both groups required similar mean Fe'Iso (1%). However, S-ket horses needed more thiopental boli. Median intraoperative cardiac index values were higher with S-ket (4.5 L minute-1  m-2 ) than Med (3.9 L minute-1  m-2 ). Overall, there were no differences in heart rate, blood pressure or dobutamine requirements; however, horses in S-ket showed higher heart rate values at 30 minutes after anaesthesia induction. Compared with Med horses, S-ket horses showed decreased PaO2 and increased pulmonary venous admixture values estimated with the Fshunt calculation. Recoveries were shorter and of poorer quality with S-ket. During infusion, S-ketamine and S-norketamine plasma concentrations lay in the ranges of 0.209-0.917 µg mL-1 and 0.250-0.723 µg mL-1 , respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Despite the higher intraoperative cardiac index with S-ket, both protocols were considered to provide acceptable cardiovascular function. However, recovery quality was significantly better in the Med group.

Evaluation of the non-calibrated pulse contour cardiac output monitor FloTrac/Vigileo against thermodilution in standing horses.

OBJECTIVE: To evaluate the non-calibrated, minimally invasive cardiac output (CO) monitor FloTrac/Vigileo (FloTrac) against thermodilution (TD) CO in standing horses. STUDY DESIGN: Prospective, experimental trial. ANIMALS: Nine adult horses weighing a median (range) of 535 (470-602) kg. METHODS: Catheters were placed in the right atrium, pulmonary artery and carotid artery under local anaesthesia. CO was measured 147 times by TD and FloTrac and indexed to body weight. Changes in CO were achieved with romifidine or xylazine and dobutamine constant rate infusions. Bland-Altman analysis, concordance and polar plot analysis were used to assess agreement and ability to track changes in CO. RESULTS: Mean ± standard deviation COTD of 48 ± 16 mL kg(-1) minute(-1) (range: 19-93 mL kg(-1) minute(-1) ) and mean COF loTrac of 9 ± 3 mL kg(-1) minute(-1) (range: 5-21 mL kg(-1) minute(-1) ) were measured. Low agreement with a large mean bias of 39 mL kg(-1) minute(-1) and wide limits of agreement of 8-70 mL kg(-1) minute(-1) were found. The percentage error of 108% and precision of TD of ± 18% resulted in an estimated precision of FloTrac of ± 106%. Comparison of changes in COF loTrac with changes in COTD gave a concordance rate of 52% in the four-quadrant plot, and a mean polar angle of -11° with radial limits of agreement of ± 61 ° in the polar plot. Mean arterial pressure (MAP) and COF loTrac were positively correlated (r = 0.5, p < 0.0001). No correlation of MAP with COTD was observed. CONCLUSIONS AND CLINICAL RELEVANCE: The FloTrac system, originally designed for use in humans, neither measured absolute CO in standing horses accurately nor tracked relative changes in CO measured by TD correctly. The false dependence of COF loTrac on arterial blood pressure further discourages the use of this technique in horses.

Evaluation of a romifidine constant rate infusion protocol with or without butorphanol for dentistry and ophthalmologic procedures in standing horses.

OBJECTIVE: To compare the clinical usefulness of constant rate infusion (CRI) protocols of romifidine with or without butorphanol for sedation of horses. STUDY DESIGN: Prospective 'blinded' controlled trial using block randomization. ANIMALS: Forty healthy Freiberger stallions. METHODS: The horses received either intravenous (IV) romifidine (loading dose: 80 µg kg(-1) ; infusion: 30 µg kg(-1)  hour(-1) ) (treatment R, n = 20) or romifidine combined with butorphanol (romifidine loading: 80 µg kg(-1) ; infusion: 29 µg kg(-1)  hour(-1) , and butorphanol loading: 18 µg kg(-1) ; infusion: 25 µg kg(-1)  hour(-1) ) (treatment RB, n = 20). Twenty-one horses underwent dentistry and ophthalmic procedures, while 19 horses underwent only ophthalmologic procedure and buccal examination. During the procedure, physiologic parameters and occurrence of head/muzzle shaking or twitching and forward movement were recorded. Whenever sedation was insufficient, additional romifidine (20 µg kg(-1) ) was administered IV. Recovery time was evaluated by assessing head height above ground. At the end of the procedure, overall quality of sedation for the procedure was scored by the dentist and anaesthetist using a visual analogue scale. Statistical analyses used two-way anova or linear mixed models as relevant. RESULTS: Sedation quality scores as assessed by the anaesthetist were R: median 7.55, range: 4.9-9.0 cm, RB: 8.8, 4.7-10.0 cm, and by the dentist R: 6.6, 3.0-8.2 cm, RB: 7.9, 6.6-8.8 cm. Horses receiving RB showed clinically more effective sedation as demonstrated by fewer poor scores and a tendency to reduced additional drug requirements. More horses showed forward movement and head shaking in treatment RB than treatment R. Three horses (two RB, one R) had symptoms of colic following sedation. CONCLUSIONS AND CLINICAL RELEVANCE: The described protocols provide effective sedation under clinical conditions but for dentistry procedures, the addition of butorphanol is advantageous.

Intravenous versus intramuscular epinephrine administration during cardiopulmonary resuscitation - a pilot study in piglets.

BACKGROUND: Early epinephrine administration in cardiac arrest seems to be advantageous to achieve return of spontaneous circulation (ROSC). Because intravenous (i.v.) or intraosseous access is not always immediately available, this study compares efficacy of early intramuscular (i.m.) epinephrine administration with early and delayed i.v. epinephrine injection in an animal cardiac arrest model. METHODS: Piglets anesthetized with sevoflurane were intoxicated by an i.v. ropivacaine infusion until circulatory arrest. After 1 min basic life support (chest compression and ventilation), epinephrine i.v. (10 µg·kg(-1), group IV) or epinephrine i.m. (100 µg·kg(-1), group IM) or normal saline (group NS) was applied. Further doses of epinephrine were given in group IV every 4 min and in group IM after 10 min if required. Twenty-one minutes after circulatory arrest, i.v. epinephrine - as necessary - was given to all animals. Thus, group NS represents late epinephrine administration. Outcomes were survival and time to ROSC. RESULTS: Twenty-four pigs aged 19.5 (median, interquartile range 16-22) days, weighing 5.4 (5.0-5.7) kg were investigated. Total amount of ropivacaine administered was 8.9 (8.1-10.1) mg·kg(-1). Cardiac rhythm before starting CPR was pulseless electric activity and asystole in 15 and 9 pigs, respectively. Eight, seven, and four pigs survived in group IV, IM, and NS. Focusing on surviving animals, time to ROSC was 2, 4 and 19.5 min in group IV, IM, and NS. CONCLUSIONS: Early i.m. epinephrine provided similar survival compared with early i.v. epinephrine and was superior to delayed epinephrine administration in resuscitation of ropivacaine-induced cardiac arrest in piglets.

Electrocardiographic and blood pressure alterations caused by intravenous injection of ropivacaine - a study in piglets.

OBJECTIVES: Objective signs to detect inadvertent intravascular injection of local anesthetics are essential in the anesthetized pediatric patient. For early detection of intravenous bupivacaine administration, it was shown that an epinephrine containing test dose reliably provoked T-wave alterations, changes in heart rate (HR) and blood pressure, whereas intravenous injection of plain bupivacaine could not be detected until high doses were applied. This study investigates electrocardiographic and hemodynamic alterations caused by intravenous ropivacaine. METHODS: Twenty-four piglets, anesthetized with sevoflurane, were randomized into two groups: Group R received as test dose plain ropivacaine 0.2% and group RE, ropivacaine 0.2% + epinephrine 5 µg·ml(-1) . Under stable conditions, 0.2 ml kg(-1) of the test solution was intravenously injected. Twenty minutes later, 0.4 ml kg(-1) was applied. A positive effect was defined as HR increase ≥ 10 bpm, increase in mean arterial pressure (MAP) ≥ 15 mmHg, T-wave increase ≥ 25% baseline. In another setting ropivacaine was intravenously infused until cardiac arrest. RESULTS: After injection of 0.2 or 0.4 ml kg(-1) test solution, a positive increase in HR and MAP was found in 0% of group R and in 100% of group RE. An increase in T-wave ≥ 25% was found in 42% of group R and in 100% of group RE. During intoxication, T-elevation was seen in 83%. CONCLUSIONS: An epinephrine containing test dose ropivacaine reliably provoked T-wave elevations and increases in HR and MAP. A small dose plain ropivacaine caused T-elevations in a remarkable percentage, whereas higher, quite toxic doses provoked T-elevations in most of the pigs.