Arterial blood gas tensions during recovery in horses anesthetized with apneustic anesthesia ventilation compared with conventional mechanical ventilation

ObjectiveTo compare PaO₂ and PaCO₂ in horses recovering from general anesthesia maintained with either apneustic anesthesia ventilation (AAV) or conventional mechanical ventilation (CMV).Study designRandomized, crossover design.AnimalsA total of 10 healthy adult horses from a university-owned herd.MethodsDorsally recumbent horses were anesthetized with isoflurane in oxygen [inspired oxygen fraction = 0.3 initially, with subsequent titration to maintain PaO₂ ≥ 85 mmHg (11.3 kPa)] and ventilated with AAV or CMV according to predefined criteria [10 mL kg^–1 tidal volume, PaCO₂ 40–45 mmHg (5.3–6.0 kPa) during CMV and < 60 mmHg (8.0 kPa) during AAV]. Horses were weaned from ventilation using a predefined protocol and transferred to a stall for unassisted recovery. Arterial blood samples were collected and analyzed at predefined time points. Tracheal oxygen insufflation at 15 L minute^–1 was provided if PaO₂ < 60 mmHg (8.0 kPa) on any analysis. Time to oxygen insufflation, first movement, sternal recumbency and standing were recorded. Data were analyzed using repeated measures anova, paired t tests and Fisher’s exact test with significance defined as p < 0.05.ResultsData from 10 horses were analyzed. Between modes, PaO₂ was significantly higher immediately after weaning from ventilation and lower at sternal recumbency for AAV than for CMV. No PaCO₂ differences were noted between ventilation modes. All horses ventilated with CMV required supplemental oxygen, whereas three horses ventilated with AAV did not. Time to first movement was shorter with AAV. Time to oxygen insufflation was not different between ventilation modes.ConclusionsAlthough horses ventilated with AAV entered the recovery period with higher PaO₂, this advantage was not sustained during recovery. Whereas fewer horses required supplemental oxygen after AAV, the use of AAV does not preclude the need for routine supplemental oxygen administration in horses recovering from general anesthesia.     

Effect of different inspired fractions of oxygen on F-shunt and arterial partial pressure of oxygen in isoflurane-anaesthetized and mechanically ventilated Shetland ponies

ObjectiveTo determine the effect of fraction of inspired oxygen (FiO₂) on intrapulmonary shunt fraction as measured by F-shunt in ponies during isoflurane anaesthesia.Study designProspective, randomized clinical study.AnimalsA group of 23 adult Shetland ponies undergoing a total of 32 anaesthetic procedures.MethodsPonies were premedicated intravenously (IV) with detomidine (0.01 mg kg^–1) and either morphine (0.1 mg kg^–1) or butorphanol (0.02 mg kg^–1). Anaesthesia was induced with ketamine (2.2 mg kg^–1) and midazolam (0.07 mg kg^–1) administered IV. Ponies were randomly allocated to maintenance of anaesthesia with isoflurane in oxygen (group TH; FiO₂ = 0.95) or a mixture of oxygen and medical air (group TL; FiO₂ = 0.65); all ponies were given a constant rate of infusion of detomidine. Animals were mechanically ventilated to maintain PaCO₂ between 40 and 50 mmHg. Arterial blood gas analysis was performed every 30 minutes. The F-shunt equation was calculated for each time point T0, T30, T60 and T90. Data were analysed using linear mixed model analysis and presented as mean ± standard deviation (p < 0.05).ResultsPaO₂ was greater in group TH than in group TL (TH: 406 ± 90, 438 ± 83, 441 ± 69 and 464 ± 53 mmHg versus TL: 202 ± 90, 186 ± 84, 172 ± 85 and 191 ± 98 mmHg at T0, T30, T60 and T90, respectively; p < 0.0001). In TH, F-shunt was < TL. Significant differences were found at T60 (TH: 13.2% ± 4.3 versus TL: 19.4% ± 8.3; p = 0.016) and T90 (TH: 11.7% ± 3.5 versus TL: 18.6% ± 9.5; p = 0.036).Conclusions and clinical relevanceOur findings do not support a beneficial effect of using a reduced FiO₂ to improve oxygenation in anaesthetized and mechanically ventilated Shetland ponies.     

Aerosolized salbutamol (albuterol) improves PaO2 in hypoxaemic anaesthetized horses – a prospective clinical trial in 81 horses

Objective To compare the arterial pH and blood gas values, heart rate and mean arterial blood pressure, in hypoxaemic anaesthetized horses, before and after treatment, with a salbutamol (albuterol) aerosol. Animal population Eighty‐one client‐owned horses weighing between 114 and 925 kg. Fifty‐seven underwent emergency abdominal surgery and 24 were anaesthetized for elective procedures. Materials and methods Pre‐anaesthetic medication included xylazine, detomidine, butorphanol and morphine, alone or in various combinations. Induction of anaesthesia was achieved with guaifenesin and ketamine, diazepam and ketamine, or guaifenesin and thiopental. The trachea of all animals was intubated and anaesthesia maintained with either halothane (33 horses) or isoflurane (48 horses) in oxygen. Heart rate and rhythm were monitored continuously. Arterial blood pressure was monitored directly, and arterial blood collected for pH and blood gas analyses. When arterial PaO₂ fell below 9.3 kPa (70 mm Hg) and failed to respond to corrective measures including positive pressure ventilation and treatment of hypotension (mean arterial blood pressures <70 mm Hg), a salbutamol aerosol (2 µg kg^?1) was delivered via the endotracheal tube. Twenty minutes later, a second arterial blood sample was analysed. Results There were no significant differences in mean arterial blood pressure, heart rate, arterial pH, base excess and bicarbonate before and after treatment. Arterial O₂ tension increased significantly from a mean ± SD of 8.3 ± 1.7 kPa (62.4 ± 13.1 mm Hg) before administration to 15.9 ± 9.8 kPa (119.4 ± 57.7 mm Hg) after treatment. There was a small but significant decrease in PaCO₂ from 7.4 ± 1.5 kPa (55.2 ± 11.2 mm Hg) to 7.0 ± 1.3 kPa (52.9 ± 9.8 mm Hg) between sample times. No changes in heart rhythm were observed. A high percentage (approximately 70%) of animals sweated following treatment. Conclusions Salbutamol administered at a dose of 2 µg kg^?1 via the endotracheal tube of anaesthetized horses with PaO₂ values less than 9.3 kPa (70 mm Hg) resulted in an almost two‐fold increase in PaO₂ values within 20 minutes of treatment. No changes in heart rate or mean arterial blood pressure were associated with the use of salbutamol in this study. The improvement in PaO₂ may be a result of bronchodilatation and improved ventilation, increased perfusion secondary to an increase in cardiac output, or a combination of these two factors. Cardiac output and ventilation–perfusion distribution were not measured in this study; therefore, the reason for the increase in PaO₂ values cannot be conclusively determined. Clinical relevance Administration of a salbutamol aerosol is a simple but effective technique that can be used to improve PaO₂ values in hypoxaemic horses during inhalant anaesthesia with no apparent detrimental side effects.     

Oxygen reserve index as a noninvasive indicator of arterial partial pressure of oxygen in anaesthetized donkeys: a preliminary study

ObjectiveTo evaluate the oxygen reserve index (ORI) as a noninvasive estimate of the PaO₂ during moderate hyperoxaemia [100–200 mmHg (13.3–26.6 kPa)], and to determine ORI values identifying PaO₂ > 100, > 150 (20.0 kPa) and > 200 mmHg in anaesthetized donkeys with an inspired fraction of oxygen (FiO₂) > 0.95.Study designProspective observational study.AnimalsA group of 28 adult standard donkeys aged (mean ± standard deviation) 4 ± 2 years and weighing 135 ± 15 kg.MethodsDonkeys were sedated intramuscularly with xylazine and butorphanol; anaesthesia was induced with ketamine and diazepam and maintained with isoflurane in oxygen. An adhesive sensor probe was applied to the donkey’s tongue and connected to a Masimo pulse co-oximeter to determine ORI values. An arterial catheter was inserted into an auricular artery. After ORI signal stabilization, the value was noted and PaO₂ determined by blood gas analysis. The Pearson correlation coefficient was used to assess the relationship between ORI and PaO₂ for oxygen tension < 200 mmHg (< 26.6 kPa). The Youden index was used to identify the value of ORI that detected PaO₂ > 150 and 200 mmHg (20.0 and 26.6 kPa) with the highest sensitivity and specificity.ResultsA total of 106 paired measurements were collected. A mild positive correlation was observed between ORI and PaO₂ for values < 200 mmHg (26.6 kPa; r = 0.52). An ORI > 0.0, > 0.1 and > 0.3 indicated a PaO₂ > 100, > 150 and > 200 mmHg (13.3, 20.0 and 26.6 kPa) with negative predictive values > 94%.Conclusions and clinical relevanceORI may provide a noninvasive indication of PaO₂ > 100, > 150 and > 200 mmHg (13.3, 20.0 and 26.6 kPa) in anaesthetized donkeys with an FiO₂ > 0.95, although it does not replace blood gas analysis for assessment of oxygenation.     

Physiologic and blood gas effects of xylazine–ketamine versus xylazine–tiletamine–zolazepam immobilization of white-tailed deer before and after oxygen supplementation: a preliminary study

ObjectiveTo compare oxygenation and ventilation in white-tailed deer (Odocoileus virginianus) anesthetized with two treatments with and without oxygen supplementation.Study designRandomized, blinded, crossover study.AnimalsA total of eight healthy adult white-tailed deer weighing 49–62 kg.MethodsEach deer was anesthetized twice intramuscularly: 1) treatment XK, xylazine (2 mg kg^–1) and ketamine (6 mg kg^–1) and 2) treatment XTZ, xylazine (2 mg kg^–1) and tiletamine–zolazepam (4 mg kg^–1). With the deer in sternal position, arterial and venous blood was collected before and at 30 minutes during administration of oxygen at 1 L minute^–1 through a face mask. PaO₂ and heart rate (HR) were compared using two-way repeated measures anova. pH, PaCO₂ and lactate concentration were analyzed using mixed-effects linear models, p < 0.05.ResultsWhen breathing air, PaO₂ was < 80 mmHg (10.7 kPa) in six and seven deer with XK and XTZ, respectively, and of these, PaO₂ was < 60 mmHg (8.0 kPa) in three and five deer, respectively. With oxygen supplementation, PaO₂ increased to 128 ± 4 and 140 ± 5 mmHg (17.1 ± 0.5 and 18.7 ± 0.7 kPa), mean ± standard error, with XK and XTZ, respectively (p < 0.001). PaO₂ was not significantly different between treatments at either time point. HR decreased during oxygen supplementation in both treatments (p < 0.001). Lactate was significantly lower (p = 0.047) with XTZ than with XK (2.2 ± 0.6 versus 3.5 ± 0.6 mmol L^–1) and decreased (p < 0.001) with oxygen supplementation (4.1 ± 0.6 versus 1.6 ± 0.6 mmol L^–1). PaCO₂ increased in XTZ during oxygen breathing.Conclusions and clinical relevanceTreatments XK and XTZ resulted in hypoxemia, which responded to oxygen supplementation. Both treatments are suitable for immobilization of white-tailed deer under the study circumstances.     

Effects of intravenous terbutaline on heart rate,arterial pressure and blood gases in anesthetized horses breathing air

Objective

To investigate the effects of intravenous (IV) administration of terbutaline on PaO₂, PaCO₂, pH, heart rate (HR) and arterial pressures in healthy, laterally recumbent horses breathing ambient air under total intravenous anesthesia (TIVA).

Effect of end-inspiratory pause on airway and physiological dead space in anesthetized horses

ObjectiveTo evaluate the impact of a 30% end-inspiratory pause (EIP) on alveolar tidal volume (V_Talv), airway (V_Daw) and physiological (V_Dphys) dead spaces in mechanically ventilated horses using volumetric capnography, and to evaluate the effect of EIP on carbon dioxide (CO₂) elimination per breath (Vco₂br^–1), PaCO_2, and the ratio of PaO₂-to-fractional inspired oxygen (PaO₂:FiO₂).Study designProspective research study.AnimalsA group of eight healthy research horses undergoing laparotomy.MethodsAnesthetized horses were mechanically ventilated as follows: 6 breaths minute^–1, tidal volume (V_T) 13 mL kg^–1, inspiratory-to-expiratory time ratio 1:2, positive end-expiratory pressure 5 cmH₂O and EIP 0%. Vco₂br^–1 and expired tidal volume (V_TE) of 10 consecutive breaths were recorded 30 minutes after induction, after adding 30% EIP and upon EIP removal to construct volumetric capnograms. A stabilization period of 15 minutes was allowed between phases. Data were analyzed using a mixed-effect linear model. Significance was set at p < 0.05.ResultsThe EIP decreased V_Daw from 6.6 (6.1–6.7) to 5.5 (5.3–6.1) mL kg^–1 (p < 0.001) and increased V_Talv from 7.7 ± 0.7 to 8.6 ± 0.6 mL kg^–1 (p = 0.002) without changing the V_TE. The V_Dphys to V_TE ratio decreased from 51.0% to 45.5% (p < 0.001) with EIP. The EIP also increased PaO₂:FiO₂ from 393.3 ± 160.7 to 450.5 ± 182.5 mmHg (52.5 ± 21.4 to 60.0 ± 24.3 kPa; p < 0.001) and Vco₂br^–1 from 0.49 (0.45–0.50) to 0.59 (0.45–0.61) mL kg^–1 (p = 0.008) without reducing PaCO₂.Conclusions and clinical relevanceThe EIP improved oxygenation and reduced V_Daw and V_Dphys, without reductions in PaCO₂. Future studies should evaluate the impact of different EIP in healthy and pathological equine populations under anesthesia.     

Hypoventilation following oxygen administration associated with alfaxalone–dexmedetomidine–midazolam anesthesia in New Zealand White rabbits

ObjectiveTo investigate the relationship between oxygen administration and ventilation in rabbits administered intramuscular alfaxalone–dexmedetomidine–midazolam.Study designProspective, randomized, blinded study.AnimalsA total of 25 New Zealand White rabbits, weighing 3.1–5.9 kg and aged 1 year.MethodsRabbits were anesthetized with intramuscular alfaxalone (4 mg kg^–1), dexmedetomidine (0.1 mg kg^–1) and midazolam (0.2 mg kg^–1) and randomized to wait 5 (n = 8) or 10 (n = 8) minutes between drug injection and oxygen (100%) administration (facemask, 1 L minute^–1). A control group (n = 9) was administered medical air 10 minutes after drug injection. Immediately before (PRE_oxy/air5/10) and 2 minutes after oxygen or medical air (POST_oxy/air5/10), respiratory rate (f_R), pH, PaCO₂, PaO₂, bicarbonate and base excess were recorded by an investigator blinded to treatment allocation. Data [median (range)] were analyzed with Wilcoxon, Mann–Whitney U and Kruskal–Wallis tests and p < 0.05 considered significant.ResultsHypoxemia (PaO₂ < 88 mmHg, 11.7 kPa) was observed at all PRE times: PRE_oxy5 [71 (61–81) mmHg, 9.5 (8.1–10.8) kPa], PRE_oxy10 [58 (36–80) mmHg, 7.7 (4.8–10.7) kPa] and PRE_air10 [48 (32–64) mmHg, 6.4 (4.3–8.5) kPa]. Hypoxemia persisted when breathing air: POST_air10 [49 (33–66) mmHg, 6.5 (4.4–8.8) kPa]. Oxygen administration corrected hypoxemia but was associated with decreased f_R (>70%; p = 0.016, both groups) and hypercapnia (p = 0.016, both groups). Two rabbits (one per oxygen treatment group) were apneic (no thoracic movements for 2.0–2.5 minutes) following oxygen administration. f_R was unchanged when breathing air (p = 0.5). PaCO₂ was higher when breathing oxygen than air (p < 0.001).Conclusions and clinical relevanceEarly oxygen administration resolved anesthesia-induced hypoxemia; however, f_R decreased and PaCO₂ increased indicating that hypoxemic respiratory drive is an important contributor to ventilation using the studied drug combination.     

Comparison of cardiopulmonary effects of etorphine and thiafentanil administered as sole agents for immobilization of impala (Aepyceros melampus)

ObjectiveTo compare the cardiopulmonary effects of the opioids etorphine and thiafentanil for immobilization of impala.Study designTwo-way crossover, randomized study.AnimalsA group of eight adult female impala.MethodsImpala were given two treatments: 0.09 mg kg^–1 etorphine or 0.09 mg kg^–1 thiafentanil via remote dart injection. Time to recumbency, quality of immobilization and recovery were assessed. Respiratory rate, heart rate (HR), mean arterial blood pressure (MAP) and arterial blood gases were measured. A linear mixed model was used to analyse the effects of treatments, treatments over time and interactions of treatment and time (p < 0.05).ResultsTime to recumbency was significantly faster with thiafentanil (2.0 ± 0.8 minutes) than with etorphine (3.9 ± 1.6 minutes; p = 0.007). Both treatments produced bradypnoea, which was more severe at 5 minutes with thiafentanil (7 ± 4 breaths minute^–1) than with etorphine (13 ± 12 breaths minute^–1; p = 0.004). HR increased with both treatments but significantly decreased over time when etorphine (132 ± 17 to 82 ± 11 beats minute^–1) was compared with thiafentanil (113 ± 22 to 107 ± 36 beats minute^–1; p < 0.001). Both treatments caused hypertension which was more profound with thiafentanil (mean overall MAP = 140 ± 14 mmHg; p < 0.001). Hypoxaemia occurred with both treatments but was greater with thiafentanil [PaO₂ 37 ± 13 mmHg (4.9 kPa)] than with etorphine [45 ± 16 mmHg (6.0 kPa)] 5 minutes after recumbency (p < 0.001). After 30 minutes, PaO₂ increased to 59 ± 10 mmHg (7.9 kPa) with both treatments (p < 0.001).Conclusions and clinical relevanceThe shorter time to recumbency with thiafentanil may allow easier and faster retrieval in the field. However, thiafentanil caused greater hypertension, and ventilatory effects during the first 10 minutes, after administration.     

Cardiovascular responses to transvenous electrical cardioversion of atrial fibrillation in anaesthetized horses

ObjectiveTo examine the influence of direct current shock application in anaesthetized horses with atrial fibrillation (AF) and to study the effects of cardioversion to sinus rhythm (SR).Study designProspective clinical study.AnimalsEight horses successfully treated for AF (transvenous electrical cardioversion after amiodarone pre-treatment).MethodsCardioversion catheters and a pacing catheter were placed under sedation [detomidine 10 μg kg^?1 intravenously (IV)]. After additional sedation (5–10 μg kg^?1 detomidine, 0.1 mg kg^?1 methadone IV), anaesthesia was induced with ketamine, 2.2 mg kg^?1 and midazolam, 0.06 mg kg^?1 (IV) in a sling and maintained with isoflurane in oxygen. Flunixin meglumine, 1.1 mg kg^?1, was administered IV. Shocks were delivered as biphasic truncated exponential waves, synchronized with the R-wave of the electrocardiogram. Monitoring included pulse oximetry, electrocardiography, capnography, inhalational anaesthetic agent concentration, arterial blood pressure, LiDCO and PulseCO cardiac index (CI) and arterial blood gases. Values before and after the first unsuccessful shock and before and after cardioversion to SR were compared.ResultsValues before the first shock were comparable to reported values in healthy, isoflurane anaesthetized horses. Reliable CI measurements could not be obtained using the PulseCO technique. Intermittent positive pressure ventilation was required in most horses (bradypnea and/or PaCO₂ >8 kPa, 60 mmHg), while dobutamine was administered in two horses (0.3–0.5 μg kg^?1 minute^?1). After the 1st unsuccessful shock application, systolic arterial pressure (SAP) was decreased (p = 0.025), other recorded values were not influenced (CI measurements not available for this analysis). SR was associated with increases in CI (p = 0.039) and stroke index (p = 0.002) and a decrease in SAP (p = 0.030).Conclusions and clinical relevanceDespite the presence of AF, cardiovascular function was well maintained during anaesthesia and was not affected by shock application. Cardiac index and stroke index increased and SAP decreased after cardioversion.     

Hyoscine‐N‐butylbromide premedication on cardiovascular variables of horses sedated with medetomidine

ObjectiveTo evaluate the effects of intravenous (IV) or intramuscular (IM) hyoscine premedication on physiologic variables following IV administration of medetomidine in horses.Study designRandomized, crossover experimental study.AnimalsEight healthy crossbred horses weighing 330 ± 39 kg and aged 7 ± 4 years.MethodsBaseline measurements of heart rate (HR), cardiac index (CI), respiratory rate, systemic vascular resistance (SVR), percentage of patients with second degree atrioventricular (2^oAV) block, mean arterial pressure (MAP), pH, and arterial partial pressures of carbon dioxide (PaCO₂) and oxygen (PaO₂) were obtained 5 minutes before administration of IV hyoscine (0.14 mg kg^?1; group HIV), IM hyoscine (0.3 mg kg^?1; group HIM), or an equal volume of physiologic saline IV (group C). Five minutes later, medetomidine (7.5 μg kg^?1) was administered IV and measurements were recorded at various time points for 130 minutes.ResultsMedetomidine induced bradycardia, 2^oAV blocks and increased SVR immediately after administration, without significant changes in CI or MAP in C. Hyoscine administration induced tachycardia and hypertension, and decreased the percentage of 2^oAV blocks induced by medetomidine. Peak HR and MAP were higher in HIV than HIM at 88 ± 18 beats minute^?1 and 241 ± 37 mmHg versus 65 ± 16 beats minute^?1 and 192 ± 38 mmHg, respectively. CI was increased significantly in HIV (p ≤ 0.05). Respiratory rate decreased significantly in all groups during the recording period. pH, PaCO₂ and PaO₂ were not significantly changed by administration of medetomidine with or without hyoscine.Conclusion and clinical relevanceHyoscine administered IV or IM before medetomidine in horses resulted in tachycardia and hypertension under the conditions of this study. The significance of these changes, and responses to other dose rates, requires further investigation.     

A clinical study on the effect in horses during medetomidine-isoflurane anaesthesia, of butorphanol constant rate infusion on isoflurane requirements, on cardiopulmonary function and on recovery characteristics

ObjectiveTo test if the addition of butorphanol by constant rate infusion (CRI) to medetomidine–isoflurane anaesthesia reduced isoflurane requirements, and influenced cardiopulmonary function and/or recovery characteristics.Study designProspective blinded randomised clinical trial.Animals61 horses undergoing elective surgery.MethodsHorses were sedated with intravenous (IV) medetomidine (7 μg kg^?1); anaesthesia was induced with IV ketamine (2.2 mg kg^?1) and diazepam (0.02 mg kg^?1) and maintained with isoflurane and a CRI of medetomidine (3.5 μg kg^?1 hour^?1). Group MB (n = 31) received butorphanol CRI (25 μg kg^?1 IV bolus then 25 μg kg^?1 hour^?1); Group M (n = 30) an equal volume of saline. Artificial ventilation maintained end-tidal CO₂ in the normal range. Horses received lactated Ringer’s solution 5 mL kg^?1 hour^?1, dobutamine <1.25 μg kg^?1 minute^?1 and colloids if required. Inspired and exhaled gases, heart rate and mean arterial blood pressure (MAP) were monitored continuously; pH and arterial blood gases were measured every 30 minutes. Recovery was timed and scored. Data were analyzed using two way repeated measures anova, independent t-tests or Mann–Whitney Rank Sum test (p < 0.05).ResultsThere was no difference between groups with respect to anaesthesia duration, end-tidal isoflurane (MB: mean 1.06 ± SD 0.11, M: 1.05 ± 0.1%), MAP (MB: 88 ± 9, M: 87 ± 7 mmHg), heart rate (MB: 33 ± 6, M: 35 ± 8 beats minute^?1), pH, PaO₂ (MB: 19.2 ± 6.6, M: 18.2 ± 6.6 kPa) or PaCO_2. Recovery times and quality did not differ between groups, but the time to extubation was significantly longer in group MB (26.9 ± 10.9 minutes) than in group M (20.4 ± 9.4 minutes).Conclusion and clinical relevanceButorphanol CRI at the dose used does not decrease isoflurane requirements in horses anaesthetised with medetomidine–isoflurane and has no influence on cardiopulmonary function or recovery.     

The influence of body mass and thoracic dimensions on arterial oxygenation in anaesthetized horses and ponies

ObjectiveTo examine the relationship between body mass and thoracic dimensions on arterial oxygen tensions (PaO₂) in anaesthetized horses and ponies positioned in dorsal recumbency.Study designProspective clinical study.AnimalsThirty six client-owned horses and ponies, mean [±SD (range)] age 8.1 ± 4.8 (1.5–20) years and mean body mass 467 ± 115 (203–656) kg.MethodsBefore general anaesthesia, food and water were withheld for 12 and 1 hours respectively. Body mass (kg), height at the withers (H), thoracic circumference (C), thoracic depth (length between dorsal spinous process and sternum; D), thoracic width (between point of shoulders; W), and thoracic diagonal length (point of shoulder to last rib; L) were measured. Pre-anaesthetic medication was with intravenous (IV) romifidine (0.1 mg kg⁻¹). Anaesthesia was induced with an IV ketamine (2.2 mg kg⁻¹) and diazepam (0.05 mg kg⁻¹) combination and maintained with halothane in 1:1 oxygen:nitrous oxide (N₂O) mixture. Animals were positioned in dorsal recumbency and allowed to breathe spontaneously. Nitrous oxide was discontinued after 10 minutes, and arterial blood samples obtained and analysed for gas tensions at 15, 30 and 60 minutes after connection to the anaesthetic breathing circuit. Data were analysed using anova and Pearson's correlation co-efficient.ResultsThe height per unit body mass (H kg⁻¹) and thoracic circumference per unit body mass (C kg⁻¹) correlated strongly (r = 0.85, p < 0.001 and r = 0.82, p < 0.001 respectively) with arterial oxygen tensions (PaO₂) at 15 minutes.ConclusionsThere is a strong positive correlation between H kg⁻¹ and C kg⁻¹ and PaO₂ after 15 minutes of anaesthesia in halothane-anaesthetized horses positioned in dorsal recumbency.Clinical relevanceReadily obtained linear measurements (height and thoracic circumference) and body mass may be used to predict the ability of horses to oxygenate during anaesthesia.     

Comparison of some cardiopulmonary effects of etorphine and thiafentanil during the chemical immobilization of blesbok (Damaliscus pygargus phillipsi)

ObjectiveTo determine the cardiopulmonary effects of etorphine and thiafentanil for immobilization of blesbok.Study designBlinded, randomized, two-way crossover study.AnimalsA group of eight adult female blesbok.MethodsAnimals were immobilized twice, once with etorphine (0.09 mg kg^–1) and once with thiafentanil (0.09 mg kg^–1) administered intramuscularly by dart. Immobilization quality was assessed and analysed by Wilcoxon signed-rank test. Time to final recumbency was compared between treatments by one-way analysis of variance. Cardiopulmonary effects including respiratory rate (?_R), arterial blood pressures and arterial blood gases were measured. A linear mixed model was used to assess the effects of drug treatments over the 40 minute immobilization period. Significant differences between treatments, for treatment over time as well as effect of treatment by time on the variables, were analysed (p < 0.05).ResultsThere was no statistical difference (p = 0.186) between treatments for time to recumbency. The mean ?_R was lower with etorphine (14 breaths minute^–1) than with thiafentanil (19 breaths minute^–1, p = 0.034). The overall mean PaCO₂ was higher with etorphine [45 mmHg (6.0 kPa)] than with thiafentanil [41 mmHg (5.5 kPa), p = 0.025], whereas PaO₂ was lower with etorphine [53 mmHg (7.1 kPa)] than with thiafentanil [64 mmHg (8.5 kPa), p < 0.001]. The systolic arterial pressure measured throughout all time points was higher with thiafentanil than with etorphine (p = 0.04). The difference varied from 30 mmHg at 20 minutes after recumbency to 14 mmHg (standard error difference 2.7 mmHg) at 40 minutes after recumbency. Mean and diastolic arterial pressures were significantly higher with thiafentanil at 20 and 25 minute measurement points only (p < 0.001).ConclusionsBoth drugs caused clinically relevant hypoxaemia; however, it was less severe with thiafentanil. Ventilation was adequate. Hypertension was greater and immobilization scores were lower with thiafentanil.     

Alfaxalone compared with ketamine for induction of anaesthesia in horses following xylazine and guaifenesin

ObjectiveTo compare anaesthesia induced with either alfaxalone or ketamine in horses following premedication with xylazine and guaifenesin.Study designRandomized blinded cross-over experimental study.AnimalsSix adult horses, five Standardbreds and one Thoroughbred; two mares and four geldings.MethodsEach horse received, on separate occasions, induction of anaesthesia with either ketamine 2.2 mg kg^?1 or alfaxalone 1 mg kg^?1. Premedication was with xylazine 0.5 mg kg^?1 and guaifenesin 35 mg kg^?1. Incidence of tremors/shaking after induction, recovery and ataxia on recovery were scored. Time to recovery was recorded. Partial pressure of arterial blood oxygen (PaO₂) and carbon dioxide (PaO₂), arterial blood pressures, heart rate (HR) and respiratory rates were recorded before premedication and at intervals during anaesthesia. Data were analyzed using Wilcoxon matched pairs signed rank test and are expressed as median (range).ResultsThere was no difference in the quality of recovery or in ataxia scores. Horses receiving alfaxalone exhibited a higher incidence of tremors/shaking on induction compared with those receiving ketamine (five and one of six horses respectively). Horses recovered to standing similarly [28 (24–47) minutes for alfaxalone; 22 (18–35) for ketamine] but took longer to recover adequately to return to the paddock after alfaxalone [44 (38–67) minutes] compared with ketamine [35 (30–47)]. There was no statistical difference between treatments in effect on HR, PaO₂ or PaCO₂ although for both regimens, PaO₂ decreased with respect to before premedication values. There was no difference between treatments in effect on blood pressure.Conclusions and clinical relevanceBoth alfaxalone and ketamine were effective at inducing anaesthesia, although at induction there were more muscle tremors after alfaxalone. As there were no differences between treatments in relation to cardiopulmonary responses or quality of recovery, and only minor differences in recovery times, both agents appear suitable for this purpose following the premedication regimen used in this study.     

Evaluation of intramuscular anesthetic protocols in healthy domestic horses

ObjectiveTo assess anesthetic induction, recovery quality and cardiopulmonary variables after intramuscular (IM) injection of three drug combinations for immobilization of horses.Study designRandomized, blinded, three-way crossover prospective design.AnimalsA total of eight healthy adult horses weighing 470–575 kg.MethodsHorses were administered three treatments IM separated by ≥1 week. Combinations were tiletamine–zolazepam (1.2 mg kg⁻¹), ketamine (1 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment TKD); ketamine (3 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment KD); and tiletamine–zolazepam (2.4 mg kg⁻¹) and detomidine (0.04 mg kg⁻¹) (treatment TD). Parametric data were analyzed using mixed model linear regression. Nonparametric data were compared using Skillings–Mack test. A p value <0.05 was considered statistically significant.ResultsAll horses in treatment TD became recumbent. In treatments KD and TKD, one horse remained standing. PaO₂ 15 minutes after recumbency was significantly lower in treatments TD (p < 0.0005) and TKD (p = 0.001) than in treatment KD. Times to first movement (25 ± 15 minutes) and sternal recumbency (55 ± 11 minutes) in treatment KD were faster than in treatments TD (57 ± 17 and 76 ± 19 minutes; p < 0.0005, p = 0.001) and TKD (45 ± 18 and 73 ± 31 minutes; p = 0.005, p = 0.021). There were no differences in induction quality, muscle relaxation score, number of attempts to stand or recovery quality.Conclusions and clinical relevanceIn domestic horses, IM injections of tiletamine–zolazepam–detomidine resulted in more reliable recumbency with a longer duration when compared with ketamine–detomidine and tiletamine–zolazepam–ketamine–detomidine. Recoveries were comparable among protocols.     

Influence of a constant rate infusion of dexmedetomidine on cardiopulmonary function and recovery quality in isoflurane anaesthetized horses

ObjectiveTo investigate the influence of a dexmedetomidine constant rate infusion (CRI) in horses anaesthetized with isoflurane.Study designProspective, randomized, blinded, clinical study.AnimalsForty adult healthy horses (weight mean 491 ± SD 102 kg) undergoing elective surgery.MethodsAfter sedation [dexmedetomidine, 3.5 μg kg^?1 intravenously (IV)] and induction IV (midazolam 0.06 mg kg^?1, ketamine 2.2 mg kg^?1), anaesthesia was maintained with isoflurane in oxygen/air (FiO₂ 55–60%). Horses were ventilated and dobutamine was administered when hypoventilation [arterial partial pressure of CO₂ > 8.00 kPa (60 mmHg)] and hypotension [arterial pressure 70 mmHg] occurred respectively. During anaesthesia, horses were randomly allocated to receive a CRI of dexmedetomidine (1.75 μg kg^?1 hour^?1) (D) or saline (S). Monitoring included end-tidal isoflurane concentration, cardiopulmonary parameters, and need for dobutamine and additional ketamine. All horses received 0.875 μg kg^?1 dexmedetomidine IV for the recovery period. Age and weight of the horses, duration of anaesthesia, additional ketamine and dobutamine, cardiopulmonary data (anova), recovery scores (Wilcoxon Rank Sum Test), duration of recovery (t-test) and attempts to stand (Mann–Whitney test) were compared between groups. Significance was set at p < 0.05.ResultsHeart rate and arterial partial pressure of oxygen were significantly lower in group D compared to group S. An interaction between treatment and time was present for cardiac index, oxygen delivery index and systemic vascular resistance. End-tidal isoflurane concentration and heart rate significantly increased over time. Packed cell volume, systolic, diastolic and mean arterial pressure, arterial oxygen content, stroke volume index and systemic vascular resistance significantly decreased over time. Recovery scores were significantly better in group D, with fewer attempts to stand and significantly longer times to sternal position and first attempt to stand.Conclusions and clinical relevance A dexmedetomidine CRI produced limited cardiopulmonary effects, but significantly improved recovery quality.     

Acute noncardiogenic pulmonary edema in an anesthetized Nubian goat kid

ObservationsA 1-month-old Nubian goat presented for sialocyst resection. Physical examination and bloodwork were unremarkable. While pre-oxygenating, the goat was sedated with midazolam and morphine (0.1 mg kg^?1 each) intravenously (IV). General anesthesia was induced 5 minutes later with 1.7 mg kg^?1 propofol. Sevoflurane was administered in oxygen without assisted ventilation via a cuffed orotracheal tube. Throughout the first 85 minutes of anesthesia, the goat was well-oxygenated (SpO₂, ≥97%), ventilating adequately (Pe′CO₂, 36–48 mmHg), and had normal mean arterial blood pressure (MAP, 60–85 mmHg). Blood-gas values at 45 minutes were consistent with adequate ventilation on oxygen. At 75 minutes, the goat moved in response to surgical stimulation, requiring additional propofol (0.4 mg kg^?1). After 10 minutes, MAP dropped precipitously to 40 mmHg and frequent multiform premature ventricular contractions (PVCs) were observed. Crystalloids, hetastarch, and dopamine (5 μg kg^?1 minute^?1) were administered to correct the hypotension. Arterial blood-gas analysis revealed that the goat had become hypoxemic (PaO₂, 50 mmHg). Intermittent positive pressure ventilation (IPPV) was initiated. Subsequent blood-gas analysis did not show significant improvement in PaO₂ (53 and 56 mmHg, respectively). Occasional PVCs were observed thereafter. Surgery ended, and sevoflurane and IPPV were discontinued. The goat was extubated within 7 minutes and received 100% oxygen by mask. Diffuse crackles were ausculted over both hemithoraces. Suspecting pulmonary edema, furosemide (1 mg kg^?1) was administered IV. Radiographs taken immediately post-operatively revealed a severe, caudodorsal airspace (alveolar) pattern, confirming the diagnosis. Respiration improved considerably within an hour with nasal oxygen and two additional doses of furosemide.ConclusionsThe goat developed acute, drug-induced, noncardiogenic pulmonary edema in response to the second dose of propofol.     

Comparative effects of three different ventilatory treatments on arterial blood gas values and oxygen extraction in healthy anaesthetized dogs

ObjectiveTo compare the effect of invasive continuous positive airway pressure (CPAP), pressure-controlled ventilation (PCV) with positive end-expiratory pressure (PEEP) and spontaneous breathing (SB) on PaO₂, PaCO₂ and arterial to central venous oxygen content difference (CaO₂-CcvO₂) in healthy anaesthetized dogs.Study designProspective randomized crossover study.AnimalsA group of 15 adult male dogs undergoing elective orchidectomy.MethodsDogs were anaesthetized [buprenorphine, medetomidine, propofol and isoflurane in an air oxygen (FiO₂= 0.5)]. All ventilatory treatments (CPAP: 4 cmH₂O; PCV: 10 cmH₂O driving pressure; PEEP, 4 cmH₂O; respiratory rate of 10 breaths minute^–1 and inspiratory-to-expiratory ratio of 1:2; SB: no pressure applied) were applied in a randomized order during the same anaesthetic. Arterial and central venous blood samples were collected immediately before the start and at 20 minutes after each treatment. Data were compared using a general linear mixed model (p < 0.05).ResultsMedian PaO₂ was significantly higher after PCV [222 mmHg (29.6 kPa)] than after CPAP [202 mmHg (26.9 kPa)] and SB [208 mmHg (27.7 kPa)] (p < 0.001). Median PaCO₂ was lower after PCV [48 mmHg (6.4 kPa)] than after CPAP [58 mmHg (7.7 kPa)] and SB [56 mmHg (7.5 kPa)] (p < 0.001). Median CaO₂-CcvO₂ was greater after PCV (4.36 mL dL^–1) than after CPAP (3.41 mL dL^–1) and SB (3.23 mL dL^–1) (p < 0.001). PaO₂, PaCO₂ and CaO₂-CcvO₂ were no different between CPAP and SB (p > 0.99, p = 0.697 and p = 0.922, respectively).Conclusions and clinical relevanceCPAP resulted in similar arterial oxygenation, CO₂ elimination and tissue oxygen extraction to SB. PCV resulted in improved arterial oxygenation and CO₂ elimination. Greater oxygen extraction occurred with PCV than with CPAP and SB, offsetting its advantage of improved arterial oxygenation. The benefit of invasive CPAP over SB in the healthy anaesthetized dog remains uncertain.     

Efficacy of a portable oxygen concentrator with pulsed delivery for treatment of hypoxemia during equine field anesthesia

ObjectiveHypoxemia is common during equine field anesthesia. Our hypothesis was that oxygen therapy from a portable oxygen concentrator would increase PaO₂ during field anesthesia compared with the breathing of ambient air.Study designProspective clinical study.AnimalsFifteen yearling (250 – 400 kg) horses during field castration.MethodsHorses were maintained in dorsal recumbency during anesthesia with an intravenous infusion of 2000 mg ketamine and 500 mg xylazine in 1 L of 5% guaifenesin. Arterial samples for blood gas analysis were collected immediately post-induction (PI), and at 15 and 30 minutes PI. The control group (n = 6) breathed ambient air. The treatment group (n = 9) were administered pulsed-flow oxygen (192 mL per bolus) by nasal insufflation during inspiration for 15 minutes PI, then breathed ambient air. The study was performed at 1300 m above sea level. One-way and two-way repeated-measures anova with post-hoc Bonferroni tests were used for within and between-group comparisons, respectively. Significance was set at p ≤ 0.05.ResultsMean ± SD PaO₂ in controls at 0, 15 and 30 minutes PI were 46 ± 7 mmHg (6.1 ± 0.9 kPa), 42 ± 9 mmHg (5.6 ± 1.1 kPa), and 48 ± 7 mmHg (6.4 ± 0.1 kPa), respectively (p = 0.4). In treatment animals, oxygen administration significantly increased PaO₂ at 15 minutes PI to 60 ± 13 mmHg (8.0 ± 1.7 kPa), compared with baseline values of 46 ± 8 mmHg (6.1 ± 1 kPa) (p = 0.007), and 30 minute PI values of 48 ± 7 mmHg (6.5 ± 0.9 kPa) (p = 0.003).ConclusionsThese data show that a pulsed-flow delivery of oxygen can increase PaO₂ in dorsally recumbent horses during field anesthesia with ketamine-xylazine-guaifenesin.Clinical relevanceThe portable oxygen concentrator may help combat hypoxemia during field anesthesia in horses.