Effect of pressure support ventilation during weaning on ventilation and oxygenation indices in healthy horses recovering from general anesthesia

ObjectiveTo determine if pressure support ventilation (PSV) weaning from general anesthesia affects ventilation or oxygenation in horses.Study designProspective randomized clinical study.AnimalsTwenty client‐owned healthy horses aged 5 ± 2 years, weighing 456 ± 90 kg.MethodsIn the control group (CG; n = 10) weaning was performed by a gradual decrease in respiratory rate (f_R) and in the PSV group (PSVG; n = 10) by a gradual decrease in f_R with PSV. The effect of weaning was considered suboptimal if PaCO₂ > 50 mmHg, arterial pH < 7.35 plus PaCO₂ > 50 mmHg or PaO₂ < 60 mmHg were observed at any time after disconnection from the ventilator until 30 minutes after the horse stood. Threshold values for each index were established and the predictive power of these values was tested.ResultsPressure support ventilation group (PSVG) had (mean ± SD) pH 7.36 ± 0.02 and PaCO₂ 41 ± 3 mmHg at weaning and the average lowest PaO₂ 69 ± 6 mmHg was observed 15 minutes post weaning. The CG had pH 7.32 ± 0.02 and PaCO₂ 57 ± 6 mmHg at weaning and the average lowest PaO₂ 48 ± 5 mmHg at 15 minutes post weaning. No accuracy in predicting weaning effect was observed for f_R (p = 0.3474), minute volume (p = 0.1153), SaO₂ (p = 0.1737) and PaO₂/PAO₂ (p = 0.1529). A high accuracy in predicting an optimal effect of weaning was observed for V_T > 10 L (p = 0.0001), f_R/V_T ratio ≤ 0.60 breaths minute^?1 L^?1 (p = 0.0001), V_T/bodyweight > 18.5 mL kg^?1 (p = 0.0001) and PaO₂/FiO₂ > 298 (p = 0.0002) at weaning. A high accuracy in predicting a suboptimal effect of weaning was observed for V_T < 10 L (p = 0.0001), f_R/V_T ratio ≥ 0.60 breaths minute^?1 L^?1 (p = 0.0001) and Pe′CO₂ ≥ 38 mmHg (p = 0.0001) at weaning.Conclusions and clinical relevancePressure support ventilation (PSV) weaning had a better respiratory outcome. A higher V_T, V_T/body weight, PaO₂/FiO₂ ratio and a lower f_R/V_T ratio and Pe′CO₂ were accurate in predicting the effect of weaning in healthy horses recovering from general anesthesia.     

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.     

The influence of atipamezole on the cardiovascular effects of detomidine in horses

The reversal of the cardiovascular effects of the α₂-adrenoceptor agonist detomidine by the α₂-antagonist atipamezole was studied. Nine horses were given detomidine 20 μg/kg iv. On a separate occasion they were given atipamezole 100 μg/kg iv 15 mins after the detomidine injection. Blood gas tensions were measured and clinical signs of sedation were also observed. Bradycardia and the frequency of heart blocks induced by detomidine were reduced after atipamezole and blood pressure decreased. These reversal effects of atipamezole were of short duration (a few minutes) at the dose level tested. Two of the nine horses exhibited premature depolarisations after administration of detomidine, but not after atipamezole injection. PaO₂ decreased and PaCO₂ increased slightly after detomidine injection, but the arterial pH was within reference values or slightly elevated. Administration of atipamezole did not alter these values. Base excess rose after detomidine, and it decreased more quickly towards the baseline level, when the horses were given detomidine alone. No clinical adverse effects were seen from the administration of atipamezole. Atipamezole may be beneficial, if detomidine-induced bradycardia needs to be reversed in horses.     

Pulsed delivery of inhaled nitric oxide counteracts hypoxaemia during 2.5 hours of inhalation anaesthesia in dorsally recumbent horses

Objective The study aimed to investigate the effect of varying pulse lengths of inhaled nitric oxide (iNO), and 2.5 hours of continuous pulse‐delivered iNO on pulmonary gas exchange in anaesthetized horses. Study Design Experimental study. Animals Six Standardbred horses. Methods Horses received acepromazine, detomidine, guaifenesin, thiopentone and isoflurane in oxygen, were positioned in dorsal recumbency and were breathing spontaneously. iNO was on average pulsed during the first 20, 30, 43 or 73% of the inspiration in 15 minute steps. The pulse length that corresponded to the highest (peak) partial pressure of arterial oxygen (PaO₂) in the individual horses was determined and delivered for a further 1.5 hours. Data measured or calculated included arterial and mixed venous partial pressures of O₂ and CO₂, heart rate, respiratory rate, expired minute ventilation, pulmonary and systemic arterial mean pressures, cardiac output and venous admixture. Data (mean ± SD) was analysed using anova with p < 0.05 considered significant. Results Although the pulse length of iNO that corresponded to peak PaO₂ varied between horses, administration of all pulse lengths of iNO increased PaO₂ compared to baseline. The shortest pulse lengths that resulted in the peak PaO₂ were 30 and 43% of the inspiration. Administration of iNO increased PaO₂ (12.6 ± 4.1 kPa [95 ± 31 mmHg] at baseline to a range of 23.0 ± 8.4 to 25.3 ± 9.0 kPa [173 to 190 mmHg]) and PaCO₂ (8.5 ± 1.2 kPa [64 ± 9 mmHg] to 9.8 ± 1.5 kPa [73 ± 11 mmHg]) and decreased venous admixture from 32 ± 6% to 25 ± 6%. The increase in PaO₂ and decrease in venous admixture was sustained for the entire 2.5 hours of iNO delivery. Conclusions The improvement in arterial oxygenation during pulsed delivery of iNO was significant and sustained throughout 2.5 hours of anaesthesia. Clinical relevance Pulsed iNO potentially could be used clinically to counteract hypoxemia in anaesthetized horses.     

Effects of Carbon Dioxide Insufflation and Body Position on Blood Gas Values in Horses Anesthetized for Laparoscopy

The objective of the study was to describe the effects of carbon dioxide pneumoperitoneum and Trendelenburg position on arterial blood gas values in horses anesthetized for laparoscopy. The study design was a prospective case series using 14 healthy adult horses anesthetized for elective laparoscopic surgery. All horses in the study were maintained under anesthesia with halothane in oxygen with intermittent positive-pressure ventilation. A pneumoperitoneum of 15 mmHg or less was achieved with carbon dioxide, and horses were tilted to a 35-degree Trendelenburg position to allow the completion of laparoscopic cryptorchidectomy (n = 13) or ovariectomy (n = 1). Heart rate, mean arterial pressure, and arterial blood gases were recorded at six time intervals throughout the procedure. Results of the study indicated a pH that decreased and partial pressure of carbon dioxide (PaCO₂) and mean arterial pressure that increased over time and differed significantly from baseline during Trendelenburg position. Partial pressure of oxygen (PaO₂) was significantly lower than baseline after assumption of Trendelenburg position and did not improve on return to normal recumbency and abdominal pressure. As body weight increased, pH and PaO₂ decreased and PaCO₂ increased. We concluded that horses placed in Trendelenburg position have changes that are transient, with the exception of PaO₂. Heavier horses have a greater change in pH, PaCO₂, and PaO₂ than lighter horses during abdominal insufflation and Trendelenburg position. The changes incurred during CO₂ abdominal insufflation and Trendelenburg position are transient, with the exception of a decreased PaO₂. Heavy horses undergoing abdominal insufflation and Trendelenburg position should be closely monitored for critical cardiopulmonary values.     

Transcutaneous monitor approximates PaCO(2) but not PaO(2) in anesthetized rabbits

ObjectiveTo compare the accuracy of transcutaneous (tc) to arterial partial pressure of carbon dioxide (PaCO₂) and partial pressure of oxygen (PaO₂) in anesthetized rabbits.Study designProspective, randomized, experimental study.AnimalsEight healthy adult female New Zealand white rabbits weighing 4.05 ± 0.30 kg.MethodsIsoflurane anesthetized rabbits received six treatments in random order; PaCO₂ < 35, 35-45, and >45 mmHg and PaO₂ < 80, 100-200, >200 mmHg. Arterial and transcutaneous measurements were taken after 15 minutes of stabilization at each condition. Linear regression, correlation and Bland-Altman analysis were performed to compare PtcCO₂ to PaCO₂ and PtcO₂ to PaO₂.ResultsOver a range of measured PaCO₂ values from 21 to 67 mmHg (n = 24) mean bias for PtcCO₂ was -1 mmHg and the 95% limits of agreement were -7 to 5 mmHg. The correlation between PtcCO₂ and PaCO₂ was strong with R² value of 0.9454. Over the entire range of measured PaO₂ values (46-508 mmHg) mean bias for PtcO₂ was -61 mmHg and the 95% limits of agreement were -226 to 104 mmHg. Correlation was poor with R² = 0.5969. Comparing PtcO₂ to PaO₂ over a narrower range [PaO₂ < 150 mmHg (n = 13)] improved the correlation, with an R² value of 0.8518, mean bias of -7 mmHg and 95% limits of agreement from -33 to 19 mmHg.Conclusions and clinical relevanceIn healthy anesthetized rabbits, PtcCO₂ closely approximated PaCO₂. In contrast PtcO₂ underestimated PaO₂, particularly at high values. The PtcCO₂ sensor may be a useful noninvasive way to assess adequacy of ventilation in anesthetized rabbits.     

Hypoxaemia during anaesthesia in seven horses with colic

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

Effect of sedation with detomidine and butorphanol on pulmonary gas exchange in the horse

Background

Sedation with α₂-agonists in the horse is reported to be accompanied by impairment of arterial oxygenation. The present study was undertaken to investigate pulmonary gas exchange using the Multiple Inert Gas Elimination Technique (MIGET), during sedation with the α₂-agonist detomidine alone and in combination with the opioid butorphanol.

Methods

Seven Standardbred trotter horses aged 3–7 years and weighing 380–520 kg, were studied. The protocol consisted of three consecutive measurements; in the unsedated horse, after intravenous administration of detomidine (0.02 mg/kg) and after subsequent butorphanol administration (0.025 mg/kg). Pulmonary function and haemodynamic effects were investigated. The distribution of ventilation-perfusion ratios (V_A/Q) was estimated with MIGET.

Results

During detomidine sedation, arterial oxygen tension (PaO₂) decreased (12.8 ± 0.7 to 10.8 ± 1.2 kPa) and arterial carbon dioxide tension (PaCO₂) increased (5.9 ± 0.3 to 6.1 ± 0.2 kPa) compared to measurements in the unsedated horse. Mismatch between ventilation and perfusion in the lungs was evident, but no increase in intrapulmonary shunt could be detected. Respiratory rate and minute ventilation did not change. Heart rate and cardiac output decreased, while pulmonary and systemic blood pressure and vascular resistance increased. Addition of butorphanol resulted in a significant decrease in ventilation and increase in PaCO₂. Alveolar-arterial oxygen content difference P(A-a)O₂ remained impaired after butorphanol administration, the V_A/Q distribution improved as the decreased ventilation and persistent low blood flow was well matched. Also after subsequent butorphanol no increase in intrapulmonary shunt was evident.

Conclusion

The results of the present study suggest that both pulmonary and cardiovascular factors contribute to the impaired pulmonary gas exchange during detomidine and butorphanol sedation in the horse.     

Apneic oxygenation in anesthetized ponies and horses

Apneic oxygenation was studied in six ponies for 30 minutes, and six horses for 10 minutes. Arterial blood was sampled at regular intervals for measurement of oxygen and carbon dioxide tensions (PaO₂ and PaCO₂) and calculation of alveolar-arterial oxygen tension difference (PAO₂-PaO₂). In both groups of animals, PaO₂ decreased rapidly during the first 3 minutes of apnea, then more slowly. Although the mean value was above 100 mmHg at 10 minutes, there was considerable inter-animal variability. Before apnea, PAO₂-PaO₂ was slightly, but not significantly, larger in horses than in ponies and increased in both groups during the first 3 minutes of apnea, after which the increase was slower. There was no significant difference between ponies and horses up to 10 minutes, suggesting that PAO₂-PaO₂ is independent of body size. In ponies, the PAO₂-PaO₂ did not change significantly between 10 and 30 minutes. Final PaO₂ could not be correlated with initial PaO₂ or initial PAO₂-PaO₂. The rate of rise of PAO₂-PaO₂ could not be predicted from baseline values. The rate of rise of PaCO₂ was similar and fairly constant in ponies and horses, and did not contribute to the rapid initial decrease in PaO₂. It appears that apneic oxygenation should not be used in the equine species, since it is impossible to predict in which animals the technique is safe for more than a few minutes.     

Effects of Intravenous Detomidine on Intraocular Pressure Readings Obtained by Applanation Tonometry in Clinically Normal Horses

This study was conducted to determine effects of intravenous detomidine on intraocular pressure (IOP) readings obtained by applanation tonometry in clinically normal horses. Twenty horses were randomly divided into two groups of 10 each (treatment and control). All horses in the treatment group received intravenous detomidine alone (20 μg/kg). The horses in the control group received only intravenous saline (0.2 mL/100 kg). The IOP values were measured before the treatment (T₀) and then at 5 (T₅), 20 (T₂₀), 60 (T₆₀), and 120 (T₁₂₀) minutes after drug administration in both groups. A significant decrease in IOP values was observed in both right and left eyes of the horses in the treatment group at T₅, T₂₀, and T₆₀ in comparison with the baseline values (P < .001). The observed decrease was only statistically significant in the right eyes of the treatment group horses at T₁₂₀ (P = .044). Mean IOP was not significantly altered at any time point during the treatment period compared with the baseline evaluations in both eyes of the horses in the control group. This study demonstrates that the use of intravenous detomidine lowers IOP quickly.     

Regional distribution of ventilation in horses in dorsal recumbency during spontaneous and mechanical ventilation assessed by electrical impedance tomography: a case series

ObjectiveTo evaluate the regional distribution of ventilation in horses during spontaneous breathing and controlled mechanical ventilation (CMV) using electrical impedance tomography (EIT).Study designProspective, experimental case series.AnimalsFour anaesthetized experimental horses.MethodsHorses were anaesthetized with isoflurane in an oxygen-air mixture and medetomidine continuous rate infusion, placed in dorsal recumbency with an EIT belt around the thorax, and allowed to breathe spontaneously until PaCO₂ reached 13.3 kPa (100 mmHg), when volume CMV was started. For each horse, the EIT signal was recorded for at least 2 minutes immediately before (T1), and at 30 (n = 3) or 60 (n = 1) minutes after the start of CMV (T2). The centre of ventilation (CoV), dependent silent spaces (DSS) (likely to represent atelectatic lung areas), non-dependent silent spaces (NSS) (likely to represent lung areas with low ventilation) and total ventilated area (TVA) were evaluated. Cardiac output (CO) was measured and venous admixture and oxygen delivery (DO₂) were calculated at T1 and T2. Data are presented as median and range.ResultsAfter the initiation of CMV, the CoV moved ventrally towards the non-dependent lung by 10% [from 57.4% (49.6–60.2%) to 48.3% (41.9–54.4%)]. DSS increased [from 4.1% (0.2–13.9%) to 18.7% (7.5–27.5%)], while NSS [21.7% (9.4–29.2%) to 9.9% (1.0–20.7%)] and TVA [920 (699–1051) to 837 (662–961) pixels] decreased. CO, venous admixture and DO₂ also decreased.Conclusions and clinical relevanceIn spontaneously breathing anaesthetized horses in dorsal recumbency, ventilation was essentially centred within the dependent dorsal lung regions and moved towards non-dependent ventral regions as soon as CMV was started. This shows a major lack of ventilation in the dependent lung, which may be indicative of atelectasis.     

Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.     

Comparison of single-breath continuous positive airway pressure manoeuvre with inhaled salbutamol to improve oxygenation in horses anaesthetized for laparotomy

ObjectiveTo compare the efficacy of single-breath continuous positive airway pressure manoeuvre (CPAP-M) with inhaled salbutamol, and a combination of both.Study designRandomized, clinical study.AnimalsA total of 62 client-owned horses (American Society of Anesthesiologists status III–V) anaesthetized for laparotomy.MethodsHorses were premedicated with intravenous (IV) xylazine (0.4–0.6 mg kg^–1), anaesthesia was induced with midazolam (0.06 mg kg^–1 IV) and ketamine (2.2 mg kg^–1 IV) and maintained with isoflurane in oxygen using volume-controlled ventilation without positive end-expiratory pressure. If PaO₂ was < 100 mmHg (13.3 kPa), either a CPAP-M (50 cmH₂O for 45 seconds) or salbutamol (0.002 mg kg^–1) was administered. The intervention was considered successful if PaO₂ reached 100 mmHg (13.3 kPa). If PaO₂ remained < 100 mmHg (13.3 kPa), treatments were switched. PaO₂/FiO₂ ratio and estimated shunt fraction (F-shunt) were derived from data obtained from arterial blood gas measurements. Dynamic compliance (C_dyn) was calculated from variables recorded at the moment of arterial blood analysis. Fisher’s exact tests compared success rates between treatments, and linear models were performed to test whether the treatment modified the values of the measurements; p < 0.05.ResultsSalbutamol was the first intervention in 28 horses and was effective in 22 horses. CPAP-M was the first intervention in 34 horses and was effective in 26 horses. CPAP-M after salbutamol was performed in six horses, with four responders, and salbutamol after CPAP-M was administered to eight horses, with one responder. Salbutamol, but not CPAP-M, significantly decreased F-shunt. Both salbutamol and CPAP-M significantly increased C_dyn.Conclusions and clinical relevanceSalbutamol and CPAP-M were comparably effective in improving oxygenation and C_dyn in anaesthetized horses with PaO₂ < 100 mmHg (13.3 kPa). Whether combining both treatments might be beneficial needs to be confirmed on a larger number of horses.     

Cardiopulmonary effects of pleural insufflation with CO2 during two-lung ventilation in dorsally recumbent anesthetized horses

Objective

To record the cardiopulmonary effects of pleural CO₂ positive pressure insufflation in anesthetized horses.

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

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

Effect of 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.     

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.     

Cardiopulmonary effects of dexmedetomidine and ketamine infusions with either propofol infusion or isoflurane for anesthesia in horses

ObjectiveTo examine the cardiopulmonary effects of two anesthetic protocols for dorsally recumbent horses undergoing carpal arthroscopy.Study designProspective, randomized, crossover study.AnimalsSix horses weighing 488.3 ± 29.1 kg.MethodsHorses were sedated with intravenous (IV) xylazine and pulmonary artery balloon and right atrial catheters inserted. More xylazine was administered prior to anesthetic induction with ketamine and propofol IV. Anesthesia was maintained for 60 minutes (or until surgery was complete) using either propofol IV infusion or isoflurane to effect. All horses were administered dexmedetomidine and ketamine infusions IV, and IV butorphanol. The endotracheal tube was attached to a large animal circle system and the lungs were ventilated with oxygen to maintain end-tidal CO₂ 40 ± 5 mmHg. Measurements of cardiac output, heart rate, pulmonary arterial and right atrial pressures, and body temperature were made under xylazine sedation. These, arterial and venous blood gas analyses were repeated 10, 30 and 60 minutes after induction. Systemic arterial blood pressures, expired and inspired gas concentrations were measured at 10, 20, 30, 40, 50 and 60 minutes after induction. Horses were recovered from anesthesia with IV romifidine. Times to extubation, sternal recumbency and standing were recorded. Data were analyzed using one and two-way anovas for repeated measures and paired t-tests. Significance was taken at p=0.05.ResultsPulmonary arterial and right atrial pressures, and body temperature decreased from pre-induction values in both groups. PaO₂ and arterial pH were lower in propofol-anesthetized horses compared to isoflurane-anesthetized horses. The lowest PaO₂ values (70–80 mmHg) occurred 10 minutes after induction in two propofol-anesthetized horses. Cardiac output decreased in isoflurane-anesthetized horses 10 minutes after induction. End-tidal isoflurane concentration ranged 0.5%–1.3%.Conclusion and clinical relevanceBoth anesthetic protocols were suitable for arthroscopy. Administration of oxygen and ability to ventilate lungs is necessary for propofol-based anesthesia.     

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.     

Blood Gas Values During Intermittent Positive Pressure Ventilation and Spontaneous Ventilation in 160 Anesthetized Horses Positioned in Lateral or Dorsal Recumbency

One hundred sixty horses were anesthetized with xylazine, guaifenesin, thiamylal, and halothane for elective soft tissue and orthopedic procedures. Horses were randomly assigned to one of four groups. Group 1 (n = 40): Horses positioned in lateral (LR_G1,; n = 20) or dorsal (DR_G1,; n = 20) recumbency breathed spontaneously throughout anesthesia. Group 2 (n = 40): Intermittent positive pressure ventilation (IPPV) was instituted throughout anesthesia in horses positioned in lateral (LR_G2; n = 20) or dorsal (DR_G2; n = 20) recumbency. Group 3 (n = 40): Horses positioned in lateral (LR_G3; n = 20) or dorsal (DR_G3; n = 20) recumbency breathed spontaneously for the first half of anesthesia and intermittent positive pressure ventilation was instituted for the second half of anesthesia. Group 4 (n = 40): Intermittent positive pressure ventilation was instituted for the first half of anesthesia in horses positioned in lateral (LR_G4; n = 20) or dorsal (DR_G4; n = 20) recumbency. Spontaneous ventilation (SV) occured for the second half of anesthesia. The mean time of anesthesia was not significantly different within or between groups. The mean time of SV and IPPV was not significantly different in groups 3 and 4. Variables analyzed included pH, PaCO₂, PaO₂, and P(A-a)O₂ (calculated). Spontaneous ventilation resulted in significantly higher PaCO₂ and P(A-a)O₂ values and significantly lower PaO₂ values in LR_G1, and DR_G1, horses compared with LR_G2 and DR_G2 horses. Intermittent positive pressure ventilation resulted in normocarbia and significantly lower P(A-a)O₂ values in LR_G2 and DR_G2 horses. In LR_G2 the Pao₂ values significantly increased from 20 minutes after induction to the end of anesthesia. The PaO₂ and P(A-a)O₂ values were not significantly different from the beginning of anesthesia after IPPV in DR_G2 or DR_G3. The PaO₂ values significantly decreased and the P(A-a)O₂ values significantly increased after return to SV in horses in LR_G4, and DR_G4. The PaO₂ values were lowest and the P(A-a)O₂ values were highest in all horses positioned in dorsal recumbency compared with lateral recumbency and in SV horses compared with IPPV horses. The pH changes paralleled the changes in PaCO₂. Blood gas values during right versus left lateral recumbency in all groups were also evaluated. The PaO₂ values were significantly lower and the P(A-a)O₂ values were significantly higher during SV in horses positioned in left lateral (LR_LG1) compared with right lateral (LR_RG1) recumbency. No other significant changes were found comparing left and right lateral recumbency. Arterial hypoxemia (PaO₂ < 60 mm Hg) developed in 35% of DR_G1 horses and 20% of DR_G2 horses at the end of anesthesia. Arterial hypercarbia (PaCO₂= 50–60 mm Hg) developed in DRoi horses. Arterial hypoxemia that developed in 20% of DR_G3 horses was not improved with IPPV. Arterial hypoxemia developed in 55% of DR_G4 horses after return to SV. Some DR_G4 horses with hypoxemia also developed hypercarbia, whereas some had PaCO₂ values within normal limits. Arterial hypoxemia developed in one LR_G1, and two LR_G4, horses. Hypercarbia developed in onlv one LR_G4 horse.