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

BACKGROUND: Sedation with alpha2-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 alpha2-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 (VA/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 VA/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.

High inspired oxygen concentrations increase intrapulmonary shunt in anaesthetized horses.

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

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

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