Effects of brotizolam as a co-agent with ketamine for induction of anaesthesia in calves.

Anaesthesia in food producing animals in the EU and UK is legally limited to a narrow choice of drugs; the only licensed benzodiazepine being brotizolam. The aim of this study was to investigate the effects of brotizolam as a co-agent with ketamine on the quality of induction, intubation, muscle relaxation and recovery from isoflurane anaesthesia. Seventeen calves were enrolled in this prospective, blinded, randomized experimental study. Calves were sedated with 0.05 mg/kg xylazine and 0.1 mg/kg butorphanol IV. After assessing the quality of sedation, anaesthesia was induced with 2 mg/kg ketamine (group KETA) or 2 mg/kg ketamine with 2 µg/kg brotizolam IV (group BROTI). An additional 1 mg/kg ketamine was administered IV every 2 min until intubation was possible. Anaesthesia was maintained with isoflurane in a mixture of oxygen and air. The amount of ketamine required, quality of induction, intubation, muscle relaxation, and recovery were scored and compared between groups using ordinal regression models (P < 0.05 was considered statistically significant). Sedation scores did not differ significantly between groups but were positively associated with the quality of recovery (P = 0.0098). Group BROTI was associated with a lower quality of induction (P < 0.0001), intubation (P = 0.0203) and muscle relaxation (P = 0.0043). The sedation score and treatment had no effect on the number of attempts of intubation, additional ketamine doses, time to extubation and recovery time. Brotizolam had a negative effect on the quality of induction, intubation, and muscle relaxation compared to ketamine alone. We do not recommend using brotizolam under these circumstances.

Double-outlet right ventricle with an intact interventricular septum and concurrent hypoplastic left ventricle in a calf.

A 3-day-old Hereford heifer calf presented for evaluation of lethargy and dyspnea, with persistent hypoxia despite supplemental oxygen therapy. A grade III/VI right apical systolic murmur was noted during cardiac auscultation. Echocardiography revealed a double-outlet right ventricle with an intact interventricular septum and concurrent hypoplastic left ventricle and tricuspid valve dysplasia. Post-mortem examination revealed additional congenital anomalies of ductus arteriosus, patent foramen ovale, and persistent left cranial vena cava. This report illustrates the use of echocardiographic images to diagnose a double-outlet right ventricle with an intact interventricular septum and a hypoplastic left ventricle in a calf.

Role of CO2 in the cerebral hyperemic response to incremental normoxic and hyperoxic exercise.

Cerebral blood flow (CBF) is temporally related to exercise-induced changes in partial pressure of end-tidal carbon dioxide (PetCO2 ); hyperoxia is known to enhance this relationship. We examined the hypothesis that preventing PetCO2 from rising (isocapnia) during submaximal exercise with and without hyperoxia [end-tidal Po2(PetO2 ) = 300 mmHg] would attenuate the increases in CBF. Additionally, we aimed to identify the magnitude that breathing, per se, influences the CBF response to normoxic and hyperoxic exercise. In 14 participants, CBF (intra- and extracranial) measurements were measured during exercise [20, 40, 60, and 80% of maximum workload (Wmax)] and during rest while ventilation (V̇e) was volitionally increased to mimic volumes achieved during exercise (isocapnic hyperpnea). While V̇ewas uncontrolled during poikilocapnic exercise, during isocapnic exercise and isocapnic hyperpnea, V̇ewas increased to prevent PetCO2 from rising above resting values (∼40 mmHg). Although PetCO2 differed by 2 ± 3 mmHg during normoxic poikilocapnic and isocapnic exercise, except for a greater poikilocapnic compared with isocapnic increase in blood velocity in the posterior cerebral artery at 60% Wmax, the between condition increases in intracranial (∼12-15%) and extracranial (15-20%) blood flow were similar at each workload. The poikilocapnic hyperoxic increases in both intra- and extracranial blood-flow (∼17-29%) were greater compared with poikilocapnic normoxia (∼8-20%) at intensities >40% Wmax(P< 0.01). During both normoxic and hyperoxic conditions, isocapnia normalized both the intracranial and extracranial blood-flow differences. Isocapnic hyperpnea did not alter CBF. Our findings demonstrate a differential effect of PetCO2 on CBF during exercise influenced by the prevailing PetO2.