Haemodynamic changes during sedation in ponies.

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (greater than 90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal. alpha 2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 micrograms/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation. Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the alpha 2-agonistic sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance. The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.