Anaesthetic management and complications of pacemaker implantation in dogs.

The aim of this study was to report the anaesthetic management and peri-anaesthetic complications of 57 dogs undergoing pacemaker implantation at a referral institution over 10 years (2002-2012). The median duration of the procedure was 135 minutes (range 25-260 minutes). Patients were classified as American Society of Anaesthesiologist (ASA) III (42 cases) and ASA IV (15 cases). Forty-three patients had third-degree atrioventricular block, and 14 patients had sick sinus syndrome. The anaesthetic protocol most frequently chosen was pethidine (41 cases), etomidate-midazolam (43 cases) and isoflurane in oxygen for maintenance (57 cases). Transthoracic external pacing was used (43 cases) until the internal pacing lead was implanted. Atracurium was administered (48 cases) and intermittent positive pressure ventilation was applied in 52 cases. Complications observed included hypothermia (19 cases) and hypotension (5 cases). Three patients died (5.8%, 95% CI 1.1% to 14.6%) within the first 48 hours after termination of anaesthesia. The outcome for this procedure in sick animals appeared generally good though a number of complications were documented.

Cardiovascular effects of romifidine in the standing horse.

The cardiovascular effects of romifidine, an alpha-2 adrenoreceptor agonist, were investigated in six horses using two doses (80 and 120 microg kg(-1)) in a cross-over study design. Cardiac index and mixed venous oxygenation were significantly decreased at 15 and 30 minutes after both doses of romifidine. Systemic vascular resistance was significantly increased with romifidine (120 microg kg(-1)). Arterial blood pressure increased initially and then gradually decreased; the doses of decrease was significant at 90 and 120 minutes with romifidine 80 and 120 microg kg(-1). There were minimal differences between the two doses of romifidine, and both should be used with care especially in horses with cardiovascular compromise, or when used in combination with other cardiovascular depressant drugs.

Effects of dopamine, dobutamine, dopexamine, phenylephrine, and saline solution on intramuscular blood flow and other cardiopulmonary variables in halothane-anesthetized ponies.

OBJECTIVE: To evaluate the effect on intramuscular blood flow (IMBF) and hemodynamic variables of 4 antihypotensive agents given during anesthesia. ANIMALS: 8 ponies. PROCEDURE: Halothane-anesthetized ponies (n = 6) positioned in lateral recumbency received, on separate occasions, infusions of each of the following 4 agents in serially increasing dosages or saline solution: phenylephrine hydrochloride (0.25, 0.5, 1, and 2 microg/kg of body weight), dopamine (2.5, 5, 10, and 20 microg/kg), dobutamine (1, 2.5, 5, and 10 microg/kg), and dopexamine (0.5, 1, 5, and 10 microg/kg). Changes in IMBF (by laser-Doppler flowmetry) in nondependent and dependent triceps brachii muscles and cardiopulmonary variables were measured. RESULTS: Phenylephrine at all dosages failed to improve IMBF or cardiac index (CI), but increased mean arterial pressure (MAP) and systemic vascular resistance (SVR); 2 ponies had forelimb lameness on recovery. Dopamine (10 microg/kg/min) increased CI, MAP, and IMBF in the dependent muscle. A higher dose (20 microg/kg/min) caused cardiac arrhythmias and muscular tremor. Dobutamine increased Cl, MAP, and IMBF of both forelimbs, effects being significant for 2.5 microg/kg/min, with further improvement as the dosage increased. In 2 ponies, 10 microg of dobutamine/kg/min caused cardiac arrhythmias. Dopexamine (1 and 5 microg/kg/min) increased CI, MAP, and IMBF in the nondependent muscle, and 10 microg/kg/min caused muscular tremor, sweating, and arrhythmias. SVR was reduced after infusion of dopamine, dobutamine, or dopexamine. CONCLUSION: During anesthesia of equids, an increase in Cl and MAP is necessary to improve IMBF in the dependent forelimb. CLINICAL RELEVANCE: Of the agents investigated, dobutamine proved the most consistent in improving IMBF.

The cardiopulmonary effects of clenbuterol when administered to dorsally recumbent halothane-anaesthetised ponies--failure to increase arterial oxygenation.

Clenbuterol (0.8 microg kg(-1) intravenously) was investigated in ponies (small horses) anaesthetised with acepromazine, detomidine and thiopentone, then halothane in oxygen alone (hyperoxic group) or with nitrous oxide (hypoxic group). Following instrumentation, ponies were placed in dorsal recumbency for 60 minutes, clenbuterol (both groups) or a saline control (hyperoxic group) given, and cardiopulmonary parameters monitored for a further 60 minutes. In the hyperoxic group, clenbuterol administration resulted in a transitory (

Effects on the intramuscular blood flow and cardiopulmonary function of anaesthetised ponies of changing from halothane to isoflurane maintenance and vice versa.

The effects on intramuscular blood flow and cardiopulmonary parameters of changing from anaesthesia with halothane to isoflurane and vice versa were investigated in six ponies (small horses). Anaesthesia was induced with xylazine, ketamine and diazepam, maintained for one hour with halothane at an end tidal concentration of 1 per cent and then with isoflurane at 1.5 per cent for a further hour (halo/iso). On another occasion the order in which the volatile agents were administered was reversed (iso/halo). After one hour of anaesthesia the mean (sd) arterial blood pressure (MAP) and cardiac output (CO) of the ponies on the two occasions did not differ significantly (iso/halo, MAP 43 [5] mmHg, CO 10.9 [2.4] litre/min; halo/iso, MAP 53 [8] mmHg, CO 8.9 [2.3] litre/min). On changing the anaesthetic, MAP rose similarly in both groups. In the halo/iso group CO remained stable (8.64 [1.4] litre/min after the hour of isoflurane), but in the iso/halo group, CO decreased significantly on the administration of halothane (6.16 [1.3] litre/min after the second hour). When halothane replaced isoflurane, the intramuscular blood flow in both the upper and lower triceps brachii decreased significantly by 23 to 35 per cent, but when isoflurane replaced halothane the changes were not significant. It is concluded that CO and intramuscular blood flow both deteriorated when isoflurane was replaced by halothane. When isoflurane replaced halothane, cardiopulmonary function did not deteriorate further, but any improvement was not statistically significant.

Cardiopulmonary effects of desflurane in ponies, after induction of anaesthesia with xylazine and ketamine.

Cardiopulmonary parameters were measured in 12 ponies (small horses) before anaesthesia and, following induction with xylazine and ketamine, during maintenance of anaesthesia with desflurane. In six of the ponies (group A) anaesthesia was maintained for three hours with desflurane at an end-tidal concentration of 7.4 per cent. In the other six ponies (group B), anaesthesia was maintained in the same way for one hour and then the effects of end-tidal desflurane concentrations of 7.4 per cent and 9.6 per cent with and without artificial ventilation were investigated. In group A ponies the arterial blood pressure and the systemic vascular resistance index (SVRI) decreased significantly during the first 45 minutes of anaesthesia but recovered with time. The cardiac index and heart rates were unchanged throughout the measurement period but arterial carbon dioxide tensions increased significantly. In group B ponies, with either mode of ventilation, increasing desflurane concentration resulted in decreases in arterial blood pressure, cardiac index and mixed venous oxygen tension, although the changes were not always statistically significant. There were marked individual differences in the cardiovascular responses to the high desflurane concentrations, the minimum mean arterial blood pressure ranging from 35 to 62 mm Hg, and the cardiac index from 23 to 50 ml/kg/min. The study concludes that during maintenance of anaesthesia with end tidal concentrations of desflurane of 7.4 per cent, cardiac index is well maintained and the initial fall in arterial blood pressures results from a fall in SVRI. However, increasing the concentration of desflurane causes a fall in blood pressure due to cardiac depression.

Cardiopulmonary effects of desflurane in the dog during spontaneous and artificial ventilation.

The cardiopulmonary effects of desflurane at end tidal concentrations of 10.3, 12.9 and 15.5 per cent during either spontaneous or artificial ventilation were studied in five beagle dogs. Desflurane anaesthesia resulted in tachycardia and a decrease in arterial blood pressure which were not significantly related to the end tidal desflurane concentrations or the mode of ventilation. At an end tidal desflurane concentration of 15.5 per cent there was a significant increase in central venous and pulmonary arterial wedge pressures and, with artificial ventilation, a reduction in cardiac output and stroke volume when compared with similar measurements at an end tidal desflurane concentration of 10.3 per cent. When allowed to breathe spontaneously, the dogs panted at times when they were lightly anaesthetised, but their respiration was depressed to a varying extent at the highest end tidal desflurane concentration. The induction of anaesthesia with desflurane was smooth, and the quality of anaesthesia during maintenance was excellent. There was one episode of a transient tachyarrhythmia associated with the measurement of cardiac output, but no other side effects were observed.

Cardiopulmonary effects of combinations of medetomidine hydrochloride and atropine sulphate in dogs.

Medetomidine and xylazine are alpha 2 adrenoceptor agonists which are used as sedatives and premedicants in small animals. However, bradycardia is a side effect and the use of atropine sulphate has been recommended to counteract it. This study investigated the effects of combining medetomidine (40 micrograms/kg) and atropine (30 micrograms/kg) on the cardiopulmonary function of six dogs. Medetomidine administered alone caused severe bradycardia, but hypertension was mild and transient. Medetomidine and atropine administered together caused an initial bradycardia, but within 15 minutes there was tachycardia accompanied by a mean arterial blood pressure of 210 mm Hg. When atropine was administered 30 minutes before medetomidine, tachycardia and hypertension were observed within five minutes of the medetomidine injection. Thus, although atropine will counteract medetomidine-induced bradycardia, its use results in prolonged and severe hypertension, in association with the tachycardia. Although atropine may be life-saving when bradycardia is profound, its indiscriminate use in combination with alpha 2 adrenoceptor agonists may be disadvantageous.