K. W. Clarke

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 μg/kg) and atropine (30 μg/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 medetomidineinduced 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.

Minimal alveolar concentration of desflurane in combination with an infusion of medetomidine for the anaesthesia of ponies

The minimum alveolar concentration of desflurane when combined with a continuous infusion of medetomidine at 3.5 μg/kg/hour was measured in seven ponies. Anaesthesia was induced with medetomidine (7 μg/kg intravenously) followed by ketamine (2 mg/kg intravenously) and maintained with desflurane in oxygen. The infusion of medetomidine was started 20 minutes after the induction of anaesthesia. The electrical test stimulus was applied at the coronary band (50 V, 10 ms bursts at 5 Hz for one minute), and heart rates and rhythms, arterial blood pressures, and arterial blood gas tensions were measured at intervals, just before the application of the stimulus. The mean (sd) minimum alveolar concentration of desflurane was 5.3 (1.04) per cent (range 3.2 to 6.4 per cent), 28 per cent less than the previously published value for desflurane alone after the induction of anaesthesia with xylazine and ketamine. The cardiopulmonary parameters remained stable throughout the period of anaesthesia. The mean (sd) time taken by the ponies to stand after the administration of desflurane ceased was 16.5 (6.17) (range 5.8 to 26) minutes, and the quality of recovery was good or excellent. However, one pony died shortly after standing; a postmortem examination revealed that it had chronic left atrial dilatation.

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 medetomidine in sheep and in ponies

Medetomidine was administered intravenously to six sheep at 5, 10 and 20 micrograms kg-1 and to one horse and four ponies at 5 and 10 micrograms kg-1. In both species medetomidine resulted in significant decreases in heart rate and cardiac output and, initially, in an increase in arterial blood pressure. In the ponies this increase in blood pressure was followed by a significant and prolonged decrease, but in the sheep the secondary decrease in blood pressure was not statistically significant. In the sheep, the three doses of medetomidine resulted in profound and significant decreases in arterial oxygen tensions, which were significantly dose related, but in the ponies the arterial blood oxygen tensions were not significantly decreased. In both species medetomidine caused a small but significant increase in arterial blood carbon dioxide tensions.

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 endtidal 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 (sviu) 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.

Characterisation of the cardiovascular pharmacology of medetomidine in the horse and sheep.

Medetomidine was administered to sheep and horses at a dose rate of 5 microg kg(-1) (i.v.). Heart rate and blood pressure were recorded. Medetomidine induced bradycardia and a biphasic blood pressure response consisting of a transient hypertension followed by hypotension. Administration of prazosin (an alpha1 adrenoceptor antagonist; 100 microg kg(-1), i.v.) had no effect on the cardiovascular response to medetomidine (5 microg kg(-1), i.v.), but inhibited the cardiovascular response of methoxamine (an alpha1 adrenoceptor agonist; 75 microg kg(-1), i.v.). L-659,066 (an alpha2 adrenoceptor antagonist which does not cross the blood brain barrier; 264 microg kg(-1), i.v.) attenuated the medetomidine induced bradycardia, but had no effect on the cardiovascular response to methoxamine. L659,066 also reduced the medetomidine induced hypertension in sheep, but had less effect on the horse. It is concluded that both alpha1 and alpha2 adrenoceptors are important in the control of cardiovascular function in horses and sheep. Medetomidine appears to act on alpha2 adrenoceptors alone in the sheep. The cardiovascular effects of medetomidine in the horse are complex and may be influenced by central alpha2 adrenoceptor regulation or effects on other receptor subtypes as well as direct stimulation of peripheral alpha2 adrenoceptors.

Maintenance of anaesthesia in sheep with isoflurane, desflurane or sevoflurane

Rapid recovery from anaesthesia is advantageous in small ruminants, to reduce the risk of regurgitation. Theoretically, the least soluble inhalation agents should result in the fastest recoveries, but using additional injectable agents may negate this advantage. This study compared three inhalation agents for the maintenance of anaesthesia in sheep. Eighteen ewes that were to undergo orthopaedic surgery were allocated to one of three groups. Each group was premedicated with xylazine (0·1 mg/kg intramuscularly), anaesthesia was induced using ketamine (2 mg/kg) and midazolam (0·03 mg/kg) intravenously and analgesia provided by buprenorphine (0·008 mg/kg intramuscularly). Anaesthesia was then maintained with either isoflurane, sevoflurane or desflurane. Cardiopulmonary parameters were monitored throughout. All three inhalation agents provided adequate stable anaesthesia and there was no significant difference between the groups in their cardiopulmonary parameters or their recovery times. The mead (sd) postanaesthetic times to first swallow, first chewing attempts and ability to maintain their head lifted for five minutes were, respectively, 3·95 (2·53), 6·37 (3·68) and 32·8 (18·1) minutes for isoflurane, 3·62 (0·98), 7·66 (0·78) and 38·8 (16·6) minutes for sevoflurane, and 4·37 (1·65), 6·95 (1·52) and 29·8 (11·5) minutes for desflurane. Two sheep had poor quality recoveries after the use of sevoflurane, but all the other sheep recovered uneventfully. All three inhalation agents were suitable for the maintenance of anaesthesia in sheep but, as used in this study, there were no differences between them in speed of recovery.

A comparison of the duration and quality of recovery from isoflurane, sevoflurane and desflurane anaesthesia in dogs undergoing magnetic resonance imaging.

OBJECTIVEnTo compare the recovery after anaesthesia with isoflurane, sevoflurane and desflurane in dogs undergoing magnetic resonance imaging (MRI) of the brain.nnnSTUDY DESIGNnProspective, randomized clinical trial.nnnANIMALSnThirty-eight dogs weighing 23.7 +/- 12.6 kg.nnnMETHODSnFollowing pre-medication with meperidine, 3 mg kg(-1) administered intramuscularly, anaesthesia was induced intravenously with propofol (mean dose 4.26 +/- 1.3 mg kg(-1)), the trachea was intubated, and an inhalational anaesthetic agent was administered in oxygen. The dogs were randomly allocated to one of three groups: group I (n = 13) received isoflurane, group S (n = 12) received sevoflurane and group D (n = 13) received desflurane. Parameters recorded included cardiopulmonary data, body temperature, end-tidal anaesthetic concentration, duration of anaesthesia, and recovery times and quality. Qualitative data were compared using chi-squared and Fishers exact tests and quantitative data with anova and Kruskal-Wallis test. Post-hoc comparisons for quantitative data were undertaken with the Mann-Whitney U-test.nnnRESULTSnThe duration of anaesthesia [mean and standard deviation (SD)] in group I was: 105.3 (27.48) minutes, group S: 120.67 (19.4) minutes, and group D: 113.69 (26.68) minutes (p = 0.32). Times to extubation [group I: 8 minutes, (interquartile range 6-9.5), group S: 7 minutes (IQR 5-7), group D: 5 minutes (IQR 3.5-7), p = 0.017] and to sternal recumbency [group I: 11 minutes (IQR 9.5-13.5), group S: 9.5 minutes (IQR 7.25-11.75), group D: 7 minutes (range 3.5-11.5), p = 0.048] were significantly different, as were times to standing. One dog, following sevoflurane, had an unacceptable quality of recovery, but most other recoveries were calm, with no significant difference between groups.nnnCONCLUSIONS AND CLINICAL RELEVANCEnAll three agents appeared suitable for use. Dogs tracheas were extubated and the dogs recovered to sternal recumbency most rapidly after desflurane. This may be advantageous for animals with some neurological diseases and for day case procedures.

The effects of ephedrine on intramuscular blood flow and other cardiopulmonary parameters in halothane‐anesthetized ponies

OBJECTIVEnTo evaluate the effect of ephedrine on intramuscular blood flow and hemodynamic parameters during equine anesthesia.nnnSTUDY DESIGNnProspective experimental study.nnnANIMALSnSix healthy adult Welsh Mountain ponies (five males, one female, mean weight: 267 kg, range: 213-347 kg).nnnMETHODSnHalothane-anesthetized ponies received an IV bolus of ephedrine (0.1 mg kg-1), followed 30 minutes later by a second IV ephedrine injection (0.2 mg kg-1). Changes in intramuscular blood flows (IMBF) in upper and lower triceps brachii were measured by laser Doppler flowmetry. Cardiopulmonary measurements were made at intervals for 30 minutes following each injection. Results were compared with values from a control group, similarly anesthetized but given saline in an earlier study.nnnRESULTSnEphedrine at either dose increased heart rate, arterial blood pressure (AP), cardiac index (CI) and intramuscular blood flow (IMBF), the effects on these parameters being significant and long-lasting following the higher dose. Systemic vascular resistance remained unchanged, and was significantly lower than in the control saline group. PaO2 decreased significantly immediately following the first injection of ephedrine, then remained unchanged for the remainder of the experiment. PaCO2 increased slowly throughout the anesthetic period. One pony developed supraventricular premature complexes following the second injection. No other side effects were seen.nnnCONCLUSIONnEphedrine at dose rates of 0.2 mg kg-1 IV consistently increased in CI, AP, and IMBF in both forelimbs.nnnCLINICAL RELEVANCEnEphedrine may be of use to improve AP, CI and IMBF during halothane anesthesia, although the occurrence of an arrhythmia in one pony is of concern.

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 (<five minutes) 15 per cent fall in arterial blood pressure and 78 per cent rise in intramuscular blood flow. Heart rate increased from a mean of 42 (SD 4) to 54 (12) beats per minute, the rise being significant for 15 minutes. Cardiac index increased from 2.1 (0.7) to 3.9 (0.7) litres m(-2) and remained significantly elevated for the remainder of the measurement period. Cardiovascular changes in the hypoxic group were similar. 30 minutes after clenbuterol administration, PaO2 had changed nonsignificantly from 32.3 (19.2) to 33.4 (17) kPa in the hyperoxic group and from 7.9 (1.8) to 8.6 (1.3) kPa in the hypoxic group. The study concludes that under these experimental conditions, clenbuterol does not cause significant improvement in arterial oxygenation, but its cardiovascular effects are minimal or advantageous.