Effects of detomidine in young water buffalo

Following preliminary studies with detomidine hydrochloride in 10 young buffaloes (Bubalus bubalis), the effects of an intramuscular injection of 40 /ixg.kg-¹ were studied in 6 healthy buffaloes of VA to 2 years of age, weighing between 85 and 140 kg. Arterial blood pressure, central venous pressure, heart rate, electrocardiogram, electroencephalogram, respiratory rate, arterial pH, arterial and venous blood gases and rectal temperature were monitored before, and for an hour after, intramuscular injection of detomidine. Marked ataxia and sternal recumbency occurred within 10 minutes of injection, and an apparent complete recovery occurred in about 90 minutes. The electroencephalograms never demonstrated the high-voltage-low-frequency wave forms normally associated with sedation, but the animals appeared well sedated.
After injection there was marked decrease in heart rate which then tended to increase but it remained significantly (P < 0.05) below pre-injection values at 60 minutes. The mean arterial pressure increased initially, especially when electrocardiogram showed AV block, but after 15 minutes it had declined to below pre-injection values. These changes in the arterial blood pressure were, however, not statistically significant. Central venous pressure tended to increase during sedation but except at 30 minutes this increase was not statistically significant.
Rectal temperature, arterial pH, arterial carbon dioxide tension, standard bicarbonate and cranial vena caval oxygen tension did not show any significant variation. Respiratory rate and arterial oxygen tension decreased significantly.     

The Cardiopulmonary Effects of Oxymorphone in Hypovolemic Dogs

Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.
Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.
Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.     

Physiological effects of etorphine, acepromazine and xylazine in the scimitar horned oryx (Oryx dammah)

Scimitar horned oryx (Oryx dammah), kept under confined and unconfined conditions were immobilised with etorphine in combination with acepromazine or xylazine or both, and with xylazine alone. Both groups of animals were successfully sedated with etorphine and xylzine, with or without acepromazine, although hypothermia and mild hypoxaemia and a fall in packed cell volume were frequently noted. Xylazine alone produced a dose dependent degree of sedation in semitame subadult animals kept in confinement, but only slight depression in their wild, unconfined counterparts. If xylazine was not included in the immobilising mixture induction was traumatic and full sedation not achieved. Heart rates and arterial pressures (systemic and pulmonary) were also monitored but no remarkable changes were noted. The only abnormalities in blood biochemistry were raised aspartate transminase and creatine kinase. Ruminal regurgitation could be a major problem if endotracheal intubation was not achieved early in the procedure.     

Effects of saffan on cardiopulmonary function in healthy cats.

The effects of saffan on cardiopulmonary function were evaluated in eight healthy adult cats. Measured values were cardiac output by thermodilution, heart rate by electrocardiogram, arterial blood gases, respiratory rate and systolic, diastolic and mean arterial blood pressures by arterial catheterization. Calculated values included cardiac index, stroke volume and systemic vascular resistance. Statistical analysis employed paired t-tests comparing pre saffan anesthetic induction and post saffan anesthetic parameters over a 120 minute time sequence. Thirty min after saffan induction, significant depression in cardiac output was evident while stroke volume was significantly depressed at 45 and 60 min, systolic blood pressure at 15 min and respiratory rate at 5, 10 and 15 min. No significant changes occurred in cardiac index, heart rate, arterial blood gases, diastolic and mean arterial blood pressure or systemic vascular resistance. It was concluded that saffan causes significant depression of cardiopulmonary function in normal adult cats.     

Cardiovascular and allied actions of xylazine and atropine in the unanaesthetized goat

The cardiovascular effects of xylazine and atropine, separately and in combination, were studied in goats. Methylatropine was used to distinguish between the central and peripheral effects of atropine. Mean arterial blood pressure and heart rate were recorded, and the sedative effect and changes in respiration and salivation noted. Intravenous infusion of xylazine (2.4-80.0 micrograms/kg) decreased mean arterial blood pressure and heart rate in a dose-dependent manner. Single intravenous injections of both atropine sulphate (0.1 mg/kg) and methylatropine bromide (0.05 mg/kg) increased blood pressure and heart rate. After methylatropine, tachycardia lasted twice as long as after atropine. Following atropinization, a potentiated rise in mean arterial blood pressure was present during the infusion of xylazine (80 micrograms/kg). Xylazine-induced bradycardia was reversed by both atropine and methylatropine. The action of atropine is presumed to be primarily peripheral because of the similar effects with methylatropine. Xylazine-induced sedation was dose dependent. At the highest dose the goats were unable to stand for 30-60 min, respiration became irregular with periods of apnoea, and saliva started to drip a few minutes after infusion without increased salivation. Atropine had no visible effect on the sedation, pattern of respiration or saliva dripping effect of xylazine.     

Hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats. ANIMALS: 12 healthy adult domestic shorthair cats. PROCEDURE: Cats were anesthetized by administration of isoflurane in oxygen. After instruments were inserted, end-tidal isoflurane concentration was set at 1.25 times the individual minimum alveolar concentration, and nitrous oxide was administered in a Latin-square design at 0, 30, 50, and 70%. Each concentration was administered for 25 minutes before measurements were obtained to allow for stabilization. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured before and during noxious stimulation for each nitrous oxide concentration. Arterial and mixed-venous bicarbonate concentrations and oxygen saturation, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, arterial and mixed-venous oxygen contents, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. RESULTS: Arterial pressure, central venous pressure, pulmonary arterial pressure, rate-pressure product, systemic and pulmonary vascular resistance indices, arterial PCO2, and PCV increased during administration of 70% nitrous oxide. Arterial and mixed-venous pH, mixed-venous PO2, and alveolar-to-arterial oxygen difference decreased during administration of 70% nitrous oxide. Results before and during noxious stimulation were similar. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of 70% nitrous oxide to isoflurane-anesthetized cats resulted in improved arterial pressure, which was related to a vasoconstrictive effect.     

Cardiopulmonary effects of xylazine in dogs.

Effects of the drug xylazine were determined on arterial pH, arterial oxygen pressure (PaO2), arterial carbon dioxide pressure (PaCO2), aortic blood pressure, aortic flow, heart rate, pulse pressure, stroke volume, and peripheral resistance of dogs. The drug was given intravenously (IV) with and without atropine and was given intramuscularly (IM) without atropine. After IV administration of xylazine (1.1 mg/kg), arterial pH, PaO2, and PaCO2 values were not changed from control values. However, the drug did produce a statistically significant decrease in heart rate, decrease in aortic flow, initial increase in blood pressure followed by decrease, and increase in peripheral resistance. Stroke volume and pulse pressure were not significantly changed. Atropine (0.02 mg/kg, IV) did not significantly change any of the effects produced by xylazine. Intramuscular administration of xylazine (2.2 mg/kg) did not produce significant changes in arterial pH, PaO2, or PaCO2. Heart rate and aortic flow decreased significantly, but statistically significant changes did not occur in aortic blood pressure or peripheral resistance; however, the changes in these last 2 values were in the same direction and were of similar magnitude as those which occurred afger IV administration of xylazine.     

Effects of anticholinergic treatment on the cardiac and respiratory systems in dogs sedated with medetomidine.

Alpha 2-adrenergic agonists are often used for sedation and, or, analgesia in dogs, but they are often associated with bradycardia and in some animals with atrioventricular heart block. In this study, atropine or glycopyrrolate either helped to maintain the heart rates or were effective in increasing reduced heart rates of dogs treated with medetomidine. In the process, however, cardiac dysrhythmias often developed. These dysrhythmias were predominantly associated with the combined responses to the medetomidine and the anticholinergic agent because there were no significant changes in respiratory function. A reduced blood oxygen content or increased blood carbon dioxide can contribute to cardiac irritability. Atropine and glycopyrrolate were more effective in preventing bradycardia and had less undesirable side effects when they were given before the administration of medetomidine.     

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.     

Effects of medetomidine premedication on propofol infusion anaesthesia in dogs

Observations of cardiovascular and respiratory parameters were made on six dogs anaesthetized on two separate occasions for 120 minutes with a propofol infusion, once without premedication and once following premedication with 10 μg kg-¹ of intramuscular medetomidine. During anaesthesia the heart rate and cardiac index tended to be lower following medetomidine premedication, while the mean arterial pressure was significantly greater (p<0.05). Although the differences were not statistically significant, the systemic vascular resistance, pulmonary vascular resistance and stroke volume index were also greater in dogs given medetomidine. The mean arterial oxygen and carbon dioxide tensions were similar under both regimens, but in 2 dogs supplementary oxygen had to be administered during anaesthesia to alleviate severe hypoxaemia on both occasions they were anaesthetized. Minute and tidal volumes of respiration tended to be greater in dogs not given medetomidine but medetomidine premedication appeared to have no effect on venous admixture. Dogs given medetomidine received intramuscular atipamezole at the end of the 120 min. propofol infusion; the mean time from induction of anaesthesia to walking without ataxia was 174. min in the unpremedicated dogs and 160 min. in the dogs given atipamezole. The mean blood propofol concentration at which the dogs walked without ataxia was higher in the unpremedicated animals (2.12 ± 0.077 μg. ml-¹ compared with 1.27 ± 0.518 μg. ml-¹ in the premedicated dogs). The oxygen delivery to the tissues was lower after medetomidine premedication (p = 0.03) and the oxygen consumption was generally lower after medetomidine premedication but the difference did not achieve statistical significance. No correlation could be demonstrated between blood propofol concentration and cardiac index, systemic or pulmonary vascular resistance indices, systolic, diastolic or mean arterial blood pressures.     

Safety and efficacy of a technique for thoracoscopically guided pulmonary wedge resection in horses

OBJECTIVE: To evaluate the safety and efficacy of thoracoscopically guided pulmonary wedge resection in horses. ANIMALS: 10 horses (5 control horses and 5 horses affected with recurrent airway obstruction [ie, heaves]). PROCEDURE: Each horse underwent a thoracoscopically guided pulmonary wedge resection. Before, during, and after surgery, heart rate, respiratory rate, arterial blood gases, and systemic and pulmonary arterial pressures were measured. Physical examination, CBC, and thoracic radiography and ultrasonography were performed 24 hours before and 2 and 48 hours after surgery. Pulmonary specimens were assessed by histologic examination. A second thoracoscopic procedure 14 days later was used to evaluate the resection site. RESULTS: The technique provided excellent specimens for histologic evaluation of the lung. Heart and respiratory rates decreased significantly after horses were administered sedatives. A significant transient decrease in Pao2 was detected immediately after pulmonary wedge resection, but we did not detect significant effects on arterial pH, Paco2, or mean arterial and pulmonary arterial pressures. All horses except 1 were clinically normal after thoracoscopic surgery; that horse developed hemothorax attributable to iatrogenic injury to the diaphragm. The second thoracoscopy revealed minimal inflammation, and there were no adhesions. CONCLUSIONS AND CLINICAL RELEVANCE: Thoracoscopically guided pulmonary wedge resection provides a minimally invasive method for use in obtaining specimens of lung tissues from healthy horses and those with lung disease. This technique may be useful for the diagnosis of diseases of the lungs and thoracic cavity.     

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.

OBJECTIVE: To evaluate the cardiovascular effects of the alpha2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats. ANIMALS: 7 clinically normal cats. PROCEDURE: Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 microg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration. RESULTS: Heart rate, cardiac index, stroke index, rate-pressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered alone to clinically normal cats, medetomidine (20 microg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central alpha2-adrenergic effect over peripheral vascular effects.     

Technical and methodological requirements for reliable haemodynamic measurements in the unsedated calf

The purpose of this study was (1) to evaluate the technical and methodological problems associated with invasive haemodynamic measurements in unsedated cattle; (2) to assess the reproducibility of such measurements both within and between days; and (3) to compare the values with those previously reported.Twenty-one healthy calves, aged from 5.5 to 12 months, were studied. The central venous, the right ventricular, the pulmonary arterial, the pulmonary capillary wedge and the systemic arterial pressures were obtained by means of fluid-filled catheters, and the cardiac output was measured by the thermodilution technique. The heart rate, the stroke volume, the pulmonary and systemic vascular resistances and the pulmonary and systemic ventricular workloads were calculated.An adverse reaction, consisting of severe pulmonary hypertension, tachycardia, tachypnoea and transient weakness, occurred in 7 calves during the catheterization procedures. Such a reaction might be due to a local reflex induced by stimulation of mechano-receptors by the catheter tip. It should be avoided by reducing the manipulation of the catheter as much as possible and by inflating the tip of the balloon when moving it forwards. A comparison of the vascular pressures with those previously reported was difficult because of methodological or technical limitations, such as, for instance, a lack of standardization of the baseline. The reproducibility of the haemodynamic measurements obtained was satisfactory, in contrast to previous studies performed in conscious animals. This was attributed to our animals being better trained to the experimental conditions and emphasizes the importance of reducing mental stress in obtaining reliable haemodynamic measurements in unsedated and potentially uncooperative animals.     

The cardiopulmonary effects of dobutamine and norepinephrine in isoflurane-anesthetized foals

OBJECTIVE: To evaluate the cardiovascular effects of norepinephrine (NE) and dobutamine (DB) in isoflurane-anesthetized foals. STUDY DESIGN: Prospective laboratory study. METHODS: Norepinephrine (0.05, 0.10, 0.20, and 0.40 microg kg(-1) minute(-1)) and dobutamine (2.5, 5.0, and 10 microg kg(-1) minute(-1)) were alternately administered to seven healthy, 1- to 2-week-old isoflurane-anesthetized foals. Arterial and pulmonary arterial blood pressure, right atrial pressure, pulmonary artery occlusion pressure, heart rate, body temperature, cardiac output, arterial and mixed venous blood pH, partial pressure of carbon dioxide, partial pressure of oxygen [arterial partial pressure of oxygen (PaO(2)) and mixed venous partial pressure of oxygen (PvO(2))], and packed cell volume were measured. Standard base excess, bicarbonate concentration, systemic and pulmonary vascular resistance, cardiac index (CI), stroke volume, left and right stroke work indices, oxygen delivery (DO(2)), consumption, and extraction were calculated. Results Norepinephrine infusion resulted in significant increases in arterial and pulmonary arterial pressure, systemic and pulmonary vascular resistance indices, and PaO(2); heart rate was decreased. Dobutamine infusion resulted in significant increases in heart rate, stroke volume index, CI, and arterial and pulmonary arterial blood pressure. Systemic and pulmonary vascular resistance indices were decreased while the ventricular stroke work indices increased. The PaO(2) decreased while DO(2) and oxygen consumption increased. Oxygen extraction decreased and PvO(2) increased. CONCLUSIONS AND CLINICAL RELEVANCE: Norepinephrine primarily augments arterial blood pressure while decreasing CI. Dobutamine primarily augments CI with only modest increases in arterial blood pressure. Both NE and DB could be useful in the hemodynamic management of anesthetized foals.     

Cardiovascular and pulmonary effects of recumbency in two conscious ponies

Respiratory dead-space, tidal volume, respiratory rate, blood gases, cardiac output, heart rate and arterial and pulmonary arterial blood pressures were measured in two conscious, trained ponies in the standing position and in left lateral recumbency. The ponies were reluctant to remain lying down for more than about 20 mins but the reason for this did not become apparent. Tidal volume was reduced during recumbency but the respiratory rate increased, tending to maintain the minute volume at about that of the standing animal. Arterial carbon dioxide tension did not change significantly from standing values but the mean arterial oxygen tension values tended to decrease in both ponies during recumbency because of a slight increase in pulmonary venous admixture. Venous admixture in these two laterally recumbent conscious animals was considerably less than previously reported for anaesthetised subjects.     

A case of spontaneous venous embolism with carbon dioxide during laparoscopic surgery in a pig

BACKGROUND: Carbon dioxide (CO2) embolism is a possible complication of capnoperitoneum during laparoscopic surgery. Experimentally induced venous CO2 embolism has been studied in pigs. In this paper we report a case of spontaneous CO2 embolism. OBSERVATIONS: A 4-month-old Large White pig weighing 20 kg underwent experimental laparoscopic surgery under general anaesthesia. Monitoring consisted of pulse oximetry, capnography, airway pressure, electrocardiography, invasive arterial and central venous blood pressures, and arterial blood-gas analysis. Shortly after the start of laparoscopy and onset of CO2 insufflation, sudden decreases in end-tidal CO2 (Pe'CO2), haemoglobin saturation of oxygen (SpO2), systolic arterial blood pressure and heart rate were observed. Airway pressure increased and pulmonary compliance decreased simultaneously. Insufflation was immediately discontinued and epinephrine (2 mg IV), atropine (0.5 mg IV) and a 50 mL bolus of a polygeline solution were administered without effect. At this time arterial blood-gas analysis revealed a pH of 7.29 and a PaCO2 of 6.8 kPa (51.2 mmHg); PaO2 was 26.6 kPa (199.5 mmHg). After 4 minutes asystole occurred. CONCLUSIONS: The sudden decrease of Pe'CO2 and lung compliance combined with the sudden decrease in systolic blood pressure, heart rate and a poor response to resuscitation suggest a case of fatal gaseous venous embolism.     

Cardiopulmonary effects of dexmedetomidine and ketamine infusions with either propofol infusion or isoflurane for anesthesia in horses

ObjectiveTo examine the cardiopulmonary effects of two anesthetic protocols for dorsally recumbent horses undergoing carpal arthroscopy.Study designProspective, randomized, crossover study.AnimalsSix horses weighing 488.3 ± 29.1 kg.MethodsHorses were sedated with intravenous (IV) xylazine and pulmonary artery balloon and right atrial catheters inserted. More xylazine was administered prior to anesthetic induction with ketamine and propofol IV. Anesthesia was maintained for 60 minutes (or until surgery was complete) using either propofol IV infusion or isoflurane to effect. All horses were administered dexmedetomidine and ketamine infusions IV, and IV butorphanol. The endotracheal tube was attached to a large animal circle system and the lungs were ventilated with oxygen to maintain end-tidal CO₂ 40 ± 5 mmHg. Measurements of cardiac output, heart rate, pulmonary arterial and right atrial pressures, and body temperature were made under xylazine sedation. These, arterial and venous blood gas analyses were repeated 10, 30 and 60 minutes after induction. Systemic arterial blood pressures, expired and inspired gas concentrations were measured at 10, 20, 30, 40, 50 and 60 minutes after induction. Horses were recovered from anesthesia with IV romifidine. Times to extubation, sternal recumbency and standing were recorded. Data were analyzed using one and two-way anovas for repeated measures and paired t-tests. Significance was taken at p=0.05.ResultsPulmonary arterial and right atrial pressures, and body temperature decreased from pre-induction values in both groups. PaO₂ and arterial pH were lower in propofol-anesthetized horses compared to isoflurane-anesthetized horses. The lowest PaO₂ values (70–80 mmHg) occurred 10 minutes after induction in two propofol-anesthetized horses. Cardiac output decreased in isoflurane-anesthetized horses 10 minutes after induction. End-tidal isoflurane concentration ranged 0.5%–1.3%.Conclusion and clinical relevanceBoth anesthetic protocols were suitable for arthroscopy. Administration of oxygen and ability to ventilate lungs is necessary for propofol-based anesthesia.     

Cardiopulmonary effects of romifidine/ketamine or xylazine/ketamine when used for short duration anesthesia in the horse

The cardiovascular changes associated with anesthesia induced and maintained with romifidine/ketamine versus xylazine/ ketamine were compared using 6 horses in a cross over design. Anesthesia was induced and maintained with romifidine (100 microg/kg, IV)/ketamine (2.0 mg/kg, IV) and ketamine (0.1 mg/kg/min, IV), respectively, in horses assigned to the romifidine/ ketamine group. Horses assigned to the xylazine/ketamine group had anesthesia induced and maintained with xylazine (1.0 mg/kg, IV)/ketamine (2.0 mg/kg, IV) and a combination of xylazine (0.05 mg/kg/min, IV) and ketamine (0.1 mg/kg/min, IV), respectively. Cardiopulmonary variables were measured at intervals up to 40 min after induction. All horses showed effective sedation following intravenous romifidine or xylazine and achieved recumbency after ketamine administration. There were no significant differences between groups in heart rate, arterial oxygen partial pressures, arterial carbon dioxide partial pressures, cardiac index, stroke index, oxygen delivery, oxygen utilization, systemic vascular resistance, left ventricular work, or any of the measured systemic arterial blood pressures. Cardiac index and left ventricular work fell significantly from baseline while systemic vascular resistance increased from baseline in both groups. The oxygen utilization ratio was higher in the xylazine group at 5 and 15 min after induction. In conclusion, the combination of romifidine/ketamine results in similar cardiopulmonary alterations as a xylazine/ketamine regime, and is a suitable alternative for clinical anesthesia of the horse from a cardiopulmonary viewpoint.     

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.     

Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs.

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.