Pharmacokinetics of intravenous and transdermal fentanyl in alpacas.

The purpose of the study was to determine pharmacokinetics of fentanyl after intravenous (i.v.) and transdermal (t.d.) administration to six adult alpacas. Fentanyl was administered i.v. (2 µg/kg) or t.d. (nominal dose: 2 µg kg-1  hr-1 ). Plasma concentrations were determined using liquid chromatography-mass spectrometry. Heart rate and respiratory rate were assessed. Extrapolated, zero-time plasma fentanyl concentrations were 6.0 ng/ml (1.7-14.6 ng/ml) after i.v. administration, total plasma clearance was 1.10 L hr-1  kg-1 (0.75-1.40 L hr-1  kg-1 ), volumes of distribution were 0.30 L/kg (0.10-0.99 L/kg), 1.10 L/kg (0.70-2.96 L/kg) and 1.5 L/kg (0.8-3.5 L/kg) for V1 , V2 , and Vss , respectively. Elimination half-life was 1.2 hr (0.5-4.3 hr). Mean residence time (range) after i.v. dosing was 1.30 hr (0.65-4.00 hr). After t.d. fentanyl administration, maximum plasma fentanyl concentration was 1.20 ng/ml (0.72-3.00 ng/ml), which occurred at 25 hr (8-48 hr) after patch placement. The area under the plasma fentanyl concentration-vs-time curve (extrapolated to infinity) after t.d. fentanyl was 61 ng*hr/ml (49-93 ng*hr/ml). The dose-normalized bioavailability of fentanyl from t.d. fentanyl in alpacas was 35.5% (27-64%). Fentanyl absorption from the t.d. fentanyl patch into the central compartment occurred at a rate of approximately 50 µg/hr (29-81 µg/hr) between 8 and 72 hr after patch placement.

Pharmacokinetics of midazolam after intravenous administration to horses.

REASONS FOR PERFORMING THE STUDY: Midazolam is used to control seizures in horses and to enhance muscle relaxation, but its pharmacokinetics are unknown. OBJECTIVE: To determine the pharmacokinetics and sedative effects of midazolam in horses. STUDY DESIGN: Blinded, randomised, crossover design. METHODS: Midazolam was administered i.v. at either 0.05 or 0.1 mg/kg bwt to 6 horses on 2 occasions at least 7 days apart using a crossover design. Blood samples were collected before and at predetermined times through 24 h after administration. Serum midazolam concentrations were determined by a liquid chromatography tandem-mass spectrometry method. Heart and respiratory rates and indices of sedation, ataxia, and sensitivity to stimuli were recorded before and at predetermined times after midazolam administration. RESULTS: Pharmacokinetic analysis was performed on samples from 5 horses in each group. Median total clearance was 10.6 ml/min/kg (range 6.1-15.2 ml/min/kg) and 10.4 ml/min/kg (range 8.4-17.6 ml/min/kg), and median volume of distribution at steady state was 2094 ml/kg (range 2076-2413 ml/kg) and 2822 ml/kg (range 2270-7064 ml/kg) after the 0.05 mg/kg and 0.1 mg/kg bwt doses, respectively. Median distribution half-life was 24 min (range 6-42 min) and 39 min (range 33.6-72 min) and median terminal half-life was 216 min (range 120-248 min) and 408 min (range 192-924 min) after the 0.05 mg/kg and 0.1 mg/kg bwt doses, respectively. Cardiorespiratory parameters and sedation scores did not change. Midazolam caused agitation, postural sway, weakness, and one horse became recumbent after the 0.1 mg/kg bwt dose. CONCLUSIONS: Midazolam produces ataxia and postural sway of short duration after i.v. administration to horses. Sedation was not evident after midazolam administration. Drug redistribution is likely the primary mechanism for the termination of effect. POTENTIAL RELEVANCE: Midazolam produces muscle relaxation but not sedation in adult horses.

The use of sedatives, analgesic and anaesthetic drugs in the horse: an electronic survey of members of the American Association of Equine Practitioners (AAEP).

REASONS FOR PERFORMING STUDY: To determine the sedative, analgesic and anaesthetic drugs and techniques that are used by equine veterinarians. HYPOTHESIS OR OBJECTIVES: To provide equine veterinarians with information concerning veterinary use of anaesthetic techniques, a reflection of the collective experiences of the profession. METHODS: A survey was conducted of those members of the American Association of Equine Practitioners (AAEP) with an electronic mail address on file with the organisation using proprietary, web-based software. The survey was comprised of 30 questions divided into 8 sections: nonsteroidal anti-inflammatory drugs; local anaesthesia; alternative techniques; standing chemical restraint; epidural anaesthesia; short-term anaesthesia; long-term anaesthesia; and a place for the respondent to make comments. RESULTS: The response rate was 13.8% (952/6911) AAEP member veterinarians primarily use phenylbutazone and flunixin as anti-inflammatory drugs, and lidocaine and mepivacaine for local anaesthesia. Combinations of drugs are preferred for standing chemical restraint. While many veterinarians frequently utilise short-term anaesthesia, longer anaesthesia is less frequently performed. CONCLUSIONS: Most AAEP member veterinarians use sedatives in combination to provide standing chemical restraint. Extra-label use of drugs is a core component of current equine sedation and anaesthetic practice. POTENTIAL RELEVANCE: Equine veterinarians can compare their choices of anaesthetic drugs with others practising equine medicine and surgery and may be stimulated to investigate alternative methods of providing comfort to horses.

Pharmacokinetics, pharmacodynamics, and analgesic effects of morphine after rectal, intramuscular, and intravenous administration in dogs.

OBJECTIVE: To compare systemic bioavailability and duration for therapeutic plasma concentrations and cardiovascular, respiratory, and analgesic effects of morphine administered per rectum, compared with IV and IM administration in dogs. ANIMALS: 6 healthy Beagles. PROCEDURE: In a randomized study, each dog received the following: morphine IV (0.5 mg/kg of body weight), morphine per rectum (1, 2, and 5 mg/kg as a suppository and 2 mg/kg as a solution), and a control treatment. Intramuscular administration of morphine (1 mg/kg) was evaluated separately. Heart and respiratory rates, systolic, diastolic, and mean blood pressures, adverse effects, and plasma morphine concentrations were measured. Analgesia was defined as an increase in response threshold, compared with baseline values, to applications of noxious mechanical (pressure) and thermal (heat) stimuli. Data were evaluated, using Friedman repeated-measures ANOVA on ranks and Student-Newman-Keuls post-hoc t-tests. RESULTS: Significant differences were not found in cardiovascular, respiratory, or analgesia values between control and morphine groups. Overall systemic bioavailability of morphine administered per rectum was 19.6%. Plasma morphine concentration after administration of the highest dose (5 mg/kg) as a suppository was significantly higher than concentrations 60 and 360 minutes after IV and IM administration, respectively. A single route of administration did not consistently fulfill our criteria for providing analgesia. CONCLUSIONS AND CLINICAL RELEVANCE: Rectal administration of morphine did not increase bioavailability above that reported for oral administration of morphine in dogs. Low bioavailability and plasma concentrations limit the clinical usefulness of morphine administered per rectum in dogs.

Effects of acepromazine and butorphanol on positive-contrast upper gastrointestinal tract examination in dogs.

OBJECTIVE: To determine whether acepromazine (ACE) and butorphanol (BUT) combination can be used for restraint of dogs during positive-contrast upper gastrointestinal tract (UGIT) examination. ANIMALS: 6 healthy dogs. PROCEDURE: In a randomized crossover design study, weekly UGIT examinations were performed on each dog for 5 weeks after administration of normal saline solution (0.5 ml), xylazine (1.0 mg/kg of body weight), or a combination of ACE (0.1 mg/kg) and 1 of 3 doses of BUT (0.05, 0.2, 1.0 mg/kg). Gastrointestinal tract emptying time, GI motility, pulse, respiratory rate, and quality of restraint were assessed. RESULTS: Total gastric emptying time was significantly prolonged by use of an ACE and BUT (0.05 mg/kg) combination. Xylazine and higher dosages of BUT significantly prolonged gastric and intestinal emptying times. All anesthetic protocols significantly decreased motility and facilitated nonmanual restraint. Xylazine and BUT (1.0 mg/kg) significantly decreased pulse and respiratory rate. CONCLUSION: The ACE and BUT combination prolonged GI tract emptying times, decreased GI motility, and facilitated nonmanual restraint for duration of the examination. Although GI motility was decreased and total gastric emptying time was prolonged, administration of ACE (0.1 mg/kg) plus BUT (0.05 mg/kg) allowed morphologic examination of the GI tract within 5 hours. Xylazine prolonged GI tract emptying, decreased GI motility, and provided good to excellent initial restraint. Clinical Relevance-The ACE and BUT combination prohibits functional examination of the GI tract; however, morphologic examination is possible when low dosages of BUT (0.05 mg/kg) are used.

[Sedation and anesthesia in dogs and cats with cardiovascular diseases. III. Ventilation, respiratory monitoring, treatment for postoperative pain]. / Sedation und Narkose bei Hund und Katze mit Herzkreislaufkrankheit. III. Teil: Ventilation, Uberwaching der Atmung, postoperative Schmerzbehandlung.

The purpose of this study was to review ventilation and postoperative analgesic technics in 137 dogs and 13 cats with congenital or acquired heart disease. The animals were referred to the Department of Veterinary Clinical Sciences at The Ohio State University, U.S.A, for the following surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch ring anomaly (3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). Controlled ventilation was used in all animals during thoracotomy. Anesthesia was maintained over 2.3 +/- 1.3 hours by using either isoflurane, halothane, propofol, or diazepam-ketamine in 64%, 32%, 2%, and 0.7% of animals, respectively. Postoperative analgesia was necessary in 20% of animals and was provided by using different technics over several hours. The technics and respective percentages of animals in which they were used, were: intravenous buprenorphine (3.3%), intercostal nerve blocks (8.7%), epidural morphine (4%), and interpleural regional analgesia (4%).

Blood gas values during intermittent positive pressure ventilation and spontaneous ventilation in 160 anesthetized horses positioned in lateral or dorsal recumbency.

One hundred sixty horses were anesthetized with xylazine, guaifenesin, thiamylal, and halothane for elective soft tissue and orthopedic procedures. Horses were randomly assigned to one of four groups. Group 1 (n = 40): Horses positioned in lateral (LRG1; n = 20) or dorsal (DRG1; n = 20) recumbency breathed spontaneously throughout anesthesia. Group 2 (n = 40): Intermittent positive pressure ventilation (IPPV) was instituted throughout anesthesia in horses positioned in lateral (LRG2; n = 20) or dorsal (DRG2; n = 20) recumbency. Group 3 (n = 40): Horses positioned in lateral (LRG3; n = 20) or dorsal (DRG3; n = 20) recumbency breathed spontaneously for the first half of anesthesia and intermittent positive pressure ventilation was instituted for the second half of anesthesia. Group 4 (n = 40): Intermittent positive pressure ventilation was instituted for the first half of anesthesia in horses positioned in lateral (LRG4; n = 20) or dorsal (DRG4; n = 20) recumbency. Spontaneous ventilation (SV) occured for the second half of anesthesia. The mean time of anesthesia was not significantly different within or between groups. The mean time of SV and IPPV was not significantly different in groups 3 and 4. Variables analyzed included pH, PaCO2, PaO2, and P(A-a)O2 (calculated). Spontaneous ventilation resulted in significantly higher PaCO2 and P(A-a)O2 values and significantly lower PaO2 values in LRG1 and DRG1 horses compared with LRG2 and DRG2 horses. Intermittent positive pressure ventilation resulted in normocarbia and significantly lower P(A-a)O2 values in LRG2 and DRG2 horses. In LRG2 the PaO2 values significantly increased from 20 minutes after induction to the end of anesthesia. The PaO2 and P(A-a)O2 values were not significantly different from the beginning of anesthesia after IPPV in DRG2 or DRG3. The PaO2 values significantly decreased and the P(A-a)O2 values significantly increased after return to SV in horses in LRG4 and DRG4. The PaO2 values were lowest and the P(A-a)O2 values were highest in all horses positioned in dorsal recumbency compared with lateral recumbency and in SV horses compared with IPPV horses. The pH changes paralleled the changes in PaCO2. Blood gas values during right versus left lateral recumbency in all groups were also evaluated. The PaO2 values were significantly lower and the P(A-a)O2 values were significantly higher during SV in horses positioned in left lateral (LRLG1) compared with right lateral (LRRG1) recumbency.(ABSTRACT TRUNCATED AT 400 WORDS)

[Sedation and anesthesia in dogs and cats with cardiovascular diseases. I. Anesthesia plan considering risk assessment, hemodynamic effects of drugs and monitoring]. / Sedation und Narkose bei Hund und Katze mit Herzkreislaufkrankheit. I. Teil: Narkoseplanung nach Risikobeurteilung, hämodynamische Wirkung der Pharmaka, Monitoring.

The purpose of this study was to review the effects of sedatives and anesthetics in 137 dogs and 13 cats with congenital or acquired heart disease which were referred for diagnostic, therapeutic, and surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart-base tumors (2%), palliative surgery for ventricular septal defect (VSD, 0.7%), and sick patients with deleterious cardiac arrhythmias (0.7%). The anesthetic plan considered the risks of anesthesia based upon preoperative patient assessment, classification scheme for functional phases of heart failure, and anesthetic drug effects of the cardiovascular system. The effects of sedatives and anesthetic drugs on determinants of cardiac output are described. The most commonly used drugs for premedication, induction, and maintenance of anesthesia were midazolam-oxymorphone (20%), thiopental or etomidate (30%), and isoflurane (64%). Prompt therapy was given to control arrhythmias and provide organ perfusion, pain relief, muscle relaxation and renal diuresis, using lidocaine, dopamine, fentanyl, atracurium, and furosemide in 17.3% 14.7%, 12%, 10%, and 8.7% of animals, respectively. Methods of routine and advanced patient monitoring are described.

Cardiorespiratory effects of acepromazine maleate and buprenorphine hydrochloride in clinically normal dogs.

Cardiorespiratory effects of the combination of acepromazine maleate (ACP) and buprenorphine hydrochloride (BPN) were studied in 11 healthy, conscious dogs. Values for systemic and pulmonary artery blood pressure, cardiac output, arterial and venous pH and blood gas tensions, and invasive and noninvasive estimates of ventricular systolic function, preload, and afterload were obtained before sedation and after administration of each drug. Acepromazine maleate (0.1 mg/kg, IV) depressed cardiac function, compared with baseline values for unsedated dogs. Cardiac output decreased from a mean (+/- SD) value of 4.2 (+/- 1.5) L/min to 3.1 (+/- 0.8) L/min (P < 0.001), a change not attributed to heart rate. Pulmonary capillary wedge pressure decreased from 8.3 (+/- 4.2) mm of Hg to 6.5 (+/- 4.3) mm of Hg (P < 0.01), but mean right atrial pressure did not change. Left ventricular measurement of the maximal positive rate of pressure change (dP/dtmax) decreased from 2,668 (+/- 356)/mm of Hg/s to 2,145 (+/- 463) mm of Hg/s (P < 0.001), and ventricular stroke volume decreased from 43.2 (+/- 15.2) ml/beat to 32.3 (+/- 8.6) ml/beat. Noninvasive indices of left ventricular function, ventricular shortening fraction, peak aortic velocity, and aortic average acceleration were decreased after ACP administration, but were not statistically different from baseline values. Mean systemic arterial blood pressure decreased from 121 +/- 12 mm of Hg to 96 +/- 13 mm of Hg 15 minutes after ACP administration (P < 0.001). Total systemic vascular resistance was not significantly different from the baseline value.(ABSTRACT TRUNCATED AT 250 WORDS)

[Sedation and anesthesia in dogs and cats with cardiovascular disease. II. Anesthesia planning with respect to pathophysiology, heart arrhythmia]. / Sedation und Narkose bei Hund und Katze mit herzkreislaufkrankheit. II. Teil: Narkoseplanung an Hand der Pathophysiologie, Herzarrhythmien.

The purpose of this study was to review the incidence of cardiac arrhythmias in 137 anesthetized dogs and 13 anesthetized cats with congenital or acquired heart disease that were referred for correction of following procedures: patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). The anesthetic plan considered the risks of anesthesia based upon the pathophysiology of cardiac lesions and the anesthetic drug effects on the cardiovascular system. Recommendations are made for dogs with decreased cardiac contractility, cardiac disease with volume overload, cardiac disease with pressure overload, and pericardial tamponade. The percentages of animals and their associated cardiac arrhythmias after premedication and during and after anesthesia were: sinus bradycardia (15.3%), sinus tachycardia (3.3%), atrial flutter (0.7%), atrial fibrillation (0.7%), premature ventricular contraction (14%), and ventricular tachycardia (1.3%). Prompt therapy was given to a percentage of animals in order to control arrhythmia and support cardiovascular system, by using atropine or glycopyrrolate (14%), lidocaine (17.3%), and dopamine (14.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of phenylephrine on hemodynamics and splenic dimensions in horses.

Pharmacologically induced splenic contraction might be useful during certain medical or surgical procedures in horses. The effects of phenylephrine, an alpha 1-adrenergic receptor agonist, on hemodynamic function and splenic dimensions were examined in 6 healthy adult horses. Phenylephrine infusion (1, 3, or 6 micrograms/kg of body weight/min for 15 minutes) resulted in a dose-related increase in mean pulmonary artery pressure; right atrial pressure; systolic, mean, and diastolic arterial pressures; and packed cell volume (P = 0.0001). Concurrent decreases in heart rate and specific cardiac output (P = 0.0001) were detected, but stroke volume did not vary significantly. The rate-pressure product was increased only at the highest phenylephrine dosage (P = 0.012). Bradycardia was observed at all dosages during drug infusion, and second-degree atrioventricular block was detected in 88% of horses during infusion. Phenylephrine administration caused dose-dependent splenic contraction, as detected by ultrasonographic measurements of splenic area and thickness (P = 0.0001). At the 3- and 6-micrograms/kg/min infusion rates, splenic area was reduced to 28 and 17% of baseline measurement, respectively. Splenic dimensions had returned to baseline values by 35 minutes after the end of infusion. Infusion of phenylephrine at a dosage of 3 micrograms/kg/min for 15 minutes can be used to induce splenic contraction in horses.

Adverse effects of administration of propofol with various preanesthetic regimens in dogs.

The effects of propofol on anesthetic induction were evaluated in 40 dogs anesthetized with isoflurane. Propofol is a rapidly acting, nonbarbiturate drug that induces anesthesia of ultrashort duration with IV administration. Four preanesthetic regimens were used: anesthesia without preanesthetic drugs; or with preanesthetic administration of acepromazine (0.1 mg/kg of body weight, IM), diazepam (0.2 mg/kg, IV), or acepromazine (0.02 mg/kg) and butorphanol (0.4 mg/kg) IM. Heart rate, systolic arterial blood pressure (SAP), respiration, quality of induction and recovery, and adverse effects were induction and recovery, and adverse effects were recorded. Intravenous propofol administration induced a variable period of apnea in 34 of 40 dogs. Cyanosis (in 2 dogs) and signs of pain on injection (in 3 dogs) were infrequently observed during induction. One dog developed ventricular premature depolarizations after propofol administration. Venous CO2 tension increased and pH decreased immediately after propofol administration, regardless of preanesthetic regimen. The SAP significantly (P < 0.05) decreased after propofol administration in dogs treated with acepromazine (SAP, 178 mm of Hg before vs 128 mm of Hg after propofol) and with acepromazine/butorphanol (SAP, 184 mm of Hg before vs 98 mm of Hg after propofol). When used for induction, propofol induces anesthetic-related adverse effects, some of which can be minimized by preanesthetic medication. Recovery characteristics varied with preanesthetic medication, independent of propofol administration.

Vaporizer in circle for delivery of isoflurane to dogs.

An in-circuit vaporizer for delivery of isoflurane was evaluated. The isoflurane concentration within an isolated circle breathing circuit was determined for 1 hour in 6 in-the-circuit vaporizers with the wicks removed. A mechanical ventilator and artificial lung were connected to the circuit. Isoflurane concentration increased as vaporizer setting increased, and delivered concentration (%) at 60 minutes (mean +/- SEM) ranged from 0.46 +/- 0.10 at tap setting 1 to 3.67 +/- 0.30 at setting 5. Temperature of the isoflurane did not change. Cardiovascular and respiratory function were maintained within a clinically acceptable range in 6 dogs anesthetized with thiamylal and maintained with 1.87% end-tidal isoflurane delivered from the in-circuit vaporizer during spontaneous ventilation, controlled ventilation, and closed-circuit anesthesia. The range of vaporizer tap settings (mean +/- SEM) was lower during closed-system anesthesia (2.5 +/- 0.1 to 3.5 +/- 0.6) and during controlled ventilation (2.6 +/- 0.2 to 3.3 +/- 0.2) than during semi-closed system anesthesia (5.4 +/- 0.3 to 6.8 +/- 0.4). The in-circuit vaporizer was used to deliver isoflurane to 36 dogs anesthetized for a variety of surgical and medical procedures. Ventilation was spontaneous, assisted, and in 1 instance, controlled. Cardiovascular function, respiratory function, and recovery times were within clinically acceptable ranges. The initial vaporizer tap setting (mean +/- SEM) was 8.2 +/- 0.4, and this corresponded to an end-tidal isoflurane concentration of 3.5 +/- 0.6. The range of vaporizer settings during the maintenance phase (mean +/- SEM) was 2.8 +/- 0.5 to 4.6 +/- 1.9.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an endtidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [PaCO2] = 35 to 45 mm of Hg), at hypercapnia (PaCO2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

Effect of xylazine on the arrhythmogenic dose of epinephrine in thiamylal/halothane-anesthetized horses.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration (MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 micrograms/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 micrograms/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 micrograms/kg/min; xylazine, 1.21 +/- 0.46 micrograms/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.

Precautions when using opioid agonists for induction of anesthesia.

Opioids produce unpredictable anesthesia that is associated with poor muscle relaxation, prolonged onset, and relatively difficult intubation. They often induce bradycardia, which must be countered with atropine or glycopyrrolate, and hypoventilation, which requires ventilatory support. Return to consciousness is often delayed, making postoperative assessment of the patient's condition difficult. Finally opioid induction is relatively expensive compared with other anesthetic induction regimens.