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Comparison of sedative and cardiorespiratory effects of medetomidine-butorphanol and medetomidine-ketamine combination in dogs
Proceedings of the American College of VeterinaryAnesthesiologists annual meeting, Dallas,Texas, 1999 The e¡ects of premedication with medetomidine on cardiopulmonary variables and cortisol concentrations were evaluated in dogs undergoing ovariohysterectomy (OHE). Twelve 2-year-old dogs, weighing 17^22.5 kg were equally divided into medetomidine (M) or saline (S) premedicated groups. Group M dogs received 40 mg kgÿ1 medetomidine intramuscularly 20 minutes before anesthetic induction. Group S dogs received saline (0.5 mL) in similar fashion. Dogs in both groups were induced with thiopental and maintained with halothane until OHE was completed. The halothane vaporizer was adjusted intraoperatively as required to maintain surgical anesthesia. All surgery was performed by an experienced surgeon. Blood samples for cortisol concentrations were collected prior to premedication, following anesthetic induction, skin incision, removal of the ovaries, extubation and then at 30, 60, 90, 120, 150, 180 and 300 minutes after extubation. Heart and respiratory rate, blood pressure and temperature were recorded at these times. ANOVA for repeated measures and Tukey's test were used for statistical analysis (p < 0.05). Heart rate was signi¢cantly lower during removal of the ovaries in the M group (80 210 beats minÿ1) than S group (130 2 20 beats minÿ1), while blood pressure did not change signi¢cantly from baseline (105 2 10 mm Hg) in the M group. Mean BP signi¢cantly decreased from baseline intra-operatively (70 2 9 mm Hg) and signi¢cantly increased at extubation (140 210 mm Hg) in the S group. Plasma cortisol concentrations increased two-fold from baseline values at extubation and reached a ¢ve-fold increase between 60 and 90 minutes after extubation in the S group. In contrast, plasma concentration did not signi¢cantly increase from baseline until 60 minutes after extubation and reached a four-fold increase at 300 minutes after extubation in the M group. The integrated cortisol value (area under the curve, ng mlÿ1 hours) was signi¢cantly lower with M (48642 2 14071) than with S (74206 2 9543). We concluded that pre-emptive administration of medetomidine attenuated pain/stress responses in dogs undergoing OHE during the ¢rst hour after extubation. Based on plasma cortisol concentrations, nonpremedicated dogs undergoing OHE require an analgesic prior to or immediately after extubation. Medetomidine premedicated dogs require an additional analgesic at 60^90 minutes following extubation.
The effect of glycopyrrolate on the cardiopulmonary response to high and low dose romi®dine sedation in dogs MD Sinclair,WN McDonell,* GR Pettifer* University of Guelph, Guelph, Ontario, Canada. The purpose of this study was to investigate the electrocardiographic (ECG) and cardiopulmonary response of VeterinaryAnaesthesia and Analgesia, 2000 , 27, 97^112
glycopyrrolate (G, 10 mg kgÿ1 IM) as a pretreatment (p) or administered concurrently (c) with romi¢dine (RO) SQ in dogs. Healthy adult dogs (3 M, 3F, 18.5^25 kg) were utilized in a randomized cross over experiment. Anesthesia was induced by face mask and maintained with iso£urane for instrumentation. Dogs were acclimatized for at least 30 minutes after recovery from anesthesia, baseline measurements were recorded and one of the treatments was administered: T1, 0.5 mL saline (S) (p) RO 40 mg kgÿ1; T2, G (p) RO (40 mg kgÿ1; T3, S (p) RO 120 mg kgÿ1; T4, G (p) RO 120 mg kgÿ1; T5, S (p) G (c) RO 120 mg kgÿ1. Measurements were repeated 15 minutes after G (p) or S (p); RO or G (c) RO were administered 20 minutes after G(p) or S(p), and further measurements were taken at 10, 20, 30, 60 and 90 minutes. A continuous lead II ECG, arterial and mixed venous blood gases, heart rate (HR), respiratory rate (RR), systemic arterial blood pressures (SAP, MAP, DAP), cardiac index (CI), pulmonary arterial (PAP) and wedge pressure (PCWP) were measured. Systemic vascular resistance (SVR), oxygen extraction ratios (VO2/DO2) and pulmonary shunt fractions were calculated. Data were analyzed by use of ANOVA for repeated measures with an LSD post-hoc test and 95% con¢dence level. Glycopyrrolate increased HR, SAP and CI. Respective values (mean 2 SD) at 30 minutes were as follows: T1, 77 2 13 (beats minÿ1), 157 220 (mm Hg), 86 2 9 (ml kg ÿ1 minÿ1); T2, 161 232, 202 268, 150 2 20; T3, 60 219, 157 228, 66 230; T4, 163 224, 267 227, 100 2 0. SVR showed a four-fold increase with all treatments. Heart block (2 AV) was noted in T1, T3 and T5, with T5 demonstrating variable conduction and high grade AV block (6 : 1) versus T1 (2 : 1) and T3 (2 : 1). T5 was associated with a higher frequency of 2 AV heart block and ventricular escape beats (2/5 dogs) at10 and 20 minutes. In conclusion, G prevented the reduction in CI associated with RO, however, the resultant tachycardia along with the increase in SAP and SVR, especially with T4, could be detrimental to myocardial function. Due to the increase in dysrhythmias, the concurrent administration of RO and G cannot be recommended.
Comparison of sedative and cardiorespiratory effects of medetomidine-butorphanol and medetomidine-ketamine combination in dogs JCH Ko,* RE Mandsager,* CJ McGrath,* SM Fox Oklahoma State University, Stillwater, OK, USA. The sedative and cardiorespiratory e¡ects of intramuscular medetomidine (M, 30 mg kgÿ1), medetomidine-butorphanol (MB, 30 mg kgÿ1 ÿ0.2 mg kg ÿ1) and medetomidineketamine (MK, 30 mg kgÿ1ÿ3 mg kg ÿ1) were compared in a randomized crossover study using six dogs (1.5 2 0.3 99
Proceedings of the American College of VeterinaryAnesthesiologists annual meeting, Dallas,Texas, 1999 years old and weighing 20.2 2 2.3 kg). Glycopyrrolate (0.01mg kgÿ1 IM) was co-administered with each drug combination. Atipamezole (150 mg kg ÿ1 IM) was given 40 minutes after each drug combination and recovery quality was assessed. One week was allowed between treatments. Direct arterial blood pressure, heart rate, respiratory rate and minute volume were recorded before and 5, 10, 20, 30 and 40 minutes after drug administration and again at 5 and 10 minutes after atipamezole injection. Samples for arterial blood gas analysis were collected at the same time intervals, and lead II of the ECG was monitored continuously. Minute volume was measured via a face mask connected to a Wright's respirometer. ANOVA for repeated measures and Tukey's test were used for analysis ( p < 0.05). All three combinations resulted in lateral recumbency within 6 minutes with the exception of one dog in the M group. Endotracheal intubation was easily achieved at 13 minutes following drug administration in both MB and MK, but was more di¤cult in M group. Analgesic duration, as assessed by tail clamp and needle prick, were 40 2 0, 38 2 4 and 34 212 minutes for MB, MK and M groups, respectively. The lowest PaO2 (60 mm Hg, 8 kPa, breathing room air) was observed in the MK group at 5 minutes after drug administration. The highest PaCO2 (61mm Hg, 8.1 kPa) was observed in MK group at 30 minutes after drug injection. Co-administration of glycopyrrolate did not prevent bradycardia in all three groups. The lowest heart rate (23 beats minÿ1) was observed at 20 minutes after MB administration. Mean blood pressure signi¢cantly increased from baseline values (100 25 mm Hg), reached peak value (190 210 mm Hg) at 30 minutes following drug administration and remained signi¢cantly elevated throughout the experiment in all three groups. Time to walking after atipamezole administration was similar between MB (21 23 minutes) and MK (24 2 3 minutes) group but was shorter with M (13 2 4 minutes). Recovery quality was reduced when atipamezole was injected IM at 40 minutes after MK administration. It was concluded that MB and MK were more e¡ective in inducing lateral recumbency, endotracheal intubation and more consistent analgesia than M alone.
Effects of pre-emptive atropine on medetomidine induced bradycardia in dogs JCH Ko,* RE Mandsager,* CJ McGrath,* SM Fox Oklahoma State University, Stillwater, OK, USA. The cardiorespiratory e¡ects of atropine (0.04 mg kgÿ1 IM) administered 10 minutes before IM administration of medetomidine (M) were assessed in 12 healthy dogs (1.5^ 2 years old, weighing 18.5^22 kg) randomly assigned to each of six treatments in a crossover study. The groups were medetomidine 10, 20 and 40 mg kgÿ1 (M10, M20, 100
M40, respectively) with either atropine (A) or saline (S). A one-week interval was allowed between treatments. Direct arterial blood pressure, heart rate, respiratory rate and minute volume were recorded before drug administration, after administration of atropine or saline, and at1, 2, 5, 10, 15, 20, 30, 40, 50, 60 and 70 minutes after administration of medetomidine. Minute volume of the dog was measured via a face mask connected to a Wright's respirometer. Samples for arterial blood gas analysis were collected at the same time intervals and lead II of the ECG was monitored continuously. Quality of sedation and recovery were assessed. ANOVA for repeated measures and Tukey's test were used for analysis ( p < 0.05). Onset and duration of lateral recumbency was medetomidine dose dependent. Atropine treated groups (M10A: 67 24 minutes; M20A: 71 24 minutes; M40A: 84 2 4 minutes) had approximately 9 minutes shorter duration of lateral recumbency than saline controls (M10S: 76 2 4 minutes; M20S: 79 25 minutes; M40S: 94 2 5 minutes). Bradycardia was seen in all 12 dogs in the M10S (45 26 beats minÿ1), M20S (31 26 beats minÿ1) and M40S (33 2 5 beats minÿ1) groups. Bradycardias were seen in 1 of 12 dogs in the M10A and M20A groups, and 2 of 12 dogs in the M40A group. Mean arterial blood pressure (MAP) did not change signi¢cantly from baseline values following M10S and M20S administration. In contrast, MAP signi¢cantly increased from baseline value (100 212 mm Hg) following M40S (130 214 mm Hg), M10A (175 28 mm Hg), M20A (190 210 mm Hg) and M40A (200 213 mm Hg) administration. Hypertension (mean BP >160 mm Hg) was observed in all atropine treated groups. Blood gas values were all within normal ranges at all times with all treatments and was not signi¢cantly di¡erent from baseline. It was concluded that administration of atropine (0.04 mg kgÿ1 IM) 10 minutes before administration of medetomidine (10 or 20 mg kg ÿ1 IM) prevented the majority of the dogs from developing bradycardia but induced hypertension.
Comparison of propofol and etomidate for anesthetic induction in bulldogs E Robinson,* S Sanderson, C Natalini, C Osborne University of Minnesota, St. Paul, MN, USA. Endotracheal intubation and anesthetic induction are high risk procedures in brachycephalic dogs. Six Bulldogs were used in a crossover study to compare propofol and etomidate as induction agents. Five English Bulldogs (4 M, 1 F, mean wt. 23.8 kg, mean age 6.6 years) and 1 French Bulldog (M, 11.8 kg, 1.8 years) were anesthetized twice at least 5 months apart. Dogs were assigned pre-anesthetic ASA physical status of III; all had clinical signs of urolithiasis and three of the English Bulldogs were under treatment for dilated cardiomyopathy (CM). Dogs received VeterinaryAnaesthesia and Analgesia, 2000 , 27, 97^112
The effect of glycopyrrolate on the cardiopulmonary response to high and low dose romi®dine sedation in dogs MD Sinclair,WN McDonell,* GR Pettifer* University of Guelph, Guelph, Ontario, Canada. The purpose of this study was to investigate the electrocardiographic (ECG) and cardiopulmonary response of VeterinaryAnaesthesia and Analgesia, 2000 , 27, 97^112
glycopyrrolate (G, 10 mg kgÿ1 IM) as a pretreatment (p) or administered concurrently (c) with romi¢dine (RO) SQ in dogs. Healthy adult dogs (3 M, 3F, 18.5^25 kg) were utilized in a randomized cross over experiment. Anesthesia was induced by face mask and maintained with iso£urane for instrumentation. Dogs were acclimatized for at least 30 minutes after recovery from anesthesia, baseline measurements were recorded and one of the treatments was administered: T1, 0.5 mL saline (S) (p) RO 40 mg kgÿ1; T2, G (p) RO (40 mg kgÿ1; T3, S (p) RO 120 mg kgÿ1; T4, G (p) RO 120 mg kgÿ1; T5, S (p) G (c) RO 120 mg kgÿ1. Measurements were repeated 15 minutes after G (p) or S (p); RO or G (c) RO were administered 20 minutes after G(p) or S(p), and further measurements were taken at 10, 20, 30, 60 and 90 minutes. A continuous lead II ECG, arterial and mixed venous blood gases, heart rate (HR), respiratory rate (RR), systemic arterial blood pressures (SAP, MAP, DAP), cardiac index (CI), pulmonary arterial (PAP) and wedge pressure (PCWP) were measured. Systemic vascular resistance (SVR), oxygen extraction ratios (VO2/DO2) and pulmonary shunt fractions were calculated. Data were analyzed by use of ANOVA for repeated measures with an LSD post-hoc test and 95% con¢dence level. Glycopyrrolate increased HR, SAP and CI. Respective values (mean 2 SD) at 30 minutes were as follows: T1, 77 2 13 (beats minÿ1), 157 220 (mm Hg), 86 2 9 (ml kg ÿ1 minÿ1); T2, 161 232, 202 268, 150 2 20; T3, 60 219, 157 228, 66 230; T4, 163 224, 267 227, 100 2 0. SVR showed a four-fold increase with all treatments. Heart block (2 AV) was noted in T1, T3 and T5, with T5 demonstrating variable conduction and high grade AV block (6 : 1) versus T1 (2 : 1) and T3 (2 : 1). T5 was associated with a higher frequency of 2 AV heart block and ventricular escape beats (2/5 dogs) at10 and 20 minutes. In conclusion, G prevented the reduction in CI associated with RO, however, the resultant tachycardia along with the increase in SAP and SVR, especially with T4, could be detrimental to myocardial function. Due to the increase in dysrhythmias, the concurrent administration of RO and G cannot be recommended.
Comparison of sedative and cardiorespiratory effects of medetomidine-butorphanol and medetomidine-ketamine combination in dogs JCH Ko,* RE Mandsager,* CJ McGrath,* SM Fox Oklahoma State University, Stillwater, OK, USA. The sedative and cardiorespiratory e¡ects of intramuscular medetomidine (M, 30 mg kgÿ1), medetomidine-butorphanol (MB, 30 mg kgÿ1 ÿ0.2 mg kg ÿ1) and medetomidineketamine (MK, 30 mg kgÿ1ÿ3 mg kg ÿ1) were compared in a randomized crossover study using six dogs (1.5 2 0.3 99
Proceedings of the American College of VeterinaryAnesthesiologists annual meeting, Dallas,Texas, 1999 years old and weighing 20.2 2 2.3 kg). Glycopyrrolate (0.01mg kgÿ1 IM) was co-administered with each drug combination. Atipamezole (150 mg kg ÿ1 IM) was given 40 minutes after each drug combination and recovery quality was assessed. One week was allowed between treatments. Direct arterial blood pressure, heart rate, respiratory rate and minute volume were recorded before and 5, 10, 20, 30 and 40 minutes after drug administration and again at 5 and 10 minutes after atipamezole injection. Samples for arterial blood gas analysis were collected at the same time intervals, and lead II of the ECG was monitored continuously. Minute volume was measured via a face mask connected to a Wright's respirometer. ANOVA for repeated measures and Tukey's test were used for analysis ( p < 0.05). All three combinations resulted in lateral recumbency within 6 minutes with the exception of one dog in the M group. Endotracheal intubation was easily achieved at 13 minutes following drug administration in both MB and MK, but was more di¤cult in M group. Analgesic duration, as assessed by tail clamp and needle prick, were 40 2 0, 38 2 4 and 34 212 minutes for MB, MK and M groups, respectively. The lowest PaO2 (60 mm Hg, 8 kPa, breathing room air) was observed in the MK group at 5 minutes after drug administration. The highest PaCO2 (61mm Hg, 8.1 kPa) was observed in MK group at 30 minutes after drug injection. Co-administration of glycopyrrolate did not prevent bradycardia in all three groups. The lowest heart rate (23 beats minÿ1) was observed at 20 minutes after MB administration. Mean blood pressure signi¢cantly increased from baseline values (100 25 mm Hg), reached peak value (190 210 mm Hg) at 30 minutes following drug administration and remained signi¢cantly elevated throughout the experiment in all three groups. Time to walking after atipamezole administration was similar between MB (21 23 minutes) and MK (24 2 3 minutes) group but was shorter with M (13 2 4 minutes). Recovery quality was reduced when atipamezole was injected IM at 40 minutes after MK administration. It was concluded that MB and MK were more e¡ective in inducing lateral recumbency, endotracheal intubation and more consistent analgesia than M alone.
Effects of pre-emptive atropine on medetomidine induced bradycardia in dogs JCH Ko,* RE Mandsager,* CJ McGrath,* SM Fox Oklahoma State University, Stillwater, OK, USA. The cardiorespiratory e¡ects of atropine (0.04 mg kgÿ1 IM) administered 10 minutes before IM administration of medetomidine (M) were assessed in 12 healthy dogs (1.5^ 2 years old, weighing 18.5^22 kg) randomly assigned to each of six treatments in a crossover study. The groups were medetomidine 10, 20 and 40 mg kgÿ1 (M10, M20, 100
M40, respectively) with either atropine (A) or saline (S). A one-week interval was allowed between treatments. Direct arterial blood pressure, heart rate, respiratory rate and minute volume were recorded before drug administration, after administration of atropine or saline, and at1, 2, 5, 10, 15, 20, 30, 40, 50, 60 and 70 minutes after administration of medetomidine. Minute volume of the dog was measured via a face mask connected to a Wright's respirometer. Samples for arterial blood gas analysis were collected at the same time intervals and lead II of the ECG was monitored continuously. Quality of sedation and recovery were assessed. ANOVA for repeated measures and Tukey's test were used for analysis ( p < 0.05). Onset and duration of lateral recumbency was medetomidine dose dependent. Atropine treated groups (M10A: 67 24 minutes; M20A: 71 24 minutes; M40A: 84 2 4 minutes) had approximately 9 minutes shorter duration of lateral recumbency than saline controls (M10S: 76 2 4 minutes; M20S: 79 25 minutes; M40S: 94 2 5 minutes). Bradycardia was seen in all 12 dogs in the M10S (45 26 beats minÿ1), M20S (31 26 beats minÿ1) and M40S (33 2 5 beats minÿ1) groups. Bradycardias were seen in 1 of 12 dogs in the M10A and M20A groups, and 2 of 12 dogs in the M40A group. Mean arterial blood pressure (MAP) did not change signi¢cantly from baseline values following M10S and M20S administration. In contrast, MAP signi¢cantly increased from baseline value (100 212 mm Hg) following M40S (130 214 mm Hg), M10A (175 28 mm Hg), M20A (190 210 mm Hg) and M40A (200 213 mm Hg) administration. Hypertension (mean BP >160 mm Hg) was observed in all atropine treated groups. Blood gas values were all within normal ranges at all times with all treatments and was not signi¢cantly di¡erent from baseline. It was concluded that administration of atropine (0.04 mg kgÿ1 IM) 10 minutes before administration of medetomidine (10 or 20 mg kg ÿ1 IM) prevented the majority of the dogs from developing bradycardia but induced hypertension.
Comparison of propofol and etomidate for anesthetic induction in bulldogs E Robinson,* S Sanderson, C Natalini, C Osborne University of Minnesota, St. Paul, MN, USA. Endotracheal intubation and anesthetic induction are high risk procedures in brachycephalic dogs. Six Bulldogs were used in a crossover study to compare propofol and etomidate as induction agents. Five English Bulldogs (4 M, 1 F, mean wt. 23.8 kg, mean age 6.6 years) and 1 French Bulldog (M, 11.8 kg, 1.8 years) were anesthetized twice at least 5 months apart. Dogs were assigned pre-anesthetic ASA physical status of III; all had clinical signs of urolithiasis and three of the English Bulldogs were under treatment for dilated cardiomyopathy (CM). Dogs received VeterinaryAnaesthesia and Analgesia, 2000 , 27, 97^112