Objective—To determine and compare levels of
sedation achieved by IM administration of diphenhydramine,
saline (0.9% NaCl) solution, and acepromazine
Design—Prospective randomized study.
Procedure—Dogs were randomly assigned to
receive diphenhydramine at 2, 4, or 8 mg/kg (0.9, 1.8,
or 3.6 mg/lb, respectively) IM; acepromazine at 0.1
mg/kg (0.05 mg/lb) IM; or saline solution at 0.05
mL/kg (0.02 mL/lb) IM. Sedation was assessed by
use of a 6-category descriptive system based on
observation and interaction.
Results—Dogs in the acepromazine group had significantly
higher sedation scores than did dogs in the
saline solution or diphenhydramine groups at 30 minutes.
Dogs in the diphenhydramine groups did not
have significantly different sedation scores from dogs
in the saline solution group at any time point.
Conclusions and Clinical Relevance—Diphenhydramine
did not cause clinically appreciable sedation in
healthy dogs. Diphenhydramine is not suitable as a sole
sedative prior to general anesthesia in dogs. (J Am Vet
Med Assoc 2005;226:1092–1094)
Objective—To determine the association among signalment, health status, other clinical variables, and treatments and events during cardiopulmonary cerebral resuscitation (CPCR) with the return of spontaneous circulation (ROSC) for animals with cardiopulmonary arrest (CPA) in a veterinary teaching hospital.
Animals—161 dogs and 43 cats with CPA.
Procedures—Data were gathered during a 60-month period on animals that had CPA and underwent CPCR. Logistic regression was used to evaluate effects of multiple predictors for ROSC.
Results—56 (35%) dogs and 19 (44%) cats had successful CPCR. Twelve (6%) animals (9 dogs and 3 cats) were discharged from the hospital. Successfully resuscitated dogs were significantly more likely to have been treated with mannitol, lidocaine, fluids, dopamine, corticosteroids, or vasopressin; had CPA while anesthetized; received chest compressions while positioned in lateral recumbency; and had a suspected cause of CPA other than hemorrhage or anemia, shock, hypoxemia, multiple organ dysfunction syndrome, cerebral trauma, malignant arrhythmia, or an anaphylactoid reaction and were less likely to have been treated with multiple doses of epinephrine, had a longer duration of CPA, or had multiple disease conditions, compared with findings in dogs that were not successfully resuscitated. Successfully resuscitated cats were significantly more likely to have had more people participate in CPCR and less likely to have had shock as the suspected cause of CPA, compared with findings in cats that were not successfully resuscitated.
Conclusions and Clinical Relevance—The prognosis was grave for animals with CPA, except for those that had CPA while anesthetized.
OBJECTIVE To determine the minimum infusion rate (MIR) of propofol required to prevent movement in response to a noxious stimulus in dogs anesthetized with propofol alone or propofol in combination with a constant rate infusion (CRI) of ketamine.
ANIMALS 6 male Beagles.
PROCEDURES Dogs were anesthetized on 3 occasions, at weekly intervals, with propofol alone (loading dose, 6 mg/kg; initial CRI, 0.45 mg/kg/min), propofol (loading dose, 5 mg/kg; initial CRI, 0.35 mg/kg/min) and a low dose of ketamine (loading dose, 2 mg/kg; CRI, 0.025 mg/kg/min), or propofol (loading dose, 4 mg/kg; initial CRI, 0.3 mg/kg/min) and a high dose of ketamine (loading dose, 3 mg/kg; CRI, 0.05 mg/kg/min). After 60 minutes, the propofol MIR required to prevent movement in response to a noxious electrical stimulus was determined in duplicate.
RESULTS Least squares mean ± SEM propofol MIRs required to prevent movement in response to the noxious stimulus were 0.76 ± 0.1 mg/kg/min, 0.60 ± 0.1 mg/kg/min, and 0.41 ± 0.1 mg/kg/min when dogs were anesthetized with propofol alone, propofol and low-dose ketamine, and propofol and high-dose ketamine, respectively. There were significant decreases in the propofol MIR required to prevent movement in response to the noxious stimulus when dogs were anesthetized with propofol and low-dose ketamine (27 ± 10%) or with propofol and high-dose ketamine (30 ± 10%).
CONCLUSIONS AND CLINICAL RELEVANCE Ketamine, at the doses studied, significantly decreased the propofol MIR required to prevent movement in response to a noxious stimulus in dogs.
Objective—To compare the effectiveness of preoperative
PO and SC administration of buprenorphine and
meloxicam for prevention of postoperative pain-associated
behaviors in cats undergoing ovariohysterectomy.
Design—Randomized controlled study.
Animals—51 female cats (4 to 60 months old; weight
range, 1.41 to 4.73 kg [3.1 to 10.4 lb]).
Procedure—Cats received 1 of 5 treatments at the time
of anesthetic induction: buprenorphine PO (0.01 mg/kg
[0.0045 mg/lb]; n = 10), buprenorphine SC (0.01 mg/kg;
10), meloxicam SC (0.3 mg/kg [0.14 mg/lb]; 10), meloxicam
PO (0.3 mg/kg; 10), or 0.3 mL of sterile saline (0.9%
NaCl) solution SC (control group; 11). Sedation scores
and visual analog scale and interactive visual analog
scale (IVAS) pain-associated behavior scores were
assigned to each cat 2 hours before and at intervals until
20 hours after surgery.
Results—Cats receiving meloxicam PO or SC had
significantly lower IVAS scores (2.91 and 2.02,
respectively), compared with IVAS scores for cats
receiving buprenorphine PO (7.55). Pain-associated
behavior scores for cats administered buprenorphine
or meloxicam PO or SC preoperatively did not differ
significantly from control group scores. Rescue analgesia
was not required by any of the cats receiving
meloxicam, whereas 3 of 10 cats receiving buprenorphine
PO, 2 of 10 cats receiving buprenorphine SC,
and 1 of 11 cats receiving the control treatment
required rescue analgesia.
Conclusions and Clinical Relevance—On the basis
of pain-associated behavior scores, cats receiving
meloxicam PO or SC before ovariohysterectomy
appeared to have less pain after surgery than those
receiving buprenorphine PO preoperatively. (J Am Vet Med Assoc 2005;227:1937–1944)
Objective—To investigate the effects of the concurrent administration of 70% N2O on the minimum alveolar concentration (MAC) for sevoflurane in dogs, the MAC derivative that blocks motor movement (MACNM), and the MAC derivative that blocks autonomic responses (MACBAR).
Animals—7 adult sexually intact male mixed-breed dogs.
Procedures—For each dog, anesthesia was induced with sevoflurane delivered via a face mask. Initially, the baseline MAC, MACNM, and MACBAR for sevoflurane were determined by use of a noxious stimulus (50 V, 50 Hz, and 10 milliseconds) applied subcutaneously over a midulnar region. Nitrous oxide (70%) was added to the breathing circuit, and MAC, MACNM, and MACBAR were determined again. Percentage changes from the respective baseline concentrations for MAC, MACNM’ and MACBAR were calculated after the administration of N2O.
Results—Baseline median values for the MAC, MACNM, and MACBAR for sevoflurane were 1.75%, 2.00%, and 2.50%, respectively. Addition of 70% N2O significantly decreased MAC, MACNM, and MACBAR by 24.4%, 25.0%, and 35.2%, respectively, and these values did not differ significantly from each other.
Conclusions and Clinical Relevance—Supplementation with 70% N2O caused a clinically important and significant decrease in the MAC, MACNM’ and MACBAR for sevoflurane in dogs.
Objective—To evaluate antinociceptive and selected effects associated with IM administration of xylazine hydrochloride in combination with tiletamine-zolazepam in llamas.
Animals—8 adult male llamas.
Procedures—Each llama received tiletamine-zolazepam (2 mg/kg) combined with either xylazine (0.1, 0.2, or 0.4 mg/kg) or saline (0.9% NaCl) solution IM (treatments designated as TZ-Xy0.1, TZ-Xy0.2, TZ-Xy0.4, and TZ-Sal, respectively) at 1-week intervals. Selected cardiorespiratory variables were assessed during lateral recumbency and anesthesia, and recovery characteristics were recorded. Duration of antinociception was evaluated by clamping a claw every 5 minutes.
Results—Interval between treatment administration and lateral recumbency for TZ-Xy0.4 was shorter than that for TZ-Xy0.1 or TZ-Sal. Mean ± SEM duration of antinociception was longer for TZ-Xy0.4 (51.3 ± 7. 0 minutes), compared with findings for TZ-Xy0.2 (31.9 ± 6.0 minutes), TZ-Xy0.1 (8.1 ± 4.0 minutes), and TZ-Sal (0.6 ± 0.6 minutes). Interval between treatment administration and standing was longer for TZ-Xy0.4 (112 ± 9 minutes) than it was for TZ-Xy0.2 (77 ± 9 minutes) or TZ-Sal (68 ± 9 minutes). Mean heart and respiratory rates during the first 30 minutes for TZ-Sal exceeded values for the other treatments. Administration of TZ-Xy0.2 and TZ-Xy0.4 resulted in Pao2 < 60 mm Hg at 5 minutes after llamas attained lateral recumbency, and values differed from TZ-Sal findings at 5, 10, and 15 minutes; Paco2 was greater for TZ-Xy0.2 and TZ-Xy0.4 than for TZ-Sal at 5, 10, 15, and 20 minutes.
Conclusions and Clinical Relevance—Xylazine (0.2 and 0.4 mg/kg) increased the duration of antinociception in llamas anesthetized with tiletamine-zolazepam.
OBJECTIVE To evaluate the effect of MgSO4, alone and in combination with propofol, on the minimum alveolar concentration preventing motor movement (MACNM) in sevoflurane-anesthetized dogs.
ANIMALS 6 healthy purpose-bred adult male Beagles (least squares mean ± SEM body weight, 12.0 ± 1.1 kg).
PROCEDURES Dogs were anesthetized 3 times at weekly intervals. The MACNM was measured 45 minutes after induction of anesthesia (baseline; MACNM-B) and was determined each time by use of a noxious electrical stimulus. Treatments were administered as a loading dose and constant rate infusion (CRI) as follows: treatment 1, MgSO4 loading dose of 45 mg/kg and CRI of 15 mg/kg/h; treatment 2, propofol loading dose of 4 mg/kg and CRI of 9 mg/kg/h; and treatment 3, MgSO4 and propofol combination (same doses used previously for each drug). A mixed-model ANOVA and Tukey-Kramer tests were used to determine effects of each treatment on the percentage decrease from MACNM-B. Data were reported as least squares mean ± SEM values.
RESULTS Decrease from MACNM-B was 3.4 ± 3.1%, 48.3 ± 3.1%, and 50.3 ± 3.1%, for treatments 1, 2, and 3, respectively. The decrease for treatments 2 and 3 was significantly different from that for treatment 1; however, no significant difference existed between results for treatments 2 and 3.
CONCLUSIONS AND CLINICAL RELEVANCE MgSO4 did not affect MACNM, nor did it potentiate the effects of propofol on MACNM. Administration of MgSO4 in this study appeared to provide no clinical advantage as an anesthetic adjuvant.
Objective—To evaluate the effect of IV administration of tramadol hydrochloride on the minimum alveolar concentration of isoflurane (ISOMAC) that prevented purposeful movement of rabbits in response to a noxious stimulus.
Animals—Six 6- to 12-month-old female New Zealand White rabbits.
Procedures—Anesthesia was induced and maintained with isoflurane in oxygen. A baseline ISOMAC was determined by clamping a pedal digit with sponge forceps until gross purposeful movement was detected or a period of 60 seconds elapsed. Subsequently, tramadol (4.4 mg/kg) was administered IV and the posttreatment ISOMAC (ISOMACT) was measured.
Results—Mean ± SD ISOMAC and ISOMACT values were 2.33 ± 0.13% and 2.12 ± 0.17%, respectively. The ISOMAC value decreased by 9 ± 4% after tramadol was administered. Plasma tramadol and its major metabolite (M1) concentrations at the time of ISOMACT determination varied widely (ranges, 181 to 636 ng/mL and 32 to 61 ng/mL, respectively). Intervals to determination of ISOMACT and plasma tramadol and M1 concentrations were not correlated with percentage change in the ISOMAC. Heart rate decreased significantly immediately after tramadol administration but by 10 minutes afterward was not different from the pretreatment value. Systolic arterial blood pressure decreased to approximately 60 mm Hg for approximately 5 minutes in 3 rabbits after tramadol administration. No adverse effects were detected.
Conclusions and Clinical Relevance—As administered, tramadol had a significant but clinically unimportant effect on the ISOMAC in rabbits. Higher doses of tramadol may provide clinically important reductions but may result in a greater degree of cardiovascular depression.
OBJECTIVE To determine effects of fentanyl, lidocaine, and a fentanyl-lidocaine combination on the minimum alveolar concentration of sevoflurane preventing motor movement (MACNM) in dogs.
ANIMALS 6 adult Beagles.
PROCEDURES Dogs were anesthetized with sevoflurane in oxygen 3 times (1-week intervals). Baseline MACNM (MACNM-B) was determined starting 45 minutes after induction of anesthesia. Dogs then received 1 of 3 treatments IV: fentanyl (loading dose, 15 μg/kg; constant rate infusion [CRI], 6 μg/kg/h), lidocaine (loading dose, 2 mg/kg; CRI, 6 mg/kg/h), and the fentanyl-lidocaine combination at the same doses. Determination of treatment MACNM (MACNM-T) was initiated 90 minutes after start of the CRI. Venous blood samples were collected at the time of each treatment MACNM measurement for determination of plasma concentrations of fentanyl and lidocaine.
RESULTS Mean ± SEM overall MACNM-B for the 3 treatments was 2.70 ± 0.27 vol%. The MACNM decreased from MACNM-B to MACNM-T by 39%, 21%, and 55% for fentanyl, lidocaine, and the fentanyl-lidocaine combination, respectively. This decrease differed significantly among treatments. Plasma fentanyl concentration was 3.25 and 2.94 ng/mL for fentanyl and the fentanyl-lidocaine combination, respectively. Plasma lidocaine concentration was 2,570 and 2,417 ng/mL for lidocaine and the fentanyl-lidocaine combination, respectively. Plasma fentanyl and lidocaine concentrations did not differ significantly between fentanyl and the fentanyl-lidocaine combination or between lidocaine and the fentanyl-lidocaine combination.
CONCLUSIONS AND CLINICAL RELEVANCE CRIs of fentanyl, lidocaine, and the fentanyl-lidocaine combination at the doses used were associated with clinically important and significant decreases in the MACNM of sevoflurane in dogs.