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- Author or Editor: Carolina H. Riccó x
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Abstract
Objective—To compare the hemodynamic responses to orotracheal intubation following induction of anesthesia with propofol, ketamine-propofol, and ketamine-diazepam in premedicated dogs.
Design—Prospective, randomized, masked study.
Animals—10 healthy adult Beagles.
Procedures—Dogs were randomly allocated to be anesthetized twice, with a 1-week wash-out interval, by means of 2 of 3 possible protocols (propofol [4 mg/kg {1.8 mg/lb}, n = 6 dogs], ketamine [2 mg/kg {0.9 mg/lb}] and propofol [2 mg/kg; 7], or ketamine [5 mg/kg {2.3 mg/lb}] and diazepam [0.2 mg/kg {0.09 mg/lb}; 6]). After instrumentation, continuous heart rate, systolic arterial blood pressure, mean arterial blood pressure, diastolic arterial blood pressure, cardiac index, stroke volume index, and systemic vascular resistance were recorded. Fifteen minutes after premedication, dogs were anesthetized; all anesthetics were administered IV. After 5 minutes, orotracheal intubation was performed without the use of a laryngoscope. Data were collected prior to intubation (baseline), at intubation, and 30, 60, 90, 120, 150, and 180 seconds thereafter. Results were compared among the 3 groups and over time.
Results—No differences among groups were observed for any variables studied. In all groups, arterial blood pressures were significantly decreased at various time points after intubation. A significant increase in systolic arterial blood pressure was observed between baseline and the 30-second time point in the ketamine-diazepam group. No significant differences were detected over time for the other variables in any group.
Conclusions and Clinical Relevance—Intubation after anesthetic induction with ketamine-diazepam caused transitory hypertension, whereas intubation after induction with propofol or ketamine-propofol did not cause cardiovascular stimulation. In dogs in which hypertension is a concern, propofol or ketamine-propofol may be a better choice for induction prior to orotracheal intubation.
Abstract
Objective—To evaluate the cardiorespiratory effects of IV administration of propofol (4 mg/kg), ketamine hydrochloride and propofol (2 mg/kg each; K-P), or ketamine hydrochloride (5 mg/kg) and diazepam (0.2 mg/kg; K-D) before and after induction of anesthesia (IoA) in dogs sedated with acepromazine maleate and oxymorphone hydrochloride.
Animals—10 healthy adult Beagles.
Procedures—Each dog was randomly allocated to receive 2 of 3 treatments (1-week interval). For instrumentation prior to each treatment, each dog was anesthetized with isoflurane. After full recovery, acepromazine (0.02 mg/kg) and oxymorphone (0.05 mg/kg) were administered IV. Fifteen minutes later (before IoA), each dog received treatment IV with propofol, K-P, or K-D. Cardiorespiratory and arterial blood gas variables were assessed before, immediately after, and 5 minutes after IoA.
Results—Compared with findings before IoA, dogs receiving the K-P or K-D treatment had increased cardiac output, oxygen delivery, and heart rate 5 minutes after IoA; K-P administration did not change mean arterial blood pressure or stroke volume and decreased systemic vascular resistance. Propofol decreased mean arterial blood pressure and systemic vascular resistance immediately after IoA but did not change heart rate, cardiac output, or oxygen delivery. All treatments caused some degree of apnea, hypoventilation, and hypoxemia (Pao 2 < 80 mm Hg).
Conclusions and Clinical Relevance—In dogs, K-P treatment maintained mean arterial blood pressure better than propofol alone and increased heart rate, cardiac output, or oxygen delivery, as did the K-D treatment. Supplemental 100% oxygen should be provided during IoA with all 3 treatments.
Abstract
OBJECTIVE
To evaluate the sedative and cardiorespiratory effects of IM administration of alfaxalone and butorphanol combined with acepromazine, midazolam, or dexmedetomidine in dogs.
ANIMALS
6 young healthy mixed-breed hounds.
PROCEDURES
Dogs received each of 3 treatments (alfaxalone [2 mg/kg] and butorphanol [0.4 mg/kg] combined with acepromazine [0.02 mg/kg; AB-ace], midazolam [0.2 mg/kg; AB-mid], or dexmedetomidine [0.005 mg/kg; AB-dex], IM) in a blinded, randomized crossover-design study with a 1-week washout period between treatments. Sedation scores and cardiorespiratory variables were recorded at predetermined time points. Data were analyzed by use of mixed-model ANOVA and linear generalized estimating equations with post hoc adjustments.
RESULTS
All treatments resulted in moderate to deep sedation (median score, ≥ 15/21) ≤ 5 minutes after injection. Sedation scores did not differ among treatments until the 40-minute time point, when the score was higher for AB-dex than for other treatments. Administration of AB-dex resulted in median scores reflecting deep sedation until 130 minutes, versus 80 and 60 minutes for AB-ace and AB-mid, respectively, after injection. Heart rate, cardiac output, and oxygen delivery decreased significantly after AB-dex, but not AB-ace or AB-mid administration. Respiratory variables remained within clinically acceptable ranges after all treatments. Undesirable recovery characteristics were observed in 4 dogs after AB-mid treatment. Four dogs required atipamezole administration 180 minutes after AB-dex injection.
CONCLUSIONS AND CLINICAL RELEVANCE
All protocols produced reliable sedation. The results indicated that in young, healthy dogs, AB-mid may produce undesirable recovery characteristics; AB-dex treatment caused cardiovascular depression and should be used with caution.
Abstract
OBJECTIVE
To evaluate the pharmacokinetics and pharmacodynamics of naloxone hydrochloride in dogs following intranasal (IN) and IV administration.
ANIMALS
6 healthy adult mixed-breed dogs.
PROCEDURES
In a blinded crossover design involving 2 experimental periods separated by a washout period (minimum of 7 days), dogs were randomly assigned to receive naloxone IN (4 mg via a commercially available fixed-dose naloxone atomizer; mean ± SD dose, 0.17 ± 0.02 mg/kg) or IV (0.04 mg/kg) in the first period and then the opposite treatment in the second period. Plasma naloxone concentrations, dog behavior, heart rate, and respiratory rate were evaluated for 24 hours/period.
RESULTS
Naloxone administered IN was well absorbed after a short lag time (mean ± SD, 2.3 ± 1.4 minutes). Mean maximum plasma concentration following IN and IV administration was 9.3 ± 2.5 ng/mL and 18.8 ± 3.9 ng/mL, respectively. Mean time to maximum concentration following IN administration was 22.5 ± 8.2 minutes. Mean terminal half-life after IN and IV administration was 47.4 ± 6.7 minutes and 37.0 ± 6.7 minutes, respectively. Mean bioavailability of naloxone administered IN was 32 ± 13%. There were no notable changes in dog behavior, heart rate, or respiratory rate following naloxone administration by either route.
CONCLUSIONS AND CLINICAL RELEVANCE
Use of a naloxone atomizer for IN naloxone administration in dogs may represent an effective alternative to IV administration in emergency situations involving opioid exposure. Future studies are needed to evaluate the efficacy of IN naloxone administration in dogs with opioid intoxication, including a determination of effective doses.
Abstract
OBJECTIVE
To compare cardiac output (CO) measurements by transesophageal echocardiography (TEECO) and esophageal Doppler monitor (EDMCO) with pulmonary artery thermodilution (PATDCO) in anesthetized dogs subjected to pharmacological interventions. The effect of treatments on EDM-derived indexes was also investigated.
ANIMALS
6 healthy male dogs (10.8 ± 0.7 kg).
METHODS
Dogs were anesthetized with propofol and isoflurane, mechanically ventilated, and monitored with invasive mean arterial pressure (MAP), end-tidal isoflurane concentration (ETISO), PATDCO, TEECO, EDMCO, and EDM-derived indexes. Four treatments were administered to all dogs by randomization. Baseline data were collected before each treatment: (1) dobutamine infusion; (2) esmolol infusion; (3) phenylephrine infusion; and (4) ETISO > 3%. Data were collected after 10-minute stabilization and after 30 minutes of washout between treatments. Statistical tests were pairwise t test, Bland-Altman analysis, Lin's concordance correlation (ρc), and polar plot analysis with P < .05 set as significance.
RESULTS
The mean ± SD relative bias (limits of agreement) for TEECO was 0.35 ± 25.2% (−49.1% to 49.8%) and for EDMCO was −27.2 ± 22.5% (−71.4% to 17%) versus PATDCO. The percent error for TEECO and EDMCO was 27.6% and 44.1%, respectively. The ρc value was 0.82 for TEECO and 0.66 for EDMCO. TEECO and EDMCO showed good trending ability. EDM-derived indexes displayed significant changes specific to the drug administered (P < .001).
CLINICAL RELEVANCE
For minimally invasive CO monitoring, TEE may provide more favorable performance than EDM in clinical settings; however, EDM-derived indexes yield valuable hemodynamic information that reliably follows trends in CO, thus supporting critical decision-making in canine patients.
Abstract
OBJECTIVE
To investigate the effects of a priming dose of alfaxalone on the total anesthetic induction dose for and cardiorespiratory function of sedated healthy cats.
ANIMALS
8 healthy adult cats.
PROCEDURES
For this crossover study, cats were sedated with dexmedetomidine and methadone administered IM. Cats next received a priming induction dose of alfaxalone (0.25 mg/kg, IV) or saline (0.9% NaCl) solution (0.025 mL/kg, IV) over 60 seconds and then an induction dose of alfaxalone (0.5 mg/kg/min, IV) until orotracheal intubation was achieved. Cardiorespiratory variables were recorded at baseline (immediately prior to priming agent administration), immediately after priming agent administration, after orotracheal intubation, and every 2 minutes until extubation. The total induction dose of alfaxalone was compared between the 2 priming agents.
RESULTS
Mean ± SD total anesthetic induction dose of alfaxalone was significantly lower when cats received a priming dose of alfaxalone (0.98 ± 0.28 mg/kg), compared with when cats received a priming dose of saline solution (1.41 ± 0.17 mg/kg). Mean arterial blood pressure was significantly higher when alfaxalone was used as the priming dose. No cats became apneic or had a hemoglobin oxygen saturation of < 90%. Expired volume per minute was not significantly different between the 2 priming agents.
CONCLUSIONS AND CLINICAL RELEVANCE
Administration of a priming dose of alfaxalone to healthy sedated cats reduced the total dose of alfaxalone needed to achieve orotracheal intubation, maintained mean arterial blood pressure, and did not adversely impact the measured respiratory variables.
Abstract
OBJECTIVE
To determine pharmacokinetic and pharmacodynamic properties of the injectable formulation of dexmedetomidine administered via the oral transmucosal (OTM) route to healthy dogs.
ANIMALS
6 healthy dogs.
PROCEDURES
Injectable dexmedetomidine was administered IV (5 μg/kg) or via the OTM route (20 μg/kg) in a blinded, single-observer, randomized crossover study. Dogs received dexmedetomidine and a sham treatment at each administration. Serial blood samples were collected from a catheter in a saphenous vein. Heart rate, respiratory rate, and subjective sedation score were assessed for 24 hours after administration. Plasma samples were analyzed for dexmedetomidine concentrations by use of ultraperformance liquid chromatography–tandem mass spectrometry.
RESULTS
For the OTM route, the mean ± SD maximum plasma concentration was 3.8 ± 1.3 ng/mL, which was detected 73 ± 33 minutes after administration. The mean maximum concentration for the IV dose, when extrapolated to the time of administration, was 18.6 ± 3.3 ng/mL. The mean terminal-phase half-life was 152 ± 146 minutes and 36 ± 6 minutes for OTM and IV administration, respectively. After IV administration, total clearance was 8.0 ± 1.6 mL/min/kg and volume of distribution at steady state was 371 ± 72 mL/kg. Bioavailability for OTM administration of dexmedetomidine was 11.2 ± 4.5%. Peak sedation scores did not differ significantly between routes of administration. Decreases in heart rate, respiratory rate, and peak sedation score were evident sooner after IV administration.
CONCLUSIONS AND CLINICAL RELEVANCE
OTM administration of the injectable formulation of dexmedetomidine resulted in a similar degree of sedation and prolonged duration of action, compared with results for IV administration, despite relatively low bioavailability.
Abstract
OBJECTIVE
To determine the effect of oral administration of gabapentin (20 mg/kg) on the minimum alveolar concentration (MAC) of isoflurane in dogs.
ANIMALS
6 healthy adult dogs (3 males and 3 females with a mean ± SD body weight of 24.8 ± 1.3 kg).
PROCEDURES
Each dog was anesthetized twice. Dogs were initially assigned to 1 of 2 treatments (gabapentin [20 mg/kg, PO] followed 2 hours later by anesthesia maintained with isoflurane or anesthesia maintained with isoflurane alone). A minimum of 7 days later, dogs received the other treatment. The MAC of isoflurane was determined by use of an iterative bracketing technique with stimulating electrodes placed in the maxillary buccal mucosa. Hemodynamic variables and vital parameters were recorded at the lowest end-tidal isoflurane concentration at which dogs did not respond to the stimulus. Effect of treatment on outcome variables was analyzed by use of a paired t test.
RESULTS
Mean ± SD MAC of isoflurane was significantly lower when dogs received gabapentin and isoflurane (0.71 ± 0.12%) than when dogs received isoflurane alone (0.91 ± 0.26%). Mean reduction in MAC of isoflurane was 20 ± 14%. Hemodynamic variables did not differ significantly between treatments. Mean time to extubation was significantly less when dogs received gabapentin and isoflurane (6 ± 4 minutes) than when dogs received isoflurane alone (23 ± 15 minutes).
CONCLUSIONS AND CLINICAL RELEVANCE
Oral administration of gabapentin 2 hours before anesthesia maintained with isoflurane had a MAC-sparing effect with no effect on hemodynamic variables or vital parameters of dogs.
Abstract
OBJECTIVE
To determine the pharmacokinetics and pharmacodynamics of dexmedetomidine after IM administration in dogs.
ANIMALS
6 healthy adult purpose-bred dogs (3 males, 3 females) with a mean ± SD body weight of 25.2 ± 1.8 kg.
PROCEDURES
Each dog received 10 µg/kg dexmedetomidine, IM. Heart rate and respiratory rate were counted via cardiac auscultation and visual assessment of chest excursions. Sedation was assessed utilizing 2 sedation scoring systems. Plasma concentrations were determined using ultra performance liquid chromatography–mass spectrometry. Plasma concentrations versus time data after IM dexmedetomidine were analyzed using noncompartmental analysis for extravascular administration.
RESULTS
Over the first 2 hours following IM injection of dexmedetomidine, plasma concentrations fluctuated in each dog. The geometric mean (range) maximum plasma concentration was 109.2 (22.4 to 211.5) ng/mL occurring at 20.5 (5 to 75) minutes, and the mean half-life was 25.5 (11.5 to 41.5) minutes. Heart rate was significantly lower than baseline from 30 minutes to 2 hours postdexmedetomidine administration, and respiratory rate was significantly lower than baseline from 45 minutes to 1.75 hours. Dogs were significantly more sedated from 30 minutes to 1.5 hours postdexmedetomidine administration. Median time to onset of sedation was 7.5 minutes (range, 2 to 10 minutes), and median time to peak sedation was 30 minutes (range, 15 to 60 minutes).
CLINICAL RELEVANCE
Variations in plasma concentrations occurred in all dogs for the 2 hours postinjection of dexmedetomidine at 10 µg/kg, IM. This was likely due to alterations in absorption due to dexmedetomidine-induced local vasoconstriction. Despite variable plasma concentrations, all dogs were sedated following IM dexmedetomidine administration.
