OBJECTIVE To evaluate effects of 2 levels of partial neuromuscular block on the ventilatory response to a hypercapnic challenge in anesthetized dogs and to evaluate effects of edrophonium for reversing partial neuromuscular block.
ANIMALS 6 healthy adult Beagles.
PROCEDURES Each dog was anesthetized twice with propofol and dexmedetomidine. End-tidal partial pressure of CO2 (Petco2), tidal volume (Vt), and peak inspiratory flow (PIF) were measured during breathing at rest. Maximal Vt and PIF (VtMAX and PIFMAX, respectively) in response to a hypercapnic challenge consisting of 10% CO2 inhaled for 1 minute were measured. Variables were measured before administration of atracurium (baseline), during moderate (train-of-four [TOF] ratio, 0.3 to 0.5) and mild (TOF ratio, 0.6 to 0.8) atracurium-induced neuromuscular block, and after neuromuscular block recovery (TOF ratio, ≥ 0.9) following administration of edrophonium or saline (0.9% NaCl) solution. Dogs for which any variable returned to < 80% of the baseline value were identified.
RESULTS Partial neuromuscular block increased Petco2; it impaired Vt at rest and VtMAX but not PIF at rest and PIFMAX. All variables except Petco2 returned to baseline values when the TOF returned to ≥ 0.9. After recovery from neuromuscular block, significantly more dogs had a VtMAX < 80% of the baseline value when edrophonium was not administered.
CONCLUSIONS AND CLINICAL RELEVANCE Partial neuromuscular block in anesthetized Beagles decreased spontaneous ventilation at rest and impaired the response to a hypercapnic challenge. Response to hypercapnic challenge might remain partially impaired after recovery of the TOF ratio to ≥ 0.9.
To evaluate the cardiovascular effects of atipamezole administered at half the volume or the same volume as dexmedetomidine to isoflurane-anesthetized cats.
6 adult (1 to 2 years old) domestic shorthair cats (body weight, 3 to 6 kg).
Each cat was anesthetized with isoflurane and rocuronium 3 times; there was a 1-week washout period between successive anesthetic procedures. For each anesthetic procedure, dexmedetomidine (5 μg/kg) was administered IV. Five minutes after dexmedetomidine was administered, atipamezole (25 or 50 μg/kg) or saline (0.9% NaCl) solution was administered IM. Pulse rate, mean arterial blood pressure (MAP), cardiac output (CO), and systemic vascular resistance (SVR) were measured during anesthesia before dexmedetomidine administration (baseline), after dexmedetomidine administration, and 15, 30, 60, and 120 minutes after administration of atipamezole or saline solution. Pulse rate and MAP were also recorded when MAP was at its lowest value. Hemodynamic variables were compared among treatments at baseline, after dexmedetomidine administration, and after administration of atipamezole or saline solution. Effects of treatment and time on all variables were assessed with mixed-effects models.
Both doses of atipamezole resulted in a significantly lower MAP than did saline solution. Pulse rate, CO, and SVR were not significantly different among treatments after atipamezole or saline solution were administered.
CONCLUSIONS AND CLINICAL RELEVANCE
Atipamezole administered IM at half the volume or the same volume as dexmedetomidine was ineffective at increasing pulse rate or CO in anesthetized cats that received dexmedetomidine. However, atipamezole caused short-lasting but severe arterial hypotension.
To create a model of transient unilateral laryngeal paralysis (LP) that will allow the study of cricoarytenoideus dorsalis dysfunction and a method for quantification of varying degrees of LP in dogs.
5 castrated male research Beagles.
Between January and February 2018, dogs were anesthetized and instrumented with a laryngeal mask airway and a flexible endoscope to record the rima glottidis. The left or right recurrent laryngeal nerve (RLn) was localized using ultrasonography and electrical stimulation, then conduction blockade was induced with perineural lidocaine. The normalized glottal gap area (NGGA) was measured before and every 15 minutes after the block. Inspired 10% carbon dioxide (CO2) was administered for 1 minute at each sampling time. The inspiratory increase in NGGA (total and each side) was measured at peak inspiration. The change in hemi-NGGA for the control side versus the anesthetized side was evaluated with a mixed-effect model.
During CO2 stimulation, the increase in inspiratory hemi-NGGA was consistently less (P < .001) for the treated side (–8% to 13%) versus the control side (49% to 82%). A compensatory increase (larger than at baseline) in the control hemi-NGGA was observed. The total NGGA remained unaffected.
Unilateral local anesthesia of the RLn produced transient unilateral LP with a compensatory increase in the hemi-NGGA for the contralateral side. This model could facilitate the evaluation of respiratory dynamics, establishment of a grading system, and collection of other important information that is otherwise difficult to obtain in dogs with LP.
OBJECTIVE To evaluate the potency of vecuronium and duration of vecuronium-induced neuromuscular blockade in dogs with centronuclear myopathy (CNM).
ANIMALS 6 Labrador Retrievers with autosomal-recessive CNM and 5 age- and weight-matched control dogs.
PROCEDURES Dogs were anesthetized on 2 occasions (1-week interval) with propofol, dexmedetomidine, and isoflurane. Neuromuscular function was monitored with acceleromyography and train-of-four (TOF) stimulation. In an initial experiment, potency of vecuronium was evaluated by a cumulative-dose method, where 2 submaximal doses of vecuronium (10 μg/kg each) were administered IV sequentially. For the TOF's first twitch (T1), baseline twitch amplitude and maximal posttreatment depression of twitch amplitude were measured. In the second experiment, dogs received vecuronium (50 μg/kg, IV) and the time of spontaneous recovery to a TOF ratio (ie, amplitude of TOF's fourth twitch divided by amplitude of T1) ≥ 0.9 and recovery index (interval between return of T1 amplitude to 25% and 75% of baseline) were measured.
RESULTS Depression of T1 after each submaximal dose of vecuronium was not different between groups. Median time to a TOF ratio ≥ 0.9 was 76.7 minutes (interquartile range [IQR; 25th to 75th percentile], 66.7 to 99.4 minutes) for dogs with CNM and 75.0 minutes (IQR, 47.8 to 96.5 minutes) for controls. Median recovery index was 18.0 minutes (IQR, 9.7 to 23.5 minutes) for dogs with CNM and 20.2 minutes (IQR, 8 to 25.1 minutes) for controls.
CONCLUSIONS AND CLINICAL RELEVANCE For the study dogs, neither potency nor duration of vecuronium-induced neuromuscular blockade was altered by CNM. Vecuronium can be used to induce neuromuscular blockade in dogs with autosomal-recessive CNM.
To elucidate the cardiovascular effects of escalating doses of phenylephrine and norepinephrine in dogs receiving acepromazine and isoflurane.
8 beagles aged 1 to 2 years (7.4 to 11.2 kg).
All dogs received acepromazine 0.01 mg/kg, propofol 4 to 5 mg/kg, and isoflurane and were mechanically ventilated. Mean arterial pressure (MAP) from a femoral artery catheter and continuous electrocardiogram were recorded. Cardiac output (CO) was measured with transpulmonary thermodilution. Systemic vascular resistance (SVR), global end-diastolic volume (GEDV), and global ejection fraction (GEF) were subsequently calculated. Phenylephrine and norepinephrine were infused in random order at 0.07, 0.3, 0.7, and 1.0 μg/kg/min. All variables were measured after 15 minutes of each infusion rate. The effects of dose, agent, and their interaction on the change of each variable were evaluated with mixed-effect models. A P < .05 was used for significance.
Atrial premature complexes occurred in 3 dogs during norepinephrine infusion at doses of 0.3, 0.7, and 1 μg/kg/min; no dysrhythmias were seen with phenylephrine administration. MAP increased during dose escalation (P < .0001) within each agent and did not differ between agents (P = .6). The decrease in HR was greater for phenylephrine (P < .0001). Phenylephrine decreased CO and GEF and increased GEDV and SVR (all P < .03). Norepinephrine decreased the SVR and increased CO, GEDV, and GEF (all P < .03).
Our results confirm that phenylephrine increases arterial pressures mainly through vasoconstriction in acepromazine-premedicated dogs while norepinephrine, historically considered a vasopressor, does so primarily through an increase in inotropism.
Objective—To determine whether dogs that received eyedrops containing phenylephrine and scopolamine would have a higher mean arterial blood pressure (MAP) when anesthetized than would dogs that did not receive the eyedrops.
Animals—37 nondiabetic and 29 diabetic dogs anesthetized for phacoemulsification and 15 nondiabetic dogs anesthetized for corneal ulcer repair (control dogs).
Procedures—Medical records were reviewed to identify study dogs. Dogs undergoing phacoemulsification received 2 types of eyedrops (10% phenylephrine hydrochloride and 0.3% scopolamine hydrobromide) 4 times during a 2-hour period prior to the procedure. Control dogs did not receive these eyedrops. Heart rate and MAP were measured before surgery in all dogs 10 and 5 minutes before, at the time of (t0), and 5 (t5) and 10 (t10) minutes after atracurium administration.
Results—MAP was greater in the 2 groups that received the eyedrops than in the control group at t0 and t5; at t10, it was greater only for the nondiabetic dogs that received eyedrops. Nine nondiabetic dogs and 1 diabetic dog anesthetized for phacoemulsification had at least 1 MAP value > 131 mm Hg; 73% of MAP values > 131 mm Hg were detected within 10 minutes after atracurium administration. At no time did a control dog have an MAP value > 131 mm Hg.
Conclusions and Clinical Relevance—Anesthetized dogs pretreated with eyedrops containing phenylephrine and scopolamine had higher MAP values than dogs that did not receive the eyedrops, suggesting the drops caused hypertension. Atracurium may interact with the eyedrops and contribute to the hypertension.
PROCEDURES Dogs were randomly assigned to receive either oxygen (Fio2 > 0.9 [100% oxygen]; n = 11; control group) or a mixture of nitrogen and oxygen (Fio2 = 0.4; 11; 40% oxygen group) as the carrier gas for isoflurane while anesthetized. All dogs were allowed to breathe spontaneously while anesthetized. For each dog, the Pao2, Paco2, other indices of oxygenation, and extent of sedation were monitored at predetermined times during and for 1 hour after anesthesia. Measured variables were compared between the 2 treatment groups and over time within each treatment group.
RESULTS None of the measured variables differed significantly between the control and 40% oxygen groups at any time during the postanesthesia period. Within each treatment group, the Paco2 and extent of sedation decreased over time during the postanesthesia period.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that indices of oxygenation did not differ significantly between healthy dogs in which the Fio2 was maintained at > 0.9 and those in which the Fio2 was maintained at 0.4 while anesthetized for ovariohysterectomy. Thus, the addition of nitrogen to the carrier gas for an inhalant anesthetic conferred neither an advantage nor disadvantage in regard to oxygenation during the first hour of anesthesia recovery.
To compare the duration of bupivacaine liposome suspension in the dog with that of bupivacaine and dexmedetomidine following a perineural injection.
8 healthy Beagles.
The left sciatic nerve of each dog was randomly assigned to an ultrasound-guided perineural injection with either bupivacaine liposome suspension (BLS) or with 0.5% bupivacaine with dexmedetomidine (1 µg/mL) (BUP-DEX). The contralateral nerve was assigned to the alternate agent. The sensory, motor, and proprioceptive functions were evaluated before the injection (baseline) and at 4, 10, 24, 48, 72, and 96 hours.
The block in 1 limb in the BLS treatment appeared to have failed (data set excluded). The motor scores of 2 individuals could not be evaluated leaving 5 limbs to evaluate in the BLS treatment and 6 in the BUP-DEX.
A total of 6 out of 7 limbs in the BLS achieved a complete sensory block. In 3 out of 5 treatments with BLS, motor block was only partial and in 2 not apparent at all. Proprioceptive block was partial in 5 out of 7 dogs in the BLS treatment. All functions were still completely obliterated at 10 hours in 6 cases in treatment BUP-DEX. All functions were restored in all cases by 96 and 24 hours after administration of BLS and BUP-DEX, respectively.
The blockade characteristics of bupivacaine liposome suspension were effective and long lasting. Motor and proprioceptive deficits may be inconsistent over time.
To compare the thermoregulatory and analgesic effects of high-dose buprenorphine versus morphine in cats undergoing ovariohysterectomy.
94 client-owned cats.
Cats were randomized to receive either buprenorphine 0.24 mg/kg or morphine 0.1 mg/kg subcutaneously (SC) during recovery from ovariohysterectomy. Body temperature measurements were obtained before anesthesia, during anesthesia (averaged), at extubation, and 2, 4, and 16 to 20 hours postoperatively. Signs of pain were assessed, and demographic characteristics were compared between groups. The effects of treatment and time on body temperature, point prevalence of hyperthermia (> 39.2 °C), and pain scores were compared with linear or generalized mixed-effect models.
Cats receiving morphine (vs. buprenorphine) were older and heavier (both, P ≤ 0.005). Other group characteristics did not differ between treatments. Cats receiving buprenorphine (vs. morphine) had higher postoperative temperatures (P = 0.03). At 2, 4, and 16 to 20 hours after extubation, the point prevalence of hyperthermia was greater (P = 0.001) for cats receiving buprenorphine (55% [26/47], 44% [21/47], and 62% [27/43], respectively) versus morphine (28% [13/46], 13% [6/46], and 47% [21/44], respectively). There were no differences in pain scores between groups or over time. Five cats receiving buprenorphine and 6 receiving morphine required rescue analgesia within the 24-hour period.
Administration of buprenorphine (0.24 mg/kg SC), compared with morphine (0.1 mg/kg SC), resulted in higher body temperatures without an apparent advantage with regard to analgesia during the first 20 postoperative hours than morphine. Opioid-induced postoperative hyperthermia could confound the diagnosis of fever from different sources.