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- Author or Editor: Kurt A. Grimm x
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Abstract
Objective—To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of sevoflurane in cats.
Animals—8 domestic cats.
Procedure—Each cat was anesthetized twice with sevoflurane. First, the MAC of sevoflurane for each cat was determined by use of the tail clamp method. Second, cats were anesthetized with sevoflurane at each of 5 MAC multiples administered in random order. Ventilation was controlled, and after a 15- minute equilibration period at each MAC multiple of sevoflurane, BIS data were collected for 5 minutes and the median value of BIS calculated.
Results—The mean (± SD) MAC of sevoflurane was 3.3 ± 0.2%. The BIS values at 0.5 MAC could not be recorded as a result of spontaneous movement in all 8 cats. The BIS values at 2.0 MAC were confounded by burst suppression in all 8 cats. Over the range of 0.8 to 1.5 MAC, BIS values decreased significantly with increasing end-tidal sevoflurane concentrations. Mean (± SD) BIS measurements were 30 ± 3, 21 ± 3, and 5 ± 2 at 0.8, 1.0, and 1.5 MAC, respectively.
Conclusions and Clinical Relevance—Values of BIS are inversely and linearly related to end-tidal sevoflurane concentrations in anesthetized cats, and BIS may be a useful predictor of CNS depression in this species. The consistently low BIS values recorded in this study suggest that clinical BIS end points used to titrate anesthetic agents in humans may not be applicable to cats. ( Am J Vet Res 2004;65:93–98)
Abstract
Objective—To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of isoflurane after IM injection of medetomidine or saline (0.9% NaCl) solution in anesthetized dogs.
Animals—6 dogs.
Procedure—Each dog was anesthetized 3 times with isoflurane. First, the MAC of isoflurane for each dog was determined by use of the tail clamp method. Second, anesthetized dogs were randomly assigned to receive an IM injection of medetomidine (8 µg · kg–1) or an equal volume of isotonic saline (0.9% NaCl) solution 30 minutes prior to beginning BIS measurements. Last, anesthetized dogs received the remaining treatment (medetomidine or isotonic saline solution). Dogs were anesthetized at each of 4 MAC multiples of isoflurane. Ventilation was controlled and atracurium (0.2 mg/kg followed by 6 µg/kg/min as a continuous infusion, IV) administered. After a 20-minute equilibration period at each MAC multiple of isoflurane, BIS data were collected for 5 minutes and median values of BIS calculated.
Results—BIS significantly decreased with increasing MAC multiples of isoflurane over the range of 0.8 to 2.0 MAC. Mean (± SD) MAC of isoflurane was 1.3 ± 0.2%. During isoflurane-saline anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 65 ± 8, 60 ± 7, 52 ± 3, and 31 ± 28, respectively. During isoflurane-medetomidine anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 77 ± 4, 53 ± 7, 31 ± 24, and 9 ± 20, respectively.
Conclusions and Clinical Relevance—BIS monitoring in dogs anesthetized with isoflurane has a predictive value in regard to degree of CNS depression. During isoflurane anesthesia, our results support a MAC-reducing effect of medetomidine. (Am J Vet Res 2003;64:316–320)
Abstract
Objective—To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO).
Animals—6 healthy dogs.
Procedure—Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 mg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 mg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, endtidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected.
Results—Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean ± SD) was 0.0 ± 0.0, 1.5 ± 1.5, 2.63 ± 0.49, and 5.58 ± 2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone.
Conclusion and Clinical Relevance—During ISOinduced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone. (Am J Vet Res 2000;61:42–47)
Abstract
Objective—To evaluate the effects of medetomidine on dynamic left ventricular outflow tract (LVOT) obstruction in cats with left ventricular hypertrophy.
Design—Clinical trial.
Animals—6 domestic shorthair cats with echocardiographic evidence of dynamic LVOT obstruction.
Procedure—Cats were restrained in lateral recumbency, and baseline M-mode and Doppler echocardiographic examinations were performed. An ECG was recorded continuously, and blood pressure was measured indirectly with Doppler instrumentation. Medetomidine (20 µg/kg [9.1 µg/lb]) was then administered IM, and examinations were repeated 15 minutes later.
Results—Significant decreases in heart rate, LVOT velocity, and the LVOT pressure gradient were documented following medetomidine administration. After adjusting for the effects of heart rate by ANCOVA, there were no significant differences in any other systolic or diastolic indices of left ventricular function.
Conclusions and Clinical Relevance—Results suggest that administration of medetomidine to cats with dynamic LVOT obstruction may result in elimination of outflow tract obstruction; medetomidine may be a suitable sedative and analgesic agent in this subpopulation of cats. (J Am Vet Med Assoc 2002;221:1276–1281)
Abstract
Objective—To evaluate the cardiovascular effects of the α2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats.
Animals—7 clinically normal cats.
Procedure—Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 µg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration.
Results—Heart rate, cardiac index, stroke index, ratepressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values.
Conclusions and Clinical Relevance—When administered alone to clinically normal cats, medetomidine (20 µg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central α2-adrenergic effect over peripheral vascular effects. (Am J Vet Res 2001;62:1745–1762)
Abstract
Objective—To determine the hemodynamic consequences of the coadministration of a continuous rate infusion (CRI) of medetomidine with a fentanyl bolus in dogs.
Animals—12 healthy sexually intact male dogs weighing 30.3 ± 4.2 kg (mean ± SD).
Procedure—Dogs received either fentanyl alone (15.0 µg/kg, IV bolus) or the same dose of fentanyl during an 11-hour CRI of medetomidine (1.5 µg/kg/h, IV). Prior to drug administration, dogs were instrumented for measurement of cardiac output, left atrial pressure, and systemic arterial blood pressures. Additionally, blood samples were collected from the pulmonary artery and left atrium for blood gas analysis.
Results—Medetomidine infusion reduced the cardiac index, heart rate, and O2 delivery while increasing left atrial pressure. Subsequent fentanyl administration further decreased the cardiac index. The PaO2 was not significantly different between the 2 treatment groups; however, fentanyl transiently decreased PaO2 from baseline values in dogs receiving a CRI of medetomidine.
Conclusions and Clinical Relevance—Because of the prolonged hemodynamic changes associated with the CRI of medetomidine, its safety should be further evaluated before being clinically implemented in dogs. (Am J Vet Res 2005;66:1222–1226)
