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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 cardiovascular effects of desflurane in mechanically ventilated calves.
Animals—8 healthy male calves.
Procedure—Calves were anesthetized by face mask administration of desflurane to permit instrumentation. Administration of desflurane was temporarily discontinued until mean arterial blood pressure increased to ≥ 100 mm Hg, at which time baseline cardiovascular values, pulmonary arterial temperature, end-tidal CO2 tension, and end-tidal desflurane concentration were recorded. Cardiac index and systemic and pulmonary vascular resistances were calculated. Arterial blood gas variables were measured and calculated. Mean end-tidal concentration of desflurane at this time was 3.4%. After collection of baseline values, administration of 10% end-tidal concentration of desflurane was resumed and calves were connected to a mechanical ventilator. Cardiovascular data were collected at 5, 10, 15, 30, and 45 minutes, whereas arterial blood gas data were collected at 15 and 45 minutes after collection of baseline data.
Results—Mean ± SD duration from beginning desflurane administration to intubation of the trachea was 151 ± 32.8 seconds. Relative to baseline, desflurane anesthesia was associated with a maximal decrease in arterial blood pressure of 35% and a decrease in systemic vascular resistance of 34%. Pulmonary arterial blood temperature was decreased from 15 through 45 minutes, compared with baseline values. There were no significant changes in other measured variables. All calves recovered from anesthesia without complications.
Conclusions and Clinical Relevance—Administration of desflurane for induction and maintenance of general anesthesia in calves was smooth, safe, and effective. Cardiopulmonary variables remained in reference ranges throughout the study period.
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)
SUMMARY
Objective
To determine whether a low dose of atropine is associated with decreased requirement for cardiovascular supportive treatment in horses given detomidine prior to maintenance of general anesthesia with halothane.
Animals
3 groups of 10 healthy horses.
Procedure
Detomidine (20 μg/kg of body weight, IM) was administered to all 30 horses. Then, 10 horses received atropine (0.006 mg/kg, IV) 1 hour after detomidine administration, 10 horses received atropine (0.012 mg/kg, IM) at the time of detomidine administration, and 10 horses served as a control group. Heart rate was measured prior to detomidine administration and at fixed intervals throughout anesthesia. The dobutamine infusion rate necessary to maintain mean arterial blood pressure between 70 and 80 mm of Hg was recorded. Systemic blood pressures, end-tidal halothane, end-tidal CO2, and arterial blood gas tensions were measured at fixed intervals.
Results
Mean heart rate was higher among horses receiving atropine IV or IM, compared with that in control horses. Horses that received atropine IV had higher systemic arterial blood pressure and required a lower dobutamine infusion rate than did horses of the other groups.
Conclusion
Detomidine-treated, halothane-anesthetized horses given atropine IV required less dobutamine, compared with horses receiving or not receiving atropine IM. Complications, such as colic and dysrhythmias, from use of higher doses of atropine, were not observed at this lower dose of atropine.
Clinical Relevance
IV administration of a low dose of atropine prior to induction of general anesthesia may result in improved blood pressure in horses that have received detomidine before anesthesia with halothane. (Am J Vet Res 1997;58:1436–1439)
Abstract
Objective
To evaluate the ability of commercial, chromogenic kits designed to measure human fibrinolytic pathway components to measure the canine plasma fibrinolytic pathway enzymes, tissue plasminogen activator (tPA) and plasminogen (PLG), and their respective inhibitors, plasminogen activator inhibitor 1 (PAI) and α2-anti-plasmim (AP).
Animals
20 healthy dogs of various ages and breeds.
Procedure
The commercial procedure was adapted to a microtitration plate. Standard curves were generated by use of a canine plasma pool.
Results
Modifications of the commercial kit consisted of change in incubation periods and the substitution of urokinase for the streptokinase. Plasminogen and AP procedures yielded intra- and interassay coefficients of variation (CV) ranging from 2 to 6.4%. The tPA activity gave an acceptable intra-assay CV of 4.2%, but an equivocal interassay CV of 18%. The PAI assay gave unacceptable intra-assay and interassay CV of 59 and 66%, respectively.
Conclusions
Modifications of the commercial PLG and AP procedures were appropriate for use with fresh and frozen canine plasma. However, equivocal results were obtained for canine plasma tPA. Although the PAI assay was able to detect the inhibitor, it gave unacceptable quantifiable results. Human and canine plasma contained similar amounts of PLG and AP, but 25% more tPA was found in canine plasma than human plasma.
Clinical Relevance
With modifications, the commercial human PLG and AP chromogenic kits may serve to elucidate such canine fibrinolytic disorders as disseminated coagulopathy. The high cost of the chromogenic substrate limits its application. (Am J Vet Res 1996;57: 1124-1130)
Abstract
Objective
To determine whether alterations in the fibrinolytic pathway analytes, plasminogen (PLG), tissue plasminogen activator, and α2-antiplasmin are significant in dogs subjected to minor and major surgical trauma.
Animals
18 dogs in 3 groups of 6 each.
Procedure
Plasma fibrinolytic pathway analytes were measured in dogs with trauma of ovariohysterectomy (minor trauma) or orthopedic surgery (major trauma) and halothane anesthesia (control group). A commercial procedure adapted to a microtitration plate was used to measure the analytes. Blood was obtained 24 hours before anesthesia, at extubation (0 hours), and again at 2, 24, and 48 hours after extubation. An analyte quality-control strategy was maintained.
Results
In the major trauma group, there was a significant, transient, postsurgical decrease in PLG activity at 0 and 24 hours and a return to presurgical values by 48 hours. The minor trauma group had a similar trend without significant changes, including an increase in PLG values at 48 hours that exceeded the reference range. Antiplasmin values changed significantly in the major trauma group only. Tissue plasminogen activator values remained within the reference range.
Conclusions
Tissue plasminogen activator was not considered a clinical marker of interest for detection of alterations in fibrinolysis after trauma. In contrast, plasma PLG and α2-antiplasmin values may be useful in the evaluation of hemostatic complications of surgery.
Clinical Relevance
Identification of altered fibrinolysis in dogs undergoing traumatic surgery may provide a baseline for preventive pre- and postsurgical hemostatic care. (Am J Vet Res 1996;57:1137-1140)
Summary
Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the eeg. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the eeg were determined for δ, θ, α, and β frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the δ band. Hypocapnia caused an increase in the absolute power of δ, θ, and α. frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.
Abstract
Cardiovascular effects of epidurally administered morphine, a morphine-xylazine combination, and saline solution (control) during isoflurane-maintained anesthesia were assessed in 6 healthy dogs. Anesthesia was induced with isoflurane in O2 and was maintained at 2.0% end-tidal isoflurane concentration. Ventilation was controlled to maintain PaCO2 at 35 to 45 mm of Hg. The dorsal pedal artery was cannulated for measurement of systolic, mean, and diastolic pressures, and for blood sample collection. Arterial blood pH and gas tensions were determined every 30 minutes. Cardiac output was determined by thermodilution. The ecg, heart rate, body temperature, central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, end-tidal isoflurane concentration, and CO2 tension were monitored. Systemic and pulmonary vascular resistance, arterial HCO3 - concentration, base excess, and cardiac index were calculated. After baseline measurements were taken, morphine (0.1 mg/kg of body weight) in 5 ml of isotonic saline solution, morphine and xylazine (0.1 mg of morphine and 0.02 mg of xylazine/kg) in 5 ml of isotonic saline solution, or 5 ml of isotonic saline solution was injected into the lumbosacral epidural space. Data were recorded at 5, 15, 30, 45, 60, 75, 90, 105, and 120 minutes after epidural injection. Statistical analysis included anova for repeated measures. Significance was set at P < 0.05. None of the measured variables was significantly different among the 3 treatments at any time. Results of the study indicated that epidural administration of morphine or morphine and xylazine is not associated with significant cardiovascular side effects during isoflurane-maintained anesthesia in dogs.
