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- Author or Editor: Stephen A Greene x
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Abstract
Objectives
To evaluate effects of strenuous exercise in adult horses immediately before anesthesia and to determine whether prior exercise affects anesthesia induction, recovery, or both.
Animals
6 healthy Thoroughbreds in good condition and trained to run on a treadmill, each horse serving as its own control.
Procedure
Horses ran on a treadmill until fatigued, then were sedated immediately with detomidine hydrochloride and anesthetized with a zolazepam hydrochloride-tiletamine combination. Anesthesia was maintained with isoflurane in oxygen for another 90 minutes. Blood samples were taken before, during, and after exercise and during anesthesia.
Results
During exercise, changes in heart rate, core body temperature, plasma lactate concentration, arterial pH, and PaCO2 were significant. Plasma ionized calcium concentration was lower after exercise, compared with baseline values, and remained lower at 30 minutes of isoflurane anesthesia. Compared with baseline values, plasma chloride concentration decreased significantly during anesthesia after exercise. Cardiac output during anesthesia was significantly lower than that during preexercise, but significant differences between experimental and control periods were not observed. Arterial blood pressure during anesthesia was significantly lower than that during preexercise and initially was maintained better during isoflurane anesthesia after exercise. Cardiac output and blood pressure values were clinically acceptable throughout anesthesia.
Conclusion
Administration of detomidine hydrochloride followed by zolazepam hydrochloride-tiletamine appeared to be safe and effective for sedation and anesthesia of horses that had just completed strenuous exercise.
Clinical Relevance
Anesthetic given in accordance with this protocol can be used to anesthetize horses that are injured during athletic competition to assess injuries, facilitate first aid, and possibly allow salvage of injured horses. (Am J Vet Res 1999;60:743–748)
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)
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
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.
SUMMARY
Fourteen adult beavers (Castor canadensis) weighing 16.5 ± 4.14 kg (mean ± sd) were anesthetized for surgical implantation of radio telemetry devices. Beavers were anesthetized with diazepam (0.1 mg/kg) and ketamine (25 mg/kg) administered im, which provided smooth anesthetic induction and facilitated tracheal intubation. Anesthesia was maintained with halothane in oxygen via a semiclosed circle anesthetic circuit. Values for heart rate, respiratory rate, esophageal temperature, direct arterial blood pressure, end-tidal halothane concentration, and end-tidal CO2 tension were recorded every 15 minutes during the surgical procedure. Arterial blood samples were collected every 30 minutes to determine pH, PaO2 , and PaCO2 . Values for plasma bicarbonate, total CO2, and base excess were calculated. Ventilation was spontaneous in 7 beavers and controlled to maintain normocapnia (PaCO2 approx 40 mm of Hg) in 7 others. Vaporizer settings were adjusted to maintain a light surgical plane of anesthesia. Throughout the surgical procedure, all beavers had mean arterial pressure < 60 mm of Hg and esophageal temperature < 35 C. Mean values for arterial pH, end-tidal CO2, PaO2 , and PaCO2 were significantly (P < 0.05) different in spontaneously ventilating beavers, compared with those in which ventilation was controlled. Respiratory acidosis during halothane anesthesia was observed in spontaneously ventilating beavers, but not in beavers maintained with controlled ventilation. All beavers recovered unremarkably from anesthesia.
Abstract
Objective
To determine the effect of craniectomy and durotomy on intracranial pressure (ICP) in clinically normal dogs.
Design
Two-part study (experiments A and B) involving craniectomy and durotomy, with and without treatments to lower ICP.
Animals
Six (experiment A) and 7 (experiment B) healthy dogs.
Procedure
In experiment A, craniectomy was performed in combination with durotomy, diuretic administration, methylprednisolone sodium succinate administration, and hyperventilation, and effect of these manipulations on ICP was determined. In experiment B, dogs had only craniectomy and durotomy without associated ICP-lowering treatments. During both experiments, ICP was monitored throughout the surgical procedure with a fiber optic ICP monitoring device.
Results
Intracranial pressure decreased after the combination of craniectomy, durotomy, and other ICP-lowering treatments in dogs of experiment A. Similar magnitude of decrease in ICP was observed in dogs of experiment B after craniectomy and durotomy.
Conclusions
Comparison of these experiments indicate that surgical removal of overlying skull and incision of the dura mater can significantly decrease ICP in clinically normal dogs.
Clinical Relevance
Craniectomy and durotomy may be useful as an adjunct treatment for increased ICP. (Am J Vet Res 1996;57:116-119)
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 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
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.
SUMMARY
Intracranial pressure and cardiovascular variables after iv administration of medetomidine (0.03 mg/kg of body weight) were evaluated in 6 healthy, mixed-breed dogs anesthetized with 1.3% end-tidal isoflurane concentration and mechanically ventilated to normocapnia (PaCO2 , 35 to 45 mm of Hg). Baseline values were determined for intracranial pressure, heart rate, arterial blood pressure, cardiac output, mean pulmonary artery pressure, pulmonary capillary wedge pressure, central venous pressure, end-tidal CO2 tension and isoflurane concentration, arterial pH and CO2 and O2 tensions, and core body temperature. Cerebral perfusion pressure, cardiac index, systemic and pulmonary vascular resistances, plasma HCO3- concentration, and base excess were calculated. Intracranial pressure was measured, using a calibrated, fiberoptic transducer placed within the brain parenchyma and secured to the calvarium by means of a subarachnoid bolt. Cardiac output was determined by thermodilution. End-tidal CO2 tension and isoflurane concentration were determined, using an infrared gas analyzer. Administration of medetomidine did not change intracranial pressure, but was associated with significant (P < 0.05) decreases in values for heart rate, cardiac index, end-tidal CO2, and HCO3- and with significant increases in systolic, mean, and diastolic pressure; pulmonary artery pressure; systemic vascular resistance; central venous pressure; and pulmonary capillary wedge pressure.