Clinical report, "Hepatic necrosis following halothane anesthesia in goats," viewed as unacceptable.
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Animals↗
Biomedical subjects
D S Hodgson
Publications and source records attributed to D S Hodgson.
Cardiopulmonary function during 5 hours of constant-dose isoflurane in laterally recumbent, spontaneously breathing horses.
Hemodynamic and respiratory effects of 5 h of unvarying 1.57%, end-tidal (1.2 MAC) isoflurane in O2 anesthesia were characterized in ten left laterally recumbent horses. Compared to base line values at 30 min of constant dose isoflurane, cardiac output, hematocrit, total plasma solids, PaCO2, and peak inspired gas flow progressively and significantly (P less than 0.05) increased over the course of study. Arterial blood pressure increased (P less than 0.05) during the first 2 h of constant dose of isoflurane then decreased and remained near base line values. Inspiratory time progressively decreased with time of anesthesia. All horses recovered from anesthesia uneventfully within 1 h of termination of isoflurane.
Anesthesia, Inhalation↗
Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses.
The effect of halothane-induced hypotension on the development of postanesthetic myopathy was studied, using 6 healthy adult horses. Horses were anesthetized with halothane in oxygen for 3.5 hours on each of 2 occasions. Intermittent positive-pressure ventilation was used to maintain PaCO2 of 45 to 55 mm of Hg throughout both anesthetic exposures. By regulating the inspired halothane concentration, a mean arterial blood pressure of 85 to 95 mm of Hg (normotension) was maintained throughout the 1st anesthetic exposure, and a mean arterial blood pressure of 55 to 65 mm of Hg (hypotension) was maintained during the 2nd anesthetic exposure. All horses recovered uneventfully from normotensive anesthesia, but all had some muscle dysfunction after prolonged hypotensive anesthesia. Because of apparent animal discomfort and lameness involving more than 1 limb, 3 horses were euthanatized soon after they recovered from hypotensive anesthesia. The 3 other horses showed a degree of lameness. In addition, 1 horse had raised, swollen plaques over the hip, rib, and facial areas which were in contact with the surgical table, and another had evidence of facial nerve paralysis. One hour after the 6 horses stood after hypotensive anesthesia was completed, values obtained for aspartate transaminase and creatinine were significantly (P less than 0.05) greater than those obtained after normotensive anesthesia was completed. Aspartate transaminase, total bilirubin, and creatinine values were significantly (P less than 0.05) increased when compared with those obtained before horses were anesthetized. A large increase was measured in creatine kinase. Twenty-four hours after hypotensive anesthesia was completed, creatine kinase and lactate dehydrogenase in the 3 surviving horses were significantly (P less than 0.05) greater than those values after normotensive anesthesia was completed.
Animals↗
Effects of spontaneous, assisted, and controlled ventilatory modes in halothane-anesthetized geldings.
Cardiopulmonary effects of spontaneous, assisted, and controlled ventilatory modes were determined with 6 young, healthy geldings anesthetized with halothane at a constant dose (1.3 minimum alveolar concentration). All horses were in lateral recumbency, and all modes of ventilation were studied at least once during each anesthetic exposure. Cardiac output did not differ between spontaneous and assisted ventilation modes, but both modes were associated with significantly (P less than 0.05) higher cardiac output than that with controlled ventilation. The PaCO2 differed significantly (P less than 0.01) between all modes of ventilation. Although controlled ventilation maintained a normal PaCO2, assisted ventilation reduced PaCO2 as compared with spontaneous ventilation with less cardiovascular depression than that with controlled ventilation. Mixed venous O2 tensions were higher with spontaneous and assisted ventilation modes than with controlled ventilation. Except for shorter inspiratory time and smaller inspiratory/expiratory ratio associated with spontaneous ventilation, there were no ventilatory mode-related effects on ventilatory variables.
Anesthesia↗
Respiratory, cardiovascular, and metabolic adjustments to exercise in the Hereford calf.
Six Hereford steers were studied before, during, and after short exercise bouts on a motor-driven treadmill (3 degrees incline) at four speeds (1.0, 1.4, 1.8, and 2.2 m X s-1). Oxygen consumption (MO2) and carbon dioxide production (MCO2) were measured by collecting the expired gas. Arterial and mixed venous blood samples were obtained simultaneously from indwelling catheters in the aorta and pulmonary artery. A 10-fold increase was observed in MO2 and MCO2 at the highest work load. Minute ventilation increased proportionately less than MO2 and MCO2 with increasing work loads, but alveolar ventilation was found to increase in proportion to both MO2 and MCO2. The highest work load produced a threefold increase in cardiac output primarily as a result of increased heart rate. A 10-fold increase in lactate and a 63% increase in serum potassium concentration were observed at the highest work load. Plasma cortisol levels were highest at 10 min postexercise and reached levels of seven times the resting values following exercise at the highest speed. The responses to exercise in the calf are qualitatively similar to those observed in other species, but quantitative differences exist in some cardiovascular and metabolic responses which may limit this animal's ability to perform strenuous exercise.
Animals↗
Monitoring oxygen concentrating devices.
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Animals↗
Pathophysiological effects of paraquat intoxication in domestic ruminants: low dose studies.
Two studies, one in mixed breed feedlot calves and one in domestic goats, evaluated the effects of low doses of parentally administered paraquat dichloride on lung function and pulmonary structure. Calves were injected IV with 5 mg/kg paraquat and studied on days 3, 5, and 7 postinfusion. Goats were intoxicated IP with 10 mg paraquat/kg and studied on days 2, 4, 8, and 10. Each animal served as its own control. The two dosage regimes in calves and goats did not alter pulmonary function or blood gases (calf study only). Only goats intoxicated at the higher dose demonstrated histopathological paraquat-related structural changes.
Animals↗
Modification of a nonrebreathing circuit adapter to prevent barotrauma in anesthetized patients.
Barotrauma, pneumothorax, and pneumomediastinum occurred in two anesthetized cats in which the waste gas outlet of a nonrebreathing circuit was occluded. To prevent any similar cases of barotrauma, we have modified our nonrebreathing circuit adapters by inserting a 15 cm H2O PEEP valve into the gas pathway of the nonrebreathing circuit adapter. This PEEP valve prevents the circuit and airway pressures from exceeding 15 cm H2O if the pop-off valve of the nonrebreathing circuit adapter is inadvertently left closed.
Anesthesia↗
The minimum alveolar concentration of desflurane in cats.
Eight adult cats, 4 male and 4 female, (3.5 +/- 0.9 [SD] kg) were used to determine the minimum alveolar concentration (MAC) of desflurane. Desflurane (DES) anesthesia was induced in a 20 L chamber with an oxygen inflow of 10 L/min and the DES vaporizer set at 18%. After 3.5 +/- 0.5 min, the cats were removed from the chamber and anesthesia was maintained via mask (14% DES, 3L/min O2) until successful intubation. Anesthesia was maintained with DES in oxygen at a flow of at least 200 mL/kg/min through a nonrebreathing circuit. The time from the start of induction to completion of intubation was 6.2 +/- 1.1 min. Esophageal temperature was maintained between 37.8 degrees C and 38.6 degrees C. Hand-collected end-tidal gas samples were obtained from a catheter positioned inside the lumen of the endotracheal tube. Inspired and end-tidal DES concentrations were measured with a Biochem 8100 anesthetic agent monitor that was calibrated with known gas standards and modified to accept hand-collected samples. A constant alveolar concentration of DES was maintained for at least 15 minutes, then a clamp was applied to the tail and the cat observed for gross purposeful movement. The end-tidal DES was then increased (if a positive response) or decreased (if a negative response) by 20% and the test repeated after 15 minutes of constant conditions. The final iteration was 10%. The MAC of DES in these cats was 9.79 +/- 0.70 vol %. The FA/FI ratio for desflurane was always greater than 0.97.
Anesthesia, Inhalation↗
Gastric myoelectric and motor activity in dogs after isoflurane anesthesia.
To characterize the effects of isoflurane on gastric motility, gastric electrical and contractile activities were assessed in six healthy adult dogs before and after recovery from anesthesia. Baseline recordings (fasting and fed state) were obtained in unanesthestized dogs 8 days after implantation of serosal electrodes and strain-gauge force transducers. After an overnight fast, dogs were anesthetized with 1.3 minimum alveolar concentration (MAC) isoflurane for 4.5 hours (approximately 6 MAC hours). No other anesthetic or sedative drugs were administered. During anesthesia, ventilation was mechanically controlled to maintain arterial carbon dioxide tension at 36 +/- 4 mm Hg. Gastric electrical and contractile activities (fasting and fed state) were recorded again 18 hours after recovery from isoflurane anesthesia. Recordings were analyzed to determine gastric slow-wave frequency, presence of slow-wave dysrhythmias, slow-wave propagation velocity, coupling of contractions to slow waves, a motility index based on relative contractile amplitudes, and onset and duration of contractions after a standardized meal. The only variable that was significantly decreased 18 hours after 6 MAC hours of isoflurane anesthesia was the gastric motility index during fasting-state phase III. This decrease was not apparent in the fed-state test periods. Our results suggest that, with the exception of gastric motility index during fasting-state phase III, variables for gastric electrical and contractile activities in dogs are unaffected by isoflurane 18 hours after anesthesia.
Anesthesia, Inhalation↗
Cardiovascular effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane in experimentally induced hypothyroidism in dogs.
This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (Q), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentration were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and PACO2 maintained between 38 to 42 mm Hg. Isoflurane caused significant (P < .05) dose-dependent reduction in Q, SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower Q, SV, SAP, and MAP PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in Q, SV, and arterial pressure.
Anesthetics, Inhalation↗