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- Author or Editor: Frank D. Galey x
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Abstract
Objective—To quantitate the effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and identify changes in selected clinicopathologic variables and serum fluoride values associated with desflurane anesthesia in horses.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized on 2 occasions: first, to determine the minimum alveolar concentration (MAC) of desflurane in O2 and second, to characterize cardiopulmonary and clinicopathologic responses to 1×, 1.5×, and 1.75× desflurane MAC during both controlled and spontaneous ventilation.
Results—Mean ± SEM MAC of desflurane in horses was 8.06 ± 0.41%; inhalation of desflurane did not appear to cause airway irritation. During spontaneous ventilation, mean PaCO2 was 69 mm Hg. Arterial blood pressure, stroke volume, and cardiac output decreased as the dose of desflurane increased. Conditions of intermittent positive pressure ventilation and eucapnia resulted in further cardiovascular depression. Horses recovered quickly from anesthesia with little transient or no clinicopathologic evidence of adverse effects. Serum fluoride concentration before and after administration of desflurane was below the limit of detection of 0.05 ppm (2.63µM/L).
Conclusions and Clinical Relevance—Results indicate that desflurane, like other inhalation anesthetics, causes profound hypoventilation in horses. The magnitude of cardiovascular depression is related to dose and mode of ventilation; cardiovascular depression is less severe at doses of 1× to 1.5× MAC, compared with known effects of other inhalation anesthetics under similar conditions. Desflurane is not metabolized to an important degree and does not appear to prominently influence renal function or hepatic cellular integrity or function. ( Am J Vet Res 2005;66:669–677)
Abstract
Objective—To quantitate effects of dose of sevoflurane and mode of ventilation on cardiovascular and respiratory function in horses and identify changes in serum biochemical values associated with sevoflurane anesthesia.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized twice: first, to determine the minimum alveolar concentration (MAC) of sevoflurane and second, to characterize cardiopulmonary and serum biochemical responses of horses to 1.0, 1.5, and 1.75 MAC multiples of sevoflurane during controlled and spontaneous ventilation.
Results—Mean (± SEM) MAC of sevoflurane was 2.84 ± 0.16%. Cardiovascular performance during anesthesia decreased as sevoflurane dose increased; the magnitude of cardiovascular depression was more severe during mechanical ventilation, compared with spontaneous ventilation. Serum inorganic fluoride concentration increased to a peak of 50.8 ± 7.1 µmol/L at the end of anesthesia. Serum creatinine concentration and sorbitol dehydrogenase activity reached their greatest values (2.0 ± 0.8 mg/dL and 10.2 ± 1.8 U/L, respectively) at 1 hour after anesthesia and then returned to baseline by 1 day after anesthesia. Serum creatine kinase, aspartate aminotransferase, and alkaline phosphatase activities reached peak values by the first (ie, creatine kinase) or second (ie, aspartate aminotransferase and alkaline phosphatase) day after anesthesia.
Conclusions and Clinical Relevance—Sevoflurane causes dose-related cardiopulmonary depression, and mode of ventilation further impacts the magnitude of this depression. Except for serum inorganic fluoride concentration, quantitative alterations in serum biochemical indices of liver- and muscle-cell disruption and kidney function were considered clinically unremarkable and similar to results from comparable studies of other inhalation anesthetics. (Am J Vet Res 2005;66:606–614)
