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Effects of ventilation and isoflurane end-tidal concentration on intracranial and cerebral perfusion pressures in horses

Robert J. BrosnanDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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 DVM, PhD
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Eugene P. SteffeyDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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 VMD, PhD
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Richard A. LeCouteurDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Ayako ImaiDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Thomas B. FarverDepartment of Population Health and Reproduction, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Gregg D. KortzDepartment of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Abstract

Objective—To measure the effects of isoflurane end-tidal concentration and mode of ventilation (spontaneous vs controlled) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in horses.

Animals—6 adult horses of various breeds.

Procedure—Anesthesia was induced and maintained with isoflurane in O2 in 6 healthy, unmedicated, adult horses. Using a subarachnoid strain gauge transducer, ICP was measured. Blood gas tensions and carotid artery pressures also were measured. Four isoflurane doses were studied, corresponding to the following multiples of the minimum alveolar concentration (MAC): 1.0 MAC, 1.2 MAC, 1.4 MAC, and 1.6 MAC. Data were collected during controlled ventilation and spontaneous ventilation at each dose.

Results—Increasing isoflurane end-tidal concentration induced significant dose-dependent decreases in mean arterial pressure (MAP) and CPP but no change in ICP. Hypercapnic spontaneous ventilation caused significant increases in MAP and ICP, compared with normocapnic controlled ventilation; no change in CPP was observed.

Conclusion and Clinical Relevance—Hypercapnia likely increases cerebral blood flow (CBF) by maintaining CPP in the face of presumed cerebral vasodilation in healthy anesthetized horses. The effect of isoflurane dose on CBF, however, remains unresolved because it depends on the opposinginfluences of a decrease in CCP and cerebral vasodilation. (Am J Vet Res 2003;64:21–25)

Abstract

Objective—To measure the effects of isoflurane end-tidal concentration and mode of ventilation (spontaneous vs controlled) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in horses.

Animals—6 adult horses of various breeds.

Procedure—Anesthesia was induced and maintained with isoflurane in O2 in 6 healthy, unmedicated, adult horses. Using a subarachnoid strain gauge transducer, ICP was measured. Blood gas tensions and carotid artery pressures also were measured. Four isoflurane doses were studied, corresponding to the following multiples of the minimum alveolar concentration (MAC): 1.0 MAC, 1.2 MAC, 1.4 MAC, and 1.6 MAC. Data were collected during controlled ventilation and spontaneous ventilation at each dose.

Results—Increasing isoflurane end-tidal concentration induced significant dose-dependent decreases in mean arterial pressure (MAP) and CPP but no change in ICP. Hypercapnic spontaneous ventilation caused significant increases in MAP and ICP, compared with normocapnic controlled ventilation; no change in CPP was observed.

Conclusion and Clinical Relevance—Hypercapnia likely increases cerebral blood flow (CBF) by maintaining CPP in the face of presumed cerebral vasodilation in healthy anesthetized horses. The effect of isoflurane dose on CBF, however, remains unresolved because it depends on the opposinginfluences of a decrease in CCP and cerebral vasodilation. (Am J Vet Res 2003;64:21–25)