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- Author or Editor: Ayako Imai x
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Objective—To determine the hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats.
Animals—12 healthy adult domestic shorthair cats.
Procedure—Cats were anesthetized by administration of isoflurane in oxygen. After instruments were inserted, end-tidal isoflurane concentration was set at 1.25 times the individual minimum alveolar concentration, and nitrous oxide was administered in a Latinsquare design at 0, 30, 50, and 70%. Each concentration was administered for 25 minutes before measurements were obtained to allow for stabilization. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured before and during noxious stimulation for each nitrous oxide concentration. Arterial and mixed-venous bicarbonate concentrations and oxygen saturation, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, arterial and mixed-venous oxygen contents, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated.
Results—Arterial pressure, central venous pressure, pulmonary arterial pressure, rate-pressure product, systemic and pulmonary vascular resistance indices, arterial PCO2, and PCV increased during administration of 70% nitrous oxide. Arterial and mixed-venous pH, mixed-venous PO2, and alveolar-to-arterial oxygen difference decreased during administration of 70% nitrous oxide. Results before and during noxious stimulation were similar.
Conclusions and Clinical Relevance—Administration of 70% nitrous oxide to isoflurane-anesthetized cats resulted in improved arterial pressure, which was related to a vasoconstrictive effect. (Am J Vet Res 2003;64:273–278)
Objective—To determine whether high intracranial pressure (ICP) during spontaneous ventilation (SV) in anesthetized horses coincides with an increase in intracranial elastance (ie, change in ICP per unit change of intracranial volume).
Animals—6 adult horses.
Procedure—Anesthesia was induced and maintained in each horse for 5 hours with isoflurane at a constant dose equal to 1.2 times the minimum alveolar concentration. Direct ICP measurements were obtained by use of a strain gauge transducer inserted in the subarachnoid space, and arterial blood pressure was measured from a carotid artery. Physiologic responses were recorded after 15 minutes of normocapnic controlled ventilation (CV) and then after 10 minutes of SV. Aliquots (3 mL) of CSF were removed from each horse during SV until ICP returned to CV values. Slopes of pressure-volume curves yielded intracranial elastance.
Results—Intracranial elastance ranged from 0.2 to 3.7 mm Hg/mL after removal of the first aliquot of CSF. Slopes of pressure-volume curves were largest following removal of the initial CSF aliquot, but shallow portions of curves were detected at relatively high ICPs (25 to 35 mm Hg). A second-order relationship between SV ICP and initial intracranial elastance was found.
Conclusions and Clinical Relevance—In horses anesthetized with isoflurane, small changes in intracranial volume can cause large changes in ICP. Increased intracranial elastance could further exacerbate preexisting intracranial hypertension. However, removal of small volumes of CSF may cause rapid compensatory replacement from other intracranial compartments, which suggests steady-state maintenance of an increase in intracranial volume during isoflurane anesthesia in horses. (Am J Vet Res 2004;65:1042–1046)
Objective—To develop a method for surgical placement of a commercial microsensor intracranial pressure (ICP) transducer and to characterize normal ICP and cerebral perfusion pressures (CPP) in conscious adult horses.
Animals—6 healthy castrated male adult horses (1 Holsteiner, 1 Quarter Horse, and 4 Thoroughbreds).
Procedure—Anesthesia was induced and maintained by use of isoflurane as the sole agent. Catheters were inserted percutaneously into the jugular vein and carotid artery. A microsensor ICP transducer was inserted in the subarachnoid space by means of right parietal craniotomy. The burr hole was then sealed with bone wax, the surgical incision was sutured, and the transducer was secured in place. Measurements were collected 1 hour after horses were able to stand during recovery from anesthesia.
Results—Mean ± SD values for ICP and CPP were 2 ± 4 and 102 ± 26 mm Hg, respectively.
Conclusion and Clinical Relevance—This report describes a relatively facile technique for obtaining direct and accurate ICP measurements for adult horses. The ICP values obtained in this study are within reference ranges established for other species and provide a point of reference for the diagnosis of abnormal ICP in adult horses. (Am J Vet Res 2002;63:1252–1256)
Objective—To test the hypothesis that isofluraneanesthetized horses during controlled ventilation and spontaneous ventilation exhibit temporal changes in cerebral hemodynamics, as measured by intracranial pressure and cerebral perfusion pressure, that reflect temporal changes in systemic arterial pressure.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized in left lateral recumbency with 1.57% isoflurane in O2 for 5 hours in 2 experiments by use of either controlled ventilation (with normocapnia) or spontaneous ventilation (with hypercapnia) in a randomized crossover design. Intracranial pressure was measured with a subarachnoid strain-gauge transducer. Carotid artery pressure, central venous pressure, airway pressures, blood gases, and minute ventilation also were measured.
Results—Intracranial pressure during controlled ventilation significantly increased during constant dose isoflurane anesthesia and thus contributed to decreasing cerebral perfusion pressure. Intracranial pressure was initially higher during spontaneous ventilation than during controlled ventilation, but this difference disappeared over time; no significant differences in cerebral perfusion pressures were observed between horses that had spontaneous or controlled ventilation.
Conclusions and Clinical Relevance—Cerebral hemodynamics and their association with ventilation mode are altered over time in isoflurane-anesthetized horses and could contribute to decreased cerebral perfusion during prolonged anesthesia. (Am J Vet Res 2003;64:1444–1448)
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)
Objective—To compare characteristics of horses recovering from 4 hours of desflurane anesthesia with and without immediate postanesthetic IV administration of propofol and xylazine.
Animals—8 healthy horses (mean ± SEM age, 6.6 ± 1.0 years; mean body weight, 551 ± 50 kg).
Procedures—Horses were anesthetized twice. Both times, anesthesia was induced with a combination of xylazine hydrochloride, diazepam, and ketamine hydrochloride and then maintained for 4 hours with desflurane in oxygen. Choice of postanesthetic treatment was randomly assigned via a crossover design such that each horse received an IV injection of propofol and xylazine or saline (0.9% NaCl) solution after the anesthetic episode. Recovery events were quantitatively and qualitatively assessed. Venous blood samples were obtained before and after anesthesia for determination of serum creatine kinase activity and plasma propofol concentration.
Results—Anesthetic induction and maintenance were unremarkable in all horses. Compared with administration of saline solution, postanesthetic administration of propofol and xylazine resulted in an increased interval to emergence from anesthesia but improved quality of recovery-related transition to standing. Compared with administration of saline solution, administration of propofol also delayed the rate of decrease of end-tidal concentrations of desflurane and carbon dioxide and added to conditions promoting hypoxemia and hypoventilation.
Conclusions and Clinical Relevance—Propofol and xylazine administered IV to horses after 4 hours of desflurane anesthesia improved the quality of transition from lateral recumbency to standing but added potential for harmful respiratory depression during the postanesthetic period.