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Sevoflurane nervous system

Inhaled anesthetics change heart rate either directly by altering the rate of sinus node depolarization or indirectly by shifting the balance of autonomic nervous system activity. Bradycardia can be seen with halothane, probably because of direct vagal stimulation. In contrast, enflurane, and sevoflurane have little effect, and both desflurane and isoflurane increase heart rate. In the case of desflurane, transient sympathetic activation with elevations in catecholamine levels can lead to marked increases in heart rate and blood pressure when high inspired gas concentrations are administered. [Pg.546]

Inhaled (volatile) anesthetics potentiate the neuromuscular blockade produced by nondepolarizing muscle relaxants in a dose-dependent fashion. Of the general anesthetics that have been studied, inhaled anesthetics augment the effects of muscle relaxants in the following order isoflurane (most) sevoflurane, desflurane, enflurane, and halothane and nitrous oxide (least) (Figure 27-9). The most important factors involved in this interaction are the following (1) nervous system depression at sites proximal to the neuromuscular junction (ie, central nervous system) (2) increased muscle blood flow (ie, due to peripheral vasodilation produced by volatile anesthetics), which allows a larger fraction of the injected muscle relaxant to reach the neuromuscular junction and (3) decreased sensitivity of the postjunctional membrane to depolarization. [Pg.589]

The effects of desflurane and sevoflurane on bronchial smooth muscle reactivity have been compared in a randomized study of 40 patients (36). Anesthesia was induced with thiopental, followed by muscle relaxation and ventilation. Airway pressures were recorded during administration of desflurane or sevoflurane at one minimal alveolar concentration (MAC). Airway resistance increased by 5% in the desflurane group and fell by 15% in the sevoflurane group. The increase in airways resistance was greater in smokers and with desflurane, but did not differ with sevoflurane. The result was a surprise, given that desflurane stimulates the sympathetic nervous system. Thiopental also increased airways resistance by 10%. The result is important, because induction of anesthesia can cause bronchospasm and desflurane can exacerbate this. [Pg.1493]

Nervous System Sevoflurane produces effects on cerebral vascular resistance, cerebral metabolic consumption, and cerebral blood flow similar to those produced by isoflurane and desflurane. Sevoflurane can increase ICP in patients with poor intracranial compliance. The response to hypocapnia is preserved during sevoflurane anesthesia, and increases in ICP can be prevented by hyperventilation. [Pg.237]

NERVOUS SYSTEM A case report describes a healthy male patient who developed involxmtary movements of the arms and head after exposure to fentanyl [31 ]. In a randomised controlled trial of 112 children undergoing anaesthesia, 14.9% experience emergence delirium after fentanyl/propofol anaesthesia as compared to 38.9% receiving sevoflurane [32 j. [Pg.109]


See other pages where Sevoflurane nervous system is mentioned: [Pg.156]    [Pg.18]    [Pg.507]    [Pg.507]    [Pg.233]    [Pg.209]   
See also in sourсe #XX -- [ Pg.143 ]




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