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Enflurane muscle effects

The anesthesiologist selects the anesthetic drug that will produce safe anesthesia, analgesia (absence of pain), and in some surgeries, effective skeletal muscle relaxation. General anesthesia is most commonly achieved when the anesthetic vapors are inhaled or administered intravenously (IV). Volatile liquid anesthetics produce anesthesia when their vapors are inhaled. Volatile liquids are liquids that evaporate on exposure to air. Examples of volatile liquids include halothane, desflurane, and enflurane. Gas anesthetics are combined with oxygen and administered by inhalation. Examples of gas anesthetics are nitrous oxide and cyclopropane. [Pg.320]

Halothane exerts a pronounced hypotensive effect, to which a negative inotropic effect contributes. Enflurane and isoflurane cause less circulatory depression. Halothane sensitizes the myocardium to catecholamines (caution serious tachyarrhythmias or ventricular fibrillation may accompany use of catecholamines as antihypotensives or toco-lytics). This effect is much less pronounced with enflurane and isoflurane. Unlike halothane, enflurane and isoflurane have a muscle-relaxant effect that is additive with that of nondepolarizing neuromuscular blockers. [Pg.218]

Enflurane potentiates the effects of non-depolarising muscle relaxants. [Pg.64]

Enflurane causes a dose-related relaxation of uterine smooth muscle. At low inspired concentrations during Caesarean section, it prevents maternal awareness without an increase in blood loss or undesirable effects on the baby. [Pg.64]

Halothane, isoflurane, and enflurane have similar depressant effects on the EEG up to doses of 1-1.5 MAC. At higher doses, the cerebral irritant effects of enflurane may lead to development of a spike-and-wave pattern and mild generalized muscle twitching (ie, myoclonic activity). However, this seizure-like activity has not been found to have any adverse clinical consequences. Seizure-like EEG activity has also been described after sevoflurane, but not desflurane. Although nitrous oxide has a much lower anesthetic potency than the volatile agents, it does possess both analgesic and amnesic properties when used alone or in combination with other agents as part of a balanced anesthesia technique. [Pg.547]

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]

Kataoka et al. (1994) studied the negative inotropic effects of sevoflurane, isoflurane, enflurane and halothane in canine blood-perfused papillary muscles. [Pg.214]

The potentiation of D-tubocurarine block produced by enflurane slowly continues to increase with time, even after the usual equilibration period has passed (SEDA-5, 132) (128). This does not occur with halothane, and the discrepancy is said to mean that more D-tubocurarine will be required in the first hour of enflurane anesthesia than during equipotent halothane anesthesia, but that thereafter less will be required during enflurane anesthesia. It has been suggested that enflurane, unhke halothane, may produce an effect on muscle that takes time to develop. This may also be part of the mechanism, in addition to the... [Pg.2494]

Electrolyte imbalance, and diseases that lead to electrolyte imbalance, such as adrenal cortical insufficiency, alter neuromuscular blockade. Depending on the nature of the imbalance, either enhancement or inhibition may be expected. Magnesium sulfate, used in the management of toxemia of pregnancy, enhances the skeletal-muscle-relaxing effects of pancuronium. Antibiotics such as aminoglycosides, tetracyclines, clindamycin, lincomycin, colistin, and sodium colistimethate augment the pancuronium-induced neuromuscular blockade. Anesthetics such as halothane, enflurane, and isoflurane enhance the action of pancuronium, whereas azathioprine will cause a reversal of neuromuscular blockade. [Pg.540]

Because diethyl ether (commonly known simply as ether) is a short-lived muscle relaxant, it has been widely used as an inhalation anesthetic. However, because it takes effect slowly and has a slow and unpleasant recovery period, other compounds, such as enflurane, isoflurane, and halothane, have replaced ether as an anesthetic. Diethyl ether is still used where there is a lack of trained anesthesiologists, since it is the safest anesthetic to administer by untrained hands. Anesthetics interact with the nonpolar molecules of cell membranes, causing the membranes to swell, which interferes with their permeability. [Pg.453]

Muscle Enflurane produces significant skeletal muscle relaxation and noticeably enhances the effects of nondepolarizing muscle relaxants. As with other inhalational agents, enflurane relaxes uterine smooth muscle. [Pg.236]

CNS effects Inhaled anesthetics decrease brain metabolic rate. They reduce vascular resistance and thus increase cerebral blood flow. This may lead to an increase in intracranial pressure. High concentrations of enflurane may cause spike-and-wave activity and muscle twitching, but this effect is unique to this drug. Though nitrous oxide has low anesthetic potency (ie. a high MAC), it exerts marked analgesic and amnestic actions. [Pg.232]

Interestingly, anticholinesterases, ACH and ion antagonize competitively pancuronium bromide effectively however, its activity is virtually enhanced by general anaesthetics, for instance halothane, ether, enflurane etc. (see Chapter 4). Therefore, the latter substantial potentiation in pharmacological activity is particularly useful to the anaesthetist due to the faet that it is administered invariably as an adjunct to the anaesthetic procedure in order to cause simultaneous relaxation of the skeletal muscle. [Pg.247]

Nitrous Oxide Mechanism unknown. Low potency as an anesthetic, but very useful as an adjunct. No muscle relaxant effects. When combined with haiothane or enflurane, much less hypotension occurs at equivalent depth of anesthesia. Little effect. [Pg.52]

It is quite potent, however, and produces good analgesia and muscle relaxation. The use of ether at present is rather limited, mainly because of its undesirable side effects. Halothane, CFsCHBrCI, comes closest to an ideal inhalation anesthetic at present, but halogenated ethers such as enflurane, CF2H—O—CF2CHCIF, are also used. [Pg.243]


See other pages where Enflurane muscle effects is mentioned: [Pg.408]    [Pg.403]    [Pg.1]    [Pg.304]    [Pg.64]    [Pg.285]    [Pg.595]    [Pg.2494]    [Pg.478]    [Pg.566]    [Pg.408]    [Pg.102]    [Pg.125]   
See also in sourсe #XX -- [ Pg.236 ]




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