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High concentrations of enflurane may cause spike-and-wave activity and muscle twitching. Most inhaled anesthetics are bronchodilators, but desflurane is a pulmonary irritant. Tomidate may cause pain and myoclonus on in ection and nausea postoperatively.
High concentrations of enflurane may cause spike-and-wave activity and muscle twitching. Most inhaled anesthetics are bronchodilators, but desflurane is a pulmonary irritant. Tomidate may cause pain and myoclonus on in ection and nausea postoperatively.
High concentrations of enflurane may cause spike-and-wave activity and muscle twitching. Most inhaled anesthetics are bronchodilators, but desflurane is a pulmonary irritant. Tomidate may cause pain and myoclonus on in ection and nausea postoperatively.
High concentrations of enflurane may cause spike-and-wave activity
and muscle twitching, but this effect is unique to this drug.
nitrous oxide has low anesthetic potency (ie, a high M!", it exerts marked analgesic and amnestic actions #nflurane and halothane are myocardial depressants that decrease cardiac output, whereas isoflurane, desflurane, and sevoflurane cause peripheral vasodilation. $itrous oxide has the smallest effect on respiration. Most inhaled anesthetics are bronchodilators, but desflurane is a pulmonary irritant and may cause bronchospasm. %he pungency of enflurane causing breath-holding limits its use in anesthesia induction &rolonged exposure to nitrous oxide decreases methionine synthase activity and may lead to megaloblastic anemia. 'antrolene is indicated for the treatment of malignant hyperthermia life-threatening condition, with supportive management Neuroleptanesthesia is a state of analgesia and amnesia is produced when fentanyl is used with droperidol and nitrous oxide (ecovery from the actions of remifentanil is faster than recovery from other opioids used in anesthesia because of its rapid metabolism by blood and tissue esterases &ropofol has antiemetic actions, Etomidate %his imida)ole derivative affords rapid induction with minimal change in cardiac function or respiratory rate and has a short duration of action. %he drug is not analgesic, and its primary advantage is in anesthesia for patients with limited cardiac or respiratory reserve. #tomidate may cause pain and myoclonus on in*ection and nausea postoperatively. &rolonged administration may cause adrenal suppression Dexmedetomidine %his centrally acting +,-adrenergic agonist has analgesic and hypnotic actions when used intravenously This can be accomplished by administration of a vasoconstrictor (usually an -agonist sympathomimetic) with the local anesthetic agent. Cocaine is an important exception because it has intrinsic sympathomimetic action due to its inhibition of norepinephrine reuptake into nerve terminals. The longer-acting agents (eg, bupivicaine, ropivicaine, tetracain) are also less dependent on the coadministration of vasoconstrictors etabolism of ester local anesthetics is carried out by plasma cholinesterases (pseudocholinesterases) and is very rapid for procaine (half-life, !"# min), slower for cocaine, and very slow for tetracaine). The amides are metaboli$ed in the liver, in part by cytochrome %&'( )so$ymes *ll local anesthetics are capable of producing a spectrum of central e+ects, including light-headedness or sedation, restlessness, nystagmus, and tonic-clonic convulsions.(,-.-T/) 0ith the exception of cocaine, all local anesthetics are vasodilators. The (,)isomer, levobupivicaine, is less cardiotoxic. 0hen cocaine is used as a drug of abuse, its cardiovascular toxicity includes severe hypertension with cerebral hemorrhage, cardiac arrhythmias, and myocardial infarction. %rilocaine is metaboli$ed to products that include o-toluidine, an agent capable of converting hemoglobin to methemoglobin The ester-type local anesthetics are metaboli$ed to products that can cause antibody formation in some patients. 1rugs that are metaboli$ed (eg, mivacurium, by plasma cholinesterase) or eliminated in the bile (eg, vecuronium) have shorter durations of action (!("#( min) than those eliminated by the kidney (eg, metocurine, pancuronium, pipecuronium, and tubocurarine), which usually have durations of action of less than 2' min )n addition to hepatic metabolism, atracurium clearance involves rapid spontaneous breakdown (3ofmann elimination) to form laudanosine and other products. *t high blood levels, laudanosine may cause sei$ures. Cisatracurium, a stereoisomer of atracurium, is also inactivated spontaneously but forms less laudanosine and currently is one of the most commonly used muscle relaxants in clinical practice. 4f the available nondepolari$ing drugs, rocuronium (5("!#( s) has the most rapid onset time ,uccinylcholine is metaboli$ed by cholinesterase (butyrylcholinesterase or pseudocholinesterase) in the liver and plasma. )t has a duration of action of only a few minutes if given as a single dose