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Depolarizing blockers

Depolarizing blockers Succinylcholine Anectine, others 1-1.5 5-8 Ultrashort... [Pg.143]

Tachycardia and a rise in blood pressure are occasionally seen. Other supraventricular and ventricular dysrhythmias are much less common. Ventricular fibrillation associated with suxamethonium is usually the result of hyperkalemia, but has also been reported in hypercalcemia (22) and is often seen in the course of malignant hyperthermia. Atropine, especially when given intravenously just before suxamethonium, is the most effective agent for the prevention of dysrhythmias. Hexafluorenium, D-tubocurarine, pancuronium, and other non-depolarizer blockers have also been reported as being effective in prevention. Severe hypotension can occur in patients with anaphylactoid reactions. [Pg.3256]

Competitive blockers (non-depolarizing blocker act by competing with acetylcholine at the nicotinic receptor, thereby blocking transmission and produdng a flaccid paralysis. The advantages are that this method does not cause muscle pain when the patient recovers from general anaesthesia. Also, the block can be reversed at the end of the... [Pg.191]

Explain the action of depolarizing blockers in skeletal muscle relaxation. [Pg.190]

What is the only depolarizing blocker currently approved for use in the United States ... [Pg.190]

Explain the physiologic response observed with the initial dose of a depolarizing blocker. [Pg.191]

Desensitization A phase of blockade by a depolarizing blocker during which the end plate repdarizes but is less than rtormally responsive to agonists (acetylcholine or succinylcholine)... [Pg.244]

Table 27-2. Comparison of a typical nondepolarizing neuromuscular blocker (tubocurarine) and a depolarizing blocker (sucdnylcholine). ... Table 27-2. Comparison of a typical nondepolarizing neuromuscular blocker (tubocurarine) and a depolarizing blocker (sucdnylcholine). ...
D. Reversal of Blockade The action of nondepolarizing blockers is readily reversed by increasing the concentration of normal transmitter at the receptors. This is best accomplished by administration of cholinesterase inhibitors such as neostigmine or pyridostigmine. In contrast, the paralysis produced by depolarizing blockers is increased by cholinesterase inhibitors during phase I. During phase II. the block produced by succinylcholine is usually reversible by cholinesterase inhibitors. [Pg.246]

The action of succinylcholine is antagonized by depolarizing blockers. To prevent fasciculations and postoperative pain caused by succinylcholine, a small nonparalyzing dose of a nondepolarizing drug is often given immediately before succinylcholine. The answer is (E). [Pg.251]


See other pages where Depolarizing blockers is mentioned: [Pg.583]    [Pg.585]    [Pg.144]    [Pg.62]    [Pg.184]    [Pg.2489]    [Pg.2489]    [Pg.3262]    [Pg.3532]    [Pg.192]    [Pg.257]    [Pg.245]    [Pg.246]    [Pg.248]    [Pg.250]    [Pg.551]    [Pg.18]   
See also in sourсe #XX -- [ Pg.143 , Pg.144 ]




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Depolarization

Depolarizer (

Depolarizers

Muscle relaxants depolarizing blockers

Neuromuscular blockers depolarizing

Non-depolarizing neuromuscular blockers

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