non-depolarizing agents that block the Ach binding site

*atracurium

*mivacurium

depolarizing agents that send the muscle into contraction and desensitize them

*succinylcholine

these bind the alpha-site on the Nm receptor found on skeletal muscle, blocking depolarization of the muscle

they competitively inhibit Ach binding

they have NO EFFECT of CNS, cardiac or smooth muscle

atracurium is safe in renal and hepatic impairment, but it is spontaneously metabolized into laudanosine, which can cause seizures once off the drug. CI in pts w Hx of seizure

mivacurium is metabolized by plasma cholinesterase, so slow metabolizers will have longer effect of drug

toxicity or effect of these drugs can be reveresed with AchE inhibitors (neostigmine)

is a depolarizing/noncompetitive nicotinic agonist

initially stimulates (phase I)contraction, so will see fasciculations then moves into (phase II) desensitization

caution: some pts have abnormal ryanodine receptor that lets out way too much Ca2+ with the initial contraction induced by succinylcholine, which can send the pt into -> malignant hyperthermia (50% of pts who suffer this rxn have the mut ryanodine gene)

some patients will be slow metabolizers with atypical pseudocholinesterases, and will have increased effect and duration

hyperkalemia can increase the effect of the drug as well

centrally!!

can use benzo's through GABAa receptors, etc