Skeletal Muscle Relaxants

Front 1

Long-duration agents - Nondepolarizing relaxing drugs

Back 1

D-tubocurarine, pancuronium

Front 2

Intermediate (most commonly used): Nondepolarizing relaxing drugs

Back 2

Vecuronium
Atracurium (metabolite laudanosine, can cross BBB and cause seizures)
Cisatracurium (stereoisomer of atracurium, does not produce laudanosine)

Front 3

Short-acting: Nondepolarizing relaxing drugs

Back 3

mivacurium

Front 4

Depolarizing relaxing drugs - Shortest duration of action (rapid hydrolysis by plasma butyrylcholinesterase). Genetic variants of BChE known, but rare; some patients experience prolonged blockade due to slower hydrolysis

Back 4

succinylcholin

Front 5

Succinylcholine binds to nicotinic receptor to open the channel and cause depolarization of motor end plate. Not metabolized at the synapse, membrane remains depolarized (unresponsive to stimuli). Repolarization of end plate is lacking, and paralysis results. Phase is augmented, not reversed by AchE inhibitors

Back 5

Phase I block (depolarizing):

Front 6

Membrane becomes repolarized, but is still desensitized (mechanism unclear). Over time, reversal with AchE inhibitors possible.

Back 6

Phase II block (desensitization):

Front 7

Reversal of nondepolarizing neuromuscular blockade - forms an inactive complex with steroidal neuromuscular blocking drugs (pancuronium, vecuronium, pipecuronium, rocuronium). Enables rapid reversal.

Back 7

Sugammadex

Front 8

Spasmolytic drugs - GABAB agonist; causes hyperpolarization of presynaptic neurons and reduces release of excitatory neurotransmitters both in brain and spinal cord). Produces less sedation than diazepam

Back 8

baclofen

Front 9

spasmolytic drug - a2 agonist that reduces spasticity with fewer cardiovascular effects than clonidine

Back 9

tizanidine

Front 10

Used for the relief of acute muscle spasm caused by the trauma or muscle strains
Act centrally at the level of brainstem; mechanism not well understood

Back 10

cyclobenzaprine