skeletal muscle relaxants Flashcards
tubocurarine
LONG ACTING
benzylisoquinolines
non-depolarizing blocker
may release histamine - give with antihistamine
may also block nicotinic receptors in ANS and adrenal medulla – hypotension and tachycardia
atracurium
INTERMED ACTING
benzylisoquinolines
non-depolarizing blocker
forms metabolite = laudanosine - may cause hypotension and seizures
(replaced by cisatracurium)
no inc in half life in pt with renal failure
cisatracurium
INTERMED ACTING
benzylisoquinolines
non-depolarizing blocker
forms less laudanosine and causes less histamine release
REPLACED atracurium
mivacurium
SHORT ACTING (only one)
benzylisoquinolines
non-depolarizing blocker
hydrolyzed by butyrylcholinesterase
pancuronium
LONG ACTING
ammonio steroids
non-depolarizing blocker
AE: mod tachycardia d/t blockade of M2
rocuronium
INTERMED ACTING
ammonio steroids
non-depolarizing blocker
most rapid == used for rapid sequence intubation
vecuronium
INTERMED ACTING
ammonio steroidsnon-depolarizing blocker
succinylcholine
only depolarizing blocker = 2 ach molecules bound
very short duration b/c of butyrylcholinesterse hydrolysis
remember butrylchoinesterase polymporphism = prolonged NM blockade
MOA - nondepolarizing blockers
competitive antagonists = overcome with inc acetylcholine (via AchE-I)
MOA - depolarizing blockers
activates nicotinic receptor depolarizes junction
causes fasiculations
not metabolizes by AchE
–> flaccid paralysis
rapid onset - short duration
NM blockers
all contain quarternary groups = doesn’t cross BBB
inactive if given PO
half life vs kidney/liver excretion
kidney = longer t 1/2 liver = shorter t 1/2
benzylisoquinolones AE
hypotension d/t histamine release and slight ganglionic blockade (only with tubocurarine)
no effect on M2 receptors
ammonio steroids AE
produce tachycardia d/t blockade of muscarinic receptors == arrhythmias
no ganglion blockade
tubocurarine AE
ganglion blockade = hypotension and tachycardia
release histamine
succinylcholine AE
activates all autonomic cholinoreceptors
nicotinic = muscle pain muscarinic = bradycardia
histamine release
d/t contractions at beginning:
hyperkalemia
increased intraocular pressure
inc intragastric pressure
malignant hyperthermia
NO CNS effects = no BBB penetration
drugs that enhance NM blockade
inhaled anesthetics
aminoglycosides
tetracyclines
aging and disease vs drug response to NM blockers
MG = inc NM blockade
adv age = prolongs blockade
severe burns and UMN dz = resistant to nondepolarizing relaxants
depolarizing blockers contraindications
hx malignant hyperthermia or myopathies
burns
trauma
denervation of skeletal muscle
UMN injury
reverse nondepolarizing NM blockade
AchE-I
atropine and glycopyrrolate are given to prevent bradycaria
spasmolytic drugs categories:
1) for chronic spasm
a: act in CNS
b: act directly on muscle
2) acute spasm
drugs that act in CNS as tx for chronic spasms
diazepam: agonist at GABA(a)
baclofen: agonist at GABA(b)
tizanidine: alpha2 agonist in CNS
baclofen
agonist at GABA(b)
used for chronic spasms tx
tizanidine
alpha2 agonist in CNS
used for chronic spamsms
botulinum toxin
act on skeletal muscle
for spastic disorders/cerebral palsy
drugs for acute spasm
centrally acting
relief of acute muscle spasm by trauma
cyclobenzaprine = prototype
AE: antimuscarinic side effects
