What are the nondepolarizing NMJ blocking drugs
cisatracurium tubocurarine pancuronium rocuronium vecuronium
which nondepolarizing blocking drugs are steroid derivatives
pancuronium
rocuronium
vecuronium
what is the depolarizing NMJ blocking drug
succinylcholine
what drugs do we have that are muscle relaxants aka spasmolytics
dantrolene
botulinum toxin
What are the AChEI
echothiophate edrophonium neostigmine physostigmine pyridostigmine
what are the antimuscarinic agents
atropine
what are the cholinesterase reactivators
pralidoxime
what are the 2 main therapeutic groups of drugs that affect skel mm function
NMJ blockers
spasmolytics
how do nondepolarizing NMJ blockers work
antagonists of nAChR
how do depolarizing NMJ blockers work
excess depolarizing agonist, so AchR taken up
What makes NMJ blockers hard to enter CNS
one or 2 quaternary nitrogens,, poorly lipid soluble
how are NMJ blockers administered
parenterally because highly polar and inactive orally
what muscles are more R to NMJ blockades
trunk, paraspinals and diaphragm
what is the last muscle to be paralyzed and quickest to recover from a NMJ blockade
diaphragm
what is the least potent nondepolarizing NMJ blocker
rocuronium
how do you reverse a NMJ blockade
Ach or succinylcholine
what cholinesterase inhibitors can antagonize nondepolarizing blockers blockade
neostigmine and pyridostigmine because increase ACh availability and increase release of NT from motor nerve terminal
why is edrophonium less effective in reversing the effects of nondepolarizing blockers
no effect on NT release
what is given to minimize adverse effects of cholinesterase inhbitors
anticholinergic agents like atropine
what are the adverse effects of cholinesterase inhibitors
bradycardia, bronchoconstriction, salivation, nausea, vomiting
adverse effects nondepolarizing NMJ blockers
histamine release which can cause wheal reaction, bronchospasm, hypotension and bronchial and salicary secretion
at large doses tubocurarine and metocurine can cause what
ACh blockade at autonomin ganglia in adrenal medulla causing a dec in BP and tachycardia
why is d tubocurarine not used anymore
long duration and caused significant histamine release
what drugs can potentiate the NMJ blockade from nondepolarizing afents
inhaled anesthetics
aminoglycosides
be careful with NMJ blockers in what population subtype
elderly because longer duration from decreased hepatic and renal clearance
what patients are resistant to nondepolarizing muscle relaxants
patients with severe burns and with UMN disease
which nondepolarizing NMJ blocker has very little to no CV effects
cisatracurium
which nodepolarizing relaxant has the shortest duration of action
mivacurium
inermediate acting steroid muscle relaxants are excreted how
biliary excretion or hepatic metabolism
what metabolizes steroid mm relaxants
3- 17- or 3,17 hydroxy derivatives
which muscle relaxant is least likely to cause histamine release
steroidal NMJ blockers
agent of choice for patients with normal renal and hepatic function requireing paralysis for more than one hour
pancuronium
adverse effects pancuronium
tachy
HTN
increased CO from vagal blockade
most rapid time onset steroidaly relaxant
rocuronium
common use rocuronium
used to facilitate a difficult tracheal intubation because rapid acting
basically no CV effects
alternative to rocuronium for intubation
vecoronium
PK of succinylcholine
short duration because rapid hydrolysis and inactivation by butyrylcholinesterase
What is the phase I block for succinylcholine
depolarizes motor end plate and spreads to adjacent membranes. remain depolarized (block)
what augments the phase I depolarizing block ofd succinylcholine
cholinesterase inhibitors
what is the phase II desensitizing block of succinylcholine
continued exposure causes intiial depolarization to decrease and membrane repolarized. R has to be desensitized until it can depolarize again
what reverses the phase II block by succinylcholine
AChE inhibitors
what occurs with standad dose IV succinylcholine
fasciculations within 30 sec then paralysis withing 90 sec
initiall arm and neck, leg muscles then respiratory muscles
when is succinylcholine used
EM surgery when need to secure airway rapidly
what degrades succinylcholine
plasma cholinesterases
CV effects of succinylcholine
cardiac arrhythmias when administered with halothane anesthesia
negative inotropic and chronotropic effects
large doses cause positive inotropic and chronotropic effects
What acid base status does succinylcholine cause
hyperkalemia
adverse effects succinylcholine
increased intraocular P
increased intragastric P
muscle pain
slight histamine release
CI to succinylcholine
personal or familial Hx of malignant hyperthermia
myopathies with elevated CPK values
acute phase injury following major burns
multiple trauma
extensive denervation of skel mm or UMN injury
black block warning on succinylcholine
acute rhabdomyolysis with hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death if administered to child with undiagnosed skel mm myopathy
what drug if used with succinulcholine can induce malignant hypertermia
volatile anesthetics