NMB Flashcards
fade during TOF is caused by
antagonism of pre-synaptic nicotinic receptors
acetylcholine - autonomic nervous system - which branch?
both! SNS and PNS but mostly Parasympathetic
how do depolarizing NMB’s work
depolarize the muscle fiber leaving it constantly stimulated and unable to be affected by Ach
how do non-depolarizers work
competitively block Ach from binding to receptors post-synaptically
non-depolarizers participate in ___ antagonism
competitive
ED95
dose of NMB necessary to produce 95% suppression of the single twitch response
ED95 when volatile anesthetic is used in conjunction with NMB
greatly reduced
use ___times the ED95 dose for tracheal intubation
2
which muscles are blocked first
small rapidly moving muscles - eyes and fingers
which muscle is blocked last
abdomen (diaphragm)
which muscle is a good predictor of laryngeal relaxation?
orbicularis
which muscles recover first?
larger muscles because they have more blood flow. (recovery in reverse order than paralysis)
ach channels are
ligand gated ion channels.
___% suppression of single twitch response is adequate for surgery
90
which non-dolparizers have a higher incidence of histamine release
benzylisoquinolinium
quaternary ammonium are ionized or lipophilic?
highly ionized.
quaternary cns effects?
none
quaternary binds to alpha sub unit ___ synaptically
post
quaternary are not completely specific, meaning they bind to
cardiac muscarinic and autonomic ganglia nicotinic
are quaternary’s highly protein bound?
no
which non-depol are long acting
panc, dox, and pipe
which non-depol are intermediate acting
atra, vec, roc, cis
which non-depol are short acting
miv
onset of succs
30-60s
duration of succs
3-5min
succs MOA
binds to one or both alpha subunits at nicotinic receptor. mimics Ach
does succs have a shorter or longer duration than ach
longer
succs increases K by
.5meq/L
tof ratio for succs
> 0.7
which recovers first.. diaphragm or peripheral muscles?
diaphragm
succs is broken down by
plasma cholinesterase in the blood
what things reduce the amt of plasma cholinesterase
severe liver dz, neostigmine, high estrogen levels. reglan
obese patients and cholinesterases
they have increased levels - so break down succs faster - need more
what kind of cardiac side effects does succs cause
arrhythmias - sinus brady, junctional rhythm, sinus arrest…. some people get tachycardia and inc BP due to ganglia stimulation (some people get sympathetic boost)
what should you give to treat the bradycardia with succs?
epi. not atropine
if something is anti-muscarinic, it is also
anticholinergic
succs causes increased pressure where
intragastric, intraocular, intracrmail.
which drug causes an increase in mortality for brain injured patients in the ED
succes
what is the TOF ratio for non-depol
<0.7
which ND’s cause histamine release
atra and miv
panc CV effects
increased HR, MAP, CO. blocks vagal/muscarinic.. so anti-parasympathetic, SNS activation
panc CV don’t give
digoxin
critical myopathy is common with which class
aminosteroids , higher risk with corticosteroids
critical myopathy what happens to pt’s
long term paralysis for mech vent >6 days
NMB’s are enhanced by
volatile anesthetics, aminoglycosides, LA’s, antiarrhymics, diuretics, Mg, Li
how do anticonvulsants affect NMB
affect cyp enzymes
how does cyclosporine affect NMB
prolonged blockade
how do corticosteroids affect NMB
compounded muscle weakness
how do sympathomimetics affect NMB
increased onset d/t changes in blood flow. argument on whether it leads to shorter or longer duration.
hypothermia ___ duration of NMB
prolongs
how does HYPOkalemia affect NMB
resistance to succs and increases sensitivity to NDNMB
how does HYPERkalemia affect NMB
increases succs effects and opposes NDNMB
how does paresis or hemiplegia affect NMB
have extra junctional receptors so need more, mega doses
are men or women more sensitive to NMB?
women
long acting panc and pipe NDNMB’s have ___ positive nitrogens
2
which long acting is a benzyl
dox
panc structure
bisquaternary aminosteriod
panc and renal failure
80% excreted unchanged in urine, renal failure reduces clearance up to 50%
panc metabolite
3-desacetylpancuronium (half as potent as panc)
how does liver disfunction effect panc
longer half life
which NMB is enhanced by resp acidosis
panc
ronium’s are
aminosteriods
curium’s are
benzyl’s
which NMB has an increased potency and shorter duration in infants
pipe
which NDNMB have only 1 positive nitrogen and what does that do
vec and roc - lipophiilc.. hepatic/renal clearance.
priming principle for roc
- small dose binds spare receptors, 4 min later deliver the rest.
which NDNMB is 82% protein bound
atra
which NDNMB’s undergo hoffman elimination
atra and cis
hoffman elimination is accelerated by ___ and slowed by ____
alkalosis, acidosis
which drugs have laudanosine as a metabolite
atra and cis. mostly atra - inactive at NMJ but may be CNS stimulant and increase MAC
laudanosine causes peripheral ____ and ___ MAC of volatile anesthetics
vasodilation, increases
atra CV
at 3x ED95 increase HR, decrease MAP. histamine release
H1 and H2’s help with
histamine release with atra
long term h2 blocker use may do what to CV effects of atra
exacerbate CV effects d/t histamine
atra infant dose
half dose of older children
cis main difference
no histamine release
how is vec eliminated
both hepatic and renal. lipid soluble!
vec and biliary excretion
40% unchanged in bile, exaggerated response with hepatic cirrhosis
vec and urinary elmin
30% unchanged in urine, half life prolonged in renal failure
cumulative effects of vec panc and atra
panc> vec> atra
which has a slight vagolytic effect… vec or roc?
roc
vec has a ___ onset in infants
rapid
vec and elderly
decreased clearance, longer recovery
onset of roc
1-2min
