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126 Cards in this Set

  • Front
  • Back
Generic name of SCH
Anectine
Generic name of rocuronium
zemuron
generic name of atracurium
tracrium
generic name of cisatracurium
nimbex
generic name of vec
norcuron
generic name of pipercuronium
arduan
induction dose of SCH
1-1.5 mg/kg
induction dose of Roc
0.6-1.2
Generic name of SCH
Anectine
induction dose of Mivacurium
0.15-0.25mg/kg
Generic name of rocuronium
zemuron
induction dose of Vecuroinum
0.1mg/kg
generic name of atracurium
tracrium
generic name of cisatracurium
nimbex
generic name of vec
norcuron
generic name of pipercuronium
arduan
induction dose of SCH
1-1.5 mg/kg
induction dose of Roc
0.6-1.2
induction dose of Mivacurium
0.15-0.25mg/kg
induction dose of Vecuroinum
0.1mg/kg
induction dose of atracurium
0.3-0.5
induction dose of cis-atracurium
0.2 mg/kg
pancuronium induction dose
0.1
d-tubo induction dose
0.6 mg/kg
onset of sux
30-60 sec
onset of roc
45-90 sec
onset of mivacurium
2-3 min
onset of atracurium
2-4 min
onset of d-tubo
3-5 min
onset of cis-atracurium
2-4 min
induction dose of atracurium
0.3-0.5
induction dose of cis-atracurium
0.2 mg/kg
pancuronium induction dose
0.1
d-tubo induction dose
0.6 mg/kg
onset of sux
30-60 sec
onset of roc
45-90 sec
onset of mivacurium
2-3 min
onset of atracurium
2-4 min
onset of d-tubo
3-5 min
onset of cis-atracurium
2-4 min
onset of pancuronium
3-5 min
duration of sux
5-8 min
duration of roc
30-40 min
duration of mivacurium
12-18 min
duration of vec
30-40 min
duration of atracurium
30-40 min
duration of cis-stracurium
40-60 min
duration of panc
45-65
d-tubo duration
60-90 min
which are histamine releasers
atracurium, sux, mivacurium, d-tubo
what things up regulate AChR
upper or lower motor neuron lesions
muscle trauma
burns
immobilization
sepsis/inf
what things down regulate AChR
myasthenia gravis
organophosphate poisoning
chronic cholinesterase inhibition
what meds decrease neuromuscular blocking effects
corticosteroids
lasix at high doses
phenytoin
methylxanthines
order of muscles that are blocked
first to last
adductor pollices
orbicular
laryngeal
diaphragm
which are benzoisoquinlinium
atracurium
cisatracurium
mivacurium

histamine release reflects presence of tertiary amine
maintenance of atracurium
0.1-0.1
priming dose of atracurium
3-5 mg
atracurium metabolism
hoffman
plasma esterases
hoffman dependent on
ph and temp
cis metabolism
hoffman
primary route of elimination is metabolism for which
suc
atracurium
cis
mivacurium
biliary excretion is the primary elimination for
vec and roc
renal is primary metabolism for
d-tubo
metocurarine
panc
gallamine
pipercuronium
mivacurium is elimated by
plasma cholinesterases
which rarely used other than defasiculation due to large histamine release
d-tubo
maintenance of mivacurium
0.01-0.1mg/kg
maintenance dose for panc
.01-0.5mg/kg
which increase HR secondary to combination of ganglionic blockade and ihibition of reuptake of NE
panc
maintenance of roc
0.06-.6mg/kg
maintenance of vec
0.01-0.05mg/kg
which anticholinergics crosses BBB
physostigmine
does atropine cross BBB
yes
dose of atropine with edrophonium
0.01mg/kg
dose of atropine with neostigmine
0.02mg/kg
duration of atropine
30 min
onset of atropine
1 min
dose of glyco
0.01 mg/kg with neo or pyrido
onset of glyco
2-3 min
duration of glyco
2-3 hours HR effect
up to 7 anticholinergic effect
edrophonium dose
0.5-1.0 mg/kg
onset of edrophonium
1-2 min
what should you give before giving edrophonium and why
atropine
to prevent brady
duration of edrophonium
10 min
dose of pyrido
0.2mg/kg
max dose of pyrido
30 mg
peak of pyrido
6-15 min
duration of pyrido
120-180 min
which anticholinesterase most potent
neo
dose of neo
0.03-0.07mg/kg
onset of neo
6 min
peak of neo
6-15 min
dur of neo
60-120 min
how many achetylcholine receptors occupied before fade seen
75%
how many receptors occupied to completely suppress twitch
95%
which produce hypotension
suc
d-tubo
metocurarine
which causes hypertension
panc
gallamine
which produces brady and why
suc
mimics action of ACH and directly stimulates M receptors of SA node
which produces autonomic ganglionic blockade
d-tubo
metocurarine
does pcn change degree of sux block
no
does VA change degree of sux block
no
does LA change sux block
yes
does anticonvulsants change degree of nondepolarizers block
yes, decreases
how do burn inj change to degree of nondepolarizers block
decreased
what decreases normal metabolism of sux
liver disease
preg
neonate
which drugs irreversibly alter metabolism of sux
echothiophate
pesticides
normal dibucaine number
80
how is sux terminated
psuedocholinesterases
mechanism for myalgia side effect
shif of Ca intracellular
muscle spindle damage
asynchronous muscle contractions
how long and how much increased intraocular pressures with sux
5-15mmHG for 10 minutes
normal K increase with sux
0.5meq/l
does LA change sux block
yes
does anticonvulsants change degree of nondepolarizers block
yes, decreases
how do burn inj change to degree of nondepolarizers block
decreased
what decreases normal metabolism of sux
liver disease
preg
neonate
which drugs irreversibly alter metabolism of sux
echothiophate
pesticides
normal dibucaine number
80
how is sux terminated
psuedocholinesterases
mechanism for myalgia side effect
shif of Ca intracellular
muscle spindle damage
asynchronous muscle contractions
how long and how much increased intraocular pressures with sux
5-15mmHG for 10 minutes
normal K increase with sux
0.5meq/l
list EKG effects of hyperkalemia
peaked T
ST depression
prolonged PR
loss of P
QRS widening
do liver disease have a abnormal dibucaine number
no
measures quality not quanity
how many receptors blocked if TV >5ml/kg
80
how many receptors blocked if no fade in TOF
70
how many receptors blocked if head lift
50
why does reversals sometimes augment phase I block
also inhibits psuedocholinesterases which prolongs depolarizers