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227 Cards in this Set
- Front
- Back
|
what occurs with Ach receptors with a burn
|
there is an INCREASED number of Ach in response to burns
(e replaced g subunits) |
|
|
how long should succinylcholine be avoided post acute burn
|
24 hours
|
|
|
hyperkalemia has been documented to occur how long post burn
|
463 days
|
|
|
the "receptor effect" with Ach and burns should subside when
|
when the skin has regrown and infection has healed
|
|
|
succinylcholine should be avoided is possible for how long after skin has healed with a significant burn
|
at least 1-2 yrs
|
|
|
hyperkalemai induced by succinylcholine with a burn is NOT associated with what factor
|
the extent of the burn
|
|
|
what conditions are associated with hyperkalemia following succinylcholine for the first 6 months after injury
|
hemiplegia and paraplegia
|
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with nerve damage or neuromuscular dz hyperkalemia associated with succinylcholine correlates with what factor
|
the extent of muscle involvement
|
|
|
with nerve damage or neuromuscular dz is hyperkalemia related to succinylcholine attentuated by prior admin of NDMB
|
NO
|
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what is the cause of hyperkalemia related to admin of succinylcholine with nerve damage or neuromuscular dz
|
prob caused by UPregulation (an increased number of receptors)
|
|
|
hyperkalemai induced by succinylcholine with a burn is NOT associated with what factor
|
the extent of the burn
|
|
|
what conditions are associated with hyperkalemia following succinylcholine for the first 6 months after injury
|
hemiplegia and paraplegia
|
|
|
with nerve damage or neuromuscular dz hyperkalemia associated with succinylcholine correlates with what factor
|
the extent of muscle involvement
|
|
|
with nerve damage or neuromuscular dz is hyperkalemia related to succinylcholine attentuated by prior admin of NDMB
|
NO
|
|
|
what conditions are associated with hyperkalemia following succinylcholine for the first 6 months after injury
|
hemiplegia and paraplegia
|
|
|
what is the cause of hyperkalemia related to admin of succinylcholine with nerve damage or neuromuscular dz
|
prob caused by UPregulation (an increased number of receptors)
|
|
|
with nerve damage or neuromuscular dz hyperkalemia associated with succinylcholine correlates with what factor
|
the extent of muscle involvement
|
|
|
with nerve damage or neuromuscular dz is hyperkalemia related to succinylcholine attentuated by prior admin of NDMB
|
NO
|
|
|
what is the cause of hyperkalemia related to admin of succinylcholine with nerve damage or neuromuscular dz
|
prob caused by UPregulation (an increased number of receptors)
|
|
|
uremic neuropathy is associated with what condition with admin of succinylcholine
|
hyperkalemia
|
|
|
pts with intra-abdominal infection longer than one week what occurs with admin of succinylcholine
|
elevations in K+ (2.5 to 3.1 mEq)
|
|
|
hyperkalemia from succinylcholine can be treated how
|
with IMMEDIATE hyperventilation, Ca chloride, and sodium bicarb
(glucose and insulin can be given as well) |
|
|
what is the dose of Ca chloride for the treatment of hyperkalemia induced by succinylcholine
|
1-2 g
|
|
|
what is the dose of sodium bicarb for the treatment of hyperkalemia induced by succinylcholine
|
1 mEq/kg
|
|
|
what are the amts of glucose and insulin given during the treatment of hyperkalemia from succinylcholine
|
*glucose= 25-50 g
*insulin= 10-20 Units |
|
|
what could be considered for pts with increased K+ or renal dz for choice of NMB
|
agents other than succinylcholine such as agents like cis-atricurium that does not rely on the kidneys for elimination
|
|
|
how is myoglobinuria a result of succinylcholine admin
|
there is relatively large proteins from muscle breakdown as a result of sustained depolarization
|
|
|
myoglobinuria is usually cleared how
|
by healthy kidneys
|
|
|
when is myoglobinuria a concern with succinylcholine admin
|
with pts with renal insufficency and/or catabolic processes that increase serum muscle breakdown
|
|
|
myotonia dz may suffer what after succinylcholine wears off
|
sustained contiual contractions
|
|
|
what pt population may be a higher risk for malignant hyperthermia with succinylcholine admin
|
myotonia pts
|
|
|
what are the pressures that can be increased by succinylcholine
|
*intraocular
*intragastric *intracranial |
|
|
when does increased intraocular pressure occur with succinylcholine
|
1 min after injection
|
|
|
when does increased intraocular pressure PEAK after succinylcholine injection
|
2-4 mins
|
|
|
when does increased intraocular pressure SUBSIDE with injection of succinylcholine
|
by 6 mins
|
|
|
what may be done to decrease/lessen the increase in intraocular pressure caused by succinylcholine
|
*3 mg dTc
*1 mg pancuronium *? SL admin of nifedipine |
|
|
what pts do not show increases in intraocular pressure with admin of succinylcholine
|
pts that are well anesthesized and not straining or coughing
|
|
|
when is succinylcholine CONTRAindicated secondary to increases in intraocular pressure
|
it is NOT contraindicated for induction unless the anterior chamber of the eye is open (open globe injury)
|
|
|
what is the increased intragastric pressure caused by with admin of succinylcholine
|
it is d/t fasiculations of abd skeletal muscle
|
|
|
with increased intragastric pressure caused by succinylcholine what is possible
|
regurge and aspiration
|
|
|
what is the cause of possible regurge and aspiration when there is an increase in intrabdomial pressure caused by succinylcholine
|
incompetence of the gastroesphageal junction
|
|
|
at what pressure should you NOT ventilate above with increased intragastric pressure secondary to succinylcholine admin
|
> 20 cm H20
|
|
|
pts who are pregnant, have abdomen distened by acites, have bowel obstruction or a hiatal hernia should be mask ventilated at what
|
< 15-20 cm H20
|
|
|
what pts should be mask ventilated at less than 15-20 cm H20
|
pts who are pregnant, of have distension of abd by ascites or have bowel obstruction or a hiatal hernia
|
|
|
which NMB agent has the potential to INCREASE intracranial pressure
|
succinylcholine
|
|
|
a possible increase in intracranial pressure with succinylcholine can be attenuated when
|
after pretreatment of NON-depolarizing NMB
|
|
|
what is masseter muscle spasm
|
it is a frequent response to succinylcholine but can NOT be used to establish a dx of MH
|
|
|
what may be an EARLY indicator of malignant hyperthermia
|
masseter muscle spasm
|
|
|
is there an indication for a change to "non-triggering" anesthetics in the presence of isolated masseter spasm
|
NO
|
|
|
is succinylcholine a trigger for malignant hyperthermia
|
YES
along with VA |
|
|
what is malignant hyperthermia
|
a genetic defect in the reuptake of Ca from the sarcoplasmic retiuculum
|
|
|
masseter muscle spasm may be what kind of response
|
may be an EARLY sign of malignant hyperthermia or NORMAL s/e in children
|
|
|
when may succinylcholine be prolonged
|
in pts with plasmacholinesterase insufficiency (atypical pseudocholinesterase)
*esp HOMOzygous type |
|
|
what should ALWAYS be done before following succinycholine with a NON-depolarizing NMB
|
perform TOF
|
|
|
extrajunctional Ach receptor up regulation occurs with what condition
|
neuromuscular dz
|
|
|
pts with neuromuscular dz have what response to Ach
|
exaggerated hyperkalemic response
|
|
|
what is a complication that can occur secondary to up-regulation and exaggerated hyperkalemic response to succinylcholine
|
cardiac arrest
|
|
|
prior to RSI with succinylcholine what can be done with a NON-depolarizer
|
a defasciulating dose can be given
|
|
|
when is a defasciculating dose given
|
2 min before succinylcholine
|
|
|
a defasciculating dose has what effects
|
*attenuates increases in intragastric and intracranial pressure
*minimizes the incidence of fasiciculations |
|
|
if a pt is resistant to succinylcholine how should the succinylcholine dose be adjusted and how may this alter the kinetics
|
*the dose should be doubled
*may slow the onset |
|
|
after admin of succinylcholine what should be given for maintenance
|
a NON-depolarizing muscle relaxant
|
|
|
what should be done after admin of succinylcholine BEFORE admin of a NON-depolarizing muscle relaxant
|
check for neuromuscular function with a twitch monitor to id pseudocholinesterase deficiencies
|
|
|
what is tetanic stimulation like with a phase 1 block
|
NO fade
|
|
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what is tetanic stimulation like with phase 2 blocks
|
fade is present
|
|
|
what is post-tetanic stimulation like with phase 1 blocks
|
there is NONE
|
|
|
is post-tetanic stimulatin present with phase 2 blocks
|
YES
|
|
|
is train of four present with phase 1 blocks
|
NO
|
|
|
what is train of four like with phase 2 blocks
|
marked fade
|
|
|
what is the train of four ratio for phase 1 blocks
|
> 0.7
|
|
|
what is the train of four ratio for phase 2 blocks
|
< 0.4
|
|
|
what does edrophonium do to phase 1 blocks
|
AUGMENTS
|
|
|
what does edrophonium do to phase 2 blocks
|
ANTGONIZES
|
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|
what is the recovery like with phase 1 blocks
|
RAPID
|
|
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what is the recovery like with phase 2 blocks
|
increasingly PROLONGED
|
|
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what are the dose requirements (mg/kg) for a phase 1 block
|
2-3
|
|
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what are the dose requirements (mg/kg) for a phase 2 block
|
<6
|
|
|
does tachyphylaxis occur with a phase 1 block
|
NO
|
|
|
does tachyphylaxis occur with a phase 2 block
|
YES
|
|
|
when can succinylcholine be given after a NON-depolarizer is reversed with a cholinesterase inhibitor
|
it should NOT
-it should be AVOIDED if possible after reversal of NDMB with CI |
|
|
neostigmine and pyridostigmine are what class of drugs
|
cholinesterase inhibtors
|
|
|
the isoquinoline NDMB consist of what kind of "backbone"
|
isoquinoline with an ester bridge
|
|
|
what is the original isoquinoline
|
curarae
|
|
|
isoquiolines as a class tend to do what
|
release histamine
|
|
|
the ester bridge of the isoquinolines is degredated how
|
by plasma esterases
|
|
|
a histamine release is manifested how clinically
|
by a decrease in BP
|
|
|
what is the "function" of the ester bridge
|
to "spread" out the 2 isoquinolines in the molecule
|
|
|
what houses the ammonium molecule in the isoquinolines
|
the isoquinoline itself
|
|
|
what are the 2 classes of the NON-depolarizing muscle relaxants
|
1-aminosteriodals
2-isoquinolines |
|
|
the aminosteriodals the distance is maintained by what
|
an androstane skeleton
|
|
|
with the benzylisoquinolinium series the distance is maintained by what
|
linear diester-containing chains OR in the case of curare benzyl ethers
|
|
|
isoquinoline DIESTER linkage is seen with what drugs
|
*mivacurium
*doxacurium |
|
|
is a NMB necessary for tracheal intubation
|
NO
-they just FACLITATE it (create optimal conditions) |
|
|
what type of muscle has MORE ablilty to contract and MORE ability to resist NMB
|
striated
|
|
|
the higher the Ach receptor count in the muscle the (lesser or greater) the amt of NMB required
|
GREATER
|
|
|
when can a NMB be reversed
|
not until a degree of spontaneous recovery has occured
|
|
|
what are the other names for curare
|
*d-Tubocurarine
*dTc |
|
|
what is the intubation dose for curarae
|
0.6 mg/kg
|
|
|
what is the onset to max block with curare
|
5.7 min
(long) |
|
|
what is the duration of action with curare
|
81 min
|
|
|
is curare classified as short, intermediate or long acting
|
LONG
|
|
|
which NMB is a ganglionic blocker
|
curare
|
|
|
does curare cause histamine release
|
YES--significant
|
|
|
what is the trade name for atracurium
|
tracrium
|
|
|
what is the intubating dose for atracurium
|
0.5 mg/kg
|
|
|
what is the onset to max block with atracurium
|
3.2 min
|
|
|
what is the duration of action with atracurium
|
46 min
|
|
|
is atracurium considered short, intermediate or long acting
|
INTERMEDIATE
|
|
|
what type of renal and hepatic metabolism does atracurium have
|
NONE
|
|
|
what are the metabolic routes of atracurium
|
*hoffman elimination
*ester hydrolysis |
|
|
does atracurium have histamine release
|
YES in larger doses
|
|
|
does atracurium have any metabolic byproducts
|
YES--laudanosine
|
|
|
what is the trade name for cis-atracurium
|
Nimbex
|
|
|
what is the intubation dose for cis-atracurium
|
.15-.4 mg/kg
|
|
|
what is the onset to max block with cis-atracurium
|
7.7-1.9 min
|
|
|
what is the duration of action with cis-atracurium
|
46-91 mins
|
|
|
is cis-atracurium short, intermediate or long acting
|
INTERMEDIATE/SHORT
|
|
|
what type of renal/hepatic metabolism does cis-atracurium have
|
NONE
|
|
|
what are the metabolic routes for cisatracurium
|
*hoffman elimination
*ester hydrolysis |
|
|
does cis-atracurium have histamine release
|
NO
|
|
|
what is the trade name for doxacurium
|
Nuromax
|
|
|
what is the intubation dose for doxacurium
|
0.04-0.06 mg/kg
|
|
|
what is the onset to max block with doxacrium
|
7.6-4.4 min
|
|
|
what is the duration of action with doxacurium
|
77-123 min
|
|
|
what is doxacurium classified as short, intermediate or long acting
|
LONG
|
|
|
what CV side effects does doxacurium have
|
MINIMAL
|
|
|
what is the metabolism of doxacurium
|
excreted 70% unchanged in the urine, also excreted in bile
|
|
|
what are the metabolites of doxacurium
|
NO active metabolites
|
|
|
what is the trade name of mivacurium
|
MIVACRON
|
|
|
what is the intubation dosage of mivacurium
|
0.15-0.25 mg/kg
|
|
|
what is the onset to max block with mivacurium
|
3.3-2.1 min
|
|
|
what is the duration of action with mivacurium
|
14.5-21 min
|
|
|
what is mivacurium classified as short, intermediate or long acting
|
INTERMEDIATE/SHORT
|
|
|
which isoquinoline is the closest to succinylcholine in DOA and recovery
|
mivacurium
|
|
|
how is mivacurium metabolized
|
by plasma cholinesterase
|
|
|
is mivacurium reversed by anticholinesterases
|
YES
|
|
|
what is the ED95 under N20/O2 for d-tubocurare
|
0.5
|
|
|
what is the ED95 under N20/O2 for doxacurium
|
0.025
|
|
|
what is the ED95 under N20/O2 for atracurium
|
0.23
|
|
|
what is the ED95 under N20/O2 for cis-atracurium
|
0.05
|
|
|
what is the ED95 under N20/O2 for mivacurium
|
0.08
|
|
|
what is the supplemental dose after intubation for d-Tubocurare
|
0.1
|
|
|
what is the supplemental dose after intubation for doxacurium
|
0.005-0.01
|
|
|
what is the supplemental dose after intubation for atracurium
|
0.1
|
|
|
what is the supplemental dose after intubation for cis-atracurium
|
0.02
|
|
|
what is the supplemental dose after intubation for mivacurium
|
0.05
|
|
|
what is the dosage for relaxation with N20 for d-Tubocurare
|
0.3
|
|
|
what is the dosage for relaxation with N20 for doxacurium
|
0.02
|
|
|
what is the dosage for relaxation with N20 for atracurium
|
0.3
|
|
|
what is the dosage for relaxation with N20 for cis-atracurium
|
0.05
|
|
|
what is the dosage for relaxation with N20 for mivacurium
|
0.1
|
|
|
what is the dosage for relaxation with VAA for d-Tubocurare
|
0.15
|
|
|
what is the dosage for relaxation with VAA for doxacurium
|
0.02
|
|
|
what is the dosage for relaxation with VAA for atracurium
|
0.15
|
|
|
what is the dosage for relaxation with VAA for cis-atracurium
|
0.04
|
|
|
what is the dosage for relaxation with VAA for mivacurium
|
0.08
|
|
|
what should be done to limit the duration of action
|
avoid excessive dosing
|
|
|
intubation dose is how many times ED 95
|
2 (3)
|
|
|
an intubating dose approximates to what of ED50
|
4 x
|
|
|
the lowest possible maintenance dose is guided by what
|
peripheral nerve stimulator
|
|
|
what should be avoided with a maintenance dosage
|
abolishing twitch or TOF
|
|
|
what is the bolus amt for a INTERMEDIATE and SHORT acting NDMR
|
1/4 initial dose
|
|
|
what is the bolus amt for a LONG acting NDMR
|
1/10 of initial dosage
|
|
|
when should boluses NOT be given
|
until clear evidence of initiation of recovery from the previous dose is apparent
|
|
|
if you use a NDMR to intubate when approximately will twitches return
|
in about 30 min
|
|
|
aminosteriodal NDMR have what type of backbone
|
steriodal
|
|
|
aminosteroidals as a class tend to do what
|
increase HR
|
|
|
aminosteriodals are metabolized how
|
primarily liver with some degree of renal excretion
|
|
|
addition of a methyl funtional group to the aminosteriodal base does what
|
increases potency
(the more methyl groups the more potent) |
|
|
what is the brand name for pancuronium
|
Pavulon
|
|
|
what is the intubation dose for pancuronium
|
.08 - .12
(.1) |
|
|
what is the onset to max block with pancuronium
|
4 min
|
|
|
what is the duration of action with pancuronium
|
100 mins
|
|
|
what is pancuronium classified as short, intermediate or long acting
|
LONG
|
|
|
what CV side effects does pancuronium have
|
it is a vagolytic
(causes tachycardia) |
|
|
does pancuronium have histamine release
|
NO
|
|
|
which NMB has butyrylcholinesterase-inhibiting properties
|
pancuronium
|
|
|
what is the trade name for vecuronium
|
norcuron
|
|
|
what is the intubation dose for vecuronium
|
0.1 - .2
|
|
|
what is the onset to max block with vecuronium
|
2.4 min
|
|
|
what is the duration of action with vecuronium
|
44 min
|
|
|
how is vecuronium classified short, intermediate or long acting
|
INTERMEDIATE
|
|
|
what kind of CV effects does vecuronium have
|
MINIMAL CV effects
(NO increase in HR) |
|
|
does vecuronium have a histamine release
|
NO
|
|
|
which NMB comes as a lypophilized powder
|
vecuronium
|
|
|
what is the trade name for pipecuronium
|
Arduan
|
|
|
what is the intubation dose for pipecuronium
|
0.08 - .1
|
|
|
what is the onset to max block for pipecuronium
|
3.6 min
|
|
|
what is the duration of action for pipecuronium
|
94 min
|
|
|
how is pipecuronium classified short, intermediate or long acting
|
LONG
|
|
|
what type of CV side effects does pipecuronium have
|
MINIMAL
(some increase in HR) |
|
|
what type of excretion does pipecuronium have
|
urine, bile and liver
|
|
|
what is the trade name for rocuronium
|
Zemuron
|
|
|
what is the intubation dose for rocuronium
|
0.6 - 1.2 mg/kg
|
|
|
what is the onset to max block for rocuronium
|
1.5-2 min
|
|
|
what is the duration of action for rocuronium
|
30-50 min
(may last longer with 1.2 dosage) |
|
|
how is rocuronium classified short, intermediate or long acting
|
INTERMEDIATE
|
|
|
what CV efffects does rocuronium have
|
some vagolytic action
-increased HR (minimal compared to pancuronium) |
|
|
what can be done with NDMR if the intubating dose is doubled
|
the speed of onset is INCREASED
|
|
|
what is significant about rapacuronium/raplon
|
it is NO longer on the market d/t bronchospasm
|
|
|
what is the ED95 under N20/02 for pancuronium
|
0.07
|
|
|
what is the ED95 under N20/02 for vecuronium
|
0.05
|
|
|
what is the ED95 under N20/02 for rocuronium
|
0.3
|
|
|
what is the supplemental dose after intubation for pancuronium
|
0.02
|
|
|
what is the supplemental dose after intubation for vecuronium
|
0.02
|
|
|
what is the supplemental dose after intubation for rocuronium
|
0.1
|
|
|
what is the dosage for relaxation with N20 for pancuronium
|
0.05
|
|
|
what is the dosage for relaxation with N20 for vecuronium
|
0.05
|
|
|
what is the dosage for relaxation with N20 for rocuronium
|
0.3
|
|
|
what is the dosage for relaxation with VA for pancuronium
|
0.03
|
|
|
what is the dosage for relaxation with VA for vecuronium
|
0.03
|
|
|
what is the dosage for relaxation with VA for rocuronium
|
0.15
|
|
|
the more potent the NMB the (slower or faster) the onset
|
SLOWER
|
|
|
the less potent the NMB the (slower or faster) the onset
|
FASTER
|
|
|
what is the structural difference b/t vecuronium and rocuronium
|
rocuronium came from vecuronium with a methyl group change
|
|
|
what area of the body has the most rapid onset of NMB
|
more central areas
|
|
|
what area of the body has slower onset of NMB
|
peripheral
|
|
|
what area of the body recovers faster from the effects of NMB
|
central areas
|
|
|
with NMB there is rapid equillbration b/t plasma and what muscles
|
CENTRAL
|
|
|
where is there greater blood flow per gram of muscle at the diapharam or larynx or at the adductor pollicus
|
the diaphragm or larynx
|
|
|
onset of NMB occurs when compared to a block in the adductor pollicus
|
1-2 min earlier
|
|
|
what muscle correlates with the diaphragm and the abd rectus
|
orbicularis oculi
|
|
|
what muscle correlates with the peripheral muscles
|
the adductor pollicus
|
|
|
what muscles are "easily" paralyzed muscles
|
peripheral muscles
|
|
|
if a NMB is given to an awake pt what would the pt experience
|
*1st thing would be diff focusing
*mandibular muscle weakness *ptosis, diplopia *dysphagia *hearing becomes more acute *NO change in LOC |
|
|
when a NMB is given to an awake pt the change that occurs with hearing occurs why
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hearing becomes MORE acute d/t relaxation of the small muscles of the ear
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does mivacurium release histamine
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YES
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