Exam 2: NMB, Reversals Flashcards
how many tof twitches need to be present before reversal drug is administered
1-2
what should tofr be to meet extubation criteria
0.7 or 0.9 depending on study
how long should tetany be to meet extubation criteria
5 seconds sustained at 50 hz
what are 2 other signs patient is a ready for extubation
strong constant hand grip
5 second head lift
what vital capacity suggests recovery from nmb
15ml/kg
what inspiratory force suggests recovery from nmb
-25-30 cmh2o
>-40
what is the goal of reversal drugs
maximize nicotinic transmission
minimize muscarinic SE
how many minutes need to be given for anticholinesterase inhibitors to fully antagonize nmb
15-30 min
what term is defined as a tofr less than 0.9
residual NMB
what is a drug class that can hinder the action of reversal agents thus prolonging nmb’s
aminoglycoside abx
what are three electrolyte imbalances that can influence reversal agents
hypermagnesemia
hypocalcemia
hypokalemia
besides certain drugs and electrolyte imbalances, what can affect reversal agents
depth of block at time of reversal
clearance/half life of reversal
resp acidosis
hypothermia
what can giving an excessive dose of acetylcholinesterase inhibitor cause
paradoxical muscle weakness
t or f- make sure to adjust dose of both ache inhibitors and nmb in patient with renal failure
f- do not adjust since doa of both is affected
t or f- neostigmine will take longer to reach peak effect with 90% twitch suppression when compared to 50% twitch suppression
true
t or f- ache inhibitors do not have a synergistic effect
false
Additive
how long can residual paralysis occur for after intermediate nmb
4 hrs
what is the term for when adequate dose of reversal is given, but blockade is re-established because reversal gets metabolized faster than nmb drug
recurarization
which receptors does ach agonize
nicotinic
muscarinic
which receptor do nondepolarizing agents antagonize
nicotinic receptors
which receptor does atropine/scopolamine/glycopyrrolate antagonize
muscarinic
what are two locations of nicotinic receptors
autonomic ganglia
skeletal muscle
what are two locations of muscarinic receptors
glands
smooth muscle (gi/bladder/bronchial)
heart
what drugs block muscarinic receptors
atropine, glycopyrolate
t or f- nicotinic and muscarinic receptors respond to ach
true
why are anticholinergic meds given with cholinesterase inhibitors
minimize muscarinic effects
what is a cv muscarinic se after anticholinesterase is given
bradycardia
what is a muscarinic se of lungs after reversal is given
bronchospasm
bronchial secretions
what is a cerebral muscarinic se after reversal is given
diffuse excitation
what is a gi muscarinic se after reversal is given
intestinal spasm
increased salivation
what is a gu muscarinic se after reversal is given
increased bladder tone
what is an ophthalmological muscarinic se after reversal is given
miosis
what is the action of cholinesterase inhibitors
indirectly increase ach to compete with non-depolarizing nmb
t or f- acetylcholinesterase inhibitors irreversibly bind to acetylcholinesterase
false
reversible
what is the supplied dose of neostigmine and physostigmine
1mg/ml
what is the reversal dose of neostigmine
0.05mg/kg
what is the onset, peak, and doa of neostig
3-5 mins, 7 mins, 1-2 hrs
what is max dose of neostig
5mg
how is neostig metabolized
liver
what is the structure of neostigmine and enlon
quaternary amine
t or f- neostig and enlon do not cross bbb
true
what are some side effects of neostig
ponv
pruritus
diarrhea
prolonged block
what do acetylcholinesterase inhibitors do to succ
prolong depolarization
what two meds inhibit pseudocholinesterase activity
neostig and physostig
what side effect should be watched for with neostig admin
cholinergic syndrome
what is the onset and doa of physostigmine
15 min, 2 hrs
How is physostigmine metabolized?
renal
what med is a tertiary amine and cross bbb
physostigmine
what reversal med should not be given with asthma
physostigmine
which reversal agent reduces post op shivering
physostigmine
what is the reversal dose for physostigmine
0.5-1mg
peds: 0.02 mg/kg
what is the supplied dose of enlon
10mg/ml
what is the reversal dose of enlon
0.5-1mg/kg
what is the onset, peak, and doa of enlon
30-60 sec
1 min
60 mins
where is the primary action of enlon
presynaptic
what is the most rapid acting cholinesterase inhibitor
enlon
t or f- enlon is recommended for a deep block
false
which should be given first, robinul or enlon and why
robinul- prevent bradycardia
what med is used to diagnose/treat myasthenia gravis
enlon
dumbbells
diarrhea
urination
miosis
bradyhcardia
bronchoconstriction
emesis
lacrimation
laxation
salivation
what are some side effects of antimuscarinics
tachyarrhythmias
nausea
constipation
dizziness
what med is a gamma cyclodextrin made of sugar that assembles in a ring
sugammadex
how does sugammadex work
encapsulates aminosteroid nmb making it inactive
what meds are sugammadex most effective for
roc, vec, pancuronium
book says roc and vec, higher affinity for roc
t or f- make sure to give antimuscarinic with sugammadex
f- you are not affecting acetylcholine
what are the uncommon se of sugammadex
anaphylaxis
bradycardia
decreased effect of hormonal birth control for 7 days
what are the pros of sugammadex
improves safety for rapid reversal
reduces risk of residual paralysis
allows for strong nmb until end of procedure
what is key before giving sugammadex
blockade depth monitoring
what is sugammadex dose for tof 2/4 or better
2mg/kg
what is sugammadex dose for tof of 0/4 and 2 ptc or better
4mg/kg
what is sugammadex dose after giving 1.2 mg/kg of roc
16 mg/kg
how long do you have to wait after giving roc to reverse
3 min
what is recommended med to give with neostig
glycopyrolate
what is recommended med to give with pyridostigmine
glycopyrolate
what is recommended med to give with enlon
atropine
what is the dose of atropine
7mcg/kg
what is the onset, peak and doa of atropine
1 min, 2min, 1 hour
what can very small doses of atropine cause
paradoxical bradycardia
which med is a tertiary ammonium
atropine
t or f- atropine cross bbb but not placenta
f- crosses both
what med is a quaternary ammonium and does not cross bbb
glycopyrolate
what is the dose of glycopyrolate
5-8 mcg/kg
what is the onset, peak, and doa of glycopyrolate
2-3 min, 5 min, 1-2 hours
which anticholinergic increases hr from most to least
atropine > glycopyrolate > scopolamine
what two anticholinergics cause the most smooth muscle relaxation
atropine, glyco
which anticholinergic causes sedation from most to least
scopolamine, atropine, glyco
which anticholinergic decreases saliva from most to least
scopolamine, glyco, atropine
which anticholinergic prevents motion induced nausea from most to least
scopolamine, atropine, glyco
which anticholinergic decreases gastric H secretion from most to least
all the same
which anticholinergic causes mydriasis from most to least
scopolamine, atropine, glyco
what rule states that volatile agents potency is proportional to their lipid solubility which is measured by oil gas partition coefficient
meyer-overton rule
t or f- males have increased mac
false
gender has no effect
what are some other factors that decrease mac
hypotension
hypoxia
anemia
metabolic acidosis
postpartum 1-3 days
paco2 > 95
what drugs cause increased mac
chronic alcohol
acute amphetamine
maoi
ephedrine
levodopa
what drugs cause decreased mac
acute alcohol
iv anesthetics
n2o
opioids
alpha 2 agonist
lithium
lidocaine
hydroxyzine
how does age influence mac
increased in infants 1-6 months
>40= mac decreases 6% per decade
what electrolyte abnormality will increase/decrease mac
increase: hypernatremia
decrease: hyponatremia
what are some of the molecular targets of volatile anesthetics
gaba- enhance inhibitory
glycine- enhance inhibitory
k channels- activate
nmda- inhibit
nicotinic ach- inhibit
ca/na channels- inhibit
what targets do volatiles enhance/activate
gaba
glycine
k channels- 2 pore and leak
what targets do volatiles inhibit
nmda
nicotinic ach
na/ca channels
t or f- nitrous oxide has a strong inhibitor action on nmda receptors
true
why do we still give opioids with volatile anesthetics
volatiles have poor control of ans response to pain
what does volatile blocking na/ca channels do
decreases action potentials/depolarizations
where do volatiles cause unconsciousness in the brain
cerebral cortex
thalamus
brain stem
t or f- volatiles cause amnesia
true
t or f- immobility from volatile anesthetics is caused by enhancing gaba receptors
f- enhancing glycine receptors
analgesia from volatiles is likely produced from disruption of ___________________ ____________ of pain transmission
spinothalamic tract
immobility occurs from effects of inhaled anesthetic on __________ __________ networks
spinal cord
what are the non-anesthetic effects of volatile gases
bronchodilation
neuromuscular effects
analgesia
how do volatiles cause bronchodilation
-block calcium channels, deplete ca stores in sarcoplasmic reticulum
-potentiate gaba
t or f- volatile anesthetics potentiate depolarizing and non-depolarizing nmb’s
true
what is the neuromuscular effect of volatile gases
skeletal muscle relaxation
which gas can have analgesic effects and how
nitrous oxide- nmda inhibitor
what do volatiles do to cmro2
decrease
what type of analgesia do volatile anesthetics provide
supraspinal
what kind of toxicity can volatiles cause
hepatotoxicity
nephrotoxcity
what are the adverse effect categories of volatiles
resp/cardiac depression
cardiac dysrhythmias
nephrotoxicity
MH
PONV
how do volatiles cause resp depression
blunt hypoxic/hypercarbic vent responses for several hours
how do volatiles cause cv depression
alter ca entry
which volatiles decrease svr
iso, sevo, des
which anesthetic has minimal cv effects
nitrous oxide
what dysrhythmia can iso/sevo/des cause
long qt–>torsades
which volatile does not contribute to MH
nitrous oxide
what receptor is involved in MH
ryr1- releases a lot of calcium
metabolism of sevo can lead to what
compound a- which is nephrotoxic
how do volatiles cause nephrotoxicity and how
metabolism leading to inorganic fluoride production or by degradation products
what can you substitute volatiles for to decrease ponv
prop
which volatile is sweet smelling
sevo
which volatile is half as potent as iso
sevo
which volatile induces least amount of cerebral vasodilation
sevo
which volatile has more favorable side effects
iso
which volatile is highly pungent and chemically stable
iso
what makes sevo better suited for inhalation inductions
minimally pungent
which volatile can cause exothermic reactions with co2
sevo
which volatile is a fluorinated methyl ethyl ether
des
what effect does fluorination have on des
decreases potency
which volatile has a low boiling point necessitating a specialized pressure vaporizer
des
which volatile has almost no metabolism so there is decreased risk of hepto/nephrotoxicity
des
which volatile is the most pungent
des
which volatile causes coughing, breathing holding, laryngospasms
des
which gas is technically not a volatile
N20
which gas is an oxidizer that supports combustion
N20
which gas has a low anesthetic potency
N20
which gas should be avoided in first trimester of pregnancy
N20
which gas promotes stable hemodynamics
N20
which gas has an insufflation risk
n20
which gas provides analgesia and euphoria
N2O
what 4 factors influence mac
age
electrolytes
temp
genetic effects on potency
opioids and volatiles have a ____________________ effect
synergistic
t or f- there is synergism between inhaled anesthetics
false
mac requirements __________________ with age
decline
mac for inhaled anesthetic decreases with decreasing body temp by ___ to ___ % per 1 degree
4-5%
which population needs for gas/adjuvants to reach 1 mac
pediatrics
what cardiac problems can volatiles cause
coronary vasodilation which can lead to coronary steal
what is the term for blood flow distal to atherosclerotic lesion decreases due to dilation, which then triggers ischemia
coronary steal
which population can volatiles cause delayed neuronal development
neonates
what are the primary binding sites for inhaled anesthetics
lipid and amphiphatic protein receptors
which effect is not associated with fentanyl
a. vasodilation
b. resp depression
c. pruritis
d. vasoconstriction
vasoconstriction
which of the following aretrue regarding zofran- Maman
a. risk for qt prolongation
b. headache is common se
c. ideally give dose pre-induction
d. 5ht3 agonist
e. all of the above
A
B
which medication can cause transient htn after rapid admin
a. clonidine
b. precedex
c. decadron
d. droperidol
precedex
how do you treat scopolamine anti cholinergic syndrome
physostigmine
What conditions are contraindications for succs
Upper/lower motor neuron injury
Spinal cord injury
Burns
Skeletal muscle trauma
Cerebrovascular accident
Tetanus
Severe sepsis
Muscular dystrophy
Prolonged chemical denervation (magnesium, long term NMB infusion, clostridial toxin)
what principle is the oil gas coefficient based on
meyer overton correlation
which two volatiles are the same except for substituting a chloride for a fluorine atom
isoflurane and desflurane
what correlation suggests that lipids were the principles target for anesthetics
meyer overton correlation
which volatiles have a chiral carbon atom
isoflurane
desflurane
what type of ion channels are though to be among the most relevant for general anesthetics
ligand gated
voltage gated
what are the two suggested mechanisms of action for general anesthetics
lipid based
protein based
according to the book, what three things compose anesthesia
reversible amnesia
loss of consciousness
immobility
what are some receptors that volatiles enhance
gaba (inhibitory)
glycine (inhibitory)
nmda (inhibitory)
nicotinic ach
k channels
what are some channels that volatiles inhibit
sodium
calcium
immobility from volatiles is due to effects on _____________ __________ networks
spinal cord
t or f- volatiles have good control of autonomic nervous system response to painful stimuli
false
how is analgesia brought about by volatiles
disruption of spinothalamic tract transmission
what receptor is likely acted on by volatiles to produce amnesia
GABA
what area of the brain are gaba receptors likely acted on to produce amnesia
frontal cortex
hippocampus
amygdala
t or f-nitrous oxide/xenon cause vasodilation and myocardial depression
false
what types of organ toxicity can volatiles cause
hepatotoxicity
nephrotoxicity
do volatiles cause bronchodilation or bronchoconstriction and how
bronchodilation- block calcium channels
t or f- volatiles potentiate non depolarizing and depolarizing nmb’s
true
which volatiles cause dose dependent respiratory depression
des
iso
sevo
anesthetics reduce minute ventilation, does it do this by effecting tidal volume or respiratory rate
tidal volume
which volatiles decrease carotid body response to hypoxia from most to least
halothane
isoflurane
des
which gases have minimal direct cv effects
nitrous oxide
xenon
which gas is reduced svr more prominent
isoflurane
which gas promotes coronary steal in coronary artery disease
isoflurane
rapid increases in what volatiles lead to increase in hr
isoflurane
desflurane
which volatile has minimal effects on heart rate
sevo
which gas increases cerebral blood flow and cmro2
N20
what part of volatile gases produces nephrotoxicity
fluoride production
seven side effects of Succs
bradycardia
tachycardia
K released
increased ocular pressure
increased ICP
increased intragastric pressure
MH
why does succs cause bradycardia
stimulation of M2 receptor in SA node
why does Succs cause tachycardia
mimics Ach at the sympathetic ganglia
which enzymes hydrolyze succs
butyrylcholinesterase
psuedocholinesterase
plasma cholinesterase
where is pseudocholinesterase produced
liver
what factors prolong succs
reglan
late stage pregnancy
esmolol
oral contraceptives
echothiophate
cyclophosphamide
neostigmine
reduce psuedocholnesterase activity
what conditions reduce psuedocholinesterase activity
atypical PChE
severe liver disease
burns
neoplasm
pregnancy (late stage)
PChE variant typical homozygous dibucaine number and succs duration
70-80
duration: 5-10 min
PChE variant heterozygous dibucaine number and succs duration
50-60
duration: 20-30 min
PChE variant atypical homozygous dibucaine number and succs duration
20-30
duration: 4-8 hrs
what primary event terminates rocuronium
biliary excretion/liver
APEX
how is pancuronium terminated
renal excretion
how is atracurium terminated
non specific ester hydrolysis
how is cisatracurium terminated
hoffmann elimination
what two NDNMBs dont produce a metabolite
roc
mivacurium
what drugs/conditions potentiate neuromuscular blockade
desflurane
gentamycin
dantrolene
aminoglycocides
clindamycin
tetracycline
verapamil
LAs
furosemide
cyclosporin
increased lithium
increased Mg
decreased K and Ca
hypothermia
why do NMB cause anaphylaxis
they contain one or more antigenic quaternary ammonium groups that interact with IgE causing mast cell and basophil degranulation
which NMBs most likely to cause allergic reactions
succs
roc
which reversal reduces post op shivering
physostigmine (40mcg/kg)
what two reversals are best paired with glycopyrrolate
neostigmine
pyridostigmine
which acetylcholinesterase inhibitor crosses the BBB
physostigmine
most to least anticholinergic HR effects
atropine most
robinol
scopolamine least
most to least anticholinergic effects on sedation
scopolamine most
atropine
robinol zero
most to least anticholinergic antisialagogue
scopolamine most
robinol
atropine least
which anticholinergics cross the BBB
atropine
scopolamine
