Exam 2 part IV Flashcards
s/e of atracurium
- dose dependent histamine release 2. may cause transient drop in SVR and increase in CI 3. severe bronchospasm 4. laudanosine toxicity
s/e of cisatracurium
- laudanosine toxicity (5x less than atracurium)
what will prolong the effects of atracurium & cisatracurium
- hypothermia 2. acidosis
atracurium is a better choice for ________________ (induction or maintenance)
maintenance
what change should you make in the dose of atracurium for neonates
decrease dose by 1/2
__________________ is a great NDMR choice for children and renal pts due to its metabolic profile
cisatracurium
what is hoffman elimination
- spontaneous, non-enzymatic chemical breakdown of drugs that occur at physiological pH and temperature 2. elimination would increase as pH and/or T increase (but should be offset by ester hydrolysis)
what is laudanosine
- an inactive metabolite of atracurium/cisatracurium 2. tertiary amine 3. metabolized by liver and excreted in bile 4. issue with hepatic failure or high doses (causes toxicity)
__________________ is a bisquaternary amine that resembles Ach enough to bind, but NOT depolarize
pancuronium
intubating dose of pancuronium
0.08 - 0.12 mg/kg
onset of pancuronium
2-3 min
DOA of pancuronium
60-90 min
ED95 of pancuronium
0.07 mg/kg
metabolism of pancuronium
in the liver (40-70%) –> active metabolite 3-desacetylpancuronium (50% reduction in potency)
which NMBA is a long acting
pancuronium
dose modification of pancuronium in peds
increase dose
s/e of pancuronium
- vagal blockade with SNS stimulation –> AV dysrhythmias 2. 10-15% increase in HR, MAP, and CO (blocks vagal muscarinic receptor of SA) 3. vagolytic esp at doses of 2x ED95 4. HTN in peds
effects of pancuronium are prolonged in those with ________________
renal failure
pt with cirrhosis, if choose to give pancuronium you should _____________ intubating dose and ___________________ maintenance dose
increase; decrease
caution use of pancuronium in what pts
- renal failure (prolonged effects) 2. CAD 3. IHSS any dz where HR increase is detrimental
why is pancuronium commonly used in cardiac anesthesia?
it counteracts the bradycardia 2/2 high dose opoids used
____________________ is a monoquaternary amine that is equal to or 1.5x as potent as pancuronium
vecuronium
intubating dose of vecuronium
0.08-0.12 mg/kg
onset of vecuronium
3 min
DOA of vecuronium
30-45 min
ED95 of vecuronium
0.04-0.05 mg/kg
excretion of vecuronium
primarily liver excretion (40-80%) then renal excretion (20-30%)
excretion of pancuronium
primarily renal (40-70%) limited liver (10%)
which patients have a slower recovery from vecuronium?
- obese 2. infants 3. neonates
females are __________% more sensitive to vecuronium than men
30
___________________ is a monoquaternary amine that is 1/6th - 1/8th as potent as vec
rocuronium
which NDMR is a steroid and has the most rapid onset due to being the least potent
rocuronium
intubating dose of rocuronium
0.45 - 0.9 mg/kg
RSI dose of rocuronium
0.9-1.2 mg/kg
pediatric intubating dose of rocuronium (ages 2-12)
0.9-1.2 mg/kg
onset of rocuronium
45-90 seconds
DOA of rocuronium
30-90 min
ED95 of rocuronium
0.3 mg/kg
metabolism of rocuronium
no metabolism
half life of rocuronium
1-2 hrs
excretion of rocuronium
primarily liver (55%) then renal (35%) most of the drug excreted in bile unchanged
DOA of rocuronium is increased in what pts?
- severe hepatic failure 2. pregnancy 3. elderly 4. obesity 5. females
rocuronium dose should be increased with what pts?
those with liver dz
a ____________mg/kg dose of rocuronium will allow for intubating conditions as fast as 1.0 mg/kg of succinylcholine
1
females appear to be ___________% more sensitive to vecuronium, pancuronium, and rocuronium
30
traditional reversal of NDMR requires maximal ________________ transmission with minimal _____________ s/e
nicotinic; muscarinic
when reversing a NDMR which medication do you give first (Anticholinergic or anticholinesterase)
anticholinergic (ex; glycopyrolate)
Anticholinesterase (neostigmine) _________________ increases the amount of Ach at the neuromuscular jx
indirectly
MOA of anticholinesterases (cholinesterase inhibitors)
- inhibit the breakdown of Ach 2. decreases the amount of AchE available to hydrolyze Ach 3. indirectly increases the amount Ach available at NMJ 4. Ach competes with NDMR for NAchR
before pharmacological reversal of NDMR is initiated or attempted, what must be present?
some evidence of spontaneous reversal
Dose of cholinesterase inhibitor for NDMR reversal is dependent on what
level of blockade
from administration of anticholinesterase (cholinesterase inhibitor); the time to reversal of NDMR depends on what?
- agent and dose of cholinesterase inhibitor 2. NDMR being reversed/antagonized 3. extent of existing block
pharmacokinetics of anticholinesterases
- water soluble 2. ionized 3. primarily excreted in the kidney
why should there be some evidence of spontaneous reversal before administration of pharmacological agents to reverse NDMR
need DOA of reversal to outlast DOA of NDMR
T/F: all patients should receive pharmacologic reversal of NDMR even if full recovery status is noted on clinical testing
TRUE
what are your anticholinesterase drugs
- edrophonium 2. neostigmine/pyridostigmine 3. organophosphates (physostigmine)
which anticholinesterase medication works via hydrogen bonding, has short DOA, and prejunctional effects (increasing Ach release)
edrophonium
Neostigmine and pyridostigmine are anticholinesterases that work via _______________ bonds causing a __________DOA
covalent; long
T/F: neostigmine is a weak agonist of nicotinic receptors
TRUE
neostigmine and pyridostigmine have _______________ junctional receptor effects
pre and post