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Flashcards in NMB and reversals Deck (62):

Atricurium MOA

competitively inhibits/blocks ACh at the post junctional nicotinic cholinergic receptor in the NMJ by binding to 2 alpha subunits, preventing opening of the channel, depolarization and contraction


Atricurium/Tracurium class

Intermediate acting bisquarternary benzyllisoquinoline NDMR


Atricurium Pharmacokinetics

PB= 82%, onset 1-3min, DOA 20-50min, E1/2 20min, water soluble, metabolized 2/3 by ester hydrolysis and 1/3 Hofmanns elimination, excreted in urine, metabolite Laudanosine- (liver metabolized) can accumulate in renal failure and cause CNS problems like sz


SE Atricurium

Histamine release; decrease bp and increase HR, skin flushing; BRONChospasm


Atricurium CI/Cautions

conscious patient, hypersensitivity, cautious with asthma and COPD &pts unable to handle histamine release- CAD, sz history, muscle weakness, metabolite can accumulate with liver/renal problems
NMB can be prolonged with IA, abc, and anti-convulsants, LA, steriods, and immunosuppressants
Resistance can occur in burn PTs- up to 3 months; resistance with muscle trauma, denervation, immobilized


Atricurium dose

initial 0.5mg/kg iv, maintanance- 0.1mg/kg q 20-45min; continuous 9-10mcg/kg/min


Cisatracurium/Nimbex class

intermediate acting NDMR; stereoisomer of Atricurium


Cisatracurium PK

Vd= .12-.2l/kg, onset 3-5min, DOA 20-90min, e1/2 20-30min, water soluble, metabolized 80% by hoffmann elimination, excreted in urine and feces, metabolite Laudanosine 1/5 that of atriucurium (can accumulate in RF and cause CNS problems like szs)


Cisatracurium SE

no histamine release, lacks cv effects, laudanosine production less likely than with atr, anaphylaxis


Cisatracurium Ci/cautions

conscious patient , hypersensitivity, electrolye/acid/base abnormalities, muscle weakness, metabolite can accumulate with liver/renal problems
enhancedNMB with some abx, LI, LA, procainamide, mg
Decreased action with PTs on phenytoin/carbamazepine


Cisatracurium dose

initial 0.2mg/kg; maintenance- 0.03mg/kgq 40-60min, continous 1-3mcg/kg/min


Rocuronium class

short/intermediate acting monoquatinary aminosteriod ND NMB


Rocuronium MOA

competes with ACh for alpha subunits on the nicotinic receptor and inhibits a conformational change which prevents depolarization and contraction


Rocuronium PK

1/6 the potency of vecuronium, Not highly protein bound- 30-50%, VD 0.25L/KG, onset 60-90 sec, DOA 30-90, E1/2t 1-2hr, metabolized in liver by deacetylation to 17-desacetylrocuronium (5-10% activity of parent) 30% excreted in the urine unchanged, 20% hepatic degradation, billary excretion is primary up to 50%- don't need to decrease dose in renal disease


Rocuronium SE

anaphylactic reactions, little affect on cardiac system- no histamine release, Hypertension or hypotension, arrhythmia, apnea, bronchospasm, hiccups, salivation


Rocuronium CI/Cautions

conscious patient, hypersensitivity, underlying neuromuscular disorder, children (2-12) need larger dose because shorter DOA, elderly prolonged effect, burns greater than 30% 3rd degree and Anticonvulsants will have resistance;
potentiated by IA, some abx, lasix, LA, antidsyrhythmics, dantroline, ketamine, anticonvulsants and Mag2+•
esmolol admin before will increase onset time
ephedrine given before will decrease onset time
Ach inhibitors diminish effects


Rocuronium dose

defaciculating- 0.06-0.1mg/kg, 0.6-1.2mg/kg intubating, maintenance 0.2mg/kg; continuous 10-12mcg/kg/min


Vecuronium/Norcuron- class

intermediate acting steriod type NDMR


Vecuronium PK

60-80% PB, Vd 0.2-0.2L/kg, onset 2-3 min, DOA 20-35min, e1/2 70min, hepatic metabolism; 30% excreted unchanged in the urine and primary excretion is billiary - active metabolite= 3-desacetyl vecuronium- 1/2 potency of parent


Vecuronium SE

No histamine release, bronchospasm, can cause SA node exit block


Vecuronium CI/cautions

hypersensitivity, caution with liver and renal disease, NMB blockade enhanced with INH Agents and increase effects of some abc (amino glycosides, anticonvulants, thiazides, and mag)


Vecuronium dose

defaciculating dose- 0.01mg/kg, 0.1mg/kg, maintenance 0.01mg/kg q25-45min, continuous 1mcg/kg/min



longacting steriod type bisquarternary aminosteriod NDMR


Pancuronium PK

little PB, onset 2-3min, DOA 60-90 min, e1/2 2hours, 10-20% hepatic metabolism with renal excretion (80% excreted unchanged), 3 active metabolites= most 3-desacetyl pancurounium ( 1/2 potency parent)


Pancuronium SE

no histamine release, not CV stable- increase hR/arrhythmias- even if beta blocked, htn, bronchospasm, allergic rxn


Pancuronium CI

hypersensitivity, conscious pt, underlying skeletal muscle disease, CV disease, hyperparathyroid, pheochromocytoma, renal disease, prolonged excretion in renal biliary or hepatic disease elderly and obese
. can be prolonged with IA, abc, BB, LI, diuretics, anticonvulsants, and TCAs


Pancuronium dose

initial 0.1mg/kg, maintenance 0.01mg/kg q 40-60min, infusion 1mcg/kg/min


Mivicurium/Mivacron class

short acting quaternary ammonium ND NMB


Mivicurium Pk

highly ionized, water soluble= decreased lipid solubility so it doesn't cross the BBB, Ed95=80mcg/kg, onset 2-3min, doa 12-20min, e1/2 55min, hydrolyzed by plasma cholinesterase's ~88% the rate of sux, 7% excreted unchanged in the urine


Mivicurium SE

slight histamine release, transient hypotension, increase HR, vasodilation, bronchospasm


Mivicurium CI

atypical plasma esterase deficiency- prolong duration, hypersensitivity, asthma, COPD


Mivicurium dose

initial 0.2mg/kg, maintenance 0.01-0.1mg/kg, continuous 6-7mcg/kg/min


succinycholine class

depolarizing NMB with rapid onset and ultrashort acting


sux MOA

mimics ACh at alpha subunits on the nicotinic receptor and produces a sustained depolarization of the post junctional membrane- keeping the channel open and unable to respond to other APs, effects are terminated when sux diffuses away from the NMJ


sux PK

onset 30-60sec, DOA 8-15min, e1/2 2-4min, small vd and little PB, rapidly hydrolyzed by plasma esterase's when diffuses away form NMJ and excreted in the urine,


sux SE

increased ICP, IOP, IGP, decrease HR and BP, histamine release, hyperkalemia, masseter muscle spasm, myalgias, fasciculations, rhabdomyolysis, myoglobuneria, systole, MH


sux ci

muscular dystrophy, pt with history or family history of MH or plasma esterase deficiency, only for emergency use in children, pts with increased K like renal pts, myopathies, pts with increased ICP, IOP, IGP, hypersensitivity, histamine release so caution with asthma/COPD, not for burns/trauma/extensive deinervation with skeletal muscle for 24-72 hours


sux dose

20-40mg for larngospasm
intubation 1-1.5mg/kg for RSI
maintenance 0.04-0.07 mg/kg q5-10min


Neostigmine class

NMB reversal/ anticholinesterase quarternary ammonia that is a competitive acetylcholinesterase inhibitor


Neostigmine MOA

competitively and irreversibly covalently binds to the carbamyl group of the acetylcholinesterases inhibiting the breakdown of Ach in the NMJ- increasing the availability of ACh at the motor end plate; used to antagonize the affects of NMBs. it's the most reliable med for a deep block


Neostigmine PK

onset 3min, peak 7-10min, DOA 1hr, e1/2 70min, metabolized by plasma and liver esterase's 50% and excreted unchanged 50% in the urine


Neostigmine SE

decrease HR, BP, SVR, N/V, increased salivation, bronchoconstriction, increase gastric secretions, seizures


Neostigmine CI

renal failure will increase DOA, GI/GU obstruction, asthma, caution in CAD


Neostigmine dose

and with glycopyrolate 0.01mg/kg IV


Pyridostigmine- class

Competitive anticholinesterase/ NMB reversal
quaternary ammonia


Pyridostigmine- MOA

reversibly binds to acetylcholinesterase, inhibiting its action and increasing the concentration of acetylcholine at the motor end plate for use on the nicotinic receptors---- attracted to the electrostatic interaction bt + charged Nitrogen and - charged catalytic site of the enzyme; forms a covalent bond to the carbamyl group on the acetylcholinesterases inhibiting the b/d of ACh @ the NMJ. increases ACh at the NMJ...... can be given orally to myasthenia gravis


Pyridostigmine PK

onset 10min, DOA 60-120, e1/2= 112 minutes, 25% hepatic metabolism by microsomal enzyme system and 75% excreted unchanged in the urine


Pyridostigmine SE

muscarinic effects- decreased HR/dysthrhythmias, BP, SVR, N/V, increased salivation, bronchospasm, increase gastric secretions, seizures


Pyridostigmine CI

hypersensitivity, Renal failure will increase DOA, GI/GU obstruction, asthma, caution with CAD
BB= potentiate decrease bp


Pyridostigmine dose

15mg PO
IV with glycopyrolate 0.01mg/kg


Edrophonium class

quaternary ammonia NMB reversal/ anticholiensterase


Edrophonium MOA

reversable H+ binding to the acetylcholinesterases forming an electrostatic attachment increasing ACh at the NMJ


Edrophonium PK

less severe muscarinic effects in this class, onset fast, DOA short at 1 receptor but binds to multiple receptors before being elimated which prolongs the DOA, peak 1-2min, 25% hepatic metabolism, 75% renal excretion unchanged


Edrophonium SE

decreases HR, BP, SVR, N/V. increases salivation and gastric secrtions, seizures


Edrophonium CI

renal failure prolongs actions, GI/GU obstruction, asthma, caution with CAD


Edrophonium dose

with atropine 0.01mg/kg


Physostigmine- class

medium duration central acting tertiary amine anticholinesterase,


Physostigmine MOA/uses

reversible binding forms a carbamyl ester complex at the esoteric site of the acetylcholinesterases increasing concentration of ACh at the NMJ; also used for atropine toxicity, MG, and glaucoma


Physostigmine PK

vd= 1L/kg- lipid soluble and crosses BBB, onset 5 min, DOA 1-5hr, e1/2 30min, hydrolyzed at ester linkage by cholinesterase's, renal excretion is minimal


Physostigmine SE

decrease HR, bp, svr, n/v. increase salivation any gastric secretions, seizures


Physostigmine CI

use with another anti cholinesterase, Gi/GU obstruction, asthma, caution with CV disease


Physostigmine dose

15-60mg/kg IV q 1-2 hours- for anticholinergic syndrome