NMB and reversals Flashcards
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
Pancuronium/Pavulon
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
0.05-0.07mg/kg
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
0.1-0.2mg/kg
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
0.5-1mg/kg
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
