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NMB and reversals Flashcards

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1
Q

Atricurium MOA

A

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

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2
Q

Atricurium/Tracurium class

A

Intermediate acting bisquarternary benzyllisoquinoline NDMR

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3
Q

Atricurium Pharmacokinetics

A

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

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4
Q

SE Atricurium

A

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

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5
Q

Atricurium CI/Cautions

A

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

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6
Q

Atricurium dose

A

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

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7
Q

Cisatracurium/Nimbex class

A

intermediate acting NDMR; stereoisomer of Atricurium

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8
Q

Cisatracurium PK

A

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)

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9
Q

Cisatracurium SE

A

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

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10
Q

Cisatracurium Ci/cautions

A

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

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11
Q

Cisatracurium dose

A

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

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12
Q

Rocuronium class

A

short/intermediate acting monoquatinary aminosteriod ND NMB

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13
Q

Rocuronium MOA

A

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

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14
Q

Rocuronium PK

A

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

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15
Q

Rocuronium SE

A

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

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16
Q

Rocuronium CI/Cautions

A

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

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17
Q

Rocuronium dose

A

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

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18
Q

Vecuronium/Norcuron- class

A

intermediate acting steriod type NDMR

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19
Q

Vecuronium PK

A

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

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20
Q

Vecuronium SE

A

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

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21
Q

Vecuronium CI/cautions

A

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)

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22
Q

Vecuronium dose

A

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

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23
Q

Pancuronium/Pavulon

A

longacting steriod type bisquarternary aminosteriod NDMR

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24
Q

Pancuronium PK

A

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)

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25
Pancuronium SE
no histamine release, not CV stable- increase hR/arrhythmias- even if beta blocked, htn, bronchospasm, allergic rxn
26
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
27
Pancuronium dose
initial 0.1mg/kg, maintenance 0.01mg/kg q 40-60min, infusion 1mcg/kg/min
28
Mivicurium/Mivacron class
short acting quaternary ammonium ND NMB
29
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
30
Mivicurium SE
slight histamine release, transient hypotension, increase HR, vasodilation, bronchospasm
31
Mivicurium CI
atypical plasma esterase deficiency- prolong duration, hypersensitivity, asthma, COPD
32
Mivicurium dose
initial 0.2mg/kg, maintenance 0.01-0.1mg/kg, continuous 6-7mcg/kg/min
33
succinycholine class
depolarizing NMB with rapid onset and ultrashort acting
34
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
35
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,
36
sux SE
increased ICP, IOP, IGP, decrease HR and BP, histamine release, hyperkalemia, masseter muscle spasm, myalgias, fasciculations, rhabdomyolysis, myoglobuneria, systole, MH
37
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
38
sux dose
20-40mg for larngospasm intubation 1-1.5mg/kg for RSI maintenance 0.04-0.07 mg/kg q5-10min
39
Neostigmine class
NMB reversal/ anticholinesterase quarternary ammonia that is a competitive acetylcholinesterase inhibitor
40
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
41
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
42
Neostigmine SE
decrease HR, BP, SVR, N/V, increased salivation, bronchoconstriction, increase gastric secretions, seizures
43
Neostigmine CI
renal failure will increase DOA, GI/GU obstruction, asthma, caution in CAD
44
Neostigmine dose
0.05-0.07mg/kg | and with glycopyrolate 0.01mg/kg IV
45
Pyridostigmine- class
Competitive anticholinesterase/ NMB reversal | quaternary ammonia
46
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
47
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
48
Pyridostigmine SE
muscarinic effects- decreased HR/dysthrhythmias, BP, SVR, N/V, increased salivation, bronchospasm, increase gastric secretions, seizures
49
Pyridostigmine CI
hypersensitivity, Renal failure will increase DOA, GI/GU obstruction, asthma, caution with CAD BB= potentiate decrease bp
50
Pyridostigmine dose
0.1-0.2mg/kg 15mg PO IV with glycopyrolate 0.01mg/kg
51
Edrophonium class
quaternary ammonia NMB reversal/ anticholiensterase
52
Edrophonium MOA
reversable H+ binding to the acetylcholinesterases forming an electrostatic attachment increasing ACh at the NMJ
53
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
54
Edrophonium SE
decreases HR, BP, SVR, N/V. increases salivation and gastric secrtions, seizures
55
Edrophonium CI
renal failure prolongs actions, GI/GU obstruction, asthma, caution with CAD
56
Edrophonium dose
0.5-1mg/kg | with atropine 0.01mg/kg
57
Physostigmine- class
medium duration central acting tertiary amine anticholinesterase,
58
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
59
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
60
Physostigmine SE
decrease HR, bp, svr, n/v. increase salivation any gastric secretions, seizures
61
Physostigmine CI
use with another anti cholinesterase, Gi/GU obstruction, asthma, caution with CV disease
62
Physostigmine dose
15-60mg/kg IV q 1-2 hours- for anticholinergic syndrome

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