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Pharmacology 1, 680 > Nondepolarizing Neuromuscular Blockade > Flashcards

Nondepolarizing Neuromuscular Blockade Flashcards

1
Q

Chemical Characteristics- 8

A

*Structurally similar to Ach
*Have one or two quaternary nitrogens
*Highly polar, highly ionized
*Making them lipid insoluble
*Prevents crossing lipid barriers
*Blood brain barrier – no CNS effects
*Placental membrane – maternal effects only
*Gastroepithelium – poor oral absorption

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2
Q

Benzylisoquinoline Class- drug name ending

A

curium
ex. d-Tubocurarine (Curare)
Atracurium (Tracrium)
Cisatracurium (Nimbex)
Doxacurium (Nuromax)
Mivacurium (Mivacron

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3
Q

Steroidal Class- drug name ending

A

Curonium
ex. Pancuronium (Pavulon)
Vecuronium (Norcuron)
Pipecuronium (Arduan)
Rocuronium (Zemuron)
Rapacuronium (Raplon

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4
Q

Mechanism of Action- Nondepolarizing Neuromuscular Blocks

A

Compete with acetylcholine to bind with the 2 alpha subunits on the postjunctional AChR = thus, prevent the ion channel from opening and prevent the muscle cell membrane from depolarizing.

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5
Q

Sequence of Relaxation

A

Small, rapidly contracting muscles
Eyes, fingers and toes
Larynx
Small muscles of the inner ear

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6
Q

Muscles composed of slow fibers

A

Adductor pollicis
Intercostal, abdomen

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7
Q

Organ that is the first to recover but last to be paralyzed

A

Diaphragm

The dose of a given NMB to produce blockade at the diaphragm is about twice the dose required to produce a similar block at the adductor pollicis.

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8
Q

Characteristics of Nondepolarizing NMB- (5)

A

*Decreased twitch response to a single stimulus
*Fade with tetanus, TOF
*Posttetanic potentiation
*Enhanced by other nondepolarizing NMB
*Antagonized by anticholinesterase drugs

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9
Q

Characteristics of NMB that determine its selection(5)

A

*Onset of agent
*Duration of agent
*Side effects of agent
*Metabolism and clearance
*Cost

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10
Q

Characteristics of the patient that determine which NMB to use (3)

A

*Co-existing diseases (renal, hepatic, cardiac, neuromuscular)
*Current medical therapy
*Surgical procedure

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11
Q

Onset-The less potent the drug the _____ the ED95 & more _____ the onset

A

higher& rapid

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12
Q

Drug Order of Onset Time(fast to slow)

A

SCh<) Rocuronium<Atracurium, Vecuronium, Mivacurium<Cisatracurium

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13
Q

ED95- Rocuronium

A

0.3

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14
Q

ED95 Atracurium

A

0.2

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15
Q

ED95 Vecuronium

A

0.05

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16
Q

ED95 -Mivacurium

A

0.08

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17
Q

ED95 Cisatracurium

A

0.05

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18
Q

Least potent drug and has highest ED

A

Rocuronium (same as Sux)

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19
Q

Priming Principle

A

To facilitate rapid intubating conditions with nondepolarizing agents, a small dose (1/10th the intubating dose or 1/3 the ED95) of the NMB is given prior to the induction to allow some receptors to be occupied and minimize the time required for the remaining receptors to be blocked by remainder of the intubating dose.

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20
Q

Disadvantage of increasing dose of NMB to speed onset is ?

A

also increases side effects and prolongs duration
ex. Vecuronium
Increased dose 0.2 mg/kg - Onset 1.5 min - Duration 60-80 min
Normal dose 0.1 mg/kg - Onset 2.3 min - Duration 45-60 min

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21
Q

Short-acting non-depolarizing NMB drug

A

Mivacurium (Mivacron)

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22
Q

Intermediate - acting non depolarizing NMB drugs

A

Atracurium (Tracrium)
Cisatracurium (Nimbex)
Vecuronium (Norcuron)
Rocuronium (Zemuron)

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23
Q

Long- acting non depolarizing NMB drugs

A

Pancuronium (Pavulon)
Doxacurium (Nuromax)
Pipecuronium (Arduan)

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24
Q

Termination of drug is when it ______ not when it is _______

A

when drug diffuses away from alpha subunit receptors=when the plasma level is low, not when it is eliminated from the body

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25
2 parts of Duration
Distribution (rapid) and Clearance (slower)
26
The _____ of elimination affects the duration of action
route
27
Excreted by the kidneys =
longer half-lives and longer duration > 60 minutes
28
Metabolism and clearance by the liver =
shorter half-lives and durations; steroid family
29
Atracurium elimination is achieved by
Hofmann elimination primarily, some hepatic
30
Mivacurium is eliminated by
plasma cholinesterase
31
Long acting non depoloarizing NMB- d- Tubocurarine (Curare)
naturally occurring benzylisoquinoline obtained from Chondodendrum plant in Amazon jungle
32
Long acting non depoloarizing NMB- d- Tubocurarine (Curare) duration and elimination:
Long-acting – eliminated both by renal and hepatic
33
Long acting non depoloarizing NMB- d- Tubocurarine (Curare) adverse reaction
Massive Histamine Release
34
Dose of d-Tubocurarine (Curare) needed for defasciculation
3 mg
35
precurarization=
a small dose of a non-depolarizing NMBD is given 2–3 min before the administration of succinylcholine which reduces the potency of succinylcholine, requiring a larger dose to produce the same effect.
36
Pancuronium (Pavulon) (most commonly used long acting NMB), ED95=
0.07 mg/kg= potent
37
Pancuronium (Pavulon) intubating dose:
0.1 mg/kg
38
Pancuronium (Pavulon) onset and duration=
onset 3-5 minutes, duration= 60-90 minutes
39
Pancuronium (Pavulon) elimination=
80% unchanged in urine (renal failure slows clearance 2-3X); 10 to 40% metabolized in the liver
40
Pancuronium cardiovascular effect=
vagolytic effects due to 1)vagal blockade at cardiac muscarinic receptors and 2)stimulation of the sympathetic nervous system (theory - by causing release of norepinephrine and preventing its uptake back into nerve endings)
41
Vagolytic effects on cardiovascular system=
*increased HR (10-15%), BP, CO, and MAP, dysrhythmias, and AV conduction *Increase is HR inversely related to baseline HR, not dose or rate of administration of pancuronium
42
Doxacurium (Nuromax) is what class of non depolarizing NMB
Benzylisoquinolone, long-acting *no cardiovascular effects
43
Doxacurium (Nuromax) ED95 & intubating dose:
ED95= 0.030= potent intubating dose= 0.05-0.08
44
Doxacurium (Nuromax) onset and duration
Onset= 4 to 6 minutes duration= 60-90 minutes
45
Doxacurium (Nuromax) elimination
mostly unchanged via the kidneys and some unchanged via the liver
46
Pipecuronium (Arduan) drug class
Long-acting, steroid family * no cardiovascular or histamine effects
47
Pipecuronium (Arduan) ED95 and intubation dose
ED95=0.050mg/kg- potent Intubation dose= 0.085 mg/kg
48
Pipecuronium (Arduan) onset and duration
onset= 3-5 minutes duration= 60-90 minutes
49
Pipecuronium (Arduan) Elimination
unchanged in the urine (ess. no metabolism); unlike pancuronium, no prolonged effect with liver disease. Prolonged duration in renal failure.
50
Vecuronium (Norcuron) drug class
Intermediate ating NMB *Monoquaternary analog of steroid class pancuronium *rarely a histamine release and n vagolytic effect
51
Vecuronium ED95 and intubating dose=
ED95= 0.05mg/kg- potent intubation dose 0.1mg/kg, same as pancuronium
52
Vecuronium onset and duration
onset= 2.3 minutes duration= 45- 60 minutes
53
Vecuronium elimination
hepatic metabolism and 40% excreted unchanged in the bile, 30% unchanged in urine (both in the first 24 hours)
54
Vecuronium is ____ ____ soluble than pancuronum which allows greater:
more lipid soluble *passage into the hepatocytes for clearance (shorter duration)
55
Vecuronium doesn't release histamine but interferes with the ____ of histamine causing more to ____ _____
*catabolism *remain active (inhibits histamine -N- methyl-transferase
56
Vecuronium has a prolonged duration of action in what patients?
*renal failure and hepatic dysfunction * and infants less than 1 yr old
57
Rocuronium drug class
Intermediate acting derivative of steroidal vecuronium
58
Rocuronium ED95 and intubating dose
ED95= 0.3 mg/kg- least potent intubating dose= 0.6 mg/kg
59
Rocuronium onset and duration
onset = 1 to 2 min duration = 20-35 minutes *sugammadex made by same company to offset duration
60
Rocuronium elimination
unchanged in the bile (50%) and in the urine (>30%)
61
Rocuronium has a prolonged duration in what patients?
liver disease- especially with infusions or repeated doses *renal failure *elderly
62
Rocuronium Drug Effects
Anaphylactoid reactions but no histamine release (also seen with SUX) *slight vagolytic effect
63
Rocuronium is indicated for a ____ but not patients with a _____ because of its _____
*rapid sequence *difficult airway *duration
64
Atracurium (Tracrium) drug class
Intermediate-acting, benzylisoquinoline diester
65
Atracurium (Tracrium) ED95 and intubating dose
ED95- 0.2 mg/kg- least potent & rapid onset intubating dose= 0.5 mg/kg
66
Atracurium (Tracrium) onset and duration
onset= 2 to 3 minutes duration 20-35 minutes
67
Atracurium (Tracrium) Elimination
Hofmann elimination *metabolism by plasma esterases not plasma cholinesterases, good for renal failure pts
68
Hofmann elimination
(spontaneous breakdown) at normal temperature and pH;
69
Laudanosine
the metabolite of both routes is a CNS stimulant (cause seizures and cerebral excitation in animals). *Clinically increased levels not reached in humans *Prolonged elimination in renal failure patients
70
Atracurium CV effects
Histamine release Increased HR, decreased MAP, decreased SVR, decreased BP, flushing (3x ED95) (bigger and more rapid the dose= increased effects)
71
How to avoid histamine release effect of Atracurium
slow administration 30 to 75 seconds and/or *pretreatment with H1 (Benadryl) and H2(Pepcid or zantac) blockers- prevents effects *give low doses of drug
72
Cisatracurium (Nimbex) drug class
Isomer of atracurium, intermediate-acting benzylisoquinoline
73
Cisatracurium (Nimbex) ED95 and intubating dose
ED95= 0.05 more potent and not for rapid onset intubating dose= 0.2 mg/kg
74
Cisatracurium (Nimbex) onset and duration
onset= 2 to 3 minutes duration= 20- 35 minutes
75
Cisatracurium (Nimbex) elimination
Hofmann elimination(organ independent) (spon. breakdown), but no ester hydrolysis
76
Cisatracurium indications:
organ failure, intermediate-length case, need to avoid histamine effects (CV or pulmonary), infusion.
77
Cisatracurium effects
No cumulative effects – good for infusions. *Production of laudanosine is less due to only one pathway. *Unlike atracurium, histamine release is MINIMAL, thus minimal CV effects.
78
Mivacurium (Mivacron) drug class
Short-acting benzylisoquinoline
79
Mivacurium (Mivacron) ED95 and intubating dose
ED95= 0.08 mg/kg- potent no fast onset intubating dose= 0.15- 0.2 mg/kg
80
Mivacurium (Mivacron) onset and duration
onset= 1.5 to 3 minutes- NOT INDICATED FOR RAPID SEQUENCE duration 12-20 minutes
81
Mivacurium (Mivacron) elimination
metabolism by plasma cholinesterase at 70-80% the rate of SCh metabolism
82
Mivacurium consists of what 3 stereoisomers
– cis-trans, trans-trans (1/2 lives of 2 minutes), cis-cis (1/2 life of 53 minutes)
83
Mivacurium causes histamine release ____ ED95, avoid by giving the dose in ____ doses
*2x-histamine release from mast cells causes hypotension and tachycardia -Prophylaxis: low doses, slow administration, pretreat *divided
84
What drug slows the recovery of Mivacurium? and how?
Neostigmine (anticholinesterase) - 20- 60 minutes *it inhibits the activity of plasma cholinesterase which is what metabolizes mivacurium. Establish that recovery is already occurring prior to giving anticholinesterase (edrophonium)
85
Mivacurium causes a prolonged blockage in patients with ____ ____ ____ due to metabolism by ___ _____
*atypical plasma cholinesterase *plasma cholinesterase
86
Mivacurium may cause prolonged duration in what other patients?
renal and hepatic failure

Pharmacology 1, 680 (3 decks)

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