Exam 2 part IV Flashcards

1
Q

s/e of atracurium

A
  1. dose dependent histamine release 2. may cause transient drop in SVR and increase in CI 3. severe bronchospasm 4. laudanosine toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

s/e of cisatracurium

A
  1. laudanosine toxicity (5x less than atracurium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what will prolong the effects of atracurium & cisatracurium

A
  1. hypothermia 2. acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

atracurium is a better choice for ________________ (induction or maintenance)

A

maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what change should you make in the dose of atracurium for neonates

A

decrease dose by 1/2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

__________________ is a great NDMR choice for children and renal pts due to its metabolic profile

A

cisatracurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is hoffman elimination

A
  1. 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is laudanosine

A
  1. 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

__________________ is a bisquaternary amine that resembles Ach enough to bind, but NOT depolarize

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

intubating dose of pancuronium

A

0.08 - 0.12 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

onset of pancuronium

A

2-3 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DOA of pancuronium

A

60-90 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ED95 of pancuronium

A

0.07 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

metabolism of pancuronium

A

in the liver (40-70%) –> active metabolite 3-desacetylpancuronium (50% reduction in potency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which NMBA is a long acting

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

dose modification of pancuronium in peds

A

increase dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

s/e of pancuronium

A
  1. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effects of pancuronium are prolonged in those with ________________

A

renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pt with cirrhosis, if choose to give pancuronium you should _____________ intubating dose and ___________________ maintenance dose

A

increase; decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

caution use of pancuronium in what pts

A
  1. renal failure (prolonged effects) 2. CAD 3. IHSS any dz where HR increase is detrimental
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why is pancuronium commonly used in cardiac anesthesia?

A

it counteracts the bradycardia 2/2 high dose opoids used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

____________________ is a monoquaternary amine that is equal to or 1.5x as potent as pancuronium

A

vecuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

intubating dose of vecuronium

A

0.08-0.12 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

onset of vecuronium

A

3 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

DOA of vecuronium

A

30-45 min

26
Q

ED95 of vecuronium

A

0.04-0.05 mg/kg

27
Q

excretion of vecuronium

A

primarily liver excretion (40-80%) then renal excretion (20-30%)

28
Q

excretion of pancuronium

A

primarily renal (40-70%) limited liver (10%)

29
Q

which patients have a slower recovery from vecuronium?

A
  1. obese 2. infants 3. neonates
30
Q

females are __________% more sensitive to vecuronium than men

A

30

31
Q

___________________ is a monoquaternary amine that is 1/6th - 1/8th as potent as vec

A

rocuronium

32
Q

which NDMR is a steroid and has the most rapid onset due to being the least potent

A

rocuronium

33
Q

intubating dose of rocuronium

A

0.45 - 0.9 mg/kg

34
Q

RSI dose of rocuronium

A

0.9-1.2 mg/kg

35
Q

pediatric intubating dose of rocuronium (ages 2-12)

A

0.9-1.2 mg/kg

36
Q

onset of rocuronium

A

45-90 seconds

37
Q

DOA of rocuronium

A

30-90 min

38
Q

ED95 of rocuronium

A

0.3 mg/kg

39
Q

metabolism of rocuronium

A

no metabolism

40
Q

half life of rocuronium

A

1-2 hrs

41
Q

excretion of rocuronium

A

primarily liver (55%) then renal (35%) most of the drug excreted in bile unchanged

42
Q

DOA of rocuronium is increased in what pts?

A
  1. severe hepatic failure 2. pregnancy 3. elderly 4. obesity 5. females
43
Q

rocuronium dose should be increased with what pts?

A

those with liver dz

44
Q

a ____________mg/kg dose of rocuronium will allow for intubating conditions as fast as 1.0 mg/kg of succinylcholine

A

1

45
Q

females appear to be ___________% more sensitive to vecuronium, pancuronium, and rocuronium

A

30

46
Q

traditional reversal of NDMR requires maximal ________________ transmission with minimal _____________ s/e

A

nicotinic; muscarinic

47
Q

when reversing a NDMR which medication do you give first (Anticholinergic or anticholinesterase)

A

anticholinergic (ex; glycopyrolate)

48
Q

Anticholinesterase (neostigmine) _________________ increases the amount of Ach at the neuromuscular jx

A

indirectly

49
Q

MOA of anticholinesterases (cholinesterase inhibitors)

A
  1. 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
50
Q

before pharmacological reversal of NDMR is initiated or attempted, what must be present?

A

some evidence of spontaneous reversal

51
Q

Dose of cholinesterase inhibitor for NDMR reversal is dependent on what

A

level of blockade

52
Q

from administration of anticholinesterase (cholinesterase inhibitor); the time to reversal of NDMR depends on what?

A
  1. agent and dose of cholinesterase inhibitor 2. NDMR being reversed/antagonized 3. extent of existing block
53
Q

pharmacokinetics of anticholinesterases

A
  1. water soluble 2. ionized 3. primarily excreted in the kidney
54
Q

why should there be some evidence of spontaneous reversal before administration of pharmacological agents to reverse NDMR

A

need DOA of reversal to outlast DOA of NDMR

55
Q

T/F: all patients should receive pharmacologic reversal of NDMR even if full recovery status is noted on clinical testing

A

TRUE

56
Q

what are your anticholinesterase drugs

A
  1. edrophonium 2. neostigmine/pyridostigmine 3. organophosphates (physostigmine)
57
Q

which anticholinesterase medication works via hydrogen bonding, has short DOA, and prejunctional effects (increasing Ach release)

A

edrophonium

58
Q

Neostigmine and pyridostigmine are anticholinesterases that work via _______________ bonds causing a __________DOA

A

covalent; long

59
Q

T/F: neostigmine is a weak agonist of nicotinic receptors

A

TRUE

60
Q

neostigmine and pyridostigmine have _______________ junctional receptor effects

A

pre and post