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Advanced Pharm 2 For NA > Nagelhout Video 3 - Exam 1 > Flashcards

Nagelhout Video 3 - Exam 1 Flashcards

1
Q

-Succinylcholine (Anectine)
-ED95
-intubation

A

ED95: 0.5-0.63mg/kg
I: 1-1.5mg/kg

per Nag, give 100mg to everyone for rest of career to keep it simple

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2
Q

Succinylcholine (Anectine)
-onset
-DOA

A

O: 30-60s
DOA: 5-15min (ultrashort)

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3
Q

Mivacurium (Mivacron)
-ED95
-intubation

A

ED95: 0.08mg/kg
I: 0.2mg

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4
Q

Mivacurium (Mivacron)
-onset
-DOA

A

O: 3 min
DOA: 20-40 min (short)

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5
Q

Atracurium (Tracrium)
-ED95
-intubation

A

ED95: 0.15mg/kg
I: 0.5mg/kg

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6
Q

Atracurium (Tracrium)
-onset
-DOA

A

O: 2-4 min
DOA: 30-60 min

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7
Q

Cisatracurium (Nimbex)
-ED95
-Intubation

A

ED95: 0.05mg/kg
I: 0.1mg/kg

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8
Q

Cisatracurium (Nimbex)
-onset
-DOA

A

O: 2-4 min
DOA: 30-60 min

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9
Q

Rocuronium (Zemuron)
-ED95
-Intubation

A

ED95: 0.3mg/kg
I: 0.6-1mg/kg

The Rock stays relevant by starring in anything he can for 0.3 of the year

The Rock stars in 0.6-1 cringe movies every year

-Nag says for intubation just keep it easy at 1mg/kg unless case is <1.5 hr

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10
Q

Rocuronium (Zemuron)
-onset
-DOA

A

O: 1-1.5min
DOA: 30-60 min

It only takes The Rock 1-1.5 min to make contact in the ring

The Rock can last 30-60 min in the ring if you make fun of his fanny pack

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11
Q

Vecuronium (Norcuron)
-ED95
-intubation

A

ED95: 0.05mg/kg
I: 0.1mg/kg

I have a tiny hand VECuum that’s effective (0.05mg)
My regular VECuum is very small too (0.1)

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12
Q

Vecuronium (Norcuron)
-onset
-DOA

A

O: 2-4 min
DOA: 30-60min

I start to VECuum after seeing 2-4 dust bunnies in the house
It takes me 30-60 min to VECuum my whole house

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13
Q

Pancuronium (Pavulon)
-ED95
-intubation

A

ED95:0.05mg/kg
I: 0.08-1.8mg/kg

0.05% of Pandas don’t prefer bambu

Panda bears range in sizes between 0.08-1.8m

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14
Q

Pancuronium (Pavulon)
-onset
-DOA

A

O: 2-4 min
DOA: 60-90min (LONG)

It takes Pandas 2-4 minutes to start eating food sitting right in front of them

Pandas eat for 60-90 minutes at a time

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15
Q

What is the priming technique for administering NMBD?

A

giving ~10% of the calculated dose to the pt RIGHT before induction, then following with the remaining NMB agent

-thought to increase speed of onset
-give induction agent asap after the 10% dose to avoid paralyzing an aware pt

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16
Q

What is the timing technique for administering NMBD?

A

-giving the FULL dose of the NMBD before the induction agents
-requires absolute precision and everything ready to go once paralyzed

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17
Q

If unable to give succinylcholine, which NDMR could you give instead?

A

Roc
-fastest onset of its class

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18
Q

Nag: “Dose for intubation with a NMBD is (roughly) _ x its ED95

A

I = ED95 x 3

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19
Q

If giving gas with NMBD:

A

just know to ease up on it before trying to reverse

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20
Q

Qualitative signs of NMBD recovery:

A

-RR smooth, unlabored
-opens eyes on command, no diplopia, purposeful tongue movement
-+ swallow, sustained bite, cough, hand grip, arm lift, head lift >5s

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21
Q

Numerical signs of NMBD recovery(not quantitative):

A

-Vt and RR WNL
-VC >/= 15mL/kg
-NIF of -25 to -30cmH2O
-sustained tetanic response to 50Hz for 5 s
-TOFR > 0.9 w/o fade
-DBS w/o fade

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22
Q

Risks of residual NMBD:

A

-aspiration ( from poor pharyngeal force, - cough, swallow, etc~airway reflexes)
-postop hypoxemia
-upper airway obstruction occurring enroute to PACU (no thanks)
-profound muscle weakness
-delays in meeting PACU discharge criteria, longer intubation times
-postop pulmonary complications (atelectasis, pneumonia)

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23
Q

Main thing we want to see when ensuring NMBD is reversed

A

TOFR >0.9

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24
Q

Pt factors contributing to residual NMBD

A

-age extremes
-gender
-pmh (renal/liver or neuromusc dysfunctions)
-meds (antiseizure meds especially)
-acidosis, hypercarbia, hypoxia, and hypothermia

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25
Q

Method of NMBD monitoring associated with LOWEST risk of residual:

A

acceleromyography

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26
Q

Which TOF count is associated with higher risk of residual NMBD, 1-2 or 2-3?

A

1-2
indicates deeper block, higher risk

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27
Q

Which method of anesthesia is more likely to be associated with residual NMBD, IA or TIVA?

A

IA

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28
Q

2 common medication classes given intraoperatively that could extend the period of paralysis:

A

opioids and abx

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29
Q

Efficacy of reversing a NMBD depends on:

A

-amount of current spont recovery? (0 twitches, 4 small twitches?)
-time between giving last paralytic (~15-30 min; should give Neostigmine anyways if <4hr since NMBD given)
-intensity of effect from NMBD given (when in doubt, wait it out -vent)

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30
Q

Neostigmine
-dose

A

25-75mcg/kg

Ne Yo has broken 25-75 mics in his career from his voice alone
(Fun fact: Ne Yo is a huge Matrix fan, hence his stage name)

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31
Q

Neostigmine
-onset
-DOA

A

O: 5-10 min
DOA: 45-90min

Ne Yo starts work 5-10 minutes late
Ne Yo will antagonize you for 45-90 min if you listen to his album

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32
Q

Neostigmine can increase the incidence of _

A

PONV

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33
Q

Edrophonium
-dose

A

500-1000mcg/kg

Ed has 500-1000 contacts in his phone

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34
Q

Edrophonium
-onset
-DOA

A

O: 5-10 min
DOA: 30-60 min

Ed is on the phone within 5-10 mins of hearing juicy gossip

Ed spends 30-60 mins on the phone spilling the tea

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35
Q

Atropine
-dose

A

15mcg/kg

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36
Q

Atropine
-onset
-DOA

A

O: 1-2 min
DOA: 1-2hr

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37
Q

Edrophonium is not ideal for _ blocks

A

deep

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38
Q

Atropine goes best with _

A

Edrophonium
-similar onset

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39
Q

Glycopyrrolate
-dose

A

10-20mcg/kg

Glyco Gecko weighs 10-20mcg

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40
Q

Glycopyrrolate
-onset
-DOA

A

O: 2min
DOA: 2-4hr

Every 2 minutes, somebody STARTS saving money by switching to Glyco
Each Glyco ad lasts 2-4hrs

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41
Q

Glycopyrrolate has _ initial tachycardia than atropine, is a _ antisecretion drug, and has _ CNS effects

A

less
better
no

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42
Q

Sugammadex
-dose

A

2-8mg/kg
-up to 16mg/kg safely

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43
Q

Sugammadex
-onset
-DOA

A

O: 1-2min
DOA: 2-16hr

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44
Q

Neostigmine
-MAX dose

A

5mg
-ceiling effect; will have 100% inhibition of AChE

45
Q

Edrophonium
-Max dose

A

1mg/kg

46
Q

Which reversal agent is a faster onset and shorter duration

A

Edrophonium
-less effective; give if pt has 4/4 twitches

47
Q

Which reversal agent is slower onset and longer duration?

A

Neostigmine

48
Q

How do AChE Inhibitors (reversal drugs) work?

A

by increasing ACh release or inhibiting degradation of ACh by AChE
-Neostigmine and others bind to active site and form carbamyolated enzyme that AChE hydrolyzes instead of ACh, this continues until enough extra ACh is made

49
Q

Why give an anticholinergic (antimuscarinics) along with AChE Inhibitors?

A

bc AChE Inhibitors often work systemically and activating the nicotinic and muscarinic cholinergic receptors will cause a large vagal/parasympathomimetic response
-bradycardia, secretions, bronchoconstriction, diarhea

50
Q

Which anticholinergics go with each AChE inhibitor?

A

Edrophonium and Atropine
Neostigmine and Glycopyrrolate (Robinul)

51
Q

What kind of drug is sugammadex?

A

gamma-cyclodextrin ; paralytic reversal drug

52
Q

How does sugammadex work?

A

Encapsulates and inactivates STEROIDAL NMBD
-encapsulates them and makes them water soluble

53
Q

Sugammadex pharmacokinetics shows a linear dose relationship in doses up to _mg/kg

A

8

54
Q

What happens if I gave my pt sugammadex but they need to go back to the OR?

A

use a different NMBD in a different class - nonsteroidal

55
Q

Which drugs does Sugammadex work on?

A

Vec and Roc; sugammadex is a selective relaxant binding agent (SRBA)
~3min

56
Q

Elimination half life of Sugammadex?

A

2.3hr

57
Q

Up to _% of Sugammadex is eliminated thru urine in 24hr

A

80

58
Q

Which pts are at higher risk for complications if not properly reversed?

A

major renal disease (NAG enzyme)
BMI>35
major resp disease
poor resp reserve
OSA
major coronary disease
hx of arrhythmias
hx PONV
major abdom/thoracic surg

-give sugammadex

59
Q

T/F Sugammadex binds to plasma proteins and erythrocytes

A

false

60
Q

Sugammadex
-dosing

A

TOFR (0.5) = 0.22mg/kg
TOF (2/4) = 2mg/kg
PTC (1-2)= 4mg/kg
RSI, high dose Roc, or can’t intubate/ventilate = 16mg/kg

61
Q

Sugammadex
A/E

A

-dry mouth, dysgeusia, N/V, cough, low BP, chills, large amt of N-acetylglucosaminidase in urine

-allergy (tachycardia, rash, at higher doses/faster admin)

-this happens within 5-10min of admin

-negates oral contraceptives (need other method for 1mo)

62
Q

2 kinds of nACh receptors exist

A

Neuronal(pre-synaptic)
Muscular (post-synaptic)

-both have 2 alpha, beta, delta, subunits

63
Q

How do NDMR and DMR differ?

A

NDMR cause blocks by blocking ACh from postsynaptic alpha subunits

DMR (sux) causes prolonged depolarization causing reduced sensitivity in post synaptic nAChr and inactivates Na+ channels to inhibit propagation

64
Q

How is a twitch and fade different?

A

Fully blocking a twitch occurs from blocking postsynaptic nAChr

Fade is caused by blocking the presynaptic nAChr

65
Q

What metabolizes Succinylcholine?

A

hydrolyzed by butyrylcholinesterase

66
Q

NDMR are classified as either:

A

steroidal or benzyl isoquinol inium

67
Q

The speed of onset is _ proportional to the potency of NDMR

A

inversely
-more potent = slower onset
-bc we’re only giving few mg at a time (hence 100mg sux vs 3-4mg Nimbex)
-molar potency is highly predictive of onset (Roc= 0.54 mcM/kg)

68
Q

Which NM units get blocked and recover quicker, central or peripheral?

A

central (laryngeal adductors, diaphragm, masseter muscle)
-hence why we watch the face first when inducing and ulnar n when emerging

69
Q

Testing facial n we’re looking for movement with the

A

orbicularis oculi and the corrugator supercilli

70
Q

Testing ulnar n we’re looking for movement with the

A

adductor pollicis

71
Q

Long acting NMBD undergo minimal metabolism and are primarily eliminated by

A

renal excretion

72
Q

Intermediate duration NMBD clear quicker than longer acting ones bc

A

they are degraded, metabolized, and eliminated

73
Q

If myalgia is a concern when giving sux, what can be done?

A

give small, rapid acting defasciculating dose of NDMR as well
OR just give Roc ~1min and ready

74
Q

Which 2 drug classes most likely cause anaphylaxis?

A

ABX and NMBD
-more common long and intermediate acting NMBD

75
Q

2 most common NMBD

A

Roc and Sux

76
Q

In terms of reversal of paralytics, what should be common practice?

A

full dose of reversal given AFTER some spontaneous reversal is seen

77
Q

Pt has increased IOP and needs surg, but sux increases IOP. What should be done?

A

-give sux anyways, propofol can decrease IOP so give it before sux
-use topical and regional anesthesia where possible

78
Q

What do Alzheimer’s drugs do?

A

weak AChE Inhibitors
-increase ACh in brain

79
Q

Examples of drugs for Alzheimers disease:

A

-Donepezil (Aricept)
-Rivastigmine (Exelon)
-Galantamine (Razadyne)
-Tacrine (Cognex)

80
Q

Will sux interact with Alzheimer drugs?

A

yes, will make NMBD last longer, but not by much ~25% inhibition

81
Q

Which NMBD will Alzheimer medications NOT interact with?

A

Neostigmine and NDMR
-these don’t cross BBB

82
Q

What is Physostigmine?

A

AChE inhibitor, increases ACh in brain CROSSES BBB
-used sometimes in PACU to wake ppl tf up

83
Q

What is Phospholine Iodide ?

A

eye gtts with AChE inhibitors used to treat glaucoma and lower IOP
-can increase duration of sux (boards question despite drug not being common now)

84
Q

What are 2 main types of local anesthetics?

A

esters and amides
-esters have 1 “i” and amides have 2 (lidocaine = amide, procaine =ester)

85
Q

3 parts of LA structure

A

Lipophilic Benzene Ring (aromatic group)

Hydrophilic Quaternary Amine (base)

Intermediate chain in between them (made of ester or amide)

-if chain has a N in it = amide
-if chain has 2 oxygen groups = ester

86
Q

Which LA have higher allergy potential?

A

esters

87
Q

T/F If pt has an allergy to an ester, they can just have a different ester

A

false

88
Q

T/F If pt has an allergy to an amide, they can just have a different amide

A

true
-can also have an ester too

89
Q

How are amide LAs metabolized?

A

in liver by CYP1A2 and CYP3A4
-if pt is ultrarapid metabolizer will have a significant blood level

90
Q

How are ester LAs metabolized?

A

catalyzed by plasma and tissue cholinesterase via hydrolysis
-does this rapidly

91
Q

Are esters synthetic or natural?

A

mostly synthetic
-except cocaine

92
Q

Which LA are longer acting and why?

A

amides
-more lipophilic and protein-bound, require transport to liver to metabolize

93
Q

Longest acting LA ester?

A

Tetracaine

94
Q

Examples of ester LAs

A

Cocaine
Procaine (Novacaine)
Chloroprocaine (Nesacaine)
Tetracaine (Pontocaine)
Benzocaine (Anbesol, Cepacol)

95
Q

Examples of amide LAs

A

Lidocaine (Xylocaine)
Prilocaine (Citanest)
Ropivacaine (Naropin)
Bupivicaine (Marcaine, Sensorcaine)
Mepivicaine (Cabocaine)

96
Q

What is N-Acetylglucosamine (NAG)?

A

biomarker for renal tubule damage
-seen as an A/E to sugammadex admin

97
Q

Common abx and paralytic drug interaction

A

Aminoglycoside abx - mycins
-can’t reverse them, just put on vent and leave in PACU

98
Q

Which complications can occur if sugammadex is given too quickly?

A

Bronchospasm, severe bradycardia
-other A/E (HoTN, rash, anaphylaxis)

99
Q

Tx for Sugammadex hypersensitivity reaction:

A

Epi 10-20mcg boluses PRN
Epi 25-50mcg for bronchospasm
LR bolus
Albuterol 4-10 puffs PRN
Hydrocortisone 100mg IV
Diphenhydramine (H1blocker) 50mg IV
Famotidine (H2 blocker) 20mg IV

100
Q

Why give an H1 and H2 blocker for sugammadex hypersensitivity?

A

H1 blocker prevents bronchoconstriction

H2 blocker prevents cardiovascular collapse

101
Q

Which NDMR are steroidal?

A

Roc
Vec
Pancuronium

102
Q

Which AChE inhibitor is likely to cause PONV

A

neostigmine

103
Q

What is best thing to document after reversal agent was given and extubated successfully before sending to PACU?

A

T1/T4 ratio >0.9
VS obviously along w Vt
“good exchange after extubation”

104
Q

H2 receptor activation causes

A

-increased gastric acid,
-systemic vasodilation and tachycardia
-+ inotrope
-+chronotrope

105
Q

H1 receptor activation causes

A

-bronchoconstriction
-increased capillary permeability (swelling)
-increases gastric contraction
-negative dromotropic effects

106
Q

Diphenhydramine blocks

A

H1 receptors

107
Q

Famotidine or zantac can block

A

H2 receptors

108
Q

Succinylcholine
-laryngospasm dose

A

0.2-2.0 mg /kg
-low for mild, high for severe

109
Q
A

Advanced Pharm 2 For NA (14 decks)

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