Nagelhout Video 3 - Exam 1 Flashcards

(109 cards)

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
Method of NMBD monitoring associated with LOWEST risk of residual:
acceleromyography
26
Which TOF count is associated with higher risk of residual NMBD, 1-2 or 2-3?
1-2 indicates deeper block, higher risk
27
Which method of anesthesia is more likely to be associated with residual NMBD, IA or TIVA?
IA
28
2 common medication classes given intraoperatively that could extend the period of paralysis:
opioids and abx
29
Efficacy of reversing a NMBD depends on:
-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)
30
Neostigmine -dose
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)
31
Neostigmine -onset -DOA
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
32
Neostigmine can increase the incidence of _
PONV
33
Edrophonium -dose
500-1000mcg/kg Ed has 500-1000 contacts in his phone
34
Edrophonium -onset -DOA
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
35
Atropine -dose
15mcg/kg
36
Atropine -onset -DOA
O: 1-2 min DOA: 1-2hr
37
Edrophonium is not ideal for _ blocks
deep
38
Atropine goes best with _
Edrophonium -similar onset
39
Glycopyrrolate -dose
10-20mcg/kg Glyco Gecko weighs 10-20mcg
40
Glycopyrrolate -onset -DOA
O: 2min DOA: 2-4hr Every 2 minutes, somebody STARTS saving money by switching to Glyco Each Glyco ad lasts 2-4hrs
41
Glycopyrrolate has _ initial tachycardia than atropine, is a _ antisecretion drug, and has _ CNS effects
less better no
42
Sugammadex -dose
2-8mg/kg -up to 16mg/kg safely
43
Sugammadex -onset -DOA
O: 1-2min DOA: 2-16hr
44
Neostigmine -MAX dose
5mg -ceiling effect; will have 100% inhibition of AChE
45
Edrophonium -Max dose
1mg/kg
46
Which reversal agent is a faster onset and shorter duration
Edrophonium -less effective; give if pt has 4/4 twitches
47
Which reversal agent is slower onset and longer duration?
Neostigmine
48
How do AChE Inhibitors (reversal drugs) work?
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
Why give an anticholinergic (antimuscarinics) along with AChE Inhibitors?
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
Which anticholinergics go with each AChE inhibitor?
Edrophonium and Atropine Neostigmine and Glycopyrrolate (Robinul)
51
What kind of drug is sugammadex?
gamma-cyclodextrin ; paralytic reversal drug
52
How does sugammadex work?
Encapsulates and inactivates STEROIDAL NMBD -encapsulates them and makes them water soluble
53
Sugammadex pharmacokinetics shows a linear dose relationship in doses up to _mg/kg
8
54
What happens if I gave my pt sugammadex but they need to go back to the OR?
use a different NMBD in a different class - nonsteroidal
55
Which drugs does Sugammadex work on?
Vec and Roc; sugammadex is a selective relaxant binding agent (SRBA) ~3min
56
Elimination half life of Sugammadex?
2.3hr
57
Up to _% of Sugammadex is eliminated thru urine in 24hr
80
58
Which pts are at higher risk for complications if not properly reversed?
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
T/F Sugammadex binds to plasma proteins and erythrocytes
false
60
Sugammadex -dosing
**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
Sugammadex A/E
-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
2 kinds of nACh receptors exist
Neuronal(pre-synaptic) Muscular (post-synaptic) -both have 2 alpha, beta, delta, subunits
63
How do NDMR and DMR differ?
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
How is a twitch and fade different?
Fully blocking a twitch occurs from blocking postsynaptic nAChr Fade is caused by blocking the presynaptic nAChr
65
What metabolizes Succinylcholine?
hydrolyzed by butyrylcholinesterase
66
NDMR are classified as either:
steroidal or benzyl isoquinol inium
67
The speed of onset is _ proportional to the potency of NDMR
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
Which NM units get blocked and recover quicker, central or peripheral?
central (laryngeal adductors, diaphragm, masseter muscle) -hence why we watch the face first when inducing and ulnar n when emerging
69
Testing facial n we're looking for movement with the
orbicularis oculi and the corrugator supercilli
70
Testing ulnar n we're looking for movement with the
adductor pollicis
71
Long acting NMBD undergo minimal metabolism and are primarily eliminated by
renal excretion
72
Intermediate duration NMBD clear quicker than longer acting ones bc
they are degraded, metabolized, and eliminated
73
If myalgia is a concern when giving sux, what can be done?
give small, rapid acting defasciculating dose of NDMR as well OR just give Roc ~1min and ready
74
Which 2 drug classes most likely cause anaphylaxis?
ABX and NMBD -more common long and intermediate acting NMBD
75
2 most common NMBD
Roc and Sux
76
In terms of reversal of paralytics, what should be common practice?
full dose of reversal given AFTER some spontaneous reversal is seen
77
Pt has increased IOP and needs surg, but sux increases IOP. What should be done?
-give sux anyways, propofol can decrease IOP so give it before sux -use topical and regional anesthesia where possible
78
What do Alzheimer's drugs do?
weak AChE Inhibitors -increase ACh in brain
79
Examples of drugs for Alzheimers disease:
-Donepezil (Aricept) -Rivastigmine (Exelon) -Galantamine (Razadyne) -Tacrine (Cognex)
80
Will sux interact with Alzheimer drugs?
yes, will make NMBD last longer, but not by much ~25% inhibition
81
Which NMBD will Alzheimer medications NOT interact with?
Neostigmine and NDMR -these don't cross BBB
82
What is Physostigmine?
AChE inhibitor, increases ACh in brain ***CROSSES BBB*** -used sometimes in PACU to wake ppl tf up
83
What is Phospholine Iodide ?
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
What are 2 main types of local anesthetics?
esters and amides -esters have 1 "i" and amides have 2 (lidocaine = amide, procaine =ester)
85
3 parts of LA structure
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
Which LA have higher allergy potential?
esters
87
T/F If pt has an allergy to an ester, they can just have a different ester
false
88
T/F If pt has an allergy to an amide, they can just have a different amide
true -can also have an ester too
89
How are amide LAs metabolized?
in liver by CYP1A2 and CYP3A4 -if pt is ultrarapid metabolizer will have a significant blood level
90
How are ester LAs metabolized?
catalyzed by plasma and tissue **cholinesterase** via **hydrolysis** -does this rapidly
91
Are esters synthetic or natural?
mostly synthetic -except cocaine
92
Which LA are longer acting and why?
amides -more lipophilic and protein-bound, require transport to liver to metabolize
93
Longest acting LA ester?
Tetracaine
94
Examples of ester LAs
Cocaine Procaine (Novacaine) Chloroprocaine (Nesacaine) Tetracaine (Pontocaine) Benzocaine (Anbesol, Cepacol)
95
Examples of amide LAs
Lidocaine (Xylocaine) Prilocaine (Citanest) Ropivacaine (Naropin) Bupivicaine (Marcaine, Sensorcaine) Mepivicaine (Cabocaine)
96
What is N-Acetylglucosamine (NAG)?
biomarker for renal tubule damage -seen as an A/E to sugammadex admin
97
Common abx and paralytic drug interaction
Aminoglycoside abx - mycins -can't reverse them, just put on vent and leave in PACU
98
Which complications can occur if sugammadex is given too quickly?
Bronchospasm, severe bradycardia -other A/E (HoTN, rash, anaphylaxis)
99
Tx for Sugammadex hypersensitivity reaction:
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
Why give an H1 and H2 blocker for sugammadex hypersensitivity?
H1 blocker prevents bronchoconstriction H2 blocker prevents cardiovascular collapse
101
Which NDMR are steroidal?
Roc Vec Pancuronium
102
Which AChE inhibitor is likely to cause PONV
neostigmine
103
What is best thing to document after reversal agent was given and extubated successfully before sending to PACU?
T1/T4 ratio >0.9 VS obviously along w Vt "good exchange after extubation"
104
H2 receptor activation causes
-increased gastric acid, -systemic vasodilation and tachycardia -+ inotrope -+chronotrope
105
H1 receptor activation causes
-bronchoconstriction -increased capillary permeability (swelling) -increases gastric contraction -negative dromotropic effects
106
Diphenhydramine blocks
H1 receptors
107
Famotidine or zantac can block
H2 receptors
108
Succinylcholine -laryngospasm dose
0.2-2.0 mg /kg -low for mild, high for severe
109