Nagelhout videos: NMB's Flashcards

1
Q

Pt can start breathing when _____% of their nicotinic cholinergic receptors are still blocked

A

80%

-only need 20% return of function to breathe

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2
Q

Smooth muscle isn’t affected by NMB… what kind of things are smooth muscle

A
  • Bronchi
  • Uterus
  • Bowel
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3
Q

T/F- GI sphincters are affected by NMB

A

True but the smooth muscle itself is not

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4
Q

if smooth muscle in the abdomen aren’t affected by NMB, why do we need to give relaxant to belly cases?

A

Think of it as a tube and toothpaste ; the way we keep the toothpaste from squeezing out of the tube, is by relaxing the tube (all the abdominal muscles surrounding the guts)

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5
Q

which way is the electric current flowing between the red and black leads on twitch monitor

A

electricity flows from positive to negative

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6
Q

What muscles are the easiest muscles to paralyze?

A

the eyelid muscles

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7
Q

Hardest muscle in the body to paralyze?

A

Diaphragm- makes sense, you need to breathe to live

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8
Q

Why shouldn’t you put the electrodes for TOF like around the eye like you sometimes might do lol

A

bc you can directly stimulate the muscle even if its 100% paralyzed- youre sending the electricity directly into the muscle- the muscle is going to contract;

& paralytics don’t paralyze the muscle, they paralyze nerve-to-muscle transmission

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9
Q

Why would you give SUX for an RSI? And don’t say bc it’s fast onset of action, what’s the real deal

A

Bc propofol makes people lose their airway reflexes, and during that time they are vulnerable to aspiration; the ability to give sux lessens the time they are a-reflexic and vulnerable to aspirating bc you can get the tube in quicker to secure the airway; whereas with roc/vec you would have to wait a much longer time for it to work

want prop to tube time to be as short as possible

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10
Q

What is a modified RSI

A

instead of not ventilating at all while waiting for relaxant to work, you gently ventilate

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11
Q

Recovery time with neostigmine based on
1 twitch:
2-3 twitches:
4 twitches:

A

1 = up to 30 minues
2-3 twitches = 4-15 mins
4 twitches = 5-10 mins

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12
Q

How is TOF ratio measured?

A

Comparing the first twitch to the 4th twitch

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13
Q

What percent is blocked with each line

A

4 twitches = 70% blocked

3 twitches = 75% blocked

2 twitches = 80% blocked

1 twitch = 90% blocked

0 twitch = 100% blocked

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14
Q

4 twitches without fade = ___% blocked, ___% recovered, TOFR:

4 twitches with fade = ____% blocked, ___% recovered, TOFR:

A
  • no fade = <70% blocked, >30% recovered; TOF > 0.9 or 90%
    • fade = 70-75% blocked, 25-30% recovered; TOF < 0.9 or 90%
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15
Q

someone asks you what the TOF ratio is on someone with 2 twitches

A

n/a - it’s a TOfour , need 4 twitches to get a TOF ratio

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16
Q

Single twitch = ____hz

TOF twitchs = _____hz

DBS = _____hz

Tetany = _______hz

A

single = 1 hz

TOF = 2 hz

DBS = 50hz

Tetanus = 50-100hz

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17
Q

DBS is 2 twitches at ___ hz with what time lapse in between

A

50hz, 3/4 of a second

18
Q

Explain why post-tetanic potentiation is a shitty way to claim someone has twitches

A

okay so you give a tetanus over 5 seconds

  • this mobilizes acetylcholine down the presynaptic nerve and floods the synapse but pt is 100% blocked and you don’t see any reaction from that ACH right away
  • After you flood the synapse with ACH and do a TOF, there hasn’t’ been enough time that lapsed for AchE to metabolize it, so it can breifly overpower the blocked receptors
  • However, that NMB is going to hop right back onto that receptor as ACH becomes more and more metabolzied by AchE.
  • So you’re only kidding yourself if you think the patient is any bit kind of recovered
19
Q

T/F- dibucaine SHOULD inhibit psedudocholinesterase

A

True

20
Q

T/F- dibucaine should NOT inhibit pseudocholinesterase

A

false - it should

if it doesn’t inhbit PchE, the patient is atypical

21
Q

T/F- the dibucaine number reflects the amount of pseudocholinesterase that was inhibited in the test tube

A

true- if it’s 80, means 80% was inhibited and 80% is normal

22
Q

1 culprit of MH

A

Sux

23
Q

2 drugs that increase IOP

A

Sux and Ketamine

24
Q

What percentage of burn injury shouldn’t you give sux to after 24 hrs?

A

>35% burned

25
Q

What should you think when you see these in a chemical structure? What are they?

A

They are ester links and it means they can be hydrolyzed by plasma esterases; since this is atracurium and cist - it would be non-specific esterases

26
Q

What should influence your decision of what muscle relaxant to use?

A

How it will be eliminated

27
Q

Stimulation of which histamine receptor results in increased capiliary permeability -> inflammation/swelling/bronchoconstriction

A

Histamine 1

28
Q

Which histamine receptor results in a great increase in gastric acid production?

A

H2 - hence why we give H2 blockers, decreases amount of gastric acid secretion

29
Q

Which histamine receptor causes systemic and cerebral vasodilation?

A

H2

30
Q

T/F- the degree of histamine release is directly propotional to how much and how fast you push a histamine-releasing drug

A

True!

-push them slow!

31
Q

If you are going to give a known histamie-releasing drug, would you pre-treat with a H1 or H2 blocker?

A

Both

H1 = benadryl

H2 = pepcid

32
Q

How does benadryl work?

A
33
Q

muscle relaxants intubating dose is ___x the maintenance dose (ED95)

ex. Roc

A

3x

ED 95 = 0.3mg/kg

intubating dose = 0.9mg/kg (1mg/kg)

34
Q

acetylcholinesterase inhibitors work by indirectly increasing the amount of acetylcholine in the synaptic cleft in excess of the blocker; this is the law of _________

A

mass action

35
Q

purpose of giving glyco with neostigmine

A

bc the acess of ACH that builds up in the synaptic cleft, also builds up around the cholinergic receptors in the PNS; so in order to block that from binding to those receptors too, an antimuscarinic is given that will work in the PNS but not block the nicotnic NMJ receptors

36
Q

max dose of edrophonium

A

1mg

37
Q

The potency is (directly/inversely) propotional to the speed of onset.

A

inversely

  • more potent = slower onset (less molecules)
  • less potent (more molecules needed) = faster onset
38
Q

anticholinesterase eyedrops

A

echothipate

Phospholine Iodide (Wyeth-Ayerst)

39
Q

T/f - echothiapate would increase the DOA of sux

A

true bc they are anticholinesterase eyed drops

40
Q
A