Lecture 4 Test 3 Flashcards

1
Q

If you want to keep tabs on your paralytics and check how deep your NM block is, what can you do?

A

Neuromuscular monitoring (TOF)

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2
Q

How does neuromuscular monitoring work?

A

Place 2 electrodes on top of a nerve and when you run a current through these, it should cause a depolarization.

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3
Q

How can you generate an action potential externally?

A

TOF

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4
Q

What does it mean when you see a reaction after running a current through the ulnar nerve?

A

Your paralytic on board isn’t that deep.

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5
Q

What does it mean when you don’t see a reaction after running a current through the ulnar nerve?

A

Your block is deep

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6
Q

What does it mean when you see a minimal reaction after running a current through the ulnar nerve?

A

Your block may be wearing off.

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7
Q

What happens when you run a current of electrons outside of the cell.

A

Generate an action potential.

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8
Q

What does polarity mean?

A

There’s a charge difference between inside and outside the cell.

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9
Q

If there’s no difference between the charges inside and outside of a cell, this mean….

A

It is depolarized!

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10
Q

Are EKG’s looking at the current inside or outside of the heart cells?

A

Outside of the heart cells

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11
Q

What is the required voltage needed to dial in for your neuromuscular monitoring called?

A

Supramaximal stimuli

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12
Q

Term for “strong enough to recruit all the motor neurons in the underlying nerve”.

A

Supramaximal stimuli

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13
Q

TOF setting

A

2Hz / 2 secs = 2 impulses/1 sec = 4 impulses / 2 secs

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14
Q

How can you tell if you’re using a non depolarizing block based on the TOF?

A

The first twitch is stronger and gets weaker each time.

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15
Q

How can you tell if you’re using a Depolarizing neuromuscular blocker?

A

Equal strength on all 4 twitches.

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16
Q

What is Tetanic contractions?

A

High frequency stimulation for a short period of time. More than 4 impulses.

Causing continuous depolarizations for a period of time.

Unable to fully relax between depolarizations.

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17
Q

Checking for impulses the muscle generates after High frequency impulses to see the health of the synapse

A

Post tetanic count

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18
Q

What is double burst stimulation?

A

High frequency stimulation for a couple of secs, lay off and then do it again. In order to check for different characteristics of the neuromuscular block.

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19
Q

What happens when the ulnar nerve is stimulated?

A

Thumb comes forward and pinky twitches.

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20
Q

What does the ulnar nerve innervate when stimulated?

A

Adductor pollicis muscle

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21
Q

What other sites for TOF

A

Facial nerve
Peroneal nerve
Posterior tibial nerve

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22
Q

Which blocking agent takes into effect faster? NDMR or DMR

A

DMR (Succs)

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23
Q

What’s another reason why Succs is good to use?

A

It’s fast onset, short acting and it’s cheap! per Dr. Schmidt

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24
Q

Based on NDMR meds, how does your twitches return as the meds wear off?

A

You get one twitch at a time, first being stronger and the others get weaker and weaker until all 4 twitches are equal.

B/A is closer to 1 = recovered

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25
Q

As the drugs wear off for an NDMR agent how do you measure the ratio of each twitch?

A

The first twitch is labeled as A and the 4th twitch is B. Initially, the B over A ratio is very small. As the drug wears off, the ratio gets closer to 1.

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26
Q

Why’s is the first twitch of the TOF always stronger in a NDMR?

A

The first twitch has enough ACh to release on the first depolarization while the next subsequent depolarizations have lesser and lesser ACh being released from the neuron.

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27
Q

What’s the difference between the B over A ratio of a DMR block vs NDMR?

A

DMR: It is always closer to 1 since the A and B twitches are the same.

NDMR: Has a B/A ratio that’s less than 1 and it gets closer to 1 the closer the meds wear off.

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28
Q

What is the target of an NDMR?

A

Motor neuron and skeletal muscle.

29
Q

What does an a3 b2 receptor do?

A

3 places to bind ACh, and 2 beta subunits. ACh is released and binds to the skeletal muscle and the others bind back to the ACh auto receptor to help complete with VP1 to VP2.

30
Q

When NDMR binds to the skeletal muscle receptor and also bind to the auto receptor (a3b2) it will prevent VP1 from becoming VP2…..

A

leads to a weaker subsequent contraction.

31
Q

Why’s does each contraction get weaker during each TOF when NDMR is used?

A

The first twitch had more time to figure out how to replace VP2 and have fewer storage vesicles available for the other twitches.

32
Q

Effects of DMR on TOF.

A

DMR affects the skeletal muscle to be constantly depolarized and no effect on the presynaptic neuron so VP1 and VP2 aren’t affected. Once the drug wears off, there’s a constant supply of VP2 for each twitch.

33
Q

How is succs broken down?

A

Plasmacholinesterase from the liver.

34
Q

Do autoreceptors have gates?

A

No, it opens when an ion binds to it.

35
Q

Are there L type calcium channels in the presynaptic cell?

A

Yes

36
Q

Does the CCBs work on L type channels in the presynaptic cell?

A

No

37
Q

T/F : If you’re hungover and shaky the L type ca channel can help settle it down.

A

True

38
Q

What happens when you give succs to a stroke Pt?

A

Prolonged depolarizations due to Fetal n-ACh-R causing increased surface area and hyperkalemia in the ECF.

39
Q

Less important muscle i.e. Adductor Pollicis muscle req. 40mcg/kg to be paralyzed.

Diaphragm (more important skeletal muscle) starts at 40mcg up to 90mcg/kg to be paralyzed.

A

Less important muscles requires less meds to be paralyzed.

The more important muscles require more drugs to block d/t more receptors.

40
Q

Which spinal nerves control the diaphragm???

A

Spinal nerves C3, C4, C5 (Phrenic nerve)!!!!!!!!!!!!!

41
Q

Can you still breathe if you have a complete lesion at T1

A

Yes

42
Q

As the block wears off, which will recover first? Diaphragm or adductor pollicis?

A

Diaphragm

43
Q

How do you know if the patient is going to be able to breathe on their own?

A

Diaphragm recovers faster than the adductor pollicis.

If the adductor pollicis has 4 strong twitches. Diaphragm has completely recovered way before the twitches occur.

44
Q

What does it mean if you have 3 of 4 TOF?

A

75%-80% nACh-R blocked

45
Q

What does it mean if you have 2 of 4 twitches?

A

85% nACh-R blocked

46
Q

What does it mean if you have 1 of 4 twitches?

A

85% - 90% nACh-R blocked

46
Q

How many % of nACh-r blocked if the Pt can lift their head?

A

70% and all 4 twitches should be present as well.

47
Q

What does it mean if all twitches are gone?

A

90% - 95% nACh blocked

48
Q

How many mA is the Stimulator settings?

A

50-80 mA

49
Q

The ocular system has several motor neurons and if paralyzed with a depolarizing muscle block it can…..

A

cause ca++ influx, increase IOP. risk for vision loss

50
Q

What is GABA used for?

A

Limit neural activity

51
Q

Inhibitory neurotransmitter in the spinal cord

A

Glycine

52
Q

What are the 2 inhibitory neurotransmitter in the spinal cord?

A

Gaba and Glycine

53
Q

What else is acetylcholine used for?

A

Makes us more awake/aware in the brain

Increase CNS; neuronal activity

54
Q

What happened when ACh is blocked in the CNS?

A

drowsiness (anticholinergic)

55
Q

ex. m-ACh-R antagonist

A

Benadryl (Anticholinergic, antihistamine)

56
Q

What can you give someone with Alzheimer’s to be more aware?

A

To increase ACh (inhibit AChesterase), give stigmines = more awareness/active

57
Q

If you give AChesterase inhibitor, one side effect could be

A

Bradycardia d/t m-Ach-R in the heart.

57
Q

If you don’t want to wake someone up but want to reverse a paralytic…

A

Might want to give an AChesterase that doesn’t cross the BBB

58
Q

What else can cause a similar affect on CNS like ACh?

A

Histamine

59
Q

Ex. of Stimulatory CNS neurotransmitter that’s also involved with pain sensors

A

Glutamate

60
Q

Potent motor inhibitor

A

Dopamine

61
Q

Disease with low dopamine = overactive motor system

A

Parkinson’s Disease

62
Q

5 ex. that increase awareness in CNS

A

Norepi
ACh
Dopamine
Glutamate
Histamine

63
Q

Acid base balance and CNS activity

A

(acidosis) low pH = low CNS activity

(alkalosis) high pH = increase CNS activity but decrease cerebral blood flow! (Co2 increases cerebral blood flow!)

64
Q

Body buffers acids in the blood with bicarb to cause CO2 and water release

A

H+ (+) HCO3- = H2CO3 = CO2 (+) H2O

65
Q

Hypoventilation (acidosis) Albumin in the blood binds to more protons H+ causing…

A

increase free Ca++ reduce CNS activity

66
Q

Hyperventilation (alkalosis). Albumin in the blood binds to more Ca++ causing…

A

decrease Ca++ in ECF > ICF is more + > increase CNS activity.

*Increase neuronal activity; decreased oxygenation to the brain d/t co2 causing increased cerebral blood flow.