Pharmacology > Nondepolarizing > Flashcards

Nondepolarizing Flashcards

(62 cards)

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1
Q

What is the intubating dose, onset of action, and duration of action for all of the intermediate ND blockers?

A

0.1 mg/kg
3-5 min
20-35 min

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2
Q

What is the RSI dose for roc? What should we know about this

A

1.2 mg/kg
Going to start working in 1-2 minutes but will last longer

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3
Q

What determines which non-depolarizing drug we will pick?

A

Onset
DOA
Offset
Metabolism (may not want to give liver dz pt a drug metabolized by liver)

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4
Q

NDMB are competitive or noncompetitive for the alpha subunits?

A

competitive (they can be booted off)!

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5
Q

Do non-depolarizing drugs cause a conformational change?

A

No! Only Sch does

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6
Q

What is the TOF ratio usually with NDMB?

A

Less than 0.7 (big change from the last one to the first one)

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7
Q

What does it mean that non-depolarizing blockers can potentiate other non-depolarizing drugs?

A

If you give Roc and then give Vec, the effect of Vec may be greater. Stick with the same one!

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8
Q

What is the antagonist to non-depolarizing drugs?

A

Acetylcholinesterase inhibitors

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9
Q

Fade suggests that ____

A

some fibers are blocked and others are not

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10
Q

What are the 3 adverse effects of non-depolarizing?

A

CV effects
critical illness myopathy
altered responses

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11
Q

CV effects with non-depolarizing are due to histamine release which will _

A

Increase HR

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12
Q

Are the CV effects of non-depolarizing drugs usually clinically significant?

A

No

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13
Q

What is the autonomic margin of safety with non-depolarizing drugs?

A

The area between the ED95 dose and the dose that causes circulatory effects. (sort of like a therapeutic index)

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14
Q

Which one of the drugs has an ED95 that is the autonomic margin of safety?

A

panceronium

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15
Q

CV effects can be offset by giving __

A

Benadryl or opioids

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16
Q

What is critical illness myopathy and what causes it? How can we adjust plan?

A

residual weakness (weeks to months after getting large doses of non depolarizing drug).

Possibly due to active metabolite sticking around longer or decreased Cl of drug.

Increase opioid/sedative use and decrease the non depolarizing drug

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17
Q

A dose dependent enhancement of non depolarizing drug can be seen if given concurrently with ___

A

Inhaled anesthetics

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18
Q

Which inhaled anesthetic may lead to enhancement of non depolarizing drugs? Next? Next?

A

Des, Sevo, Iso

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19
Q

What are the 4 kinds of drugs that enhance the blockade of nondepolarizing drugs?

A

Diuretics, local anesthetics, corticosteroids, Reglan

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20
Q

What does Magnesium do when you add it to the regimen when paralyzing a pt? What are the 2 ways that happens?

A

Enhances the block
Decreases the presynaptic release of Ach
Decrease the sensitivity of the Ach-R on the post synaptic membrane

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21
Q

What do drugs that increase SNS do to non-depolarizing drugs?

A

The SNS drug will lead to an increase in CO (such as Ephedrine) leading to the drug working SOONER!

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22
Q

What would an SNS blocking drug such as Esmolol do the effects of non depolarizing drug?

A

Decrease HR, BP, CO, slower delivery of the drug to the site of action. Delay the onset

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23
Q

Which 2 drugs are to some degree metabolized by the liver?

A

Veceronium and Pacneroinum

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24
Q

If the pt is cold, what happens to their CYP450’s?

A

There will be a decrease in the # of enzymes to metabolize the drug, it will end up sticking around for double the time

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25
DECREASED TEMP LEADS TO __ ACTIVITY OF CYP450'S
Decreased
26
Temperature affects CYP450's, Hoffman elimination and _
Ester hydrolysis
27
Atra and Cis are dependent on being metabolized via Hoffman and Ester hydrolysis, are those temp dependent?
Yes
28
What effects do hypokalemia have on depolarizing and nondepolarizing drugs?
D: Increased resistance ND: Increased sensitivity to ND
29
What effects do hyperkalemia have on depolarizing and nondepolarizing drugs?
D: Increased effects ND: Resistance
30
If the pt has been burned. Usually > 30% BSA and starting at day 10 up to day 30, there is ____ to the use of NDMB, why?
Resistance Probably leads to decreased affinity of the nAch-R
31
If the pt does have an extensive brun, which ND MB may you want to use? Why?
Roc at the doubled dose (1.2 mg/kg)
32
If the pt has hemiperalisis, what response does the paretic arm have to the NDMB? Why?
It will have resisntance to the drug compared to the "normal" side Proliferation of extrajunctinal nAch-R. (more available!)
33
If the pt has hemiperalisis, what response does the normal arm have to the NDMB?
Resistance compared to pt's who have had no stroke at all
34
Which neuromuscular blocking drug has the highest potential for an allergy? Which is the least likely?
Sch Nimbex
35
If the pt is allergic to one of the NDMB does that mean they have a greater chance for allergy to another?
Yes! Cross sensitivity in the quaternary ammonium group
36
The pt can have a cross sensitivity of soap or perfume that is a quaternary ammonium to NDMB. This is more common in M or F?
F
37
Women need ___ % less Roc
30
38
Women need ___% less Vec
22
39
What is the intubating dose, onset, and DOA for Pancuronium?
0.1 mg/kg 3-5 min 60-90 min
40
How is Pan metabolized?
80% is eliminated unchanged into the urine and there is a small amount of liver metabolism.
41
What causes the sympathomimetic response in Pan?
Also blocks muscarinic-R (at SA node) --> increased HR, therefore increase BP and CO
42
Panceronium not only causes vagal blockade but also cause SNS activation leading to _ and _
Release of NE Blocking NE reuptake
43
Does panceronium affect SVR and inotropy?
No
44
Do the intermediate NDMB have CV effects like Panceronium?
No- minimal CV effects
45
What drugs can antagonize intermediate blocking drugs?
Acetylcholinesterase inhibitors
46
How is Vec metabolized? What is the active metabolite that is 1/2 as potent?
By the liver. 3-desacetylvecuronium
47
How much of Vec is excreted into the urine unchanged?
30% so 70% is metabolized by the liver
48
Since Vec has an active metabolite what would you think would be true for the cumulative effects?
Repeated doses can lead to cumulative effects.
49
Is Vec safe for vabies? (babies)
Yes.
50
Vec can be affected by acid-base changes. (explain before and after)
If the change happens before administering the drug: no effect If the change happens after administering the drug: prolongs blockade
51
Which of the non-depolarizing drugs do we worry about most to cause CV effects?
Pan
52
How is Roc metabolized? When would the drug hang around longer?
Excreted unchanged in the bile If the pt had liver dz, if the pt were old with a high VD due to less plasma proteins
53
What is behind the name of Cisatracurium?
It is the cis-isomer
54
Is Cisatracurim affected by the length of time that the gtt has been running?
No, probably why it is so commonly used as a gtt in the ICU
55
How is Cisatracurium metabolized?
Hoffman elimination (which is temp and pH dependent)
56
All of the NDMB should be dosed based off of: ideal or actual BW?
Ideal. If dosed on actual --> could lead to OD
57
What is the intubating dose of Mivacurium?
0.15 mg/kg
58
What is the onset of Mivacurium?
2-3 minutes
59
What is the duration of action of mivacurium?
12-20 min (not much time to get anything done)
60
Mivacurium has 3 stereoisomers. Which 2 actually have NM blocking ability?
Both except for Cis-cis So, cis-trans and trans-trans
61
How is Mivacurium metabolized?
By plasma cholinesterase!
62
Is Mivacurium currently on the market?
No

Pharmacology (6 decks)

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