NMB part two Flashcards

0
Q

what dose for roc if you want it to work quick?

A

1-1.2 mg/kg

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1
Q

Out of vec, roc, and cis, which has the least cumulative effects?

A

cis

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2
Q

Supposedly, why does roc work faster?

A

“lack of potency”

since it is less potent than vec or cis, we inject 5x the dose / molecules (0.6-1.2 mg/kg) therefore more receptors are blocked faster due to greater number of roc molecules

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3
Q

tell me about a “priming dose”

A

give 10% of the ED95 about 4 minutes before the main dose to speed onset, the priming dose will occupy the spare receptors leaving the main dose to get right to work

not really applicable for roc

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4
Q

vec drug class, concentration, onset, duration

A

monoquaternary aminosteroid
0.1 mg/kg
3-5 minute onset
20-35 minute duration

“pancuronium minus the quaternary methyl group in the A-ring of the steroid nucleus”

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5
Q

vec metabolites and potency

A

3-desacetyl vec, 50% potent

3,17-desacetyl vec, less than 10% potent

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6
Q

since vec undergoes __ metabolism and __ excretion, if your patient doesn’t have those organs it’s probably not the best choice

A

hepatic metabolism

renal excretion

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7
Q

tell me about hypoventilation enhancing vec postop, or why you should always reverse your patients

A

let’s say you don’t reverse the vec, take the patient to the pacu where they get snowed with morphine and hypoventilate, become acidotic and re-paralyze

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8
Q

does vec has cardiovascular effects?

is vec a good choice for infusion?

A

no cv effects

not a good choice for infusion due to large Vd and cumulative effects

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9
Q

Can vec cross the placental barrier?

A

nope

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10
Q

should you dose vec on actual or ideal body weight?

A

ideal

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11
Q

does vec alter intraocular pressure or trigger MH?

A

no and no

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12
Q

what is roc’s drug class, dose, onset, and duration?

A

monoquaternary aminosteroid- basically vec with a hydroxyl group instead of an acetyl group on the A-ring of the steroid nucleus

0.6-1.2 mg/kg
1-2 minutes onset
20-35 minutes duration

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13
Q

what is the only non-depolarizer that serves as an alternative to succs for rapid sequence?

A

roc

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14
Q

roc metabolism and excretion

A

50% excreted unchanged in bile

hepatic metabolism and renal excretion, so duration prolonged with ESRD and lived dsfxn

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15
Q

Cis drug class, dose, onset, duration, concentration

A
benzylisoquinolinium
0.1 mg/kg
onset 3-5 minutes
duration 20-35 min
2mg/ml concentration
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16
Q

Is cis good for constant infusion?

A

yes, rate of recovery not influenced by prolonged infusion

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17
Q

How is cis metabolized? Metabolites?

A

(Cari) Hoffman elimination (77%)

laudanosine and a monoquaternary acrylate

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18
Q

Succs onset, duration, dose

A

30-60 seconds onset
3-5 minutes duration
1-1.5 mg/kg for intubation

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19
Q

is succs degraded by acetylcholinesterase like ACH or by pseudocholinesterase?

A

pseudocholinesterase- slower hydrolysis than ACH by acetylcholinesterase = prolonged depolarization

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20
Q

most succs is hydrolyzed before reaching junction, however because pseudo cholinesterase is not found in the junction, end of succs blockade is due to succs ___ away from the junction

A

diffusion

21
Q

how much can succs raise your K+

A

average 0.5 mEq per liter, due to K+ leakage from sustained ion channel opening

22
Q

succs doses >2mg/kg, repeated doses, or infusions may cause __ of response to succs, leading to a phase 2 block

A

inhibition/desensitization

23
Q

metabolites and potency of metabolites of succs

A

hydrolyzed by plasma cholinesterase to succinylmonocholine then to succinic acid and choline, not active

24
Q

succs dosing for infants and small children?

A

2mg/kg

may result in profound brady or asystole, pretreat with atropine

25
Q

who is succs contraindicated for?

A
major burns
multiple trauma
extensive denervation of skeletal muscle
upper motor neuron injury
= severe hyperK = cardiac arrest
26
Q

how does succs cause bradycardia / arrest?

A

ACH is the primary neurotransmitter of the parasympathetic nervous system, so give a big dose of a drug that mimics ACH (succs) and you will have a huge parasympathetic response (brady or arrest). Pretreat with vagolytic.

27
Q

Let’s say your IV just died and your patient is suddenly having laryngospasm, what do you do?

A

IM succs 3-4 mg/kg, onset at laryngeal muscles will be faster than complete flaccidity which will take 2-3 minutes

28
Q

How many days after a burn covering >30% of your patient’s body will their risk of hyperK be highest?

A

7-10 days

29
Q

Will pretreatment with non-depolarizers prevent hyperK?

A

NO NO NO

30
Q

succs adverse effects

A

dysrhythmias, hyperK, myalgia, myoglobinuria, increased intragastric pressure, increased ICP, increased IOP, sustained skeletal muscle contractions

31
Q

can succs cause MH?

A

yes

32
Q

if your patient is on digoxin and you don’t know their current dig level (they could be dig toxic) should you use succs?

A

best to avoid it

33
Q

Two ways succs can alter your heart rhythm

A
  • vagal stimulation (stimulation of cardiac muscarinic cholinergic receptors by mimic ACH) (most likely to occur with second dose, atropine will NOT prevent this brady)
  • hyperK
34
Q

how to treat a hyperK cardiac arrest

A

IV calcium
bicarb
glucose/insulin
hyperventilate

35
Q

for PEDS, don’t use succs unless it is

A
an emergency intubation
laryngospasm
difficult airway
full stomach
IM use

“when seconds matter”

36
Q

symptoms of histamine release following succs administration includes

A

flushing, hypotension, bronchoconstriction

37
Q

your patient has an eye injury, should you use succs?

A

if you want their vitreous humor to squirt out of their eye

38
Q

If your patient has a full stomach, why should you pretreat them with a non-depolarizer before giving succs?

A

Because succs can increase intragastric pressures greater than 20 cmH2O leading to reflux back through lower esophageal sphincter.

39
Q

Will a phase 1 block exhibit post-tetanic potentiation?

A

NO

slide 87

40
Q

A phase 2 block with succs looks __ like a non-depolarizer block

A

exactly

41
Q

What is more sensitive, single twitch or fade on TOF/tetanus?

A

fade on TOF/tetanus

42
Q

What is the % blockade and clinical significance of no twitches?

A

100% blocked, suitable for intubation

43
Q

What is the % blockade and clinical significance of 1 twitch?

A

90%, suitable for mechanical ventilation

44
Q

What is the % blockade and clinical significance of 2 twitches?

A

80-90% blocked, mech. ventilation some patients, short term relaxation

45
Q

What is the % blockade and clinical significance of three twitches?

A

75-80%, maintenance doses needed.

46
Q

What is the % blockade and clinical significance of 4 twitches?

A

0-75% blocked, suitable for reversal

47
Q

Why should you check TOF after giving succs and before giving non-depolarizers?

A

To make sure you’re not in a phase 2 block, which is indistinguishable from a non-depolarizer block. The treatment is different for the two. Phase 2 block from succs = go sleep it off in the ICU for 12 hours. Non-depolarizer block = give anticholinesterase and anticholinergics.

48
Q

How to reverse a phase 2 block.

A

Do not give anticholinesterases until 20 minutes of spontaneous recovery has passed and a plateau has been reached. Giving it before this time could lead to prolongation of a mis-diagnosed phase 1 block. Try edrophonium first to confirm phase 2, then if reversal occurs use a longer acting like neostigmine.

49
Q

Obese patients have __ plasma cholinesterase activity and therefore may require __ amounts of succs.

A

increased plasma cholinesterase

increased succs

50
Q

Dibucaine number of 80%? 60%? 20%?

A

80% normal
60% reduced quality, 30 minute paralysis
20% greatly reduced quality, prolonged paralysis

dibucaine number is indicative of the QUALITY, not the QUANTITY of plasma cholinesterase.

51
Q

plasma cholinesterase activity is diminished with…

A
genetics
pregnancy
severe liver or kidney dz
malignant tumor
infection
burns
anemia
decompensated heart dz