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Pharmacology of Anesthesia > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

0
Q

What is the main purpose of giving muscle relaxants?

A
  • To relax skeletal muscles
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1
Q

What is the only depolarizing NMBA that we currently have?

A

Succinylcholine

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2
Q

Why do we need to relax skeletal muscles for surgery?

A
  • We don’t want the patient to move, makes surgeon job easier and they will do a better job
  • We could never get complete immobility with the inhalation agents b/c of blood pressure issues, so we get just above the MAC awake point with the inhalation agents and then add NMBA to prevent pt movement
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3
Q

Which type of muscle relaxant will best achieve the effects we desire?

A
  • We typically use a rapid NMBA like SUX for intubation and then if we need muscle relaxant after that we will use a non-depolarizer
  • If we have a longer case sometimes we will give a heavy dose of the non-depolarizer up front knowing that we may get paralysis for a long time after
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4
Q

What are the benefits of muscle relaxation?

A
  1. Improve surgical conditions - allow for CV, Neuro, transplant surgeries
  2. Facilitate endotracheal intubation
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5
Q

What properties/effects are not associated with NMBAs?

A
  • They have no analgesic or anesthetic properties by themselves
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6
Q

How do non-depolarizing NMBAs work?

A
  • Binds to one of the two alpha subunits and prevents 2 ACh molecules from binding to the nAChR to open the channel
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7
Q

What is the ED50 refer to?

A
  • It is the dose at which a muscle relaxant produces a 50% depression of twitch tension in the nAChR.
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8
Q

What are the 3 effects of depolarizing NMBA (SUX)?

A
  1. Desensitizes the nAChR
  2. Inactivates the voltage gated sodium channel and the NMJ
  3. Increases potassium permeability in the surrounding membrane
    - ->These effects prevent an action potential from being generated and nAChR blockade occurs
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9
Q

What is the basic structure of Succinylcholine?

A
  • It is basically 2 ACh molecules connected end to end.
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10
Q

Acetylcholinesterase hydrolyzes ACH to:________ and _________.

A
  1. Choline

2. Acetic acid

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11
Q

Fetal nAChR receptors are resistant to ____________ NMBAs.

A

Non-depolarizing NMBAs

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12
Q

Fetal nAChR are more sensitive to ___________.

A

Succinylcholine

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13
Q

Explain the phenomenon of fade seen with NMJ monitoring.

A
  • Pre-junctional nicotinic receptors have a positive feedback role in making ACh available to the nAChR when needed.
  • Blockade of these receptors appears to explain the phenomenon of fade
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14
Q

Pre-junctional nicotinic receptors are involved in?

A
  • the mobilization of ACh, but not the release process
  • blockade of pre-junctional nicotinic receptors by non-depolarizing agents will affect the availability of ACh when needed fast as in TOF or tetanic contraction monitoring .
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15
Q

Pre-junctional muscarinic receptors are involved in?

A
  • the facilitation and inhibition of the release of ACH through modulation of Ca influx.
  • non-depolarizers do not appear to block the pre-junctional Muscarinic receptors
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16
Q

Neuromuscular blockade develops faster, is less profound, and wears off sooner in …?

A
  • in centrally located muscles like the larynx and the diaphragm than peripheral muscles lie the adductor pollicis.
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17
Q

What is the assumption when using the twitch monitor?

A
  • If the twitch monitor is showing that the muscle relaxant effects have worn off at the adductor pollicis, it is safe to think that they have worn off at the diaphragm and other larger central muscle groups
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18
Q

Fade on the neuromuscular twitch monitor tells us that…?

A
  • a significant portion of the muscle fibers are completely blocked, NOT that the muscle is partially blocked.
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19
Q

You shouldn’t give a reversal agent unless you have at least one or two twitches present because why?

A
  • the duration of the blockade may outlast the duration of the reversal agent
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20
Q

What is the TOF ratio?

A
  • Compares the 4th twitch to the 1st twitch

- Must have 4 responses

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21
Q

A TOF ratio greater than _________ is required for extubation and spontaneous respiration?

A
  • 80-90%
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22
Q

What allows NMBAs to attach to the nicotinic acetylcholine (nAChR) receptor at the NMJ?

A
  • They are all quaternary ammonium compounds

- Positive charges at these sites mimic the quaternary nitrogen atom of ACh and allow then to attach to nAChR.

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23
Q

What does the ED95 refer to?

A
  • the dose causing 95% suppression of neuromuscular response on average
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24
Q

Butrylcholinesterase metabolizes SUX to ________ and _________?

A
  • Succinylmonocholine & choline

- Succinylmonocholine (weaker NMB effects than SUX) is further metabolized to succinic acid and choline

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25
Q

Butrycholinesterase is sucha powerful metabolizer that …?

A
  • Only about 10% of the SUX dose reaches the neuromuscular junction
  • There is virtually no Butrycholinesterase at the NMJ, so the action of SUX is terminated via diffusion away from the NMJ back into circulation where BCE finishes the metabolism.
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26
Q

Where is BCE synthesized?

A
  • Liver
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27
Q

What have been found to decrease BCE activity?

A
  • Liver disease
  • Advanced age
  • Malnutrition
  • Pregnancy
  • Burns
  • Oral contraceptives
  • MAOIs
  • Metoclopramide
  • Anticholinesterases
  • tetrahydroaminacrine
  • Hexafluorenium
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28
Q

People that have an atypical BCE genetic variant will have…?

A
  • a significantly prolonged duration of action from a “normal” dose of SUX
29
Q

What does the Dibucaine number mean?

A
  • The Dibucaine number indicates the percentage of BCE that is inhibited by Dibucaine
  • Dibucaine is very good at inhibiting normal BCE activity
30
Q

A homozygous atypical BCE person will have a dibucaine number of what?

A
  • 20-30: meaning that dibucaine only inhibited about 20-30 percent of the BCE activity
  • Will have a prolonged action of SUX up to 4-8 hours to 24 hours
31
Q

A heterozygous atypical BCE patient will have a dibucaine number of what?

A
  • 50-60: meaning that they will have a 50-100% longer duration of action of SUX (15-30 mins)
32
Q

When administering SUX, sinus bradycardia can develop d/t stimulation of cardiac Muscarinic receptors in the sinus node. What can be given to help prevent the bradycardia?

A
  • It can be pretreated with a small dose of atropine
33
Q

Why can junctional rhythms occurs after administration of SUX?

A
  • Stimulation of Muscarinic receptors in the sinus node can suppress the sinus rhythm and the AV pacemaker takes over momentarily.
34
Q

What causes ventricular dysrhythmias when SUX is administered?

A
  • Circulating catecholamines increase fourfold and potassium increases 33% after a dose of SUX
  • Endotracheal intubation, hypoxia, hypercapnia, and surgery may also increase the likelihood of dysrhythmias
35
Q

What are the side effects of SUX?

A
  1. Cardiac dysrhythmias, sinus bradycardia, junctional
  2. Hyperkalemia
  3. Increased Intra-Ocular Pressure
  4. Increased Intra-gastric Pressure
  5. Increased Intra-cranial Pressure (ICP)
  6. Myalgias
  7. Masseter Spasm
  8. Malignant Hyperthermia (MH)
36
Q

What cause the hyperkalemia side effect of SUX?

A
  • Via depolarization of the NMJ (Na moves into the cells and K moves out of the cells)
  • SUX causes a temporary 0.5 mEq/L increase in K levels
37
Q

What is the treatment for severe rapid onset Hyperkalemia?

A
  1. Hyperventilation
  2. 1-2 grams Calcium Chloride IV
  3. 50 cc D50W IV + 10 units IV insulin (Adults) or 1.0 ml/kg D50W + 0.15 U/kg insulin
  4. Sodium Bicarbonate 1 mEq/kg
38
Q

SUX is contraindicated in …?

A
  • eye injuries that result in an open anterior chamber
39
Q

What is typical IGP?

A

20 cm H2O

40
Q

What IGP induces vomiting by overcoming the gastric sphincter pressure?

A

28 cm H2O

41
Q

This hypermetabolic state is first recognized by an abrupt increase in end-tidal CO2 and late in the syndrome with an elevation in core temperature.

A

Malignant Hyperthermia

42
Q

What are the symptoms of MH?

A
  1. tachycardia
  2. acidosis
  3. hyperkalemia
  4. hypercarbia
  5. dramatic increases in temperature
  6. muscle rigidity
43
Q

What drug treats MH and how does it work?

A
  • Dantrolene - inhibits calcium release from the sarcoplasmic reticulum
44
Q

How is Dantrolene administered?

A
  • Initial dose: 2 mg/kg

- Repeat 2 mg/kg up to 10 mg/kg if required to stop the MH crisis

45
Q

What clinical signs indicate that enough Dantrolene has been given?

A
  • Decrease in temperature

- Decrease in ETCO2

46
Q

What should be verified before giving a dose of Non-depolarizing muscle relaxant?

A
  • Verify that relaxation is desired for the case
47
Q

What is a Phase I block?

A
  • Depolarizing neuromuscular blockade
48
Q

What is a Phase II block?

A
  • is present when the post-junctional membrane has become repolaized but still does not respond normally to ACh (desensitization NM blockade)
49
Q

Excessively large doses, repeated doses, or infusions of SUX can result in …?

A
  • a Phase II block, which acts more like a non-depolarizing blockade of the NMJ
50
Q

Anticholinesterases (Neostigmine, Pyridostigmine)are given to prevent ACh breakdown and reverse non-depolarizing muscle relaxants, but they also inhibit BCE. What is the significance of this?

A
  • BCE is responsible for terminating the action of SUX
  • If Neostigmine has been given at the end of surgery and the pt needs rapid relaxation for whatever reason and SUX is given, its action will be prolonged by 30-60 minutes from baseline.
51
Q

How do Non-depolarizing muscle relaxants work?

A
  • they competitively bind with one of the two alpha subunits on the post-junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh
  • this prevents the opening of the ion channel and prevents depolarization of the membrane
  • since this is competitive antagonism, as long as there is more ACh at the NMJ, there is no contraction of the muscle spindles
52
Q

What are the 2 classes of Non-depolarizing agents and name 1 drug in each?

A
  • Benzylisoquinolinium: Cisatracurium

- Aminosteroid: Rocuronium

53
Q

What is typical intubation dosing?

A
  • 1.5 - 2x the ED95 to ensure that patients who may be resistant to the effects of the particular relaxant develop at least a 90% neuromuscular blockade.
54
Q

What is ideal body weight?

A
  • we give everybody 100 lbs for 5 feet

* If your over 5 feet - women get 5 lbs/inch, men get 7 lbs/inch

55
Q

For BZQ, as potency increases, the speed of onset of action ________.

A
  • Decreases
  • Less potent = fast onset
  • More potent = slow onset
  • As potency increases, side effects decrease
56
Q

BZQs lack vagolytic properties. What does this mean?

A
  • No increase in heart rate is seen with a standard intubating dose
57
Q

What is a side effect seen more with BZQs than aminosteroids?

A
  • BZQs have an increased histamine release compared to other available non-depolarizing muscle relaxants.
  • Histamine can cause bronchospasm in an asthmatic or significant hypotension r/t capillary vasodilation
  • Histamine release is dependent on the total dose given and the speed of injection
58
Q

Cisatracurium

A
  • 4x as potent as Atracurium
  • Does not cause histamine release at typical anesthetic dose ranges
  • Undergoes Hofmann elimination
  • Virtually no CV side effects d/t no histamine release
59
Q

Vecuronium

A
  • Only available for pediatric ICU infusions

- Has no CV side effects

60
Q

Why do we give muscle relaxation for intubation?

A
  1. Prevent laryngospasm because we will be irritating the airways and we are not deeply anesthetized at that point
  2. Balanced medication approach so we don’t give high doses of the induction and opioid agent to decrease hypotensive effects
  3. We are in a hurry- if we waited for the anesthetic to be deep enough we wouldn’t need the muscle relaxant
61
Q

Rocuronium

A
  • eliminated un-metabolized by both the liver and kidneys - renal or liver failure will increase duration of action
  • Mild vagolytic properties with rare increases in heart rate
62
Q

Why don’t we do quantitative monitoring with SUX?

A
  • With SUX either the patient is paralyzed or they are not - no fade with SUX
63
Q

What is the maximum dose of neostigmine?

A
  • 0.06 - 0.08 mg/kg or a total dose of 5 mg
64
Q

What is the maximum dose of Edrophonium?

A
  • 1 - 1.5 mg/kg
65
Q

Neostigmine & Pyridostigmine bind to….?

A
  • they bind to the anionic and esteratic site on AChE
66
Q

What are the benefits of Neostigmine?

A
  • Longer duration than edrophonium

- Better for deep blockade reversal

67
Q

What is the onset and peak for Neostigmine?

A
  • Onset - 5 min

- Peak - 10 min

68
Q

What is the duration of Neostigmine?

A
  • Duration - 60 min
69
Q

What drug is also administered with Neostigmine and why?

A
  • Glycopyrrolate (0.2 mg/mg of Neostigmine), blocks the Muscarinic effects of ACh
70
Q

Suggamedex

A
  • Not yet approved in the US

- Encapsulates the rocuronium molecule to render it unavailable to the nAChR at the NMJ

Pharmacology of Anesthesia (6 decks)

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