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Neuromuscular Blockers > Neuromuscular > Flashcards

Neuromuscular Flashcards

1
Q

What are the two types of nicotinic receptors in the neuromuscular junction?

A

Nn on the presynaptic

Nm on the postsynaptic (Ligand gated)

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2
Q

What are the five subunits on the Postsynaptic receptor?

A

Two alpha
One beta
One Delta
One Epsilon

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3
Q

What is the process of sending a signal through the neuromuscular junction?

A
  1. Nerve impulse travels down the neuron through the myelinated sheath
  2. Positively charged Na floods into the neuron
  3. Calcium follows, binds, and releases acetylcholine into the synaptic cleft
  4. Acetylcholine diffuses down its concentration gradient, across the synaptic cleft, and two molecules bind to the Alpha subunits.
  5. Once activated Na an Ca enter the cell and K leaves which depolarizes the cell
  6. Depolarization of the myocyte instructs the SR to release Ca into the cytoplasm thus initiating the actin and myosin to contract
  7. ATP is needed to release the actin and myosin
  8. Acetylcholinesterase hydrolyzes Ach immediately into Acetyl Coa and Choline
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4
Q

How many extra junctional receptors are there?

A

Two:
-Alpha7 which has 5 alpha subunits
-A gamma that replaces the epsilon subunit

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5
Q

When are extrajunctional receptors present?

A

-Early in fetal development
-Denervation
-Prolonged immobility

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6
Q

Contradictions of Succ

A

-Upper or lower motor neuron injury
-Spinal cord injury
-Burns
-Cerebrovascular accident
-Tetanus
-Severe sepsis
-Muscular dystrophy
-Skeletal muscle trauma

-Prolonged chemical denervation (Mag, long term NMB infusion, clostridial toxin)

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7
Q

How much and how long will Succ raise serum potassium?

A

0.5-1.0

10-15 minutes

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8
Q

How long should Succ be avoided with a patient that has extrajunctional receptors?

A

24-48 hours

Some texts say up to a year

BURNS up to several years

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9
Q

How is Succ induced hyperkalemia treated?

A

Calcium
Hyperventilation
Sodium Bicarb
Glucose + Insulin

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10
Q

How do extrajunctional receptors affect nondepolarizers?

A

They are resistant so need an increased dose

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11
Q

What does the stimulation of presynaptic Nn receptors do?

A

Moves stockpiled Ach toward the motor endplate

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12
Q

Why do you see no fade with phase 1 blocks?

A

There is always Ach available for release. When a non depolarizing medication is used, it blocks the presynaptic receptor which blocks the stockpiled Ach from moving to the motor endplate

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13
Q

What produces a phase 1 block? Phase 2?

A

Phase 1 - Succ

Phase 2 - Non depolarizers and high dose succ

Dose > 7mg/kg or greater than 30 minutes of a continuous infusion

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14
Q

Best place to monitor for onset of blockade?

A

Orbicularis Oculi (CN 7)

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15
Q

Best place to monitor recovery of blockade?

A

Adductor Pollicis or flexor hallicus

(Ulnar or Posterior tibial nerve)

Don’t rely on the 5th finger for recovery - this overestimates recovery

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16
Q

What is defined as full TOF recovery?

A

> 0.9 at the adductor pollicus

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17
Q

What’s the best qualitative test to assess neuromuscular function ?

A

Tongue blade test

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18
Q

What’s better qualitative test or quantitative?

A

Quantitative but not available

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19
Q

Acceptable clinical end point of TOF and what percent of receptors are occupied?

A

No fade - 70%

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20
Q

What are side effects of Succ?

A

-Bradycardia from stimulation of M2

-Tachycardia from Ach at the sympathetic ganglia (MORE COMMON)

-Potassium release

-5-10 mmHg increase in Intraocular pressure for up to 10 minutes

-Increase in intracranial pressure

-Increase intragastric pressure however the lower esophageal sphincter tone is increased

-Malignant hyperthermia and may increase masseter muscle tone

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21
Q

What metabolizes Ach? Succ?

A

Ach - Type 1 or acetylcholinesterase or true

Succ- Pseudo or type 2 or plasma or false

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22
Q

Facts about pseudocholinesterase?

A

-Produced in the liver and serves as a liver function

-2900 to 7100 units/L in the plasma

-Neuromuscular symptoms begin at 60% and are serious at 20%

-Not located in the CSF

-Located in the smooth muscle, intestines, white matter of brain, heart, pancreas

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23
Q

What diseases reduce pseudocholinesterase ?

A

Liver and Kidney disease
Burns and Cancer
Malnutrition
Old age and Pregnancy
Organophosphate poisoning
Atypical pseudocholinesterase

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24
Q

What drugs reduce pseudocholinesterase?

A

Reglan
Esmolol
Neostigmine
Birth control
MAOI
Nitrogen

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25
Q

What is a Dibucaine test? What is normal?

A

Amide local that inhibits normal plasma cholinesterase and no effect on atypical.

Normal is 80 or above

Does not show quantity JUST QUALITY

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26
Q

Dibucaine chart?

A
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27
Q

What is Myalgia?

A

Muscle soreness from Succ that lasts 24-48 hours

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28
Q

Who is at the highest/lowest risk for Myalgia?

A

Highest - young adults, women, lazy people

Lowest- Children, elderly, pregnant

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29
Q

How can we reduce the risk of myalgia?

A

-Can minimize but not eliminate

-Non depolarizers 3-5 minutes before
-Higher dose of succ
-NSAID
-Lidocaine 1.5mg/kg

-opioids do not

30
Q

What is the black box warning for Succ?

A

In children - risk for sudden cardiac death, secondary to hyperkalemia, related to undiagnosed skeletal myopathy

31
Q

What are common skeletal muscle disorders?

A

Duchenne muscular dystrophy (most common)

Becker
Emery-Dreifuss
Facioscapulohumeral

32
Q

What is dystrophin?

A

Critical structural component of the cytoskeleton of skeletal and cardiac muscle cells

Helps anchor the actin and myosin

33
Q

What happens in the absence of dystrophin ?

A

-Destabilizes the sarcolemma during muscle contraction which increases membrane permeability

-This creates creatine phosphokinase and myoglobin into the systemic circulation

-Also allows calcium to enter into the cell which allows proteases that destroy the cell.

Observed as weakness, conduction abnormalities, cognitive impairment, and cardiomyopathy

34
Q

What is the treatment for hyperkalemia ?

A
35
Q

Neuromuscular chart for neuromuscular blockers

A
36
Q

Do you need higher or lower doses for low potency drugs?

A

The less potent, the more drug you need.

37
Q

What is the ED95?

A

An inverse measure of potency.

Means there is a 95% decrease in twitch height

38
Q

Does a higher or lower ED95 mean more or less potent?

A

Higher ED95 means more potent

39
Q

When comparing the ED95 to intubation, what is the dose required to achieve optimal intubating conditions?

A

2-3 times ED95

40
Q

Class, dose, time to block, and time to return for Mivacurium?

A

-Short acting
-.15mg/kg
-Onset 3.3 minutes
-Return in 16.8 minutes

41
Q

Class, dose, time to block, and time to return for Cisatracurium ?

A

-Intermediate
-.1mg/kg
-5.2 minute onset
-45 minute return

42
Q

Class, dose, time to block, and time to return for Vecuronium?

A

-Intermediate
-.1mg/kg
-Onset 2.4 minutes
-45 minute return

43
Q

Class, dose, time to block, and time to return for Atracurium?

A

-Intermediate
-.5mg/kg
-Onset 3.2 minutes
-45 minute return

44
Q

Class, dose, time to block, and time to return for Rocuronium?

A

-Intermediate
-.6mg/kg
-Onset 1.7 minutes
-35 minute return

45
Q

Class, dose, time to block, and time to return for Pancuronium?

A

-Long
-.08mg/kg
-Onset 2.9 minutes
-85 minute return

46
Q

Potency from lowest to highest for Non Depolarizers

A

-Roc
-Succ
-Atracurium
-Panc
-Miv
-Vec
-Cis

47
Q

How are benzylisoquinolinium compounds are metabolized?

A

Spontaneous degradation in the plasma. NON dependent on hepatic or renal function for metabolization or elimination

48
Q

How is atracurium broken down? active metabolite?

A

33% Hoffman
66% Non-specific plasma esterases

Same esterases as esmolol and remi, pseudocholinesterase deficiency does not affect.

-Metabolite is laudanosine

49
Q

How is cisatracurium broken down? Metabolite?

A

77% Hoffman

-Metabolite is Laudanosine

50
Q

How is mivacurium broken down? Metabolite?

A

Metabolized by pseudocholinesterase

No metabolite

51
Q

What is Laudanosine?

A

Active metabolite of cisatracurium and atracurium

Can produce seizure with prolonged infusions

No muscle relaxant properties

52
Q

What is Hoffman elimination? What is it dependent on?

A

-Base catalyzed reaction dependent on pH and temperature

Faster with Alkalosis and hyperthermia

Slower with Acidosis and hypothermia

53
Q

How are aminosteroids metabolized?

A

Liver, Renal, and Biliary

54
Q

How is Roc metabolized and eliminated? Metabolite?

A

It is not metabolized or have any metabolites.

70% Liver
25% Kidney

55
Q

How is Vec metabolized and eliminated? Metabolite?

A

Metabolized 30% by the liver into 3-OH Vec

Excreted 50% liver and 50% Kidney

56
Q

How is Panc metabolized and eliminated? Metabolite?

A

Metabolized 20% by the liver into 3-OH Panc

Excreted 15% liver and 85% Kidney

57
Q

Factors that potentiate NM blockade?

A
58
Q

Which NMB’s release Histamine?

A

Succ, Atra and Mivacurium

59
Q

Which NMB has the greatest affect on the heart?

A

Panc - inhibits M2 so increases HR and stimulates the release catecholamines.

DO NOT GIVE WITH HYPERTROPHIC CARDIOMYOPATHY

60
Q

What NMB may lower the HR?

A

Vec and atracurium

61
Q

What affect does Succ have on the heart?

A

Can cause tachy and bradycardia (Equal out)

62
Q

What two NMB are most likely to cause anaphylaxis?

A
  1. Succ
  2. Roc

(varying literature)

63
Q

Which conditions require a dose reduction for roc?

A

Duchenne Muscular Dystrophy
MS

64
Q

Which NMB do not produce an active metabolite?

A

Roc

Mivacurium

65
Q

What’s the first treatment after a child experiences cardiovascular collapse from succ?

A

Calcium to treat the hyperkalemia

66
Q

What is the most sensitive clinical end point of recovery from a NMB ?

A

Thumb and Toe

67
Q

What is the most sensitive clinical end point from NMB recovery?

A

Inspiratory force >40cm H2O suggests that no more than 60% blockade

68
Q

Which ion does not pass through the nicotinic receptor?

A

Chloride

69
Q

Which enzymes metabolize succ and mivacurium?

A

Type 2
False
Butyrylcholenesterase
Plasma
Pseudo

70
Q

Order from most to least ;
inhaled anesthetics potentiation of nondepolarizing NMB

A

Des
Sevo
Iso
N2O
Prop

71
Q

What is the best lab level for anaphylaxis to NMB?

A

Tryptase and histamine

Neuromuscular Blockers (2 decks)

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