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IV Induction Agent/ NMBD > Neuromuscular Blocker General Info > Flashcards

Neuromuscular Blocker General Info Flashcards

1
Q

Types of Neuromuscular Blockers

A
  1. Depolarizing
  2. Non Depolarizing
    * Aminosteroids
    * Benzylisoquinoliniums
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2
Q

Depolarizing NMBDs

A
  1. Succinylcholine
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3
Q

Nondepolarizing NMBDs

A
  1. Aminosteroids
    * Rocuronium
    * Vecuronium
    * Pancuronium
  2. Benzylisoquinoliniums
    * Atracurium
    * Cisatracurium
    * Mivacurium
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4
Q

NMBD Main Site of Action

A

Nicotinic chloinergic receptor at the post junctional motor end plate

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5
Q

Adult Postjunctional Ach Receptor Subunits

A
  • 2 alpha
  • 1 beta
  • 1 delta
  • 1 epsilon

  • only the alpha subunits of the nicotinic cholinergic receptor can bind acetylcholine
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6
Q

Fetal Postjunctional Ach Receptor Subunits

A

2 alpha
1 beta
1 delta
1 gamma

  • only alpha subunits of the nicotinic cholinergic receptor can bind acetylcholine
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7
Q

Dibucaine Number Values

A

Homozygous Typical
2 normal gene copies
dibucaine number 70 - 80
normal response to Sch
Heterozygous Atypical
1 abnormal gene copy
dibucaine number 50 - 60
Sch response prolonged by 50 - 100%
Homozygous Atypical
2 abnormal gene copies
dibucaine number 20 - 30
Sch response prolonged by 4 to 8 hours

Refelcts the QUALITY of pseudocholinesterase, NOT the QUANTITY

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8
Q

What Does Dibucaine Number Mean

A

Uses amide local anesthetic (dibucaine) to test the ability of pseudocholinesterase to be inhibited, indicating if there is a pseudocholinesterase abnormality or genetic variation

  • normal pseduocholinesterase is highly inhibited by dibucaine
  • abnormal pseudocholinesterase is not inhibited by dibucaine

Can indicate if someone will have a prolonged muscle relaxation from succinylcholine use due to a genetic variation in the enzyme that breaks down Sch in the plasma (psuedocholinesterase)

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9
Q

Acetylcholine Receptor Upregulation

A

Results in an increase in the number of extrajunctional acetylcholine receptors

Caused by:
* Chronic decreased stimulation of the NMJ (body craves Ach stimulation and will increase number of receptors)
* Severe burns
* Immobilization
* Infection/ sepsis
* Prolonged use of NMBDs
* CVA
* Trauma

Results in Increased sensitivity to Sch and Decreased sensitivity to non-depolarizers

**High risk of hyperkalemia with the use of Sch in patients with increased number of extrajunctional Ach receptors (potassium moves out of the cell during depolarization)

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10
Q

Acetylcholine Receptor Downregulation

A

Results in a decrease in the number of acetylcholine receptors (in an attempt to compensate for overstimulation of Ach receptors)

Causes
* Chronic neostigmine use (myasthenia gravis patients)

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11
Q

Non-depolarizing NMBDs Causing Histamine Release

A

Rocuronium: Rare
Vecuronium: None
Pancuronium: None
Mivacurium: Yes
Atracurium: Some
Cisatracurium: None

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12
Q

Metabolism of Succinylcholine

A
  • Broken down via hydrolysis in the plasma by the pseudocholinesterase enzyme
  • Only ~ 10% of administered succinylcholine actually reaches the NMJ due to rapid metabolism in the plasma
  • Abnormalities in pseudocholinesterase can lead to prolonged muscle relaxation
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13
Q

Succinylcholine Types of Blocks

A

Phase I Block
* NO fade
* Most common type of block with Sch

Phase II Block
* Fade IS present (similar to non-depolarizing NMB)
* Can result from subsequent or continued dosing of Sch

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14
Q

Hyperkalemia in Succinylcholine Use

A

Serum potassium can increase by about 0.5 meq/ dL in normal healthy patients after administration (due to potassium moving out of the cell during depolarization)

Conditions causing increase in extrajunctional receptors (upregulation) can result in profound/ severe hyperkalemia
* Hemiplegia/ paraplegia
* Muscular dystrophy
* Guillian Barre
* Burns

**Sch use in children (undiagnosed muscular dystrophies?) can be very harmful

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15
Q

MOA of Depolarizing NMBs

A
  • Succinylcholine mimics acetylcholine (2 Ach molecules joined together)
  • When administered, Sch floods the NMJ and binds to post junctional Ach receptors, causing prolonged opening of of the Ach receptor, prolonged flow of Na and Ca into the cell, causing prolonged depolarization of the motor end plate (muscle is unable to repolarize and achieve another action potential)
  • Sch also stimulates prejunctional receptors to release more Ach
  • Fasciculations may be present from depolarization of the muscles
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16
Q

MOA of Non-depolarizing NMBs

A
  • Competitive antagonist at the alpha subunits of the postjunctional acetylcholine receptors- preventing the binding of ach to the postjunctional nicotinic cholinergic receptor at the motor end plate and preventing depolarization of the muscle cell
  • Also competitively antagonize the prejunctional acetylcholine receptors to prevent the release of Ach across the NMJ
17
Q

Hoffmann Elimination

A

Spontaneous, non-enzymatic, non organ dependent chemical breakdown of medications in the plasma
* Drug “falls apart”

Dependent on physiologic temperature and pH
If temp and pH increase - increased metabolism
If temp and pH decrease - decreased metabolism

18
Q

Acetylcholinesterase

A
  • Responsible for the rapid hydrolysis and breakdown of acetylcholine that has been released from presynaptic nerve terminals
  • 50% of Ach is hydrolyzed during its diffusion across the synaptic cleft before reaching its receptor
  • AchAse can catalyze Ach at 4,000 molecules per active site per second
19
Q

Types of Reversal Agents

A

Acetylcholinesterase Inhibitors
* Neostigmine
* Edrophonium
* Pyridostigmine

Selective Relaxant Binding Agent
* Suggamadex

20
Q

Acetylcholinesterase Inhibitors

A
  • Neuromuscular blocker reversal
  • Blocks the breakdown of acetylcholine by acetylcholinesterase, allowing more Ach to be present at the NMJ to compete with the non-depolarizing agents for binding to the alpha subnuits of the nicotinic cholinergic receptors (nondepolarizing agents)
  • Can cause muscarinic side effects (N/V, bradycardia) when administered alone - must be given with antimuscarinic (glycopyrrolate) to prevent the muscarinic effects of Ach inhibitors
21
Q

Ceiling Effect (neostigmine)

A
  • Occurs when all of the acetylcholinesterase has been inhibited
  • Giving more acetylcholinesterase inhibitor will cause no additional effect
  • Max dose (neostigmine) = 5 mg
22
Q

Physostigmine

A
  • Not used for reversal of NMBD
  • Used to treat anticholinergic toxicity
  • Tertiary amine - only anticholinesterase that crosses the BBB
23
Q

Cholinergic Crisis

A

Excessive use/ overdose of cholinesterase inhibitors or exposure to organic pesticides
Excessive amounts of Ach centrally and peripherally
Treatment: Atropine 30 - 70 mcg/ kg, Pralidoxime 15 mcg q 15 minutes, Benzodiazepenes

24
Q

S/S of Cholinergic Crisis

A

Muscarinic Symptoms (SLUDGE)
Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis

Nicotinic Symptoms (MTWTF)
Muscle cramps, Tachycardia, Weakness, Twitching, Fasciculations

Also: Bradycardia, miosis, salivation, abdominal cramping, confusion, seizure, coma

25
Q

Myasthenic Crisis

A

Decrease in acetylcholine activity due to autoreactive antibodies that attack the nicotinic acetylcholine receptors on postsynaptic membranes

26
Q

S/S Myasthenic Crisis

A
  • Normal secretions
  • Tachycardia
  • Normal or dilated pupils
  • Muscle weakness
27
Q

Differentiation Between Myasthenic Crisis and Cholinergic Crisis

A

Tensilon Test
Administer edrophonium (enlon)

Myasthenic Crisis
Muscle strength will improve with enlon

Cholinergic Crisis
Symptoms worsen with cholinergic crisis

28
Q

Clinical Signs of Prolonged Muscular Relaxation

A

Blurry/ double vision
Facial weakness, facial numbness
Generalized weakness
* Indicates ocular and pharyngeal weakness

Most common signs in PACU
Generalized weakness
Difficulty with 5 second eye opening
Difficulty visually tracking or speaking

29
Q

Clinical Signs of Neuromuscular Relaxation Recovery

A

Adequate spontaneous tidal volumes
Negative inspiratory force
5 second head lift
Grip strength
Ability to protrude the tongue

  • These are clinical indicators but unreliable signs of return of muscle strength
30
Q

Causes of Altered Responses to NMBA

A

Acid/ base and electrolyte imbalance
Hyperkalemia: potentiates NMBAs and can decrease anticholinesterase (reversal) effectiveness
Hypermagnesemia: prolongs block (inhibits calcium channels)
Acidosis: interferes with effects of anticholinesterase reversal agents
Hypercarbia: leads to acidosis and interferes with antagonism
Organ dysfunction
Liver and kidney dysfunction
Myasthenia Gravis

31
Q

Neostigmine

General Information

A
  • Anticholinesterase
  • Quaternary ammonium compound - does not cross the BBB
  • Used in deep blocks
  • More effective with moderate blocks but slower
  • Recommended to wait until 4/4 twitches until administering neostigmine
32
Q

Factors that Enhance NMBD Effects

A
  • Inhalational agents (postjunctional receptor effects)
  • Local anesthetics (potentiate depolarizers and nondepolarizers)
  • Antibiotics (streptomycin, neomycin, aminoglycosides - depress the NMJ)
  • Hypercarbia
  • Acidosis
  • Hypothermia
  • Anticonvulsants
  • Magnesium

IV Induction Agent/ NMBD (3 decks)

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