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Pharmacology Exam 3 > NMBD Intro > Flashcards

NMBD Intro Flashcards

1
Q

dTc and SCh (Anectine)

A
  • 1940 - 1960
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2
Q

Pancuronium (Pavulon)

A
  • 1960
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3
Q

Atracurium (tracrium) and Vecuronium (Norcuron)

A
  • 1980
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4
Q

Rocuronium (Zemuron)

A
  • 1994
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5
Q

Cisatracurium (Nimbex) and Mivacurium (Mivacron)

A
  • 1995 and 1997
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6
Q

Rapacurium (Raplon)

A
  • 2001
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7
Q

Define the Effect of NMBD

A
  • Interrupt transmission of nerve impulses at neuromuscular junction (NMJ)
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8
Q

Actions of a Depolarizing NMB

A
  • Mimics the action of acetylcholine
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9
Q

Name the only Depolarizing Paralytic on market.

A

Succinycholine

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10
Q

Actions of Non-depolarizoing NMB

A
  • Interferes with the actions of acetylcholine
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11
Q

Name (3) ways NMB minimize incidences of tissue trauma

A
  1. Decreased airway trauma
  2. Facilitates surgical exposure
  3. Minimizes injury from patient movement
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12
Q

Name the #1 Purpose of NMB

A
  • Minimize incidence of tissue trauma
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13
Q

Name (3) common airway trauma symptoms

A
  1. airway edema
  2. hoarsness
  3. vocal cord injury
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14
Q

What are the (5) Clinical Classifications of NMB

A
  1. Depolarizing
  2. Non-depolarizing
  3. Long-Acting
  4. Intermediate Acting
  5. Short Acting
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15
Q

Name (1) Depolarizing NMB

A
  • Succinylcholine ( Anectine)
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16
Q

Name () Non- Depolarizing NMB

A
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17
Q

Name (3) Long-Acting NMB

A
  1. Pancuronium (Pavulan)
  2. Doxacurium
  3. Pipecuronium
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18
Q

Name (4) Intermediate Acting NMB

A
  1. Atracurium (Tracrium)
  2. Vecuronium (Norcuraon)
  3. Rocuronium (Zemuron)
  4. Cisatracurium (Nimbex)
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19
Q

Name (1) Short Acting NMB

A
  1. Mivacurium (Mivacron)
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20
Q

Describe the potency of neuromuscular blocking drug (NMBD)

A
  • ED95
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21
Q

Equal Potency of NMB

A
  • Dose necessary to produce 95% suppression of single twitch
  • In the presense of nitrous/barbituate/opioid anesthesia
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22
Q

ED95: Adductor pollicis muscle

A
  • Single twitch at 1 Hz
  • Ulnar nerve stimulated
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23
Q

Order of the NMB depends on (4) Factors

A
  1. # of presynaptic Ach containing vesicles released
  2. # of postsynaptic Ach receptors
  3. Blood flow to area
  4. Drug potency
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24
Q

________, ___________ moving muscles block faster than __________ muscles

A
  • Small
  • rapidly
  • large
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25
Q

Smaller muscles blocks are more _____________, but less ______________.

A
  • rapid
  • intense
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26
Q
A
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27
Q

Name the (2) preferred monitoring sites

A
  • Orbicularis oculi
  • adductor pollicis
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28
Q

Monitoring site: Orbicularis Oculi

A
  • Mores closely reflects diaphragm and laryngeal muscle blockade
  • Underestimate residual paralysis
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29
Q

Monitor Site: Adductor pollicis

A
  • Poor indicator of laryngeal relaxation
  • Gold Standard for recovery
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30
Q

Ulnar Nerve Stimulation

A
  • Place negative electrode (black) on wrist in line with the smallest 1-2 cm below skin crease
  • postive electrode (red) 2-3 cms proximal to the negative electrode
  • Response: Adductor pollicis muscle – thumb adduction
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31
Q

TOF: Single Twitch

A
  • Usually 1 Hz/second decreasing to 0.1 Hz q 10 seconds
  • Continously
  • Onset of block = fade with each stimulus
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32
Q

Double Burst

A
  • 2-3 short twitches following 2-3 short twitches
  • Use 50 Hz (supramaximal current)
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33
Q

Why was the Double Burst developed?

A

Developed to improve detection of residual block
* Fade in 2nd response vs 1st
* Qualitatively better than TO4

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34
Q

Train of Four (TOF)

A
  • 4 stimuli at 2 Hz in 1/2 second
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35
Q

When should TOF be used?

A
  • Prior to NMBD: 4th twitch = 1st twitch …. TOFR 1
  • After administration and return of 4 twitches
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36
Q

Amplitude of 4th twitch to 1st twitch

A
  • If amplitude of 4th twitch 50% of 1st…. TOFR 0.5
  • Experienced anesthetists’ unable to detect fade TOFR > 0.4
  • May choose not administer reversal….poor choice
  • Significant residual TOFR 0.7-0.9
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37
Q

Describe Tetanic Stimulation

A
  • Very rapid. 50 Hz for 5 seconds
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38
Q

Name (1) cause of Tentanic Stimulation: Sustained Muscle Response

A
  • Depolarizing blocks
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39
Q

Name (1) cause of Tetanic Stimulation: Non-Sustained Response

A
  • non-depolarizing block
  • Phase 2 block w. Succs
  • Fade related to:
    (1) presynaptic deplation of Ach or inhibition of release
    (2) Frequency and length of stimulation
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40
Q

Define a Post-Tetanic Stimulation

A
  • single twitch 3 seconds after tetanic stimulation
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41
Q

Why does post-tetanic stimulation occur?

A
  • accumulation of calcium during ‘tetany”
  • Excess calcium stimulates Ach release
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42
Q

What does it mean if their is no Post- Stimulation response?

A
  • Intense Block
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43
Q

Effects of NMBD

A
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44
Q

Bedside evaluation of criteria to extubate

A
  • Head lift
  • Negative PIP 25 - 30 cmH20
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45
Q

Baillard, Clec’h, Catineua et al. Br J Anaesth….. 2 studies

A
  • No anticholinesterace drugs used
  • No nerve stimulators
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46
Q

Baillard, Clec’h, Catineua et al. Br J Anaesth…..: 1st study

A
  • 1st study: 568 patients over 3 months
  • 1/3 of patients extubated in OR
  • Postop blockade 42%
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47
Q

Baillard, Clec’h, Catineua et al. Br J Anaesth….. : 2nd Study

A
  • 2nd study: Use of nerve stimulators increased from 2%-60%
  • Neostigmine use increased 6%-42%
  • Postop blockade decreased to < 4%
48
Q

Anatomy of a NMJ: Synaptic Cleft

A
  • Synaptic cleft 20-50 nm wide with fluid
  • Contain collagen, acetylcholinesterase
49
Q

Synaptic Cleft: Vesicles

A
  • 5,000-10,000 vesicles release ACh
  • Ready pool (increased demand)
  • Calcium dependent
50
Q

Synaptic Cleft: Acetylcholinesterase

A
  1. hydrolysis of Ach
  2. to acetic acid and choline
51
Q

Anatomy of a NMJ: Post synaptic

A

Membrane with multiple folds
* -90 mv resting membrane potential
* Maintained by sodium/potassium
* nAChRs directly opposite

52
Q
A
  • N-ACHR
53
Q

NACHR Subunit: Pentameric Unit

A

Penameric unit
* 5 sub pores
* Transmembrane

54
Q

What happens to a NACHR subunit if ACH binds?

A
  • Conformational change
  • Pores open, sodium/calcium/potassium flow
55
Q

What happends to a NACHR subunit when NMBD binds?

A
  • No conformational change
  • No ion flow
  • Probability of binding d/t concentration of NMBD vs Ach
  • Sch only requires binding at 1 alpha subunit —- can leave 1 receptor and attach to other nACHRs ill hydrolyzed …..fasciculations
56
Q

Name the only depolarizing NMBD in clinical practice

A
  • Succinylcholine
57
Q

Name (2) unique characteristics of Succinulcholine

A
  1. Intense, rapid paralysis
  2. Offset of effects prior to hypoxia
58
Q

What is the main use of Succinylcholine

A
  • Useful for tracheal intubation
  • Rapid sequence induction
59
Q

Name (1) con of succinylcholine

A
  • Releases histamine
60
Q

Name the dose, onset and duration of Succinycholine

A
  • I mg/kg IV
  • onset: 30 - 60 seconds
  • Duration: 3 - 5 minutes
61
Q

MOA of Succinylcholine

A
  • Attaches to 1 or both alpha subunits
  • mimics effects of ACh
62
Q

Succinycholine: Hydrolysis is slower than Ach

A
  • Sustained opening of receptor ion channels
  • Leakage of potassium ions = 0.5 mEq/liter serum increases
63
Q

Succinylcholine Depolarization is called

A
  • Phase 1 block
64
Q

Succinylcholine: Phase 1 Block Characteristics

A
  • ⬇️ contraction to single twitch stimulation
  • ⬇️ amplitude to continuous stimulation
  • TOF ratio > 0.7
  • Absence of post-tetanic facilitation
  • Skeletal muscle fasciculations
65
Q

Phase II Block

A
  • Responses typical of non-depolarizing NMBD
  • Can be antagonized by anticholinesterase drug
66
Q

Phase II Block: Abrupt transition

A
  • SCh dose 2-4 mg/kg
  • Lack of/poorly functioning pseudocholinesterase
  • Relative “overdose”….desensitization
67
Q

Phase II Block: Duration of Action

A

Normal: 3 - 5 minutes

68
Q

Phase II Block: Hydrolyzed by butyrylcholinesterase (plasma cholinesterase)

A
  • Synthesized in liver
  • Terminated by diffusion out of NMJ into plasma
  • Succinylmonocholine (less potent) and choline
69
Q

Phase II Block: Pseudocholinesterase activity

A
  • Decreased hepatic production (⬇️ 75% before apparent)
  • Drug-induced decreases (Neostigmine, Reglan, chemo, insectides)
  • Genetically atypical
  • Chronic diseases (renal): ↓ activity
  • Pregnancy (high estrogen levels): ↓activity
  • Obese: ↑ activity
70
Q

Characteristics of Dibucaine

A
  • Amide local anesthetic
  • Inhibits activity of normal variant butyrylcholinesterase (pseudocholinesterase)
  • % inhibition = dibucaine number
71
Q

Dibucaine Numbers

A
  • Reflects quality not quantity of enzyme
  • 20: SCh 1mg/kg lasts 3 hours
72
Q

Side Effects of SCH

A
  • Cardiac dysrhythmias
  • Hyperkalemia
  • Myalgia
  • Myoglobinuria
  • ⬆️ intragastric pressure
  • ⬆️ intraocular pressure
  • ⬆️ intracranial pressure
  • Masseter spasm
73
Q

What can you do to prevent side effects of SCH?

A
  • Pretreatment with non-depolarizing NMBD
74
Q

Name (6) effects of Defasiculating d/t Patient symptoms

A
  • Loss of visual focus
  • Mandibular muscle weakness
  • Ptosis
  • Diplopia
  • Dysphagia
  • Increased hearing acuity
75
Q

name the (3) Cardiac Dysrhythmias w/ SCH

A
  1. SB
  2. JR
  3. Sinus Arrest
76
Q

Actions of cardiac muscarinic, cholinergic receptors w/ SCH

A
  • Mimics action of ACh
  • Most likely on 2nd dose, 5 minutes post 1st
  • Due to metabolites: succinylmonocholine and choline???
77
Q

SCH: Actions at ANS ganglia

A
  • ⬆️ Heart rate and blood pressure
  • Mimics action of Ach
  • Usually occurs with large doses
78
Q

Cause of Hyperkalemia with SCH

A
  • Patient’s with extrajunctional sites (more ion channels)
79
Q

Name (5) conditions that can cause hyperkalemia in SCH use:

A
  • Unrecognized muscular dystrophy
    Duchenne’s: Diagnoseis 2-6 y/o
  • Unhealed 3rd degree burns
  • Denervation of skeletal muscles (atrophy): 96 hrs - 6 months
  • Skeletal Muscles trauma
  • Upper motor neuron lesions
80
Q

Can you alter Hyperkalemia with pretreatment with non-depolarizers

A

No

81
Q

Myalgia

A
  • Young adults
  • Neck, back, abdomen
  • Confused with pharyngitis d/t intubation?
82
Q

Myoglobinuria

A

Damage to skeletal muscles
* Especially pediatrics

  • Usually found later to have MH or muscular dystrophy
83
Q

Intragastric pressure and LES pressure with Succinylcholine

A
  • Inconsistent increases r/t
    1) intensity of fasciculations
    2) direct increase in vagal tone
84
Q

Is Intragastric pressure and LES pressure seen in children?

A
  • Not seen in children d/t minimal fasciculations
85
Q

Succinycholine: Intragastric pressure and LES pressure: Passage of gastric fluid into esophagus and pharynx

A
  • Aspiration?
  • Some texts refute this concern stating gastric pressure doesn’t exceed LES pressure
86
Q

Succinylcholine Intraocular pressure

A
  • Maximum increase 2-4 minutes after administration
  • Lasts 5-10 minutes
87
Q

Succinylcholine Intraocular Pressure: MOA

A

MOA unknown
* Contraction of EOM and globe distortion
* Resistance to outflow of aqueous humor and dilation of vessels

88
Q

When is Succinylcholine counterindicated d/t intraoccular pressure?

A
  • Open anterior chamber injury
89
Q

Succinycholine: Intraocular Pressure controversial

A
  • Efficacy of defasciculation controversial
90
Q

Succinycholine: Intracranial Pressure increase with patients with……

A
  • intracranial tumors or CHI
  • Not consistently observed in studies
91
Q

Succinycholine: Intracranial Pressure Attenuated

A
  • Attenuated by hyperventilation prior to SCh
  • RSI not ventilated
92
Q

Succ: Sustained Skeletal Muscle Contraction

A
  • Incomplete jaw relaxation/masseter muscle spasm
  • Inadequate dosage given? (children)
  • Early indicator of Malignant Hyperthermia?
93
Q

Malignant Hyperthermia

A

Hereditary rhabdomyolysis associated with anesthetics

  • Muscle destruction
  • Hyperkalemia
  • Acidosis
  • Dysrhythmia
  • Renal failure
  • DIC
94
Q

Malignant Hyperthermia: Triggers

A
  • ALL volatile anesthetics
  • Succinycholine
95
Q

Malignant Hyperthermia: Causes

A
  • Mutations in skeletal muscle calcium release
  • Ryanodine receptor (RyR1)
    (1) 50-70% of MH patients
    (2)Native Americans
96
Q

Maligant Hyperthermia: Ryanodine Receptors Mutations

A

*50-70% of MH patients
*Native Americans

97
Q

What is the Maligant Hyperthermia Test?

A
  • Skeletal muscle caffeine contracture testing
  • Muscle biopsy
98
Q

Symptoms of Malignant Hyperthermia

A
  • Acute increased skeletal muscle metabolism
  • Increased oxygen consumption
  • Lactate formation
  • Heat production
  • Rhabdomyolysis
99
Q

Signs of Maligant Hyperthermia

A
  • ↑ ETCO2
  • ↑ temp 1 degree C/5 minutes
  • Arrhythmias
  • Skeletal muscle rigidity
100
Q

Treatment of Malignant Hyperthermia: ABCD (A)

A
  • Agents- stop all triggering agents
  • Administer non-triggering anesthetics
  • Ask for help
  • Ask for MH Cart
101
Q

Treatment of Malignant Hyperthermia: ABCD (B)

A
  • Breathing - hyperventilation with 100% oxygen
102
Q

Treatment of Malignant Hyperthermia: ABCD (C)

A
  • Cooling procedures is patient is > 102.2
103
Q

Treatment of Malignant Hyperthermia: ABCD (D)

A
  • Dantrolene - continous rapid IV push
104
Q

How much does dantrolene decrease mortality with MH?

A
  • 80% –> 10%
105
Q

Dantrolene Dose

A
  • 2mg/kg IV
  • Respeat doses until symptoms subside or 10 mg/kg IV
106
Q

Dantrolene MOA

A
  • Inhibits calcium release into SR
  • By affecting the ryanodine receptors
107
Q

Dantrolene Metabolism

A
  • 5-hydroxydantrolene
  • Muscle relaxant properties
  • 50% c/o weakness…grip strength
  • Verapamil, Cardizem
  • Cardiovascular collapse
108
Q

Most Common Side Effects with Dantrolene

A
  • Weakness
  • Phlebitis
  • Respiratory failure
  • GI upset
109
Q

Less Common side effects of Dantrolene

A
  • Confusion
  • Dizziness
  • Drowsiness
110
Q

NM Diseases: Myasthenia Gravis

A

Autoimmune Disease
* Antibodies against Ach receptor
* ↓ Ach receptors

111
Q

Myasthenia Gravis: S/E

A

Increasing weakness/fatique
* Diplopia
* Ptosis
* Extremity and respiratory muscle weakness
* Tx: Cholinesterase Inhibitors

112
Q

Myasthenia Gravis and Succinycholine

A
  • Resistant to Sch… 1.5-2.0 mg/kg
  • fewer receptors….ED95 2.5 times higher
113
Q

NM Disease: Lambert- Eton

A

Autoimmune diease
* Small-cell lung cancer
* Antibodies against calcium channels
* Decreases release of Ach pre-junctionally

114
Q

Lambert-Eton: Increases sensitivity

A
  • Depolarizers
  • Non-depolarizers
115
Q

NMB with the Chemical Classification of Amiosteroid

A
  • Pancuronium
  • Doxacurium
  • Pipecuronium
  • Vecuronium
  • Rocuronium
116
Q

NMB with Chemical Classification of Benzylisoquinoline

A
  • Atracuronium
  • Cisatracurum
  • Mivacurium

Pharmacology Exam 3 (4 decks)

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