NMBD intro and sux - test 3 Flashcards
1
Q
What is the main effect of NMBDs?
A
Interrupt transmission of nerve impulses at neuromuscular junction
2
Q
Action of depolarizing NMBD
A
Mimics the action of acetylcholine
3
Q
Action of non-depolarizing NMBD
A
Interferes with the action of acetylcholine
4
Q
What is the purpose of NMBD for anesthesia?
A
- Decrease airway trauma
- airway edema
- hoarseness
- vocal cord injury - Facilitates surgical exposure
- Minimizes injury from patient movement
5
Q
Classifications of NMBDs:
A
6
Q
Classification of succinylcholine:
A
Depolarizing
7
Q
List the long acting NMBDs:
A
- Pancuronium
- Doxacurium
- Pipecuronium
8
Q
What is the chemical classification of pancuronium?
A
Aminosteroid
9
Q
What is the classification of Doxacurium?
A
Aminosteroid
10
Q
What is the classification of Pipecuronium?
A
Aminosteroid
11
Q
List the intermediate acting NMBDs:
A
- Atracurium
- Vecuronium
- Rocuronium
- Cisatracurium
12
Q
What is the chemical classification of Atracurium?
A
Benzylisoquinoline
13
Q
What is the chemical classification of Vecuronium?
A
Aminosteroid
14
Q
What is the chemical classification of Rocuronium?
A
Aminosteroid
15
Q
What is the chemical classification of Cisatracurium?
A
Benzylisoquinoline
16
Q
What is the clincal and chemical classification of Mivacurium?
A
Short acting; Benzylisoquinoline
17
Q
What is ED95?
A
Potency of NMBD. Dose that is necessary to produce 95% suppression of a single twitch in the presence of nitrous/barbiturate/opioids
18
Q
Which nerve is stimulated so that the adductor pollicis muscle will produce 1 twitch at 1Hz
A
Ulnar nerve
19
Q
What is the order of block dependent on?
A
- # of presynaptic Ach containing vesicles released
- # of postsynaptic Ach receptors
- Blood flow to the area
- Drug potency
20
Q
Which muscles block faster, small or large?
A
Small, rapidly moving muscles block faster than large muscles
- onset more rapid, less intense
21
Q
Larynx effects vs thumb effects:
A
The larynx wasn’t 100% paralyzed before it started wearing off - started wearing off faster than the peripheral
*this is why we watch the larynx for induction but adductor for emergence
22
Q
What is the preferred central monitoring location for NMBDs?
A
Orbicularis Oculi
- More closely reflects diaphragm and laryngeal muscle blockade
- Underestimate residual paralysis
23
Q
What is the preferred peripheral monitoring location for NMBDs?
A
Adductor pollicis
- Poor indicator of laryngeal relaxation
- Gold standard for recovery
24
Q
Ulnar nerve NMBD monitoring:
A
25
Which muscle is the gold standard to check a twitch on for recovery?
Adductor pollicis
26
A single twitch nerve stimulator starts at _____ Hz/second decreasing to ______ Hz/10 secs.
1 Hz/sec to 0.1 Hz/10 secs
27
With an onset of a block a single twitch will ______ with each stimulus.
Fade
28
What is double burst stimulator?
What Hz?
- 2-3 short twitches followed by 2-3 short twitches
- Use 50 Hz
29
Why was the double burst stimulator developed?
To improve detection of residual block
30
Double twitch stimulator will ____ in 2nd response vs 1st
Fade; qualitatively better than the TOF
31
Train of Four is ________ stimuli at _______ Hz with ______ seconds between each burst.
4 stimuli at 2 Hz w/ 0.5 seconds between each burst
32
TOF reflects events at ____ membrane
presynaptic
33
Prior to NMBD what will be your twitches on the TOF?
What will be the TOF ratio (Twitch 4 : Twitch 1)?
4/4 twitches
Ratio 1
34
What happens to the twitches after administration and return of 4 twitches?
- Amplitude of 4th twitch to 1st twitch
35
What is the TOF ratio if the amplitude of the 4th twitch is 50% of 1st?
TOFR = 0.5
36
Experienced anesthetists are unable to detect fade TOFR > ___
0.4
- may choose to not administer reversal - poor choice
37
There will still be significant residual block if the TOFR is ____
0.7-0.9
38
Tetanic stimulation is very rapid, it will be ________ Hz for _____ seconds.
50 Hz; 5 seconds
39
Tetanic stimulation has a sustained muscle response with which block?
Depolarizing
40
If a _____ NMBD is given, a tetanic stimulation will result in a a non-sustained muscle response (fade).
Nondepolarizing NMBD (Roc/Vec)
The fade is a result of presynaptic depletion of ACh or inhibition of release
41
What is the fade in tetanic stimulation related to?
- Presynaptic depletion of Ach or inhibition of release
- Frequency and length of stimulation
42
What is post-tetanic stimulation?
- A single twitch 3 seconds after tetanic stimulation
- Occurs due to accumulation of calcium during "tetany"
43
No response in post-tetanic stimulation will mean ______.
intense blockade
44
Characteristics of a presynaptic motor neuron:
- Large, myelinated
- From spinal cord or medulla
45
Characteristics of a presynaptic motor nerve ending:
- unmyelinated
- innervate single muscle mfiber
46
What is responsible for Ach in the presynaptic NMJ?
- Synthesis and release
- Reuptake and storage of choline
47
How big is the synaptic cleft?
What does it contain?
- 20-55mm wide with fluid
- Contains collagen and acetylcholinesterase
48
How many vesicles in the synaptic cleft release Ach?
5,000-10,000
49
What electrolyte is Ach release dependent on?
Calcium
50
What does acetylcholinesterase do to Ach?
Hydrolyzes Ach to acetic acid and choline
51
What is the anatomy of the post-synaptic membrane?
Membrane with multiple folds
52
Characteristics of the post-synaptic membrane:
-90 mV resting membrane potential
- Maintained by sodium/potassium
- nAchR dirrectly opposite
53
nAchR picture:
54
Characteristics of a nAchR subunit:
- Pentameric unit
- 5 sub pores (2 alpha, beta, gamma, delta)
- Transmembrane
55
What happens to the nAchR subunit when Ach binds?
- Conformational change
- Pores open
- Sodium influx
- Calcium influx
- Potassium efflux
56
What happens to the nAchR subunit when an NMBD binds:
- No conformational change
- No ion flow
- Probability of binding due to concentration of NMBD vs Ach
57
How is sux different when binding to the nAchR subunit?
It only requires binding at 1 alpha subunit
- it can leave one receptor and attach to other nAchRs until hydrolyzed - this is what causes fasiculations
58
What are the two unique characteristics of sux?
- Intense rapid paralysis
- Offset of effects prior to hypoxia
59
When is sux the most useful?
RSI - full stomach, code, trauma, pregnancy, emesis, etc.
60
Does sux release histamine?
Yes
61
What is the dose for Sux?
Onset?
Duration?
Dose = 1mg/kg IV for actual body weight
Onset: 30-60 seconds
Duration: 3-5 minutes
62
MOA of Sux:
- Attaches to 1 or both alpha subunits
- Mimics effects of Ach
- Hydrolysis is slower than Ach - keeps ion channels open (leaks potassium)
63
What is the sux depolarization called?
Phase I block
64
Characteristics of a phase I block:
- decreased contraction to single twitch stimulation
- decreased amplitude to continuous stimulation
- TOF ratio > 0.7
- Absence of post-tetanic facilitation
- Skeletal muscle fasciculations
65
Characteristics of a phase II block:
- Responses typical of non-depolarizing NMBD
- can be antagonized by anticholinesterase drug
- abrupt transition
66
How can a phase I block transition to a phase II block?
- Sux dose 2-4 mg/kg
- Lack of/poorly functioning pseudocholinesterase
- Relative "overdose" - desensitization
67
How is sux hydrolyzed?
- Butyrylcholinesterase
- Synthesized in liver
- terminated by diffusion out of NMJ into plasma
68
What things can effect pseudocholinesterase activity?
- Decreased hepatic function
- Drug induced decreases (neostigmine, reglan, chemo, insectides)
- Genetically atypical
- Chronic disease (renal) - decreased activity
- Pregnancy (high estrogen levels) = decreased activity
- Obese = increased activity
69
What is dibucaine?
- Amide local anesthetic
- inhibits activity of normal variant butyrylcholinesterase
- % inhibition = dibucaine number
70
What is the dibucaine number?
- Reflects quality not quantity of the enzyme to inhibit butyrylcholinesterase
20: Sux 1mg/kg lasts 3 hours
71
Dibucaine number:
72
Side effects of Sux:
- Cardiac dysrhythmias
- Hyperkalemia
- Myalgia
- Myoglobinuria
- increased intragastric pressure
- increased intraocular pressure
- Masseter spasm
73
What is pretreatment with non-depolarizing NMBD?
Giving a small dose of Roc early on to block the alpha subunit enough that you don't see fasciculations - prevents an increase in pressures
74
Defasiculating d/t patient symptoms:
- loss of visual focus/blurry
- mandibular muscle weakness
- ptosis
- diplopia
- dysphagia
- increased hearing acuity
75
What cardiac dysrhythmias can occur with sux?
- Sinus brady
- Junctional rhythm
- Sinus arrest
76
What actions does sux cause at the ANS ganglia?
- increased heart rate and blood pressure
- mimics action of ach
- usually occurs with large doses
77
Cardiac dysrhythmias most likely present on ____ dose of Sux.
2nd dose - 5 minutes after 1st
78
What patients will have hyperkalemia with sux?
What causes this?
- Unrecognized muscular dystrophy
- Unhealed 3rd degree burns
- Denervation of skeletal muscles (atrophy) - 96hrs-6 months
- Skeletal muscle trauma
- Upper motor neuron lesions
*caused by extrajunctional sites
79
Who will experience myalgia with Sch?
Where will the myalgia be located?
Young adults;
Neck, back, abdomen
80
What are pediatric patients more at risk for when given sux?
Myoglobinuria (damage to skeletal muscles)
81
Inconsistent increases in intragastric and LES pressure are related to:
- intensity of fasciculations
- direct increase in vagal tone
82
Sch will increase intragastric pressure and LES pressure, this will increase the risk of _______.
Aspiration
83
When does maximum increase in intraocular pressure occur after adminstering sux?
How long does it last?
Max increase = 2-4 minutes after admin;
Lasts 5-10 minutes
84
Intraocular pressure and sux:
- MOA unknown
- Contraction of EOM and globe distortion?
- Resistance to outflow of aqueous humor and dilation of vessels
- Efficacy of defasciculation controversial
85
Intraocular pressure graph:
86
What eye condition is sux contraindicated?
Open anterior chamber injury
87
What patients are at risk for intracranial pressure with sux?
Patients with intracranial tumors or or CHI
88
How can you attenuate the increase of ICP with sux?
Hyperventilating the patient prior to sux to cause cerebral vasoconstriction and decrease CBF and ICP
89
Sustained skeletal muscle contraction, incomplete jaw relaxation, and/or masseter muscle spasm d/t sux could be an indication of what conditions?
Early indicator of Malignant Hyperthermia
Inadequate dosage given in children
90
Definition of malignant hyperthermia:
Hereditary rhabdomyolysis associated with anesthetics
91
What can MH lead to if untreated?
- Muscle destruction
- Hyperkalemia
- Acidosis
- Dysrhythmia
- Renal failure
- DIC
92
Triggers for MH:
- ALL volatile anesthetics
- Sux
92
93
MH causes mutations in what?
- Skeletal muscle calcium release
- Ryanodine receptor (RyR1) 50-70% of MH patients
94
What population is susceptible to MH?
Native americans
95
How is MH diagnosed?
- Skeletal muscle caffeine contracture testing
- Muscle biopsy
96
Symptoms of MH:
- Acute increased skeletal muscle metabolism
- Increased oxygen consumption
- Lactate formation
- Heat production
- Rhabdomyolysis
97
Symptoms of rhabdo present in MH:
-↑ ETCO2 that you can’t bag fast enough to reverse
- ↑ temp 1 degree C/5 minutes
- Arrhythmias
- Skeletal muscle rigidity
98
What is the A for in Emergency ABCDs of MH?
- Agents: stop all triggering agents
- Administer non-triggering anesthetics
- Ask for help
- Ask for MH cart
99
What is the B for in the Emergency ABCDs of MH?
Breathing: hyperventilation with 100% oxygen
100
What is the C for in the Emergency ABCDs of MH?
Cooling procedures if patient is >102.2
101
What is the D for in the Emergency ABCDs of MH?
Dantrolene: continuous rapid IV push
102
MOA of Dantrolene:
CCB: inhibits calcium release into SR
- By affecting the ryanodine receptor
103
How much does Dantrolene decrease mortality?
From 80% → 10%
104
What is the dose for dantrolene?
2 mg/kg IV
- repeat doses until symptoms subside or 10 mg/kg IV
105
How is dantrolene metabolized?
- In the liver
- Metabolite = 5-hydroxydantrolene
106
Patients on calcium channel blockers (verapamil, Cardizem) that receive dantrolene as a treatment can result in __________
Cardiovascular Collapse (d/t synergistic effects)
107
What are the most common side effects of dantrolene?
- Weakness
- Phlebitis
- Respiratory failure
- GI upset
108
What do 50% of MH patients complain of?
Weakness in grip strength - be careful if they're already on CCB
109
What are the less common side effects of dantrolene?
- Confusion
- Dizziness
- Drowiness
110
What autoimmune disease develops Antibodies against the ACh receptor?
Myasthenia Gravis
111
Symptoms of Myasthenia gravis:
What is the treatment?
- increasing weakness/fatigue
- Diplopia
- Ptosis
- Extremity and respiratory muscle weakness
Treat with cholinesterase inhibitors
112
Myasthenia Gravis patients are _________ to Succinylcholine? Why?
What is the dose of sux for MG patients?
Resistant to Sux. More Sux is needed because the ACh receptors that are left do not function as well.
1.5-2.0 mg/kg
ED95 is 2.5 times higher
113
What is Lambert-Eton (LE) disease?
LE has an increased sensitivity to which type of NMBD?
An autoimmune disease that can result from small-cell lung cancers. LE can produce antibodies against calcium channels and decrease the release of ACh pre-junctionally.
LE has a sensitivity to both depolarizing and nondepolarizing NMBD.
