Lecture 13 (Exam3) - Neuromuscular Blockade Flashcards
1
Q
S/E of SCh
Why could you see Myalgia with with SCh adminstration?
What population commonly c/o this?
What three areas are typically affected?
A
Because of the fasciculations = muscle pain.
Young adults.
Neck, back, abdomen
Slide 40
2
Q
Your patient you gave SCh to c/o bilateral neck & throat pain after waking up.
What could have caused this?
A
SCh can cause myalgia from the fasciculations OR it could be from your botched intubation attempts bc you’re a baby SRNA.
Slide 40
3
Q
S/E of SCh
You start to see amber urine in your patients foley bag post SCh administration. What is happening?
What population do you see ⬆ incidence of this?
A
Myoglobinuria - Damage to skeletal muscles from the SCh administration.
Pediatrics.
Slide 41
4
Q
What two things have an ⬆ correlation with myoglobinuria in pediatrics?
A
MH instance & muscular dystrophy diagnoses. :(
Slide 41
5
Q
S/E of SCh
Which GI S/E probably DOES HAPPEN from SCh admin?
Why is this bad?
A
⬆ in Intragastric Pressure & LES Pressure
Can cause vomiting/aspiration. 🤮
Slide 42
6
Q
S/E of SCh
What do intragastric and LES pressure ⬆’s depend on? (2 things)
What population is this seen the least in?
A
1) intensity of fasciculation
2) direct ⬆ in vagal tone
Seen less in children d/t minimal fasciculations.
Side 42
7
Q
S/E of SCh
Why don’t we clinically worry too much about ⬆ pressures in intragastric and LES?
Why do we still give SCh knowing this may happen?
A
Bc LES pressure > intragastric pressure = blockage of stomach acid being ejected into esophagus.
*ON BOARDS: ✅ S/E of SCh; BUT not as clinically important bc giving SCh overpowers not giving SCh. (Pros outweigh Cons)
Slide 42
8
Q
S/E of SCh
What is an ABSOLUTE C/I for SCh in relevance to eyes? 👀
A
Open Anterior Chamber injury
(can cause the eye to pop out)
Slide 43
9
Q
S/E of SCh
Why does intraocular pressure ⬆ with SCh?
Maximum increase in IOP seen how long after administration: ?
Duration of IOP: ?
A
Unknown - but speculated d/t globe distortion from fasciculations - can cause outflow blockage of aqueous humor and dilation of vessels
Onset: 2-4 mins
Duration: 5-10 mins
Slide 43
10
Q
S/E of SCh
SCh can ______ ICP in pt’s with tumors or CHI (Closed Head Injury).
How ‘could’ you fix this?
But why would you NOT want to do this post SCh administration?
A
SCh can ⬆ ICP
**not consistently observed in studies 🙄
Hyperventilation = ⬇ CO2 = vasoconstrics = ⬇ ICP
BUTTTTT you wouldn’t want to put more gas/pressure in the stomach = ⬆ aspiration risk Not Appropriate fix
Slide 44
11
Q
The order of block is dependent on what four things?
A
- Number of presynaptic Ach-containing vesicles released
- Number of post-synaptic Ach receptors
- Blood flow to the area
- Drug potency
Slide 8
12
Q
Small, rapidly moving muscles block ____________ than large muscles
A
Faster
Slide 8
13
Q
Which muscle would become paralyzed first, muscles in the eyes or the diaphragm?
A
Eyes
Slide 8
14
Q
S/E of SCh
What is a very serious S/E of SCh involving some skeletal muscles? 😶 (not the diaphragm 😅)
What would you do in this instance?
A
Masseter muscle spasm 😬
-you cant intubate them…orally. (Could you nasally??)
“Mask ventilate, wait till it wears off” per Kane.
I asked her after class, if it were an emergent intubation - you would give more SCh to hopefully relax the spasm (if they were young, healthy adult)
Slide 45
15
Q
No question just a graph…
A
The graph shows the difference between smaller muscles (adductor pollicis) and large muscles (larynx) after a dose of Rocuronium was given. The adductor pollicis continued to be blocked, and the laryngeal muscles were not fully paralyzed. <– this is why we want thumb twitches before we send to PACU/extubate 😁
Slide 9
16
Q
What are the two preferred nerve monitoring sites?
A
Orbicularis oculi and Adductor Pollicis
Slide 10
17
Q
The orbicularis oculi more closely reflects __________ and ___________ muscle blockade
A
Diaphragm and Laryngeal
Slide 10
18
Q
What nerve monitoring site is the gold standard for recovery and a good indicator of peripheral recovery?
A
Adductor Pollicis
Slide 10
19
Q
The black electrode (negative) is always placed __________ to the red, positive electrode.
A
Distal
Slide 11
20
Q
What are three additional options for nerve monitoring discussed in lecture?
A
Ulnar nerve, Facial nerve, Posterior tibial
Slides 11-13
21
Q
When would you use posterior tibial monitoring?
A
Any time you can not get to the head of the bed
Shoulder surgeries, craniotomies, etc.
Slide 13
22
Q
Do you see a fade with Succinylcholine when using a peripheral nerve stimulator?
A
No. You get equal but lower height, depressed response.
Slide 21
23
Q
When giving succinylcholine, what kind of response do you expect to see with post-tetanic potentiation?
A
Short, no fade and post-tetanic twitch is not potentiated. It’s the same height as other twitches.
Slide 21
24
Q
When non-depolarizing NMB is given, what do you expect to see in tetany, TOF, DBS, and post-tetanic potentiation?
A
You see fade in all of it. In post-tetanic potentiation, you see fade and the potentiation of the last twitch after tetany.
Slide 21
25
Do we really have to use an NMB reversal instead of bedside criteria for extubation?
Yes, they still have postop residual NMB in their body.
Slide 22
(They will look like a fish, unable to breathe and will need to be reintubated) 🐟🐟🐟
26
Bedside criteria for extubation are: (in Dr. Kane's slides)
Head lift
Negative PIP 25-30 cmH2O (taking a deep breath)
Slide 22
27
According to the study, how much percentage of the patients still had postop blockade after extubation without anticholinesterase and no nerve stimulators?
42% of the extubated patients who did not receive NMB reversal still had postop blockade.
Slide 22
28
According to the study, use of nerve stimulator increased from 2% to 60% and after giving neostigmine to 42% of the patients, how much percentage postop blockade was resulted?
Postop blockade decreased to <4%.
Slide 22
29
Motor neuron are _____ and ________.
Large and myelinated. It runs from spinal cord or medulla.
Slide 24
30
Motor nerve endings are ______. It innervates______.
Unmyelinated. It innervates single muscle fiber.
Slide 24
31
Where do Ach synthesis, release, and reuptake of choline occur in NMJ?
Presynaptic neuron
Slide 24
(Ach is stored in vesicles in presynaptic neuron after it is synthesized.)
32
Synaptic cleft is _____ wide and filled with fluid that contains _____.
20-50 nm wide
collagen and acetylcholinesterase
Slide 25
33
How many molecules of Ach are contained in each vesicle?
5000 - 10,000 molecules of Ach
Slide 25
34
_____ vesicles are aligned in an active zone that contains readily releasable stores.
active pool
Slide 25/from book
Ready pool vesicles are released with increased demand.
35
_____ ion plays role in release of ready pool/active pool vesicles in the synaptic cleft.
Calcium
Slide 25
36
Where is acetylcholinesterase located in NMJ and what is the function of it?
Its located in the synaptic cleft nearby the Ach receptors.
Its breaks down Ach in synaptic cleft via hydrolysis to acetic acid and choline.
(♻️ Presynaptic neuron reuptake acetic acid and choline to rebuild Ach)
Slide 25
37
What is the resting membrane potential of post synaptic membrane and what are the two ions that maintain the membrane potential of post-synaptic membrane?
-90mv
Sodium and potassium ions
Slide 26
38
Post-synaptic membrane comprise of ______ that increases the surface area of the muscle plasma membrane.
multiple folds/ invaginations
Slide 26
(nAch receptors are concentrated at the crest of the folds directly opposite to the active zones where active pool/ready pools Ach are released.)
39
How can succinylcholine cause a phase II block?
1. You give too much succinylcholine, **dose 2-4 mg/kg**
2. Lack of/poorly functioning pseudocholinesterase (breaks down succinylcholine).
If they have this and you give them a normal dose of succinylcholine, then you relatively “overdosed” your patient......
(Slide 34)
40
Describe a phase II block!
Responses typical of non-depolarizing NMBD.
Can be antagonized by anticholinesterase drug.
(Slide 34)
41
What is the duration of action of succinylcholine?
Normally 3-5mins in duration.
(Slide 35)
42
What clears succinylcholine from the body?
It is hydrolyzed by butyrylcholinesterase (plasma cholinesterase) (Pseudocholinesterase )
Butyrylcholinesterase:
*Synthesized in liver
*Terminated by diffusion out of NMJ into plasma
*Byproducts are: Succinylmonocholine (less potent) and choline
(Slide 35)
43
What can alter the activity of Pseudocholinesterase activity?
Decrease:
*Decreased hepatic production of Pseudocholinesterase (⬇️ 75% of liver function before apparent) (Sux lasts longer in these patients.)
*Drug-induced decreases (Neostigmine, Reglan, chemo, insectides)
*Genetically atypical (People don’t have the same quality of functioning pseudocholinesterase)
*Chronic diseases (renal): ↓ activity (pseudocholinesterase does not work as well.)
*Pregnancy (high estrogen levels): ↓activity
Increase:
*Obesity: ↑ activity of plasma cholinesterase.
(Slide 35)
44
Why was Electroconvulsive therapy used and what is it?
ECT is where a generalized seizure is electrically induced to manage refractory mental disorders
It is used to stimulate the release of mood enhancing hormones.
Example: used for extreme depression on the boarder of suicide and manic depressive episodes.
Treatment may be once a week to twice a week. We give them succinylcholine to paralyze them while we induce the seizure, so we gotta make sure they have normal working butyrylcholinesterase or else they will be paralyzed longer.....
(Slide 36)
45
What is Dibucaine?
*Amide local anesthetic
*Inhibits breakdown of butyrylcholinesterase
*% inhibition = dibucaine number
(Slide 36)
46
What does the Dibucaine number reflect?
What # would indicate we would have prolonged blockade?
*Reflects quality not quantity of butylcholinsterase enzyme
*20: SCh 1mg/kg lasts 3 hours
* The lower the Dibucaine number is, the longer succinylcholine will last!
- Think of Dibucaine as a protector - if the Dibucaine # is low (20) that means it was used bc our crappy Butyrylcholinsterase sucks-ass and cant get the job done...
- If the # was normal/high - it means we dont need protection bc our Butyrlcholinesterase is good 😎
(Slide 36)
47
What are the side effects of succinylcholine?
1. Cardiac dysrhythmias
2. Hyperkalemia ( +0.5 mEq/L to K+ level)
3. Myalgia
4. Myoglobinuria
5. ⬆️ intragastric pressure
6. ⬆️ intraocular pressure
7. ⬆️ intracranial pressure
8. Masseter spasm (Cannot open mouth to intubate)
(Slide 37)
48
Pretreatment with a non-depolarizing NMBD before giving succinylcholine (Defisciculating dose) can be problematic bc?
It can mask the side effects of succinylcholine.
(Slide 37)
49
What are the cardiac dysrhythmias caused by succinylcholine?
SB, JR, & Sinus arrest!
**Think ACh slows the heart down & SCh is 2 ACh together 👬**
(Slide 38)
50
What two receptor sites does succinylcholine work on to cause cardiac dysrhythmias?
Actions at **cardiac muscarinic, cholinergic receptors**
1. Mimics action of ACh
2. Dysrhythmias most likely on 2nd dose, 5 minutes post 1st
3. Due to metabolites: succinylmonocholine and choline.
Actions at **ANS ganglia**
1. ⬆️ Heart rate and blood pressure
2. Mimics action of Ach
3. Usually occurs with large doses
(Slide 38)
51
Why does hyperkalemia occur with succinylcholine?
Activation of ACh receptor from succinylcholine causes an influx of sodium and calcium to the cytoplasm and an **efflux of potassium** to the extracellular space.
( +0.5 mEq/L with each dose)
***** K+ levels not altered by pretreatment with non-depolarizers (Defasiculating dose)*****
(Slide 39)
52
Question 1:
In what diseases should you avoid giving succinylcholine?
Question 2:
1. Unrecognized muscular dystrophy
-Duchenne’s
2. Unhealed 3rd degree burns
3. Denervation of skeletal muscles (atrophy) (Stroke)
-96 hrs-6 months
4. Skeletal muscle trauma
5. Upper motor neuron lesions
These patients have extra junctional sites!
(More ion channels = more K+ out)
(Slide 39)
53
The _____ is a pentameric unit neurotransmitter receptor with a transmembrane pore and has how many subunits?
How many of each subunit are there?
nAChR
5 subunits: 2-alphas, beta, delta, and gamma
(gamma is fetal nACH-r, swapped out with Epsilon when mature)
(slide 28)
54
With the binding of ACh to a nAChR, a ______________ change occurs.
Pores open, allowing what to flow through?
confirmational change
sodium, calcium to flow into the cell, potassium dueces out ✌️
(slide 28)
55
What happens if a NDNMBD binds to the nAChR? (2 answers)
Which muscular blocking agent only requires binding to 1 alpha subunit?
no confirmational change
no ion flow
Succ's only requires binding to 1 alpha subunit
(slide 28)
56
You administer Succ's and understand that the succ's molecule will bind to a nAChR subunit. What happens after that?
T/F: Fasciculations occur as a direct result of a succ's molecule attaching to a single receptor and remaining attached until the succ's is hydrolyzed.
Bonus question: What's a succ's molecule comprised of? (This was from Schmidt)
The nAChR channel remains open
False: Fasciculations occur because that one succ's molecule can attach to one unit at a time but can leave and attach to another nAChR until it's hydrolyzed.
Essentially a succ's molecule is 2 ACh molecules stuck together
(slide 28)
57
Malignant hyperthermia is triggered by ___ . (2)
Volatile anesthetics, Succinylcholine (slide 48)
58
Definition of malignant hyperthermia and cause.
“Hereditary rhabdomyolysis associated with anesthetics.”
Caused by a mutation in the RYR-1 receptor.
-mutation is found in 50 - 70% of MH pts and often found in Native Americans. (Slide 47, 49)
59
Malignant hyperthermia leads to ….(6 things).
Muscle destruction, hyperkalemia, acidosis, arrhythmias, renal failure, DIC (slide 47)
60
Signs and symptoms of malignant hyperthermia?
1. Acute increased skeletal muscle metabolism.
2. Increased O2 consumption.
3. Lactate formation
4. Heat production
5. Rhabdomyolysis —> ⬆️ ETCO2, ⬆️ temp 1 degree C every 5 min, arrhythmias, skel muscle rigidity
(Slide 50)
61
What are the “ABCD” of malignant hyperthermia treatment?
A = agents, administer, ask. Stop all triggering agents, administer non triggering agents (basically TIVA), ask for help, ask for MH cart.
B = breathing = hyperventilation w/ 100% O2
C = Cooling procedure if pt > 102.2 F. (39 C)
D = Dantrolene = continuous rapid IVP
(Slide 51)
62
Succinylcholine is the only DEPOLARIZING NMBD in clinical practice
What 2 characteristics make it the ideal choice for Rapid Sequence Intubation (RSI)?
What 2 side effects are we not too thrilled about when using Succ's?
2 characteristics: intense rapid paralysis; offset of effects prior to hypoxia
2 unwanted S/E: histamine release and ~0.5 ⬆️ in serum K+ (exponentially more K+ efflux in specific health conditions)
(slide 30 + 32)
63
How can we test for malignant hyperthermia?
A muscle biopsy is done, and that sample undergoes the skeletal muscle caffeine contracture test.
(Slide 49)
64
Succ's is ideal for RSI and also what type of situations that Kane mentioned in lecture?
Succ's is great for prevention of __________ and rapid offset prevents _____
Succ is good to consider in pts who may have...
(Hint: 7 criteria markers but can be summed up to 2)
"Can't oxygenate and can't ventilate" situations
aspiration; death (secondary to hypoxia) (Kane)
edematous airway, MP grade IV, broken jaw, full stomachs, obesity, trauma, pregnancy. Basically any time where we're concerned about accessing a possibly difficult airway or aspiration
(slide 30 + Kane)
65
Dantrolene dose? MOA? Metabolite?
Dose: 2mg/kg IV, up to a max of 10 mg/kg IV.
MOA: inhibits intracellular Ca release
Metabolized by liver into 5 hydroxydantrolene.
- metabolite has muscle relaxant effect!
(Slide 52)
66
Succinylcholine Dose:
Onset:
Duration:
1 mg/kg IV
30-60 seconds
3-5 mins
(slide 31)
67
What are side effects of dantrolene?
Common SE: weakness, phlebitis, respiratory failure, GI upset
Less common: confusion, dizziness, drowsiness.
(Slide 53)
68
When is the ideal OR time for myasthenia gravis pts?
Beginning of the day! This is when they have the most available ACh, so extubation and breathing will be better post op.
“These are 7 am fools, not 4 pm folks.” - Dr. Kane
(Slide 54)
69
How do we adjust Succinylcholine dosing in myasthenia gravis pts?
Pts will need MORE Succinylcholine (less working receptors).
Dose = 1.5 - 2 mg/kg (recall normal succ dose is 1mg/kg)
(Slide 54)
70
You push lidocaine, fentanyl, propofol, and lastly succ's. When do we know when to ventilate?
Why?
Ventilate via intubation AFTER the 30 sec passes post succ's admin
If you attempt to BMV after succ's has been given, you risk insufflating the stomach, therefore, increasing risk of a not-so-pleasant bile bath and aspiration
(Kane)
71
How do we adjust the dosing of NMBD in pts with Lambert - Eton dz?
These pts have increased sensitivity to depolarizing and nondepolarizing NMBDs , so you will need to DECREASE dose of your NMBD. Some say decrease by 20%.
(Slide 55)
72
Antibodies form against ____ in myasthenia gravis and ____ in lambert Eton.
Myasthenia gravis = antibodies against ACh receptors.
Lamber Eton = antibodies against P-type calcium channels.
(Slide 54, 55)
73
Dantrolene + what med taken in preop = severe CV collapse.
Calcium channel blockers. (Slide 52)
74
Dantrolene decreased mortality of MH from ____ to ____ %.
Mortality decreased from 80 to 10 %. (Slide 52)
75
Succ's mimics the actions of what neurotransmitter?
Succ's is hydrolyzed by what?
T/F: Succ's molecule is hydrolyzed slower than ACh. And this means the receptor ion channel remains open longer.
ACh
plasma cholinesterase (butyrylcholinesterase)
True
(slide 32)
76
Succ's causes what degree of block?
Phase 1 block
(slide 32)
77
Characteristics of a Phase 1 block:
__ contraction to a _______ twitch stimulation
__ amplitude to __________ stimulation
TOF ratio of ____ (meaning no "____")
_______ of ____-_______ facilitation
________ muscle fasciculations
⬇️ contraction to single twitch stim.
⬇️ amplitude to continuous stim.
TOF ratio of >0.7 (meaning no "fade")
Absence of post-tetanic facilitation
Skeletal muscle fasciculations
(slide 33)
78
According to the History of neuromuscular blocking agents, what is the chronological years these agents were founded in?
1. dTc and SCh (Anectine)
2. Pancuronium (Pavulon)
3. Atracurium (Tracrium) and Vecuronium (Norcuron)
4. Rocuronium (Zemuron)
5. Cisatracurium (Nimbex) and Mivacurium (Mivacron)
6. Rapacurium (Raplon)
1. 1940-1960
2. 1960
3. 1980
4. 1994
5. 1995 and 1997
6. 2001
(slide 2)
79
What are the 2 most common NMBD that we use today?
Vecuronium (Norcuron)
Rocuronium (Zemuron)
(slide 2)
80
Mivacurium (Mivacron) is "nicknamed" as what according to Dr. Kane?
And how does it get reversed in the body?
And is it still used today?
"move-a-cron"
because it is not a very dense medication and of a very short duration of action of about 12 min.
It reversed by plasma cholinesterases
It was removed strictly due to the big pharma not making enough money off of it (costs too much to make even though it's a good drug. there are rumors that it may come back!)
(slide 2)
81
What is the effect of NMBDs?
To Interrupt transmission of nerve impulses at neuromuscular junction (NMJ)
(slide 3)
82
What are the 2 MOA of NMBDs? (2 groups)
Depolarizing
-Mimics the action of acetylcholine
Non-depolarizing
-Interferes with the action of acetylcholine
(slide 4)
83
What is the purpose we give NMBDs? (3 main reasons)
Minimizes incidence of tissue trauma (do not want them to buck or cough with intubation)
1. Decreased airway trauma
- Airway edema
- Hoarseness
- Vocal cord injury
2. Facilitates surgical exposure:
- (Ex: cases with open chest or belly that needs the uses of retractors during surgery to open the cavity so we want those muscle to be relaxed)
3. Minimizes injury from patient movement
(slide 5)
84
What are the classifications of NMBDs?
And name the drugs in each (what's an easy way to remember?)
Depolarizing
* Succinylcholine (Anectine)
Non-depolarizing
- Long acting : * Pancuronium (Pavulon) (the other 2 drugs we don't use)
- Intermediate acting: (everything else)
- Short acting: * Mivacurium (Mivacron) (AKA- "Move-a-cron")
(chart on Slide 6)
85
With the classifications of NMBDs, what are the 2 chemical classifications of the non-depolarizing drugs?
How can we remember?
*Aminosteroid*
*Benzylisoquinoline*
- There's only 3 of these drugs: Atracurium (Tracrium), Cisatracurium (Nimbex), Mivacurium (Mivacron)
-- remember AMC (like the movie theater- preferably not like Jeffery Dahmer)
(slide 6)
86
When we dosing our NMBDs, we use ED95. What does this mean?
And what is this dose based off of?
Is potency (or dose) of neuromuscular blocking drug (NMBD) necessary to produced 95% suppression of single twitch
This is based off of the pts having a general anesthetics (In the presence of nitrous/barbiturate/opioid anesthesia) So, NOT awake patients.
(Slide 7)
87
What muscle do we use when assessing the ED95 dose of a NMBD? what nerve is stimulated?
Adductor pollicis muscle
-Single twitch at 1Hz
-Ulnar nerve stimulated
(slide 7)
88
What are some common symptoms of receiving a defasciculating dose of an NMBD?
Loss of visual focus
Mandibular muscle weakness
Ptosis
Diplopia
Dysphagia
Increased hearing acuity
(Slide 14)
89
What do we do when patients experience symptoms from a defasciculating dose?
Guide them through the symptoms. (Close eyes, relax, etc.)
(Slide 14)
90
Describe the function of single twitch stimulation. (Strength, duration, etc.)
1 Hz/second decreasing to 0.1 Hz every 10 seconds. 1 transmission is delivered every time the button is pushed. The stimulator automatically decreases the strength every time if pushed rapidly.
(Slide 16)
91
Single twitch is rarely used now. In what scenario, mentioned in lecture, was it used for?
During a Succinylcholine infusion. The medication wears off so quickly that twitches would be different minute to minute. The single twitch stimulation would run continuously.
(Slide 16)
92
Describe double burst stimulation.
3 short bursts followed by 3 short bursts.
50Hz
(Slide 17)
93
Why was double burst stimulation developed?
To improve detection of residual block.
Detect a fade in responses
Better at detecting the quality of responses than TO4.
(Slide 17)
94
Describe train of 4 stimulation
4 stimuli at 2 Hz in 1/2 second.
(Slide 18)
95
How is the TO4 ratio determined?
Compare the amplitude of the 4th twitch to the 1st twitch.
(Slide 18)
96
What TO4 ratio is usually needed before you can detect the difference in twitches?
< 0.4
Experienced anesthetists unable to detect fade at TOF > 0.4
(Slide 18)
97
What TO4 ratio can still be present with residual paralysis?
0.7 - 0.9
(Slide 18)
98
Describe Tetanic Stimulation
very rapid
50 Hz for 5 seconds
(Slide 19)
99
How does a depolarizing and non depolarizing agent react to tetanic stimulation?
Depolarizing = constant amplitude
Non depolarizing = fade amplitude
(Slide 19)
100
What creates the fade with nondepolarizing agents?
presynpatic depletion of ACh or inhibition of its release.
(Slide 19)
101
Describe post-tetanic stimulation
Single twitch 3 seconds after tetanic stimulation
(Slide 20)
102
Why would a post-tetanic stimulation occur?
Accumulation of calcium and ACh during tetany.
Excess calcium stimulates ACh release
(Slide 20)
103
The patient does not have a post-tetanic stimulation. Why?
Intense blockade. They aint moving for awhile.
(Slide 20)
