Lecture 13 (Exam3) - Neuromuscular Blockade Flashcards
S/E of SCh
Why could you see Myalgia with SCh adminstration?
What population commonly c/o this?
What three areas are typically affected?
Because of the fasciculations = muscle pain.
Young adults.
Neck, back, abdomen
Slide 40
Your patient you gave SCh to c/o bilateral neck & throat pain after waking up.
What could have caused this?
SCh can cause myalgia from the fasciculations OR it could be from your botched intubation attempts bc you’re a baby SRNA.
Slide 40
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?
Myoglobinuria - Damage to skeletal muscles from the SCh administration.
Pediatrics.
Slide 41
What two things have an ⬆ correlation with myoglobinuria in pediatrics?
MH instance & muscular dystrophy diagnoses. :(
Slide 41
S/E of SCh
Which GI S/E probably DOES HAPPEN from SCh admin?
What could resut from this?
⬆ in Intragastric Pressure & LES (lower esophageal sphincter) Pressure
Can cause vomiting/aspiration. 🤮
Slide 42
S/E of SCh
What do intragastric and LES pressure ⬆’s depend on? (2 things)
What population is this seen the least in?
1) intensity of fasciculation
2) direct ⬆ in vagal tone
Seen less in children d/t minimal fasciculations.
Side 42
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?
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
S/E of SCh
What is an ABSOLUTE C/I for SCh in relevance to eyes? 👀
Open Anterior Chamber injury
(can cause the eye to pop out)
Slide 43
S/E of SCh
Why does intraocular pressure ⬆ with SCh?
Maximum increase in IOP seen how long after administration: ?
Duration of IOP: ?
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
S/E of SCh
SCh can ______ ICP in pt’s with tumors or CHI (Closed Head Injury).
How ‘could’ you fix this?
What negative effects could this cause and likely affect airway with post SCh administration?
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
The order of block is dependent on what four things?
- Number of presynaptic Ach-containing vesicles released
- Number of post-synaptic Ach receptors
- Blood flow to the area
- Drug potency
Slide 8
Small, rapidly moving muscles block ____________ than large muscles
Faster
Slide 8
Which muscle would become paralyzed first, muscles in the eyes or the diaphragm?
Eyes
Slide 8
S/E of SCh
What is a very serious S/E of SCh involving some skeletal muscles that could affect RSI/DLI? 😶 (not the diaphragm 😅)
What would you do in this instance?
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
No question just a graph…
The graph shows the difference between smaller muscles (larynx) v. large muscles (adductor pollicis) 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
What are the two preferred nerve monitoring sites?
Orbicularis oculi and Adductor Pollicis
Slide 10
The orbicularis oculi more closely reflects __________ and ___________ muscle blockade
Diaphragm and Laryngeal
Slide 10
What nerve monitoring site is the gold standard for recovery and a good indicator of peripheral recovery?
Adductor Pollicis
Slide 10
The black electrode (negative) is always placed __________ to the red, positive electrode.
Distal
Slide 11
What are three additional options for nerve monitoring discussed in lecture?
Ulnar nerve, Facial nerve, Posterior tibial
Slides 11-13
When would you use posterior tibial monitoring?
Which types of surgeries?
Any time you can not get to the head of the bed
Shoulder surgeries, craniotomies, etc.
Slide 13
Do you see a fade with Succinylcholine when using a peripheral nerve stimulator?
No. You get equal but lower height, depressed response.
Slide 21
When giving succinylcholine, what kind of response do you expect to see with post-tetanic potentiation?
Short, no fade and post-tetanic twitch is not potentiated. It’s the same height as other twitches.
Slide 21
When non-depolarizing NMB is given, what do you expect to see in tetany, TOF, DBS, and post-tetanic potentiation?
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
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) 🐟🐟🐟
Bedside criteria for extubation are: (in Dr. Kane’s slides)
Head lift
Negative PIP 25-30 cmH2O (taking a deep breath)
Slide 22
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
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
Motor neurons are _____ and ________. They run from the _______ or the ________.
Large and myelinated. It runs from spinal cord or medulla.
Slide 24
Motor nerve endings are ______. It innervates______.
Unmyelinated. It innervates single muscle fiber.
Slide 24
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.)
Synaptic cleft is _____ wide and filled with fluid that contains _____ and ______.
20-50 nm wide
collagen and acetylcholinesterase
Slide 25
How many molecules of Ach are contained in each vesicle?
5000 - 10,000 molecules of Ach
Slide 25
_____ vesicles are aligned in an active zone that contains readily releasable stores.
_________ are released on increased demand.
Active pool
Ready pool vesicles are released with increased demand.
Slide 25/from book
_____ ion plays role in release of ready pool/active pool vesicles in the synaptic cleft.
Calcium
Slide 25
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
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
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.)
How can succinylcholine cause a phase II block?
- You give too much succinylcholine, dose 2-4 mg/kg
- 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)
Describe a phase II block!
Responses typical of non-depolarizing NMBD.
Can be antagonized by anticholinesterase drug.
(Slide 34)
What is the duration of action of succinylcholine?
Normally 3-5mins in duration.
(Slide 35)
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!
(Slide 36)
ChatGPT:
Dibucaine is a local anesthetic that inhibits sodium channels, preventing the initiation and propagation of nerve impulses, which leads to the loss of sensation in the area it is applied to. Its relationship with succinylcholine and the dibucaine number involves the enzyme pseudocholinesterase (also known as butyrylcholinesterase), which is responsible for the hydrolysis and inactivation of succinylcholine.
Succinylcholine is a muscle relaxant used in anesthesia that is quickly broken down by pseudocholinesterase in the blood, leading to a short duration of action. However, some individuals have a genetic variant of pseudocholinesterase that is less efficient at metabolizing succinylcholine, resulting in prolonged muscle paralysis and recovery time after administration of the drug.
The dibucaine number is a measure of the inhibitory effect of dibucaine on pseudocholinesterase activity. It is used to detect atypical forms of the enzyme that are resistant to inhibition by dibucaine. A normal dibucaine number indicates a typical response, where dibucaine effectively inhibits the enzyme’s activity, while a lower dibucaine number suggests the presence of an atypical enzyme variant with decreased sensitivity to inhibition by dibucaine. This test helps identify patients at risk of experiencing prolonged effects from succinylcholine due to atypical pseudocholinesterase activity.
Question 1:
In what diseases should you avoid giving succinylcholine?
DUUUS
Question 2:
- Unrecognized muscular dystrophy
-Duchenne’s - Unhealed 3rd degree burns
- Denervation of skeletal muscles (atrophy) (Stroke)
-96 hrs-6 months - Skeletal muscle trauma
- Upper motor neuron lesions
These patients have extra junctional sites!
(More ion channels = more K+ out)
(Slide 39)
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)
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)
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)
