NMBDs: Physiology/Succinylcholine Exam III Flashcards
(100 cards)
1
Q
Which of the following is the newest NMBD?
A. Atracurium
B. Vecuronium
C. Pancuronium
D. Cistracurium
A
A. Atracurium (1980)
B. Vecuronium (1980)
C. Pancuronium (1960)
D. Cistracurium (1995)
S2
2
Q
Why was Rapacurium (Raplon) discontinued in 2001?
A
Massive laryngospasm and bronchospasm leading to death.
S2
3
Q
The effect of NMBD is to interrupt the transmission of nerve impulses at the _____.
A
Neuromuscular Junction (NMJ)
S3
4
Q
The MOA of NMBD is either depolarizing or non-depolarizing.
Deploarizing NMBD will _________ the action of ACh.
Non-depolarizing NMBD will ______ the action of ACh.
A
Depolarizing NMBD will mimic the action of ACh.
Non-depolarizing NMBD will interfere with the action of ACh.
S4
5
Q
Purpose of NMBD for anesthesia.
A
- Decrease airway trauma
- Facilitate surgical exposure
- Minimize injury from patient movement
S5
6
Q
What classification of NMBD is Succinylcholine (Anectine)?
A
Depolarizing NMBD
Only depolarizing agent used in anesthesia.
S6
7
Q
Name a long-acting non-depolarizing NMBD.
A
Pancuronium (Pavulon)
S6
8
Q
Name a short-acting non-depolarizing NMBD.
A
Mivacurium (Mivacron)
Move a lot, short-acting
S6
9
Q
What is the chemical classification of Pancuronium?
A
Aminosteroid
S6
10
Q
What is the chemical classification of Mivacurium?
A
Benzylisoquinoline
S6
11
Q
What is the chemical classification of Pancuronium (Pavulon)?
A
Aminosteroid
S6
12
Q
Which intermediate-acting NMBDs are Benzylisoquinolines?
A
Atracurium (Tracrium)
Cisatracurium (Nimbex)
S6
13
Q
Which intermediate-acting NMBD are Aminosteroids?
A
Vecuronium (Nocuron)
Rocuronium (Zemuron)
S6
14
Q
What is ED95 in regards to NMBDs?
A
The potency of NMBD. The dose that is necessary to produce a 95% suppression of a single twitch in the presence of nitrous/ barbiturate/ opioid anesthesia.
S7
15
Q
What nerve is stimulated so that the adductor pollicis muscle will produce a single twitch at 1 Hz (thumb adduction)?
A
Ulnar nerve
S7
16
Q
The order of block for NMBD is dependent on:
A
- Number of presynaptic ACh-containing vesicles released.
- Number of ACh receptors.
- Blood Flow to the area.
- Drug potency
S8
17
Q
Low potency NMBD will onset _________ than higher potency NMBD.
A
Faster
Lower potency NMBD will have more molecules than higher potency NMBD. This will create a higher concentration gradient and result in a faster onset.
S8
18
Q
Small, rapidly moving muscles will be blocked ________ than large muscles.
A
Faster
Eyes will be paralyzed first before diaphragm.
S8
19
Q
What does this graph show?
A
- Both Larynx and Adductor Pollicis muscle received 0.5 mg/kg of Rocuronium.
- Both muscles experience a dramatic decrease in twitch percent height, but the adductor pollicis is completley blocked while the larynx got down to a twitch height of 20%.
- Both muscles recovered at the same rate. Almost 100% twitch response returned by minute 40.
S9
20
Q
Checking a twitch in which muscle will assess the diaphragm and laryngeal muscle blockade.
A
Orbicularis Oculi
If there are no twitches to the facial nerve, the diaphragm and laryngeal muscles are adequately blocked. Best indicator of intubating conditions.
S10
21
Q
The orbicularis oculi underestimates _____________.
A
residual paralysis.
S10
22
Q
Is checking a twitch in the adductor pollicis a good indicator for laryngeal relaxation?
A
No, it is not a good indicator of laryngeal relaxation.
Checking a twitch of the adductor pollicis is a good indicator or peripheral recovery.
S10
23
Q
Which muscle is the gold standard to check a twitch on for recovery?
A
Adductor pollicis (Ulnar Nerve)
S10
24
Q
What is the placement of electrodes on ulnar nerve?
What will the response be?
A
S11
25
SLIDE 12
26
SLIDE 13
27
What is a defasciculating dose of NMBD?
What symptoms will the patient experience with a defasciculating dose?
Where 20% of intubating dose is given early (primer) to prevent fasciculation.
Blurred Vision
Ptosis (droopy eyes)
Diplopia (double vision)
Mandibular weakness
Dysphagia
**Increased hearing acuity** - people need to be quiet
*Let patient know they might start to feel week and get blurry vision. Encourage them to close their eyes.*
28
A single twitch nerve stimulator starts at _____ Hz/second decreasing to ______ Hz/10 secs.
1 Hz/sec to 0.1 Hz/10 secs
## Footnote
S15
29
With an onset of a block a single twitch will ______.
fade with each stimulus
## Footnote
S15
30
Double burst stimulator is _____ short bursts followed by ______ short bursts.
The double burst stimulator setting uses ________ Hz
2, 3
50 Hz (supramaximal current)
## Footnote
S16
31
Why was the double burst stimulator developed?
Developed to improve detection of residual block (fade).
Fade in 2nd response vs 1st response.
Qualitatively better than TOF.
## Footnote
S16
32
Train of Four is ________ stimuli at _______ Hz with ______ seconds between each burst.
4 stimuli at 2 Hz with ½ seconds between each burst
## Footnote
S17
33
TOF reflects events at _________ membrane.
Presynaptic
## Footnote
S17
34
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
## Footnote
S17
35
Experienced anesthetist are unable to qualitatively detect the fade of a TOFR > ______.
0.4
*The twitch will have to go from unblocked to completely blocked in order to tell a difference*
## Footnote
S17
36
There will be significant residual block with a TOFR of ______ to _____.
0.7 to 0.9
*You will not feel a fade, but there will still be blockade at the NMJ. Patient will still need reversal agent.*
## Footnote
S17
37
Tetanic stimulation is very rapid, it will be ________ Hz for _____ seconds.
50 Hz for 5 seconds
## Footnote
S18
38
If a _____ NMBD is given, a tetanic stimulation will result in a sustained muscle response.
Depolarizing NMBD (Succinylcholine)
## Footnote
S18
39
If a _____ NMBD is given, a tetanic stimulation will result in a non-sustained muscle response (fade).
Nondepolarizing NMBD (Roc/Vec)
*The fade is a result of presynaptic depletion of ACh or inhibition of release*
## Footnote
S18
40
What is post-tetanic stimulation?
Single twitch 3 seconds after tetanic stimulation.
*The post-tetanic stimulation will occur **d/t accumulation of calcium during tetany, the excess calcium will stimulate ACh release.***
## Footnote
S19
41
No response in post-tetanic stimulation will mean ______.
intense blockade
## Footnote
S19
42
What kind of blocks are in column A, B, and C?
What kind of nerve stimulation is performed in row 1 through 4?
## Footnote
S20
43
S22
44
A study performed showed that _____ % of patients that were not given anticholinesterase drugs for NMBD reversal and no use of nerve stimulator had post-op blockade once extubated.
42%
## Footnote
S21
45
A study performed showed that less than ____ % of patients that were given anticholinesterase drugs for NMBD reversal and use of nerve stimulator had post-op blockade once extubated.
<4%
## Footnote
S21
46
The presynaptic motor neuron is large and _________ which helps with transmission of nerve impulses.
myelinated
## Footnote
S23
47
The motor nerve ending is ________ and innervates single muscle fibers.
unmyelinated
## Footnote
S23
48
The presynaptic motor neuron is responsible for what three things involving ACh?
- ACh synthesis
- ACh uptake and storage in vesicles
- ACh release and uptake of choline
## Footnote
S23
49
The synaptic cleft is _______ nm wide with fluid that contains ________ and _________.
20-50 nm
Collagen and acetylcholinesterase (plasma cholinesterase, butyrylcholinesterase)
## Footnote
S24
50
ACh release is dependent on what electrolyte?
Calcium
## Footnote
S24
51
What does Acetylcholinesterase do to ACh?
Hydrolyze ACh to acetic acid and choline
## Footnote
S24
52
Post-synaptically, the membrane has multiple _______.
Post-synaptically, the resting membrane potential is _______.
Membrane potential is largely maintained by what two electrolytes?
folds
-90 mV
Na+ and K+
## Footnote
S25
53
How many subunits are on a transmembrane nicotinic acetylcholine receptor (nAChR)?
Name them.
Five subunits. (Pentameric unit)
2 alphas, beta, delta, gamma
## Footnote
S26/27
54
If NMBD (non-depolarizer) binds to nACh, there will be no __________ change and no ion flow.
conformational change
## Footnote
S27
55
Succinylcholine only requires binding at one ________ subunit. It is postulated that this will cause ________ before total blockade.
one alpha subunit
fasciculation
## Footnote
S29
56
_________ is the only depolarizing NMBD in clinical practice.
What are two unique characteristics of this drug?
What is this NMBD most useful for?
What is the downside of this NMBD?
- Succinylcholine
- Provides very intense and rapid paralysis
- Offsets of effects prior to hypoxia
- Rapid Sequence Induction
- Histamine Release (tachycardia, rash, welps)
## Footnote
S29
57
What is the dose of Succinylcholine?
Onset:
Duration:
Dose: 1 mg/kg IV
Onset: 30-60 seconds
Duration: 3-5 minutes
## Footnote
S30
58
What is the MOA of succinylcholine (Sch)?
- **Attaches to one or both alpha subunits **of the nAChR.
- Mimics the effect of ACh, but has a sustained opening of the receptor channel (hydrolysis is slower than ACh).
## Footnote
S31
59
SCh will cause how much increase in serum K+?
0.5 mEq/L
## Footnote
S31
60
What are characteristics of a phase I block?
Decrease contraction to single twitch stimulation.
Decrease amplitude to continuous stimulation.
TOF ratio > 0.7 (no fade)
Absence of post-tetanic facilitation
Skeletal muscle fasciculation
## Footnote
S32
61
Phase II Blocks are typical of ___________ NMBD.
non-depolarizing
## Footnote
S33
62
How can a Phase I block transition to a Phase II block?
Essentially an overdose
- Large dose of SCh (2-4 mg/kg)
- Lack of/ poorly functioning pseudocholinesterase
## Footnote
S33
63
Succinylcholine is hydrolyzed by __________.
Butyrylcholinesterase (plasma cholinesterase)
## Footnote
S34
64
What factors can decrease pseudocholinesterase activity?
- Hepatic disease
- Drugs (neostigmine, reglan, chemo)
- Genetics
- CKD
- Estrogen (think pregnancy)
## Footnote
S34
65
What factor can increase pseudocholinesterase activity?
What does this mean clinically?
- Obesity
- Higher dosing of succinylcholine is necessary for obese patients.
## Footnote
S34
66
What does dibucaine number mean?
What does it mean in extremely simple terms?
Dibucaine number reflects the quality of the enzyme that inhibits the breakdown of butyrylcholinesterase.
- ↑ Dibucaine number = Fast succinylcholine metabolism
- ↓ Dibucaine number = Slow succinylcholine metabolism
## Footnote
S35
67
What is normal dibucaine number?
80
*More butyrylcholinesterase will stick around and break down Sch*
## Footnote
S35
68
What will a dibucaine number of 20 mean for Sch?
1 mg/kg of SCh will last 3 hours
*Less butyrylcholinesterase will stick around*
## Footnote
S35
69
What are the side effects of Succinylcholine?
- Cardiac dysrhythmias
- Hyperkalemia
- Myalgia
- Myoglobinuria
- ↑ Gastric pressure
- ↑ IOP
- ↑ ICP
- Masseter spasm
## Footnote
S36
70
What is the pre-treatment to the side effects of SCh?
- Pre-treatment with non-depolarizing NMBD (5mg of Roc).
*This defasciculating dose either decreases, prevents, or mask the side effects of SCh.*
## Footnote
S36
71
What dysrhythmias can occur with succinylcholine administration?
- ↓HR
- Junctional Rhythm
- Sinus Arrest
## Footnote
S38
72
Cardiac dysrhythmia's will usually present on the 1st dose of succinylcholine. T/F?
False. If dysrhythmias occur, it will be with the 2ⁿᵈ dose.
## Footnote
S38
73
What are succinylcholine's actions at the ANS ganglia?
- ↑HR
- mimic ACh
*This usually occurs with large doses.*
## Footnote
S38
74
Patient's with _________ sites will have true hyperkalemia when given SCh.
Extrajunctional NMJ sites (more ion channels)
## Footnote
S39
75
What patient populations are more susceptible to the hyperkalemic effects of succinylcholine?
- Individuals with unrecognized muscular dystrophy (Duchenne's)
- Unhealed 3rd degree burns
- Denervation of Skeletal Muscles (bed-ridden patients)
- Upper motor lesions
## Footnote
S39
76
Who will experience myalgia with Sch?
Where will the myalgia be located?
## Footnote
S40
Young adults
Neck, back, abdomen
## Footnote
S40
77
S40 with soreness
78
Pediatric patients more frequently experience this with succinylcholine administration.
**Myoglobinuria** (damaged to skeletal muscles), usually found later to have MH or muscular dystrophy.
No succinylcholine for children
## Footnote
S41
79
Sch will increase intragastric pressure and LES pressure, this will increase risk of _______.
Aspiration
*This is related to the intensity of the fasciculation and the direct increase in vagal tone.*
## Footnote
S42S
80
Sch will increase intraocular pressure _________ minutes (range) after administration and last _________ minutes (range).
2-4 minutes after admin
last 5-10 minutes
## Footnote
S43
81
Sch will be contraindicated in ______________ chamber injury.
open anterior
## Footnote
S43
82
Succinylcholine will increase ICP transiently, how can this effect be attenuated?
**By hyperventilating the patient**, the PaCO2 will decrease leading to cerebral vasoconstriction. This will decrease CBF and decrease ICP before Succinylcholine administration.
## Footnote
S44
83
Sustained skeletal muscle contraction, incomplete jaw relaxation, and/or masseter muscle spasm d/t Sch could be an indication of what conditions?
Early indicator of Malignant Hyperthermia
Inadequate dosage given in children
## Footnote
S45
84
What is the hereditary rhabdomyolysis associated with all volatile anesthetics and SCh?
Malignant Hyperthermia (MH)
## Footnote
S47
85
If MH is untreated what can it lead to?
Muscle destruction
Hyperkalemia
Acidosis
Dysrhythmia
Renal Failure
DIC
## Footnote
S47
86
MH causes mutations in what receptor that causes excessive calcium release from the SR?
Ryanodine Receptor (RyR1)
## Footnote
S49
87
What ethnicity/nationality are susceptible to MH?
Native Americans
| plus people from Wisconsin area
## Footnote
S49
88
MH testing
## Footnote
S49
89
What are the symptoms of MH?
An acute increase in skeletal muscle metabolism
Increase O2 consumption
Lactate formation
Heat Production
Rhabdomyolysis (*Spiked increase ETCO2, Increase temp 1C/5mins, arrhythmias, rigidity.*)
## Footnote
S50
90
What are the emergency ABCDs of malignant hyperthermia?
## Footnote
S51
91
Dantrolene has decreased the mortality of MH from 80% to ________%.
10%
## Footnote
S52
92
What is the dose of dantrolene?
2mg/kg IV
Repeat doses until symptoms subside or 10mg/kg IV
## Footnote
S52
93
How does dantrolene work?
How is dantrolene metabolized?
- Inhibits the Ca2+ release from the SR and produces a muscle relaxant effect.
- Dantrolene is metabolized in the liver to 5-hydroxydantrolene
## Footnote
S52
94
Patients on calcium channel blockers (verapamil, Cardizem) that receive dantrolene as a treatment can result in __________
Cardiovascular Collapse (*d/t synergistic effects*)
## Footnote
S52
95
What are the most common side effects of dantrolene?
What are less common S/Es?
Most Common: Weakness, Phlebitis, Respiratory Failure, GI upset
Less Common: Confusion, Dizziness, Drowsiness
## Footnote
S53
96
What autoimmune disease develops Antibodies against the ACh receptor?
Symptoms (Sx)
Treatment (Sx)
Myasthenia Gravis (MG)
Sx:
Increasing weakness and fatigue throughout the day
Diplopia
Ptosis
Extremity and Resp muscle weakness
Tx: Cholinesterase Inhibitor
## Footnote
S54
97
What part of the day would a Myasthenia Gravis patient be scheduled for surgery?
Should be the first of the day. When they have the most ACh and their ACh receptors are not worn out.
## Footnote
S54
98
Myasthenia Gravis patients are _________ to Succinylcholine. Why?
What is the dose of SCh for MG patients?
**Resistant to SCh.** More SCh is needed because the ACh receptors that are left do not function as well.
1.5-2.0 mg/kg
## Footnote
S54
99
What is Lambert-Eton (LE) disease?
LE has an increased sensitivity to which type of NMBD?
Autoimmune disease: 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.
## Footnote
S55
100
Why does Lambert-Eton disease often develop?
Often results from small-cell lung cancers.
