PHARMACOLOGY-neuromuscular blockers AND reversal agents Flashcards
(166 cards)
1
Q
What components make up the neuromuscular junction
A
Axon terminal (presynapse) Synaptic cleft (space between) Motor end plate (postsynapse)
2
Q
What are the 2 types of nicotinic ACh receptors at the neuromuscular junction
A
- Prejunctional Nn, on the presynaptic nerve
2. Postsynaptic Nm on motor endplate
3
Q
Describe the structure of a postsynaptic nicotinic receptor
A
Pentameric
Ligand-gated ion channel
5 subunits around ion-conducting pore
Subunits = 2 alpha, 1 beta, 1 delta, 1 epsilon
4
Q
How does a nicotinic ACh receptor become active
A
1 ACh molecule binds to each alpha subunit
The pore channel opens when both subunits are occupied
Na+ and Ca++ enter the cell and K+ exits
5
Q
Which ions are conducted through the nicotinic ACh channel
A
Na+ and Ca++ in
K+ out
6
Q
Once the nicotinic receptor is activated by ACh, what happens to the charge of the neuron
A
When ions pass through the pore, the inside of the neuron becomes positive and activates an action potential
7
Q
How do nicotinic receptors initiate action potentials
A
Once the pore opens and conducts Na+ and Ca++ inside, the positive charge activates voltage-gated Na+ channels causing depolarization and an action potential
8
Q
After depolarization of the myocyte occurs, what happens next
A
Depol instructs the sarcoplasmic reticulum to release Ca++ into the cytoplasm
Ca++ engages with myofilaments and initiate muscle contraction
9
Q
How are nicotinic receptors turned off
A
Acetylcholinesterase is positioned around the receptors and hydrolyzes ACh into choline and acetate. This occurs almost immediately after ACh binds the nicotinic receptor
10
Q
Describe 2 pathologic variants of nicotinic receptors
A
- has a gamma subunit instead of an epsilon
2. Has 7 alpha subunits
11
Q
What factors increase the presence of extra-junctional nicotinic receptors
A
Denervation
Prolonged immobility
12
Q
Where are extrajunctional nicotinic receptors located
A
NOT at the NMJ site
13
Q
What are patients with extrajunctional receptors at risk for with succinylcholine administration
A
Hyperkalemia
Serum K+ can increase by 0.5 - 1.0 mEq/L
14
Q
In what conditions is succinylcholine contraindicated (9)
A
- Upper or lower motor neuron injury
- Spinal cord injury
- Burns
- Skeletal muscle trauma
- CVA
- Tetanus
- Severe sepsis
- Muscular dystrophy
- Prolonged chemical denervation (Mg, long term NMB)
15
Q
How do extrajunctional nicotinic receptors respond differently to succinylcholine
A
They remain open for a longer time, allowing more Na+ to enter the cell
16
Q
Why can extrajunctional nicotinic receptors increase K+
A
The receptors are open for longer time allowing more K+ to leak out
17
Q
What can depolarize the a7 type of nicotinic receptor
A
Succinylcholine AND choline (succ metabolite)
18
Q
How is succinylcholine-induced hyperkalemia treated (4)
A
- IV calcium chloride
- Hyperventilation
- Sodium bicarb
- glucose + insulin
19
Q
How do patients with upregulated extrajunctional receptors respond to nondepolarizers
A
The receptors are resistant to ND-NMB
The nondepolarizers have decreased potency
More receptors = more drug needed
20
Q
What causes fade during train-of-four stimulation
A
Antagonism of the presynaptic nerve nicotinic receptor (nondepolarizer)
This blocks the mobilization of ACh for potential release with stimulation
21
Q
What action occurs when ACh binds to receptors of the presynaptic nerve
A
It mobilizes more ACh in the nerve terminal
22
Q
Why doesn’t succinylcholine produce fade
A
Because it agonizes the presynaptic nicotinic receptor, mobilizing ACh vesicles for immediate release
23
Q
What triggers ACh vesicles to release ACh into the synaptic cleft
A
An action potential opens VG gated Ca++ channels allowing Ca++ into the nerve terminal
Increased Ca++ destabilizes the proteins holding ACh vesicles
The vesicles exit the nerve terminal via exocytosis
24
Q
What action does ACh take in the synaptic cleft
A
- Binds to postynaptic Nm receptors, opening ion channels
2. Binds to presynaptic Nn receptors, mobilizing more ACh vesicles for immediate release
25
How do nondepolarizing NMB act on presynaptic Nn receptors
The competitively antagonize the receptor, inhibiting the ability of more mobilization of ACh vesicles for release
26
Does succinylcholine block cause fade?
NO because it is an agonist that mimics the action of ACh
27
What distinguishes the difference between phase 1 and phase 2 block
The presence or absence of fade
28
Describe a phase 1 block
It is produced by succinylcholine which agonizes the presynaptic Nn receptors and allows for normal ACh mobilization in the nerve terminal. The result is plenty of ACh for release with TOF stimulation
29
Describe a phase 2 block
It is produced with nondepolarizers or excessive succinylcholine dose
The ACh mobilization mechanism is impaired due to antagonism at the presynaptic Nn receptors. Since the Nn receptors don't function to mobilize ACh, there is less ACh available and the supply is exhausted quickly producing fade
30
How can succinylcholine produce a phase 2 block
1. High dose >7 - 10 mg/kg
| 2. continuous exposure >30 - 60 minutes
31
How is a phase 1 block distinguished from a phase 2 block with a nerve stimulator
There is no fade with a phase 1 block. All responses have the same intensity
32
What characteristic responses are seen with a phase 2 block
1. Fade with tetany
| 2. Prolonged duration
33
Describe how post-tetanic potentiation is affected by phase 1 block
Post-tetanic potentiation is absent
34
Describe how double burst stimulation is affected by phase 1 block
Constant but diminished response to double burst stimulation
35
Describe how post-tetanic potentiation is affected by phase 2 block
It is present unlike with a phase 1 block where it is absent
36
```
Describe the corresponding percentage of receptors still blocked with each bedside test of NMB recovery
Vt 6 mL/kg
VC >20 mL/kg
4/4 twitches w/o fade
Inspiratory force -40 cmH2O
```
Vt 6 mL/kg = 80%
VC >20 mL/kg = 70%
4/4 twitches w/o fade = 70-75%
Inspiratory force -40 cmH2O = 50%
37
What is the sequence of muscles types blocked by neuromuscular blockers
central muscles are more resistant to NMB effects and recover sooner than peripheral muscles
38
Which muscle causes eyebrow twitch
corrugator supercilii
39
Which muscle closes the eyelid
Orbicularis oculi
40
Which nerve is stimulated when assessing the corrugator supercilli and orbicularis occuli
the facial nerve (CN 7)
41
Which location is best to measure onset of block with nerve stimulation (muscle and nerve)
```
Orbicularis oculi or corrugator supercilii
Facial nerve (CN 7)
```
42
Which location is best to measure recovery of blockade with nerve stimulation (muscle and nerve)
```
M = Adductor pollicis or flexor hallucis
N = Ulnar nerve or posterior tibial
```
43
Which muscle adducts the thumb
Adductor pollicis
44
Which muscle causes big toe flexion
Flexor hallucis
45
When the adductor pollicis is stimulated with TOF, what can be assumed for recovery from NMB
The return of upper airway muscle function
46
At what ratio is residual NMB defined
TOF < 0.9
47
Patients who have inadequately recovered from NMB are at risk for 2 problems
1. Airway obstruction
| 2. Aspiration (d/t pharyngeal dysfunction)
48
What are 4 of the most sensitive bedside recovery tests for NMB recovery
What is the max percentage of occupied receptors
1. Inspiratory force -40 cmH2O
2. Head lift >5 s
3. Hand grip same as preinduction
4. Holding tongue blade against force
50% receptors occupied
49
What clinical assessment is normal with a max percentage of occupied receptors at...
80%
70%
60%
```
80% = normal Vt
70% = No TOF fade VC normal
60% = No fade with sustained tetanus or DBS
```
50
How can succinylcholine illicit bradycardia
Stimulating the M2 receptor in the SA node
| A second dose increases the risk for bradycardia or asystole
51
How can bradycardia with succinylcholine be prevented or treated
Don't repeat the dose
| Give an antimuscarinic/anticholinergic like atropine
52
How can succinylcholine cause tachycardia
It mimics ACh action at the sympathetic ganglia causing tachycardia and HTN
53
How can succinylcholine increase serum K+
Upregulation of extrajunctional nicotinic receptors increases K+ release
Hyperkalemia increases resting membrane potential and raises the risk of dysrhythmias
54
How does succinylcholine affect intraocular pressure
Transiently increases IOP 5 - 15 mmHg for 10 minutes
This can be significant in patients with an open globe injury
55
How does succinylcholine affect intracranial pressure
Temporarily increased
| Can be minimized with defasciculating dose
56
How does succinylcholine affect intragastric pressure
Causes contraction of abdominal muscles increasing intragastric pressure
It raises lower esophageal sphincter tone
These cancel each other out
57
How can succinylcholine-induced malignant hyperthermia be assessed
Increased masseter muscle tone and spasm can be an initial sign of MH
If this occurs in the absence of other MH d/dx, then there is no risk for Mh
58
What are 5 terms for the mechanism of succinylcholine metabolism.
Primary location =
1. Butyrylcholinesterase
2. Pseudocholinesterase
3. Type 2 cholinesterase
4. False cholinesterase
5. Plasma cholinesterase
Primary location = plasma
59
What are 5 terms for the mechanism of acetylcholine metabolism
Primary location =
1. Acetylcholinesterase
2. Genuine cholinesterase
3. True cholinesterase
4. Type 1 cholinesterase
5. Specific cholinesterase
Location = NMJ
60
Where is pseudocholinesterase produced
In the liver
61
How does reduced pseudocholinesterase activity affect succinylcholine
Prolongs the duration
62
Name 5 drugs that can prolong succinylcholine duration and why
1. Metoclopramide
2. Esmolol
3. Neostigmine
4. Oral contraceptives/estrogen
5. MAO inhibitors
Why = they reduce pseudocholinesterase activity
63
Name 5 conditions that can prolong succinylcholine duration and why
1. Atypical PChE
2. Severe liver disease
3. Burns
4. Neoplasm
5. Late-stage pregnancy
These conditions reduce PChE activity
64
What variant of pseudocholinesterase cannot hydrolyze succinylcholine?
What is the result?
Atypical PChE
Result = prolong succs duration
65
What is the dibucaine test
Dibucaine is an amide LA that inhibits normal plasma cholinesterase. It has no effect on atypical PChE
The number reflects the percentage of NORMAL enzyme that is inhibited by dibucaine
66
What is a normal dibucaine number and test
Normal = 80
| Dibucaine inhibits 80% of PChE
67
What is an abnormal dibucaine number and test
Atypical pseudocholinesterase is not inhibited
| Any number <70
68
What is succinylcholine duration with a dibucaine number of 50 - 60
Duration = 20 - 30 minutes
69
What is succinylcholine duration with a dibucaine number of 20 - 30
Duration = 4 - 8 hours
70
What does heterozygous PChE variant mean
The dibucaine number is 50 - 60 and succinylcholine duration can last 20 - 30 minutes
71
What does atypical homozygous PChE variant mean
the dibucaine number is 20 - 30 and succinylcholine duration is 4 - 8 hours
72
Why is Ca++ used in the treatment of hyperkalemia
Because it increases the threshold potential making action potential propagation harder to attain with the higher resting membrane potential
73
What is the most likely cause of cardiac arrest following succinylcholine administration in children <8.
Undiagnosed Duchenne Muscular Dystrophy
74
What is the treatment for hyperkalemic cardiac arrest in children who received succinylcholine
1. Stabilize myocardium
- Calcium chloride 20 mg/kg
- Calcium gluconate 60 mg/kg
2. Shift K+ into cells
- Hyperventilation
- Glucose + insulin
- Sodium bicarb
- Albuterol
3. Enhance K+ elimination
- Furosemide
- Volume resuscitation
- Hemodialysis
- Hemofiltration
75
What is the origin of myalgia following succinylcholine use
The uncoordinated muscle contraction (from depolarizing) before flaccid paralysis
76
Who is at risk for myalgias following succinylcholine
1. Young adults
2. Women > men
3. Those that don't routinely perform strenuous activity
77
What populations are at lowest risk for succinylcholine induced myalgia
Children
Elderly
Pregnant
78
What are some methods to minimize succinylcholine induced myalgias
1. Pretreat w/ nondepolarizer
2. NSAIDS
3. Lidocaine 1.5 mg/kg
4. Higher dose of succs
79
What medications do not decrease the incidence of succinylcholine induced myalgias
opioids
80
What dose of nondepolarizer can be given to minimize myalgias from succinylcholine
One-tenth of the ED95 for ND-NMBD
Rocuronium = 2 mg
Atracurium = 1.5 mg
Vecuronium = 0.3 mg
81
How is dosing for succinylcholine affected when a defasciculating dose of a nondepolarizer given
Why
Succs dose should be increased 1.5 - 2.0 mg/kg
B/c the nondepolarizer competitively antagonizes the nicotinic receptor more succs is needed to outcompete the ND
82
When should a defasciculating dose be avoided
Pre-existing skeletal muscle weakness
| Myasthenia gravis
83
Name 5 conditions that can increase the risk of succinylcholine-induced hyperkalemia
1. Guillain-Barre
2. Hyperkalemic periodic paralysis
3. Malignant hyperthermia
4. Multiple sclerosis
5. up-regulation of ACh receptors
84
Name 4 conditions that increase sensitivity to nondepolarizing NMB
1. Guillain-Barre
2. Huntington chorea
3. Multiple sclerosis
4. Myasthenia gravis
85
What are the 2 classes of nondepolarizing NMB
Benzylisoquinolinium
| Aminosteroid
86
Which nodepolarizers belong to the benzylisoquinolinium class
1. Atracurium
2. Cisatracurium
3. Micavurium
87
Which nodepolarizers belong to the aminosteroid class
1. Rocuronium
2. Vecuronium
3. Pancuronium
88
How are benzylisoquinolinium compounds metabolized
Spontaneous degradation in the plasma via Hofmann elimination or non-specific plasma esterases
89
What is the metabolite of atracurium and cisatracurium. Describe possible side effects of metabolite
Laudanosine
CNS stimulation which can produce seizures
90
Why does renal insufficiency prolong the duration of nondepolarizers
Because they are ionized and undergo renal elimination as an unchanged drug
91
Which nondepolarizers are a good choice in patients with renal or hepatic insufficiency and why
Benzylisoquinolinium class
They are degraded in the plasma and not dependent on hepatic or renal function
92
How is atracurium metabolized
33% Hofmann elimination
| 66% non-specific plasma esterase (NOT pseudocholinesterase)
93
How is cisatracurium metabolized
Hofmann elimination
94
How is mivacurium metabolized
Pseudocholinesterase (similar to succs)
95
What altered physiology affects Hofmann elimination
Alkalosis/hyperthermia = FASTER reaction
Acidosis/hypothermia = SLOWER reaction
96
What is Hofmann elimination dependent on
Blood pH
| Temperature
97
What is the primary method of rocuronium metabolism and elimination
```
Metabolism = NONE
Elimination = Biliary excretion
```
98
What is the primary method of vecuronium metabolism and elimination
```
Metabolism = Liver
Elimination = 50/50 Liver and renal
```
99
What is the primary method of pancuronium metabolism and elimination
```
Metabolism = Liver (20%)
Elimination = Renal > liver
```
100
What are the metabolites of
Rocuronium
Vecuronium
Pancuronium
```
Rocuronium = NONE
Vecuronium = 3-OH vecuronium
Pancuronium = 3-OH pancuronium
```
101
Which 2 nondepolarizing NMB don't produce a metabolite
Rocuronium
| Mivacurium
102
Which 2 nondepolarizers produce laudanosine metabolite
Atracurium
| Cisatracurium
103
Name 4 NMB that undergo organ-independent elimination
Atracurium
Cisatracurium
Mivacurium
Succinylcholine
104
Which drugs can potentiate nondepolarizing NMB
```
Volatile anesthetics
Abx
Antidysrhythmics
Local anesthetics
Diuretics
Dantrolene
Cyclosporin
Tamoxifen
Lithium
```
105
List, from greatest to least, the potentiation effect of volatile anesthetics on nondepolarizers
Des > sevo > Iso > N2O
106
Which antibiotics can prolong nondepolarizing NMB duration (5)
```
Aminoglycosides
Polymyxins
Clindamycin
Lincomycin
Tetracycline
```
107
Which antidysrhythmics can prolong nondepolarizing NMB duration (4)
Verapamil
Amlodipine
Lidocaine
Quinidine
108
How does lithium affect the duration of action for nondepolarizers
Activation of the potassium channels alters resting membrane potential
109
Which electrolytes can prolong nondepolarizer NMB duration and why
Increase Magnesium = decreases ACh release
Decreased Calcium = decreases ACh release
Decreased potassium = Decreases RMP
110
How can temperature affect the duration of nondepolarizing NMB
Hypothermia decreases metabolism and clearance
111
How does succinylcholine produce tachycardia
By stimulating the autonomic ganglia
112
Which NMB drugs release histamine
| What are the effects
Succinylcholine
Atracurium
Mivacurium
Effects = tachycardia and vasodilation
113
In which patients should histamine releasing NMB drugs be avoided
Patients who are sensitive to higher HR or reduced afterload
114
What are 3 unique CV effects of pancuronium
Vagolytic effects
1. Inhibition of M2 receptors at the SA node
2. Stimulates catecholamine release
3. Inhibits catecholamine reuptake in adrenergic nerves
115
In what condition should pancuronium be avoided and why
Hypertrophic cardiomyopathy
The anterior leaflet of the mitral valve can occlude the LVOT with forceful ventricular contraction causing systolic anterior motion (SAM). This prohibits CO through aortic valve
116
Which NMB can alter HR independent of histamine release due to autonomic effects
1. Succinylcholine
2. Pancuronium
3. Rocuronium (minimally)
117
Which NMB drug can cause tachycardia by stimulating the autonomic ganglia
Succinylcholine
118
How does the chemical structure of NMB drugs preclude this class to allergic reactions
They contain one or more antigenic quaternary ammonium group (charged), which interact with IgE causing mast cell and basophil degranulation
119
Which 2 NMB drugs have the highest incidence of anaphylaxis
Succinylcholine
| Rocuronium
120
How do AChE inhibitors increase available ACh
Indirectly allowing increased ACh concentration at the NMJ to outcompete the concentration of the NMB
121
What happens to the duration of succinylcholine if given after neostigmine
It is prolonged because neostigmine inhibits pesudocholinesterase in the plasma
122
What are the 2 mechanism AChE inhibitors increase the concentration of ACh at the NMJ
1. Enzyme inhibition
| 2. Presynaptic effects
123
How doe AChE inhibitors (reversal agents), bind to acetylcholinesterase sites
1. Electrostatic attachment
2. Formation of carbamyl ester
3. Phosphorylation
124
What interaction does neostigmine have at acetylcholinesterase site
It forms a carbamyl ester complex with the positive esteratic site (cleavage site)
125
What interaction does edrophonium have with acetylcholinesterase
1. Binds an electrostatic bond with the anionic site (holds ACh)
2. Forms a hydrogen bond with the esteratic site (cleaves ACh)
126
What are 3 examples of AChE inhibitors that form carbamyl ester inhibition
Neostigmine
Pyridostigmine
Physostigmine
127
What is an example of AChE inhibitor that forms an electrostatic attachment with acetylcholinesterase
Edrophonium
128
What are 2 possible presynaptic mechanisms of AChE inhibitor effects
1. Stimulation of presynaptic receptor, causing release of ACh
2. Inhibiting AChE near presynaptic receptor sites, increasing ACh concentration
129
```
Edrophonium
Dose =
Onset =
Duration =
Metabolism =
Elimination =
Anticholinergic =
```
```
Dose = 0.5 - 1.0 mg/kg
Onset = 1 - 2 min
Duration = 30 - 60 min
Metabolism = RENAL 75%
Elimination = LIVER 25%
Anticholinergic = Atropine
```
130
```
Neostigmine
Dose =
Onset =
Duration =
Metabolism =
Elimination =
Anticholinergic =
```
```
Dose = 0.02 - 0.07 mg/kg
Onset = 5 - 15 min
Duration = 45 - 90 min
Metabolism = Renal 50%
Elimination = Liver 50%
Anticholinergic = Glycopyrrolate
```
131
```
Pyridostigmine
Dose =
Onset =
Duration =
Metabolism =
Elimination =
Anticholinergic =
```
```
Dose = 0.1 - 0.3 mg/kg
Onset = 10 - 20 min
Duration = 60 - 120 min
Metabolism = Renal 75%
Elimination = Liver 35%
Anticholinergic = glycopyrrolate
```
132
How are cholinergic side effects reduced when giving AChE inhibitors
Administer anticholinergic drug before AChE inhibitor
133
How does renal failure affect duration of AChE inhibiors
It prolongs the duration of the reversal agent AND NMB
134
What effect do AChE inhibitors have when the dose administered exceeds the dose required for reversal
There is a ceiling effect and dose not produce a better recovery from paralytic
135
How does the degree of neuromuscular blockade affect the onset of AChE inhibitors
The deeper the block the longer the onset time for the reversal agent
136
What type of effect occurs when AChE inhibitors are mixed
ADDITIVE effect (not synergistic)
137
Which AChE inhibitors pass through the BBB and why
Physostigmine passes through the BBB because it is a tertiary amine
138
Which AChE inhibitors do NOT pass through the BBB and why
Edrophonium, neostigmine, pyridostigmine
They are quaternary amines (+ charge)
139
At what TOF ratio is risk of airway obstruction, hypoxemic events, and postop pulmonary complications increased
TOF < 0.9
140
What use and effect does intrathecal neostigmine ellicit
Produces analgesia
Side Effects = N/V, pruritus, prolonged sensory and motor block
141
In addition to physostigmine's reversal effects, what postoperative benefits does it have
When dosed at 40 mcg/kg, it reduces the incidence of postop shivering
142
List 4 drugs that reduce the incidence of shivering in the PACU
1. Meperidine
2. Clonidine
3. Dexmedetomidine
4. Physostigmine
143
Which 2 AChE inhibitors are best paired with glycopyrrolate
Neostigmine
| Pyridostigmine
144
Which AChE inhibitor has a tertiary amine structure
Physostigmine
145
What type of effects are elicited from increased ACh concentration
Parasympathetic side effects
146
List 9 parasympathetic side effects of AChE inhibitors
DUMBBELLS
1. Diarrhea
2. Urination
3. Miosis
4. Bradycardia
5. Bronchoconstriction
6. Emesis
7. Lacrimation
8. Laxation
9. Salivation
147
What class of drugs are reversal agents (3)
1. Acetylcholinesterase inhibitors
2. Cholinergics
3. Muscarinics
148
What class of drugs antagonize the effects of reversal agents (2)
1. Anticholinergics
| 2. Muscarinic antagonists
149
Which muscarinic antagonist increases HR the most
Atropine > glycopyrrolate > scopolamine
150
Describe the sedating effects of the following anticholinergics
Atropine
Scopolamine
Glycopyrrolate
```
Atropine = minimal
Scopolamine = Greatest sedative
Glycopyrrolate = non-sedating
```
151
From greatest to least, compare the antisialagogue effect of atropine, glycopyrrolate and scopolamine
Scopolamine > Glyco > atropine
152
From greatest to least, compare the antiemetic effects of atropine, glycopyrrolate, and scopolamine
Scop > Atropine
| glyco has no antiemetic effects
153
Describe the effects of muscarinic agents on pupil diameter
Antimuscarinics cause dilated pupils (mydriasis)
Scop produces mydriasis greater than atropine
Glyco has no dilating effects
154
How does the structure of atropine and scopolamine compare to glycopyrrolate
Atropine/Scop = tertiary amine
Glyco = quaternary ammonium (ionized)
155
How does the differing structure between atropine/scopolamine vs glycopyrrolate have on each drugs effect
Atropine/Scop:
Lipophilic, non-ionized
Cross lipid membrane i.e. placenta, GI tract, and BBB causing CNS side effects
Glyco:
Ionized, limited ability to cross membranes
No CNS or placental effect
156
What effect do antimuscarinics have on patients with a heart transplant
The heart is denervated so there is no effect on the patients HR
they do still have other cholinergic effects from AChE inhibitors and should receive antimuscarinics
157
Describe the structure of sugammadex
Gamma-cyclodextrin made up of eight sugars assembled in a ring
158
Which NMB does sugammadex have NO effect on
Succinylcholine
| Benzylisoquinolines (atracurium, cisatracurium, mivacurium)
159
What is the mechanism of action for sugammadex
The ring structure encapsulates the NMB making it inactive and unable to engage at the nicotinic receptor
160
How does sugammadex augment NMB transfer from the NMJ to the plasma
by encapsulating NMB the free concentration is reduced. The concentration gradient between the NMJ and plasma is increased increasing NMB transfer away from the NMJ
161
From greatest to least, compare the affinity of sugammadex to vecuronium, pancuronium, and rocuronium
Rocuronium > vecuronium > pancuronium
162
How is the sugammadex-NMB complex excreted
Unchanged via the kidneys
163
What is the dosing for sugammadex
TOF 2+/4 = 2 mg/kg
TOF 0+/4 = 4 mg/kg
Immediately after Roc 1.2 mg/kg dosing = 16 mg/kg
164
What are the options for re-paralysis if sugammadex <4 mg/kg has been given in the last 24 hours
1. If it's between 5 min and 4 hrs of dosing, re-administer rocuronium at 1.2 mg/kg
2. If it has been >4 hrs, rocuronium 0.6 mg/kg or vecuronium at 0.1 mg/kg
165
If >16 mg/kg of sugammadex has been used within 24 hours and a patient requires re-paralysis, which drug is the best choice.
Benzylisoquinolinium (non-aminosteroid)
- Cisatracurium
- Atracurium
- Mivacurium
Succinylcholine
166
What are 3 risks associated with sugammadex
1. Anaphylaxis (0.3% of pts)
2. Bradycardia and arrest
3. Reduced oral contraceptive effectiveness for <7 days
