Nmba Flashcards
(149 cards)
1
Q
What is the structure of succinylcholine?
A
2 joined Ach molecules
2
Q
What is the dosage of succinylcholine ?
A
1-1.5 mg/kg
3
Q
What is the intubating dose of suc if you use a defasciculating dose of roc?
A
1.5-2 mg/kg
4
Q
What is the defasciculating dose of roc?
A
0.03mg/kg
5
Q
How is succinylcholine metabolized?
A
By pseudocholinesterases
6
Q
How long can paralysis last in someone homozygous for pseudocholinesterase deficiency?
A
3-8 hours
7
Q
How can you tell if they have pseudocholinesterase deficiency?
A
Dibucaine inhibits normal pseudocholinesterase by 80% but only 20% in abnormal
8
Q
What drug prolongs neuromuscular blockade?
A
Cyclosporine (has solvent polyethoxylated castor oil) Aminoglycosides Tetracyclines Polymixin Clindamycin
9
Q
What drug prolongs the action of succinylcholine?
A
Echothiophate
10
Q
How does Echothiophate prolong succinylcholine ?
A
By inhibiting pseudocholinesterase
Can cause 95% decrease in plasma butyrylcholinesterase for 4-6 weeks after stopping the drug
11
Q
What is Echothiophate?
A
A topical eye medication for glaucoma- an acetylcholinesterase inhibitor
12
Q
How do all neuromuscular blocking agents work?
A
They are quaternary ammonium compounds with a positively charged nitrogen that has an affinity for the nicotinic receptors
13
Q
What is a phase I block?
A
When a depolarizing muscle blocker is bound to Ach receptors the perijunctional voltage gated Na channels close after a certain amount of time so you get the initial excitation (propagation of signal via the sodium channels and then release of calcium from the sarcoplasmic reticulum) and then the sodium channel closes again. The endplate cannot repolarize while the muscle blocker is bound to the Ach receptors
14
Q
How do nondepolarizing muscle relaxants work?
A
Competitive antagonism
They do not produce a conformational change for ion channel opening
15
Q
What are the two subunits on the neuromuscular Ach receptors that bind acetylcholine?
A
Two identical alpha subunits
16
Q
How many binding sites have to be occupied by acetylcholine to elicit a conformational change?
A
The 2 alpha subunits
17
Q
What is the difference in the fetal form of Ach receptor?
A
It has a gamma unit instead of epsilon
Low channel conductance
18
Q
What happens in conditions of chronically decreased acetylcholine release?
A
More expression of the extrajudicial all Ach receptor.
19
Q
Why do states with more extrajunctional receptors have prolonged blockade with depolarizing muscle relaxants?
A
Because there are more receptors being depolarized
20
Q
What is the sensitivity of neuromuscular blockade in myasthenia gravis.
A
A resistance to depolarizing relaxants (because there are fewer receptors)
Increased sensitivity to nondepolarizing relaxants (only takes one subunit to bind to cause muscle relaxation)
21
Q
What are other ways of causing neuromuscular blockade?
A
Channel blockade
22
Q
What drugs may cause channel blockade?
A
Neostigmine
Antibiotics
Cocaine
Quinidine
23
Q
What is sugammadex
A
A cyclodextrin that binds tightly in a 1:1 ratio with steroidal nondepolarizing agents (roc, vec)
24
Q
How much current should a peripheral nerve monitor be able to create for muscle contraction?
A
50 mA across 1000 ohm load
25
How long is the stimulus of a peripheral nerve monitor?
200 nanoseconds
26
What is the train of four stimulation?
Four successive 200 nanosecond stimuli in 2 seconds
27
What happens to the train of four as the block increases?
Train of four decreases
28
How much block do you after disappearance of the fourth twitch (3)?
75%
29
How much block do you have after disappearance of the third twitch? (Two twitches)
80%
30
How much block do you have with disappearance of the second twitch?
90%
31
How much block does clinical relaxation require?
75-95% so 1-3 twitches
32
What is tetany a test of?
Neuromuscular function
33
What is double burst more sensitive than?
More sensitive than train of four for fade
34
What does 5 second tetany indicate?
Adequate but not full reversal
35
What muscles recover faster than adductor pollicis?
Diaphragm
Rectus abdominis
Laryngeal adductors
Orbicularis ocular
36
What is tetany
A sustained stimulus 50-100 Hz usually lasting 5 seconds
37
What is fade indicative of?
A nondepolarizing block (phase 2 block)
38
What does the absence of fade indicate?
Adequate clinical recovery
39
What is fade due to?
Prejunctional effect of NMBs that reduces the amount of acetylcholine available for release (the higher the calcium influx, the more quanta of Ach released - nondepolarizing agents don't allow for influx)
40
What is posttetanic potentiation?
The ability of theta if stimulation to increase the evoked response to a subsequent twitch during a partial nondepolarizing block
41
Why is post-tetanic potentiation possible?
Transient increase in Ach mobilization due to tetany
42
What is the lipid solubility of succinylcholine
Low
43
How does succinylcholine stop working?
It diffuses away from the membrane and gets broken done by pseudocholinesterase
44
What does hypothermia due to succinylcholine metabolism?
Decreases the rate of its hydrolysis so prolongs its action
45
In what conditions are there reduced levels of pseudocholinesterase?
Pregnancy
Liver disease
Renal failure
46
What is dibucaine
A local anesthetic that inhibits normal pseudocholinesterase by 80%
47
Why is dibucaine used to test for pseudocholinesterase deficiency?
Because abnormal pseudocholinesterase is only inhibited 20% by dibucaine as opposed to normal which is 80%
48
What is a normal dibucaine number?
80
49
How long will a heterozygote of pseudocholinesterase deficiency have a block from succinylcholine
20-30 minutes
50
How long will a homozygous of pseudocholinesterase deficiency have a block from succinylcholine
4-8 hours
51
How do acetylcholinesterase inhibitors prolong depolarizing blockade?
1. Inhibit acetylcholinesterase so that more acetylcholine is in the junction causing more polarization
2. Reduce hydrolysis of succinylcholine by inhibiting pseudocholinesterase
52
How do nondepolarizing agents antagonize a phase 1 block?
They occupy some acetylcholine receptors
53
Why do children require higher doses of succinylcholine?
Because they have a larger extra cellular space than adults and succinylcholine is not lipid soluble
54
Why isn't succinylcholine used in children?
May cause a systole in children with undiagnosed myopathies or prolonged paralysis
55
Where does succinylcholine work?
At ALL acetylcholine receptors
56
What are the CV effects of succinylcholine in children?
Profound bradycardia
57
What are the CV effects of low dose succinylcholine in an adult?
Negative chronograph and inotropy due to stimulation of parasympathetic ganglia to SA node
58
What are the CV effects of high dose succinylcholine in an adult?
Increased heart rate and contractility
Increased catecholamines
Due to SNS stimulation in Heart
59
What may happen to heart rate in an adult after second dose of succinylcholine?
Bradycardia due to succinylmonocholine (hydrolyzed succinylcholine) sensitization of muscarinic cholinergic receptors in the heart
60
How long after a spinal cord or burn injury can you use succinylcholine before it becomes unsafe?
24 hours
61
Why is using succinylcholine unsafe in burn or spinal cord patients?
Because of hyperkalemia cardiac arrest refractory to treatment
62
When is the risk of hyperkalemia the highest after injury?
7-10 days
63
How do you prevent myalgia from succinylcholine?
Pretreatment with 0.06 mg/kg - 0.1 mg/kg of or uranium
64
How do you treat myalgias
NSAID
65
How does succinylcholine increase intraocular pressure?
Extra ocular muscles have more motor end-plates on each cell
66
What is a premonitory sign of malignant hyperthermia?
Increased tone of the masseter muscle preventing malignant hyperthermia
67
Can you give succinylcholine to someone with NMS
Yes
68
What does succinylcholine do to CBF?
Increases it
69
What does succinylcholine do to ICP?
Increases it
70
Is succinylcholine contraindicated in patients with hig ICP?
No
71
How can increased ICP with succinylcholine be avoided?
Pretreatment with rocuronium and lidocaine
| Hyperventilating
72
Which nondepolarizing muscle relaxant is vagolytic?
Pancuronium
73
What kind of nondepolarizing agents cause histamine release ?
Benzylisoquinolones (atracurium, gantacurium)
74
What is the purpose of a priming dose?
To produce intubating conditions within 60-90 seconds
75
What is the dose of a priming dose?
10-15% of the usual intubating dose
76
How much do volatile agents decrease nondepolarizing dosage requirements?
By at least 15%
77
Do the newer nondepolarizing agents affect the autonomic systems?
No
78
Which nondepolarizing agents are metabolized significantly by the liver?
Pancuronium and vecuronium
79
Which 2 nondepolarizing agents are excreted via the biliary system?
Roc and vec
80
Which 2 nondepolarizing agents have prolonged effect in liver failure?
Pancuronium and rocuronium
81
Which nondepolarizing agents are excreted by the kidney?
Pancuronium
Vecuronium
Doxacurium
Pipecurium
82
How does hypothermia prolong blockade?
By decreasing metabolism and excretion
83
How does respiratory acidosis affect nondepolarizing blockade?
Prolongs it and antagonizes its reversal
84
How does hypermagnesemia affect nondepolarizing blockade?
Prolongs it because mg competes with calcium at the motor end plate
85
How does hypokalemia and hypocalcemia affect nondepolarizing blockade?
Increases the block
86
What is special about vec in the pediatric population?
Longer acting in neonate X
87
Which nondepolarizing agent is not prolonged in the elderly?
Cisatracurium
88
What do you have to do to the dosage of nondepolarizing agents in the obese population?
Increase by 20% of lean body weight
89
What kind of nondepolarizing agent is atracurium?
Benzylisoquinolone
90
How is atracurium metabolized?
Ester hydrolysis and spontaneous chemical breakdown (Hoffman elimination)
91
What is the intubating dose of atracurium?
0.5mg/kg
92
What are the side effects of atracurium?
Bronchospasm
Transient drop in SVR and increase in CO
Seizure (laudanosine toxicity)
Anaphylaxis (acrylate immune activation)
93
What is laudanosine toxicity?
It is a tertiary amine that is a breakdown product of atracurium which causes CNS excitation
94
What happens to atracurium if you run it with lidocaine or thiopental?
It will precipitate as a free acid because those are bases
95
What is acrylate?
Metabolite of atracurium that can cause anaphylaxis
96
What is cisatracurium?
A stereoisomers of atracurium that is 4 times more potent
97
How is cisatracurium metabolized?
Hoffman elimination only
98
What is the intubating dose of cisatracurium?
0.1-0.15 mg/kg within 2 minutes
99
What does pancuronium look like?
Steroid ring with two modified Ach molecules
It resembles Ach enough to bind the nicotinic receptor but not activate it
100
How is pancuronium metabolized?
By the liver
101
How is pancuronium excreted?
Renally
102
What is the induction dose of pancuronium?
.08-.12 mg/kg
103
What are the side effects of pancuronium?
Vagolytic - tachycardia
SNS stimulation - HTN
Arrhythmias due increased catecholamines and decreased uptake
104
What drugs should pancuronium not be used with and why?
Halothane and TCAs because of ventricular arrhythmias
105
What allergy should you avoid using pancuronium with?
Bromide
106
How long does pancuronium last?
60-120 minutes
107
How is vecuronium metabolized?
Liver a little
| But then excreted in biliary and renal systems
108
What is vecuronium linked to in ICU?
Polyneuropathy from prolonged blockade
109
What is the intubating dose of vecuronium?
0.08-0.12 mg/kg
110
What is interesting about women and men with vecuronium?
Women are 30% more sensitive than men (greater and longer blockade) same with roc and pan
111
What changes about the dosage of vec in the anhepatic phase of liver transplantation?
They are reduced
112
How is rocuronium metabolized?
It's not
113
How is roc eliminate?
Primarily by liver through the biliary system
114
What conditions prolong roc?
Liver disease
| Pregnancy
115
What kind of nondepolarizing agents are pan, roc, and vec?
Steroids
116
What is the intubating dose of rocuronium?
0.6-1.2 mg/kg
117
What is gantacurium?
A nondepolarizing agent that has a ultra short duration of action and comes in a powder
118
How is gantacurium metabolized?
Ester hydrolysis
| Cysteine adduction
119
What ion is responsible for neuron depolarization?
Sodium influx
120
What does sodium influx into a neuron lead to in the nerve terminal?
Calcium influx in the nerve terminal
121
What does influx of calcium do at the nerve terminal?
Facilitates the release of Ach molecules out of the presynaptic nerve into the NMJ
122
What do the Ach molecules in the NMJ do?
Bind nicotinic Ach receptors on the motor end plate which depolarizers the muscle
123
What is the titanic fade due to?
Blockade of pre-junctional receptors
Due to blocking of the positive feedback system (normally release more acetylcholine in response to stimulation, but cannot when blocked by NMB)
124
How should succinylcholine be dosed?
Using TBW
125
How should NMBs be dosed?
IBW or LBW
126
How much reversal should be given for a phase II block from succinylcholine?
0.03 mg/kg
127
Why must the minimum amount of neostigmine be used to reverse a patient with pseudocholinesterase deficiency?
Because neostigmine inhibits pseudocholinesterase as well and at higher doses will do this which will prolong blockade cause by succinylcholine and acetylcholinesterase inhibition
128
What does phenytoin do to NMBs?
Enhances the blockade if acute
| Chronically reduces duration of blockade action
129
What does a phase II block mean?
Means the postjunctional membrane has become repolarized, but it is desensitized to acetylcholine
130
How would you reverse succinylcholine apnea in a patient with abnormal pseudocholinesterase?
Low dose neostigmine after phase II blocks occurs
- low dose because neostigmine preferentially inhibits acetylcholinesterase, but higher dose inhibits pseudocholinesterase which would impair metabolism of sux even further
131
What is the dosage of sugammadex for routine reversal?
2 mg/kg of actual body weight
132
How much sugammadex for no twitches?
4 mg/kg
133
What is the dosage of sugammadex for immediate reversal aft RSI dose of roc?
16 mg/kg
134
What is the advantage of double burst stimulation of train of four?
It allows better tactile and visual assessment of neuromuscular blockade
135
What are the clinical signs of a TOF ratio greater than 0.7?
```
Head lift greater than 5 seconds
Leg lift
Hand grip
Tidal volume of 15-20ml/kg
Effective cough
Negative inspiratory pressure of -25 cmH2O
```
136
What side effect of succinylcholine cannot be blunted with a defasciculating dose of roc?
Increased IOP
137
How much does IOP increase with succinylcholine?
5-15 mm Hg
138
What does carbamazepine do to P450?
Induces it so it may cause decrease NMB by vec, roc
139
How do amino glycosides prolong the NMB?
Inhibit the release of acetylcholine from alpha motor neurons
140
How does clindamycin prolong NMB?
Prevents prejunctionsl release of Ach and decreases postjunctional nicotinic Ach receptors to Ach
141
How do tetracyclines prolong NMB?
Postjunctional inhibitor
142
How does cyclophosphamide affect NMB?
It is a pseudocholinesterase inhibitor so causes prolonged apnea after succinylcholine administration
143
How long do the anti-pseudocholinesterase activities of cyclophosphamide last?
3-4 weeks after administration
144
Which volatile augments NMB the most?
Desflurane
145
What drugs potentiate NMBs?
```
Aminoglycosides
Tetracyclines
Clindamycin
Lincomycin
Polymixin
Volatile
Lithium
Anticonvulsant
```
146
Which volatile potentiates NMB the most?
Desflurane
147
How is gantacurium metabolized?
Ester hydrolysis
148
How is gantacurium inactivated?
By L-cysteine which replaces a chlorine atom
149
Which NMB has an active metabolite?
Vecuronium
| Metabolite = 3-desacetyl and has 80% activity, can accumulate in renal disease
