NMBAs Flashcards
(258 cards)
1
Q
Do muscle relaxants provide amnesia?
A
NO
2
Q
Neuromuscular junction consists of:
A
-Prejunctional: motor nerve ending
-cleft: AChAse
-Postjunctional: Highly folded muscle fiber
3
Q
what causes a muscle contraction?
A
-ACh binds to nicotinic cholinergic receptor (postsynaptic)
4
Q
Nerve stimulation
A
-Depolarization reaches nerve terminal
-voltage-gated Ca channels open
-calcium enters the nerve terminal
-Storage quanta Vesicles (presynaptic) release acetylcholine (ACh) into the cleft
-ACh diffuses cleft
-ACh binds to nicotinic cholinergic receptor at postsyn. end plate
-muscle contraction
5
Q
each quanta contains ____ ACh molecules
A
5,000 to 10,000
6
Q
⭐️
Which subunits do NMBs work on?
A
the 2 alpha subunits
7
Q
Only ___ subunits are capable of binding ACh
A
the 2 alpha
8
Q
If both the alpha subunits are occupied, what happens?
A
conformational change
central channel opens
9
Q
What ions enter and exit when the 2 alpha subunits are occupied?
A
Na & Ca in
K out
10
Q
____ occurs, and a muscle contraction happens
A
action potential
11
Q
Postjunctional receptors have ___ subunits
A
5
2 alpha, 1 beta, 1 delta, and 1 epsilon (ADULT)
12
Q
How many ACh molecules are needed to open the post jxnl receptor channel?
A
TWO
one or none = closed
13
Q
causes vesicles of acetylcholine to fuse with the nerve membrane
A
influx of calcium within the terminal
14
Q
ACh combines with and activates which receptor?
A
nicotinic receptors on motor end plate
15
Q
release of ___ from intracellular stores stimulates an interaction between __ and ___. This results in a muscle contraction.
A
Ca
myosin
actin
16
Q
Why do we use muscle relaxants?
A
-Optimize surgical conditions
-Prevent unwanted movement
-Facilitate tracheal intubation **
-Improve mechanical ventilation
17
Q
The primary purpose of using NMB is to
A
achieve adequate relaxation of the upper airway, vocal cords, and diaphragm to facilitate intubation and surgery
18
Q
Prolonged opening and increased ion flow (Hyperkalemia) can occur with (up/down) regulation.
A
up
19
Q
Increased Extrajunctional Receptors
(up regulation or down?)
A
upregulation
20
Q
Upregulation
A
stimulation of NMJ decreases over days (severe burns, immobilization, infxn, sepsis, prolonged use of NMBAs in ICU, CVAs)
increased immature nAChrs
21
Q
immature nAChRs will have increased sensitivity to ____ but decreased sensitivity to ___.
A
-increased sensitivity to ACh and SCh (more nACHr’s being depolarized)
-decreased sensitivity to Nondepolarizers (more nACHr’s to block
22
Q
Chronic neostigmine use will affect jxnl receptors by…
A
downregulating them
23
Q
Pts w/ myasthenia gravis may experience (up/down) regulation due to chronic neostigmine use.
A
down-regulation
(Neostigmine: cholinesterase inhibitor; increases ACh levels at nerve terminals)
24
Q
T/F
NMBAs are anesthetics
A
NO
not anesthetics
do not cause amnesia
25
Which causes awareness?
NMBA
not enough anesthesia
not enough anesthesia
26
T/F
Complete paralysis is required for all surgical cases
false
27
⭐️
Main site of action of NMBA
nicotinic cholinergic receptor (nAChRs)
at the endplate, which connects to the muscle
28
T/F
Neuromuscular Blocking Agents is synonymous with paralytic.
True
29
Most poisonous creature on planet
Golden Poison Frog
30
T/F
Paralytics exist in nature.
True
pufferfish
Golden Poison Frog
31
all 4 twitches will be full-strength if...
No muscle relaxation
32
With muscle relaxation....
there will be decreased strength
33
depolarizer or non?
depolarizer block
34
depolarizer or non?
non-depolarizer block
35
Which NMBAs show fade?
non-depolarizers
36
Potency
the relationship between twitch depression and dose
37
median dose that corresponds to 50% twitch reduction (among average population)
ED50
38
ED95
corresponds to 95% block (useful relaxation when twitch abolished)
39
Do we use ED50 or ED95 more when deciding doses for NMBAs?
ED95
we want what will get pt adequately paralyzed, full relaxed
40
Duration of Action
Time of injection to return of ___% twitch height
25 or 1 twitch (1 twitch out of 4 twitches)
41
T/F
Duration of action is dose-dependent
True
42
T/F
Inhalational agents & NMBAs have a synergistic effect.
True
IA can prolong NMB duration
43
Recovery Index
Time interval between 25% and 75% twitch height
Speed of recovery
44
Only depolarizing agent
Succinylcholine
45
Depolarizing a muscle actually ____ it and keeps it in a relaxed state.
fatigues
46
Succinylcholine
“Depolarizes” at postsynaptic nAChRs
47
Nondepolarizing
"Competes” for active binding sites on nAChRs
Aminosteroid (Rocuronium, Vecuronium, Pancuronium)
Benzylisoquinolinium (Mivacurium, Atracurium, Cisatracurium)
48
How does depolarizing NMB work?
Depolarizes:
**occupies 2 alpha subunits**
**opens channel**
ions in
depolarizes muscles
muscle is fatigued
stays in relaxed state
49
How does non-depolarizing NMB work?
competes for nicotinic sites
**binds to 1 alpha subunit**
**prevents opening**
muscle cannot contract
50
Mimics ACh
depolarizing/succinylcholine
51
Prolonged depolarization of the motor end-plate will....
inactivate Na channels
increases influx of K
52
Can a muscle contract while ACh is bound to the receptor?
No
can only contract once it diffuses off receptor
53
What is the resemblance between ACh and Suxx?
Suxx = two ACh molecules
allows Suxx to sit on top of receptor and bind two alpha subunits
54
When given may cause fasciculations before total paralysis
Succinylcholine
55
⭐️
Succinylcholine dosing (adult)
1 -1.5 mg/kg IV
56
Succinylcholine onset
1 min
57
Succinylcholine duration
5-15 mins
58
T/F
We can achieve paralysis even if one of the alpha subunits is occupied by succinylcholine and the other by ACh.
True
Both alpha subunits must be occupied, can be 1 ACh and 1 suxx; or both occupied by suxx
59
fastest onset, the shortest duration, and greatest reliability (i.e., narrowest onset variability around the mean) of any NMBA
Succinylcholine
60
All NMBAs interact with ____ and block muscle membrane ____, leading to ___ paralysis.
α subunits of the nicotinic cholinergic receptors
depolarization
flaccid
61
reversal of ____ block is limited
nondepolarizing
(cholinesterase inhibitors have a ceiling effect)
62
___% of the IV dose of Suxx is hydrolyzed in the plasma before reaching the myoneural junction.
90
plasma cholinesterase eats it up before it gets to the receptor
63
pseudocholinesterase breaks suxx into...
succinylmonocholine and choline
64
Recovery from suxx occurs when...
SCh diffuses away from the NMJ
5-6 mins
SCh = succinylcholine
65
____% of administered suxx reaches the NMJ
10%
66
Plasmacholinesterase is also called:
Butyrylcholinesterase
Pseudocholinesterase
67
Factors that lower pseudocholinesterase
severe liver disease
old
pregnancy
malnutrition
burns
anticholinesterase drugs
Reglan
oral contraceptives
68
Plasmacholinesterase
Synthesized in the ___ and found in the ___.
liver
plasma
69
Which drug decreases plasma cholinesterase (PChE) activity more?
Edrophonium
neostigmine
neostigmine
70
Abnormal Plasma Cholinesterase testing
Dibucaine number
reflects **quality** of cholinesterase enzyme (ability to hydrolyze SCh) not the quantity that is circulating in plasma
71
T/F
Dibucaine number reflects quantity of cholinesterase enzyme
False
quality (ability to hydrolyze SCh)
72
Lower dibucaine numbers mean (shorter/longer) duration of drug action.
longer
73
How do anesthesia providers usually determine that their pt has abnormal PChE (plasma cholinesterase)?
On the spot. The patient will not recover from paralytic. Twitches not returning when expected.
Will have to recover in ICU
74
Which type of PChE are we most concerned with?
-homozy. typical
-heterozy. atypical
-homozy. atypical
homozygous atypical
both genes are mutated
75
T/F
Succinylcholine can be given as an infusion.
False
Will cause Phase II block
76
What causes Phase II block?
(Suxx)
continued dosing, a phase I block can develop into a phase II block
77
⭐️
T/F
Succinylcholine is an antagonist, making it a paralytic.
False
NMJ nicotinic AGONIST
78
Succinylcholine prevents (depolarization/repolarization).
repolarization
79
Phase II block
(Repeated SCh doses or an IV continuous infusion)
muscles are **no longer receptive to acetylcholine released by the motor neurons**
"I'm phase 2 faded"
80
Suxx
CV effects
Sinus bradycardia
junctional
arrest (esp peds)
81
When giving suxx to kids, mix it with ____.
atropine
82
Suxx
if a second dose is given within 5 minutes of first dose, we increase the risk of...
cardiac arrest
83
CV effects of suxx are due to...
its action @ **cardiac muscarinic cholinergic (M2)** receptors
mimics ACh
84
Preventing myalgias from SChE (suxx)
pretreat with non-depolarizer or NSAIDs
85
SChE myalgias are usually due to _____, and affect ____ muscles.
fasciculations
big skeletal muscles
86
SCh can elevate plasma potassium by ___ mEq/dL in healthy patients.
0.5
caution in renal pts (K already high)
87
Conditions to avoid SChE
renal Dz
burns
severe abdominal Infections
severe metabolic acidosis
upregulation of AChR
hemiplegia, paraplegia, muscular dystrophies, Guillian-Barre syndrome
88
Which paralytic should we avoid in a pt with a recent diagnosis of Guillian-Barre syndrome?
SChE (suxx)
89
Conditions associated with upregulation of extrajunctional AChR
hemiplegia
paraplegia
muscular dystrophies
Guillian-Barre syndrome
burns
90
Succinylcholine risk specific to children
massive rhabdomyolysis --> renal failure
91
Which paralytic is better for children?
succinylcholine
rocuronium
rocuronium
suxx risks:
-asystole
-hyperK
-massive rhabdomyolysis --> renal failure
92
Which paralytic is associated w/ MH?
SchE
93
Primary sign of MH
Masseter/jaw spasm
Jaw will lock up
cannot scissor jaw open
94
Best NMB for full stomach
Suxx
Increases intragastric pressure
**increases lower esophageal tone (LES)** helps prevent vomitus entering airway
95
NMB to avoid in open eye injury
Suxx
increases IOP
96
SChE (increases/decreases) ICP.
increases
97
Malignant Hyperthermia triggers
halogenated agents & succinylcholine
Activates Ryanodine receptor from the sarcoplasmic reticulum
98
Malignant Hyperthermia
-Massive uncontrolled release of Ca++ from the sarcoplasmic reticulum
-activates uncontrolled – constant (hypermetabolic) muscle contraction state
99
T/F
ACh is more competitive and more easily bound to alpha subunits than non-depolarizing NMB.
False
NDNMB are more competitive than ACh
can push ACh off receptors
100
T/F
Non-depNMB only need to occupy one of the alpa subunits to elicit their paralytic effect.
True
2 NDNMB = closed
1 NDNMB + ACh = closed
2 ACh = open
101
Classes of Non-depolarizing muscle relaxant (NDMR)
**Aminosteroid**
(Rocuronium, Vecuronium, Pancuronium)
**Benzylisoquinolinium**
(Mivacurium, Atracurium, Cisatracurium)
102
Know dis
-dose
-onset
-duration
103
Nondepolarizing Muscle Relaxants
MoA
Competitively **antagonize** the presynaptic receptors (one or both alpha subunits) to decrease release of Ach (fade on TO4)
104
Depolarizing NMB are ____.
Non-depolarizaing are ____.
(agonist/antagonist)
Depo = agonIst
non-depo = competitive antagonist
(Every home DEPO has a mansplainer, who thinks he's some AGONIST to women)
105
Almost always given IV
NonDepoMB
106
Rocuronium (Zemuron) is ____ acting.
intermediate
107
T/F
Rocuronium (Zemuron) is know to cause histamine release.
True
rare tho
108
Rocuronium (Zemuron)
CV effects
no effect of BP or HR
109
Using Rocuronium with suxx
use rocuronium to defasciculate
110
Rocuronium is (high/low) potency.
low
takes more molecules for effect
111
Rocuronium
intubating dose
0.6 mg/kg
112
Rocuronium
RSI dose
1.2 mg/kg
113
Rocuronium
defiscic dose
5 mg
114
Rocuronium
maintenance/repeat dosing
0.1 mg/kg PRN
115
Rocuronium
onset
1-2 mins (dose-dependent)
116
Rocuronium
duration
30 min or up to 70 minutes after RSI dose
117
Rocuronium elimination
___% hepatic
___% renal
70% liver
30% renal
118
Best NMB for short laparoscopic procedures
Rocuronium
119
Has greatest assoc. w/ anaphylaxis than any other drug given in anesthesia
Rocuronium
(stats could be inflated b/c we give rocuronium A LOT)
120
T/F
We must be aware of active metabolites with Rocuronium.
False
no real metabolites
121
Vecuronium (Norcuron) benefits
No histamine release
Cardiac stable
122
Vecuronium (Norcuron) is ___ potency
medium
123
Vecuronium (Norcuron) is ____ acting.
intermediate
124
Vecuronium (Norcuron) precipitates with ____.
thiopental
125
Vecuronium (Norcuron)
induction/intubation dose
0.1 mg/kg
126
Vecuronium
Pretreatment/priming with ___% of intubation dose given ___ min before intubation dose.
10%
3-5 min
127
Which NMB agent do we see pre-dosing before intubation?
Vecuronium
onset of action is longer than rocuronium
128
Vecuronium
recovery
25-40 min (25% recovery)
45-60 min(95% recovery)
129
Vecuronium metabolite has ___% potency of parent drug.
(3-desacetyl): 60% potency of vecuronium
130
What's unique about a patient's response to Vecuronium?
same dose will give same, predictable duration of action (on that given day, may change next day)
131
Pancuronium (Pavulon)
initial dose
0.1 mg/kg
132
longest acting aminosteroid NMB
Pancuronium (Pavulon)
133
Pancuronium (Pavulon)
CV effects
Vagolytic effects: modest tachycardia due to M2 antimuscarinic stimulation
Direct sympathomimetic effects: norepine release and reduced uptake of norepinephrine by adrenergic nerves
134
T/F
Histamine release occurs with Pancuronium.
False
135
T/F
Pancuronium increases HR and CO.
True
136
Used in Cardiac surgery to counteract the bradycardia associated with high-dose opioid dosing
Pancuronium
137
Potential for significant postoperative residual blockade
Pancuronium
very long acting
138
Pancuronium
Maintenance dose
0.02 mg/kg
139
Pancuronium
onset
2-5 min
140
Pancuronium
duration
60-100 min
141
T/F
Pancuronium is mostly metabolized by the liver
False
Hepatic metabolism 20%
Urinary excretion (40-70%)
142
Pancuronium metabolite
(3-OH pancuronium): 50% potency
143
NMB best for renal and liver Dz
Benzylisoquinolines
144
Potency: relationship between ____ ___ and dose.
twitch depression
145
ED50
median dose that corresponds to 50% twitch reduction
146
ED95
corresponds to 95% block (useful relaxation when twitch abolished)
147
Undergoes Hoffman elimination
Benzylisoquinolines
148
Hofmann Elimination
Spontaneous, non-enzymatic, non-organ dependent chemical breakdown at physiologic temperature and pH
149
____ increases Hofmann Elimination.
Increased Temp = increased Hoff Elim
150
Beware of histamine release, esp if giving quickly
Mivacurium (Mivacron)
151
Mivacurium (Mivacron)
recovery
rapid
152
Mivacurium (Mivacron)
metabolism
Hydrolysis by plasma cholinesterase
153
Atracurium metabolism is by the same enzymes that degrade ___ and ___.
esmolol and remifentanil
154
Mivacurium (Mivacron)
onset
1 min
| "MIV only takes a MIN!"
155
Mivacurium (Mivacron)
duration
10-20 min
156
Mivacurium (Mivacron)
intubation dose
0.2 mg/kg
157
Mivacurium (Mivacron)
infusion dose
5-8 mcg/kg/min infusion
158
Atracurium (Tracrium) is ____ acting.
intermed
159
Atracurium (Tracrium)
metab
Hofmann Elimination 30% and ester hydrolysis 60%
160
Laudanosine
Primary metabolite of Atracurium
-seizure activity
-tertiary amine
-CNS stimulant
161
Atracurium (Tracrium)
dose
0.5 mg/kg
162
Atracurium (Tracrium)
histamine release?
some
potential for skin flushing, tachycardia and hypotension
163
Atracurium (Tracrium)
onset
2-3 min
164
Atracurium (Tracrium)
duration
20-35 min
165
Atracurium (Tracrium)
recovery
60-70 min = 95% recovery
166
Cisatracurium (Nimbex) is __ acting
intermed
167
Potent cis-cis isomer of Atracurium
**Cis**atracurium (Nimbex)
168
Cisatracurium (Nimbex)
metabolism
30% Hofmann elimination
metabolite breakdown by nonspecific esterase metabolism
169
Cisatracurium (Nimbex)
dose
0.15-0.2 mg/kg IV
170
Cisatracurium (Nimbex)
onset
2-3 min
peak: 4-7 min
171
Cisatracurium (Nimbex)
peak effect
4-7 min
172
Cisatracurium (Nimbex)
duration
40-70 min
173
Cisatracurium (Nimbex)
recovery
20-35 min
93 min = 90%
174
Why use cistracurium or atracurium instead of rocuronium or vecuronium?
ESRD
dialysis
175
drugs that enhance NMBA effects(8)
Inhalational agents (direct effect on postjunctional receptors)
Local anesthetics: potentiate both NDMA and depolarizers
Antibiotics (streptomycin/neomycin/aminoglycosides): depress the NMJ
Hypercarbia
Acidosis
Hypothermia
Anticonvulsants (Acute administration)
Magnesium
176
How do volatiles enhance NMBs?
direct effect on postjunctional receptors
177
How do L.A.'s enhance NMBs?
potentiate both NMDA and depolarizers
**NMDA: N-methyl D-aspartate (like ketamine)
178
How do antibiotics enhance NMBs?
depress the NMJ
streptomycin/neomycin/aminoglycosides
179
We would expect (longer/shorter) NMB action in an acidotic patient.
longer
hypercarbia & acidosis enhances NMBA effects
180
We would expect (longer/shorter) NMB action in a patient being treated for acute seizures.
longer
Anticonvulsants (Acute administration) enhance NMBA
181
We would expect (longer/shorter) NMB action in a parturient patient being treated with magnesium.
longer
Mag enhances NMBA effects
182
How would hypothermia affect NMB activity?
prolongs
decreasing receptor sensitivity and ACh mobilization
183
T/F
ED95 values are safe for older ppl.
False
Decreased total body water and serum albumin… reduced volume of distribution
184
old ppl require (higher/lower) NMB doses
lower
185
How would hypoK affect NMB activity?
prolongs
potentiates NMBA
can decrease the effectiveness of anticholinesterases on reversal
186
How would hypermag affect NMB activity?
prolongs duration
by inhibiting calcium channels
187
Acidosis prolongs NMB effects by...
interfering with effects of anticholinesterases
188
Hypercarbia prolongs NMB effects by...
leads to acidosis
interferes with antagonism
189
used to diagnose myasthenia gravis
edrophonium
if weakness resolves after giving it = + diagnosis
190
the enzyme responsible for rapid hydrolysis of released ACh
AChASe
acetylcholinesterase
191
AChASe can catalyze ACh at ___ molecules per active site per second
4,000
note: a quanta is ~5,000-10,000 ACh molecules
192
__% of released ACh is hydrolyzed during its diffusion across the synaptic cleft before reaching the nicotinic receptor
50%
193
Anticholinesterase/Acetylcholinesterase Inhibitors
Neostigmine
Edrophonium
Pyridostigmine
194
Selective Relaxant Binding Agent
Sugammadex
195
Mechanisms to reverse NMBA (5)
-Diffuse away
-Metabolized
-Excreted
-Encapsulated (sugammadex)
-Reversed with an Anticholinesterase
196
Acetylcholinesterase Inhibiting Agents/Anticholinesterase
MoA
-Block ACh breakdown by AChAse
-increase ACh [ ] in cleft
-more ACh to compete with remaining NMBA
-Causes normal muscle contraction
197
Anticholinesterases have (PNS/SNS) effects due to....
PNS
stimulate muscarinic Ach receptors in the heart, lungs, and GI tract
198
Anticholinesterase
PNS side effects
Bronchoconstriction
increased salivation
increased bowel motility
199
Acetylcholinesterase Inhibiting Agents are usually given with ___.
an Anticholinergic (Antimuscarinic)
glycopyrrolate
atropine
200
T/F
Acetylcholinesterase Inhibiting Agents have no ceiling effect.
False
they do
Maximal inhibition: when 100% of acetylcholinesterase has been inhibited
201
Acetylcholinesterase Inhibiting Agents
maximal inhibition:
-more doses will not improve recovery
-risk paradoxical muscle weakness
-weakness: desensitization of Ach receptors --> transmission failure --> depolarization block
202
Why do we see paradoxical muscle weakness at max Anticholinesterase effect?
desensitization of Ach receptors --> transmission failure --> depolarization block
203
Neostigmine (Prostigmin)
Inhibits hydrolysis of ACh by AChAsE
Blocks AChAse at all cholinergic synapses --> PNS (bradycardia, GI effects)
204
Neostig is a ____ amine.
QUAT amine (does not cross BBB)
205
glycopyrrolate decreases _____ side effects of Neostigmine
muscarinic
206
T/F
Neostig reduces risk of PONV
False
may increase
207
When to Reverse with Neostigmine
moderate & deep block
only if spontaneous NMB recovery (4 tactile TOF counts are visible at the adductor pollicis)
208
T/F
Neostig is fast acting.
False
slow
209
Neostigmine
dose
0.04-0.08 mg/kg (max 5mg)
210
Glyco + Neostig
For every 1 mg of Neostigmine mix with 0.2 mg Glyco (sometimes less)
mix or give separately
211
Neostigmine
onset
15 mins
depends on twitches
212
Neostigmine
duration
1-2 Hours
213
Neostigmine
metab & excretion
Hepatic metabolism
urinary excretion
214
What happens if we don't give atropine with edrophonium?
bradycardia!
215
T/F
atropine crosses the BBB
True
216
Sugammadex (Bridion)
mechanism
Eight sugars arranged in a ring specifically designed to ENCAPSULATE
217
Sugammadex is a modified γ-
______.
cyclodextrin
218
Sugammadex
solubility
-highly water soluble
-hydrophobic cavity: encapsulate steroidal NMBAs, especially rocuronium > vecuronium
219
T/F
Sugammadex has no effect on Acetylcholinesterase or cholinergic receptors.
True
220
T/F
Sugammadex efficacy depends on depth of the NM blockade.
False
Independent of depth of neuromuscular blockade
221
Sugammadex vs. other reversal agents
No real undesirable effects like anticholinesterases
222
T/F
Sugammadex is an anticholinesterase.
False
modified γ-cyclodextrin
223
Sugammadex dosing
Immediate reversal: 16 mg/kg
routine (deep block): 4 mg/kg
routine (moderate): 2 mg/kg
224
Sugammadex has no interaction with which medications?
succinylcholine & benzylisoquinolines
225
Sugammadex immediate reversal dosing (16 mg/kg) may cause:
-bradycardia (cardiac arrest)
-headache
-hypoTN
-N/V
-anaphylaxis
-hypersensitivity (pruritus and urticaria)
226
Using ____ may inactive birth control.
Sugammadex
must tell pt to use alt. contraception for 1 week
227
___ mg of Sugammedex is needed to encapsulate 1 mg of rocuronium.
4
228
T/F
Sugammadex works well for renal Dz pts.
False
not recommended
229
Sugammadex is incompatible with....
verapamil
ondansetron
ranitidine
230
We must wait ____ before giving Roc/Vec if Sugammadex was used for NMB reversal.
24 H
Suga is still removing aminosteroids
231
What NMBA should we use if we need to reparalyze after using Sugammadex?
Ie: emergent return to OR <24 H postop
nonsteroidal
Suxx
232
T/F
High dose Sugammadex decreases aPTT, PT, and INR.
False
increases
233
Sugammadex anaphylaxis
Airway edema
bronchospasm
CV collapse
esp higher doses
Within 5 minutes of administration
234
Sugammadex anaphylaxis treatment
-titrated to response: small boluses of epinephrine (10-20 mcg)
-Benadryl
-dexamethasone
-famotidine
235
T/F
Physostigmine crosses the BBB.
True
tertiary amine
236
T/F
Quaternary amines cross the BBB.
False
tertiary amines cross the BBB
"Trespassing tertiaries"
| they are "quarentined" out!
237
only anticholinesterase that crosses the blood brain barrier
Physostigmine
tertiary amine
238
Organophosphate poisoning
What do we give?
Atropine first
Then Physostigmine (must be given w/in timeframe or else toxic changes in brain will kill pt)
239
T/F
Physostigmine is used for reversal of muscle relaxants
False
Not used for reversal of muscle relaxants
240
Physostigmine use
treat anticholinergic toxicity
241
anticholinergic toxicity
S/S
-flushing
-dry skin
-mucous membranes
-mydriasis + loss of accomdtn
-AMS
-fever
-urinary retention
"cant see, cant pee, cant spit, cant shit"
242
anticholinergic toxicity
CNS effects
restless, shivers, agitation, disoriented
243
(anticholinergic toxicity)
Types of anticholinergics
-atropine
-scopolamine
-antihistamines
-antipsychotics
-cyclic antidepressants
244
Cholinergic Crisis/Syndrome
-Excessive use/overdose of cholinesterase inhibitors or **organic pesticides**
245
Cholinergic Crisis/Syndrome
mechanism
**Excessive ACh** peripherally and centrally
246
Cholinergic Crisis/Syndrome
S/S
miosis, salivation, bronchoconstriction, bradycardia, abdominal cramping, weakness, lacrimation,
dysphoria, confusion, seizures, coma
247
Cholinergic Crisis/Syndrome
Treatment
Atropine 35-70 mcg/kg
Pralidoxime 15 mcg/kg Q20 min
Benzos
248
Cholinergic Crisis
Muscarinic & Nicotinic Sx
249
How do your differentiate Cholinergic vs Myasthenic Crisis?
Give edrophonium
muscle strength improves = MG
no improvement/worse = Cholinergic crisis
250
Cholinergic vs Myasthenic Crisis
S/S
**Tensilon = edrophonium
251
T/F
Every pt that gets a NMBA should get a reversal agent.
True
252
Clinical Signs of Muscle Weakness
-Blurry/double vision
-Face weak/numb
-general weakness
PACU:
-Gen. weakness
-reported difficulty completing 5-second eye opening
-Difficult visually tracking/ speaking
253
Residual neuromuscular blockade
-reintubation
-**Impaired oxygenation and ventilation (may be blamed on Opioids)**
-Impaired pulmonary fxn
-risk of aspiration & pneumonia
-Pharyngeal dysfunction
-Delayed PACU discharge
254
Signs of Neuromuscular Recovery
-Tidal volume
-Negative inspiratory force
-Grip strength
-5-second head lift (not a sensitive test for residual block)
-Ability to protrude the tongue
255
T/F
5-second head lift is a sensitive test for residual block.
False
it is not
256
Are these reliable signs of return of muscle strength
NO
257
Cholinergic vs Myasthenic Crisis
(definition)
Cholinergic crisis: **excess** activity of Ach
Myasthenia Gravis: **decrease** in Ach activity d/t auto-reactive antibodies attacking nicotinic Ach receptors on postsynaptic membranes
258
Endrophonium (does/doesn't) cross the blood-brain barrier bc...
does NOT
it is a quaternary amine.
