NMB agents Flashcards
Endrophonium (does/doesn’t) cross the blood-brain barrier bc…
does NOT
it is a quaternary amine.
Do muscle relaxants provide amnesia?
NO
Neuromuscular junction consists of:
-Prejunctional: motor nerve ending
-cleft: AChAse
-Postjunctional: Highly folded muscle fiber
what causes a muscle contraction?
-ACh binds to nicotinic cholinergic receptor (postsynaptic)
Nerve stimulation
-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
each quanta contains ____ ACh molecules
5,000 to 10,000
⭐️
Which subunits do NMBs work on?
the 2 alpha subunits
Only ___ subunits are capable of binding ACh
the 2 alpha
If both the alpha subunits are occupied, what happens?
conformational change
central channel opens
What ions enter and exit when the 2 alpha subunits are occupied?
Na & Ca in
K out
____ occurs, and a muscle contraction happens
action potential
Postjunctional receptors have ___ subunits
5
2 alpha, 1 beta, 1 delta, and 1 epsilon (ADULT)
How many ACh molecules are needed to open the post jxnl receptor channel?
TWO
one or none = closed
causes vesicles of acetylcholine to fuse with the nerve membrane
influx of calcium within the terminal
ACh combines with and activates which receptor?
nicotinic receptors on motor end plate
release of ___ from intracellular stores stimulates an interaction between __ and ___. This results in a muscle contraction.
Ca
myosin
actin
Why do we use muscle relaxants?
-Optimize surgical conditions
-Prevent unwanted movement
-Facilitate tracheal intubation **
-Improve mechanical ventilation
The primary purpose of using NMB is to
achieve adequate relaxation of the upper airway, vocal cords, and diaphragm to facilitate intubation and surgery
Prolonged opening and increased ion flow (Hyperkalemia) can occur with (up/down) regulation.
up
Increased Extrajunctional Receptors
(up regulation or down?)
upregulation
Upregulation
stimulation of NMJ decreases over days (severe burns, immobilization, infxn, sepsis, prolonged use of NMBAs in ICU, CVAs)
increased immature nAChrs
immature nAChRs will have increased sensitivity to ____ but decreased sensitivity to ___.
-increased sensitivity to ACh and SCh (more nACHr’s being depolarized)
-decreased sensitivity to Nondepolarizers (more nACHr’s to block
Chronic neostigmine use will affect jxnl receptors by…
downregulating them
Pts w/ myasthenia gravis may experience (up/down) regulation due to chronic neostigmine use.
down-regulation
(Neostigmine: cholinesterase inhibitor; increases ACh levels at nerve terminals)
T/F
NMBAs are anesthetics
NO
not anesthetics
do not cause amnesia
Which causes awareness?
NMBA
not enough anesthesia
not enough anesthesia
T/F
Complete paralysis is required for all surgical cases
false
⭐️
Main site of action of NMBA
nicotinic cholinergic receptor (nAChRs)
at the endplate, which connects to the muscle
T/F
Neuromuscular Blocking Agents is synonymous with paralytic.
True
Most poisonous creature on planet
Golden PoisonFrog
T/F
Paralytics exist in nature.
True
pufferfish
Golden PoisonFrog
all 4 twitches will be full-strength if…
No muscle relaxation
With muscle relaxation….
there will be decreased strength
depolarizer or non?
depolarizer block
depolarizer or non?
non-depolarizer block
Which NMBAs show fade?
non-depolarizers
Potency
the relationship between twitch depression and dose
median dose that corresponds to 50% twitch reduction (among average population)
ED50
ED95
corresponds to 95% block (useful relaxation when twitch abolished)
Do we use ED50 or ED95 more when deciding doses for NMBAs?
ED95
we want what will get pt adequately paralyzed, full relaxed
Duration of Action
Time of injection to return of ___% twitch height
25 or 1 twitch (1 twitch out of 4 twitches)
T/F
Duration of action is dose-dependent
True
T/F
Inhalational agents & NMBAs have a synergistic effect.
True
IA can prolong NMB duration
Recovery Index
Time interval between 25% and 75% twitch height
Speed of recovery
Only depolarizing agent
Succinylcholine
Depolarizing a muscle actually ____ it and keeps it in a relaxed state.
fatigues
Succinylcholine
“Depolarizes” at postsynaptic nAChRs
Nondepolarizing
“Competes” for active binding sites on nAChRs
Aminosteroid (Rocuronium, Vecuronium, Pancuronium)
Benzylisoquinolinium (Mivacurium, Atracurium, Cisatracurium)
How does depolarizing NMB work?
Depolarizes:
occupies 2 alpha subunits
opens channel
ions in
depolarizes muscles
muscle is fatigued
stays in relaxed state
How does non-depolarizing NMB work?
competes for nicotinic sites
binds to 1 alpha subunit
prevents opening
muscle cannot contract
Mimics ACh
depolarizing/succinylcholine
Prolonged depolarization of the motor end-plate will….
inactivate Na channels
increases influx of K
Can a muscle contract while ACh is bound to the receptor?
No
can only contract once it diffuses off receptor
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
When given may cause fasciculations before total paralysis
Succinylcholine
⭐️
Succinylcholine dosing (adult)
1 -1.5 mg/kg IV
Succinylcholine onset
1 min
Succinylcholine duration
5-15 mins
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
fastest onset, the shortest duration, and greatest reliability (i.e., narrowest onset variability around the mean) of any NMBA
Succinylcholine
All NMBAs interact with ____ and block muscle membrane ____, leading to ___ paralysis.
α subunits of the nicotinic cholinergic receptors
depolarization
flaccid
reversal of ____ block is limited
nondepolarizing
(cholinesterase inhibitors have a ceiling effect)
___% 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
pseudocholinesterase breaks suxx into…
succinylmonocholine and choline
Recovery from suxx occurs when…
SCh diffuses away from the NMJ
5-6 mins
SCh = succinylcholine
____% of administered suxx reaches the NMJ
10%
Plasmacholinesterase is also called:
Butyrylcholinesterase
Pseudocholinesterase
Factors that lower pseudocholinesterase
severe liver disease
old
pregnancy
malnutrition
burns
anticholinesterase drugs
Reglan
oral contraceptives
Plasmacholinesterase
Synthesized in the ___ and found in the ___.
liver
plasma
Which drug decreases plasma cholinesterase (PChE) activity more?
Edrophonium
neostigmine
neostigmine
Abnormal Plasma Cholinesterase testing
Dibucaine number
reflects quality of cholinesterase enzyme (ability to hydrolyze SCh) not the quantity that is circulating in plasma
T/F
Dibucaine number reflects quantity of cholinesterase enzyme
False
quality (ability to hydrolyze SCh)
Lower dibucaine numbers mean (shorter/longer) duration of drug action.
longer
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
Which type of PChE are we most concerned with?
-homozy. typical
-heterozy. atypical
-homozy. atypical
homozygous atypical
both genes are mutated
T/F
Succinylcholine can be given as an infusion.
False
Will cause Phase II block
What causes Phase II block?
(Suxx)
continued dosing, a phase I block can develop into a phase II block
⭐️
T/F
Succinylcholine is an antagonist, making it a paralytic.
False
NMJ nicotinic AGONIST
Succinylcholine prevents (depolarization/repolarization).
repolarization
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”
Suxx
CV effects
Sinus bradycardia
junctional
arrest (esp peds)
When giving suxx to kids, mix it with ____.
atropine
Suxx
if a second dose is given within 5 minutes of first dose, we increase the risk of…
cardiac arrest
CV effects of suxx are due to…
its action @ cardiac muscarinic cholinergic (M2) receptors
mimics ACh
Preventing myalgias from SChE (suxx)
pretreat with non-depolarizer or NSAIDs
SChE myalgias are usually due to _____, and affect ____ muscles.
fasciculations
big skeletal muscles
SCh can elevate plasma potassium by ___ mEq/dL in healthy patients.
0.5
caution in renal pts (K already high)
Conditions to avoid SChE
renal Dz
burns
severe abdominal Infections
severe metabolic acidosis
upregulation of AChR
hemiplegia, paraplegia, muscular dystrophies, Guillian-Barre syndrome
Which paralytic should we avoid in a pt with a recent diagnosis of Guillian-Barre syndrome?
SChE (suxx)
Conditions associated with upregulation of extrajunctional AChR
hemiplegia
paraplegia
muscular dystrophies
Guillian-Barre syndrome
burns
Succinylcholine risk specific to children
massive rhabdomyolysis –> renal failure
Which paralytic is better for children?
succinylcholine
rocuronium
rocuronium
suxx risks:
-asystole
-hyperK
-massive rhabdomyolysis –> renal failure
Which paralytic is associated w/ MH?
SchE
Primary sign of MH
Masseter/jaw spasm
Jaw will lock up
cannot scissor jaw open
Best NMB for full stomach
Suxx
Increases intragastric pressure
increases lower esophageal tone (LES) helps prevent vomitus entering airway
NMB to avoid in open eye injury
Suxx
increases IOP
SChE (increases/decreases) ICP.
increases
Malignant Hyperthermia triggers
halogenated agents & succinylcholine
Activates Ryanodine receptor from the sarcoplasmic reticulum
Malignant Hyperthermia
-Massive uncontrolled release of Ca++ from the sarcoplasmic reticulum
-activates uncontrolled – constant (hypermetabolic) muscle contraction state
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
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
Classes of Non-depolarizing muscle relaxant (NDMR)
Aminosteroid
(Rocuronium, Vecuronium, Pancuronium)
Benzylisoquinolinium
(Mivacurium, Atracurium, Cisatracurium)
Know dis
-dose
-onset
-duration
Nondepolarizing Muscle Relaxants
MoA
Competitively antagonize the presynaptic receptors (one or both alpha subunits) to decrease release of Ach (fade on TO4)
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)
Almost always given IV
NonDepoMB
Rocuronium (Zemuron) is ____ acting.
intermediate
T/F
Rocuronium (Zemuron) is know to cause histamine release.
True
rare tho
Rocuronium (Zemuron)
CV effects
no effect of BP or HR
Using Rocuronium with suxx
use rocuronium to defasciculate
Rocuronium is (high/low) potency.
low
takes more molecules for effect
Rocuronium
intubating dose
0.6 mg/kg
Rocuronium
RSI dose
1.2 mg/kg
Rocuronium
defiscic dose
5 mg
Rocuronium
maintenance/repeat dosing
0.1 mg/kg PRN
Rocuronium
onset
1-2 mins (dose-dependent)
Rocuronium
duration
30 min or up to 70 minutes after RSI dose
Rocuronium elimination
___% hepatic
___% renal
70% liver
30% renal
Best NMB for short laparoscopic procedures
Rocuronium
Has greatest assoc. w/ anaphylaxis than any other drug given in anesthesia
Rocuronium
(stats could be inflated b/c we give rocuronium A LOT)
T/F
We must be aware of active metabolites with Rocuronium.
False
no real metabolites
Vecuronium (Norcuron) benefits
No histamine release
Cardiac stable
Vecuronium (Norcuron) is ___ potency
medium
Vecuronium (Norcuron) is ____ acting.
intermediate
Vecuronium (Norcuron) precipitates with ____.
thiopental
Vecuronium (Norcuron)
induction/intubation dose
0.1 mg/kg
Vecuronium
Pretreatment/priming with ___% of intubation dose given ___ min before intubation dose.
10%
3-5 min
Which NMB agent do we see pre-dosing before intubation?
Vecuronium
onset of action is longer than rocuronium
Vecuronium
recovery
25-40 min (25% recovery)
45-60 min(95% recovery)
Vecuronium metabolite has ___% potency of parent drug.
(3-desacetyl): 60% potency of vecuronium
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)
Pancuronium (Pavulon)
initial dose
0.1 mg/kg
longest acting aminosteroid NMB
Pancuronium (Pavulon)
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
T/F
Histamine release occurs with Pancuronium.
False
T/F
Pancuronium increases HR and CO.
True
Used in Cardiac surgery to counteract the bradycardia associated with high-dose opioid dosing
Pancuronium
Potential for significant postoperative residual blockade
Pancuronium
very long acting
Pancuronium
Maintenance dose
0.02 mg/kg
Pancuronium
onset
2-5 min
Pancuronium
duration
60-100 min
T/F
Pancuronium is mostly metabolized by the liver
False
Hepatic metabolism 20%
Urinary excretion (40-70%)
Pancuronium metabolite
(3-OH pancuronium): 50% potency
NMB best for renal and liver Dz
Benzylisoquinolines
Potency: relationship between ____ ___ and dose.
twitch depression
ED50
median dose that corresponds to 50% twitch reduction
ED95
corresponds to 95% block (useful relaxation when twitch abolished)
Undergoes Hoffman elimination
Benzylisoquinolines
Hofmann Elimination
Spontaneous, non-enzymatic, non-organ dependent chemical breakdown at physiologic temperature and pH
____ increases Hofmann Elimination.
Increased Temp = increased Hoff Elim
Beware of histamine release, esp if giving quickly
Mivacurium (Mivacron)
Mivacurium (Mivacron)
recovery
rapid
Mivacurium (Mivacron)
metabolism
Hydrolysis by plasma cholinesterase
Atracurium metabolism is by the same enzymes that degrade ___ and ___.
esmolol and remifentanil
Mivacurium (Mivacron)
onset
1 min
“MIV only takes a MIN!”
Mivacurium (Mivacron)
duration
10-20 min
Mivacurium (Mivacron)
intubation dose
0.2 mg/kg
Mivacurium (Mivacron)
infusion dose
5-8 mcg/kg/min infusion
Atracurium (Tracrium) is ____ acting.
intermed
Atracurium (Tracrium)
metab
Hofmann Elimination 30% and ester hydrolysis 60%
Laudanosine
Primary metabolite of Atracurium
-seizure activity
-tertiary amine
-CNS stimulant
Atracurium (Tracrium)
dose
0.5 mg/kg
Atracurium (Tracrium)
histamine release?
some
potential for skin flushing, tachycardia and hypotension
Atracurium (Tracrium)
onset
2-3 min
Atracurium (Tracrium)
duration
20-35 min
Atracurium (Tracrium)
recovery
60-70 min = 95% recovery
Cisatracurium (Nimbex) is __ acting
intermed
Potent cis-cis isomer of Atracurium
Cisatracurium (Nimbex)
Cisatracurium (Nimbex)
metabolism
30% Hofmann elimination
metabolite breakdown by nonspecific esterase metabolism
Cisatracurium (Nimbex)
dose
0.15-0.2 mg/kg IV
Cisatracurium (Nimbex)
onset
2-3 min
peak: 4-7 min
Cisatracurium (Nimbex)
peak effect
4-7 min
Cisatracurium (Nimbex)
duration
40-70 min
Cisatracurium (Nimbex)
recovery
20-35 min
93 min = 90%
Why use cistracurium or atracurium instead of rocuronium or vecuronium?
ESRD
dialysis
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
How do volatiles enhance NMBs?
direct effect on postjunctional receptors
How do L.A.’s enhance NMBs?
potentiate both NMDA and depolarizers
**NMDA: N-methyl D-aspartate (like ketamine)
How do antibiotics enhance NMBs?
depress the NMJ
streptomycin/neomycin/aminoglycosides
We would expect (longer/shorter) NMB action in an acidotic patient.
longer
hypercarbia & acidosis enhances NMBA effects
We would expect (longer/shorter) NMB action in a patient being treated for acute seizures.
longer
Anticonvulsants (Acute administration) enhance NMBA
We would expect (longer/shorter) NMB action in a parturient patient being treated with magnesium.
longer
Mag enhances NMBA effects
How would hypothermia affect NMB activity?
prolongs
decreasing receptor sensitivity and ACh mobilization
T/F
ED95 values are safe for older ppl.
False
Decreased total body water and serum albumin… reduced volume of distribution
old ppl require (higher/lower) NMB doses
lower
How would hypoK affect NMB activity?
prolongs
potentiates NMBA
can decrease the effectiveness of anticholinesterases on reversal
How would hypermag affect NMB activity?
prolongs duration
by inhibiting calcium channels
Acidosis prolongs NMB effects by…
interfering with effects of anticholinesterases
Hypercarbia prolongs NMB effects by…
leads to acidosis
interferes with antagonism
used to diagnose myasthenia gravis
edrophonium
if weakness resolves after giving it = + diagnosis
the enzyme responsible for rapid hydrolysis of released ACh
AChASe
acetylcholinesterase
AChASe can catalyze ACh at ___ molecules per active site per second
4,000
note: a quanta is ~5,000-10,000 ACh molecules
__% of released ACh is hydrolyzed during its diffusion across the synaptic cleft before reaching the nicotinic receptor
50%
Anticholinesterase/Acetylcholinesterase Inhibitors
Neostigmine
Edrophonium
Pyridostigmine
Selective Relaxant Binding Agent
Sugammadex
Mechanisms to reverse NMBA (5)
-Diffuse away
-Metabolized
-Excreted
-Encapsulated (sugammadex)
-Reversed with an Anticholinesterase
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
Anticholinesterases have (PNS/SNS) effects due to….
PNS
stimulate muscarinic Ach receptors in the heart, lungs, and GI tract
Anticholinesterase
PNS side effects
Bronchoconstriction
increased salivation
increased bowel motility
Acetylcholinesterase Inhibiting Agents are usually given with ___.
an Anticholinergic (Antimuscarinic)
glycopyrrolate
atropine
T/F
Acetylcholinesterase Inhibiting Agents have no ceiling effect.
False
they do
Maximal inhibition: when 100% of acetylcholinesterase has been inhibited
Acetylcholinesterase Inhibiting Agents
maximal inhibition:
-more doses will not improve recovery
-risk paradoxical muscle weakness
-weakness: desensitization of Ach receptors –> transmission failure –> depolarization block
Why do we see paradoxical muscle weakness at max Anticholinesterase effect?
desensitization of Ach receptors –> transmission failure –> depolarization block
Neostigmine (Prostigmin)
Inhibits hydrolysis of ACh by AChAsE
Blocks AChAse at all cholinergic synapses –> PNS (bradycardia, GI effects)
Neostig is a ____ amine.
QUAT amine (does not cross BBB)
glycopyrrolate decreases _____ side effects of Neostigmine
muscarinic
T/F
Neostig reduces risk of PONV
False
may increase
When to Reverse with Neostigmine
moderate & deep block
only if spontaneous NMB recovery (4 tactile TOF counts are visible at the adductor pollicis)
T/F
Neostig is fast acting.
False
slow
Neostigmine
dose
0.04-0.08 mg/kg (max 5mg)
Glyco + Neostig
For every 1 mg of Neostigmine mix with 0.2 mg Glyco (sometimes less)
mix or give separately
Neostigmine
onset
15 mins
depends on twitches
Neostigmine
duration
1-2 Hours
Neostigmine
metab & excretion
Hepatic metabolism
urinary excretion
What happens if we don’t give atropine with edrophonium?
bradycardia!
T/F
atropine crosses the BBB
True
Sugammadex (Bridion)
mechanism
Eight sugars arranged in a ring specifically designed to ENCAPSULATE
Sugammadex is a modified γ-
______.
cyclodextrin
Sugammadex
solubility
-highly water soluble
-hydrophobic cavity: encapsulate steroidal NMBAs, especially rocuronium > vecuronium
T/F
Sugammadex has no effect on Acetylcholinesterase or cholinergic receptors.
True
T/F
Sugammadex efficacy depends on depth of the NM blockade.
False
Independent of depth of neuromuscular blockade
Sugammadex vs. other reversal agents
No real undesirable effects like anticholinesterases
T/F
Sugammadex is an anticholinesterase.
False
modifiedγ-cyclodextrin
Sugammadex dosing
Immediate reversal: 16 mg/kg
routine (deep block): 4 mg/kg
routine (moderate): 2 mg/kg
Sugammadex has no interaction with which medications?
succinylcholine & benzylisoquinolines
Sugammadex immediate reversal dosing (16 mg/kg) may cause:
-bradycardia (cardiac arrest)
-headache
-hypoTN
-N/V
-anaphylaxis
-hypersensitivity (pruritus and urticaria)
Using ____ may inactive birth control.
Sugammadex
must tell pt to use alt. contraception for 1 week
___ mg of Sugammedex is needed to encapsulate 1 mg of rocuronium.
4
T/F
Sugammadex works well for renal Dz pts.
False
not recommended
Sugammadex is incompatible with….
verapamil
ondansetron
ranitidine
We must wait ____ before giving Roc/Vec if Sugammadex was used for NMB reversal.
24 H
Suga is still removing aminosteroids
What NMBA should we use if we need to reparalyze after using Sugammadex?
Ie: emergent return to OR <24 H postop
nonsteroidal
Suxx
T/F
High dose Sugammadex decreases aPTT, PT, and INR.
False
increases
Sugammadex anaphylaxis
Airway edema
bronchospasm
CV collapse
esp higher doses
Within 5 minutes of administration
Sugammadex anaphylaxis treatment
-titrated to response: small boluses of epinephrine (10-20 mcg)
-Benadryl
-dexamethasone
-famotidine
T/F
Physostigmine crosses the BBB.
True
tertiary amine
T/F
Quaternary amines cross the BBB.
False
tertiary amines cross the BBB
“Trespassing tertiaries”
they are “quarentined” out!
only anticholinesterase that crosses the blood brain barrier
Physostigmine
tertiary amine
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)
T/F
Physostigmine is used for reversal of muscle relaxants
False
Not used for reversal of muscle relaxants
Physostigmine use
treat anticholinergic toxicity
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”
anticholinergic toxicity
CNS effects
restless, shivers, agitation, disoriented
(anticholinergic toxicity)
Types of anticholinergics
-atropine
-scopolamine
-antihistamines
-antipsychotics
-cyclic antidepressants
Cholinergic Crisis/Syndrome
-Excessive use/overdose of cholinesterase inhibitors or organic pesticides
Cholinergic Crisis/Syndrome
mechanism
Excessive ACh peripherally and centrally
Cholinergic Crisis/Syndrome
S/S
miosis, salivation, bronchoconstriction, bradycardia, abdominal cramping, weakness, lacrimation,
dysphoria, confusion, seizures, coma
Cholinergic Crisis/Syndrome
Treatment
Atropine 35-70 mcg/kg
Pralidoxime 15 mcg/kg Q20 min
Benzos
Cholinergic Crisis
Muscarinic & Nicotinic Sx
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
How do your differentiate Cholinergic vs Myasthenic Crisis?
Give edrophonium
muscle strength improves = MG
no improvement/worse = Cholinergic crisis
Cholinergic vs Myasthenic Crisis
S/S
**Tensilon = edrophonium
T/F
Every pt that gets a NMBA should get a reversal agent.
True
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
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
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
T/F
5-second head lift is a sensitive test for residual block.
False
it is not
Are these reliable signs of return of muscle strength
NO
