NMB Reversals Flashcards
Acetylcholine is broken down by what? what are the byproducts?
acetylcholinesterase breaks it down into choline and acetate
Do AchE inhibitors eliminate need to eliminate NMBs from the body?
No, just increase Ach concentration at NMJ, NMB still have to be eliminated from the body
How does AchE work?
- enzyme inhibition
- pre-synpatic effects
describe the three bonds that can occur with enzyme inhibition of AchE which are competitive antagonism vs non-competative?
electrostatic attachment-competitive
formation of carabmol esters-competitive
phosphorylation non-competitive
which AchE inhibitors use each form of enzyme inhibition?
edrophonium - electrostatic attachment
neostigmine, pyridostigmine, physostigmine - carbamol esters
organophosphates and echothiopate - phosphyrlation
What is the mech of action for AchE pre-synaptic effects
- AchE stimulate presynpatic R (like sux) causing increased Ach release
or
- AchE increases Ach in the NMJ which then binds the presynaptic R itself.
How do anti-AchE affect psuedocholinesterase?
neostigmine and pyridostigmine inhibit it. Can lead to prolonged block from sux if given after neostigmine or pyridostigmine.
Edrophonium has no effect.
Do you need dose adjustments for AchE inhibitors in renal failure?
no, renal failure prolongs both NMBs and Anti-AchEs so no need to change doses
in which populations does neostigmine work the most quickly?
works faster in infants and children than adults
What happens if you give a huge dose of AchE inhibitor?
AchE inhibitors have a ceiling effect, so all yo get beyond max dose is more side effects
Do quaternary amines or tertiary amines cross the BBB?
tertiary amines. Quaternary amines do not cross BBB
which AchE inhibitors are quaternary amines?
edrophonium
neostigmine
phyridostgmine
what AchE inhibitors ar tertiary amines?
physiostigmine
what TOF ratio increases risk of PPC?
<0.9
when can AchE inhibitors caues muscle weakness
this can occur paradoxically if AchE inhibitor is given after full recovery from NMB is acheived
which antimuscarnics pair best with the following AchE inhibitors?
Edrophonium
neostigmine
pryidostgmine
atropine
glyocpyrrolate
glyocpyrrolate
respectively
Edrophonium dose, onset, doa, and metabolim/elimination
dose: 0.5-1.0mg/kg
onset: 1-2min
doa: 30-60min
metabolism/elimination
renal 75%
liver 25%
neostigminedose, onset, doa, and metabolim/elimination
0.02-0.07mg/kg
onset: 5-15min
doa: 45-90min
M/E: 50/50 renal/liver
pyridostigmine dose, onset, doa, and metabolim/elimination
dose: 0.1-0.3mg/kg
onset: 10-20min
doa: 60-120min
M/E: renal 75% liver 25%
can neostigmine be used intrathecally? if so what is the dose and associated side effects?
yes
50-100mcg
produces analgesia
SE: n/v, pruritis, prolongation of sensory and motor block
which AchE inhibitor can be used for post-op shivering? what is the dose? how does it compare to other options to stop shivering?
physostigmine 40mcg/kg
efficacy matches meperidine and clonidine for anishivering effects
Classic AchE Inhibitor side effects?
Dumbbells
diarrhea
urination
miosis
bradycardia
bronchoconstriction
emesis
lacrimation
laxation (defecation)
salivation
which antimuscarnics increase HR the most?
atropine > glyco > scopolamine
which antimuscarnics cause sedation? which causes the most?
scopolamine > atropine
which antimuscarnics cause the most dry mouth?
scopolamine > glyco > atropine
which antimuscarnics cause the most mydriasis and cycloplegia?
scopolamine > atropine
cycloplegia: temporary paralyzed ciliary m. causing blurry vision
how do anti muscarnics affect gastric H+ secretion?
they all decrease it by the same magnitude (equally)
which antimuscarinics cross the BBB? which do not?
atropine and scopolamine, tertiary amines cross BBB
glyco, quaternary amine does not cross the BBB
do tertiaty or quarternary amines cross the BBB
tertiary amines cross the BBB
what can a small dose of atropine cause? what is the mech of action?
paradoxical bradycardia
inhibits presynaptic M1 receptors on vagal nerve endings, blocking the negative feedback loop > continued Ach release and bradycardia
antimuscarnic considerations in patients who have undergone heart transplant
anti-muscarinics will not effect heart rate, still give them with AchE inhibitors when reversing NMB though to prevent the other side effects.
sugammadex med class
gamma-cyclodextrin
sugammadex SE
anaphylaxis 0.3% of patients
bradycardia
decrease effectiveness of hormonal birth control for up to 7 days
sugammadex can be used to reverse which NMBs?
Roc Vec and Pacuronium. Works the best for Roc though
What if you need to re-paralyze after using suggamadex?
Can always use steroid not from amino steroid class. Sux, cisatracurium, etc.
if dose was < or equal to 4mg/kg
5min-4hrs after Roc at 1.2mg/kg
if >4hrs Roc at 0.6mg/kg
If 16mg/kg given within 24hrs must use NMB outside of aminosteroid class
what molar concentration between Roc and sugammadex do you need? How does this affect dosing?
Need 1:1 molar concentration between Roc and suggamadex.
this is why sugammadex dose is based on block density
how are suggamadex-roc complex metabolised/eliminated?
excreted unchanged by the kidneys
is the affinity of suggamadex for roc reversible?
technically yes, affinity is very strong but it is reversible.
Sugammadex dosing
TOF 2/4 2mg/kg
TOF 0/4 with 2 PTC or more 4mg/kg
after 1.2mg Roc, wait 3 min then 16mg/kg
