Miscellaneous
definition of residual neuromuscular blockade
TOF < 0.9
S&S of muscle weakness
MOA of AchE inhibitors
•Inhibit AChE located at the NMJ causing great amount of ACh to become available to nicotinic & muscarinic receptors in CNS
•Ach accumulates at the NMJ and competes with NMB for the occupation of unblocked nicotinic Ach receptors
where anticholinergics exert their effects
Occurs at the cholinergic postganglionic sites called muscarinic receptors (M1-M5)
Muscarinic receptors located in heart, salivary glands, smooth muscle of GI & GU tracts
Anticholinergics reversibly combine w/muscarinic receptors and prevent ACh access to these sites
80kg patient has a moderate level of rocuronium induced block with a TOF count of 2. What is the sugammadex dose?
2mg/kg
160mg
full reversal combo
neo 5 mg + glyco 1 mg in same syringe
Cation in the presynaptic membrane that destabilizes the proteins that hold ACh vesicles in place and help them mobilize to reach the junction
Calcium
AchE inhibitors that are poorly lipid-soluble
quaternary ammonium group:
edrophonium
neostigmine
pyridostigmine
anticholinergics with greater lipid solubility
tertiary amines:
atropine
scopolamine
after administering 50mg of rocuronium to an 80kg patient, the CRNA encounters a "can't intubate and can't ventilate" scenario. How much sugammadex should be adminstered at this time?
16mg/kg
80kg x 16 = 1280mg
this drug can be used to antagonize effects of benzos and ketamine
physostimine
how does AChE terminates the effects of ACh?
by hydrolyzing it into choline and acetate
These receptors require less ACh to produce its effects (bradycardia, hypersalivation, hyperperistalsis)
Muscarinic
large dose of which inhaled anticholinergic that is useful for COPD and blocks which receptor...?
Ipratropium in large dose blocks M3 receptors causing bronchodilation
MOA of sugammadex
gamma-cyclodextrin that encapsulates aminosteroid nondepolarizing NMB, which renders them inactive and provides a swift reversal of neuromuscular blockade.
•3D structure:
•Shaped like donut (hollow center)
•hydrophobic center
•hydrophilic exterior
Drugs that Rely on AChE for Metabolism
•Succinylcholine
•Remifentanil
•2-chloroprocaine (Nesacaine)
•Glaucoma medications (echothiopate)
•Myasthenia gravis drugs
•Dementia drugs (Aricept)
treatment of anticholinesterase overdose
supportive
atropine 35-70mcg/kg q 3-10min until muscarinic sx disappear
Pralidoxime 15mg/kg
common side effects caused by AchE inhibitors
DUMBBELLS
Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Emesis
Lacrimation
Laxation
Salivation
*cholinergic crisis, anticholinesterase overdose...*
scopolamine
which NMB is most effectively antagonized by sugammadex?
rocuronium
if you need to reparalyze the patient after administering sugammadex, which NMB would be better to be administered?
One outside the aminosteroid class, so a benzylisoquinoline or depolarizing.
atracurium, cisatracurium, succinylcholine...
this preexisting condition prolongs the duration of action for AChE inhibitors
renal failure
3 forms of binding interactions for AChE inhibiting drugs
1. electrostatic attachment
2. formation of carbamyl esters
3. phosphorylation (irreversible)
s&s of central anticholinergic syndrome
•“Red as a beet, blind as a bat, dry as a bone, mad as a hatter, hot as a hare”
Flushed skin
Mydriasis
Dry mouth
Urinary retention
Hallucinations
Confusion
Hyperthermia
Tachycardia
Tremors
Rocuronium 1.2mg/kg
this anticholinergic does not prevent motion induced nausea
glycopyrrolate