Depolarizing NMB - SCh Flashcards
binds to the alpha subunit of the postsynaptic nicotinic receptor and mimics ACh and causes the muscle cell membrane to depolarize
depolarizing NMB
competes with ACh to bind with the alpha subunits to prevent the ion channel from opening and preventing the muscle cell membrane from depolarizing
nondepolarizing
two acetylcholine molecules linked by acetate methyl groups
SCh
what ACh receptors are affected by SCh
- cholinergic receptors at NMJ
- parasympathetic nervous system
- sympathetic ganglions
- muscarininc receptors in the SA node
Why use SCh?
- rapid intubation
- desire for short duration of action
Causes depolarization – initial contractions (fasciculations) — then paralysis – diffuses away from NMJ — repolarizes for later use
Phase I SCh Block
- Fasciculations
- decreased single twitch
- NO FADE W TETANUS/TOF/DOUBLE BURST
- blockade enhanced by anticholinesterase
- rapid recovery, short duration of action
Characteristics of Phase I SCh block
- FADE OF TETANUS/TOF/DOUBLE BURST
- posttetanic twitch
- prolonged duration
- reversible with anticholinesterase
Phase II SCh block
SCh: You give a small dose of edrophonium (.1-.2 mg/kg) and block becomes weaker. Should you give remainder of reversal dose? Is this indicative of a phase I or Phase II block
Give remainder, Phase II block
SCh: You give small dose of endrophonium (.1-.2 mg/kg), block becomes stronger. Should you give remainder of dose and is this indicative of phase I or phase II block?
Avoid additional dose and phase I block
What is SCh metabolized by
plasma choinesterase at 80 mg/min
what organ is responsible for SCh elimination
kidneys
where is pseudocholinesterase produced
liver
anticipated in patients with severe liver disease, pregnancy, malignancies, malnutrition, collagen vascular disease, and hypothyroidism
deficit of plasma cholinesterase
these patients can decrease plasma cholinesterase activity up to 40%, but at term there is no prolonged effect due to the increase volume of distribution of blood (high plasma volume)
pregnant patients
two genes dictate quality and quantity of plasma cholinesterase
atypical plasma cholinesterase
96% homozygous for normal genes - SCh duration is?
5-10 mins
3.96% heterozygous atypical - duration of SCh?
30 mins
.04% homozygous for atypical genes- duration of SCh
3 hrs or more
How can you test for issues with SCh metabolism
dibucaine
Inhibits normal plasma cholinesterase activity by 80%
dibucaine number of 80
normal 5-10 min duration
inhibits homozygous atypical activity by 20%
dibucaine number 20
duration 3 hrs or longer
inhibits heterozygous atypical activity by 40 to 60%
dibucaine number 40-60
duration 30 mins
causes a decrease in plasma cholinesterase activity
neostigmine and edrophonium (to a lesser degree)
- anticholinesterase drugs used in insecticides
- treatment of glaucoma
- myasthenia gravis
- chemo drugs like nitrogen mustard
- metoclopramide
cause decrease in plasma cholinesterase activity
tacrine (cognex), donepezil (aricept), rivastigmine (exelon), galantamine (razadyne)
anticholinesterase drugs used to treat alzheimer’s and some forms of dementia that increase ACh levels in the CNS that may prolong SCh
tachycardia muscle rigidity
bradycardia prolonged relaxation
hyperkalemia increased IOP
fasciculations increased ICP
myoglobinuria increased intragastric pressure
MH histamine release
sustained muscle contractions
complications of SCh
what patients should you not use SCh with?
damaged muscle membranes, guillain-barre, crush injury, MVA, burns
ED95 SCh
0.3 mg/kg
intubating dose SCh
1 mg/kg
1.5 mg/kg with pretreatment
IM dose SCh
4-5 mg/kg
Onset SCh
45 to 90 seconds
Durations SCh
5-10 mins
