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45 Cards in this Set

  • Front
  • Back
what do NMB's do?
antagonize the effects of aCh
Benzylisoquinolines [4]
Mivacurium, Atracurium, Cisatracurium, Doxacurium
Aminosteroids [4]
Vecuronium, Rocuronium, Pancuronium, Pipecuronium
Respiratory acidosis ________ blockade and _________ its reversal

Succinylcholine structure?
two molecules of acetylcholine
aCh mimetics have...
have a quat. amine and some a second tertiary amine that is protonated at physiological pH
prototype NMB?
Newer NMB's– cause less toxicities (histamine release, autonomic side effects) [4]
doxacurium, mivacurium, rocuronium, vecuronium
There is often more than one nitrogen, if the additional are tertiary, then they add _______ character
_________ has about the same onset and so could be used in place of succinylcholine (has many side effects) but will sacrifice for longer duration
selection of NMB's?
Onset of Action
Rocuronium vs succinylcholine
Duration of Action
Degree of changes in BP and HR
Short and intermediate have minimal changes
Non-depolarizing- mech of action
Competitive Antagonist
Curariform Agents
Phase II Block
Depolarizing - mech of action
Phase I Block
Nicotinic receptor is a...
(ligand gated ion channel)
competitive agent onset?
Small rapidly moving muscles of eyes and face THEN 2. Larger muscles of limbs and trunk THEN 3. intercostal muscles and diaphragm (so can relax without apnea if choose)
All due to differences in blood flow, distance from central circulation and different fiber types.
Acetlycholine receptors are
multi-subunit membrane spanning proteins consisting of five distinct subunits; (a,b,d,g).
Acetylcholine binds to the ______ subunits, of which there are _____ on each of the acetylcholine receptor ion channels.

Once bound, acetylcholine causes ligand-gated ion channels in the post synaptic membrane to ______.
These channels are relatively ________, so the passage of different ions
Depolarizing (succinylcholine) mechanism
Binds to nicotinic receptor
Influx/outflux of ions leads to persistent depolarization
Initially have involuntary muscle contractions (fasciculations)
Paralysis sets in
Time dependent gate closes but voltage gate remains open. The end plate cannot repolarize because an agonist is bound keeping upper gate open.
Receptor becomes inactive and desensitized (channel will remain closed even with agonist). Mechanism is not clear we ‘exhaust’ the receptor
______ and ______ may change sux response.
Hypokalemia and hypocalcemia
Speed of onset - Most potent have _______ onset
potency facts
Speed of onset - Most potent have longer onset
Potency measured by ED95
ED95 is different for different muscles
Takes more drug for intubation than facial relaxation
Wide variability in dosages

More potent so must give less, give less takes longer to get to site, longer to get to site, longer onset.
what is an Antagonist?
a ligand that binds and nothing happens, we keep the membrane at its resting state
Duration of Action
Parallel metabolism
Succinylcholine, mivacurium
Parallel elimination
Usually redistribution
Gradual metabolism
absorption for quat. amines?

Not well absorbed from gut (limits delivery, can still eat meat of animals killed)
Do not cross BBB
NMB's hepatic metabolism [2]
Pancuronium/Vecuronium (vecuronium active 3-hydroxy)
Acetylcholinesterase metab [3]
Acetylcholine (somewhat mivacurium/cisatracurium/atracurium)
Pseudocholinesterase metab
Non-specific cholinesterase/plasma cholinesterase/ butyrylcholinesterase
Succinylcholine (also mivacurium/cisatracurium/atracurium)
Other drugs decrease psudochbolinesterase activity
Many not metabolized and eliminated unchanged..[4]
effect of hypothermia on metabolism?
Decreased temperature decreases metabolism
Because of significant esterase metabolism of all of the compounds, should screen for?
“atypical chlolinesterase”
Drugs reducing psuedocholinesterase activity
include echothiophate (glaucoma), neostigmine/pyridostigmine (cholinesterase inhibitors), Phenylzine (MAOI), Cyclophosphamide (antineoplastic), Esmolol (beta-blocker), Pancuronium (non-depolarizing muscle blocker), oral contraceptives.
renal excretion [4]
Doxacurium, Pancuronium, Vercuronium, Pipecuronium
Biliary Excretion
renal failure/liver failure effects
So if have renal failure and prolonged action and increased volume of distribution
Liver disease also have increased volume of distribution

May need greater initial dose to compensate for increased volume of distribution but then lower maintenance doses
Hyperthermia delays ?
Prolonged NM paralysis (atypical esterase levels)
Release Histamine from mast cells
Curariform compounds
Cause bronchospasm
Block autonomic ganglia
Hypotension, tachycardia
Block Cardiac Muscarinic receptors
Less pronounced toxicities with the new drugs [4]
doxacurium, mivacurium, rocuronium, vecuronium
hyperkalemia effects?
Hyperkalemia – during succinylcholine depolarization potassium is still released by muscle and raises serum potassium by 0.5 mEq/L which is ok for normal but in those patients with burn, massive trauma and other neurological and other disorders, this causes hyperkalemia. See cardiac arrest, V.fib, heart block, bradycardia
Prolonged blockade
active metabolites or development of polyneuropathy
Vagal blockade and catecholamine release
Hypertesion and tachycardia
Inhibits Psueodocholiesterases
Succinylcholine (*contraindicated for children and adolescents)
*Cardiac Arrest
Postoperative Myalgia
Bradycardia (stimulate vagal ganglia)
Hypertension/tachycardia (stimulate sympathetic ganglia)
Prolonged activity (atypical esterase levels)
Other drugs act at receptor (potentiate effects)
Volatile anesthetics, local anesthetics, ketamine
Neostigmine, antibiotics (aminoglycoside/ tetracycline), cocaine, quinidine, calcium channel blockers.
Others (table 9-4 Lange’s text)
Effects pronounced with disorders (Myasthenia gravis, etc, see table 9-8, Lange’s text)
Effects reversed by cholinesterase inhibitors (neostigmine)
No reversal for succinylcholine
why no reversal for sux?
Cholinesterase inhibitors allow for increase in Ach concentration at end plate and allow for agonism.