Term
NEUROMUSCULAR
BLOCKING DRUGS
Characteristics/Functions |
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Definition
nAKA “muscle relaxants”/”NMB’s”/ “paralytics”
¨Interfere with the transmission of nerve impulses at the neuromuscular junction
¨Help facilitate endotracheal intubation
¨Provide optimal surgical conditions and pt safety
¨They are NOT anesthetics:
n*Should not be used to ensure lack of movement in an under anesthetized pt.
¨Not always a part of anesthetic plan
nCan often achieve relaxation with regional or deep inhalational anesthetic, or mixed anesthetic technique
nSome surgeries (thyroid, breast, facial) may necessitate that you NOT use muscle relaxants |
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Term
NEUROMUSCULAR
TRANSMISSION |
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Definition
nConsists of:
¨Prejunctional motor nerve ending
¨Synaptic cleft
¨Highly folded post junctional membrane
nAction potential
¨Moves along nerve terminal
nCauses an influx of Ca into the nerve cytoplasm and allows storage vesicles to release acetylcholine (Ach) |
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Term
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Definition
nACh molecules diffuse across synaptic cleft and bind with nicotinic cholinergic receptors
nThese receptors have 5 subunits- 2 alpha, 1 beta, 1 gamma, and 1 delta
nOnly the 2 alpha subunits are capable of binding ACh , and as such capable of binding Succs.
¨If both alpha subunits are occupied; there is a conformational change in the subunits opening up a central channel (postsynaptic nerve)
nNa (and Ca) flow in and K flows out
nAction potential spreads and ultimately causes a muscle contraction |
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Term
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Definition
nACh is rapidly metabolized (hydrolyzed) by the enzyme acetylcholinesterase (true cholinesterase)
nAcetylcholinesterase is found in the folds of the endplates
nReceptor ion channels close and cause the end plate to repolarize
nACh is hydrolyzed into acetic acid and choline |
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Term
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Definition
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Ach is metabolized VERY RAPIDLY (milliseconds) in the Neuromuscular Junction by acetylcholinesterase – also referred to as TRUE cholinesterase – found in the NMJ in the folds of the Endplate.
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As Ach is metabolized (off of the alpha subunits) the ion channels close bc of repolarization of the nerve and becomes ready for the next impulse (depolarized).
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Ach byproducts of metabolism, some of that is taken back to the presynaptic nerve (where vesicles are – Ach storage) and used to make Ach again for later release.
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Term
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Definition
nDepolarizers: Synonymous with SUCCs
¨Resemble Ach: mimic the action of Ach
nBind to ACh receptors and generate an action potentialà muscle contraction
nNOT metabolized by acetylcholinesterase therefore concentration in synaptic cleft high for longer period…… prolonged depolarization of end plate
¨Depolarizers act as ACh receptor agonists |
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Term
ACTIONS
OF
SUCCS/ANECTINE |
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Definition
Depolarizer (SUCCS/Anectine)– resembles Ach – mimics action of Ach – may here it called an Ach agonist.
Depolarizes the nerve ending – causing contraction – SUSTAINED – where that another impulse CANNOT come in – so it cannot be depolarized again – causes FASICULATIONS – then relaxation because Succs does not move off as fast, the nerve cannot be stimulated again.
Paralysis ocuurs with the depolarizer because there is a prolonged refractory period. |
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Term
ADVANTAGE/
DISADVANTAGE
OF
SUCCS |
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Definition
MAIN ADVANTAGE- short duration of action, rapid onset of relaxation of muscles for intubation.
DISADVANTAGE – side effects – HYPERKALEMIA
Nondepolarizers (all other NMB) block the receptors so depolarization CANNOT occur |
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Term
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Definition
nOnly depolarizing agent in clinical use today
nRapid onset: 30-60 sec
nShort duration: 3-10 min
nDose: 1-1.5 mg/kg IV
4-5 mg/kg IM in children
nUpon entering circulation metabolized by psuedocholinesterase into succinylmonocholine |
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Term
RECOMMENDATION
OF
SUCCS IN CHILDREN |
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Definition
SUCCS is not recommended in children because it has a HIGH INCIDENCE of Cardiac arrest.
Requires larger dose because of larger distribution. |
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Term
SUCCS
More Characteristics |
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Definition
nLittle of actual original dose gets to the receptors
-Amount that gets to receptors, binds to 2-alpha subunits and causes depolarization
-It is a sustained depolarization because metabolism is slower than ACh
-Succs vs Roc: Rocuronium – next closest onset – 60-90 seconds – The CATCH is that it has a LONGER DURATION of action before pt will breathe again
-Metabolized by pseudocholinesterase – AKA plasma cholinesterase – found in plasma (blood) NOT in the end plates of the NMJ.
-NMB – hydrophillic, don’t cross the placenta (good thing), repel against lipid membranes, does not cross blood-brain barrier |
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Term
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Definition
Phase I block – normal/intended block seen with Succs. Fasciculations, lasts 3-10 mins. NORMAL effects.
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Term
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Definition
Phase II block – Succs drips/boluses. This block is caused by a large single dose, a repeated dose or a continuous dose of Succs.
nCaused by a depolarizer
nPost-junctional membrane has repolarized but still does not respond normally to ACh
nDue to ionic and conformational changes that accompany a prolonged membrane depolarization
nUsually with doses >3-5mg/kg IV
nResembles a non-depolarizer block - Test on peripheral nerve stimulator mimics a nondepolarizing block. This is thought to happen because of a temporary conformational change in the membrane. |
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