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what is the only depolarizing NMB in clinical use
SCh
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SCh produces
intense paralysis rapids, and effects are likely to wane before preoxygenated patient becomes hypoxic
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how is SCh supplied
20mg/ml
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what is induction dose of SCh
1-2 mg/kg
3-4 x's the ED95
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What is onset of Sch
30 seconds
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What is duration of Sch
- 5-10 minutes
- because of hydrolysis by plasma cholinesterase enzyme.
- -hydrolyzed at such a fast rate only a small fraction of original iv dose reaches NMJ
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SCh has slight _____ release, moderate ______ stimulation, and modest _____ stimulation
- histamine
- muscarinic -cardiac
- nicotinic- nmj
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pre oxygenated adults can experience ____ minutes of apnea before sat drops below 90%
8 minutes
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MOA of SCh
- attaches to 1 or both alpha subunits of nAChRs and mimics the action of ACh (partial agonist) thus depolarizing the post junctional membrane
- -compared with Ach the hydrolysis of Sch is slow resulting in sustained depolarization of receptor ion channels
- -NM blockade develops b/c a depolarized post junctional membrane can not respond to subsequent Ach release
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depolarizing NM blockade is also referred to as
phase I blockade
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electically evoked mechanical responses using PNS that are characteristic of phase I blockade are
- decreased contraction in response to single twitch stimulation
- -decreased amplitude but sustained response to continuous stimulation
- -TOF ration >0.7
- absence of posttetanic faciculation
- - enhancement of NM blockade if anticholinesterase drug given
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the onset of phase I blockade is accompanied by
skeletal muscle fasiculations that reflect the generalized depolarization of post junctional membrane produced by SCh
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phase II blockade cause from
- a single large dose of SCh (>2 mg/kg IV), repeated doses, or continuous infusion
- -this causes post junctional membrane to no respond to Ach even after they have become repolarized
- -similar to nondepolarizing blockade
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giving anticholinergic in phase I blockade will what
enhancement of existing NM blockade
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Phase II blockade can be antagonized by what
anticholinesterase drugs
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acceptable approach to administering anticholinergic in phase II blockade
- give small dose of drug such as edriphonium 0.1-0.2 mg/kg IV and see if small dose improves neuromuscular transmission by using PNS if it does an additional dose will antagonize the NM blockade rather than enhance it ( enhanced if still in phase I)
- -this is best way to distinguish between
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plasma cholinesterase
- influnces the duration of action of SCH by controlling the amount of NMBD that is hydrolyzed before reaching the NMJ
- -decrease in this results in slowed or absent hydrolysis of SCh and prolongation of NM blockade.
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neuromuscular blockade is terminated by
diffusion away from NMJ into the ECF
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plasma cholinesterase produced by
- liver
- -liver disease must be severe before decreases in plasma cholinesterase are sufficient to prolong NM blockade
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what drugs decrease plasma cholinesterase leading to prolonged effects of Sch
- neostigmine
- anticholinesterase drugs (used in glaucoma and MG)
- chemo drugs
- reglan (metoclopramide)
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what causes increase in plasma cholinesterase increasing the needs for SCh
obesity
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atypical plasma cholinesterase
presence often only recognized after an healthy pt experiences prolonged NM blockade (1-3 hours) after a conventional dose of SCh is given.
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dibucaine
a local anesthetic that inhibits the activity of normal plasma cholinesterase activity by 80% compared with 20% atypical enzyme
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dibucaine number of 80
- confirms the presence of normal plasma cholinesterase activity
- -
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dibucaine number of 20
indicates atypical plasma cholinesterase and that blockade could last for 3 hours or longer after normal dose.
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adverse side effects of SCh
- cardiac dysrhythmias
- hyperkalemia
- myalgia
- myoglobinuria
- increased gastric pressure
- increased intraocular pressure
- increased ICP
- sustained skeletal muscle contractions
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cadiac dysrhythmias and SCh
- SB junctional rhythm and even cardiac arrest can follow administration of SCh because of acton it has on muscarinic repectors
- - most likely to occur when 2nd dose is given 5 minutes after first
- -atropine will not help this response to 2nd dose.
- -increased heart rate and BP also reported
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hyperkalemia and SCh
- may occur after administration to patient with clinically unrecognized muscular dystrophy, unhealed 3rd degree burns, denervation, leading to skeletal muscle atrophy, severe skeletal muscle trauma and upper motor lesions.
- -usually develops within 96 hours and may persist for up to 6 months.
- -sustained opening of receptor ion channels causes leakage of potassium ion concentration enough to produce a 0.5 meq/L increase
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do not give SCh to kids under 6 why?
some forms of muscular dystrophy do not appear until children are 6 years old.
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myalgia and SCh
- post skeletal muscle myalgia especially in skeletal muscles of neck, back, and abdomen can occur after administration.
- -especially in young adults undergoing minor procedures that permit ambulation
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giving non paralyzing dose of non-depolarizer in preop may decrease risk of
- cardiac dysrhythmias
- myalgia
- increased intragastric and intraocular pressure
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myoglobinuria and Sch
- damage to skeletal muscle is suggested by occurrence of myoglobinuria after administration
- -mostly seen in peds
- -rarely seen in adults
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increased gastric pressure and SCh
- related to intensity of fasiculations
- -give non paralyzing dose of non depolarizer and this may decreased risk of aspiration
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increased intraocular pressure and SCh
- increase in pressure 2-4 min after administration and lasts 5-10 min
- -do not use with open eye injury
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incomplete jaw relaxation and masseter jaw rigidity seen in patients after halothane, SCh administration
- not uncommon in kids and considered normal response
- -the difficulty is separating the normal response from the masseter muscle rigidity that may be associated with MH
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what are the 2 life threatening side effects of SCh that Rickey talked about in class
- hyperkalemia
- malignant hyperthermia- SCh is biggest trigger for this
- tx with dantrolene
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