NMB Succinylcholine

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  1. what is the only depolarizing NMB in clinical use
  2. SCh produces
    intense paralysis rapids, and effects are likely to wane before preoxygenated patient becomes hypoxic
  3. how is SCh supplied
  4. what is induction dose of SCh
    1-2 mg/kg

    3-4 x's the ED95
  5. What is onset of Sch
    30 seconds
  6. 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
  7. SCh has slight _____ release, moderate ______ stimulation, and modest _____ stimulation
    • histamine
    • muscarinic -cardiac
    • nicotinic- nmj
  8. pre oxygenated adults can experience ____ minutes of apnea before sat drops below 90%
    8 minutes
  9. 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
  10. depolarizing NM blockade is also referred to as
    phase I blockade
  11. 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
  12. the onset of phase I blockade is accompanied by
    skeletal muscle fasiculations that reflect the generalized depolarization of post junctional membrane produced by SCh
  13. 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
  14. giving anticholinergic in phase I blockade will what
    enhancement of existing NM blockade
  15. Phase II blockade can be antagonized by what
    anticholinesterase drugs
  16. 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
  17. 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.
  18. neuromuscular blockade is terminated by
    diffusion away from NMJ into the ECF
  19. plasma cholinesterase produced by
    • liver
    • -liver disease must be severe before decreases in plasma cholinesterase are sufficient to prolong NM blockade
  20. what drugs decrease plasma cholinesterase leading to  prolonged effects of Sch
    • neostigmine
    • anticholinesterase drugs (used in glaucoma and MG)
    • chemo drugs
    • reglan (metoclopramide)
  21. what causes increase in plasma cholinesterase increasing the needs for SCh
  22. 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.
  23. dibucaine
    a local anesthetic that inhibits the activity of normal plasma cholinesterase activity by 80% compared with 20% atypical enzyme
  24. dibucaine number of 80
    • confirms the presence of normal plasma cholinesterase activity
    • -
  25. dibucaine number of 20
    indicates atypical plasma cholinesterase and that blockade could last for 3 hours or longer after normal dose.
  26. adverse side effects of SCh
    • cardiac dysrhythmias
    • hyperkalemia
    • myalgia
    • myoglobinuria
    • increased gastric pressure
    • increased intraocular pressure
    • increased ICP
    • sustained skeletal muscle contractions
  27. 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
  28. 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
  29. do not give SCh to kids under 6 why?
    some forms of muscular dystrophy do not appear until children are 6 years old.
  30. 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
  31. giving non paralyzing dose of non-depolarizer in preop may decrease risk of
    • cardiac dysrhythmias
    • myalgia
    • increased intragastric and intraocular pressure
  32. myoglobinuria and Sch
    • damage to skeletal muscle is suggested by occurrence of myoglobinuria after administration
    • -mostly seen in peds
    • -rarely seen in adults
  33. increased gastric pressure and SCh
    • related to intensity of fasiculations
    • -give non paralyzing dose of non depolarizer and this may decreased risk of aspiration
  34. 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
  35. 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
  36. 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
Card Set:
NMB Succinylcholine
2014-01-31 20:05:12
anesthesia pharm
anesthesia pharm test 1
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