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Anesthesia > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

Depolarizing NMBD

A

Succinylcholine (only one) - mimics action of ACh

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2
Q

Major characteristics of succinylcholine

A

rapid onset

ultrashort acting

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3
Q

Long acting non-depol NMBD

A

pancuronium

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4
Q

Intermediate acting non-depolar NMBD

A

vecuronium
rocuronium
atracurium
cisatracurium

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5
Q

short acting non-depolar NMBD

A

mivacurium

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6
Q

Which non-depolar NMBD time to onset is similar to succinylcholine?

A

rocuronium

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7
Q

Best NMBD(s) for tracheal intubation

A

succinycholine (rapid onset, short duration)

rocuronium (rapid onset, much longer action)

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8
Q

NMBDs given when longer surgery requiring paralysis

A

non-depolars

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9
Q

NMBD most likely to cause an allergic reaction

A

succinylcholine (most likely to cause hypersensitivity of all anesthetic drugs)

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10
Q

Site with highest concentration of acetylcholinesterase

A

folds of post-synaptic end-plate region of NMJ (close proximity to site of action of ACh)

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11
Q

physiologically, why is there a fade in response to high frequency repetative stimulation (ie train of 4 stim)

A

binding and inhibition of presynatpic nAChRs (cannot uptake ACh back into nerve terminal so diminishing amount available to act)

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12
Q

subunits of postjunctional NMJ rectpros that ACH and NMBDs bind

A

two alpha subunits

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13
Q

How do non-depolarizing NMBDs work?

A

bind to 1 or both of alpha receptors = ion channel bloked/closed = no depolarization can occur

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14
Q

How do depolarizing NMBDs (SCh) work?

A

attaches to alpha site = ion channel remains open = prolonged depolarization

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15
Q

What is the importance of extrajunctional receptors?

location
action

A

Location - projectional receptors and throughout skeletal muscle

Synthesis is normaly suppressed by neural activity

Prolonged inactivity, sepsis, denervation (ALS, etc), trauma/burn = increase proliferation of extrajunctional

***Activated extrajunctional receptors = allow extra ion flow = HYPERKALEMIA IN RESPONSE TO SCh

**Proliferation = resistance/tolerance to non-depol NMBDs in burn patients/mech vent pts

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16
Q

Structure of NMBDs as relates to function

A

Quaternary ammonium compound with 1+ nitrogen charged attoms = binds with alpha subunit of postsynaptic ACh receptor

SCh = 2 ACh bound by methyl group (smaller/flexible vs non-depolar NMBDs = can activate as opposed to block)

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17
Q

Nondepolar NMBD most similar to ACh structurally

A

pancuronium

similarity confers high degree of NMB activity

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18
Q

NMBDs most likely to evoke a histamine response? Why?

A

atracurium, cisatracarium, mivacurium (Benzylisoquinolinium compounds)

presence of tertiary amine confers this activity

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19
Q

Dosing of SCh?

A

0.5-1.5mg/kg IV (typically 1-1.5mg/kg for tracheal intubation)

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20
Q

SCh time to onset? Duration?

A

30-60sec

5-10 min

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21
Q

How should doses of SCh be adjusted if you give non-depolar NMBD prior to SCh for intubation (avoid fasiculations)?

A

increase dose by 70%

NMBD dosing for this would be 5-10% of the effective paralytic dosing given 2-4 min before SCh

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22
Q

Dosing of Roccuronium (for equivalent onset time of SCh)?

A

1.0-1.2mg/kg IV

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23
Q

Describe NM blockade by SCh

  • PHASE 1
  • PHASE 2
A
  • depolarized postjunctional membrane and inactivated Na channels cannot respond to subsequent release of ACh = PHASE I BLOCK

PHASE 2 BLOCK:
postjunctional membrane repolarized by does not respond normally to ACh (desensitization block)= similar to non-depolar NMBDs

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24
Q

Signs of phase 2 blockade

A

fade to tetanic stimulation

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25
Q

Dose of SCH required for predominant phase 2 block

A

3-5 mg/kg IV

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26
Q

Metabolism of SCh

A
  • hydrolysis by plasma cholinesterase (pseudocholinesterase) = rapid (only small fraction of original dose reaches site of action, controls duration of effect by nature of how much reaches NMJ)
  • termination of effect = diffusion away from NMJ (no plasma cholinesterase at NMJ)
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27
Q

S/sx of atypical plasma cholinesterase?

A

otherwise healthy pt experiences prolonged skeletal muscle paralysis (> 1 hr) after conventional dose of SCh or mivacurium (cannot metabolize ester bond)

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28
Q

Major side effects of SCh (8)

A
  1. Cardiac dysrhhythmias
  2. fasiculations
  3. hyperkalemia
  4. myalgia
  5. myoglobinuria
  6. increased intraocular pressure
  7. increased ICP
  8. Trismus
  9. increased intracastric pressure
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29
Q

Types of cardiac dysrrhythmias caused by SCh?

MOA of effect?

A

sinus brady

junctional rythm

sinus arrest

MOA- effect of action of SCh at cardiac postganglionic muscarinic receptor (mimic ACh = increased parasymp effect)

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30
Q

When are dyssrhtymia associated with SCH most likely to occur? tx?

A

2nd dose sch 5 min after first dose

tx- atropine IV 1-3min before SCh

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31
Q

factors predisposing to massive hyperkalemia w/ SCh?

A

burns
trauma
spinal cord/neurologic damage (ALS, etc)
immobility/critical care patients

32
Q

Myalgia effects which sites most often 2/2 SCh

A

neck/ back/ abdomen

give NSAIDS

33
Q

time frame of increased intraoccular pressure with sch

A

2-4 min after administration, lats 5-10 min

avoid SCh in open eye injuries

34
Q

consequence of increased icp from sch

A

minimal, does not effect decisions clinically

35
Q

Drug combination with highest risk of trismus in children?

A

halothane + SCh

36
Q

Drug combination with highest risk of trismus in children?

A

halothane + SCh

can make determination of trismus vs malignant hyperthermia difficult

SCH not recommended in children except for emergency airway control

37
Q

best non-depol nmbd for kidney injury/failure pts

A

cisatricurium (no dependence on kidney for elim)

38
Q

non-depol nmbd antagonized by sugammadex

A

rocuronium

vecuronium

39
Q

intubating dose of pancuronium mg/kg

A

0.1mg/kg ( ED95 0.07 mg/kg)

40
Q

intubating dose vecuronium mg/kg

A

0.08-0.1 mg/kg (ED95 0.05mg/kg)

41
Q

intubating dose rocuronium mg/kg

A

0.6-1.2mg/kg ( ED95 0.3mg/kg)

42
Q

intubating dose atracurium mg/kg

A

0.4-0.5 mg/kg ( ED95 0.2mg/kg)

43
Q

intubating dose cisatricurium dosing

A

0.1 mg/kg ( ED95 0.05mg/kg)

44
Q

time to onset non-dpolar nmbd

A

rocuronium (1-2 min) > mivacurium (2-3 min) > the rest (3-5min)

45
Q

renal disease effects which non-depolar nmbds most?

A

pancuronium (long acting)

46
Q

liver disease effects which non-depolar nmbds?

A

intermediate acting (rocuronium)

47
Q

hoffman elimination for which non-depolar nmbds?

A

atricarium and cisatricarium

48
Q

plasma cholinesterases effects which non-depolar nmbds?

A

mivacirium

49
Q

Drugs that can decrease required NMBD (non-depolar) conc needed for effect?

A

volatile anesthetics

local anesthetics

aminoglycoside antibiotics

cardiac antiarrhythmics

dantrolene

magnesium

lithium

tamoxifen

50
Q

drugs that diminish the effect of non-depolar nmbds?

A

calcium

corticosteroids

anticonvulsants (phenytoin)

51
Q

cardiovascular effects of non-depolar nmbds?

A

minimal- some hypotension via histamine/muscarinic and nicotininc ACh effects

variable depending on underlying factor (autonimic, volume status, preop meds, etc)

52
Q

How long maximally should NMBDs be used for?

A

2 days max to decrease risk of prolonged myopathy

only with concurrent use of analgesics, sedatives, and adjusted ventilator settings to decrease their use

53
Q

Duration of effect of pancuronium

A

60-90 min

54
Q

cardiac effects of pancuronium

A

modest increase in HR, MAP, and CO (block muscarinic = acts like atropine at SA node)

55
Q

intermediate acting nmbd that has cardiac effects

A

atriciurium

56
Q

duration of vecuronium
metabolism
cardiac effects

A

20-35 min

hepatic/renal

minimal/no cardiac effects

57
Q

duration of rocuronium
metabolism
cardiac effects

A

20-35 min (longer ~60-90 min if using SCh onset equivalent dosing of 1.2mg/kg)

liver/renal

little to no cardiac effects

58
Q

Atracurium duration
metabolism
cardiac effects

A

20-35 min

chemical/hofmann elimination (nonenzmatic degradation) + enzymatic ester hydrolysis

CNS stimulation occurs by metabolite laudanosine

histamine release = hypotension and tachycardia (if dose >2x ED95)

59
Q

Duration of cisatricurium
metabolism
cardiac effects

A

20-35 min

hofmann elimination primary

no histamine effects = no cardiac changes

60
Q

duration of mivaciurium
metabolism
cardiac effects

A

12-20 min

plasma cholinesterase

not available in USA

61
Q

nerves typically used for peripheral nerve monitoring of nondepol nmbds

A 
facial nerve (orbicularis oculi)
ulnar nerve (adductor pollicus) - closely reflects blockade at larynx (clinically important for reversal)
62
Q

types of evoked responses used to monitor nmbds

A 
single twitch response
train of four (TOF) ratio
double burst suppression
tetanus
post-tetanic stim
63
Q

Questions answered by PN stim

A
  • is block adequate for surgery
  • is block excessive?
  • can block be reversed?
64
Q

Adequate block response per single twitch and TOF stim?

A

single twitch- depressed by greater than 90%

TOF - elimination of 2-3 twitches

65
Q

All TOF twitches are absent? what to do next?

A

don’t give more nmbd until some twitch is present

66
Q

Some twitches are present on TOF stim…should you reverse or give more?

A

reversal is likely to be successful

67
Q

Does tetanus stimulation fade completely or incompletely with phase 1 block of Sch?

A

incompletely

phase 2 - similar to non-depol - completely fade

68
Q

anticholinesterase typically used for nmbd reversal

A

neostigmine

69
Q

all tests are normal (TOF, burst suppresion, etc), how many receptors could still be blocked by nmbd?

A

up to 50% - need more than this for skeletal muscle strength

70
Q

tests that help determine skeletal muscle strength after nmbds

A

sustained head or leg lift for 5 sec

tongue depressor test

TOF > 0.9 (first twitch and 4th twitch nearly the same)

71
Q

Why does neostigmine help reverse nmj blockade by non-depol nmbds?

A

decrease activity of acetylcholinesterase = increase ACh = increased chance ACh will bind to NMJ and not drug (increased competition) = restore NM transmission

72
Q

side effects of neostigmine? how to tx it?

A

bradycardia (muscarinic effect)

simultaneous admin of atropine or glycopyrrolate (must be given)

73
Q

Factors influencing success of antagonism of nmbds

A
  1. intensity of blockade at time of administration
  2. choice of drug
  3. dose of drug
  4. rate of concurrent spontaneous recovery
  5. conc of inhaled anesthetic
74
Q

max dose of neostigmine

A

60-70ug/kg

75
Q

what is sugammedex?

A

drug that encapsulate and inactivates steroidal nmbds (rocuronium)

no effect on nmj itself

rapidly reverse effect, 2-3 min, and is complete

no CV effects

Anesthesia (9 decks)

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