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Flashcards in Neuromuscular Blocking Drugs Deck (75):
1

Depolarizing NMBD

Succinylcholine (only one) - mimics action of ACh

2

Major characteristics of succinylcholine

rapid onset
ultrashort acting

3

Long acting non-depol NMBD

pancuronium

4

Intermediate acting non-depolar NMBD

vecuronium
rocuronium
atracurium
cisatracurium

5

short acting non-depolar NMBD

mivacurium

6

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

rocuronium

7

Best NMBD(s) for tracheal intubation

succinycholine (rapid onset, short duration)
rocuronium (rapid onset, much longer action)

8

NMBDs given when longer surgery requiring paralysis

non-depolars

9

NMBD most likely to cause an allergic reaction

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

10

Site with highest concentration of acetylcholinesterase

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

11

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

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

12

subunits of postjunctional NMJ rectpros that ACH and NMBDs bind

two alpha subunits

13

How do non-depolarizing NMBDs work?

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

14

How do depolarizing NMBDs (SCh) work?

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

15

What is the importance of extrajunctional receptors?

location
action

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

16

Structure of NMBDs as relates to function

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)

17

Nondepolar NMBD most similar to ACh structurally

pancuronium

similarity confers high degree of NMB activity

18

NMBDs most likely to evoke a histamine response? Why?

atracurium, cisatracarium, mivacurium (Benzylisoquinolinium compounds)

presence of tertiary amine confers this activity

19

Dosing of SCh?

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

20

SCh time to onset? Duration?

30-60sec

5-10 min

21

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

increase dose by 70%

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

22

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

1.0-1.2mg/kg IV

23

Describe NM blockade by SCh
- PHASE 1
- PHASE 2

- 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

24

Signs of phase 2 blockade

fade to tetanic stimulation

25

Dose of SCH required for predominant phase 2 block

3-5 mg/kg IV

26

Metabolism of SCh

-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)

27

S/sx of atypical plasma cholinesterase?

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

28

Major side effects of SCh (8)

1. Cardiac dysrhhythmias

2. fasiculations

3. hyperkalemia

4. myalgia

5. myoglobinuria

6. increased intraocular pressure

7. increased ICP

8. Trismus

9. increased intracastric pressure

29

Types of cardiac dysrrhythmias caused by SCh?

MOA of effect?

sinus brady

junctional rythm

sinus arrest

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

30

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

2nd dose sch 5 min after first dose

tx- atropine IV 1-3min before SCh

31

factors predisposing to massive hyperkalemia w/ SCh?

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

32

Myalgia effects which sites most often 2/2 SCh

neck/ back/ abdomen

give NSAIDS

33

time frame of increased intraoccular pressure with sch

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

avoid SCh in open eye injuries

34

consequence of increased icp from sch

minimal, does not effect decisions clinically

35

Drug combination with highest risk of trismus in children?

halothane + SCh

36

Drug combination with highest risk of trismus in children?

halothane + SCh

can make determination of trismus vs malignant hyperthermia difficult

SCH not recommended in children except for emergency airway control

37

best non-depol nmbd for kidney injury/failure pts

cisatricurium (no dependence on kidney for elim)

38

non-depol nmbd antagonized by sugammadex

rocuronium

vecuronium

39

intubating dose of pancuronium mg/kg

0.1mg/kg ( ED95 0.07 mg/kg)

40

intubating dose vecuronium mg/kg

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

41

intubating dose rocuronium mg/kg

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

42

intubating dose atracurium mg/kg

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

43

intubating dose cisatricurium dosing

0.1 mg/kg ( ED95 0.05mg/kg)

44

time to onset non-dpolar nmbd

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

45

renal disease effects which non-depolar nmbds most?

pancuronium (long acting)

46

liver disease effects which non-depolar nmbds?

intermediate acting (rocuronium)

47

hoffman elimination for which non-depolar nmbds?

atricarium and cisatricarium

48

plasma cholinesterases effects which non-depolar nmbds?

mivacirium

49

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

volatile anesthetics

local anesthetics

aminoglycoside antibiotics

cardiac antiarrhythmics

dantrolene

magnesium

lithium

tamoxifen

50

drugs that diminish the effect of non-depolar nmbds?

calcium

corticosteroids

anticonvulsants (phenytoin)

51

cardiovascular effects of non-depolar nmbds?

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

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

52

How long maximally should NMBDs be used for?

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

Duration of effect of pancuronium

60-90 min

54

cardiac effects of pancuronium

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

55

intermediate acting nmbd that has cardiac effects

atriciurium

56

duration of vecuronium
metabolism
cardiac effects

20-35 min

hepatic/renal

minimal/no cardiac effects

57

duration of rocuronium
metabolism
cardiac effects

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

Atracurium duration
metabolism
cardiac effects

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

Duration of cisatricurium
metabolism
cardiac effects

20-35 min

hofmann elimination primary

no histamine effects = no cardiac changes

60

duration of mivaciurium
metabolism
cardiac effects

12-20 min

plasma cholinesterase


not available in USA

61

nerves typically used for peripheral nerve monitoring of nondepol nmbds

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

62

types of evoked responses used to monitor nmbds

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

63

Questions answered by PN stim

- is block adequate for surgery

- is block excessive?

- can block be reversed?

64

Adequate block response per single twitch and TOF stim?

single twitch- depressed by greater than 90%

TOF - elimination of 2-3 twitches

65

All TOF twitches are absent? what to do next?

don't give more nmbd until some twitch is present

66

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

reversal is likely to be successful

67

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

incompletely

phase 2 - similar to non-depol - completely fade

68

anticholinesterase typically used for nmbd reversal

neostigmine

69

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

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

70

tests that help determine skeletal muscle strength after nmbds

sustained head or leg lift for 5 sec

tongue depressor test

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

71

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

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

72

side effects of neostigmine? how to tx it?

bradycardia (muscarinic effect)

simultaneous admin of atropine or glycopyrrolate (must be given)

73

Factors influencing success of antagonism of nmbds

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

max dose of neostigmine

60-70ug/kg

75

what is sugammedex?

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