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5230 > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

What a patient can do when 50% of their neuromuscular receptors are still occupied

A
  • Head lift
  • Sustained bite
  • Hand grip
  • Inspiratory force >40cmH2O
  • Sustained tetanus at 100Hz without fade
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2
Q

What a patient can do when still 60-70% of their neuromuscular receptors are occupied

A
  • Sustained tetanus at 50Hz for 5 seconds without fade
  • Vital capacity at least 20mL/kg
  • Double-burst stimulation without fade
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3
Q

What TOF will do when 70-75% receptors are occupied

A

No palpable fade

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4
Q

What patient can do when 80% of receptors are still occupied

A

Tidal volume of at least 5mL/kg

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5
Q

Train of four

A

Series of four twitches at 2Hz given every half second

  • Reflects blockade from 70-100%
  • Train of four ratio determined by comparing T1 to T4
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6
Q

Double-burst stimulation

A

Two short bursts of 50Hz tetanus separated by 0.75 second

-May be easier to detect fade than To4

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7
Q

Tetanus

A

Rapid delivery of 30 50 or 100Hz for 5 seconds

  • Use sparingly for deep block assessment, painful
  • Have to hold button down for 5 seconds manually, safety feature
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8
Q

Posttetanic count (PTC)

A

50Hz tetanus for 5 seconds, then 3 second pause, then single twitches at 1Hz up to 20x
-Used when To4 or double burst stimulation is absent
-At 7-9 posttetanic twitches you should get a To4 1/4
-Used to dose sugammadex for deep blocks
Tetanus stimulates acetylcholine to come out (even though you won’t get a response to the tetanus, the AcH is then mobilized in the neuromuscular junction to temporarily complete with the NMBD in the junction

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9
Q

Clinical duration vs total duration of action of NMBDs

A

Clinical duration: Time from drug administration to 25% recovery of twitch response (still 75% paralyzed)
Total duration of action: Time from drug administration to 90% recovery of twitch response

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10
Q

When is recovery indicated per To4

A

When the fourth twitch is 90% of the first

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11
Q

Chemical structure of succinylcholine, mechanism of action

A

2 Acetylcholine molecules attached to each other

  • Depolarize the nerve, stimulating muscle contraction just like acetylcholine
  • But stays on the receptor much longer than acetylcholine, during which it cannot repolarize and is refractory to another contraction
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12
Q

Function of cholinesterase, 2 types

A

Terminate the action of acetylcholine at cholinergic nerve endings in synapses or in effector organs
Type 1: Acetylcholinesterase (in nerve endings)
Type 2: Pseudocholinesterase (in plasma, >11 enzyme variants)

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13
Q

Dibucaine inhibition test

A

Dibucaine=LA that inhibits typical pseudocholinesterase but not atypical

  • Normal=80 (80% PchE activity inhibited)
  • Result of 20 means patient has atypical enzyme (dibucaine didn’t inhibit the patients enzyme activity)
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14
Q

If prolonged apnea, what do these results indicate:

  • Low dibucaine number, normal activity
  • Normal dibucaine number, low activity
  • Low dibucaine number, low activity
  • Normal dibucaine number, normal activity
A
  • Low dibucaine number, normal acitivity=atypical enzyme
  • Normal dibucaine number, low activity=normal enzyme with low levels present
  • Low dibucaine number, low activity=atypical enzyme with low levels present
  • Normal dibucaine number, normal activity=normal enzyme and amount (different reason for apnea)
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15
Q

Hyperkalemia and succinylcholine (normal increase, pt population which will increase more)

A

Normally K increases by 0.5mEq/L (K leaks from depolarized muscles)

  • May rise higher in patients after crush injuries, burns, denervating injuries, or malignant hyperthermia
  • Also patients with disuse atrophy (quad or paraplegic, bedridden patient) or severe sepsis
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16
Q

Dysrhythmias and succinylcholine

A

Wide ECG complexes leading to cardiac arrest have been seen in children with muscular dystrophy

  • Contraindicated in peds until their teenage years (may have muscular dystrophy and haven’t been diagnosed yet)
  • Still used in peds laryngospasm
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17
Q

Malignant hyperthermia and succinylcholine

A

Succinylcholine triggers MH, not understood why

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18
Q

Masseter spasm and succinylcholine

A

Rare, seen more in children than adults

-Sometimes followed by MH

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19
Q

Succinylcholine use in burn patients

A

Acetylcholine receptors are greatly upregulated post burn for >1 year+, K can rise much higher than 0.5 in these patients, succinylcholine is contraindicated

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20
Q

2 chemical structures of non-depolarizing muscle relaxants

A

Benzylisoquinolines
-Cisatracurium (same as > but doesn’t cause histamine release), atracurium, mivacurium
Steroidal
-Rocuronium, vecuronium, pancuronium

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21
Q

Hoffman elimination

A

Requires a change in temperature and pH to start metabolism

  • Drug in vial=room temp, pH 5.5 -> body=36C, pH 7.4
  • Metabolizes the same in everyone, predictable
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22
Q

Succinylcholine metabolism

A

Plasma cholinesterase

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23
Q

Cisatracurium metabolism, elimination, and metabolite

A

Metabolism: Hoffman elimination and non-specific ester hydrolysis
Elimination: Renal clearance 16% total elimination
Metabolite: Laudanosine, can be CNS toxic but because cis is so potent the quantity of metabolite produced isn’t an issue

24
Q

Vecuronium metabolism, elimination, metabolite

A

Metabolism: Liver 30-40%
Elimination: Kidney 20-40%, Liver 60-80%
Metabolite: 3-OH, accumulates in renal failure, may be responsible for delayed recovery in ICU patients

25
Q

Rocuronium metabolism, elimination, metabolite

A

Metabolism: <1%
Elimination: Kidney 10-25%, Liver 70%
Metabolite: None

26
Q

Which NMBDs may be prolonged with renal disease

A

Pancuronium, rocuronium

27
Q

Which NMBDs may be prolonged with hepatic disease

A

Rocuronium, vecuronium

28
Q

Which NMBDs will be prolonged with cholinesterase deficiency

A

Succinylcholine, mivacurium

29
Q

Which NMBDs will cause histamine release

A

Atracurium and mivacurium, slight release may occur with succinylcholine

30
Q

Cardiac effects of NMBDs (which cause hypotension/tachycardia, vagolytic, tachycardia->bradycardia)

A

Hypotension/tachycardia: Atracurium and mivacurium (because of histamine release)
Vagolytic: Pancuronium (slight catecholamine release/indirect sympathomimetic) -> tachycardia (no BP change)
Tachycardia: Usually slight with succinylcholine, repeat dosing in adults/any dose in children can produce sudden bradycardia

31
Q

Effects of stimulation of histamine receptors by NMBDs

A 
Increased capillary permeability
Bronchoconstriction
Increased gastric acid production
Systemic and cerebral vasodilation
Positive inotropic and chronotropic
Negative dromotropic (slow conduction)
32
Q

Prophylaxis against histamine release

A

Block H1 and H2 receptors
H1: Benadryl
H2: Zantac

33
Q

Factors related to anesthesia that might prolong paralysis

A 
Cholinesterase deficiency or variance
Hypothermia
Steroids
Volatile anesthetics 
Dantrolene
34
Q

Antibiotics, muscle relaxants, neostigmine, and calcium

A

Abx can cause neuromuscular blockade without NMBDs
-When combined with NMBDs they can potentiate block
(cephalosporin’s and penicillin’s haven’t been reported to potentiate block)
Neostigmine sometimes doesn’t work, and calcium shouldn’t be used to speed recovery
Wait until block terminates spontaneously

35
Q

Intubating dose of Vecuronium, time to onset, and duration of action

A

0.1 mg/kg
Onset: 2-4 minutes
Duration of action: 30-60 minutes

36
Q

Intubating dose of Cisatracurium, time to onset, and duration of action

A

0.1 mg/kg
Onset: 2-4 minutes
Duration of action: 30-60 minutes

37
Q

Intubating dose of Rocuronium, time to onset, and duration of action

A

0.6-1.2 mg/kg (RSI=1.2 mg/kg)
Onset: 1-1.5 minutes
Duration of action: 30-60 minutes

38
Q

Intubating dose of Succinylcholine (& RSI dose), time to onset, and duration of action

A

1-1.5 mg/kg (100 mg is standard)
RSI: 2 mg/kg
Onset: 30-60 seconds
Duration of action: 5-15 minutes

39
Q

Time frame since NMBDs were given when reversal should still be given

A

If time since relaxant was given is <4 hours reversal should be given

40
Q

Neostigmine dose, onset, duration, common side effect

A

Dose: .05 mg/kg (25-75mcg/kg)
Onset: 5-15 minutes
Duration: 45-90 minutes
May increase PONV

41
Q

Edrophonium dose, onset, duration, indication

A

Dose: .5-1 mg/kg
Onset: 5-10 minutes (faster than neostigmine)
Duration: 30-60 minutes
Indication: Lower efficacy, only works if block is already wearing off (not for deep block), rapid onset

42
Q

Atropine with reversal dose, onset, duration, indication

A 
Dose: 15 mcg/kg
Onset: 1-2 minutes
Duration: 1-2 hours
Indication: Anti muscarinic, given with edrophonium (more rapid onset)
*Crosses BBB
43
Q

Glycopyrrolate with reversal dose, onset, duration, indication

A 
Dose: 10-20 mcg/kg
Onset: 2 minutes
Duration: 2-4 hours
Indication: Anti muscarinic, given with neostigmine (not fast enough onset for edrophonium), less initial tachycardia than atropine
*No CNS effects (doesn't cross BBB)
44
Q

Sugammadex general dosing, onset, duration, indication

A

Dose: 2-8 mg/kg (up to 16 safely used)
Onset: 1-2 minutes
Duration: 2-16 hours
Indication: Reversal of steroidal NMBDs (works better for roc than vec)

45
Q

Sugammadex specific dosing based on To4

A

Immediate roc RSI: 16 mg/kg
1-2 PTC after 5 seconds tetanus: 4 mg/kg
To4 second twitch: 2 mg/kg (most common dose)
To4 ratio of 0.5: 0.22 mg/kg

46
Q

Max doses of neostigmine and edrophonium

A

Neostigmine: 5mg
Edrophonium: 1 mg/kg
100% of cholinesterase inhibited at these doses

47
Q

Neostigmine mechanism of action

A

Normal process: Cholinesterase binds to acetylcholine in synapse and metabolizes it
Neostigmine: Attaches to cholinesterase in the synapse so it metabolizes it instead of acetylcholine (takes 45 minutes to metabolize vs seconds for acetylcholine), acetylcholine builds up in the synapse more than the muscle relaxant to bind to receptors

48
Q

Sequence of muscles to get paralyzes

A

1: Eye lids
2: Extremities
3: Chest/intercostals
4: Abdominal muscles
5: Diaphragm
* Muscle function returns in the opposite order

49
Q

Train of four ratio to be considered “recovered”

A

90%

50
Q

Percent paralysis when train of four results are..

4/3/2/1/0 twitches

A 
4 twitches: <70%
4 twitches (with To4 ratio<90%): 70-75%
3 twitches: 75-80%
2 twitches: 80-85%
1 twitch: 90-95%
0 twitches: 100%
51
Q

“Fade” on train of four (why it happens, what it means)

A

Normal physiology: to sustain a muscle contraction there is a positive feedback mechanism on the presynaptic acetylcholine receptors to continue releasing acetylcholine
Nondepolarizing muscle relaxants block these presynaptic receptors

52
Q

Unique train of four results for succinylcholine

A

No fade, called a “sustained response”

  • Will have 4 twitches but they will all get smaller and smaller until no twitch
  • Can’t get a train of four ratio
53
Q

Posttetanic potentiation/stimulation/facilitation

A

Exaggerated response to twitches after tetanus hold (doesn’t happen with succs)

54
Q

Pretreating succs with non depolarizer (why do you do it, what happens to the dose you need to give)

A

Given to prevent fasciculations

-Antagonize block, need to give ~20% more succs

55
Q

Anticholinesterase drugs and succinylcholine

A

Block is potentiated

Succinylcholine relies on metabolism by cholinesterase just like AcH

5230 (13 decks)

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