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AS - N926 Pharmacology > Neuromuscular Blocking > Flashcards

Neuromuscular Blocking Flashcards

1
Q

Choline Hydrolysis

A

Acetylcholinesterase (“true” cholinesterase)
VS.
Butyrylcholinesterase (plasma cholinesterase)
PChe - pseudocholinesterase
Synthesized in liver
Succinylcholine hydrolysis in plasma

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2
Q

Muscle Relaxation Onset

A

Eye muscles > extremities > trunk > abdominal muscles > diaphragm

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3
Q

Neuromuscular Function Clinical Tests

A 
TOF
Tetanus
Post-tetanic count
Single twitch
Double-burst suppression
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4
Q

Train of Four

A

Most widely used
Four separate stimuli every 0.5sec at 2Hz
T1-T4 comparison
Non-depolarizing onset = fade
4 twitches 75-80% receptors can still be blocked
Zero twitches = 100% blocked

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5
Q

Tetany

A

Continuous electrical stimulation for 5sec at 50-100Hz
Reliable for detecting fade
Sustained contraction w/out fade = paralysis unlikely

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6
Q

Post-Tetanic Count

A

Tetany followed in 3sec by single twitch stimulations

Higher the count (>8) less intense the block

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7
Q

Single Twitch

A

Single twitch at 0.1-1Hz for 0.1-0.2sec

Determine when 100% paralysis present

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8
Q

Double-Burst Suppression

A

Seems to improve ability to detect residual paralysis

Evaluate 2 rather than 4 twitches

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9
Q

Extubation Conditions

A

5 second head life

Generate peak negative inspiratory pressure 20-30cm H2O

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10
Q

Neuromuscular Blocking Structure

A

Quaternary ammoniums = ionized
Low Vd - does not cross blood-brain or placenta
Structurally r/t ACh
Primarily synthetic alkaloids

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11
Q

Non-Depolarizing Blockade

A

Decrease in twitch tension (strength)
Fade during repetitive stimulation
Post-tetanic potentiation

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12
Q

Fade

A

Concentration
Twitch depression results from blocking post-synaptic nicotinic ACh receptors
Post-tetanic or TOF fade results from blocking PRE-synaptic nAChR ↓ACh released

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13
Q

Depolarizing Blockade

A

Phase 1 often preceded by muscle fasciculation
Decrease in twitch tension
NO fade during repetitive stimulation
NO post-tetanic potentiation

Phase 2 not commonly seen
Repeated or long-term administration
Doses >6mg/kg
Inhibit pre-synaptic nAChR

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14
Q

Succinylcholine

A

ONLY depolarizing NMBD
Two ACh molecules linked by acetate methyl groups
Intubating conditions w/in 60sec
Duration 4-5min
Recovery to 90% muscle strength 9-13min (offset)
Short action d/t rapid hydrolysis by butyrylcholinesterase

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15
Q

Butyrylcholinesterase (PChE)

A

Psuedocholinesterase
Metabolized in liver & found in plasma
Genetic variations prolong effects d/t unable to metabolize succinylcholine

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16
Q

Dibucaine

A

Local anesthetic than inhibits typical PChE
Number indicates cholinesterase quality NOT quantity
80 = 80% PChE enzyme inhibited

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17
Q

Dibucaine Number

A 
Normal genotype >70
Heterogenous for atypical gene = 40-60
→ Prolongs block 1.5-2x longer
Homogenous for atypical gene < 30
→ Block prolonged 4-8hrs (unable to extubate)
→ Overnight ICU admission
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18
Q

Succinylcholine SE

A

Bradycardia, junctional rhythm, sinus arrest
Ventricular dysrhythmias, tachycardia, ↑ BP d/t autonomic ganglia stimulation
Hyperkalemia - severe in burn, abdominal infections, metabolic acidosis, closed head injury, & nAChR upregulation
Myoglobinuria - damage to skeletal muscle (especially in pediatric patients MD or malignant hyperthermia susceptible)
↑ intraocular pressure NOT commonly used in eye surgery
↑ gastric and lower esophageal pressures (↑ gastric contents)
↑ ICP r/t head injury
Masseter spasm (early indicator) - KNOWN TRIGGER for malignant hyperthermia
Myalgias - prominent in neck, back, & abdomen skeletal muscle
Elderly: Slower onset d/t ↓ circulation & reduced PChE levels
Pediatrics: Avoided in patients <5yo, Duchenne muscular dystrophy, cardiac arrest d/t hyperkalemic rhabdomyolysis

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19
Q

Malignant Hyperthermia

A

Pharmacogenetic disorder triggered by volatile anesthetics, succinylcholine, & stress
Ryanodine receptor gene mutation (chromosome 19)
S/S: ↑ CO2 production (1st sign), muscle rigidity, ↑ peak airway pressure, ↓ TV, metabolic acidosis, ↑ temp (late sign)

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20
Q

Succinylcholine Dose

A

Intubation 1mg/kg based on ideal body weight

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21
Q

Non-Depolarizing NMBDs Classifications

A

*Steroidal - Pancuronium, Vecuronium, & Rocuronium
Most common

Benzylisoquinoliniums - Atracurium & Cisatracurium

22
Q

Atracurium

A

Benzylisoquinoliniums
Intermediate onset & action
Ester hydrolysis & spontaneous degradation
-Hoffmann elimination
Metabolite: Laudanosine (tertiary amine) implicated in convulsions
HISTAMINE RELEASE

23
Q

Atracurium Dose

A

Intubation 0.5mg/kg

24
Q

Cisatracurium

A 
Benzylisoquinoliniums
Atracurium cis-isomer
Intermediate onset &amp; action
Metabolism - Hoffmann elimination
NO histamine release
Acceptable option for liver and/or renal failure
25
Q

Cisatracurium Dose

A

Intubation 0.1mg/kg

26
Q

Mivacurium

A

Only available short-acting non-depolarizing drug available
Not used in the USA (only Europe)
Metabolized by butyrylcholinesterase in plasma
Histamine release possible

27
Q

Mivacurium Dose

A

Intubation 0.15mg/kg

28
Q

Pancuronium

A

Steroidal
Potent long-acting NMBD
Vagolytic (maintain HR & BP) and butyrylcholinesterase properties
Clearance via kidney
Small amount de-acetylated by liver
3-OH metabolite accumulation responsible for block prolongation

29
Q

Pancuronium Dose

A

Intubation 0.08mg/kg (most potent steroidal NMBD)

30
Q

Pancuronium Onset

A

SLOWEST

Onset time to maximum block 2.9min

31
Q

Vecuronium

A

Steroidal
Intermediate-acting (as compared to Pancuronium) NMBD
Essentially Pancuronium w/out quaternized methyl group - slight potency decrease, loss vagolytic properties, molecular instability (shorter duration), ↑ lipid solubility
Metabolized primarily by liver
3-OH metabolite 80% neuromuscular potency

32
Q

Vecuronium Dose

A

Intubation 0.1mg/kg

33
Q

Vecuronium Onset

A

Onset time to maximum block 2.4min

34
Q

Rocuronium

A

Steroidal
Intermediate-acting NMBD
Metabolized primarily by liver
Approximately 30% excreted in urine

35
Q

Rocuronium Dose

A

Intubation 0.6mg/kg (least potent steroidal NMBD)

6x less potent than Vecuronium

36
Q

Rocuronium Onset

A

FASTEST

Onset time to maximum block 1.7min

37
Q

Steroidal Compounds

A

Acetyl ester facilitates interaction w/ nAChR
No conformational change
Essential that 1/2 nitrogen atoms quaternized
Pancuronium, Vecuronium, Rocuroniuam
Liver & renal impact

38
Q

NMBD Potency

A

Increase: Inhalation agents, antibiotics, hypothermia, Magnesium sulfate (Ca2+ antagonist), local anesthetics, Quinidine (anti-arrythmic)

Decrease: Chronic anticonvulsant administration, hyperparathyroidism, hypercalcemia

INVERSE relationship w/ onset
Low potency = quick onset

39
Q

NMBDs Adverse Effects

A

Autonomic - block nicotinic receptors w/in SNS & PSNS → bradycardia & hypotension

Histamine - flushing, hypotension, reflex tachycardia, bronchospasm, ↑ HR, ↓ SVR
Usually short duration (1-5min)
Pre-treat w/ H1 & H2 blockers to ↓ CV effects

Respiratory r/t histamine release in patients w/ reactive airway disease ↑ airway resistance & bronchospasm

Allergic reactions - cross reactivity b/w NMBDs & food, cosmetics, disinfectants, industrial materials
Roc & Succ most common cause (also ↑ prevalence/administration)
Treatment: 100% FiO2, IV epi, intubation, fluid admin (crystalloid vs. colloid), sympathomimetic drugs (pressers)

40
Q

NMBD Reversal

A 
Acetylhcholinesterase hydrolyzes ACh - reversal dependent on ACh vs. NMBD concentration at NMJ
AChE inhibitors (Neostigmine, Edrophonium, Pyridostigmine) - antagonize residual effects, accelerate recovery, cause ACh build-up to compete w/ residual NMBD
Antagonism depends on blockage depth when reversal attempted, inhibitor chosen, dose, spontaneous clearance rate, &amp; anesthesia choice/depth
41
Q

Neostigmine

A

Ceiling effect - once reached additional doses have no effect
Maximum block depth antagonist corresponds to 4th twitch return
Cannot antagonize profound or deep blockade levels
Administering more inhibitor can have detrimental effects

42
Q

Neostigmine Dose

A

40-80mcg/kg

Maximum dose 6mg

43
Q

Edrophonium Dose

A

1-1.5mg/kg
Based on block %
Twitches number, strength, & fade

44
Q

ACh Inhibitor SE

A

Cardiovascular: Muscarinic effects MUST be blocked by anticholinergic
Pulmonary: Bronchoconstriction (↑ airway resistance & ↑ salivation)
GI: ↑ bowel motility w/ no effect on PONV incidence
Effects reduced by co-administration w/ anticholinergics

45
Q

Glycopyrrolate +

A 
NEOSTIGMINE
Similar onset times
*Match dosages*
Small w/ small
Moderate w/ moderate
Large w/ large
MAX w/ MAX
46
Q

Glycopyrrolate Dose

A

5-10mcg/kg
200mcg per 1mg Neostigmine OR
0.4mg per 2mg Neostigmine

47
Q

Atropine +

A

EDROPHONIUM
Similar onset times
Match dosages

48
Q

Atropine Dose

A

7-10mcg/kg OR 0.01mg/kg

49
Q

Only True Objective NMBD Monitoring

A 
Qualitative monitoring
Need 4/4 twitches to assess
% fade from 1st to last twitch
TOF >0.9 (90%)
Less than 0.9 associated w/ difficulty speaking &amp; swallowing, visual disturbances, &amp; aspiration risk
50
Q

Sugammadex

A

Modified gamma-cyclodextrin
Aminosteroid-induced reversal (Roc, Vec, & Panc)
Selective relaxant-binding
NO effect on acetylcholinesterase - not r/t ratio
Attaches in plasma to encapsulate NMBD therefore unable to work (inactivates)
Also encapsulates progesterone - birth control ineffective for 1wk
Ineffective against succinylcholine & benzylisoquinoliniums
Possible allergic reactions or bleeding

51
Q

Sugammadex Dose

A

Based on TOF response
TOF >2 = 2mg/kg
1-2 = 4mg/kg
0 = 8-16mg/kg

AS - N926 Pharmacology (18 decks)

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