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N926 Pharmacology > NMBD > Flashcards

NMBD Flashcards

1
Q

NEUROMUSCULAR JUNCTION

  • The neuromuscular junction (NMJ) or endplate:
  • Presynaptic motor nerve ending meets ____ _____ of skeletal muscle
  • Designed to transmit impulses from_____ to _____ via ______
  • Three components:
  • ____
  • ____
  • ____
A

NEUROMUSCULAR JUNCTION

  • The neuromuscular junction (NMJ) or endplate:
  • Presynaptic motor nerve ending meets postsynaptic membranes of skeletal muscle
  • Designed to transmit impulses from nerve terminal to muscle via acetylcholine (ACh)
  • Three components:
  • Presynaptic nerve terminal
  • Synaptic cleft
  • Postsynaptic muscle membrane
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2
Q

CHOLINE HYDROLYSIS

  • _______ (“True” cholinesterase)
  • Present at the NMJ
  • Rapid ____ of acetylcholine (ACh)
  • ________ (“plasma cholinesterase”)
  • AKA… “______” (_____)
  • Synthesized in the _____
  • Hydrolysis of______ in the plasma
A

CHOLINE HYDROLYSIS

  • Acetylcholinesterase (“True” cholinesterase)
  • Present at the NMJ
  • Rapid hydrolysis of acetylcholine (ACh)
  • Butyrylcholinesterase (“plasma cholinesterase”)
  • AKA… “pseudocholinesterase” (PChE)
  • Synthesized in the liver
  • Hydrolysis of succinylcholine in the plasma
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3
Q

MONITORING

Standard of care in patients who receive a neuromuscular blocking drug (NMBD)

• Many practitioners do not monitor neuromuscular blockade:

  • Quantitative monitors are ____and ____
  • Qualitative monitoring is _____

• Residual paralysis is not an issue in “my practice”

  • May be as high as __%
  • Represents significant ____ and _____ risk
A

MONITORING

Standard of care in patients who receive a neuromuscular blocking drug (NMBD)

• Many practitioners do not monitor neuromuscular blockade:

  • Quantitative monitors are cumbersome and difficult
  • Qualitative monitoring is unreliable

• Residual paralysis is not an issue in “my practice”

  • May be as high as 25%
  • Represents significant airway and aspiration risk
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4
Q

MONITORING

Proper administration of NMBDs is essential to surgery

  • Underdosing
  • Overdosing

Contraction of the ____ muscle of the thumb (____nerve) is the preferred method of determining level of blockade

Facial nerve monitoring generally involves stimulation of the ____ _____ muscle (____ nerve)

A

MONITORING

Proper administration of NMBDs is essential to surgery

  • Underdosing
  • Overdosing

Contraction of the adductor muscle of the thumb (ulnar nerve) is the preferred method of determining level of blockade

Facial nerve monitoring generally involves stimulation of the orbicularis oculi muscle (facial nerve)

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5
Q

MONITORING

Assess the ulnar nerve or face?

Onset of relaxation

• ____ > _____ > _____ > _____ > _____

Blood flow is greatest to the ___ ____ and ____

• More drug distributed to these areas

  • Onset measured in ____nerves
  • Recovery best measured in the ______
A

MONITORING

Assess the ulnar nerve or face?

Onset of relaxation

• Eye muscles > extremities > trunk > abdominal muscles > diaphragm

Blood flow is greatest to the head neck and diaphragm

• More drug distributed to these areas

  • Onset measured in facial nerves
  • Recovery best measured in the hand
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6
Q

There are five clinical tests of neuromuscular function:

  • ____
  • ____
  • ____
  • ____
  • ____
A

There are five clinical tests of neuromuscular function:

  • Single twitch
  • Train-of-four (TOF)
  • Double-burst suppression (DBS)
  • Tetanus
  • Posttetanic count
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7
Q

MONITORING

  • TOF – most widely used means of stimulation
  • Four separate stimuli every___seconds at____Hz
  • Comparison made between the four twitches; T1-T4
  • With onset of paralysis in ______ agent there is a successive decrease in twitch response between T1-T4 (____)
  • TOF can aid in determining ______

• Most sensitive between ______% paralysis

  • T4 – ____%
  • T3-4 –____%
  • T2-4 –____%

• Zero twitches – ____%

A

MONITORING

  • TOF – most widely used means of stimulation
  • Four separate stimuli every 0.5 seconds at 2Hz
  • Comparison made between the four twitches; T1-T4
  • With onset of paralysis in non-depolarizing agent there is a successive decrease in twitch response between T1-T4 (fade)
  • TOF can aid in determining degree of block

• Most sensitive between 70-100% paralysis

  • T4 – 75-80%
  • T3-4 – 80-85%
  • T2-4 – 90-95%

• Zero twitches – 100%

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8
Q

MONITORING

Tetany – continuous electrical stimulation for___ seconds at ___- ___Hz

  • Reliable for detecting ___
  • Sustained ___ without ___; significant ___ unlikely

Posttetanic count – Tetany followed in ___seconds by ___stimulations

• The ____ the count (> ___) the ___ intense the block

A

MONITORING

Tetany – continuous electrical stimulation for 5 seconds at 50- 100Hz

  • Reliable for detecting fade
  • Sustained contraction without fade; significant paralysis unlikely

Posttetanic count – Tetany followed in 3 seconds by single twitch stimulations

• The higher the count (> 8) the less intense the block

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9
Q

MONITORING

Single twitch – single twitch at __-___ Hz for __-___ milliseconds

• Determine whether ____ is present

Double-burst suppression

  • Seems to improve ability to detect ____
  • Evaluating ___ rather than ___twitches facilitates detection
A

MONITORING

Single twitch – single twitch at 0.1-1 Hz for 0.1-0.2 milliseconds

• Determine whether 100% paralysis is present

Double-burst suppression

  • Seems to improve ability to detect residual paralysis
  • Evaluating 2 rather than 4 twitches facilitates detection
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10
Q

Not reliable indicator for ___

  • __-second head lift
  • TOF ratio < ____
  • Generate peak negative inspiratory pressure: ___-___ cmH2O
A

Not reliable indicator for endotracheal extubation

  • 5-second head lift
  • TOF ratio < 0.60
  • Generate peak negative inspiratory pressure - 20-30 cmH2O
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11
Q

NON-DEPOLARIZING BLOCKADE

Non-depolarizing neuromuscular blockade is characterized by:

  • Decrease in ____
  • ____ during repetitive stimulation
  • _____ potentiation
A

NON-DEPOLARIZING BLOCKADE

Non-depolarizing neuromuscular blockade is characterized by:

  • Decrease in twitch tension
  • Fade during repetitive stimulation
  • Posttetanic potentiation
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12
Q

FADE

Twitch depression results from block of ____ nicotinic acetylcholine receptors

___ or ____ fade results from blocking _____ nicotinic acetylcholine receptors

• Amount of ____ ACh does not match the ____

A

FADE

Twitch depression results from block of postsynaptic nicotinic acetylcholine receptors

Posttetanic or TOF fade results from blocking presynaptic nicotinic acetylcholine receptors

• Amount of released ACh does not match the demand

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13
Q

SUCCINYLCHOLINE

Only ___ NMBD
• Two ___ molecules linked by _____groups

  • Dose for tracheal intubation ____ (more towards ___ body wt)
  • Creates____ conditions in approximately___seconds
  • ____ approximately ____seconds

• Recovery to ___% muscle strength __-___ minutes

A

SUCCINYLCHOLINE

Only depolarizing NMBD
• Two ACh molecules linked by acetate methyl groups

  • Dose for tracheal intubation 1.0 mg/kg (more towards ideal body wt)
  • Creates intubating conditions in approximately 60 seconds
  • Larynx approximately 34 seconds

• Recovery to 90% muscle strength 9-13 minutes

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14
Q

SUCCINYLCHOLINE

Short action due to rapid ___ by ____

  • Into ___ and ____
  • ___ is weak ___

-further into ___ and ____

Recovery from succinylcholine motor blockade occurs as it ____ from the NMJ down a ___ _____

A

SUCCINYLCHOLINE

Short action due to rapid hydrolysis by butyrylcholinesterase

  • Into Succinylmonocholine and choline
  • Succinylmonocholine is weak NMBD

-further into Succinic acid and choline

Recovery from succinylcholine motor blockade occurs as it drifts away from the NMJ down a concentration gradient

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15
Q

BUTYRYLCHOLINESTERASE (PChE)

  • Metabolized in the ____ and found in the _____
  • Responsible for the metabolism of:

• [____]

  • Factors decreasing PChE activity include:
  • [____]
  • _____ cause a mild prolongation of succinylcholine
A

BUTYRYLCHOLINESTERASE (PChE)

  • Metabolized in the liver and found in the plasma
  • Responsible for the metabolism of:

• Succinylcholine, mivacurium, procaine, chloroprocaine, tetracaine, cocaine and heroin

  • Factors decreasing PChE activity include:
  • Advanced liver disease, age, malnutrition, pregnancy, burns, oral contraceptives, MAO inhibitors, echothiophate, cytotoxic drugs, neoplastic disease and anticholinesterase drugs
  • Beta blockers cause a mild prolongation of succinylcholine
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16
Q

BUTYRYLCHOLINESTERASE (PChE)

  • Genetic variations can cause significant prolongation of succinylcholine effects
  • ____ – local anesthetic that inhibits typical PChE
  • Dibucaine number reflects the ___ of cholinesterase not ____ (e.g. – Dibucaine of 80 infers ___of enzyme ___)
  • Normal genotype = Dibucaine number ____
  • Heterogenous for atypical gene = Dibucaine number ___
  • Prolongs block ____ times longer

• Homogeneous for atypical gene = Dibucaine number___

  • Block prolonged for ____
A

BUTYRYLCHOLINESTERASE (PChE)

  • Genetic variations can cause significant prolongation of succinylcholine effects
  • Dibucaine – local anesthetic that inhibits typical PChE
  • Dibucaine number reflects the quality of cholinesterase not quantity (e.g. – Dibucaine of 80 infers 80% of enzyme inhibited)
  • Normal genotype = Dibucaine number > 70
  • Heterogenous for atypical gene = Dibucaine number 40-60
  • Prolongs block 1.5-2 times longer

• Homogeneous for atypical gene = Dibucaine number < 30

  • Block prolonged for 4-8 hours
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17
Q

SUCCINYLCHOLINE SIDE-EFFECTS

Cardiac

  • ____, ___ rhythm or ___ arrest

• Actions of succinylcholine on ___ ____ receptors

  • More likely to occur:
  • Second dose given within ___minutes of first dose
  • ___ patients

Stimulation of ___ _____may cause:

• ___ dysrhythmias

  • ____cardia
  • Increased ____
A

SUCCINYLCHOLINE SIDE-EFFECTS

Cardiac

  • Bradycardia, junctional rhythm or sinus arrest

• Actions of succinylcholine on cardiac muscarinic receptors

  • More likely to occur:
  • Second dose given within 5 minutes of first dose
  • Pediatric patients

Stimulation of autonomic ganglia may cause:

• Ventricular dysrhythmias

  • Tachycardia
  • Increased blood pressure
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18
Q

SUCCINYLCHOLINE SIDE-EFFECTS

Hyper____

  • ______ increase in plasma concentration in healthy individuals
  • May be severe in:
  • [_______] and conditions associated with ___regulation of _____(____, _____, ____)
  • Should be avoided in _____ except for_____

_______uria

  • Damage to _____; especially ____ patients
  • Most found to have muscular _____ or be _____ susceptible
A

SUCCINYLCHOLINE SIDE-EFFECTS

Hyperkalemia

  • 0.5 mEq/dL increase in plasma concentration in healthy individuals
  • May be severe in:
  • Burn patients, abdominal infections, metabolic acidosis, closed head injury and conditions associated with upregulation of nAChR (paraplegia, muscular dystrophy, Guillain-Barre’)
  • Should be avoided in children except for emergency intubation

Myoglobinuria

  • Damage to skeletal muscle; especially pediatric patients
  • Most found to have muscular dystrophy or be malignant hyperthermia susceptible
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19
Q

SUCCINYLCHOLINE SIDE-EFFECTS

Increased _____ pressure

  • Peaks at __-____ minutes; pressure returns to normal by ____ minutes
  • Not widely accepted in open eye injury

Increased ____ and lower _____ pressures

  • Related to intensity of ____ of ____ muscles
  • Prevented by prior administration of _____ drug
  • Does not increase risk of _____

Increased ____ pressure

• Can be attenuated with pretreatment of ______ drug

A

SUCCINYLCHOLINE SIDE-EFFECTS

Increased intraocular pressure

  • Peaks at 2-4 minutes; pressure returns to normal by 6 minutes
  • Not widely accepted in open eye injury

Increased intragastric and lower esophageal pressures

  • Related to intensity of fasciculations of abdominal muscles
  • Prevented by prior administration of non-depolarizing drug
  • Does not increase risk of regurgitation

Increased intracranial pressure

• Can be attenuated with pretreatment of non-depolarizing drug

20
Q

SUCCINYLCHOLINE SIDE-EFFECTS

____ spasm

  • Succinylcholine is a known trigger for ______
  • ____ ____ may be an early indicator of ___, however not consistently seen
  • Possibly due to ____ dosing

_____gias

  • Prominent in skeletal muscle of the ___, ____ and ____
  • Greater in ____, _____ and _____patients
  • Not well understood; possible muscle injury due to ____

-Pretreatment with_____, _____ or _____

*_____ occur even in absence of ______

A

SUCCINYLCHOLINE SIDE-EFFECTS

Masseter spasm

  • Succinylcholine is a known trigger for malignant hyperthermia
  • Masseter spasm may be an early indicator of MH, however not consistently seen
  • Possibly due to inadequate dosing

Myalgias

  • Prominent in skeletal muscle of the neck, back and abdomen
  • Greater in young adults, females and ambulatory surgery patients
  • Not well understood; possible muscle injury due to fasciculations

-Pretreatment with non-depolarizing drug, lidocaine or NSAIDs

*Myalgias occur even in absence of succinylcholine

21
Q

SUCCINYLCHOLINE SIDE-EFFECTS

Special populations

  • _____
  • Onsets lower due to decreased _____
  • Reduced levels of ____
  • Certain ____ medications may prolong actions
  • _____
  • Avoided in ___ patients < ____years-old
  • _______ (DMD)
  • _____ from hyperkalemic; _____lysis
A

SUCCINYLCHOLINE SIDE-EFFECTS

Special populations

  • Elderly
  • Onsets lower due to decreased circulation
  • Reduced levels of PChE
  • Certain Alzheimer medications may prolong actions
  • Pediatrics
  • Avoided in pediatric patients < 5 years-old
  • Duchene muscular dystrophy (DMD)
  • Cardiac arrest from hyperkalemic; rhabdomyolysis
22
Q

MALIGNANT HYPERTHERMIA

  • Pharmacogenetic disorder triggered by:

• ____

  • ____
  • _____
  • _____ receptor gene mutation (chromosome ____)
  • Signs and symptoms include:

• Increase in _____ production

  • Muscle ____
  • Metabolic _____
  • ____ (late sign)
A

MALIGNANT HYPERTHERMIA

  • Pharmacogenetic disorder triggered by:

• Volatile anesthetics

  • Succinylcholine
  • Stress
  • Ryanodine receptor gene mutation (chromosome 19)
  • Signs and symptoms include:

• Increase in carbon dioxide production

  • Muscle rigidity
  • Metabolic acidosis
  • High temperature (late sign)
23
Q

NON-DEPOLARIZING NMBDs

Classification by structure

  • _____
  • _____

• Other

Classification by action

  • ____
  • ____

• ____

A

NON-DEPOLARIZING NMBDs

Classification by structure

  • Steroidal
  • Benzylisoquinolinium

• Other

Classification by action

  • Long-acting
  • Intermediate-acting

• Short-acting

24
Q

ATRACURIUM

________ RELEASE

  • Racemic mixture of ___ stereoisomers separated into three geometrical isomer groups:

• ___, ____, ____

  • _____e-acting and onset

• Intubating dose____

  • Undergoes ____ and ____ degradation

• _____ elimination

______ (tertiary amine) metabolite implicated in convulsions

• Doses given in anesthesia not capable of producing this

A

ATRACURIUM

HISTAMINE RELEASE

  • Racemic mixture of 10 stereoisomers separated into three geometrical isomer groups:

• cis-cis, cis-trans, trans-trans

  • Intermediate-acting and onset

• Intubating dose 0.5 mg/kg

  • Undergoes ester hydrolysis and spontaneous degradation

• Hoffmann elimination

Laudanosine (tertiary amine) metabolite implicated in convulsions• Doses given in anesthesia not capable of producing this

25
Q

CISATRICURIUM

The____ isomer of atracurium

______ onset and action

• Intubating dose ______

Metabolized by _____elimination

• There is no ______

Unlike atracurium, it does not cause_______

A

CISATRICURIUM

The cis isomer of atracurium

Intermediate onset and action

• Intubating dose 0.1 mg/kg

Metabolized by Hoffman elimination

• There is no ester hydrolysis

Unlike atracurium, it does not cause histamine release

26
Q

MIVACURIUM

Only available _______ non-depolarizer available

  • Not used in ____
  • Intubating dose ______

Metabolized by ________

  • ______ rate of succinylcholine
  • _____, ____ acid

May produce _______

A

MIVACURIUM

Only available short-acting non-depolarizer available

  • Not used in the United States
  • Intubating dose 0.15 mg/kg

Metabolized by butyrylcholinesterase

  • 70-88% rate of succinylcholine
  • Monoester, dicarboxylic acid

May produce histamine release

27
Q

STEROIDAL COMPOUNDS

  • ______ thought to facilitate interaction with _____
  • Essential that one of two______ atoms are _____

Steroidal compounds include:

  • _____
  • _____
  • _____
A

STEROIDAL COMPOUNDS

  • Acetyl ester thought to facilitate interaction with nAChR
  • Essential that one of two nitrogen atoms are quaternized

Steroidal compounds include:

  • Pancuronium
  • Vecuronium
  • Rocuronium
28
Q

PANCURONIUM

Potent ____-acting neuromuscular blocking drug

  • Intubating dose –_____
  • Onset time to maximum block – ____ minutes

___lytic and _____-inhibiting properties

Majority cleared by the ____

  • Small amount _____ by the liver
  • Accumulation of ______ responsible for block prolongation
A

PANCURONIUM

Potent long-acting neuromuscular blocking drug

  • Intubating dose – 0.08 mg/kg
  • Onset time to maximum block – 2.9 minutes

Vagolytic and butyrylcholinesterase-inhibiting properties

Majority cleared by the kidney

  • Small amount deacetylated by the liver
  • Accumulation of 3-OH metabolite responsible for block prolongation
29
Q

VECURONIUM

____-acting neuromuscular blocking drug

  • Intubating dose – ____
  • Onset time to maximum block – ____

Essentially Pancuronium without_______group

  • Slight _____ in potency
  • Loss of ______ properties
  • Molecular _____ (_____ duration of action)

• ______ lipid solubility

Metabolized principally by the _____

• 3-OH metabolite has _____ of neuromuscular potency

A

VECURONIUM

Intermediate-acting neuromuscular blocking drug

  • Intubating dose – 0.1 mg/kg
  • Onset time to maximum block – 2.4 minutes

Essentially Pancuronium without quaternized methyl group

  • Slight decrease in potency
  • Loss of vagolytic properties
  • Molecular instability (shorter duration of action)

• Increased lipid solubility

Metabolized principally by the liver

• 3-OH metabolite has 80% of neuromuscular potency

30
Q

ROCURONIUM

______-acting neuromuscular blocker

  • Intubating dose – _____
  • Time to maximum block – _____

_____ onset of action than ___ or ____

• ____ times ____ potent than vecuronium

Primarily metabolized in the _____

• Approximately ____% is excreted in the ____

A

ROCURONIUM

Intermediate-acting neuromuscular blocker

  • Intubating dose – 0.6 mg/kg
  • Time to maximum block – 1.7 minutes

Faster onset of action than pancuronium or vecuronium

• Six times less potent than vecuronium

Primarily metabolized in the liver

• Approximately 30% is excreted in the urine

31
Q

NMBD POTENCY

Factors that increase potency include:

  • _____ agents:
  • _____ of _____ anesthesia
  • Type of agent

____>____>____>_____>______

  • Antibiotics:
  • Type of abx ______: for example ____
  • ______thermia
  • _______ (calcium antagonist)
  • _____ anesthetics
  • _______
A

NMBD POTENCY

Factors that increase potency include:

  • Inhalational agents:
  • Length of inhalational anesthesia
  • Type of agent

desflurane>sevoflurane>isoflurane>nitrous oxide>IV anesthesia

  • Antibiotics:
  • Aminoglycosides: Clindamycin
  • Hypothermia
  • Magnesium sulfate (calcium antagonist)
  • Local anesthetics
  • Quinidine
32
Q

NMBD POTENCY

Factors that decrease potency include:

  • Chronic _____ administration
  • ______parathyroidism and hyper_____
  • Decreased _______ sensitivity
A

NMBD POTENCY

Factors that decrease potency include:

  • Chronic anticonvulsant administration
  • Hyperparathyroidism and hypercalcemia
  • Decreased atracurium sensitivity
33
Q

POTENCY AND ONSET

  • Potency and onset of action have an _____ relationship

• ____ potency = _____ onset

  • Buffered diffusion seen with high potency drugs

• Drug diffusion is impeded because it binds to high-density receptors in a confined space

A

POTENCY AND ONSET

  • Potency and onset of action have an inverse relationship

• Low potency = fast onset

  • Buffered diffusion seen with high potency drugs

• Drug diffusion is impeded because it binds to high-density receptors in a confined space

34
Q

ADVERSE EFFECTS OF NMBDs

Autonomic effects:

• May also block ____ receptors within ____ and _____ nervous system

  • ___cardia and ____tension
  • ____ release – ____, ____, reflex ___ and ___
  • _____ has direct vagolytic effects
  • Block _____ receptors
  • Inhibition of ____ feedback system where ____ release is ____ or ____
A

ADVERSE EFFECTS OF NMBDs

Autonomic effects:

• May also block nicotinic receptors within sympathetic and parasympathetic nervous system

  • Bradycardia and hypotension
  • Histamine release – flushing, hypotension, reflex tachycardia and bronchospasm
  • Pancuronium has direct vagolytic effects
  • Block muscarinic receptors
  • Inhibition of negative feedback system where catecholamine release is modulated or prevented
35
Q

ADVERSE EFFECTS OF NMBDs

Histamine release

Skin ____, ____, decrease in ___ ___ ___, increased _____

Seen in ____
• ___, ____ and ____

Usually ___ duration (__ to __minutes)

_____ administration or pretreatment with___and___blockers to reduce ______ effects

A

ADVERSE EFFECTS OF NMBDs

Histamine release

Skin flushing, hypotension, decrease in systemic vascular resistance, increased heart rate

Seen in benzylisoquinolinium
• Mivacurium, atracurium and tubocurarine

Usually short duration (1 to 5 minutes)

Slow administration or pretreatment with H1 and H2 blockers to reduce cardiovascular effects

36
Q

ADVERSE EFFECTS OF NMBDs

Respiratory effects

  • Related to _____ release in patients with ____ _____ disease
  • Increased ____ _____ and ______
A

ADVERSE EFFECTS OF NMBDs

Respiratory effects

  • Related to histamine release in patients with reactive airway disease
  • Increased airway resistance and bronchospasm
37
Q

ADVERSE EFFECTS OF NMBDs

Allergic reactions

  • NMBD are a common cause of ____ allergic reactions
  • ____ and ______
  • 1:___ – _____
  • ____ reactivity between NMBDs and:

___, ____, ____ and ____ materials

• Treatment includes:

  • ___
  • ____
  • ____
  • ____

• ____

A

ADVERSE EFFECTS OF NMBDs

Allergic reactions

  • NMBD are a common cause of perioperative allergic reactions
  • Rocuronium and succinylcholine
  • 1:1,000 – 25,000
  • Cross reactivity between NMBDs and:

Food, cosmetics, disinfectants and industrial materials

• Treatment includes:

  • 100% oxygen
  • Intravenous epinephrine
  • Early tracheal intubation
  • Fluid administration (crystalloid vs. colloid)

• Sympathomimetic drug

38
Q

NMBD REVERSAL

____ (_____) rapidly ____ ACh

• Reversal of NMBD is predicated on creating ___-____ of ACh at _____

AChE inhibitors:

  • _____ residual effects of NMBD
  • Accelerate recovery from ___-_____ drugs

AChE inhibitors include:

  • _____
  • _____

• ______

A

NMBD REVERSAL

Acetylcholinesterase (AChE) rapidly hydrolyzes ACh

• Reversal of NMBD is predicated on creating build-up of ACh at NMJ

AChE inhibitors:

  • Antagonize residual effects of NMBD
  • Accelerate recovery from non-depolarizing drugs

AChE inhibitors include:

  • Neostigmine
  • Edrophonium

• Pyridostigmine

39
Q

NMBD REVERSAL

AChE inhibitors cause a build-up of ____ in NMJ

• Compete with ___ _____ for unoccupied ______

Neostigmine has a _____ effect, once reached additional doses have ___ effect

  • Maximum block depth that can be antagonized corresponds to return of _____ twitch in TOF
  • Cannot antagonize ____ or _____ levels of blockade
  • Administering more _____ may be ________
A

NMBD REVERSAL

AChE inhibitors cause a build-up of ACh in NMJ

• Compete with residual NMBD for unoccupied nAChR

Neostigmine has a ceiling effect, once reached additional doses have no effect

  • Maximum block depth that can be antagonized corresponds to return of fourth twitch in TOF
  • Cannot antagonize profound or deep levels of blockade
  • Administering more inhibitor may be detrimental
40
Q

NMBD REVERSAL

Antagonism of NMBDs depends on:

  • _____ of blockade when reversal is attempted
  • ____ chosen
  • _____
  • Rate of _____ of NMBD
  • ___ and ____ of anesthesia

Maximum effective doses:

  • Neostigmine – _____
  • Edrophonium –______
A

NMBD REVERSAL

Antagonism of NMBDs depends on:

  • Depth of blockade when reversal is attempted
  • Inhibitor chosen
  • Dose
  • Rate of spontaneous clear of NMBD
  • Choice and depth of anesthesia

Maximum effective doses:

  • Neostigmine – 0.06-0.08 mg/kg
  • Edrophonium – 1.0-1.5 mg/kg
41
Q

ACh INHIBITOR SIDE-EFFECTS

  • Cardiovascular

• Muscarinic effects must be blocked by anticholinergic

  • Glycopyrrolate – ____
  • Atropine – _______
  • Administered with AChE inhibitor
  • ____ and _____
  • ____ and _____
A

ACh INHIBITOR SIDE-EFFECTS

  • Cardiovascular

• Muscarinic effects must be blocked by anticholinergic

  • Glycopyrrolate – 5-10 mcg/kg
  • Atropine – 7-10 mcg/kg
  • Administered with AChE inhibitor
  • Edrophonium and atropine
  • Neostigmine and glycopyrrolate
42
Q

AChE INHIBITOR SIDE-EFFECTS

Pulmonary

• ____

* Increased airway ____

* Increased _____

Effects reduced by coadministration of ____

• Gastrointestinal

* Increased ____
* ?____ effect on incidence of _____?

A

AChE INHIBITOR SIDE-EFFECTS

Pulmonary

• Bronchoconstriction

* Increased airway resistance

* Increased salivation

Effects reduced by coadministration of anticholinergics

• Gastrointestinal

* Increased bowel motility
* ?No effect on incidence of PONV?

43
Q

MONITORING CRITERIA

Following administration of NMBD it is essential to ensure adequate reversal

  • TOF > ___
  • Less than ____ is associated with:
  • Difficulty ____
  • Difficulty _____
  • _____ disturbances
  • ______ risk
A

MONITORING CRITERIA

Following administration of NMBD it is essential to ensure adequate reversal

  • TOF > 0.9
  • Less than 0.9 is associated with:
  • Difficulty speaking
  • Difficulty swallowing
  • Visual disturbances
  • Aspiration risk
44
Q

SUGAMMADEX

Dosing

  • TOF > _
  • TOF __ – ____
  • TOF __ – _____

Ineffective against ___ or ____ Possible ___ reactions and ____

A

SUGAMMADEX

Dosing

  • TOF>2–2mg/kg
  • TOF 1-2 – 4 mg/kg
  • TOF 0 – 8-16 mg/kg

Ineffective against succinylcholine or benzylisoquinoliniums Possible allergic reactions and bleeding

45
Q

NMB STRUCTURE

All neuromuscular blockers are ____ ____

  • Structurally related to ____
  • Majority are ____ _____

• ______ is the exception

A

NMB STRUCTURE

All neuromuscular blockers are quaternary ammoniums

  • Structurally related to ACh
  • Majority are synthetic alkaloids

• Tubocurarine is the exception

46
Q

DEPOLARIZING BLOCKADE

Aka “_____” is often preceded by___ _____

Depolarizing block is characterized by:

  • Decrease in __ ____
  • No ___ during repetitive stimulation
  • No _____ ____

”Phase II block” seen in ___ or ____administration

  • Doses > ____
  • Inhibit _____AChR
A

DEPOLARIZING BLOCKADE

Aka “phase I block” is often preceded by muscle fasciculation

Depolarizing block is characterized by:

  • Decrease in twitch tension
  • No fade during repetitive stimulation
  • No posttetanic potentiation

”Phase II block” seen in repeated or long-term administration

  • Doses > 6 mg/kg
  • Inhibit pre-synaptic AChR
47
Q

SUGAMMADEX

Modified ___-____

Reversal of ____ and _____ _____-induced blockade

• ____ > ____ >> _____
-_____forces, _____bonds and _____ actions

Selective _____-binding

• No effect on _____

A

SUGAMMADEX

Modified gamma-cyclodextrin

Reversal of shallow and profound aminosteroid-induced blockade

• Rocuronium > vecuronium >> pancuronium
-Van der Waals forces, hydrogen bonds and hydrophobic actions

Selective relaxant-binding

• No effect on acetylcholinesterase

N926 Pharmacology (16 decks)

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