NMBD Flashcards
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:
- ____
- ____
- ____
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
CHOLINE HYDROLYSIS
- _______ (“True” cholinesterase)
- Present at the NMJ
- Rapid ____ of acetylcholine (ACh)
- ________ (“plasma cholinesterase”)
- AKA… “______” (_____)
- Synthesized in the _____
- Hydrolysis of______ in the plasma
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
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
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
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)
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)
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 ______
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
There are five clinical tests of neuromuscular function:
- ____
- ____
- ____
- ____
- ____
There are five clinical tests of neuromuscular function:
- Single twitch
- Train-of-four (TOF)
- Double-burst suppression (DBS)
- Tetanus
- Posttetanic count
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 – ____%
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%
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
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
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
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
Not reliable indicator for ___
- __-second head lift
- TOF ratio < ____
- Generate peak negative inspiratory pressure: ___-___ cmH2O
Not reliable indicator for endotracheal extubation
- 5-second head lift
- TOF ratio < 0.60
- Generate peak negative inspiratory pressure - 20-30 cmH2O
NON-DEPOLARIZING BLOCKADE
Non-depolarizing neuromuscular blockade is characterized by:
- Decrease in ____
- ____ during repetitive stimulation
- _____ potentiation
NON-DEPOLARIZING BLOCKADE
Non-depolarizing neuromuscular blockade is characterized by:
- Decrease in twitch tension
- Fade during repetitive stimulation
- Posttetanic potentiation
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 ____
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
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
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
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 ___ _____
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
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
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
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 ____
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
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 ____
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
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
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
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
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
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 ______
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
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
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
MALIGNANT HYPERTHERMIA
- Pharmacogenetic disorder triggered by:
• ____
- ____
- _____
- _____ receptor gene mutation (chromosome ____)
- Signs and symptoms include:
• Increase in _____ production
- Muscle ____
- Metabolic _____
- ____ (late sign)
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)
NON-DEPOLARIZING NMBDs
Classification by structure
- _____
- _____
• Other
Classification by action
- ____
- ____
• ____
NON-DEPOLARIZING NMBDs
Classification by structure
- Steroidal
- Benzylisoquinolinium
• Other
Classification by action
- Long-acting
- Intermediate-acting
• Short-acting
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
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
CISATRICURIUM
The____ isomer of atracurium
______ onset and action
• Intubating dose ______
Metabolized by _____elimination
• There is no ______
Unlike atracurium, it does not cause_______
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
MIVACURIUM
Only available _______ non-depolarizer available
- Not used in ____
- Intubating dose ______
Metabolized by ________
- ______ rate of succinylcholine
- _____, ____ acid
May produce _______
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
STEROIDAL COMPOUNDS
- ______ thought to facilitate interaction with _____
- Essential that one of two______ atoms are _____
Steroidal compounds include:
- _____
- _____
- _____
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
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
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
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
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
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 ____
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
NMBD POTENCY
Factors that increase potency include:
- _____ agents:
- _____ of _____ anesthesia
- Type of agent
____>____>____>_____>______
- Antibiotics:
- Type of abx ______: for example ____
- ______thermia
- _______ (calcium antagonist)
- _____ anesthetics
- _______
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
NMBD POTENCY
Factors that decrease potency include:
- Chronic _____ administration
- ______parathyroidism and hyper_____
- Decreased _______ sensitivity
NMBD POTENCY
Factors that decrease potency include:
- Chronic anticonvulsant administration
- Hyperparathyroidism and hypercalcemia
- Decreased atracurium sensitivity
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
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
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 ____
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
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
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
ADVERSE EFFECTS OF NMBDs
Respiratory effects
- Related to _____ release in patients with ____ _____ disease
- Increased ____ _____ and ______
ADVERSE EFFECTS OF NMBDs
Respiratory effects
- Related to histamine release in patients with reactive airway disease
- Increased airway resistance and bronchospasm
ADVERSE EFFECTS OF NMBDs
Allergic reactions
- NMBD are a common cause of ____ allergic reactions
- ____ and ______
- 1:___ – _____
- ____ reactivity between NMBDs and:
___, ____, ____ and ____ materials
• Treatment includes:
- ___
- ____
- ____
- ____
• ____
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
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:
- _____
- _____
• ______
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
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 ________
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
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 –______
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
ACh INHIBITOR SIDE-EFFECTS
- Cardiovascular
• Muscarinic effects must be blocked by anticholinergic
- Glycopyrrolate – ____
- Atropine – _______
- Administered with AChE inhibitor
- ____ and _____
- ____ and _____
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
AChE INHIBITOR SIDE-EFFECTS
Pulmonary
• ____
* Increased airway ____
* Increased _____
Effects reduced by coadministration of ____
• Gastrointestinal
* Increased ____
* ?____ effect on incidence of _____?
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?
MONITORING CRITERIA
Following administration of NMBD it is essential to ensure adequate reversal
- TOF > ___
- Less than ____ is associated with:
- Difficulty ____
- Difficulty _____
- _____ disturbances
- ______ risk
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
SUGAMMADEX
Dosing
- TOF > _
- TOF __ – ____
- TOF __ – _____
Ineffective against ___ or ____ Possible ___ reactions and ____
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
NMB STRUCTURE
All neuromuscular blockers are ____ ____
- Structurally related to ____
- Majority are ____ _____
• ______ is the exception
NMB STRUCTURE
All neuromuscular blockers are quaternary ammoniums
- Structurally related to ACh
- Majority are synthetic alkaloids
• Tubocurarine is the exception
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
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
SUGAMMADEX
Modified ___-____
Reversal of ____ and _____ _____-induced blockade
• ____ > ____ >> _____
-_____forces, _____bonds and _____ actions
Selective _____-binding
• No effect on _____
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
