Neuromuscular Blockade Flashcards by Tara Betts

Neuromuscular blocking drugs are used in ___________ to cause muscle relaxation

Anesthesia

How well did you know this?

Not at all

Perfectly

Neuromuscular blocking drugs target the _____________ _____________ to enable light anesthesia to be used with adequate relaxation of the abdomen and diaphragm

Neuromuscular junction (NMJ)

How well did you know this?

Not at all

Perfectly

Neuromuscular blocking drugs relax the _________ ________ to allow passage of a ____________ _______

Vocal cords

Tracheal tube

How well did you know this?

Not at all

Perfectly

Neuromuscular blocking drugs differ from muscle relaxants used in MSK disorders that act on the ________ or ________

Spinal cord

Brain

How well did you know this?

Not at all

Perfectly

Patients who have received a neuromuscular blocking drug should always have their __________ assisted or controlled until the drug has been inactivated or antagonised.

respiration

How well did you know this?

Not at all

Perfectly

Patients who are given neuromuscular blocking drugs should also receive sufficient concomitant inhalation or IV ____________ or ___________ drugs to prevent _____________

Anesthetic

Sedative

Awareness

How well did you know this?

Not at all

Perfectly

What are the two major classes of neuromuscular blocking agents?

Non-depolarizing (AKA competitive muscle relaxants)

2. Depolarizing

How well did you know this?

Not at all

Perfectly

What is the mechanism of action of non-depolarizing neuromuscular blocking drugs?

Non-depolarizing neuromuscular blocking drugs (also known as competitive muscle relaxants) compete with acetylcholine for receptor sites at the neuromuscular junction

How well did you know this?

Not at all

Perfectly

Non-depolarizing neuromuscular blocking drugs can be reversed with ________________ such as ___________

AchE inhibitors

Neostigmine

How well did you know this?

Not at all

Perfectly

Non-depolarising neuromuscular blocking drugs can be divided into the __________ group and the ___________ group

aminosteroid

benzylisoquinolinium

How well did you know this?

Not at all

Perfectly

Aminosteroid non-depolarizing neuromuscular blocking drugs include…? (3)

pancuronium bromide
rocuronium bromide
vecuronium bromide

How well did you know this?

Not at all

Perfectly

Benzylisoquinolinium non-depolarizing neuromuscular blocking drugs include…? (3)

atracurium besilate
cisatracurium
mivacurium

How well did you know this?

Not at all

Perfectly

Non-depolarising neuromuscular blocking drugs have a __________ (faster/slower) onset of action than suxamethonium chloride (a depolarizing neuromuscular blocking agent).

Slower

How well did you know this?

Not at all

Perfectly

Non-depolarizing neuromuscular blocking drugs can be classified by their duration of action as short-acting ( ________ minutes), intermediate-acting ( _______ minutes), and long-acting ( _______ minutes), although duration of action is dose-dependent

15–30

30–40

60–120

How well did you know this?

Not at all

Perfectly

Non-depolarizing neuromuscular blocking drugs that have a shorter or intermediate duration of action include…? (2)

Atracurium
Vecuronium

*more widely used than those with a longer duration (eg. pancuronium)

How well did you know this?

Not at all

Perfectly

Which non-depolarizing neuromuscular blocking drug has a longer duration of action?

Pancuronium

How well did you know this?

Not at all

Perfectly

Do non-depolarising neuromuscular blocking drugs have sedative or analgesic effects?

How well did you know this?

Not at all

Perfectly

Do non-depolarizing neuromuscular blocking drugs trigger malignant hyperthermia?

NO, unlike depolarizing

How well did you know this?

Not at all

Perfectly

For patients receiving intensive care and who require tracheal intubation and mechanical ventilation, a ___________ (depolarizing/non-depolarising) neuromuscular blocking drug is chosen according to its onset of effect, duration of action, and side-effects

Non-depolarizing

How well did you know this?

Not at all

Perfectly

______________, with a rapid onset of effect, may facilitate intubation

Rocuronium bromide

How well did you know this?

Not at all

Perfectly

_____________ or ___________ may be suitable for long-term neuromuscular blockade since their duration of action is not dependent on elimination by the liver or the kidneys

Atracurium besilate

cisatracurium

How well did you know this?

Not at all

Perfectly

Atracurium besilate or cisatracurium may be suitable for long-term neuromuscular blockade since their duration of action _______ (is/is not) dependent on elimination by the liver or the kidneys

Is NOT

How well did you know this?

Not at all

Perfectly

Atracurium besilate, a mixture of 10 isomers, is a benzylisoquinolinium neuromuscular blocking drug with an __________ duration of action

intermediate

A non-depolarizing neuromuscular blocking drug

How well did you know this?

Not at all

Perfectly

_____________ undergoes non-enzymatic metabolism which is independent of liver and kidney function, thus allowing its use in patients with hepatic or renal impairment

Atracurium besilate

How well did you know this?

Not at all

Perfectly

Cardiovascular effects associated with _____________ (non-depolarizing neuromuscular blocking drug) include significant histamine release; histamine release can be minimised by administering slowly or in divided doses over at least 1 minute.

Atracurium besilate

_____________ is a single isomer of atracurium besilate. It is more potent and has a slightly longer duration of action than atracurium besilate and provides greater cardiovascular stability because it lacks histamine-releasing effects

Cisatracurium

Cisatracurium is a single isomer of atracurium besilate. It is ________ (more/less) potent and has a slightly ________ (longer/shorter) duration of action than atracurium besilate and provides _________ (greater/less) cardiovascular stability because it lacks histamine-releasing effects

More Longer Greater

Mivacurium, a benzylisoquinolinium neuromuscular blocking drug, has a _______ (long/short) duration of action

Short

___________ (a benzylisoquinolimium neuromuscular blocking drug) is metabolised by plasma cholinesterase and muscle paralysis is prolonged in individuals deficient in this enzyme.

Mivacurium

Mivacurium ______ (is/is not) associated with vagolytic activity or ganglionic blockade; histamine release can occur, particularly with rapid injection

Is NOT

Pancuronium bromide, an aminosteroid neuromuscular blocking drug, has a ________ (long/short) duration of action and is often used in patients receiving long-term mechanical ventilation in intensive care units

Long

Pancuronium bromide, an aminosteroid neuromuscular blocking drug, has a long duration of action and is often used in patients receiving long-term ___________ in _____________

mechanical ventilation intensive care units

Pancuronium _______ (does/does not) cause a histamine-releasing effect, but __________ (does/does not) cause vagolytic and sympathomimetic effects

Does NOT DOES; may cause tachycardia and hypertension

________________, an aminosteroid neuromuscular blocking drug, exerts an effect within 2 minutes and has the most rapid onset of any of the non-depolarising neuromuscular blocking drugs

Rocuronium bromide

Rocuronium bromide, a non-depolarizing neuromuscular blocking drug, has a/an _________ duration of action

Intermediate *But most rapid onset (within 2 min)

Does rocuronium have CV and/or vagolytic effects?

Minimal CV effects High doses may produce mild vagolytic activity

Vecuronium, an aminosteroid neuromuscular blocking drug, has a/an ________ duration of action

Intermediate

Does vecuronium produce histamine release or CV effects?

Generally no histamine release Lacks CV effects

What is the mechanism of action of depolarizing neuromuscular blocking drugs?

Binding to ACh receptors to generate an action potential; because they are not metabolized by AChE, the binding of this drug to the receptor is prolonged resulting in an extended depolarization of the muscle end-plate

Depolarizing neuromuscular blocking drugs first cause _______ then ________

Muscle contraction Paralysis

What is the most commonly-used depolarizing neuromuscular blocking agent?

Suxamethonium chloride (aka succinylcholine)

Suxamethonium chloride (succinylcholine) should be given _______ (before/after) anaesthetic induction because paralysis is usually preceded by painful muscle fasciculations

After

_________________ has the most rapid onset of action of any of the neuromuscular blocking drugs and is ideal if fast onset and brief duration of action are required, e.g. with tracheal intubation

Suxamethonium chloride (succinylcholine)

Unlike the non-depolarising neuromuscular blocking drugs, the action of suxamethonium (succinylcholine) ________ (can/cannot) be reversed

Cannot; recovery is spontaneous

Anticholinesterases such as neostigmine ____________ (reverse/potentiate) the neuromuscular block generated by suxamethonium (succinylcholine)

Potentiate Unlike non-depolarizing neuromuscular blocking drugs which are reversed by agents like neostigmine that increase the amount of ACh in the synaptic cleft leading to displacement of these drugs from receptors

While ____________ (bradycardia/tachycardia) occurs with single use of suxamethonium (succinylcholine), ____________ (bradycardia/tachycardia) may occur with repeated doses in adults and with the first dose in children

Tachycardia Bradycardia *Premedication with atropine reduces bradycardia as well as the excessive salivation associated with suxamethonium chloride use

____________ may occur in dual block, which occurs with high or repeated doses of suxamethonium chloride and is caused by the development of a non-depolarising block following the initial depolarising block

Prolonged paralysis

Prolonged paralysis may occur in __________, which occurs with high or repeated doses of suxamethonium chloride and is caused by the development of a non-depolarising block following the initial depolarising block

dual block

Prolonged paralysis may occur in dual block, which occurs with _________ or ________ doses of suxamethonium chloride and is caused by the development of a non-depolarising block following the initial depolarising block

High repeated

Prolonged paralysis may occur in dual block, which occurs with high or repeated doses of suxamethonium chloride and is caused by the development of a ____________ (depolarizing/non-depolarising) block following the initial ___________ (depolarising/non-depolarizing) block

Non-depolarizing Depolarizing

Individuals with _____________ are resistant to suxamethonium chloride but can develop dual block resulting in delayed recovery.

myasthenia gravis

Individuals with myasthenia gravis are resistant to __________________ but can develop dual block resulting in delayed recovery.

suxamethonium chloride (succinylcholine)

Individuals with myasthenia gravis are resistant to suxamethonium chloride but can develop dual block resulting in ____________

delayed recovery

Prolonged paralysis may occur in those treated with suxamethonium (succinylcholine) with _________ or _________ plasma cholinesterase

Low Atypical *Assisted ventilation should be continued until muscle function is restored

How is dose calculated when prescribing non-depolarizing neuromuscular blocking drugs?

Based on ideal body-weight

Non-depolarizing neuromuscular blocking drugs should be prescribed with caution in which patients? (6)

Patients with: 1. Burns (resistance can develop) 2. CVD (reduce rate of administration) 3. Fluid and electrolyte disturbances (response unpredictable) 4. Hypothermia (activity prolonged, lower dose required) 5. MG (activity prolonged, lower dose required) 6. Neuromuscular disorders (response unpredictable)

What are the side effects of non-depolarizing neuromuscular blocking drugs? (8)

1. Flushing (histamine release) 2. Hypotension (histamine release) 3. Bronchospasm (histamine release) 4. Circulatory collapse (histamine release) 5. Muscle weakness and myopathy (after prolonged use in ICU) 6. Shock 7. Cardiac arrest 8. Seizures **pancuronium lacks histamine-releasing effects, but vagolytic and sympathomimetic effects can cause tachycardia

What are the symptoms of histamine release associated with rapid administration of non-depolarizing neuromuscular blocking agents? (4)

1. Flushing 2. Hypotension 3. Bronchospasm 4. Circulatory collapse Manufacturer advises minimising effects of histamine release by administering over 1 minute in patients with cardiovascular disease or sensitivity to hypotension.

Do non-depolarizing neuromuscular blocking drugs cross the placent?

No; Non-depolarising neuromuscular blocking drugs are highly ionised at physiological pH and are therefore unlikely to cross the placenta in significant amounts

What side effects are associated with pancuronium bromide specifically? (5)

1. Apnea 2. Arrhythmia 3. Hypersalivation 4. Increased CO 5. Miosis **lacks histamine-releasing effects, but vagolytic and sympathomimetic effects can cause tachycardia

What are the contraindications to use of suxamethonium (succinylcholine)? (9)

1. Hyperkalemia 2. Low plasma-cholinesterase activity (including severe liver disease) 3. Major trauma 4. Neurological disease involving acute wasting of major muscle 5. Personal or family history of malignant hyperthermia 6. Personal or family history of congenital myotonic disease 7. Prolonged immobilisation (risk of hyperkalemia) 8. Severe burns 9. Skeletal muscle myopathies (eg Duchenne MD)

What is malignant hyperthermia?

A severe reaction to all inhalation anesthetics EXCEPT nitrous oxide AND depolarizing neuromuscular junction blocking agent, suxamethonium chloride (succinylcholine)

What is the cause of malignant hyperthermia?

Genetic defect leading to an abnormal ryanodine receptor in skeletal muscle This abnormality interferes with regulation of calcium in the muscles, leading to buildup of calcium in skeletal muscles and a clinical syndrome of hypermetabolism

What are the symptoms of malignant hyperthermia? (7)

1. Severe muscle rigidity or spasm 2. Rapid shallow breathing and secondary respiratory failure 3. Tachycardia 4. Arrhythmia 5. Hyperthermia 6. Excessive sweating 7. Mottled skin

What is the route of administration of neuromuscular blocking drugs?

In which patients should suxamethonium (succinylcholine) be administered with caution? (5)

Patients with: 1. Cardiac disease 2. Neuromuscular disease 3. Raised IOP (avoid in penetrating eye injury) 4. Respiratory disease 5. Severe sepsis (risk of hyperkalemia)

What are the side effects of suxamethonium chloride (succinylcholine)? (14)

1. Arrhythmias 2. Bradycardia (with repeated doses) 3. Flushing 4. Involuntary muscle contractions 5. Myoglobinemia 6. Myoglobinuria 7. Post-procedural muscle pain 8. Rash 9. Apnea 10. Cardiac arrest 11. Hypersensitivity 12. Malignant hyperthermia 13. Respiratory disorders 14. Trismus

Premedication with ________ reduces bradycardia associated with suxamethonium use.

atropine

How does pregnancy affect the effect of suxamethonium?

Mildly prolonged maternal neuromuscular blockade

Does hepatic impairment affect the effect of suxamethonium (succinylcholine)?

Yes, increased risk of prolonged apnoea due to reduced hepatic synthesis of plasma cholinesterase Manufacturer advises caution, particularly in end stage hepatic failure

Anticholinesterase inhibitors reverse the effects of ______________ (depolarizing/non-depolarizing) neuromuscular blocking drugs such as ___________ but they prolong the action of ____________ (depolarizing/non-depolarizing) neuromuscular blocking drugs such as _____________.

non-depolarising (competitive); pancuronium depolarising; suxamethonium chloride

____________ is used specifically for reversal of non-depolarising (competitive) blockade

Neostigmine

Neostigmine acts within ___________ of intravenous injection and its effects last for __________; a second dose may then be necessary

one minute 20 to 30 minutes

_______________ or alternatively _________, given before or with neostigmine, prevent bradycardia, excessive salivation, and other muscarinic effects of neostigmine.

Glycopyrronium bromide atropine sulfate

____________ is a modified gamma cyclodextrin that can be used for rapid reversal of neuromuscular blockade induced by rocuronium bromide or vecuronium bromide

Sugammadex; in practice, sugammadex is used mainly for rapid reversal of neuromuscular blockade in an emergency.

What is the mechanism of action of neostigmine?

AChE inhibitor In the context of non-depolarizing neuromuscular blockade reversal, inhibition of AChE leads to build-up of ACh at the NMJ and displacement of muscle relaxants from ACh receptors

In addition to reversing the action of non-depolarizing neuromuscular blockade, neostigmine is also used in the treatment of ___________

Myasthenia gravis

AChE inhibitors, including neostigmine, are contraindicated in ___________ and ____________

Intestinal and urinary obstruction

AChE inhibitors, including neostigmine, should be used with extreme caution in which patients? (10)

Patients with: 1. Arrhythmias 2. Asthma (extreme caution) 3. Bradycardia 4. Epilepsy 5. Hypothyroidism 6. Hypotension 7. Parkinsonism 8. Peptic ulceration 9. Recent MI 10. Vagotonia

Why isn’t atropine given routinely with neostigmine?

Because it may mask signs of overdosage

What are the signs and symptoms of ACh toxicity (AChE inhibitor overdose)? (11)

1. Cramps and muscle weakness 2. Hypersalivation 3. Lacrimation 4. Paralysis 5. Muscle fasciculations 6. Diarrhea, involuntary defecation 7. Blurry vision, miosis, nystagmus 8. Bradycardia, hypotension 9. Bronchospasm, increased bronchial secretions 10. Excess sweating 11. Involuntary micturition May be remembered by DUMBBEELLS or SLUDGE (Think parasympathetic hyperstimulation)

___________ or ____________ should also be given when reversing neuromuscular blockade with IV neostigmine

Glycopyrronium atropine

Neuromuscular Blockade Flashcards

(82 cards)