Neuromuscular Blockers (NMBs)

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Questions and Answers

How do neuromuscular blocking agents (NMBs) primarily exert their effect?

  • By enhancing the degradation of acetylcholine in the synaptic cleft.
  • By directly stimulating skeletal muscle contraction.
  • By increasing acetylcholine release at the neuromuscular junction.
  • By interfering with the nicotinic receptors at the neuromuscular junction. (correct)

Succinylcholine's mechanism of action primarily involves:

  • Inhibiting the release of acetylcholine from the presynaptic neuron.
  • Acting as a competitive antagonist at the acetylcholine receptor.
  • Increasing the activity of acetylcholinesterase.
  • Causing prolonged depolarization of the muscle endplate. (correct)

A patient undergoing surgery experiences prolonged muscle paralysis after succinylcholine administration. Which condition is most likely contributing to this prolonged effect?

  • Genetic deficiency in plasma cholinesterase (correct)
  • Increased pseudocholinesterase activity
  • Decreased sensitivity to acetylcholine
  • Concurrent administration of a non-depolarizing NMB

How do non-depolarizing neuromuscular blocking agents (NMBs) elicit muscle paralysis?

<p>By preventing acetylcholine from binding to its receptors. (A)</p>
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Which of the following best describes the main clinical difference between depolarizing and non-depolarizing neuromuscular blockers?

<p>Depolarizing blockers cause muscle fasciculations before paralysis, while non-depolarizing blockers do not. (D)</p>
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Which of the following neuromuscular blocking agents is most likely to be used for rapid sequence intubation due to its quick onset and short duration of action?

<p>Succinylcholine (D)</p>
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What is the primary mechanism by which fresh frozen plasma can reverse the effects of succinylcholine?

<p>By supplying functional pseudocholinesterase to metabolize succinylcholine. (B)</p>
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Why is neostigmine sometimes used to reverse the effects of non-depolarizing neuromuscular blocking agents?

<p>It increases acetylcholine levels at the neuromuscular junction. (D)</p>
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What is a primary therapeutic application of neuromuscular blocking agents?

<p>To facilitate endotracheal intubation during surgery. (D)</p>
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Why are neuromuscular blocking agents used during electroconvulsive therapy (ECT)?

<p>To prevent severe muscle contractions and physical injury. (B)</p>
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A patient receiving succinylcholine experiences a rapid and significant increase in serum potassium levels. What is the most likely explanation for this adverse effect?

<p>Release of potassium from damaged muscle cells due to depolarization (A)</p>
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A patient with glaucoma is scheduled for a surgical procedure requiring neuromuscular blockade. Which neuromuscular blocking agent should be used with caution?

<p>Succinylcholine (B)</p>
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Why is succinylcholine known to sometimes cause postoperative muscle pain?

<p>Associated with the unsynchronized contractions of muscle fibers. (D)</p>
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Which of the following best describes the effect of pancuronium on heart rate?

<p>Causes tachycardia due to its atropine-like effect (C)</p>
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What is an idiosyncratic reaction associated with succinylcholine administration potentially leading to prolonged muscle paralysis and apnea?

<p>Deficiency of pseudocholinesterase enzyme (A)</p>
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A patient with myasthenia gravis requires neuromuscular blockade. Which consideration is most important when selecting a neuromuscular blocking agent?

<p>Avoiding depolarizing blockers due to increased sensitivity. (C)</p>
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A patient with severe liver and kidney disease requires neuromuscular blockade. Which agent is safest to use in this situation?

<p>Atracurium (D)</p>
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Which of the following best describes the metabolism of vecuronium?

<p>Metabolized by the liver (C)</p>
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Why should aminoglycosides be avoided or used with caution in patients receiving neuromuscular blocking agents?

<p>They can potentiate the neuromuscular blockade, leading to prolonged paralysis. (A)</p>
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What is the specific mechanism of action of Sugammadex?

<p>Encapsulates rocuronium and vecuronium (C)</p>
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Flashcards

Neuromuscular Blockers (NMBs)

Blockers that inhibit skeletal muscle contraction by interfering with Nm receptors.

Depolarizing NMBs Mechanism

Type of NMB that causes prolonged depolarization of the muscle.

Non-depolarizing NMBs action

Binds to Ach receptors but do not activate them, prevents AcH from binding and causing depolarization.

Succinylcholine Mechanism

Neuromuscular blocker with a mechanism that depolarizes membrane like acetylcholine, leading to longer-lasting depolarization

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Therapeutic Uses of NMBs

Short surgical procedures, endotracheal intubation, and controlling convulsions during ECT.

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Succinylcholine Metabolism

Succinylcholine broken down very quickly in the plasma by this enzyme.

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IOP Increase

Extraocular muscle contraction leading to increased pressure.

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Hyperkalemia

High potassium levels in the blood, caused by muscle cell depolarization.

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Reversal of Neuromuscular Block

Fresh frozen plasma transfusion, Neostigmine.

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Succinylcholine Use

Rapid-onset NMB used in short procedures, metabolized by plasma cholinesterase.

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NMBs Contraindications

Myasthenia Gravis, Bronchial Asthma, and use with Aminoglycosides .

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Atracurium Metabolism

Spontaneous hydrolysis in the plasma (Hoffman degradation).

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Neostigmine Action

Reverses non-depolarizing neuromuscular blockade by increasing acetylcholine levels at the NMJ.

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Histamine Release

Non-depolarizing agent that cause release of inflammatory mediator, resulting in hypotension and bronchospasm .

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Pancuronium Adverse Effect

Pancuronium causes this side effect through an atropine-like effect.

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Study Notes

  • Neuromuscular blockers (NMBs) inhibit skeletal muscle contraction by interfering with Nm receptors

Classification of Neuromuscular Blockers (NMBs)

  • Depolarizing NMBs cause prolonged depolarization
    • Example: Succinylcholine (Suxamethonium)
  • Non-depolarizing NMBs act as competitive antagonists of Ach at Nm receptors
    • Example: Curare (prototype), no longer used clinically
  • Non-depolarizing NMBs include drugs with names ending in "-curium" or "-curonium"
    • "-Curium" examples: Mivacurium, Atracurium, Cisatracurium
    • "-Curonium" examples: Pancuronium, Vecuronium, Rocuronium

Succinylcholine

  • Used to depolarize the membrane by opening channels like acetylcholine
  • Action persists longer at the neuromuscular junction, resulting in prolonged depolarization
  • Causes a brief period of repetitive muscle excitation (fasciculations), followed by neuromuscular transmission blocking and flaccid paralysis (phase I block)
  • High concentrations over time convert the block from a depolarizing phase I to a non-depolarizing phase II block
  • Pharmacokinetics: Quaternary amine, given parentally because it cant cross into the CNS
  • Metabolism: Metabolized by plasma pseudo-cholinesterase
  • Duration: Has short effects, only lasting a few minutes

Succinylcholine Reversal:

  • Fresh frozen plasma transfusion (contains pseudo-cholinesterase) can be used
    • Use this in cases of succinylcholine apnea
  • Neostigmine can be used
    • can reverse the block in phase 2 only
    • The two phases of block are hard to differentiate clinically

Succinylcholine: Therapeutic Uses

  • During surgical operations for short procedures like endotracheal intubation due to its shorter duration
  • During electroconvulsive (ECT) therapy to control convulsions

Succinylcholine: Adverse Effects

  • Sudden increase in IOP (intraocular pressure) from extra-ocular muscle contraction in phase 1
    • Contraindicated in patients with glaucoma or recent eye surgery
  • Acute hyperkalemia due to efflux of muscle K+ during depolarization
  • Postoperative muscle pain
  • Bradycardia via cardiac M Re +++ (as ACh)
  • Succinylcholine apnea
    • Idiosyncratic reaction due to deficiency of PsChE enzyme
    • Treated by artificial respiration and plasma transfusion

Non-depolarizing NMBs: Pharmacokinetics

  • Quaternary amine
    • Poorly absorbed from the GIT (given parentally) and can't pass to CNS.
  • Metabolism of Atracurium
    • Spontaneous plasma hydrolysis
    • Breakdown products may cause seizures, but less so with cisatracurium
    • It is the drug of choice in patients with severe renal or hepatic disease
  • Vecuronium is metabolized by the liver
  • Mivacurium is metabolized by Pseudo-cholinesterase

Reversal of Non-depolarizing NMBs:

  • Block can be reversed spontaneosly
  • Reversal of block through Neostigmine
    • Increase Ach level at NMJ, which displaces competitive blockers from the receptor
  • Sugammadex reverses the effects of Rocuronium & Vecuronium

Non-depolarizing NMBs: Therapeutic Uses

  • Used during surgical operations
  • Used during electroconvulsive (ECT) therapy to control convulsions

Non-depolarizing NMBs: Adverse Effects

  • Histamine release causes Hypotension & Bronchospasm
  • High doses can cause Respiratory paralysis
  • Pancuronium can have an atropine-like effect on the heart, leading to Tachycardia

Non-depolarizing NMBs: Contraindications & Precautions

  • Contraindicated in patients with Myasthenia Gravis, Bronchial Asthma
  • Use with caution with Aminoglycosides as they can aggravate MS paralysis.

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