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Related Concept Videos

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
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Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
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All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
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Depolarizing Blockers: Pharmocokinetics01:19

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Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
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Skeletal Muscle Relaxants: Therapeutic Uses01:31

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Skeletal muscle relaxants are used to relax muscle tone and alleviate painful muscle contractions. However, the choice of skeletal muscle relaxants depends on the duration of the surgical procedure in order to minimize potential side effects. Skeletal muscle relaxants like neuromuscular blocking agents [NMBAs] are commonly employed as adjuvants alongside general anesthetics in clinical settings. NMBAs are also used to maintain controlled ventilation during surgery of the larynx or pharynx...
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Sustained Neuromuscular Blockade after Vecuronium Use in a Premature Infant.

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Prolonged neuromuscular blockade (NMBA) use in preterm infants is common but risky. Avoid concurrent NMBA use with aminoglycosides and steroids, especially in infants with renal failure.

Keywords:
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Area of Science:

  • Pediatric Critical Care Medicine
  • Neonatal Intensive Care
  • Pharmacology

Background:

  • Neuromuscular blocking agents (NMBAs) are frequently used in critically ill children.
  • Limited safety data and no US guidelines exist for NMBA use in pediatric and neonatal populations.
  • NMBAs are essential for managing respiratory failure and facilitating mechanical ventilation in intensive care settings.

Observation:

  • A case of prolonged neuromuscular blockade is presented in a premature infant.
  • The infant received a neuromuscular blocking agent concurrently with aminoglycosides and steroids.
  • The infant also experienced renal failure, complicating the clinical picture.

Findings:

  • Concurrent administration of NMBAs with aminoglycosides and steroids can potentiate neuromuscular blockade.
  • Renal failure exacerbates the risk and duration of neuromuscular blockade.
  • Prolonged NMBA use in preterm infants requires careful consideration of drug interactions and organ function.

Implications:

  • Avoid prolonged NMBA use in preterm infants whenever possible.
  • If NMBA use is necessary, restrict it to the shortest effective duration and lowest effective dose.
  • Avoid concurrent NMBA administration with aminoglycosides and steroids, particularly in neonates with renal impairment.