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Related Concept Videos

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics01:11

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics

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.
Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

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...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

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

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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...
Parenteral Anesthetics: Overview01:24

Parenteral Anesthetics: Overview

Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

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 succinylcholine...

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Related Experiment Video

Updated: May 28, 2026

Deep Neuromuscular Blockade Leads to a Larger Intraabdominal Volume During Laparoscopy
08:50

Deep Neuromuscular Blockade Leads to a Larger Intraabdominal Volume During Laparoscopy

Published on: June 25, 2013

Induction-Phase Peripheral Perfusion Dynamics and Rocuronium Neuromuscular Blockade Onset: A Retrospective Cohort

Su Yeon Cho1,2, Dong Joon Kim1, Ki Tae Jung1,2,3

  • 1Department of Anesthesiology and Pain Medicine, Chosun University Hospital, College of Medicine, Chosun University, Gwangju 61453, Republic of Korea.

Journal of Clinical Medicine
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

The change in peripheral perfusion index (PI) within 60 seconds of propofol administration is a strong predictor of rocuronium onset time. Faster PI changes indicate quicker rocuronium onset, regardless of anesthetic method.

Keywords:
anesthesia inductionhemodynamicsneuromuscular blockadeperfusion indexphotoplethysmographyrocuronium

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Area of Science:

  • Anesthesiology
  • Cardiovascular Physiology
  • Pharmacodynamics

Background:

  • Rocuronium onset time exhibits significant interindividual variability, with hemodynamic determinants not fully understood.
  • Peripheral perfusion index (PI) is a non-invasive measure reflecting cardiac output and vascular tone.
  • Early PI dynamics during anesthesia induction may correlate with rocuronium onset.

Purpose of the Study:

  • To investigate the association between early peripheral perfusion index (PI) dynamics and rocuronium onset time during anesthesia induction.
  • To determine if PI changes after propofol administration can predict rocuronium onset.
  • To assess the influence of baseline PI and anesthetic method on this relationship.

Main Methods:

  • Retrospective observational cohort study of 1377 adult patients.
  • Standardized anesthesia induction with quantitative electromyographic train-of-four monitoring.
  • Analysis of baseline PI categories and the 60-second PI change (ΔPI60) after propofol, stratified by anesthetic technique (TIVA vs. volatile).

Main Results:

  • ΔPI60 tertiles were significantly associated with rocuronium onset time in both TIVA and volatile anesthesia groups (p < 0.001).
  • Patients with faster ΔPI60 (Fast-Rise) had shorter median onset times (170 s) compared to Slow-Rise (211 s).
  • ΔPI60 tertile provided the largest increase in model fit (adjusted R2 Δ0.060, p < 0.001), indicating its strong independent contribution.

Conclusions:

  • The 60-second change in peripheral perfusion index (ΔPI60) is strongly associated with rocuronium onset time.
  • ΔPI60 serves as a potential non-invasive marker for rocuronium delivery conditions, independent of baseline factors and anesthetic method.
  • Prospective validation is warranted to confirm PI dynamics as a predictor of rocuronium onset.