BIOS5140 - anaesthesia
University of Kent: BIOS5140
Focus: Pharmacology of Anaesthesia, Analgesia, and Opioids
Local Anaesthesia
Definition: Local anaesthetics target the electrical excitability of neurons.
Mechanism:
They inhibit voltage-gated sodium ion channels (VGSC), reducing sodium ion entry into axons.
This impairment affects the opening of ion channels, decreasing the ability of axons to reach the threshold level for depolarization.
Primarily impacts neurons involved in nociception (pain perception), specifically Ad and C fibres, due to their small diameter.
Delivered via methods such as topical application, injection, or dural space injection.
Preferred over general anaesthesia for patient safety and outpatient surgical procedures.
Action Potential and Ion Channel Behavior
Sodium and Potassium Channels:
Rapid opening of sodium channels during action potential upstroke, followed by delayed potassium channel opening and sodium channel inactivation during repolarisation.
Membrane Potential:
Em (membrane potential): rapid change upon sodium channel activation.
gNa (membrane conductance to Na+), gK (membrane conductance to K+).
Action Potential Characteristics:
Depolarisation occurs as sodium ions enter the axon, leading to local depolarisation.
Action potential threshold: adjacent sodium channel opens at -50 mV, reaching -20 mV.
Potassium efflux results in repolarisation back to resting potential (-80 mV).
Voltage-Gated Ion Channels
Conformations of Channels:
Resting State: m-gate closed, h-gate open (at -70 mV).
Active State: both gates open (at -50 mV).
Inactivated State: m-gate open, h-gate closed (at -20 mV).
Cycles among these states depending on membrane depolarisation during action potentials.
Gating Mechanism
Functionality of m-gate and h-gate:
m-gate as voltage sensor opens at -50 mV; h-gate (physical closure) at -20 mV.
Following potassium efflux, both gates reset to their resting states (-70 mV).
Mechanism of Action for Local Anaesthetics
Drug Properties:
Must be lipid-soluble to penetrate membranes; enter as protonated, activated form post-membrane entry.
Binds to inactivated sodium channel state, blocking further action potential propagation by keeping h-gate closed.
Local Anaesthetic Structure
Weak Bases with Three Chemical Regions:
Lipophilic Region: Usually aromatic, facilitating plasma membrane penetration.
Hydrophilic Region: Typically a secondary/tertiary amine for protonation and activation in the axon.
Ester or Amide Linker: Key for the structural integrity of the local anaesthetic.
Active once protonated in the acidic intracellular environment where they inhibit sodium channel cycling.
Interactions and Use Dependence of Local Anaesthetics
Lipid Solubility Impact: Determines how effectively they can block sodium channels, with ion interaction pathways.
Highly active neurons frequently open sodium channels, impacting effectiveness.
Clinical Applications of Local Anaesthetics
Variability in Effectiveness: Speed of onset and duration differ across agents.
Examples:
Lidocaine, Prilocaine, Articaine: Rapid onset, short-to-medium duration; ideal for minor surgeries.
Bupivacaine: Slow onset, long duration; used in epidural anaesthesia in labour.
Potential Side Effects:
Primarily cardiovascular due to off-target effects; minimized with local application.
General Anaesthesia Overview
General Mechanism: Operate through various targets, correlated with lipid solubility.
Functionality: Primarily reduces synaptic transmission in specific CNS regions and can affect cardiac/respiratory functions.
Preferred Protocol for In-Patient Surgeries:
Administration of pre-med anxiolytics, injected anaesthetics, peri-operative opioids, inhaled general anaesthetics, neuromuscular blockers, antiemetics, muscarinic antagonists, and acetylcholinesterase inhibitors post-surgery.
Close patient monitoring is essential throughout surgical procedures.