Local Anaesthetic Agents

In this video we look at local anaesthetic agents and how their physicochemical properties effect potency, duration of action and speed of onset. This video follows on from 'The Henderson-Hasselbalch Equation and pKa'.
This is a favourite topic in the FRCA as questions can be targeted at both basic sciences and clinical application. Easy marks if you've nailed the theory!

[@rajeevkaparthi190]

Thank you.
Please explain the concept of "frequency dependent blockade" (i.e the block intensifies with more frequent rates of nerve firing)

[@PrimaryConcepts]

No worries!
The frequency-dependant blockade is attributed to the fact that local anaesthetics only block the sodium channels when they are in their 'open' configuration. So nerves which fire more rapidly will have a greater degree of open sodium channels and therefore be blocked to a greater extent.
See this great summary from LITFL:
www.bjaed.org/article/S2058-5349(19)30152-0/fulltext

[@rajeevkaparthi190]

Thank you. It is clear to some extent. We can explain the anti arrhythmic property of lignocaine with this concept.i e during tachyarrhythmia nerve fibers fire more rapidly which will keep more sodium channels in opened state, allowing more lignocaine to bind and block the nerve. And in case of chronic pain there will be continuous firing of concerned nerve, such nerve get blocked more intensively.
But... How can we apply this concept to spinal anaesthesia and nerve blocks where there is no rapid firing of nerves as there is no surgical stimulus? Still we are getting block. How? If there is no firing of nerve fibre,I.e when sodium channels are in resting phase, can't we block nerve fibre? Am I missing any primary concept?
I am eagerly waiting for your reply... Thank you.