Local anaesthetics work by inhibiting the conduction of electrical impulses in peripheral nerves. They do this by preventing the entry of sodium ions needed to produce the depolarization stage of the action potential. There are two theories for how this is accomplished - the non-specific membrane expansion theory, where the local anaesthetic attaches to and swells the cell membrane to block sodium channels, and the specific receptor theory, where the local anaesthetic binds to specific sodium channel receptors to prevent ion flow. Common local anaesthetics include lidocaine, prilocaine, articaine, and bupivacaine, which each have varying properties in terms of onset time, duration of effect, formulations, and maximum safe dosages.

2. Local Anaesthetics produce loss of pain
sensation in a circumscribed area of
the body by inhibiting the conduction
process in the peripheral nerves.

3. In order for us to understand how
local anaesthetics work, we first have
to look at how electrical impulses are
generated and take you back to first
year physiology!!

5. This picture shows
how membrane
potential changes
with an action
potential.

6. As we have learnt, nerve
impulses are conducted by a
wave of action potentials.
When a stimulus is great
enough to reach the
threshold potential of -55mV,
sodium ions flow into the
neurone.
It does so via sodium gates
to produce depolarisation.

7. When depolarised, the
membrane potential is
reversed to +40 mV
from -70mV.
At the same time, there
is passive outward
diffusion of potassium
ions to bring about
repolarisation and the
membrane potential is
again restored to -70mV.

8. Local anaesthetics work by
preventing the entry of sodium ions
to inhibit the propagation of action
potentials.

9. There are two theories on the subject
of how sodium channels are blocked:
1. Non-specific membrane expansion
theory
2. Specific receptor theory

10. Non-specific membrane expansion theory:
The lipophilic part of the local anaesthetic
attaches to the cell membrane to cause swelling.
This then reduces the size of the sodium channel
to obstruct the flow of sodium ions.

11. Specific receptor theory:
The hydrophilic charged amino terminal
binds to specific receptors of the sodium
gates to block the passage of sodium ions.

12.  Lignocaine(Xylocaine)
 Prilocaine(Citanest)
 Articaine(Septocaine)
 Bupivacaine(Marcaine)

13. First found by Nils Lofgren in 1943, and has been in
clinical use since 1948
used as 2% plain or 2% with 1: 80000 adrenaline
Short onset of 2-3 minutes
Duration of action for ~ 2hrs
Each 2.2ml cartridge contains 44mg of lidocaine
Max dose with vasoconstrictor is 7mg/Kg

14. Less toxic and metabolises quicker than lignocaine.
Used as 4% plain or 3% with IU/ml Felypressin;
Felypressin is an analogue of Oxytocin. Oxytocin induces
labour hence its use should be avoided in pregnant women.
Slower onset of 4 minutes.
Max dose is 6mg/Kg.
A metabolite of prilocaine can very rarely oxidise heme to
cause methemoglobinemia. This of course, reduces the
oxygen carrying capacity of haemoglobin. Consequently
the patient becomes hypoxic.

15. The molecular structure of articaine is different from other
local anaesthetics due to the presence of a thiophene ring.
It also contains an additional ester group which is
metabolized by estearases found in the blood and tissues.
For this reason. Articaine is hydrolysed quicker than other
anaesthetics.
-used as 4% solution with 1:100000 or 1:200000
adrenaline.
More rapid onset.
Anaesthesia is more profound.
Maximum dose 7mg/kg.

16. used as 0.25% or 5% solution with
1: 200000adrenaline.
Onset of 5 minutes.
Can last for ~8 hours.
Used for longer duration surgery, post-
operative pain control and pain control for
intractable facial pain.
Maximum dose 1.3mg/kg.

17. THIS IS THE END OF THE SLIDE
SHOW ON LOCAL ANAESTHETICS