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Local Anaesthetics produce loss of
sensation to pain in a circumscribed
area of the body by inhibiting the
conduction process in the peripheral
nerves.
In order for us to understand how
local anaesthetics work, we first have
to look at the the electrical impulse
and take you back to first year
physiology
This picture shows how membrane
potential changes with an action
potential.
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.
When depolarised, the membrane
potential is reversed to +40 mV.
At the same time, there is passive
outwards diffusion of potassium ions
to bring about repolarisation and the
membrane potential is again reversed
to -70mV
Local anaesthetics work by
preventing the entry of sodium ions
to prevent the propagation of
action potentials.
There are two theories on the subject
of how sodium channels are blocked:
1. Non-specific membrane expansion
theory
2. Specific receptor theory
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.
Specific receptor theory:
The hydrophilic charged amino terminal
binds to specific receptors of the sodium
gates to block the passage of sodium ions
 Lignocaine
 Prilocaine(Citanest)
 Articaine
 Bupivacaine(Marcaine)
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
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.
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
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
THIS IS THE END OF THE SLIDE
SHOW ON LOCAL ANAESTHETICS

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Local anaesthesia

  • 1.
  • 2. Local Anaesthetics produce loss of sensation to pain 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 the the electrical impulse and take you back to first year physiology
  • 4.
  • 5. This picture shows how membrane potential changes with an action potential. 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. When depolarised, the membrane potential is reversed to +40 mV. At the same time, there is passive outwards diffusion of potassium ions to bring about repolarisation and the membrane potential is again reversed to -70mV
  • 6. Local anaesthetics work by preventing the entry of sodium ions to prevent the propagation of action potentials.
  • 7. There are two theories on the subject of how sodium channels are blocked: 1. Non-specific membrane expansion theory 2. Specific receptor theory
  • 8. 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.
  • 9. Specific receptor theory: The hydrophilic charged amino terminal binds to specific receptors of the sodium gates to block the passage of sodium ions
  • 10.  Lignocaine  Prilocaine(Citanest)  Articaine  Bupivacaine(Marcaine)
  • 11. 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
  • 12. 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.
  • 13. 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
  • 14. 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
  • 15. THIS IS THE END OF THE SLIDE SHOW ON LOCAL ANAESTHETICS