Local Anaesthetics produce loss of pain
sensation in a circumscribed area of
the body by inhibiting the conduction
process...
In order for us to understand how
local anaesthetics work, we first have
to look at how electrical impulses are
generated ...
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
...
When depolarised, the
membrane potential is
reversed to +40 mV
from -70mV.
At the same time, there
is passive outward
diff...
Local anaesthetics work by
preventing the entry of sodium ions
to inhibit 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. Spe...
Non-specific membrane expansion theory:
The lipophilic part of the local anaesthetic
attaches to the cell membrane to caus...
Specific receptor theory:
The hydrophilic charged amino terminal
binds to specific receptors of the sodium
gates to block ...





Lignocaine(Xylocaine)
Prilocaine(Citanest)
Articaine(Septocaine)
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 adrenali...
Less toxic and metabolises quicker than lignocaine.

Used as 4% plain or 3% with IU/ml Felypressin;
Felypressin is an anal...
The molecular structure of articaine is different from other
local anaesthetics due to the presence of a thiophene ring.
I...
used as 0.25% or 5% solution with
1: 200000adrenaline.

Onset of 5 minutes.
Can last for ~8 hours.

Used for longer durati...
THIS IS THE END OF THE SLIDE
SHOW ON LOCAL ANAESTHETICS
Local anaesthesia
Local anaesthesia
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Local anaesthesia

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Local anaesthesia

  1. 1. Local Anaesthetics produce loss of pain sensation in a circumscribed area of the body by inhibiting the conduction process in the peripheral nerves.
  2. 2. 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!!
  3. 3. This picture shows how membrane potential changes with an action potential.
  4. 4. 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.
  5. 5. 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.
  6. 6. Local anaesthetics work by preventing the entry of sodium ions to inhibit the propagation of action potentials.
  7. 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. 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. 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. 10.     Lignocaine(Xylocaine) Prilocaine(Citanest) Articaine(Septocaine) Bupivacaine(Marcaine)
  11. 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. 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. 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. 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, postoperative pain control and pain control for intractable facial pain. Maximum dose 1.3mg/kg.
  15. 15. THIS IS THE END OF THE SLIDE SHOW ON LOCAL ANAESTHETICS
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