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Flashcards in Local Anaesthetic Agent Deck (12)
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1

Definition

A local anaesthetic (LA) is a drug that causes reversible local anaesthesia and analgesia.
Have a range of effects from analgesia
alone (sensory block) to a complete motor block with paralysis.

2

Classification of nerve fibres

A-alpha= motor funtion
A-beta= Touch and pressure/ Proprioception
A-gamma= muscle spindle (tone)
A-delta= pain and temperature
B=pre-ganglionic autonomic
C= pain and temperature, post-ganglionic autonomic
Arrange based on Myelin

3

Sequence of blockage by LA

1) Peripheral vasodilatation and elevation of skin temperature (C & B fibres)
2) Loss of pain and temperature sensation (C & Ad fibres)
3) Loss of proprioception (Ab fibres)
4) Loss of touch and pressure sensation (Ab fibres)
5) Motor paralysis (Aa fibres)
THE thinner the neuron the QUICKER IT IS TO BLOCK.

4

Pharmacology

Chemical structure
The local anaesthetics consist of a lipophilic aromatic group (benzene ring) connected to a
hydrophilic tertiary group (tertiary amide) via an intermediate chain. They are classified into 2
groups based on the linking group in the intermediate chain: ESTERS or AMIDES.
ESTERS: Amethocaine AMIDES: Lignocaine
Cocaine Bupivacaine
Benzocaine Ropivacaine
Tetracaine Levobupivacaine
Procaine Prilocaine

5

Factors influencing activity of local anaesthetics

1) Lipid solubility
The more lipophilic the agent, the more drug crosses the lipid bilayer of the neuronal membrane.
This increases potency, onset of action and duration of action of the LA.
2) Intermediate chain
Lengthening of the intermediate chain increases potency.
3) Protein binding
The higher the degree of protein binding, the longer the duration of action.
4) pKa
The pKa represents the pH value at which the local anaesthetic is 50 % ionised and 50 %
unionised.
The lower the pKa, the less ionisation for any given pH and the faster the onset of action.
5) pH
Acidosis increases the proportion of ionised drug in the interstitial fluid, and reduces the
proportion of unionised drug available to cross the neuronal membrane. This reduces the
potency of the drug. This might explain why LA’s do not work so well in areas of infection. The pH is too low outside the nerve as a result of the infection, therefore the drug will be more ionised
and less will reach the target site in the neuron.

6

Clinical effects LA

As mentioned, the opening of the fast sodium channels and the influx of sodium are essential for
the development and propagation of the action potential. As more and more sodium channels
become blocked by the LA agent, the sharp upstroke of the action potential is attenuated until
depolarisation does not generate sufficient currents to depolarise neighbouring cell membranes.
At this point neuronal transmission will stop. Sodium channels are found throughout the whole
body. It is not surprising, therefore, that the local anaesthetics have a capability for systemic
toxicity.

7

Local anaesthetic toxicity

Toxic effects can occur in organs with excitable membranes. The BRAIN and HEART are most
at risk.
Systemic toxicity is a rare, but catastrophic event; especially if a cardiac arrest is the end result.
Toxicity of the central nervous system (CNS) occurs first. Cardiovascular system (CVS) toxicity
occurs due to the slowed myocardial conduction and myocardial depression, plus peripheral
vasodilatation (due to the vascular smooth muscle relaxant effects of the LA).
Cardiac toxicity is usually only evident clinically after 2 - 4 x the plasma concentration required to
cause a convulsion. Exception to the rule: CVS toxicity due to Bupivacaine occurs at low plasma
levels.
Resistant ventricular fibrillation (VF) may occur with intravenous injection.

8

Prevention of systemic toxicity

Avoiding excessive doses. Consider site of injection (vascularity) and size of patient.
Use vasoconstrictors if not contra-indicated.
Avoid intravascular injections (aspirate prior to injection)
Use test doses where appropriate.

9

Anaphylactic reactions

Anaphylactic reactions to local anaesthetics are very rare. It is the esters that are
implicated more frequently than the amides. Esters are metabolised by plasma
cholinesterase. The degradation product of ester metabolism is p-aminobenzoic acid
(PABA); a compound associated with hypersensitivity and anaphylaxis.

10

Additives to local anaesthetics

Vasoconstrictors
pH manipulation: Alkalinisation
Glucose
Additives with analgesic activity (Opiates, ketamine, clonidine, midazolam, neostigmine and adrenaline)

11

Lignocaine

Maximum
dose: 3 mg kg-1
without
Adrenaline
or
7 mg kg-1
with
Adrenaline
Remains the most versatile and (Topical, Infiltration, Peripheral
Epidural, Biers block
Spinal)
widely used local anaesthetic
Relatively low systemic toxicity
Rapid onset, moderate potency and
moderate duration of action
Addition of adrenaline ↓ toxicity
An anti-dysrhythmic drug
pKa = 7,9 & protein binding = 64 %

12

Bupivacaine

Maximum
dose: 2 mg kg-1
with or
without
Adrenaline
Only modest increase in duration of
action with adrenaline.
Popular due to:-
- Potency (3 – 4 x lignocaine)
- Relatively low toxicity
- Long duration of action
- Safe in obstetrics
Low concentrations produce mostly a
sensory block.
Severe cardiotoxicity if given IV
Contra-indicated in Bier's (IV) block.
pKa = 8,1 & protein binding = 96 %