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Local Anaesthetics (LA)

Mechanism of action

- Bind to sodium channels to block transmission of action potentials

They also bind to potassium and calcium channels and have effects on local G-protein coupled receptors


- The more 'open' and active Na+ channels are, the more the LA will bind (called a 'use-dependant or 'phasic' block)


- LA stabilises the receptor in its 'inactive' state - preventing it opening

- This is obviously also reversible

- Response is concentration dependant. Higher concentrations selectively either reduce APs, slow conduction, or cause refractory period to lengthen


- A-delta fibres are more responsive to LA than C-fibres

- This is called differential sensitivity


This is most easily seen in epidural anaesthesia. Fibres are generally blocked in the following order:

- Sympathetic --> Cold and pinprick --> proprioception --> Motor fibres


Pharmacology

- They are water soluble salts of lipid soluble alkaloids

- They are lipophilic aromatic group connected via bridge to hydrophilic amine group

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Pharmacodynamics



Pharmacokinetics

The type of tissue that the LA enters also impacts upon its concentration. For example intrapleural > epidural > sciatic.


Types

- Speed of onset, potency and duration depends upon the pKa, lipid solubility and protein binding respectively



Ropivicaine causes local vasodilation at clinical doses - which may be why the max dose with adrenaline remains the same.




- Ropivicaine has lower lipid solubility than bupivicaine which means it has a better selective sensory blockade than bupivicaine

- Ropivicaine is a levo-enantiomer of bupivicaine


- Bupivicaine lasts longer in effect than lidocaine because it has a higher affinity for binding and dissociates more slowly. This is also why it can accumulate in diastole and cause cardiac issues.


Bupivicaine particularly binds cardiac Na+ channels causing prolonged diastole.


Metabolism

Esters are hydrolysted in plasma to a metabolite called PABA. This can cause allergic reactions.


Amide local anaesthetics undergo aromatic hydroxylation, amide hydrolysis and N-dealkylation. It is much slower than for esters and is more prone to accumulation in hepatic dysfunction. Amides have very low allergic potential.


Clearance values and elimination half times for amides is mainly due to hepatic metabolism. Renal excretion of unchanged drug is minimal and accumulation of metabolites can occur in renal failure. Lidocaine actually depends more on total blood flow to the liver rather than the enzymes themselves.


Interesting fact: EMLA cream is called a eutectic mixture! Because it has both lidocaine and prilocaine in an oil/water emulsion. It is used this way because it has a lower melting point than the two LA's seperately allowing higher concentrations to be used.


Contraindications:

Local anaesthetics can be toxic to nerves and other tissues but LA induced neurotoxicity is rare.


LA in the intra-articular space is chondrotoxic so needs to be used with caution


Other uses:

Anti-inflammatory/antibacterial: They reduce polymorphonuclear leukocyte adherence, migration and accumulation and alter macrophage and monocyte functions. At high concentrations they have anti-bacterial effects however these are rarely reached in clinical practice.


Antimetastatic properties:


LAST


References:

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