Local Anaesthetics Flashcards
What is local anaesthesia?
Any technique to induce absence of sensation in a specific part of the body, generally for the aim of inducing local analgesia. I.e. local insensitivity to pain
Use of local anaesthesia/ why LA:
- Good for surgical n dental procedures to reduce pain and distress
- As effective & safer, superior to GA in cases such as caesarean section
- Relief of non-surgical pain + enable diagnosis of the cause of some chronic pain conditions
Name the various techniques/extents of local anaesthesia:
- Topical anaesthesia (surface)
- Infiltration (injection to target area)
- Plexus block (LA to entire area)
- Epidural (whole CNS including spine)
- Spinal anaesthesia (subarachnoid block)
Most local anaesthetics consist of:
-
lipophilic group connected via an ester or amide to an ionizable group
- ester links are more prone to hydrolysis, they have shorter duration of action - Most are weak bases
- charged form is the most active as it cannot readily exit closed Na channels
- uncharged form is impt for rapid penetration of lipid membranes
Name LA drugs and their duration of effect:
Procaine: short acting cuz its less hydrophobic/more hydrophilic
Lidocaine: medium acting
Bupivacaine: long acting (cuz more hydrophobic => more likely to penetrate lipid membrane)
How can you prolong effect of LA?
- increase dose
- Add vasoconstrictor => minimise systemic distribution
How can you accelerate onset of action of LA?
- use LA w rapid penetration of skin
- add sodium bicarbonate => increase pH => higher proportion uncharged=> can better penetrate lipid membrane
LA is injected into acidic tissue, effect is?
LA becomes less effective, cuz it is now in its charged form.
Charged form: more active, cannot readily exit closed Na+ channels
Uncharged form: impt for rapid penetration into lipid membranes
- the uncharged basic form (B) and the charged form (BH+).
How are amide-type LAs metabolised?
In the liver, by CYP450 isoenzymes
Thus! Better not use in pxs w:
- liver disease (e.g. liver cirrhosis, decreased hepatic blood flow), as metabolism of the LA will be impaired
- concomitant medications competing for/inhibiting CYP450 => decreased metabolism
How are ester-type LAs metabolised?
- in blood, by circulating butyrylcholinesterase
- rapidly hydrolysed into inactive metabolites, including PABA(which can cause hypersensitivity)
- shorter plasma half life
Which type of LA is more prone to hypersensitivity in patients? ester type or amide type?
Ester type more prone hypersensitivity (allergies, e.g. erythematous reaction) bcuz it gets hydrolysed into PABA which is a known allergen.
- usually patients if allergic to one type, will not be allergic to the other type
What are the adverse effects of LAs? (systemic toxicity)
- CVS (most extensively affected)
- arteriolar dilation & depression of myocardial contractility => systemic hypotension
- arrythmia - CNS
- sleepy, lightheaded, restless, visual & auditory disturbances
- at higher conc: nystagmus, muscle twitching, seizures, coma - Haematology
- metabolites of prilocaine accumulate => methemoglobinemia (oxidation of a type of haemoglobin=> oxygen delivery impaired) - Allergic rxns
- metabolites of ester type LA (PABA thing)
What is the most common reason for overdose on LA?
Accidental intravascular administration
(when u accidentally inject into a blood vessel instead of the local nerves then it goes into systemic circulation)
What LA is more likely to cause CVS side effects?
Longer acting LAs such as bupivacaine.
- cuz itll stay in the blood longer then itll more likely bind to the cardiovascular receptors
List out the ester-type LAs:
- Cocaine
- Procaine
- Tetracaine
- Chloroprocaine
