Local Anaesthesia/Analgesia Flashcards
What is the triad of GA? Which 2 are involved in local anaesthesia?
- narcosis (unconciousness)
- analgesia (antinocieption)
- muscle relaxation
> local = lack of narcosis uncocnoiusness
3 drugs that can acheive local analgesia?
> ocal anaesthetics
- opioids (see aanlgesia)
- a2 agonists (see sedation lecture)
What are local anaesthetics?
- reversibly block the transmission of action potentials along the axon
- interfere with NA channels
- wears off after time
Which nerve fibres are most and least sensitive to local anaesthesia?
> B fibres most sensitive (sympathetic)
then ‘ad’ fibres (sensory PAIN)
least sensitive ‘ab’ and ‘Aa’ fibres (motor and proprioceptive)
sensitivity o f C fibres (unmyelinated) overlaps
WHat nerve groups exist and what are their fibre sizes, function and signs of blockade? Priority of blockade? [See table for fibre types and info]
- B fibres (vasoconstriction) preganglionic SnS. Fibres 1-3 w/ light myelination, ^ skin temp
- C fibres (pain) post ganglionic SnS. 0.13-1.3 w/ NO myelin. analgesia and loss of temp and sensation
- A-delta (pain and temperature) 2-5 w/ light myelination. Analgesia, loss of temp and sensation
- A-gamma (muscle spindles) 3-6 moderate. Loss of proprioception.
- A-beta (touch and pressure) 5-12 moderate myelin. loss of sensation touch/pressure.
- A-alpha (somatic motor, proprioception) 12-20 heavy myelination. Loss of motor func and proprioception
What order are sensations lost? “Differential block”
- pain
- cold
- warmth
- touch
- deep pressure
2 main pharmacological classes of local anesthesia
> esters
- metabolites by plasma pseudocholinesterases
- allergenergic
- eg. procaine (only LIC product in FPA,) tetracaine
- less commonly used
amides
- metabolised in liver by amidases
- allergies rare
- eg. lidocaine, bupivicaine, ropivacaine
- common
- 2 “i”s in name = amide!!
How does lipid solubility affect pharacology?
- potency
- axonal membranes predominantly lipid
How does protein binding affect pharmacology?
- duration of action
- bind to protein (Na channel) within axonal membranes
How does pKa affect pharmacology?
- speed of onset
- must diffuse across axon sheath in uncharged base form
(pH at which drug is 50% ionised, 50% unionised) - pKa close to PH of tissue -> ^ diffusion
Which form of drug blocks the Na channels?
Ionised form (must become re-ionised after crossing membane in unionised form)
Give an eg. of a high and low potency drug, how can this be calculated? Eg. slow, fast and medium onset drug, how is this calc? Eg. short and long lasting drug, how is this calc?
[See table for local anaesthetics, potency, onset and duratio nof action.]
> Potency = lipid solubility - high: procaine - low: tetracaine > Onset = pKa - slow: procaine - medium: ropivicaine - mepivicaine: fast > duration = protein binding % - ~1hr: procaine - ~2hrs: mepivicaine - - ~2.5-7hrs: bupivacaine
Which drug is lic FPA UK?
procaine (cattle only)
Which locals can be used in horses in UK?
- all (if LIC or on positive list)
- not FPA here
- skin and subcut swelling reported after lidocaine
- mepivicaine mainly used
What are the 2 main causes of local anesthetic toxicity?
> accidental IV injection
- always draw back before injecting
overdose
- always check weight and calculate maximum dose
3 complications of local anaesthesia?
> nerve damage - low incidence - providing not injecting inside the nerve, will be ok - if feel ^ pressure, likely inside nerve!! > systemic toxicity - right dose - draw back > local toxicity - very rare
How ca pharmacokinetics of local aneasthetic be manipulated?
- addition of vasoconstrictor (adrenaline)
- reduces systemic absorption
- reduce local blood flow
- ^ duration of action
