Local Anaesthesia Flashcards
(19 cards)
Local anaesthesia
- Reversibly prevents transmission of the nerve impulse
- Works at the site it is injected into either the peripheral nerve or the spinal cord
o We don’t inject regional anaesthetic drugs into the IV space / system unless it is lignocaine if we require it as an anti-arrhythmic or as a lignocaine infusion
No effect on consciousness
Classification of local anaesthetic: very NB!
- Lipid-soluble hydrophobic aromatic group and a charged, hydrophilic tertiary amide group
o Weak base with slightly alkaline pH
o The lipid-soluble part renders the drug more potent
o The lipophilic part is attached to an intermediate chain the longer the chain, the longer the duration
Amides:
- Contains an amide-link between the aromatic- and hydrophilic ends
- eg. lignocaine, mepivacaine, prilocaine, ropivacaine, bupivacaine, levo-bupivacaine
Esters:
- Contains an ester-link between the aromatic- and hydrophilic ends
- More heat-labile
- Easily broken-down
- Less stable in solution
- Cannot be stored for a long time
- Para-aminobenzoate (PABA) allergic reaction
eg. cocaine, procaine, 2-chloroprocaine, tetracaine
Mechanism of action of local anaesthesia NB
Local anaesthetics work on the cell membranes of nerves
- The local anaesthetic stops action potential impulse from happening it essentially acts as sodium-channel blockers
o They are injected and initially they are extracellularly (in an ionised form)
o In order to move intracellularly, it needs to be unionised
o When they move intracellularly to work inside the cell, it blocks sodium influx
Functional consequences of sodium-channel blockade by local anaesthetics:
- Vascular smooth muscle vasodilatation
- Heart decrease excitability
- Central nervous system increase excitability
- Nerves abolish the conduction of action potentials (obviously)
Physiochemical properties: of local anaesthetics
- Weak bases
- The terminal amine may exist in a tertiary form (3 bonds) that is lipid soluble or as a quaternary form (4 bonds) that is positively charged and renders the molecule water soluble
- The aromatic ring determines degree of lipid solubility if unionised, but the terminal amine acts as an “on-off switch” for lipid-solubility
- Potency correlates with lipid solubility
- Onset of action influenced by Pka
- Duration of action determined by protein binding and intermediate chain = NB!
Measure of potency patient factors
- pH = acidic pH antagonizes block
- Frequency of the nerve stimulation
- Electrolyte concentrations decr K & incr Ca antagonize block
Measure of potency nerve factors
- Fibre size & type the smaller the fibre, the quicker it is to block
o Type A-delta fibres are your smallest fibres and are the quickest to block these are the fibres that control pain, temperature, and touch
o Your motor nerves are bigger nerves and takes longer to block - Myelination
The significance in the use of adrenaline with the local
Presence of vasoconstrictors = prolong action and decrease systemic toxicity (3 mg/kg if used alone but 7 mg/kg if adrenaline is added)
Metabolism/ Excretion of Esters
Predominantly via pseudocholinesterases
- Ester hydrolysis is rapid
- Water soluble metabolites excreted via the kidney
- Procaine / benzocaine has p-aminobenzoic acid allergic reactions
- Cocaine partially metabolised in the liver and partially excreted unchanged in the kidney
Metabolism / Excretion of Amides
- They do not undergo tissue enzyme degradation; they go directly through the cytochrome P450 n-dealkylation and hydroxylation
o Need to adjust your dose in patients with hepatic / renal failure - Rate of metabolism = prilocaine > lignocaine > ropivacaine > bupivacaine
Eg. of local anaesthesia drugs
Lignocaine (T1/2 = 90min)
Bupivacaine (never IV t1/2 = 2.7 hrs)
Complications of local
- Local anaesthetic systemic toxicity (LAST)
- Bleeding
- Nerve injury
- Haematoma formation
- Infection
Significance of thrombolytics and local anaesthesia
Absolute contra-indication!
Local anaesthetic systemic toxicity (LAST)
- Accidental intravascular injection
- Rapid absorption of local anaesthetic
- Determined by peak plasma level
- Excessive dose or rate of injection
- Give intralipid! Rx
- prolonged anaesthesia
- progressing neuropraxia
Treatment of LAST
- Resuscitation ABC
o Continue CPR = reversible cause - Intralipid = 1.5 ml/kg followed by infusion
- Terminate convulsion = benzodiazepines / thiopentone
CNS symptoms of Local Anaesthesia
Initially CNS excitation but then CNS depression
o Peri-oral and / or tongue numbness
o Metallic taste
o Tinnitus
o Dizziness
o Visual and auditory disturbances (difficulty focusing)
o Disorientation
o Drowsiness
o Muscle twitching
o Convulsions terminate with benzodiazepines & thiopentone
o Coma
Cardiovascular Symptoms of local anaesthesia
In the heart, this depresses Vmax (the rate of depolarization)
may lead to re-entrant arrhythmias
- Chest pain
- Shortness of breath
- Palpitations
- Light-headedness
- Diaphoresis
- Arrhythmias
- Hypotension
- Arrest
