Local Anaesthesia Flashcards
Definition of a LA?
A drug that causes REVERSIBLE local anaesthesia and analgesia.
When applied to specific nerve pathways they have a range of effects from analgesia alone to a complete motor block with paralysis.
The physiology of nerve conduction?
Action potential generated by altered Na permeability across the membrane
Slow rise in membrane potential until threshold potential is reached (-50mV)
Voltage sensitive Na channels open, and Na floods in
Membrane potential peaks at 30mV
Voltage sensitive Na channels close
Na-K ATPase restores normal resting membrane potential (K channels open and K leaks out of the cell)
Classify the different nerve fibres by size and conduction?
A (alpha, beta, gamma, delta):
Most myelin
Thickest diameter
Slowest conduction
B:
Some myelin
Medium diameter
Moderate conduction speed
C:
No myelin
Thinnest
Fastest conduction
What are the different functions of the various nerve fibres?
A alpha: motor A beta: touch, pressure, proprioception A gamma: muscle tone A delta: pain and temperature B: pre-ganglionic autonomic C: pain and temperature, post-ganglionic autonomic
What is the sequence of nerve fibre blockade from first effect to last effect?
- Peripheral vasodilation and elevation of skin temperature
- Loss of pain and temperature sensation
- Loss of proprioception
- Loss of touch and pressure sensation
- Motor paralysis
What is the chemical structure of a LA?
Lipophilic ring, connected to a hydrophilic amine, via an intermediate chain
The intermediate chain may be an ester or an amide.
Give examples of LA that are ESTERS, and their common use?
Amethocaine (high potency and toxicity):
Topical
Eye drops or cream
Useful for venepuncture
Cocaine (high potency):
Topical
Used in ENT
Increases BP and HR
Give examples of LA that are AMIDES?
Lignocaine (topical, infiltrative, peripheral, epidural, Bier’s block or spinal) - rapid onset, moderate potency, moderate duration of action
Bupivicaine (infiltrative, peripheral, epidural or spinal)
Ropivicaine
Levobupivicaine
(The above 3 have slow onset of action (if infiltrative), high potency and long duration of action)
Prilocaine (a topical agent)
MoA of local anaesthetics?
Once injected, the acidic pH of the drug is elevated (made more basic) by tissue buffers and unionised basic drug is released
The unionised lipid-soluble drug passes through the neuronal membrane
Inside the neuron, it is ionised by the low intracellular pH to its active form
LA’s work from inside the nerve by inhibiting sodium influx
Factors that influence the activity of LA?
Lipid solubility: the more lipophilic the agent the more that crosses the neuronal membrane and thus the more potent it is
Intermediate chain length: >length = >potency
Protein binding: higher degree of protein binding, the longer the duration of action
pKa (the pH value at which LA is 50% unionised and 50% ionised): lower the pKa, the less ionisation for any given pH and the faster the onset of action
pH: acidosis increases the proportion of ionised drug and reduces potency
Which organs are most at risk for LA toxicity?
Brain and heart (organs with the most excitable membranes)
In which system does LA toxicity occur first, and what is the exception?
Central nervous system usually first
The exception is with bupvicaine, in which CVS toxicity occurs first
When is cardiac toxicity usually only evident?
2-4x the plasma concentration required to cause a convulsion
Describe the phases of CNS toxicity?
Initial:
Parasthesia, metallic taste, tinnitus, visual distubance
Confusion
Slurred speech
Excitatory:
Muscle twitching and convulsions
Depressive phase:
LOC
Coma
Respiratory depression and apnoea
Describe the phases of CVS toxicity?
Initial:
Hypertension and tachycardia (occurs during CNS excitatory phase)
Intermediate phase:
Myocardial depression
Decreased CO
Hypotension
Terminal phase: Peripheral vasodilation SEVERE hypotension Sinus bradycardia Conduction defects Dysrythmias
What is the immediate management in the case of LA toxicity?
STOP the drug
Call for help
ABC’s:
Maintain airway, intubate if necessary
Give 100% O2
Instruct patient to hyperventilate (blow off excess CO2 and reduce any acidosis)
Confirm or establish venous access
Control convulsions if they are present and do not terminate within 20s (IV midaz, diazapem or thiopentone)
Assess cardiovascular status throughout
If hypotensive, give IV fluid and vasoconstrictors (ephidrine, phenylephrine or adrenaline)
What is Intralipid and what are it’s uses?
A lipid emulsion consisting of soya oil, glycerol and egg phospholipids.
Lipid substance of total parenteral nutrition.
Solvent for propofol.
“Antidote” for bupivicaine (acts as a circulating lipid sink, drawing bupivicaine out of the plasma and binding it so that no more free fraction exist to bind receptors)
How to prevent LA systemic toxicity?
Avoid using excessive doses
Use vasoconstrictors if not contra-indicated
Avoid intravascular injections (always aspirate before administering LA)
Use test doses where appropriate
Anaphylactic reactions to LA?
Occurs most commonly with ESTERS
Degradation product of esters by plasma cholinesterase is PABA, which is associated with hypersensitivity and anaphylaxis
When are additive vasoconstrictors with LA contraindicated?
Nerve blocks in areas that lack collateral blood supply
IV regional anaesthesia
Unstable angina
Dysrhythmias
Uncontrolled hypertension
Utero-placental insufficiency
Patient on tricyclic antidepressants and MAOI’s
The benefit of adding vasoconstrictors (i.e. adrenaline) to LA?
Decreases rate of absorption, therefore enhances amount of drug available for neuronal uptake Enhances quality of analgesia Prolongs duration of action Limits toxic side-effects Decreases surgical bleeding
What are other additives to LA?
(Vasoconstrictors)
Bicarbonate (increases tissue pH resulting in a higher proportio of unionised drug available to enter nerve)(also reduces burning sensation)
Glucose (in spinal anaesthesia, makes LA “heavy”)
Additives with analgesia activity (i.e. opioids, ketamine, midazolam)(in neuraxial blocks only)
Max dose of Lignocaine?
Without adrenaline: 3 mg/kg
With adrenaline: 7 mg/kg
Max dose of Bupivicaine?
Without adrenaline: 2 mg/kg
With adrenaline: 2 mg/kg
Max dose of Amethocaine?
1 mg/kg
