Local Anaesthesia Flashcards
Definition of local anaesthetic
A drug that causes reversible local anaesthesia and analgesia
Which nerve fibre type transmits somatic motor impulses?
A-alpha
Which nerve fibre type is responsible for muscle tone and which neuromuscular organs do they innervate?
A-gamma
Innervate muscle spindles
Which nerve fibre type is responsible for pre-ganglionic autonomic innervation?
B
Which nerve fibre types are responsible for pain and temperature sensation?
A-delta (faster) and C (slower)
Which nerve fibre type is responsible for touch, pressure and proprioception, and where do these fibres run in the spinal cord?
A-beta
Run in the dorsal columns of the spinal cord
What are the functions of type C nerve fibres?
Pain and temperature sensation
Post-ganglionic autonomic nerves
What is the general rule of which nerve fibres are easiest to block with local anaesthetic agents?
Thin nerves are easier to block than thicker nerves (effective dose reached more easily)
Myelinated nerves are easier to block than unmyelinated nerves of same size (saltatory conduction - only requires block at 3 consecutive nodes of Ranvier)
What characteristics of local anaesthetics make them ideal agents for anaesthesia?
Rapid onset Long duration of action Minimal systemic toxicity Selective blockade of regions, as well as sensory block without motor blockade Reversibility
Where are ester local anaesthetics primarily metabolised?
In the plasma, by plasma cholinesterases
Where are amide local anaesthetics primarily metabolised?
In the liver
What is pKa?
The dissociation constant of a chemical.
pKa = pH at which a substance is in equilibrium i.e. half is in neutral base form/unionised (salt) and half is in acid/ionised state (cation)
List the sequence of nerve fibre blockade in order of first to last effect (effect and fibres involved)
- Peripheral vasodilatation with elevation of skin temperature (C + B)
- Loss of pain and temperature sensation (C + A-delta)
- Loss of proprioception (A-beta)
- Loss of touch and pressure sensation (A-beta)
- Motor paralysis (A-alpha)
What is selective blockade?
Blockade of selected nerve fibre functions, while preserving others e.g. block pain and temperature (C + A-delta) sensation while motor function remains in tact (A-alpha)
What are the 2 main groups of local anaesthetics?
Esters
Amides
What is the basic structure of local anaesthetic agents?
Aromatic ring (lipophilic)
Intermediate chain
- Ester: -C O O-
- Amide: -N H C O-
Amino group (hydrophilic)What are some basic chemical characteristics of local anaesthetics?
Amphipathic - has both hydrophilic and hydrophobic moeities
Weak bases
What chemical state must local anaesthetic agents exist at to cross the cell membrane and exert their effects?
Unionised (=basic salt)
Why are local anaesthetics prepared as salts of hydrochloric acid?
Enhances chemical stability and prolongs shelf-life
How do local anaesthetic agents work?
- Unionized, lipid-soluble drug crosses neuron cell membrane
- Drug is ionized by low intracellular pH into its active form
- Drug inhibits sodium influx through Na channels (reversibly)
- Neuron membrane is stabilised and becomes resistant to depolarisation and repolarisation, thus inhibiting nerve conduction
Examples of ester local anaesthetics
Amethocaine
Cocaine
Examples of amide local anaesthetics
Lignocaine Bupivocaine Ropivacaine Levobupivacaine Prilocaine
5 factors affecting the activity of local anaesthetics
- Lipid solubility: more lipophilic (increases dose that crosses cell membrane) = more potent, quicker onset of action, longer duration of action
- Intermediate chain: Lengthening intermediate chain = more potency
- Protein binding: more protein binding = longer duration of action
- pKa: lower pKa = less ionisation of drug required at any pH = faster onset of action
- pH: lower/acidic pH = higher ionised drug in interstitium = reduced uptake of drug into cell = lower potency
Which two organs are potential sites of systemic toxicity of local anaesthetics? Why?
Brain (occurs first)
Heart
These organs have excitable membranes required for normal functioning, which is inhibited by the action of local anaesthetics
What are the 3 phases of CNS toxicity due to systemic toxicity of local anaesthetics?
Initial phase:
- Circumoral parasthesiae + metallic taste
- Tinnitus + visual disturbances
- Confusion + slurred speech
Excitatory phase:
- Muscle twitching
- Convulsions
Depressive phase:
- Loss of consciousness
- Coma
- Respiratory depression and apnoea
What are the 3 phases of cardiovascular toxicity due to systemic toxicity of local anaesthetics?
Initial phase:
- Hypertension
- Tachycardia during CNS excitatory phase
Intermediary phase:
- Myocardial depression
- Decreased cardiac output
- Hypotension
Terminal phase:
- Peripheral vasodilatation
- Severe hypotension
- Sinus bradycardia
- Dysrhythmias
Immediate management of systemic toxicity of a local anaesthetic
- Stop injecting the drug
- Call for help
- ABC
- Maintain airway, intubate if necessary (full stomach etc)
- Give 100% O2
- Hyperventilation of patient to reduce acidotic state resulting from apnoea and convulsions
- Control convulsions: if >20 seconds, give IV diazepam, midazolam, thiopentone or propofol (beware CVS instability)
- Assess CVS status continuously
- Manage hypotension: give IV fluids and vasoconstrictors (start with ephedrine or phenylephrine, move to adrenaline if unresponsive)
- Intralipid if unresponsive to routine measures
Management of cardiac arrest secondary to systemic toxicity caused by a local anaesthetic agent
- Start CPR (may require prolonged CPR if toxicity due to bupivacaine)
- If toxicity due to bupivacaine: may respond to hyperventilation, defibrillation, MgSO4 and Intralipid
- Intralipid 20%: IV bolus 1,5ml/kg over 1 min, repeat every 3-5min x 2
- Cardiopulmonary bypass until drug effects subside (impractical)
Prevention of systemic toxicity due to a local anaesthetic agent
- Avoid excessive doses of local anaesthetics: consider site of injection (vascularity) and size of patient
- Use vasoconstrictors if not contra-indicated
- Avoid IV injections (aspirate before injecting)
- Use test doses if appropriate
What are the 2 main ways in which systemic toxicity results from a local anaesthetic?
- IV injection
- Excessive doses used
Roughly what serum level of local anaesthetics causes clinically evident cardiac toxicity
2-4 x plasma concentrations required to cause a convulsion
Exception: Bupivacaine causes CVS toxicity at low levels - may lead to resistant ventricular fibrillation
What is Intralipid?
- Lipid emulsion of soya oil, glycerol and egg phosholipids
- Used commonly as lipid substance of total parenteral nutrition
- Solvent for propofol
- Acts as a circulating “lipid sink”, drawing local anaesthetic drugs out of the plasma and binding them, thus inactivating them
Which local anaesthetics may cause an anaphylactic reaction?
Most commonly esters - plasma cholinesterases degrade them to form PABA, which is associated with hypersensitivity and anaphylaxis
Amides can also cause anaphylaxis, but less common
Why might you add a vasoconstrictor to a local anaesthetic?
- Decreases rate of absorption, so increases amount of drug available for neuronal uptake
- Enhances quality of analgesia
- Prolongs duration of action (depending on site and drug)
- Limits toxic side effects
- Decreases surgical bleeding
- Typically use adrenaline 1:80 000 - 1:200 000 (sometimes is pre-mixed)
What are contra-indications to using a vasoconstrictor in combination with a local anaesthetic?
- Nerve block in area lacking collateral blood supply e.g. digits, eyes, penis
- IV regional anaesthesia (Bier’s block)
- Unstable angina, dysrhythmia, uncontrolled HPT
- Utero-placental insufficiency
- Patients on TCA’s or MAOI’s, as may promote HPT or dysrhythmia
Why might you alkalinise a mix that includes a local anaesthetic?
- Adding bicarbonate increases the tissue pH = more unionised anaesthetic = greater diffusion into cell
- Decreases burning sensation when lignocaine infiltrated
Standard mixes of bicarbonate with local anaesthetic agents?
1ml NaHCO3 8,5% added to 10ml lignocaine
0,1ml NaHCO3 8,5% added to 10ml bupivacaine (precipitates if too alkaline)
Why might you add glucose to a mix that includes a local anaesthetic?
- Important for spinal anaesthetics
- Local anaesthetics are slightly hypobaric in relation to CSF at normal body temperatures, hence tend to move up CSF column
- Dextrose added to solution to make it hyperbaric and sink
Why might you add other analgesics to a local anaesthetic mix?
- Useful in spinals and epidurals
- Synergy between the two drugs used increases the quality and duration of analgesia
- Opiates are typically added, which act on their usual receptors in the spinal cord
What are the characteristics of lignocaine as a topical anaesthetic?
2 - 10% concentration used
Fast onset
0,5 - 1 hour duration
What are the characteristics of lignocaine as an infiltration?
0,5 - 1% concentration used
Fast onset
1 - 2 hour duration
What is the maximum dose of lignocaine?
- 3mg/kg without adrenaline
- 7mg/kg with adrenaline
What are the characteristics of lignocaine as a peripheral nerve block?
1 - 1,5% concentration used
Fast onset
1 - 3 hour duration
What are the characteristics of lignocaine as an epidural?
1 -2% concentration used
Fast onset
1 - 2 hour duration
What are the characteristics of lignocaine as a Bier’s block?
0,5% concentration used
Fast onset
Up to 2 hour duration
What are the characteristics of lignocaine as a spinal?
2 - 5% concentration used
Fast onset
0,5 - 1,5 hour duration
What are the characteristics of bupivacaine as an infiltration?
0,2 - 0,5% concentration used
Slow onset
4 - 12 hour duration
What are the characteristics of bupivacaine as a peripheral nerve block?
0,2 - 0,5% concentration used
Moderate onset
4 - 12 hour duration
What are the characteristics of bupivacaine as an epidural?
0,2 - 0,5% concentration used
Fast onset
2 - 4 hour duration
What are the characteristics of bupivacaine as a spinal?
0,5% concentration used
Fast onset
2- 4 hour duration
What is the maximum dose of bupivacaine?
2mg/kg with OR without adrenaline
