Local Anaesthesia

Question 1

What is local anaesthesia?

Answer 1

A drug that causes reversible local anaesthesia and analgesia

Question 2

What do A- alpha receptors modulate

Answer 2

Motor and proprioception

Question 3

What do A delta receptors modulate?

Answer 3

Pain and temperature

Question 4

C fibers?

Answer 4

Pain and temp

Question 5

The sequence of nerve fiber blockade from first effect to last effect?

Answer 5

Peripheral vasodilation and elevation of skin temp
Loss of pain and temp sensation 
Loss of proprioception
Loss of tough and pressure sensation
Motor paralysis

Question 6

Which fibers are easier to block?

Answer 6

Thin nerve fibers

Question 7

Which fibers are more readily blocked and why- myelinated or non-myelinated?

Answer 7

Myelinated- because only the sodium channels at the node of Ranvier need to be inactivated

Question 8

What is the chemical structure of LA?

Answer 8

Lipophilic ring connected to a hydrophilic amine via an intermediate chain

Question 9

How many classified groups are there and what are they?

Answer 9

2, based on the linking group in the intermediate chain: ESTER or AMIDES

Question 10

Which LA are esters?

Answer 10

Amethocaine

Cocaine

Question 11

Which LA are amides?

Answer 11

Lignocaine
Bupivacaine
Ropivacaine
Levobupivacaine
Prilocaine

Question 12

What determines the state of LA?

Answer 12

pH
pK
Henderson-Hasselbach equation

Question 13

What can unionized drug do?

Answer 13

Cross the neuronal membrane and exert effect

Question 14

What are LA?

Answer 14

Weak bases

Question 15

Preparation of LA?

Answer 15

Must be water soluble and stable in solution

Question 16

What enhances chemical stability of LA?

Answer 16

pH adjustment to acidic side

LA are formulated as salts of hydrochloric acid to give stability and prolong shelf-life

Question 17

Mechanism of action of LA?

Answer 17

All LA are membrane stabilizing drugs and they reversibly decrease the rate of depol and depol.

They inhibit sodium influx through channels in the neuronal membrane

Once injected it’s acidic ph is elevated by tissue buffers and unionized basic drug is released

Only unionized lipid soluble drug is able to pass through the neuronal membrane

Question 18

What happened to the LA in the cell?

Answer 18

Inside the neuron, it is ionized by low intracellular pH into its active form

Question 19

Where does LA work?

Answer 19

Within the nerve, the inner portion of the sodium channel

Question 20

What are the factors influencing activity of local anaesthesics?

Answer 20

Lipid solubility
Intermediate chain
Protein binding
pKa
pH

Question 21

Systemic toxicity of LA?

Answer 21

Can occur in organs with excitable membranes heart and brain most at risk

Question 22

Which toxicity comes first brain or heart?

Answer 22

Brain

Question 23

Why does cardiac toxicity occur?

Answer 23

Slowed myocardial condition and myocardial depression. Plus peripheral vasodilation ( due to vascular SM relaxant effect of LA

Question 24

Which drug causes CVS to cuff at low plasma volumes

Answer 24

BUPIVACAINE

Question 25

What are the stages of CNS toxicity?

Answer 25

Initial phase: Circumoral parasthesia + metallic taste Tinnitus + visual disturbances Confusion + slurred speech Excitatory phase Mm twitching Convulsions Depressive phase Loss of consciousness Coma Resp depression and apnoea

Question 26

CVS stages go toxicity?

Answer 26

Initial phase Hypertension Tachycardia during CNS excitatory phase Intermediary phase Myocardial depression Decreased CO Hypotension ``` Terminal phase Peripheral vasodilation Severe hypotension Sinus bradycardia Conduction defects Dysrhythmias ```

Question 27

Immediate management of systemic toxicity of LA

Answer 27

STOP La Call for help ABC Maintain airway and ETT intub if necessary 100% O2 Confirm IV access Control convulsions IV diazepam (0,1mgkg) midazolam (0,1mgkg) thiopentone (2mgkg) Propofol (1-2mgkg) Assess cv status throughout Hypotension give IV fluids and vasoconstrictors- starts ephedrine or phenylephrine Use adrenaline if unresponsive

Question 28

Why is apnoea and convulsions a problem with systemic toxicity?

Answer 28

Apnoea and convulsions cause hypoxia, hyper arnica and metabolic acidosis This acidosis increase the ionised portion of the drug in the cytoplasm and reduced the amount of drug that can diffuse out the cell ---> prolonging the toxic effect

Question 29

How would we treat the apnoe?

Answer 29

Hyperventilate patient

Question 30

Management of cardiac arrest?

Answer 30

CPR BUPIVACAINE induced VF may require prolonged CPR due to drug's long duration of actions and slow dissociation from Na channels May respond to hyperventilation with O2 (to cause hypercarbia), defibrillation, MgSO4 and intralipid

Question 31

What is the drug treatment of BUPIVACAINE OD?

Answer 31

Intralipid

Question 32

What is the protocol of intralipid?

Answer 32

IV bolus of 1,5mgkg over 1min, repeated every 3-5mins (X2) Start an infusion- 0,25-0,5mg kg min MAX of 8mgkg Stored in fridge

Question 33

What is intralipid and what else can it be used for?

Answer 33

It's is a lipid emulsion contains soya oil, glycerol and egg phospholipids Can also be used as lipid substance of total parenteral nutrition (TPN), and as a propofol solvent

Question 34

What is the action of intralipid?

Answer 34

It acts as a circulating lipid sink, drawing bupivacaine out of theplasma and binding to it so that no more free fraction exist to bind to receptors

Question 35

Preventing systemic toxicity?

Answer 35

Results from intravascular injection or excessive doses Prevented by: Avoiding excessive doses. Consider site of injection and size of patient Use vasoconstrictors if not contraindicated Avoid intravascular injections Use test dose where appropriate

Question 36

Which LA are at risk of anaphylactic reactions?

Answer 36

Esters as they are metabolized by plasma cholinesterase and the product of metabolism is PABA which is associated with hypersensitivity

Question 37

How do vasoconstrictors aid LA?

Answer 37

Adrenaline 1:80 000- 1:200 000 Some come premixed Decreased rate of absorption therefore enhances amounts of drug available for neuronal uptake Enhances quality of analgesia Prolongs duration of action but depend on the: - agent lignocaine is more effective (shorter acting) than bupivacaine ( longer acting) - site more effective with infiltration than epidurals Limits toxicity Decreases surgical bleeding

Question 38

Vasoconstrictor are contra-indicated in?

Answer 38

Nerve blocks of areas without collaterals (penis, digits, eyes) Intravenous regional (bier's block) Unstable angina, dysrhymias, uncontrolled hypertension Utero-placental insufficiency Patient on tricyclics and MOAS- promote hypertension and/dysrhymias

Question 39

How can pH manipulation aid LA?

Answer 39

Alkalinisation Adding bicarbonate increased the tissue pH, higher proportion of unionized drug - accelerates diffusion across the neuronal membrane Also decreased the burning sensation often felt when lignocaine is given How much: 1ml NaHCO3 8,5% added to 10ml lignocaine 0,1ml NaHCO3 8,5% added to 10ml bupivacaine

Question 40

Glucose added to LA?

Answer 40

Spinal with LA solutions are slightly hypobaric ( at body temp), when compared to CSF- this will cause it to move upwards in the CSF away from the gravitional pull Adding dextrose makes the solution "heavy" or hyperbaric, causing it to sink in relation to the CSF

Question 41

Adding analgesic drugs?

Answer 41

Can be used with neuraxial procedures They have a synergistic effect improving - the quality - duration of analgesia These work on there respective receptors in the spinal cord Opioates, ketaminem clonidine, midazolam, neostigmine and adrenaline

Question 42

What is lignocaine's range of usual concentration, onset and max dose?

Answer 42

2-5% Fast onset Duration from 0,5-1,5hr Max dose = 3mgkg, 7mgkg with adrenaline

Question 43

What is bupivacaine's range of usual concentration, onset and max dose?

Answer 43

0,2-0,5% Slow-fast 2-12hrs Max dose is 2mgkg with or without adrenaline