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Anaethetics 2 > Local Anaesthesia > Flashcards

Local Anaesthesia Flashcards

1
Q

What is local anaesthesia?

A

A drug that causes reversible local anaesthesia and analgesia

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2
Q

What do A- alpha receptors modulate

A

Motor and proprioception

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3
Q

What do A delta receptors modulate?

A

Pain and temperature

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4
Q

C fibers?

A

Pain and temp

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5
Q

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

A 
Peripheral vasodilation and elevation of skin temp
Loss of pain and temp sensation 
Loss of proprioception
Loss of tough and pressure sensation
Motor paralysis
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6
Q

Which fibers are easier to block?

A

Thin nerve fibers

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7
Q

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

A

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

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8
Q

What is the chemical structure of LA?

A

Lipophilic ring connected to a hydrophilic amine via an intermediate chain

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9
Q

How many classified groups are there and what are they?

A

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

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10
Q

Which LA are esters?

A

Amethocaine

Cocaine

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11
Q

Which LA are amides?

A 
Lignocaine
Bupivacaine
Ropivacaine
Levobupivacaine
Prilocaine
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12
Q

What determines the state of LA?

A

pH
pK
Henderson-Hasselbach equation

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13
Q

What can unionized drug do?

A

Cross the neuronal membrane and exert effect

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14
Q

What are LA?

A

Weak bases

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15
Q

Preparation of LA?

A

Must be water soluble and stable in solution

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16
Q

What enhances chemical stability of LA?

A

pH adjustment to acidic side

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

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17
Q

Mechanism of action of LA?

A

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

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18
Q

What happened to the LA in the cell?

A

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

19
Q

Where does LA work?

A

Within the nerve, the inner portion of the sodium channel

20
Q

What are the factors influencing activity of local anaesthesics?

A 
Lipid solubility
Intermediate chain
Protein binding
pKa
pH
21
Q

Systemic toxicity of LA?

A

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

22
Q

Which toxicity comes first brain or heart?

A

Brain

23
Q

Why does cardiac toxicity occur?

A

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

24
Q

Which drug causes CVS to cuff at low plasma volumes

A

BUPIVACAINE

25
Q

What are the stages of CNS toxicity?

A

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

26
Q

CVS stages go toxicity?

A

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
27
Q

Immediate management of systemic toxicity of LA

A

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

28
Q

Why is apnoea and convulsions a problem with systemic toxicity?

A

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

29
Q

How would we treat the apnoe?

A

Hyperventilate patient

30
Q

Management of cardiac arrest?

A

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

31
Q

What is the drug treatment of BUPIVACAINE OD?

A

Intralipid

32
Q

What is the protocol of intralipid?

A

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

33
Q

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

A

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

34
Q

What is the action of intralipid?

A

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

35
Q

Preventing systemic toxicity?

A

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

36
Q

Which LA are at risk of anaphylactic reactions?

A

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

37
Q

How do vasoconstrictors aid LA?

A

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

38
Q

Vasoconstrictor are contra-indicated in?

A

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

39
Q

How can pH manipulation aid LA?

A

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

40
Q

Glucose added to LA?

A

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

41
Q

Adding analgesic drugs?

A

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

42
Q

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

A

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

43
Q

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

A

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

Anaethetics 2 (10 decks)

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