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ACVN - ANAESTHESIA > Local Anaesthetics > Flashcards

Local Anaesthetics Flashcards

1
Q

What is the action potential?

A

Conduction of impulse through nerves occurs as an all-or-nothing
event

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2
Q

What is the action potential caused by?

A

voltage-dependant opening of Na+ and K+ channels in the cell membrane

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3
Q

What does it mean by the rate of Na+ entry exceeds K+ exit?

A

the membrane becomes depolarized so there is a loss of electrical gradient

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4
Q

What happens during depolarization?

A

sets off a Na + positive feedback whereby more voltagegated Na + channels open and membrane becomes more depolarized

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5
Q

When is an action potential generated?

A

If a threshold is reached (about 15mV higher than RMP)

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6
Q

When does the membrane repolarize?

A

when Na + channels become inactivated and a special set of K + channels open and K + leaves the axon

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7
Q

Where are voltage operated Na+ channels present?

A

in all excitable tissues

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8
Q

What do voltage operated Na+ channels do?

A

Selectively passes Na+ ions

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9
Q

What does local anaesrthetics do to voltage operated Na+ chanels?

A

block the Na+ channel and therefore block nerve
conduction and have a membrane stabilising effect

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10
Q

What are the motor nerve types?

A

Aα, Aβ, Aγ

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11
Q

What are the sensory nerve types?

A

Proprioceptors Aα, Aβ; Mechanoreceptors Aβ, Aδ; Nociceptors
Aδ,C

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12
Q

What are the autonomic nerve types?

A

preganglionic B, postganglionic C

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13
Q

Which axons are more resistant to LA block?

A

larger diameter axons that are more heavily myelinated

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14
Q

Which fibres are more susceptible to LA block?

A

C fibres are unmyelinated and Aδ fibres are thinly myelinated

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15
Q

Whcih fibres are preferentially blocked?

A

C fibres and Aδ fibres

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16
Q

What will C fibres and Aδ fibres get when blocked?

A

get a nociceptive blockade before proprioceptive,
mechanoreceptive and motor
blockade

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17
Q

What must the LA penetrate to bind to the Na+ channel?

A

the nerve

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18
Q

What is the pKa of lidocaine

A

7.8

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19
Q

What is the pKa of bupivacaine?

A

8.1

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20
Q

When is bupivacaine ionized?

A

at plasma pH 7.4

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21
Q

Does bupivacaine or lidocaine have a slower onsey of action?

A

bupivacaine

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22
Q

What happens when pH decreases?

A

greater proportion
of the drug is ionized and therefore less drug can penetrate the nerve membrane to bind to the sodium channel

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23
Q

Which type of tissue is LA less effective in?

A

inflammed

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24
Q

What is potency?

A

a measure of drug activity
expressed in terms of the
amount required to produce an effect of given intensity

25
Q

What is the potency for procaine/

A

1

26
Q

What is the potency for lidocaine?

A

2

27
Q

What is the potency for bupivacaine?

A

8

28
Q

What is the potency for ropivacaine?

A

6

29
Q

What are the factors of duration of action?

A
  • The ease of penetration and
    amount of drug reaching the
    sodium channel: lipid solubility
  • Strength of binding to the
    channel: property of some
    drugs
  • Speed of removal: dependent on tissue perfusion (addition of
    vasoconstrictors)
  • Metabolism of LA: ester versus amide
30
Q

What is ester linkage?

A

-no i in the name before the caine
- relatively unstable
- rapidly broken down by plasma pseudocholinesterase
- Leads to a short plasma half life of the LA

31
Q

What is amide linkage?

A

i in the name before the caine
- more stable
- LAs subject to biotransformation with conjugation in the liver
- longer plasma half life

32
Q

How are esters metabolised?

A
  • Hydrolysis of the ester link by plasma esterases such as cholinesterases
    ▪-PABA is formed as a product of hydrolysis (can provoke allergic reactions)
  • CSF does not contain
    esterases
33
Q

How are amides metabolised?

A

Broken down by the cytochrome P450 enzymes
- Hepatic disease can prolong or limit metabolism
- Drugs such as barbiturates that induce enzymes can increase drug breakdown
- Drugs that inhibit the P450 enzyme

34
Q

What are the formulations of lidocaine?

A

– Sterile solutions for parenteral use
– Aerosol sprays for nasal / airway use
– Topical patches

35
Q

What does making local anaesthetics more water soluble by making a salt solution do?

A

Lowers the pH of the solution if a hydrochloride salt – can cause stinging on injection

36
Q

What is baricity?

A

the weight of one substance compared with the weight of an equal volume of another substance. For spinal anaesthesia, the comparator substance is cerebrospinal fluid

37
Q

What vasoconstrictors are often used with LAs?

A

adrenaline

38
Q

What do vasoconstrictors do when given with an LA?

A
  • reduce the speed of systemic absorption and therefore prolong duration
    of action
  • Reduces the risk of toxicity
  • Reduces bleeding at the injection site
39
Q

What can patients get if they have a vasoconstrictor added to their LA through end arterial sites?

A

can get ischemia

40
Q

How do drugs become systemically active?

A

drug must be unbound + unionised

41
Q

What is the onset of action for lidocaine?

A

2-5 minutes

42
Q

What is the duration of action for lidocaine?

A

20-40minutes

43
Q

Which has a lower cariotoxicity, lidocaine or bupivacaine?

A

lidocaine

44
Q

What is the duration of action for bupivacaine?

A

up to 6 hours

45
Q

What drugs are found in EMLA cream?

A

lidocaine and prilocaine

46
Q

What is the duration of onset for EMLA topical cream?

A

30-45 minutes

47
Q

What will you see with central nervous system toxicity?

A
  • Minor behavioural changes
    – Muscle twitching and tremors
    – Tonic-clonic convulsions
    – CNS depression / respiratory depression & death
48
Q

How do you treat CNS toxicity?

A
  • Symptomatic
  • Benzodiazepines (BDZs) to control seizures
  • O2 supplementation
  • Intubation and controlled ventilation if needed
49
Q

What can cardiovascular toxicity cause?

A

hypotension and dysrhythmias

50
Q

What can you see with CVS hypotension?

A

– Depression of myocardial contractility
– Direct relaxation of vascular smooth muscle
– Loss of vasomotor sympathetic tone

51
Q

What can you see with CVS dysrhythmias?

A

– Most commonly seen with bupivacaine
– Lipophilicity means rapid entry to open sodium channels during systole
– Drug remains bound to the sodium channel during diastole
– Presents as re-entrant arrythmias

52
Q

How do you treat CVS toxicity?

A
  • Symptomatic treatment
  • Manage bradycardias with an anticholinergic
  • Fluid therapy with inotropic support if needed
  • Intralipid IV may be successful (mop up the LA)
53
Q

How can you prevent toxicity?

A
  • Don’t exceed “safe” maximum dose
  • If greater volume needed dilute the LA with NaCl 0.9%
  • Use appropriately sized syringes to draw up dose (accuracy)
  • Use appropriately sized needles to minimise tissue trauma
  • Aspirate before injection to confirm you are not in a blood vessel
54
Q

What are the loco-regional techniques for LAs?

A

▪ Epidural
▪ Regional/ Local
▪ Topical
▪ Infiltration

55
Q

What is the difference between spinal and epidural anaesthesia?

A
  • In the vertebral canal
  • Spinal cord and nerves are in a sac of CSF
    – Injection into this sac containing CSF = spinal anaesthesia
  • Space around the sac is the epidural space
    – Injection into the epidural space = epidural anaesthesia
56
Q

What is epidural anaesthesia

A
  • Technically difficult technique – should only be performed by trained
    individuals
  • More difficult in obese and pregnant animals and any other patients where
    anatomical landmarks are affected – ideally use X-ray or U/S
  • Must have sterile prep of area
  • Do not do if skin infection at puncture site, sepsis, coagulation impairments
  • Need sterile and preservative free LA preparation
  • May also add/ use opioids, medetomidine, ketamine
57
Q

What are the possible side effects after epidural given?

A

▪ Hypotension
▪ Hypothermia
▪ Urinary retention
▪ Infections
▪ (slowed hair regrowth)

58
Q

What is regional blocking

A

blocking a larger area

59
Q

What is local blocking?

A

something like an infiltration small and sidcrete action

ACVN - ANAESTHESIA (12 decks)

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