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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
What is the potency for procaine/
1
26
What is the potency for lidocaine?
2
27
What is the potency for bupivacaine?
8
28
What is the potency for ropivacaine?
6
29
What are the factors of duration of action?
- 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
What is ester linkage?
-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
What is amide linkage?
i in the name before the caine - more stable - LAs subject to biotransformation with conjugation in the liver - longer plasma half life
32
How are esters metabolised?
- 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
How are amides metabolised?
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
What are the formulations of lidocaine?
– Sterile solutions for parenteral use – Aerosol sprays for nasal / airway use – Topical patches
35
What does making local anaesthetics more water soluble by making a salt solution do?
Lowers the pH of the solution if a hydrochloride salt – can cause stinging on injection
36
What is baricity?
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
What vasoconstrictors are often used with LAs?
adrenaline
38
What do vasoconstrictors do when given with an LA?
- reduce the speed of systemic absorption and therefore prolong duration of action - Reduces the risk of toxicity - Reduces bleeding at the injection site
39
What can patients get if they have a vasoconstrictor added to their LA through end arterial sites?
can get ischemia
40
How do drugs become systemically active?
drug must be unbound + unionised
41
What is the onset of action for lidocaine?
2-5 minutes
42
What is the duration of action for lidocaine?
20-40minutes
43
Which has a lower cariotoxicity, lidocaine or bupivacaine?
lidocaine
44
What is the duration of action for bupivacaine?
up to 6 hours
45
What drugs are found in EMLA cream?
lidocaine and prilocaine
46
What is the duration of onset for EMLA topical cream?
30-45 minutes
47
What will you see with central nervous system toxicity?
- Minor behavioural changes – Muscle twitching and tremors – Tonic-clonic convulsions – CNS depression / respiratory depression & death
48
How do you treat CNS toxicity?
- Symptomatic - Benzodiazepines (BDZs) to control seizures - O2 supplementation - Intubation and controlled ventilation if needed
49
What can cardiovascular toxicity cause?
hypotension and dysrhythmias
50
What can you see with CVS hypotension?
– Depression of myocardial contractility – Direct relaxation of vascular smooth muscle – Loss of vasomotor sympathetic tone
51
What can you see with CVS dysrhythmias?
– 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
How do you treat CVS toxicity?
- Symptomatic treatment - Manage bradycardias with an anticholinergic - Fluid therapy with inotropic support if needed - Intralipid IV may be successful (mop up the LA)
53
How can you prevent toxicity?
- 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
What are the loco-regional techniques for LAs?
▪ Epidural ▪ Regional/ Local ▪ Topical ▪ Infiltration
55
What is the difference between spinal and epidural anaesthesia?
- 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
What is epidural anaesthesia
- 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
What are the possible side effects after epidural given?
▪ Hypotension ▪ Hypothermia ▪ Urinary retention ▪ Infections ▪ (slowed hair regrowth)
58
What is regional blocking
blocking a larger area
59
What is local blocking?
something like an infiltration small and sidcrete action

ACVN - ANAESTHESIA (12 decks)

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