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Applied Clinical Veterinary Nursing > Local Anaesthetics > Flashcards

Local Anaesthetics Flashcards

1
Q

What is the mechanism of LAs?

A

Block Na+ channel to block nerve conduction (action potentials)
“Membrane-stabilising effect”

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2
Q

Describe preferential/differential block.

A

Larger diameter axons are more heavily myelinated so less susceptible to LA block
Will get nociceptive block before proprioceptive, mechanoreceptive and motor blockade

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3
Q

Describe the structure of LAs.

A

Aromatic group (lipophilic end)
Basic side chain/tertiary amine (hydrophilic end)
EITHER ester OR amide linkage

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4
Q

How does pKa affect onset of action of LAs?

A

Plasma pH = 7.4
pKa further from 7.4 = greater proportion of LA ionised
Greater ionisation = slower onset of action

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5
Q

How does pH affect action of LAs?

A

Plasma pH = 7.4
pH decreases in inflamed tissue
Greater proportion of drug is ionised so less drug can penetrate nerve membrane to bind to Na+ channel
So LAs less effective in inflamed tissue

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6
Q

Define potency.

A

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

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7
Q

What is the relationship between toxicity and potency of LAs?

A

LA toxicity increases as potency increases

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8
Q

What factors affect duration of action of LAs?

A

Ease of penetration and amount of drug reaching Na+ channel (lipid solubility)
Strength of binding to channel
Speed of removal - dependent on tissue perfusion (addition of vasoconstrictors)
Metabolism of LA (ester vs amide)

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9
Q

Describe ester linkages.

A

No ‘i’ in name before ‘caine’
Relatively unstable
Rapidly broken down by plasma psuedocholinesterase
Leads to a short plasma half-life

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10
Q

Describe amide linkages.

A

‘i’ in name before ‘caine’
More stable than ester linkages
Subject to biotransformation with conjugation in liver
Longer plasma half-life

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11
Q

How are ester linkages metabolised?

A

Hydrolysis of ester link by plasma esterases (e.g. cholinesterases)
PABA is formed as a product of hydrolysis (can provoke allergic reactions)

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12
Q

How are amide linkages metabolised?

A

Broken down by cytochrome P450 enzymes
Hepatic disease can prolong or limit metabolism
Drugs such as barbiturates (that induce enzymes) can increase drug breakdown
Drugs that inhibit P450 enzymes (e.g. midazolam) can inhibit breakdown

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13
Q

How are LAs formulated?

A

Generally poorly water soluble
Overcome this by making salt solution
Lowers pH of solution if hydrochloride salt (can cause stinging on injection)

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14
Q

Define baricity.

A

Weight of one substance compared with weight of equal volume of another substance
e.g. for spinal anaesthesia, comparator substance is CSF

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15
Q

How do we balance baricity for spinal anaesthesia?

A

Glucose added to solutions to make them heavier
To ensure LAs do not spread too high into epidural space (to avoid affecting muscles of respiration)

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16
Q

Describe the addition of vasoconstrictors to LAs.

A

Reduce risk of toxicity
Reduce bleeding at injection site
Care with end arterial sites as can get ischaemia
Adrenaline commonly added

17
Q

Why are vasoconstrictors added to LAs?

A

To reduce speed of systemic absorption
Prolong duration of action

18
Q

Describe plasma protein binding.

A

LAs are absorbed systemically so available for systemic effects e.g. toxicity
Drug must be unbound and unionised to be systemically active
Plasma protein binding is concentration- and pH-dependent
(% binding decreases as concentration rises or pH falls)

19
Q

Describe lidocaine.

A

Rapid onset of action (2-5 mins)
Intermediate duration of action (20-40 mins)
Lower cardiotoxicity than bupivacaine

20
Q

Describe bupivacaine.

A

Longer onset of action than lidocaine
Longer duration of action (up to 6 hours)
Greater CVS toxicity than lidocaine

21
Q

Describe EMLA.

A

Mixture of lidocaine and prilocaine in a cream
Topical anaesthesia - good for IV catheterisation
Onset of action 30-45 mins before full effect

22
Q

What are the risk factors for LA toxicity?

A

Dose!
Site of injection (determines rate of uptake into systemic circulation)
Smaller animals (essential to give correct dose so use appropriately-sized syringes)

23
Q

Describe CNS toxicity.

A

Seen at lower concentrations than CVS toxicity
Generalised CNS depression proportional to unbound drug

24
Q

What are the symptoms of CNS toxicity?

A

Minor behavioural changes
Muscle twitching/tremors
Tonic-clonic convulsions
CNS/respiratory depression
Death

25
Q

How do we treat CNS toxicity?

A

Symptomatic treatment
Benzodiazepines to control seizures
Oxygen supplementation
Intubation and controlled ventilation if required

26
Q

Describe hypotension as a symptom of CVS toxicity.

A

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

27
Q

Describe dysrhythmias as a symptom of CVS toxicity.

A

Most commonly seen with bupivacaine
Lipophilicity means rapid entry to Na+ channels during systole
Drug remains bound during diastole
Presents as re-entrant arrhythmias

28
Q

How do we 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)

29
Q

How can we prevent LA toxicity?

A

Do not exceed max. “safe” dose
If greater volume needed, dilute with 0.9% NaCl
Use appropriately-sized syringes for accuracy
Use appropriately-sized needles to minimise tissue trauma
Aspirate before injection to confirm not in blood vessel

30
Q

What are the possible loco-regional LA techniques?

A

Epidural
Regional/local
Topical
Infiltration

31
Q

What is the difference between spinal and epidural anaesthesia?

A

Spinal anaesthesia = injection into sac containing spinal cord, nerves and CSF
Epidural anaesthesia = injection into space around sac containing spinal cord, nerves and CSF

32
Q

Can RVNs carry out an epidural?

A

No! - into a body cavity

33
Q

What are the possible side effects of epidural anaesthesia?

A

Hypotension
Hypothermia
Urinarry retention
Infections
(Slowed hair regrowth)

34
Q

What is the difference between local and regional anaesthesia?

A

Arguably the same thing - may differ in size of affected area
Local e.g. infiltration = small discrete action
Regional = blocking a larger area

35
Q

Give some examples of local and regional anaesthesia.

A

Ophthalmic block
Dental block
Limb nerve block
IV regional anaesthesia
Intra-articular
Wound soaker catheters

36
Q

Give some examples of topical anaesthesia.

A

LA eye drops
Lidocaine spray for ET intubation of cats
EMLA cream for IV catheterisation

37
Q

Give some examples of infiltration anaesthesia.

A

Testicular
Ovarian ligament
Ring block
Incisional line block
Intraperitoneal

38
Q

How do you carry out infiltration anaesthesia?

A

Usually blind inject in a ‘V’ or inverse pyramid shape
Desensitises this ‘V’ of tissue

Applied Clinical Veterinary Nursing (40 decks)

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