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The vet med 1 > 2 - Premeds and sedation > Flashcards

2 - Premeds and sedation Flashcards

1
Q

Give the definition of premedication

A

The administration of medication before anaesthesia

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2
Q

What is an anxiolytic?

A

A drug that produces a mental calming effect characterised by reduced motor activity, anxiety and interest in the environment

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3
Q

What is a sedative?

A

A drug that produces a mental calming effect characterised by sleepiness as well as disinterest in the environment

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4
Q

What is narcosis

A

Sedation produced by opioid analgesics

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5
Q

What are the 3 aims of premedication?

And what do they aim to do

A

Anxiolysis - to reduce stress and anxiety
Analgesia
Anaesthetic dose sparing (to reduce the dose of induction and maintenance agents needed for GA)

They aim to make animals easier and safer to handle, smooth induction, maintenance and recovery phases of anaesthesia, help create muscle relaxation to facilitate surgery and prevent adverse effects

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6
Q

What are the desirable properties of premedication drugs?

A
  1. To reduce fear and anxiety
  2. Should be easy to administer by different routes and be permissible with other drugs
  3. Quick onset of action
  4. Reasonable duration of action
  5. Antagonisable (so we can reverse them)
  6. They should have a predictable, reliable and dose dependent sedative effect
  7. Have minimal cardiovascular and rep effects
  8. Be analgesic
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7
Q

What is the definition of neuroleptanalgesia?

A

Sedation achieved wit a combination of an opioid and sedative drug

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8
Q

Is the effect of neuroleptanalgesia additive or synergistic and what does this mean? and why?

A

Its synergistic so the effect of the combination of drugs is greater than the effect of the sum of the individual drugs - this is because we choose drugs that act at different receptors.

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9
Q

Is sedation safer than anaesthesia and why?

A

People often think so but the 2 are on a continuum of CNS depression.
The response of an individual can be unpredictable, if you aim for sedation you may accidently get anaesthesia.
So whenever you sedate you need to be prepped to provide oxygen and ventilation, the same way you would if going for GA

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10
Q

How should we monitor sedated patients in comparison to GA patients?

A

The same

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11
Q

When is procedural sedation appropriate?

A

In a healthy patient for a non painful procedure like diagnostic imaging OR a painful procedure when using LA.

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12
Q

When is procedural sedation not appropriate?

A
  1. In patients who cant compensate for cardiovascular effects of sedative drugs - like those with cardiac disease or hypovolaemia
  2. When there is the potential for unrecognised stress and or pain in a ‘locked in’ patient - like with some sedatives the sedation lasts longer than the analgesic effect so they may be sedated but in pain
  3. Patients at risk of airway complications (like obstruction or aspiration) e.g. brachycephalic dogs, and patients undergoing airway surgery or dentistry
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13
Q

Name 3 classes of drugs that can be used for neuroleptanalgesia

A
  1. Phenothiazine (acepromazine)
  2. Alpha 2 adrenoreceptor agonists
  3. Benzodiazepines
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14
Q

What drug class is acepromazine?

A

Phenothiazine

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15
Q

What are acepromazines mechanisms of action?

A
  • A dopamine receptor antagonist
  • An alpha 1 adrenoceptor antagonist
  • A histamine (H1) blockade
  • Its antithrombotic
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16
Q

How is acepromazine eliminated from the body

A

Its metabolised by hepatic metabolism

Renal and biliary excretion

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17
Q

How long is acepromazines onset?

A

30-40 mins

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18
Q

How long is acepromazines duration?

A

6-8 hours

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19
Q

What are the routes of administration for acepromazine?

A

IV, IM, PO

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20
Q

What are the 5 effects of acepromazine?

And what are these things a result of?

A
  • Effects on CNS: sedation (which is a result of central dopamine receptor blockade)
  • Cardiovascular effects: hypotension (due to peripheral alpha 1 receptor antagonism causing vasodilation) AND its antiarrhythmic (so reduces catecholamine induced arrhythmias)
  • Its antiemetic (due t reduced dopamine activity in the chemoreceptor trigger zone)
  • Antihistamine (its direct histamine 1 receptor antagonism makes it a mild antihistamine so its not a good sedative for intradermal skin testing)
  • Haematological effects: reduced PCV ( due to sequestration of RBCs in the spleen) AND it causes reduced platelet count and function - but isnt associated with haemorrhage in normal patients, but should be avoided in those with platelet disorders
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21
Q

Why is acepromazine not a good sedative for intradermal skin testing?

A

Because its a mild antihistamine

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22
Q

What are the considerations of using acepromazine?

A
  1. Size - large breeds are more susceptible to its effects because its allometric scaling so we dose on body surface area rather than bodyweight
  2. It may reduce the seizure threshold, but its probs ok at clinical doses
  3. In boxers it causes syncope and fainting - probs vasovagal syncope
  4. It can cause aggression - its anxiolysis results in disinhibition so the animal may be more likely to attach you when its not anxious
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23
Q

Why is acepromazine significant in boxers and what is the solution to this?

A

It can cause syncope and fainting.

The solution is to avoid ACP or to give half the normal dose or to give the normal dose combined with an anticholinergic

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24
Q

What are the names of the alpha 2 adrenoceptor agonists and which species are they licenced in?

A

Medetomidine, dexmedetomidine (dogs and cats)
Detomidine, xylazine (cattle and horses)
Romifidine (horses)

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25
Q

What is the mechanism of action of the alpha 2 adrenoceptor agonists?

A

They are alpha 2 agonists and they have some alpha 1 agonism too.

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26
Q

How are alpha 2 adrenoceptor agonists eliminated from the body?

A

Hepatic metabolism

Renal excretion

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27
Q

How long is the onset of alpha 2s?

A

5 mins - but is dose and drug dependent

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28
Q

How long is the duration of action of alpha 2s?

A

30-180 mins but is dose and drug dependent

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29
Q

What are the routes of administration of alpha 2s?

A

IV, IM, transmucosal

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30
Q

What are the CNS effects of alpha 2 agonists?

A

Sedation (its profound and reliable) - this is a direct effect of the alpha 2 effects on the CNS
Analgesia
Muscle relaxation

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31
Q

Describe the cardiovascular effects of alpha 2 agonists

A

The effects are biphasic.
Phase 1: peripheral vasoconstriction –> hypertension –> reflex bradycardia
Phase 2: central alpha 2 actions –> reduced sympathetic tone –> normotension

The overall effect is: vasoconstriction, reduced cardiac output and occasional bradyarrhythmia’s.

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32
Q

Why shouldnt we treat bradyarrhythmias caused by drugs like anticholinergics?

A

Because the bradycardia is a defence mechanism so if you increase heart rate while the patient is still vasoconstricted you can cause fatal ventricular tachyarrhythmia.

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33
Q

What are some other effects of alpha 2 agonists (not including cardiovascular and CNS effects)?

A

Endocrine effects:

  • Reduced ADH and renin –> leads to diuresis
  • Reduced insulin –> gluconeogenesis –> increased blood glucose
  • Reduced ACTH –> reduced cortisol
  • Reduced catecholamines

Emesis - due to the direct alpha 2 effect at the chemoreceptor trigger zone.

Sweating (in horses)

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34
Q

What is a special consideration when using alpha 2 agonists?

A

Accidental self administration: alpha 2s are absorbed across mucous membranes and in humans they cause severe cardiovascular and resp depression

35
Q

What can alpha 2 agonists be antagonised by and describe this

A

Atipamezole
It is an alpha 2 antagonist
Its licenced for use with medetomidine and dexmedetomidine but works for the other alpha 2s
It reverses all effects - even the ones you want

36
Q

What drugs are in the benzodiazepines class of drugs?

A

Diazepam

Midazolam

37
Q

What are benzodiazepines mechanism of action?

A

They enhance action of GABA at GABAa receptors in the brain and spinal cord

38
Q

How are benzodiazepines eliminated from the body?

A

Hepatic metabolism

Renal and biliary excretion (but they have active metabolites)

39
Q

What are the routes of administration for benzodiazepines?

A

IV, IM (midazolam only)

40
Q

What are the effects of benzodiazepines?

A

Anxiolysis –> sedation (which you get depends on dose)
Anticonvulsant
Central muscle relaxation
Cardiovascular and resp depression (but its minimal at clinical doses)

41
Q

What are the considerations when using benzodiazepines?

A

Their sedation is unreliable and you can get paradoxical excitation - this is less likely if old, young or sick.

And if animals have a portosystemic shunt the drugs can be pro-convulsant.

42
Q

What is the best way to use benzodiazepines and why?

A

As a co-induction agent - so given immediately before the IV induction so we still get the anaesthetic dose sparing effect but it avoids risk of paradoxical excitement

43
Q

How do opioids work?

A

They alter modulation and perception of noxious stimuli.
They can be agonists, partial agonists or antagonists at mu, delta or kappa opioid receptors.
And they may have a combination of actions at one or more receptor types.

44
Q

What routes can opioids be administered?

A

PO, IM, SC, IV

45
Q

How are opioids metabolised?

A

Hepatic metabolism

- They undergo extensive first pass hepatic metabolism making oral bioavailability poor

46
Q

Describe the adverse effects of opioids

A

They are more common in healthy/pain free animals and systemic side effects can be minimised by administering the drug at the site of action

47
Q

What is the beneficial effect of opioids - describe it

A

Sedation - they have synergy with sedatives (so enhance the effect of sedatives which is good in premeds - hence they are useful in premedication.
But they can cause excitation in some species - like cats, horses and ruminants but at clinical doses usually this isnt an issue

48
Q

What are the cardiovascular and resp effects of opioids?

A
  1. Respiratory depression: its frequently seen as an adverse effect, at clinical doses its not normally an issue an isnt usually clinically significant.
    Its more likely when large doses of mu agonists are given to anaesthetised patients.
    And opioids improve resp function in animals with thoracic pain - because it hurts less to breathe

Bradycardia: opioids are cardiovascular safe becaue their only effect is bradycardia. This is caused by increased parasympathetic tone.
This is easily treated with a anticholinergic e.g. atropine

49
Q

Other than the resp and cardio effects, what other adverse effects can opioids cause (and describe them)?

A

Nausea and vomiting - because there are mu opioid receptors in the CTZ
This is only really seen with morphine in dogs and cats

Urinary retention - especially seen post-epidural but is seen after systemic opioid use too.

Reduced MI motility: which can lead to constipation and potentially post op colic - but preanesthetic use of opioids doesnt lead to it

Histamine release - especially morphine and pethidine. Mild reactions include cutaneous signs, or may be severe like anaphylactoid acute hypersensitivity and may result in cardiac pulmonary arrest.
We can avoid histamine release by giving morphine slowly and never giving pethidine IV

50
Q

How do we avoid histamine release from opioids?

A

We can avoid histamine release by giving morphine slowly and never giving pethidine IV

51
Q

Which is the gold standard opioid?

A

Morphine

52
Q

Which receptors does morphine have an effect on and is it agonist, partial agonist or antagonist?

A

Mu and kappa agonist

53
Q

What strength of analgesia does morphine provide?

A

Profound analgesia

54
Q

Is morphine licenced for use in animals?

A

No but we can use it under the perscribing cascade in some situations: epidural, intrathecal and intraarticular injections where its poor lipid solubility means it gets trapped in those spaces.

55
Q

Which control drug is morphine?

A

A schedule 2 controlled drug

56
Q

What are the 2 licenced mu agonists and what control drug are they?

A

Methadone
Fentadon
Pethidine
All schedule 3 control drugs

57
Q

Which receptors does methadone have an effect on and is it agonist, partial agonist or antagonist?

A

Mu and kappa agonist

58
Q

What is methadones potency compared to morphine?

A

1x morphine

59
Q

How long is methodones onset?

A

10-15 mins if IV, 20-30 mins if IM

60
Q

How long is methodones duration of action?

A

4 hours

61
Q

What species is methodone licenced for use in?

A

Dogs and cats

62
Q

Which receptors does pethidine have an effect on and is it agonist, partial agonist or antagonist?

A

Mu and kappa - agonist

63
Q

How long is prthidines onset?

A

Under 10 mins IM

64
Q

How long is pethidines mechanism of action?

A

Under 2 hours

65
Q

What are 2 considerations of pethidine?

A

It has anticholinergic activity and causes histamine release

66
Q

What species is pethidine licenced in?

A

Dogs cats and horses

67
Q

Which receptors does fentanyl have an effect on and is it agonist, partial agonist or antagonist?

A

mu and kappa - agonist

68
Q

What is fentanyls potency compared to morphine?

A

50x morphine

69
Q

How long is fentanyls onset?

A

1-2 mins

70
Q

How long is fentanyls duration of action?

What is the benefit of this

A

20 mins

It makes it ideal for titration of analgesia to effect and administration by constant infusion during anaesthesia

71
Q

Which species is fentanyl licenced in?

A

Dogs

72
Q

What is a negative of using fentanyl?

A

It can accumulate following long series because it is very lipid soluble
And when we use high doses we get marked respiratory depression requiring controlled ventilation and we get bradycardia

73
Q

Which receptors does buprenorphine have an effect on and is it agonist, partial agonist or antagonist?

A

mu partial agonist

74
Q

Does buprenorphine cause mild, moderate or marked analgesia?

A

Moderate

75
Q

How long is buprenorphines onset?

A

45-60 mins

76
Q

How long is buprenorphines duration of action?

A

Between 6-24 hours:
- 6-8 hours in SA
12-24 hours in horses

77
Q

What animals is buprenorphine licenced in?

A

Dogs cats and horses

78
Q

What is the limitation when using buprenorphine?

A

Its hard to top up the analgesia, because increasing the dose doesnt improve the analgesia because its a partial agonist.

79
Q

What happens if we administer a full mu agonist along side buprenorphine and why?

A

The full mu agonist will struggle to compete with buprenorphine for receptor binding because buprenorphine has very high affinity

80
Q

Which species can have an oral-transmucosal buprenorphine?
Why?
And what is the benefit of this?

A

Cats
Because of the specific combination of the chemical properties of buprenorphine and the oral pH of cats
Benefit: it will have 100% bioavailability in cats so its as good as giving it IV but can be given at home

81
Q

Which receptors does butorphanol have an effect on and is it agonist, partial agonist or antagonist?

A

its a mixed mu antagonist and kappa agonist

82
Q

Does butorphanol provide mild, moderate or marked analgesia?
Does butorphanol provide good or bad sedation?
And what is the relevance of these

A

Mild
Good

Its probably best for non painful procedures where its often given with ACP or an alpha 2 agonist to create good sedation.

83
Q

How long is butorphanols onset

A

5-15 mins

84
Q

How long is the duration of action of butorphanol?

A

Controversial

The vet med 1 (3 decks)

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