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Anesthesia > Test 1- Pre-meds > Flashcards

Test 1- Pre-meds Flashcards

1
Q

Purposes of premedication

A

Sedation, analgesia
Anesthetic sparing effect
Reduction of stress and catecholamine release Reduction of O2 demand
Increased safety for animals and humans!
Decreasing parasympathetic tone
Others: antibiotics, antihistamines

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2
Q

Anticholinergics

A

Atropine and Glycopyrrolate

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3
Q

Atropine

A

Lipid soluble
Absorbs well IM, SC, PO
Crosses the BBB and placental barrier Dose: 0.01 – 0.04 mg/kg iv

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4
Q

Glycopyrrolate

A

Water soluble
Absorbs slowly IM, SC, PO
Onset of effect is slower than atropine even IV Doesn’t cross the BBB and placental barrier
Dose: half of that of atropine
Advantage over atropine is debated

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5
Q

What are indications of anticholinergics?

A

Increasing heart rate
o Treatment of opioid induced bradycardia

o Prevention/treatment of reflex bradycardia

o Young animals and brachycephalic breeds

o Routine use is not recommended!

Decreasing salivation and bronchial secretion o Smaller amount but thicker mucus is not better

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6
Q

What are the contraindications of anticholergenics?

A

Tachycardia

Hyperthyroidism

Most heart diseases
o Except when needed for treatment of bradycardia

Narrow angle glaucoma

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7
Q

CV S/E of Anticholingerics

A

IT’S ALL ABOUT THE AV NODE!

2o AV block, bradycardia, cardiac arrest Tachycardia, hypertension

SA node: atrial conduction (p wave)

AV node: ventricular conduction (QRS)

Anticholinergics easily affect on the SA node o Lot’s of P waves

Effect on AV node is weaker and comes later o AV blocks, bradycardia (vagal tone increased?)

When the AV node finally conducts o Excessive tachycardia

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8
Q

What can you not use with atropine?

A

alpha 2 agonist

though you can use medetomidine +atropine— but measure the bp before giving atropine

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9
Q

What are anticholergics used for?

A

Treatment of bradycardia

Be careful and think before you act!

Is there a problem? Yes or no?

o Consider species, age and disease of the patient.

o Is the patient hypotensive?

o Is the ET CO2 adequate (assuming constant ventilation)?

Treatment plan:
o Drugs: atropine, naloxone, othersH o Dose? Monitoring? Plan B?

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10
Q

Alpha 2 agonists

A

Strongest available sedatives (except pigs)

Have important cardiovascular side effects

Myriad of other effects
Have specific antagonists

Appropriate use is debated (crashing opinions)

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11
Q

MOA of alpha 2 agonist

A

Competitive agonist of α2 adrenergic receptors

Location
o CNS: presynaptic membrane (autoreceptor)

o Post-synaptic membrane (vascular smooth muscle) o Extra-synaptic sites (e.g. pancreas, lipocytes etc.)

sedation, vasoconstriction

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12
Q

what are the CNS effects of alpha agonist

A

Sedative effect is species specific

o Strong: dogs, cats, horses, ruminants o Weak: pigs

Some analgesic effect o Synergistic with opioids

Muscle relaxation

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13
Q

CV effects of alpha 2 agonist

A

Strong vasoconstriction
Leads to high SVR and BP
Reflex bradycardia develops
Result: low CO and tissue perfusion
BP may decrease later on (hypotension)

Common recommendation
o Don’t use atropine
o If necessary, give specific antidote (e.g. atipamezole)

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14
Q

Respiratory effects of alpha 2 agonists

A

Mild respiratory depression

RR decreases but tidal volume increases

Upper airway resistance increases
o Relaxation of larynx, pharynx and nares o Head dropping in horses: nasal edema

V/Q mismatch in horses
o Low V/Q resulting in decreased PaO2

Mostly with xylazine in sheep

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15
Q

α2 agonists: indications

A

Sedation of aggressive animals

Sedation in the ICU

Sedation to manage post operative airway

obstruction (e.g. after brachycephalic surgery) Prevention/treatment of seizures (epilepsy)

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16
Q

α2 agonists: contraindications

A

Too young or too old
Hemodynamic instability
Severely debilitated patient
Not suitable for most risk patients

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17
Q

Available α2 adrenergic agents

A

Agonists

Xylazine

Medetomidine

Dexmedetomidine

Detomidine

Romifidin

Antagonist

Atipamezole Yohimbine Tolazoline

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18
Q

α2 agonists

A

Specificity to α2/α1 receptor differ
Medetomidine >>> detomidine > xylazine
Most effects are mediated by α2 receptors
The main effects are very similar
Pharmacokinetics and purchase price may differ

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19
Q

Xylazine

A

Dog: 0.25 – 2 mg/kg
Horse: 0.5 – 1 mg/kg
Cattle: 10% of the horse’s dose
Small ruminants: between dogs and horses The dose of medetomidine does not differ Duration: 20-40 min

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20
Q

Detomidine

A

Used for large animals
Dose: 0.01-0.02 mg/kg

Route: IM, IV, sublinqual

Duration: 90-120 min

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21
Q

What is the main indication to use an anticholergic during anesthesia?

A

Increase HR and inhibit PSNS

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22
Q

What are the main indications to give an alpha 2 agonist?

A

SEDATION

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23
Q

What are the biggest SE of alpha 2 agonists?

A
  1. reflex bradycardia
  2. vasoconstriction—> decreased CO, decreased tissue perfussion
  3. increased bp, increased vascular resisitance
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24
Q

Which is more potent dexmedetomine or Medetomidine?

A

Dexmedetomidine is about twice as potent as medetomidine, but they act the same

25
Q

Phenothiazines

A

Acepromazine, (chlorpromazine, etc.)

Acting as antagonist on multiple receptors o Dopamine

o Serotonine o α1
o Histamine

26
Q

Acepromazine

A

Long acting drug (depending on dose) o 4–8hours

o 48 hours for liver patients
o Shorter if given in low doses (e.g. 10 μg/kg)

27
Q

Phenothiazines: CNS effects

A

Actions on dopamine and serotonine receptors
Weaker sedative effects compared to α2 agonists

No analgesic effect
Antiemetic effect
Mild respiratory depression

28
Q

Phenothiazines: CV effects

A

Actions on α1 receptors
Vasodilation and hypotension
Especially in hypovolemic animals
May cause death of hypovolemic patients

Measure blood pressure, give fluids!

29
Q

Phenothiazines: indications

A

Mild sedation for premedication or post OP

Prevention / treatment of opioid dysphoria

Prevention of emesis caused by morphine

Sedation for dogs with laryngeal paralysis

Enhance the sedative effect of xylazine in

horses

30
Q

Phenothiazines: contraindications

A

Hypovolemia, hemodynamic instability

Very young or very old patient
Von-Willebrand disease (Doberman)
Boxers may be sensitive (bradycardia)

Breeding stallions

31
Q

Butyrophenones

A

Similar drug family to phenothiazines

Drugs: droperidol and azaperone (Stresnil)

Sedative effect is similar to acepromazine

More likely to cause behavioral side effects

Less hypotensive and stronger antiemetic then acepromazine

Less effect on platelets

Anti arrhythmogenic, not seizurogenic

32
Q

Benzodiazepines

A

GABA receptor agonists
Sedative, anticonvulsant, muscle relaxant effects

Minimal CV and respiratory effects
No analgesia

Sedative is species specific

33
Q

Benzodiazepines

A

Agonists
o Diazepam

o Midazolam
o Zolazepam (Zoletil or Telazol)

Agonists
o Diazepam

o Midazolam
o Zolazepam (Zoletil or Telazol)
34
Q

Benzodiazepines: sedation

A

Species specific effect

Dogs, cats horses: disorientation, excitation may

occur when used alone

Better sedative effects in ruminants, camelids, pigs, birds, and ferrets

Rarely used alone

35
Q

Benzodiazepines: indications

A

Premedication: combine with

o Opioids

o α2 agonist o Or both

Induction: combine with
o Dissociative anesthetics (ketamine)

o Barbiturates or propofol

Treatment of seizures (status epilepticus)

36
Q

Diazepam

A

Lipid soluble

Formulated in propylene glycol or lipid emulsion

Chemical compatibility is limited

Give slowly IV

Poor absorption and pain on IM injection

Metabolized in liver and duration of action is 1 to 4 hours

37
Q

Midazolam

A

Water soluble (no propylene glycol)

Good chemical compatibility

More potent than diazepam

Shorter acting than diazepam

Metabolized in liver, but metabolites are inactive (unlike diazepam).

Can be given IM, IV or via mucus membranes

Better choice than diazepam

38
Q

Opioids

A

Exogenous substances that bind to opioid receptors and activate them

Strongest available systemic analgesics

Best choice for treatment of acute pain (e.g.

surgery!)

Decreases the doses of anesthetics

Minimal CV side effects

Suitable for most risk patients

39
Q

Opioid receptors

A

μ: strong analgesia, resp. depression, dependency

κ: weaker analgesia
δ: weaker analgesia (human relevance)

Location o Brain

o Spinal cord (dorsal horn)
o Peripheral nerves
o Inflamed organs (e.g. arthritis)

40
Q

Classification of opioids

A

Full agonists: activate receptors and trigger full tissue response

Partial agonists: activate receptors but do not trigger full tissue response even at high doses

Antagonists: bind to receptors but do not activate them

These drugs concentration dependently compete for receptor binding

41
Q

Potency

A

Potency: tells you the dose

42
Q

Efficacy:

A

Efficacy: tells you the strength of the effect

43
Q

Pharmacokinetics:

A

Pharmacokinetics: onset, duration of effect, administration strategy etc.

44
Q

Opioids: CNS effects

A

Analgesia
o Excellent for acute pain
o Less good for chronic pain

Decreasing the MAC of inhalants
o Species dependent
o Primates > dogs > cats > pigs > horses o May increase the MAC in horses

Sedation depends on
o Species: primates and dogs sedate better o Pain level: stronger if there was pain

Excitation, dysphoria
o Cats may become excited o Horses after high doses

Tolerance
Dependence

45
Q

Opoids cause what clinic sign?

A

Opioids may trigger or may inhibit vomiting

They stimulate the chemoreceptor trigger zone

outside of the BBB and may trigger vomiting

After entering the brain they inhibit the vomiting center

Water soluble opioids (morphine) enter the brain slowly: cause more vomiting

Lipid soluble opioids (e.g. fentanyl) enter the brain fast, vomiting does not occur.

46
Q

Opioids: CV effects

A

No direct negative inotropy or vasodilation

Indirectly may reduce sympathetic outflow

from the brain and reduce Bp that way

Increase parasympathetic tone and may cause bradycardia, this is treatable with atropine

Suitable for most risk patients

Improves CV function by allowing to reduce the doses of anesthetics

47
Q

Opioids: respiratory effects

A

May depress respiration but not as strongly as in humans and primates

Healthy small animals tolerate high doses well

Be careful with combinations and sick patients

Opioids have antitussive effect: therapy

May inhibit airway protective reflexes (e.g. coughing)

48
Q

Opioids: GI effects

A

Nausea, vomiting

Defecation

Obstipation

Spasm of the sphincter of Oddi (hepatopancreatic sphincter)

49
Q

Opioids: other effects

A

Hypothermia
Post OP hyperthermia (in cats)

Myosis (dogs), mydriasis (cats)

Inhibition of urination
Noise sensitivity

50
Q

Morphine

A

Cheap and strong analgesic, water soluble

Slow onset (30-45 min) long duration (4-6 hours)

High individual variability in elimination

Metabolized in the liver to an active metabolite

Elimination is slow in liver and renal patients

May cause histamine release, especially after high iv doses

Duration of epidural analgesia is 12-24 hours

51
Q

Hydromorphone, oxymorphone

A

Strong analgesics (full μ agonists)

Duration is about 4 hours
Reliable metabolism
No histamine release

Better choices than morphine

52
Q

Fentanyl

A

Strong analgesic (full μ agonist)

Fast onset short duration (15-20 min)

No histamine release

May accumulate after long infusions

53
Q

Remifentanil

A

Similarly potent to fentanyl

Very short acting (5 min) and does not

cumulate, ideal for CRI

Metabolized by non-specific esterases in muscles and intestines

Caution: accidental disruption of administration may trigger strong pain

Boluses may cause sudden bradycardia

54
Q

Butorphanol

A

Butorphanol is a mu ANTAGONIST and kappa agonist

Weak and short acting analgesic

It may worsen pain sensation in case of strong

pain
May be used for premedication in combination

with benzodiazepines or α2 agonists if there is no

strong pain (e.g. radiology)
May partially antagonize full μ agonists
55
Q

Buprenorphine

A

Partial μ agonist

Stronger analgesic than butorphanol

Relatively long acting: 6-8 hours

Onset is slow (20-40 min iv)

Often given to cats because may cause less excitation than full μ agonists

The owner of cats may continue giving is via the oral mucosa

56
Q

Tramadol

A

Weak analgesic

Metabolizes in the liver and its metabolite is μ

opioid agonist Inhibits
Tramadol itself inhibits NE and serotonin

reuptake (analgesia)

Not scheduled drug

Can be given PO

57
Q

Opioid antagonists

A

Naloxone: 30 min duration
o May be used in small animals to reverse respiratory

depression

o Routine use is not recommended (reverses analgesia)

Naltrexone: long acting (~10 hours). Used to antagonize wild animals after long acting opioids e.g. carfentanyl or etorphine

58
Q
A

Anesthesia (14 decks)

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