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Anesthesia > Support Drugs used in anesthesia > Flashcards

Support Drugs used in anesthesia Flashcards

1
Q

Support drugs used in anesthesia

A
  1. analgesics
  2. Fluids
  3. Resp stimulants
  4. Cardiovascular support
  5. Neuromuscular blocking agents
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2
Q

Effects of general anesthesia

A
  1. CNS depression
  2. CVS depression
  3. Respiratory depression
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3
Q

CNS depression from anesthesia

A
  1. Loss of consciousness
  2. Damping of reflexes
    -cardiovascular= hypotension
    -respiratory= hypoventilation
    -thermoregulatory= hypothermia
    -postural= reduced muscle tone
  3. Central modulation of nociception
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4
Q

Cardiovascular system Depression

A

-Reflex suppression (central and peripheral)
-changes in autonomic balance
-changes in vasomotor tone (drug effects, centrally and peripherally)
-myocardial depression (direct drugs, indirect hypoxemia, hypercapnia)

**OVERALL= hypotension

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5
Q

Respiratory depression

A

Reflex suppression:
-Decrease ventilatory response to increase CO2 pressure. Leads to decrease in pH and O2 pressure

-reduced muscle activity
-alveolar collapse/small airway closure (atelectasis)
-reduced functional residual capacity
-entilation/perfusion mismatch

OVERALL EFFECT: hypoventilation (hypercapia/hypoxemia)

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6
Q

Analgesics drugs

A

-nociceptive pathways can be stimulated during anesthesia
-sympathetic nervous system stimulation
-may require higher doses of anesthetic drugs= increased side effects

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7
Q

What is the only drug with both anesthetic and analgesic properties?

A

Ketamine

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8
Q

Fluid therapy rates

A

Dogs: 5ml/kg/hr

Cats: 3ml/kg/hr

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9
Q

Why supply fluid therapy?

A
  1. Replace losses due to:
    -evaporation from body surfaces
    -bleeding from surgical sites
    -urine production
  2. To offset hypotension:
    -vasodilation common side effect of inhalant anesthetic
    -increase venous return and CO
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10
Q

Fluids to use during anesthesia

A
  1. Isotonic crystalloid solution
  2. Colloids
  3. Blood products
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11
Q

Isotonic crystalloid solution

A

-balanced electrolyte

-lactated ringers
-normosol R/plasmalyte

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12
Q

Colloids

A

-larger molecules provide oncotic pressure similar to albumin
-stay in circulation longer than crystalloids
-starches (hetastarch)
-Gelatin- based **not in Canada

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13
Q

Blood products as fluids

A

-whole blood
-plasma
-packed red cells

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14
Q

Respiratory stimulants

A

-not often used during anesthesia- best to ventilate lungs using anesthetic breathing system and O2

-may use in field situations where no apparatus to ventilate lungs and for some rests for laryngeal paralysis

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15
Q

what does Doxapram cause?

A

-directly stimulates the CNS and respiratory center
-increases the sensitivity of peripheral and central chemoreceptors to CO2 and O2
-increases tidal volume and resp rate
- increases cerebral and myocardial oxygen demand which can be detrimental with patient not breathing or already hypoxemic
-stimulates vasomotor center= increase in BP
-increase plasma catecholamine concentration

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16
Q

Doxapram timing

A

-Can be given IM, IV, buccal
-onset immediate, effect lasts 1-2 mins

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17
Q

Hypotension during anesthesia

A
  1. Reduced CO
  2. Vasodilation
  3. Bradycardia
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18
Q

Reduced cardiac output

A

-depressed cardiac contractility
-reduced venous return (relaxation of great veins)
-position of animal, procedure and use of IPPV will also affect venous return

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19
Q

Vasodilation

A

-depress vasomotor control= vasodilation throughout the entire body

-directly relax vascular smooth muscle as well as skeletal muscle

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20
Q

Bradycardia

A

CO= HR x SV

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21
Q

Treatment for reduced CO

A
  1. Fluid therapy- improves CO by increasing venous return
  2. Improve cardiac contractility and heart rate through beta 1 adrenergic receptor stimulation
    -catecholamine drugs
    -short half life (similar to endogenous)
    -usually administer as in infusion
22
Q

Drugs used to treat reduced CO

A
  1. Dobutamine- most commonly used inotrope
  2. Epinephrine- reserved for CPR use
23
Q

Treatment of excessive vasodilation

A

Use alpha 1 adrenergic catecholamines to increase vascular tone
-short elimination lives; infusions required

24
Q

What does too much vasoconstriction limit?

A

-renal vascular supply

-skeletal muscle perfusion

25
Q

What pathological conditions cause excessive vasodilation?

A

-vasodilatory shock
-sepsis
-anaphylaxis

26
Q

Drugs used to treat vasodilation

A
  1. Phenylephrine
  2. NE
  3. high infusion rate of dopamine
  4. Epi
27
Q

Action of phenylephrine

A

alpha 1 action only

28
Q

Action of NE

A

mainly alpha 1, some beta 1

29
Q

Action of Dopamine

A

-mainly alpha 1, some beta 1

30
Q

Action of Epi

A

alpha 1, some beta 1 and beta 2 effects

31
Q

Ephedrine

A

-direct effect (beta 1 and alpha 1), but mainly acts on adrenal gland which then releases endogenous NE (alpha 1, some beta 1)

-long duration (10-15mins); bolus and infusion
**repeat bolus injection can exhaust ability to replenish NE so use infusions to overcome this effect

32
Q

Benefits to ephedrine

A

-preserves tissue perfusion
-useful effect
-inexpensive

33
Q

What drugs are used to treat bradycardia?

A

Anticholinergics
-act on muscarinic/cholinergic sites
NOT nicotinic

34
Q

Actions of Anticholinergics

A
  1. prevent action of acetylcholine
    2.prevents increases in vagal tone (opioids, head and neck surgery from oculo-cardiac reflex)
  2. prevents excessive secretions and drooling
35
Q

Anticholinergics and herbivores

A

not routinely used!

36
Q

Side effects of anticholinergics

A
  • bronchodilation

-secretions become thicker because only the water producing cells are affects

-increased HR, some increase in BP= increase in myocardial oxygen demand/work of the heart

-increases intra-ocular pressure through mydriasis

-reduced tear productions

-reduced GI motility and GI tract secretion

-reduced lower esophageal sphincter tone

37
Q

Routine use of anticholinergics?

A

Know when a drug cannot be used/not routinely used because it allows you to avoid:
-tachycardia
-glaucoma

** not with alpha 2 agonists unless the blood pressure has been lowered by use of other drugs such as isoflurane

38
Q

Use when required?

A

-use if excessive parasympathomimetic action is likely (concurrent use of potent opioid)

-if blood pressure is already low and has become heart rate dependent

39
Q

Atropine timing and specifics

A

Duration of action: 30-40mins

Onset of action: 1-2mins

**increases HR more than glycopyrrolate

**crosses CNS

40
Q

Glycopyrrolate timing and specifics

A

Duration of action: 2 hrs

Onset of action: 15-20mins

**does not increase HR as much as atropine

**does not cross CNS

**strong action to dry secretions

41
Q

Skeletal muscle relaxation under anesthesia

A

-tone reduced; some procedures need no muscle tone

42
Q

Eye surgery under anesthesia

A

Eye rotations in cats and dogs occur during surgery making intra-ocular surgery difficult because centrally acting drugs sill allow eye rotation even though they reduce muscle tone

**Need to use peropheral acting neuromuscular blocking agents (NMBAs)

43
Q

NMBAs

A

-not lipophilic so cannot cross CNS or placenta

-no sedative or analgesic properties; never used in animals alone

44
Q

Action of NMBAs

A

Paralyze all skeletal muscles
-must ventilate patient
-cannot use some monitoring signs based on muscle tone or muscle action (because they may maintain central eye)
-must ensure full reversal before recovery (laryngeal function)

45
Q

Depolarizing NMBAs

A

-act similar to Ach
-remain on receptor longer
-depolarization= flaccid paralysis
-broken down by plasma cholinesterase
-no reversal drug available

46
Q

Succinylcholine

A

Used in medical anesthesia to relax laryngeal muscles and allow endotracheal intubation
**animals not too hard to incubate, so not used often

Also may be used to prevent limb paddling in horses when combined with euthanasia

47
Q

Succinylcholine timing

A

Duration: short time in most species except dog

Onset: 20secs

48
Q

Non-depolarizing NMDAs

A

-based on CURARE
-competition inhibition with Ach; prevents 2 Ach molecules from reaching receptors. NMBA stays in receptor

Onset: 1-2 mins
Duration: 15-20 mins

49
Q

Reversing non-depolarizing NMBAs

A

Need to increase the number of Ach molecules in the area by blocking Acetylcholinesterase (Neostigmine)

Will increase Ach concentration all over body
-Nicotinic: ganglion, skeletal NMJ
-Muscarinic: post ganglion parasympathetic

**means need to give atropine to prevent undesirable side effects (bradycardia, drooling, bronchoconstriction)

50
Q

Atracurium (NMBA)

A

Spontaneously broken down at normal body temp and pH by plasma esterases
-store in fridge
-duration of action increases with hypothermia

**cannot get this drug anymore

51
Q

Rocuronium (NMBA)

A

-liver metabolism
-duration of action not changing with temp
-may increase HR on administration

52
Q

Neostigmine

A

-strong effects at muscarinic sites
-Allows for a build up of Acetylcholine at clefts and allows them to outcompete the NMBAs allowing for reversal
-consider using with atropine in cats and dogs

Duration: 40mins

Anesthesia (24 decks)

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