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ANESTHESIA > 19 – Support Drugs > Flashcards

19 – Support Drugs Flashcards

1
Q

What are some support drugs used in anesthesia?

A
  • Analgesics
  • Fluids
  • Respiratory stimulants
  • CV support
  • Neuromuscular blocking agents
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2
Q

What are the 3 general effects of general anesthesia?

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

CNS depression

A
  • Loss of consciousness
  • Damping reflexes
    o Hypotension
    o Hypoventilation
    o Hypothermia
    o Reduced muscle tone
  • Central modulation of nociception
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4
Q

CVS depression

A
  • Reflex suppression
  • Changes in autonomic balance
  • Changes in vasomotor tone
  • Myocardial depression (direct=drugs, indirect=hypoxemia, hypercapnia)
  • *HYPOTENSION
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5
Q

Respiratory depression

A
  • Reflex suppression
  • Reduced muscle activity
  • Alveolar collapse
  • Reduced functional residual capacity
  • Ventilation/perfusion mismatch
  • *HYPOVENTILATION
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6
Q

What is the only general anesthetic with analgesic properties?

A
  • Ketamine
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7
Q

Fluid therapy: recommended surgical fluid rate for dogs

A
  • 5ml/kg/hr
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8
Q

Fluid therapy: recommended surgical fluid rate for cats

A
  • 3ml/kg/hr
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9
Q

What are the reasons to provide fluid therapy for all anesthetized animals?

A
  1. Replace losses due to various reasons
  2. To offset hypotension
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10
Q

Fluid therapy to replace losses due to

A
  • Evaporation from body surfaces
  • Bleeding from surgical sites
  • Urine production
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11
Q

Fluid therapy to offset hypotension

A
  • Vasodilation common side effect of IH anesthetic
  • Increase venous return and CO
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12
Q

What are examples of fluids to use during anesthesia (3)?

A
  • Isotonic crystalloid solution (balance electrolyte)
  • Colloids
  • Blood products
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13
Q

Isotonic crystalloid solution (balanced electrolyte): fluid therapy

A
  • Lactated ringers
  • Normosol R/plasmalyte
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14
Q

Colloids: fluid therapy

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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15
Q

Blood products: fluid therapy

A
  • Whole blood
  • Plasma
  • Packed red cells
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16
Q

Respiratory stimulants

A
  • Not often used during anesthesia
  • *best to ventilate lungs using anesthetic breathing system and O2
  • Ex. Doxapram
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17
Q

Possible indications of when you would use respiratory stimulants

A
  • Field situations where no apparatus to ventilate lungs
  • Some tests for laryngeal paralysis
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18
Q

Doxapram (respiratory stimulant): ‘effects’

A
  • Directly stimulates the CNS and respiratory center
  • Increases sensitivity of peripheral and central chemoreceptors to CO2 and O2
  • Increases tidal volume and RR
  • *increases cerebral and myocardial O2 demand
  • Stimulates vasomotor centre=increase BP
  • Increases plasma catecholamine concentration
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19
Q

Doxapram (respiratory stimulant) can be given

A
  • IM
  • IV
  • Buccal
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20
Q

Doxapram onset and duration

A
  • Immediate onset
  • Lasts 1-2 mins
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21
Q

Vasomotor control

A
  • Vasomotor center in lower barin
  • Outflow to body via SYMPATHETIC NS
  • NT=NE (acts on post-synaptic alpha1 adrenergic receptors)
  • At rest: midway between vasodilation and vasoconstriction
  • Adrenal glands release E into circulation for longer: sustained response (STRESS)
  • In skeletal muscle beds: beta-2=vasodilation
  • *baroreceptor reflex arc
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22
Q

What are 3 reasons for hypotension during anesthesia?

A
  1. Reduced CO
  2. Vasodilation
  3. Bradycardia (CO=HRxSV)
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23
Q

Reduced CO contributing to hypotension during anesthesia

A
  • Depressed cardiac contractility
  • Reduced venous return
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24
Q

What are some factors that can affect venous return?

A
  • Position of animal
  • procedure
  • use of IPPV will affect venous return
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25
Q

vasodilation contributing to hypotension during anesthesia

A
  • depression of vasomotor center=vasodilation throughout body
  • directly relax vascular smooth muscle as well as skeletal muscle
26
Q

What are some ways to treat reduced CO?

A
  • fluid therapy=increases venous return
  • improve cardiac contractility and HR through beta-1 adrenergic receptor STIMULATION
  • *DRUGS: Dobutamine, epinephrine
27
Q

Improve cardiac contractility and HR through beta-1 adrenergic receptor STIMULATION

A
  • Use catecholamine drugs
  • Have a short half-life (similar to endogenous)
  • Usually administer as an infusion
28
Q

Dobutamine to increase CO

A
  • Most commonly used inotrope
29
Q

Epinephrine to increase CO

A
  • Reserved for CPR use
30
Q

What do you use for treatment of excessive vasodilation?

A
  • *Alpha-1 adrenergic catecholamines
    o Increase vascular tone
    o Don’t use aggressively=limit duration
    o Useful for pathological conditions
    o Short elimination lives
    o Infusions required
31
Q

What can happen if there is too much vasoconstriction?

A
  • Can LIMIT
    o Renal vascular supply
    o Skeletal muscle perfusion
32
Q

Examples of patholocial conditions that cause excessive vasodilation?

A
  • Vasodilatory shock
  • Sepsis
  • Anaphylaxis
33
Q

Other drugs used to treat vasodilation (4)

A
  1. Phenylephrine
  2. NE
  3. High infusion rate Dopamine
  4. E
34
Q

Phenylephrine: acts on

A
  • alpha-1 action only
35
Q

NE: acts on

A
  • mainly alpha-1, some beta-1
36
Q

High infusion rate of Dopamine: acts on

A
  • mainly alpha-1, some beta-1
37
Q

E: acts on

A
  • alpha 1, beta-1 and beta-2 effects
38
Q

Ephedrine

A
  • longer duration (10-15mins)
    o bolus AND infusion
  • direct effect (beta-1 and alpha-1), but mainly acts on ADRENAL GLAND
    o release of endogenous NE (alpha1, some beta1)
  • preserves tissue perfusion
  • useful effect, inexpensive
  • *band aid solution (get time to fix what is happening)
39
Q

What can happen with repeat bolus injection of ephedrine?

A
  • Can exhaust ability to REPLENISH NE
  • *infusions can overcome this exhaustion effect
40
Q

What is the basis of drugs used to treat bradycardia?

A
  • Anticholinergics
    o Prevent action of ACh
    o Not routinely used in herbivores
  • *act on muscarinic/cholinergic sites, NOT nicotinic
  • *mainly PS action=decrease PS tone
41
Q

Anticholinergics are used to prevent

A
  • Increases in vagal tone
    o Opioids
    o Head and neck surgery
  • Excessive secretions (ex. drooling)
42
Q

What are some side effects of anticholinergics?

A
  • Bronchodilation
  • Secretions become thicker=only water producing cells are affected
  • Increase HR, with some increase in BP (increase in myocardial O2 demand/work of heart)
  • Increases intra-ocular pressure through mydriasis
  • Reduce tear production
  • Reduced GI motility and GIT secretion
  • Reduced lower esophageal sphincter
43
Q

When can anticholinergics not be used in cats and dogs? (‘use routinely’ school of thought’)

A
  • Tachycardia
  • Glaucoma
  • Not with alpha2 agonists unless BP has been lowered by use of other drugs (ex. isoflurane)
44
Q

‘use when required’ school of through for anticholinergics in dogs and cats

A
  • If excessive PS action is likely (concurrent use of potent opioid)
  • If BP is already low and has become HR dependent
45
Q

Atropine vs. Glycopyrrolate: duration of action

A
  • Atropine: 30-40mins
  • Glycopyrrolate: 2 hrs
46
Q

Atropine vs. Glycopyrrolate: onset of action

A
  • Atropine: 1-2 mins
  • Glycopyrrolate: 15-20mins
47
Q

Atropine vs. Glycopyrrolate: effect

A
  • Atropine may increase HR higher than glycopyrrolate
  • *atropine crosses into CNS (glycopyrrolate does not)
  • Glycopyrrolate has stronger action to dry secretions
48
Q

Overview of skeletal muscle relaxation

A
  • Skeletal muscle tone is REDUCED under anesthesia
  • Some procedures require NO muscle tone
  • Eye rotation makes intra-ocular surgery difficult
    o Centrally-acting drugs which lower muscle tone can still allow eye rotation
    o *use peripheral-acting neuromuscular blocking agents (NMBAs)
49
Q

Neuromuscular junction review

A
  • 2 ACh molecules required to open the nicotinic receptor
  • ACh drifts away after stimulating receptor
  • AChesterase breaks down ACh to prevent over-stimulation
50
Q

Points about NMBAs

A
  • Not lipophilic molecules
  • Do NOT cross into CNS or cross placenta
  • No sedative OR analgesic properties
  • Never used alone in animals (INHUMANE)
  • *paralyze ALL skeletal muscle
51
Q

NMBAs paralyze all skeletal muscles

A
  • Must VENTILATE
  • Cannot use some monitoring signs based on muscle tone
  • *will MAINTAIN central eye
  • Must ensure full reversal before recovery (laryngeal function)
52
Q

Depolarizing NMDAs

A
  • act similar to ACh
  • remain on receptor longer
  • depolarization=flaccid paralysis
  • broken down by PLASMA CHOLINESTERASE=shorter acting
  • no reversal drug available
  • Ex. succinylcholine
53
Q

Succinylcholine

A
  • Used to relax laryngeal muscles and allow endotracheal intubation
  • Animals not as difficult to intubate=not routinely using NMBAs
  • Fast onset of action=20s
  • Lasts short time in most species (except dog)
  • May be combined with euthanasia drugs to prevent limb paddling in horses
54
Q

Non-depolarizing NMBAs

A
  • Based on CURARE (plant, put on arrow heads)
  • Longer onset time: 1-2 mins
  • Duration of action: 15-20mins
  • Competitive inhibition with ACh
  • Prevents 2 ACh molecules from reaching receptors
  • NMBA stays on receptor
55
Q

How to reverse non-depolarizing NMBAs?

A
  • Increase in number of ACh molecules in area by BLOCKING ACETYLCHOLINESTERASE (Neostigmine)
56
Q

What are some NMBAs used in Vet Med?

A
  • Atracurium
  • Rocuronium
57
Q

Atracurium

A
  • Spontaneously broken down at normal body T and pH by plasma esterases
  • Store in refrigerator
  • Duration of action increases with hypothermia
58
Q

Rocuronium

A
  • Liver metabolism
  • Duration of action does NOT change with change in body T
  • May increase HR on administration
59
Q

Reversal agents for non-depolarizing NMBAs, increases Ach within all areas of body including

A
  • Nicotinic sites: ganglion, skeletal NMJ
  • Muscarinic sites: post-ganglion PS
60
Q

What may be required with reversal agents of non-depolarizing NMBAs?

A
  • Atropine to prevent undesirable side effects
    o Bradycardia
    o Drooling
    o Bronchoconstriction
61
Q

What is an example of a reversal agent of a non-depolarizing NMBAs?

A
  • Neostigmine
62
Q

Neostigmine

A
  • Strong effects at MUSCARINIC sites
  • Consider using with atropine (dogs and cats)
  • Duration of action=40 mins

ANESTHESIA (27 decks)

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