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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
vasodilation contributing to hypotension during anesthesia
- depression of vasomotor center=vasodilation throughout body - directly relax vascular smooth muscle as well as skeletal muscle
26
What are some ways to treat reduced CO?
- fluid therapy=increases venous return - improve cardiac contractility and HR through beta-1 adrenergic receptor STIMULATION - *DRUGS: Dobutamine, epinephrine
27
Improve cardiac contractility and HR through beta-1 adrenergic receptor STIMULATION
- Use catecholamine drugs - Have a short half-life (similar to endogenous) - Usually administer as an infusion
28
Dobutamine to increase CO
- Most commonly used inotrope
29
Epinephrine to increase CO
- Reserved for CPR use
30
What do you use for treatment of excessive vasodilation?
- *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
What can happen if there is too much vasoconstriction?
- Can LIMIT o Renal vascular supply o Skeletal muscle perfusion
32
Examples of patholocial conditions that cause excessive vasodilation?
- Vasodilatory shock - Sepsis - Anaphylaxis
33
Other drugs used to treat vasodilation (4)
1. Phenylephrine 2. NE 3. High infusion rate Dopamine 4. E
34
Phenylephrine: acts on
- alpha-1 action only
35
NE: acts on
- mainly alpha-1, some beta-1
36
High infusion rate of Dopamine: acts on
- mainly alpha-1, some beta-1
37
E: acts on
- alpha 1, beta-1 and beta-2 effects
38
Ephedrine
- 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
What can happen with repeat bolus injection of ephedrine?
- Can exhaust ability to REPLENISH NE - *infusions can overcome this exhaustion effect
40
What is the basis of drugs used to treat bradycardia?
- 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
Anticholinergics are used to prevent
- Increases in vagal tone o Opioids o Head and neck surgery - Excessive secretions (ex. drooling)
42
What are some side effects of anticholinergics?
- 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
When can anticholinergics not be used in cats and dogs? (‘use routinely’ school of thought’)
- Tachycardia - Glaucoma - Not with alpha2 agonists unless BP has been lowered by use of other drugs (ex. isoflurane)
44
‘use when required’ school of through for anticholinergics in dogs and cats
- If excessive PS action is likely (concurrent use of potent opioid) - If BP is already low and has become HR dependent
45
Atropine vs. Glycopyrrolate: duration of action
- Atropine: 30-40mins - Glycopyrrolate: 2 hrs
46
Atropine vs. Glycopyrrolate: onset of action
- Atropine: 1-2 mins - Glycopyrrolate: 15-20mins
47
Atropine vs. Glycopyrrolate: effect
- Atropine may increase HR higher than glycopyrrolate - *atropine crosses into CNS (glycopyrrolate does not) - Glycopyrrolate has stronger action to dry secretions
48
Overview of skeletal muscle relaxation
- 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
Neuromuscular junction review
- 2 ACh molecules required to open the nicotinic receptor - ACh drifts away after stimulating receptor - AChesterase breaks down ACh to prevent over-stimulation
50
Points about NMBAs
- 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
NMBAs paralyze all skeletal muscles
- Must VENTILATE - Cannot use some monitoring signs based on muscle tone - *will MAINTAIN central eye - Must ensure full reversal before recovery (laryngeal function)
52
Depolarizing NMDAs
- 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
Succinylcholine
- 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
Non-depolarizing NMBAs
- 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
How to reverse non-depolarizing NMBAs?
- Increase in number of ACh molecules in area by BLOCKING ACETYLCHOLINESTERASE (Neostigmine)
56
What are some NMBAs used in Vet Med?
- Atracurium - Rocuronium
57
Atracurium
- Spontaneously broken down at normal body T and pH by plasma esterases - Store in refrigerator - Duration of action increases with hypothermia
58
Rocuronium
- Liver metabolism - Duration of action does NOT change with change in body T - May increase HR on administration
59
Reversal agents for non-depolarizing NMBAs, increases Ach within all areas of body including
- Nicotinic sites: ganglion, skeletal NMJ - Muscarinic sites: post-ganglion PS
60
What may be required with reversal agents of non-depolarizing NMBAs?
- Atropine to prevent undesirable side effects o Bradycardia o Drooling o Bronchoconstriction
61
What is an example of a reversal agent of a non-depolarizing NMBAs?
- Neostigmine
62
Neostigmine
- Strong effects at MUSCARINIC sites - Consider using with atropine (dogs and cats) - Duration of action=40 mins

ANESTHESIA (27 decks)

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