19 – Support Drugs Flashcards
What are some support drugs used in anesthesia?
- Analgesics
- Fluids
- Respiratory stimulants
- CV support
- Neuromuscular blocking agents
What are the 3 general effects of general anesthesia?
- CNS depression
- CVS depression
- Respiratory depression
CNS depression
- Loss of consciousness
- Damping reflexes
o Hypotension
o Hypoventilation
o Hypothermia
o Reduced muscle tone - Central modulation of nociception
CVS depression
- Reflex suppression
- Changes in autonomic balance
- Changes in vasomotor tone
- Myocardial depression (direct=drugs, indirect=hypoxemia, hypercapnia)
- *HYPOTENSION
Respiratory depression
- Reflex suppression
- Reduced muscle activity
- Alveolar collapse
- Reduced functional residual capacity
- Ventilation/perfusion mismatch
- *HYPOVENTILATION
What is the only general anesthetic with analgesic properties?
- Ketamine
Fluid therapy: recommended surgical fluid rate for dogs
- 5ml/kg/hr
Fluid therapy: recommended surgical fluid rate for cats
- 3ml/kg/hr
What are the reasons to provide fluid therapy for all anesthetized animals?
- Replace losses due to various reasons
- To offset hypotension
Fluid therapy to replace losses due to
- Evaporation from body surfaces
- Bleeding from surgical sites
- Urine production
Fluid therapy to offset hypotension
- Vasodilation common side effect of IH anesthetic
- Increase venous return and CO
What are examples of fluids to use during anesthesia (3)?
- Isotonic crystalloid solution (balance electrolyte)
- Colloids
- Blood products
Isotonic crystalloid solution (balanced electrolyte): fluid therapy
- Lactated ringers
- Normosol R/plasmalyte
Colloids: fluid therapy
- Larger molecules provide oncotic pressure (similar to albumin)
- Stay in circulation longer than crystalloids
- Starches (Hetastarch)
- Gelatin: based (not in Canada)
Blood products: fluid therapy
- Whole blood
- Plasma
- Packed red cells
Respiratory stimulants
- Not often used during anesthesia
- *best to ventilate lungs using anesthetic breathing system and O2
- Ex. Doxapram
Possible indications of when you would use respiratory stimulants
- Field situations where no apparatus to ventilate lungs
- Some tests for laryngeal paralysis
Doxapram (respiratory stimulant): ‘effects’
- 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
Doxapram (respiratory stimulant) can be given
- IM
- IV
- Buccal
Doxapram onset and duration
- Immediate onset
- Lasts 1-2 mins
Vasomotor control
- 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
What are 3 reasons for hypotension during anesthesia?
- Reduced CO
- Vasodilation
- Bradycardia (CO=HRxSV)
Reduced CO contributing to hypotension during anesthesia
- Depressed cardiac contractility
- Reduced venous return
What are some factors that can affect venous return?
- Position of animal
- procedure
- use of IPPV will affect venous return
vasodilation contributing to hypotension during anesthesia
- depression of vasomotor center=vasodilation throughout body
- directly relax vascular smooth muscle as well as skeletal muscle
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
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
Dobutamine to increase CO
- Most commonly used inotrope
Epinephrine to increase CO
- Reserved for CPR use
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
What can happen if there is too much vasoconstriction?
- Can LIMIT
o Renal vascular supply
o Skeletal muscle perfusion
Examples of patholocial conditions that cause excessive vasodilation?
- Vasodilatory shock
- Sepsis
- Anaphylaxis
Other drugs used to treat vasodilation (4)
- Phenylephrine
- NE
- High infusion rate Dopamine
- E
Phenylephrine: acts on
- alpha-1 action only
NE: acts on
- mainly alpha-1, some beta-1
High infusion rate of Dopamine: acts on
- mainly alpha-1, some beta-1
E: acts on
- alpha 1, beta-1 and beta-2 effects
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)
What can happen with repeat bolus injection of ephedrine?
- Can exhaust ability to REPLENISH NE
- *infusions can overcome this exhaustion effect
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
Anticholinergics are used to prevent
- Increases in vagal tone
o Opioids
o Head and neck surgery - Excessive secretions (ex. drooling)
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
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)
‘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
Atropine vs. Glycopyrrolate: duration of action
- Atropine: 30-40mins
- Glycopyrrolate: 2 hrs
Atropine vs. Glycopyrrolate: onset of action
- Atropine: 1-2 mins
- Glycopyrrolate: 15-20mins
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
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)
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
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
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)
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
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
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
How to reverse non-depolarizing NMBAs?
- Increase in number of ACh molecules in area by BLOCKING ACETYLCHOLINESTERASE (Neostigmine)
What are some NMBAs used in Vet Med?
- Atracurium
- Rocuronium
Atracurium
- Spontaneously broken down at normal body T and pH by plasma esterases
- Store in refrigerator
- Duration of action increases with hypothermia
Rocuronium
- Liver metabolism
- Duration of action does NOT change with change in body T
- May increase HR on administration
Reversal agents for non-depolarizing NMBAs, increases Ach within all areas of body including
- Nicotinic sites: ganglion, skeletal NMJ
- Muscarinic sites: post-ganglion PS
What may be required with reversal agents of non-depolarizing NMBAs?
- Atropine to prevent undesirable side effects
o Bradycardia
o Drooling
o Bronchoconstriction
What is an example of a reversal agent of a non-depolarizing NMBAs?
- Neostigmine
Neostigmine
- Strong effects at MUSCARINIC sites
- Consider using with atropine (dogs and cats)
- Duration of action=40 mins
