Support Drugs used in anesthesia Flashcards
Support drugs used in anesthesia
- analgesics
- Fluids
- Resp stimulants
- Cardiovascular support
- Neuromuscular blocking agents
Effects of general anesthesia
- CNS depression
- CVS depression
- Respiratory depression
CNS depression from anesthesia
- Loss of consciousness
- Damping of reflexes
-cardiovascular= hypotension
-respiratory= hypoventilation
-thermoregulatory= hypothermia
-postural= reduced muscle tone - Central modulation of nociception
Cardiovascular system Depression
-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
Respiratory depression
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)
Analgesics drugs
-nociceptive pathways can be stimulated during anesthesia
-sympathetic nervous system stimulation
-may require higher doses of anesthetic drugs= increased side effects
What is the only drug with both anesthetic and analgesic properties?
Ketamine
Fluid therapy rates
Dogs: 5ml/kg/hr
Cats: 3ml/kg/hr
Why supply fluid therapy?
- Replace losses due to:
-evaporation from body surfaces
-bleeding from surgical sites
-urine production - To offset hypotension:
-vasodilation common side effect of inhalant anesthetic
-increase venous return and CO
Fluids to use during anesthesia
- Isotonic crystalloid solution
- Colloids
- Blood products
Isotonic crystalloid solution
-balanced electrolyte
-lactated ringers
-normosol R/plasmalyte
Colloids
-larger molecules provide oncotic pressure similar to albumin
-stay in circulation longer than crystalloids
-starches (hetastarch)
-Gelatin- based **not in Canada
Blood products as fluids
-whole blood
-plasma
-packed red cells
Respiratory stimulants
-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
what does Doxapram cause?
-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
Doxapram timing
-Can be given IM, IV, buccal
-onset immediate, effect lasts 1-2 mins
Hypotension during anesthesia
- Reduced CO
- Vasodilation
- Bradycardia
Reduced cardiac output
-depressed cardiac contractility
-reduced venous return (relaxation of great veins)
-position of animal, procedure and use of IPPV will also affect venous return
Vasodilation
-depress vasomotor control= vasodilation throughout the entire body
-directly relax vascular smooth muscle as well as skeletal muscle
Bradycardia
CO= HR x SV
Treatment for reduced CO
- Fluid therapy- improves CO by increasing venous return
- 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
Drugs used to treat reduced CO
- Dobutamine- most commonly used inotrope
- Epinephrine- reserved for CPR use
Treatment of excessive vasodilation
Use alpha 1 adrenergic catecholamines to increase vascular tone
-short elimination lives; infusions required
What does too much vasoconstriction limit?
-renal vascular supply
-skeletal muscle perfusion
What pathological conditions cause excessive vasodilation?
-vasodilatory shock
-sepsis
-anaphylaxis
Drugs used to treat vasodilation
- Phenylephrine
- NE
- high infusion rate of dopamine
- Epi
Action of phenylephrine
alpha 1 action only
Action of NE
mainly alpha 1, some beta 1
Action of Dopamine
-mainly alpha 1, some beta 1
Action of Epi
alpha 1, some beta 1 and beta 2 effects
Ephedrine
-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
Benefits to ephedrine
-preserves tissue perfusion
-useful effect
-inexpensive
What drugs are used to treat bradycardia?
Anticholinergics
-act on muscarinic/cholinergic sites
NOT nicotinic
Actions of Anticholinergics
- prevent action of acetylcholine
2.prevents increases in vagal tone (opioids, head and neck surgery from oculo-cardiac reflex) - prevents excessive secretions and drooling
Anticholinergics and herbivores
not routinely used!
Side effects of anticholinergics
- 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
Routine use of anticholinergics?
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
Use when required?
-use if excessive parasympathomimetic action is likely (concurrent use of potent opioid)
-if blood pressure is already low and has become heart rate dependent
Atropine timing and specifics
Duration of action: 30-40mins
Onset of action: 1-2mins
**increases HR more than glycopyrrolate
**crosses CNS
Glycopyrrolate timing and specifics
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
Skeletal muscle relaxation under anesthesia
-tone reduced; some procedures need no muscle tone
Eye surgery under anesthesia
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)
NMBAs
-not lipophilic so cannot cross CNS or placenta
-no sedative or analgesic properties; never used in animals alone
Action of NMBAs
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)
Depolarizing NMBAs
-act similar to Ach
-remain on receptor longer
-depolarization= flaccid paralysis
-broken down by plasma cholinesterase
-no reversal drug available
Succinylcholine
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
Succinylcholine timing
Duration: short time in most species except dog
Onset: 20secs
Non-depolarizing NMDAs
-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
Reversing non-depolarizing NMBAs
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)
Atracurium (NMBA)
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
Rocuronium (NMBA)
-liver metabolism
-duration of action not changing with temp
-may increase HR on administration
Neostigmine
-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
