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544 Cards in this Set

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Problem w/gas induction
-Inhalation slower- excitement stages
-Adrenaline release -dysrhythmias
-Increased oxygen demand
-Harm by restraint
-Non protected airway
-More pollution
-Irritant, breath holding
problem w/IV induction
-drug calculations
-respiratory depression
what determines the effects of IV drugs?
-blood flow to the brain (cardiac output)
-pKa of the drug (amt of non-ionized drug bc non-ionized form crosses to the brain and is fat soluble)
pKa of Propofol and at what pH is it fully ionized?
-pKa = 11
-ionized at pH of 7.4
the four pharmacokinetic and physiochemical properties of the ideal injectable agent
–water soluble
–long shelf life
–stable
–potent
which part of the drug is used: protein bound or non-protein bound?
non-protein bound
Define: Therapeutic index
a comparison of the amount of a therapeutic agent that causes the THERAPEUTIC effect to the amount that causes TOXIC effects.
4 things that cause reduced drug-protein binding
-low protein amt
-renal dz
-liver dz
-old age
which is wakeup due to: redistribution or metabolism?
redistribution
ketamine, phencyclidine, & tiletamine are all what?
dissociative agents (reduce of block signals to the conscious mind from other parts of the brain)
1. short-acting barbituate:
2. long-acting barbituate:
1. thiopental
2. pentobarbital (euthanasia)
barbituates have a relatively ___ therapeutic index
low
which ion channel do they work on and what do they cause?
-chloride channel
-they increase the duration of GABA dependent chloride channel opening --> hyperpolarisation
Thiopental is very acidic or alkaline? in a 2.5% soln, what is the pH?

--the only way it is given?
very alkaline (weak acid)
-10

--IV
40% of dogs on thiopental develop what?
bigeminal rhythm
Thiopental: side effects
-may have a dose-dependent reduction in CP and SVR
-may see tachycardia
-respiratory depression
Thiopentone: in what type of dog do we NOT use this in and why?
-Sighthounds

--prolonged recovery
--genetic hepatic metabolic defect – first step of hepatic metabolism
--contribution from low % body fat
--slow recovery in thin animals
why is it relevant that Propofol is a "phenol ‘Propyl phenol"
bc cats cannot get rid of phenols
W/ drugs, you wake from __1__ and
recover by __2__?
1. redistribution
2. metabolism
Propofol: side effects
-HUGE respiratory depressant (worse than thiopental)
-cardiac depressent
-decr BP by vasodilation
--NO cardiac dysrhythmias, analgesia
Propofol: problem w/injection
-marked pain, venus spasm, and thrombophlebitis
the "Key point" Propofol reaction
extended rigid forelimbs, flaccid hindlimbs
alfaxalone/alphadolon is licensed for use in what spp?
--do not use in what spp?
cats (also used in sheep, goats, pigs, monkeys)
--do NOT use in dogs (the new Alfaxan can be used in dogs)
Alfaxalone: what can it cause?
histamine release
swollen paws, ears
What is so beneficial about Alfaxalone/Alfaxan?
-it LACKS depressant effects on the myocardium
-it does NOT induce cardiac arrhythmias NOR sensitize the conductive tissue of the heart
-it has MINIMAL effects on peripheral tissue vascular resistance and blood flow
-causes LITTLE respiratory depression at clinical doses in either dogs or cats
-LACKS a dose-dependent increase in respiratory depression until doses exceed 3 times the labeled dose
Alfaxalone: pharmacokinetics are similar to what other drug?
--meaning ?
propofol
--rapid induction (< 30s IV) (--> also effective administered IM
-rapid hepatic metabolism
-short duration of action
-rapid recovery (through both redistribution and metabolism)
-no accumulation (so suitable for TIVA and CRI)
-renal excretion
-wide safety margin
Difference between injection propofol IV and alfaxalone IV
alfaxalone causes no tissue irritation if extravasated
Alfaxalone: effects and side effects
-good muscle relaxation
-mild respiratory depression
-decr tidal volume and rate
-animals disturbed during recovery may paddle and twitch violently (so sedate for recovery and recover in quiet tranquil environment)
what do dissociative anesthetics do?

--examples
"separate" thalamic and limbic systems
-good analgesics (poor muscle relaxants, poor hypnotics)

--ketamine, tiletamine, phencyclidine
Ketamine:
1. what type of drug is it?
2. routes
3. very good in which spp/animals
1. NMDA antagonist
2. all (including oral)
3. exotics, fractious animals
what does a patient look like on ketamine?
-BUT
--what do we often do with ketamine?
may appear conscious (eye opening, muscle contraction, swallowing)

-BUT is unable to process or respond to sensory input

--combine it with a 2nd drug as a muscle relaxant
CNS effects of ketamine:
-muscle rigidity
-laryngeal swallowing/coughing while intubating
-hypersalivation
-analgesia
ocular effects of ketamine
-dilated central pupils
-nystagmus
-corneal reflexes maintained
-eyes remain open - risk of drying
-increased intraocular pressure
cardiovascular system effects of ketamine
-stimulates the sympathetic nervous system and inhibits noradrenaline uptake --> so stimulates the cardiovascular system
-BUT has direct myocardial depressive effects --> more seen in shocked patients
-MAY RAISE INTRACRANIAL PRESSURE
respiratory effects of ketamine
-reflexes may remain intact
-bronchodilation
-breathing supported but rapid IV bolus can cause apnea
what is in the classic triple drip (TIVA) in field anesthesia?
guaifenesin, ketamine, and xylazine
ration os Tiletamine and zolazapam in Telazol/Zoletil
1:1
Telazol/Zoletil: side effects
salivation
muscular spasms
vomiting
vocalisation
apnea
hypertension and tachycardia
unpleasant recoveries
what spp is telazol/zoletil used for mostly?
pigs and wildlife capture
why is heavy premed prefered when using Etomidate?
Myoclonic activity can occur post-induction
what is the safety margin of etomidate?
large - lethal dose is 16 times higher than the hypnotic dose
good CV effect of etomidate
maintains hemodynamic stability better than any other agent
endocrine effects of etomidate
Marked inhibition of adrenal synthesis of cortisol, aldosterone, corticosterone (but no problems with a single dose)
when is etomidate not recommended?
-in animals w/pre-existing adrenocortical suppression
-not recommended for CRI (continuous rate infusions)
when is etomidate recommended?
Mainly used in small animal anaesthesia:
-High risk patients
-Patients with cardiovascular instability
-Animals scheduled for interventional cardiac surgery
give a brand name for Fentanyl + Fluanisone (Opioid/Butyrophenone)

--what does it do
---side effects
----in what spp is it used and what is it used with?
-Hypnorm

--neuroleptic (major tranquilizer)

---severe respiratory depression

----in rabbits w/diazepam/midazolam
What is Immobilon?

--side effects


---who is it a risk to?
-Etorphine + Phenothiazine

--Marked CV and Respiratory effects

---Risk to personnel
ideal agent for TIVA (total intravenous anesthesia)
Non cumulative
Rapidly metabolized
No active metabolites
Non-irritant
No side-effects
common TIVA combination used in horses
guafenesin (muscle relaxant), alpha-2 agonist (hypnotic and analgesic) (xylazine, romifidine, detomidine), and ketamine (analgesic/anesthetic)
maximum infusion for TIVA
2 hours (every drug accumulates)
Agents used for TIVA in small animals
mainly propofol based agents, plus opioids and ketamine
"Vapors are NOT ____"
gases (they are liquids which are vaporized in a carrier)
vaporization: define equilibrium
the number of molecules entering gaseous state equals the number leaving it
what is SVP? define it
-static vapor pressure: the static pressure of vapour in equilibrium with liquid
Vaoprization is...
-totally temperature dependent
-the evaporation of a volatile liquid in a ‘closed’ container
the higher the SVP...

--most inhalational agents have what? what does this require?
-the more volatile the agent

a very high SVP; vaporisers are required
SVP of:
1. Sevoflurane
2. Halothane
3. Isoflurane
4. Desflurane
1. S: 160 mm Hg
2. H: 239 mm Hg
3. I:240 mm Hg
4. D: 664 mm Hg
benefits of a modern vaporiser
-Temperature compensated
-Flow compensated
the rate at which inhalant anesthetics rise in the plasma/blood stream depends on:
-Ventilation
-Concentration of agent in carrier gas
-Cardiac output (inversely)
-Solubility of agent in the
body (inversely)
the blood:gas partition coefficient is:
solubility
-the ratio of the amount of anaesthetic in blood and gas when the two phases are of equal pressure and volume
(where does the anesthetic want to be)
blood:gas coefficient - what happens w/the less soluble agents?
the less soluble they are, the less they are washed away, and the faster the alveolar concentration rises
uptake of an agent is determined by:
-the rate and depth of ventilation
(hyperventilation will accelerate uptake)
(respiratory depression will slow uptake)
which will wake up slower: a fat animal or a thin one?
a fat one (holds onto an anesthetic agent) (depends on the agent's solubility in fat)
what is: end-tidal concentration
-concentration in the last bit of breath breathed out
what is MAC?

---what is it used to compare?
-minimal alveolar concentration
-minimal end-tidal concentration that prevents 50% animals responding from a supramaximal stimulus.

---the potency of an agent
**average MAC of halothane
0.08 - 0.09
** average MAC of isoflurane
1.4
**average MAC of sevoflurane
2.3
**average MAC of desflurane
8
what increases MAC?
Neonate
Hyperthermia
Hyperthyroidism
Catacholamines
what decreases MAC?
Age
Pregnancy
Hypotension
Hypothermia
Hypothyroidism
Opioids and Alpha-2 agonists
what happens to MAC, induction, and recovery w/a high fat soluble agent?
-low MAC
-slow induction and recovery
what happens to MAC, induction, and recovery w/a low fat soluble agent?
-higher MAC
-fast induction and recovery
negative affects of inhalational agents on the animal
-Cardio and respiratory depression
-Formation of carbon monoxide with soda lime
-(Formation of other toxic gases)
what is the only inhalation agent that has a negative effect on the anesthetist? what does it do?
-Nitrous oxide
-bone marrow suppression, teratogenesis
effects of nitrous oxide

--high or low MAC?
-minimal respiratory and CV effects
-analgesia

--Very high MAC
why use Nitrous Oxide?
-'second gas effect’
-‘adjunctive anaesthesia’
-reduces concentration of other inhalational agents
-analgesic effect
what is the "second gas effect?"
where administration of one gas will accelerate initial uptake of another anaesthetic gas given at the same time
why does N2O make such a good agent to use to get the 'second gas effect?'
it is associated with low blood gas solubility and high MAC of N2O
how does N2O cause "diffusion hypoxia?"

--when can this happen?

---how do you prevent it?
-N20 washes out down a concentration gradient into the alveolus and dilutes the oxygen concentration
--at the end of anesthesia
---always provide an enriched oxygen source for ten minutes after turning off nitrous oxide
difference between the MAC of N2O in cats and in dogs
MAC of nitrous oxide in cats may be higher than in dogs
advantages of N2O
-second gas effect accelerates anaesthetic uptake
-reduces requirements for more depressant agents; ‘adjunctive anaesthetic’
-analgesia
disadvantages of N2O
-low potency in animals
-potential for hypoxia
-diffusion into gas-filled spaces
-expensive
-potential for human abuse
Halothane has metabolic hepatic hypoxia in what spp?
guinea pigs
solubility of iso

--CV effect

---safer to use in what spp?
-Lower solubility

--Different CV depression

---SAFER in dog
what do animals do with sevo that cause a problem w/induction?
breath holding
between iso and sevo, which one is the irritant?

--which one has a faster induction in cats?

---which one has a faster recovery in horses?
iso

--sevo

---sevo
CV effects of Halothane, iso, and sevo:
1. which cause dose-dependent cardiac depression?
2. which cause vasodilation --> hypotension?
1. ALL 3
2. Isoflurane and Sevoflurane –vasodilation, hypotension. Do not sensitise to cardiac arrhythmias. Little difference in cardiac depression.

Individual responses in relation to cardiac depression (large SDs)
When doing a study on the respiratory effects of halo, iso, and sevo, what problem did most studies have?
maintaining spontaneous ventilation at 2 MAC
the most clinically used local anesthetics are ___

--examples
amides

--lidocaine, bupivacaine, ropivacaine, mepivacaine
halflife of amides vs half life of esters

--how are they both metabolized
-amides: a few hours
-esters: a few minutes

--amides: hepatic metabolism w/renal excretion
--esters: pseudocholinesterases (PABA)
examples of esters used for local anesthetics
-prilocaine, tetracaine, cocaine
**MOA of local anesthetics
block sodium channels in the ‘closed state’ to prevent sodium ion influx during an action potential ("membrane stabilizing")
2 ways local anesthetics block Na channels
1. impair propagation of the action potential in the axon
2. interact directly with specific receptors on the sodium channel, inhibiting sodium ion influx
3. (also perturb the lipid membrane of the neuron)
what happens to vascular uptake and duration of action to drugs that cause vasodilation (ex lidocaine)
-more rapid vascular uptake
-shorter duration of action
local anesthetics w/ a pKa close to 7.4 have what?
a faster onset of action
how much of lidocaine is protein bound?

--bupivicaine?
-lidocaine: 64%
--bupivacaine: 96%
vasoactivity influences:

--meaning:
speed of onset, duration of action and potency

--vasodilators cause a more rapid vascular uptake and a shorter duration of action
problem w/using epinephrine (vasoconstrictor) and local anesthetics
vasoconstrictors prolong the action of local anesthetics (don't use together for ring blocks or spinal anesthesia)
2 ways local anesthetics block peripheral and central sensitization (analgesia)
1. block transmission of impulses to the spinal relay station
2. block transduction of noxious stimuli into electrical signals at nerve endings
what influences the toxicity of local anesthetics?
-dose
-route of administration (interpleural > intercostals > epidural > infiltration)
-rate of absorption from injection site
-acid-base status (acidosis incr risk of toxicity (rare))
-rate of metabolism of specific drug
p-resence of adrenaline
first sign of systemic overdose w/LAs
-CNS signs: sedation followed by convulsions
signs of systemic OD w/LAs
1. CNS: sedation followed by convulsions
2. CVS: cardiovascular depression and arrhythmias
3. Respiratory depression: depress ventilatory response to hypoxia
bupivicaine has a strong affinity for what type of tissue?
cardiac
CVS effects of a systemic OD of LAs
-direct myocardial depression
-hypotension (local vasodilation and autonomic impairment)
-Arrhythmias - conduction delay and heart block
CNS effects of a systemic OD of LAs
-initial transient depression
-agitation, muscle twitching, convulsions
-initial state of excitement due to blockade of inhibitory centers in cortex
what does adding opioids do to local anesthetics effects?

--most common ones used for articular and epidural blocks
-Increase efficacy and extend duration of block

--Morphine, buprenorphine
what does adding alpha2 agonists do to local anesthetics effects?

--which two?
-may extend duration and incr efficacy of local blocks

--Medetomidine and dexmedetomidine
1. onset time of lidocaine
2. duration of action of lidocaine
3. onset time of bupivicaine
4. duration of action of bupivicaine
1. 10-15 minutes
2. 1-2 hours
3. 20-30 minutes
4. 2.5-6 hours
where does lidocaine act?
-onset (slow or rapid)
--duration of action (short of long)
centrally acting analgesic
-rapid
--relatively short
what can develop w/lidocaine?
tachyphylaxis
when is lidocaine used as an IV infusion?
--what will you see w/i 2 min of a bolus inj? when will it disappear?
---which spp is very sensitive to the toxic effects of lidocaine?
-for treatment of ventricular tachyarrhythmias, central analgesia, prokinetic effects
--anti-arrhythmic effects; within 10 to 20 minutes
---cats
two things mepivicaine is used for
-equine nerve blocks
-intra-synovial anesthesia
pKa of bupivicaine and what it means
--is it long or short lasting? why?

---more of less potent than lidocaine? why?
8.1 - means slow onset of action
--long acting bc highly protein bound
---4x more potent bc high lipid solubility
which is more cardiotoxic: lidocaine or bupivicaine?
bupivicaine is SIGNIFICANTLY more cardiotoxic (may cause cardiotoxicity before neurotoxicity)
significance of L-bupivicaine
significantly less neurotoxic and cardiotoxic than racemic bupivicaine
why use Ropivacaine (naropin) over bupivicaine
less cardiotoxic
quicker return of full motor function (selective for sensory fibers over motor fibers)
systemic lidocaine infusion is standardly used in what spp?

--effects
-dogs and horses

-central analgesia and prokinetic effects
when do you use local anesthetics as "splash blocks?"
on ovarian ligaments, peritoneum or abdominal wall; or on surgical wounds
what can you use to reduce pain on injection of LAs?
sodium bicarbonate (1:9)
for cruciate surgery, what do you use:
1. pre-incisional
2. post-surgical

3. problem using bupivicaine
1. mepivicaine + morphine
2. bupivicaine + morphine

3. might be toxic to synovial tissues
what agent do you use for intrapleural/intraperitonial LA?

--how long does it last?
bupivicaine or ropivicaine

--4-6 hours
what do you use for IV regional analgesia (Bier block)
lidocaine
where do you place the needle for proximal/distal paravertebral nerve blocks?

-how long does it last?
dorsal aspect of the T13, L1, L2

-90 minutes
what do you do in an intercostal nerve block?

-what do you use?
block at least 2-3 adjacent intercostal spaces

-bupivicaine
where do the nerves cme from for a brachial plexus block?

--what nerves must you block?

---what is this good for?
-derives from spinal nerves C6, C7, C8, T1
--must block radial, ulnar, musculocutaneous, median and axillary nerves
---useful for all surgery including and distal to the elbow
two ways to do a digital nerve block
1. block superficial branches of radial and median nerve, dorsal and palmar branches of the ulnar nerve
2. ring block is alternative
what do each of these blocks desensitize:
1. Infraorbital and maxillary
2. Mental
3. Mandibular-alveolar
4. Retrobulbar - be careful of what?
1. upper lip, nose and upper rostral teeth
2. anterior mandible
3. skin, mucosa and teeth of mandible
4. must take care to avoid intravenous injection or damage to the globe
large animals nerve blocks:
1. Mandibular - what does it desensitize?
2. Mental - what do you use it for?
3. Supraorbital - what does it block?
4. Auriculopalpebral - what does it do?
1. practically the whole of the lower jaw and all of the teeth and alveoli on that side.
2. to suture wounds of the lower lip
3. sensory fibres to the upper eyelid and in part to the skin of the forehead
4. prevents voluntary closure of the eyelids but doesn’t in any way desensitize them
two nerve blocks for ocular sx
retrobulbar ner block
Peterson's nerve block (cattle and horses)
Spinal anesthesia: where to inject?
1. Subarachnoid block
2. Epidural block
1. inject into cerebrospinal fluid bathing spinal cord
2. inject into extradural space
agents used for epidurals
lidocaine
bupivicaine
morphine
‘triple combination’
potential adverse effects of epidurals
hypotension (common)
-respiratory depression
-coagulopathies and skin infections
-dural puncture
-coat abnormalities
-pruritus (opioids)
-bradycardia (rare)
what can extradural anethesia produce?
produces ‘chemical sympathectomy’ at level of extradural spread
does extradural anesthesia cause hyper or hypotension?
--what happens to peripheral resistance? by what %?
is it a combined α and β blockade that produces both arteriolar and venous dilation (mostly venous)
--total peripheral resistance drops by 18-20%
how do you treat hypotension from extradural anesthesia?
-usually managed with supportive IV fluid therapy
-best choice for treatment is ephedrine (alpha1 agonist)
what agent do you use for epidural catheter?
bupivicaine
Classical Triad of anesthesia (the three things you want to produce)
unconsciousness
reflex suppression / analgesia
muscle relaxation
what is Guaifenesin

--mainly in which spp?
centrally acting NMB w/no action at neuromuscular jnct

--cattle and horses
what does guaifenesin cause

--side effects

---metabolism
-tranquillisation, ataxia, recumbency

--no major CVS or respiratory changes

---hepatic metabolism
*** 3 risks of usingguaifenesin
Irritation, hemolysis, thrombophlebitis
the 3 prerequisites of muscle relaxation
Ensure unconsciousness!
Ensure adequate analgesia
Ensure you can provide artificial ventilation
NMBAs are NOT...
anesthetics nor analgesics
if an animal is too light under anesthesia WITHOUT neuromuscular block, you will see...
Changes in ventilation: faster, deeper
Changes in eye position: the eye will rotate upwards
Palpebral reflex
If an animal is paralyzed (neuromuscular blocker) but NOT unconscious
muscle twitching of head - paradoxical jaw tone and tongue twitching, mydriasis, lacrimation, salivation, tachycardia, hypertension, arrhythmias, increased ETCO2
what % of post-junctional nicotinic receptors must be blocked before transmission begins to fail?
75% (still have mm fn)
when ___% are blocked, transmission ceases completely
90%
order in which mm are affected
1. muscles of expression, jaw and tail
2. muscles of neck and distal limb
3. muscles of proximal limb
4. muscles of swallowing and phonation (pharynx, larynx)
5. muscles of abdominal wall
6. intercostal muscles
7. diaphragm
what do depolarizing agents do?
mimic the action of acetylcholine at the neuromuscular junction but remain bound to post-junctional receptors (unlike ACh)
example of a depolarizing agent

--what will you see?
suxamethonium/succinylcholine

--initial muscle contraction (fasciculations) followed by muscle relaxation
advantages of suxamethonium

--was used to facilitate intubation in what spp?
-fastest onset of all NMDAs
-spontaneous recovery w/o need for reversal
-short acting
--cat and pigs
disadvantages of suxemthonium
-painful muscle fasciculations
-myalgia
-hyperkalaemia and arrhythmias
-anaphylactic reactions
-**assoc w/malignant hyperthermia
-muscarinic cardiac effects
non-depolarizing relaxants
-Quaternary ammonium compounds (BIG compounds) structurally related to ACh
-Aminosteroids (vecuronium, rocuronium)
-Benzylquinolium (curariform) derivatives: atracurium
advantages of non-depol agents
-incremental doses can be given
-relatively easily reversed
-duration fairly predictable
-fewer side-effects than suxamethonium
-no painful initial fasiculations
-can "top off" to maintain paralysis as drug wears off
advantage of amino-steroids (vecuronium, rocuronium)
no histamine release
advantages of vecuronium
-no histamine release
-very cardiostable
-can give w/renal disease - little effect on clearance
-minor hepatic metabolism (depends on biliary excretion for termination of effect)
what happens w/hepatic dz when using vecuronium?

--what is vecuronium also called?
-duration of action is prolonged

--the "cleanest" of the currently available NMDAs
what's special about Rocuronium?
it's the fastest of the non-depol agents
problem w/benzylquinolium compounds
-tendency to cause histamine release
- < 10% of the drug is excreted unchanged by the liver and kidneys
-partially degraded by Hoffman elimination
-also eliminated by hepatic pathways
-laudanosine metabolite - epileptiform (looks like seizures)
most commonly used benzylquinolium in horses?

--used in what patients?
atracurium

-those w/liver and renal dz
how to reverse the non-depol agents
--commonly used anticholinesterase agents
--new reversal agent? used to reverse ?
-classic: anticholinesterase: blocks ACh breakdown so that [ACh] rises and displaces NMB combined with an antimuscarinic
--neostigmine and edrophonium
---Suggamadex;reverses rocuronium
why do we need to combine anticholinesterases with anticholinergics?

--what are these?
bc increased plasma concentrations of ACh cause muscarinic side-effects

--salivation, bradycardia, bronchospasm, defaecation, urination
what is the most potent non-depolarizing agent reversal agent?
--what do you need to combine it with?
---potential side effect?
-Neostigmine (drug of choice in profound blockade)
--an anticholinergic
---cardiac arrhythmias (especially if animal is hypercapnic)
non-depol agent reversal agent of choice in horses
--why?
---more or less potent than neostigmine?
Edrophonium
--doesn't slow the heartrate and doesn't cause central excitement
---less potent (fewer muscarinic affects)
when is reversal/recovery complete?

--what is recurarization? when does it happen?
-good jaw tone and brisk palpebral reflex
-beware “fish-eye” appearance
--return of neuromuscular blockade - ‘recurarisation’; can happen if reversal agent starts to wear off (may need another dose)
peripheral nerve stimulation:
1. when is it used?
2. what does it do?
3. what does it allow?
1. ONLY used to monitor non -depolarising agents
2. gives an idea of how “occupied” the NMJ is by relaxant, ‘how deep is the paralysis’
3. allows titration of NMBA intra-operatively & assessment of recovery post-operatively
where do you put the peripheral nerve stimulator to monitor these nerves:
1. Ulnar nerve
2. Peroneal nerve
3. Facial nerve
1. medial aspect of elbow
2. lateral cranial tibia
3. lateral aspect of the face
the most common stimulation pattern from the peripheral nerve stimulator is called ___?
Train of Four
rank the spp from msot to least anesthetic risk: cats, dogs, rabbits
rabbit > cats > dogs
how is a cat's metabolism different than a dog's?

--what does this mean for administering drugs?
-cats are deficient in glucuronide synthase
-inability to ‘conjugate’

--results in major differences in dose and duration of many drugs.
which NSAID cannot be used in cats? why?
Acetaminophen (paracetamol)
--VERY toxic, very prolonged effect, liver damage, methaemoglobin
Slow elimination of NSAIDS in cats means what?
you give lower doses less frequently.
cats: why is the metabolism of Propofol slow?
-cats lack the enzymes to conjugate glucuronides
-have problems metabolizing triglycerides produced by metabolism of the lipid in original versions
cats: will Propo-clear be less toxic?
still won't metabolize but no lipids
three problems w/using opioids in cats
-High doses cause increased muscle tone and dysphoria
-Dilated pupils may cause panic.
Occasional hyperthermia
when using local anesthetics (lidocaine, bupivicaine), which spp has a higher risk of systemic OD: dogs or cats?
cats
what is the "shock response" triad in cats?
-bradycardia
-hypothermia
-hypotension
what two things do you use for pre-an meds in cats?

--what do you add if the cat is crazy?
ace + morphine or buprenorphine

--ketamine IM
Cats: what meds do you use for skin testing?
Medetomidine/midazolam
Cats: what meds do you use when critical?
Fentanyl/midazolam
Cats: which med combination can cause excitement? Esp in what age/breed?
Ketamine and midazolam
--you adults, Bengals, and Oriental cats
Cats: what can oral ketamine be used for? And can is cause?
Use in killer cats
--causes hypersalivation, corneal ulceration
What can you use to facilitate intubation in catatonic cats?
supplementary IV propofol/ sevo by mask
Cats: IV induction drugs
--what does the dose of each of these depend on?
Propofol
thiopental
ketamine
alfaxalone

--what was used to sedate/premed
Cats: what CANNOT be used to help w/laryngospasm on intubation?
Astra-Zeneca Xylocaine Spray
Cats: what type of breathing system is used for anesthesia?

--what are cat’s prone to under GA?
non-rebreathing system (Ayre’s T-piece, Bain)

-- hypothermia (Bair huggers, warming devices )
Cats: 60% of deaths happen when?
Recovery (from lack of care)
Equine: how can you cut the anesthetic death rate in half?
Ace as premed
Equine: difference between halothane and isoflurane?
None
Equine: what happens to the anesthetic death rate when you give romifidine?
Slight incr
Equine: when do emergencies from anesthesia show and how to they present?
-during anaesthesia (induction and during maintenance)
-during the immediate recovery period (airway obstruction, Physical damage, myopathy etc)
-over the next few days (resultant physical problems, post-op colic etc)
Equine: problem w/standing sedation in stallions
penile relaxation
Equine: why would field anesthesia (TIVA) be considered safer?
only because it is only used for short procedures
Equine: what needs to be available when doing field anesthesia?
ET tube, oxygen cylinder and Hudson valve
Equine: 2 ways to do field anesthesia
repeated bolus injections OR infusion
Equine: what are the 3 options for surgical anesthesia?
Standing, field, and surgical suite
Equine: what can you use when doing surgical anesthesia in a sx suite rather than standing of field?
Inhalational anesthesia or TIVA w/O2 and ventilator support
Equine: prolonged use of alpha2s, even for sedation, can cause ___?
reduce gut motility --> prolonged use can cause ileus
Equine: starvation for how long for prolonged anesthesia?
8-12 hours
Equine: T/F in many clinics, hematology and biochem are done before elexctive sx
False: in many clinics, no bloodwork is done before elective sx
Equine: hematology and biochem are mandatory before what type of sx? What are they testing for?
emergency colic surgery
-evaluating hypovolaemia, endotoxaemia
Equine: opioids used in horses
Morphine
Methadone
meperidine (im only)
Fentanyl
Butorphanol
Buprenorphine
Equine: pros of opioids
-effective and essential pre-emptive analgesia
-effective and essential analgesic agents
-effective (slow onset) given by epidural injection
Equine: 2 side effects of opioids in horses
-overdose in unsedated horses may cause excitement and stereotypic behaviour
-repeated doses impair GI motility
Equine: how do opioids help intra-operatively
Effective in stabilizing anesthesia
Equine: T/F itra-operative opioids significantly reduce the MAC of inhalational agents
False: opiods do NOT significantly reduce MAC of inhalation agents
Equine: drugs used for sedation
-acepromazine
-alpha2 agonists
--either (or both) plus
opioids
Equine: effects of acepromazine
--effect on GI
---long or short acting?
----effect on BP
-effect less obvious than alpha 2 agonists.
-mild ‘tranquilliser’:
-Mood altering. Needs time to effect
--antispasmodic
---long acting
----depressed for 6-8hrs
Equine: risk of ace in stallions
penile priapism/relaxation
Equine: when do you use ace
-to calm the frightenedapprehensive animal
-training – low doses only (ex shoeing)
-for premedication
Equine: which agents are the mainstay of sedation in horses?
--what can horses do even when deeply sedated w/these agents?
---these drugs are routinely combined w/what?
alpha2 agonists
--respond to touch and kick
---opioids
Equine: alpha 2 agonists uesd in horses
xylazine
detomidine
Romifidine
(medetomidine)
Equine: IM dose is how much higher than the IV dose?

--how much time?
2-3xs

--30 min
Equine: drug combination of choice to feisty, unmanageable horses

--how long do you wait?
IM acepromazine, detomidine, butorphanol mixed

--wait 30-45 mins
Equine: choosing between aloha2 agonists (medetomidine, detomidine, romifidine, and xylazine):
1. selectivity (rank)
2. duration of action (rank)
3. muscle relaxation
4. analgesia
5. infusion
1. medetomidine > detomidine > romifidine > xylazine
2. romifidine > detomidine > medetomidine> xylazine
3. romifidine is LESS of a muscle relaxant
4. xylazine or medetomidine is best
5. detomidine, medetomidine
Equine: which alpha2 has less ataxia
romifidine
Equine: which alpha2 (+ opiod) do you use for standing sx?
Xylazine or detomidine
Equine: problems w/GA in a horse
Cardiac arrest
Hypoxia
Hypercarbia
Post-operative complications (myopathy, neuropathy, spinal damage)
Equine: anesthetic induction in adults always given...
IV
Equine: 5 induction combinations used (can be after ace premed)
-Alpha 2/ketamine ± benzodiazepine
-Alpha 2 /Guiaphenesin/ Ketamine
-Alpha 2 and/or ACP plus thiopental
-Guiaphenesin /thiopental or ketamine
-Propofol or alfaxalone (currently not practicable)
Equine: RVC rule w/Ketamine use
DO NOT draw up or give BEFORE alpha2 is given
Equine: guaifenesin is NOT a ___?

-useful for ___

--side effects
an anesthetic (IS a m relaxant)
-in combinations for induction and maintenance of anaesthesia in horses
--irritant if injected peri-vascularly - haemolysis, phlebitis
Equine: why do we use ketamine (+/- diazepam) for field induction
-Good quality induction
-Minimal cardiopulmonary depression
-High safety margin
-Can top up or infuse to prolong
-Excellent Recovery (especially if no benzodiazepine)
Equine: 3 different drugs/combinations used for field top ups
-Ketamine (alpha2): 25 – 50% of induction dose - (limit the xylazine)
-Thiopental (will impair recovery if used repeatedly)
-Ketamine/midazolam (25 % of induction dose) - beware too much midazolam gives a poor recovery
Equine: ideal time period for use of TIVA
short (up to 1 hour)
Equine: what do horses look like/appear on a tripla drip
'light' - strong palpebral reflex, lacrimation, swallowing, vocalisation, gentle purposeful responses to sx stim (use local to prevent)
Equine: paradoxical signs of trip drip OD
rigid limbs, opisthotonus
Equine: what is known as "the ultimate in sedative/opioid combinations"
-what drug is it?
--what is the reversal agent?
---when can you NOT use it?
Immobilon
-etorphine + acepromazine
--diprenorphine (Revivon)
---in animals intended for food
Equine: what type of system is used for inhalational anesthesia?
Closed system w/minimum flow rates oxygen consumption
(5mls/kg/min)
Equine: basic guidelines for anesthesia
-plenty of eye lubrication
-support limbs
-optimize ventilation
-catheterize bladder
Equine: what do you do w/a horse's legs in:
1. lateral recumbency
2. dorsal recumbency
1. under-forelimb forward, under-hindlimb back, upper limbs supported
2. DO NOT extend hindlimbs (mm and nn damage is stifles locked for long)
Equine: what do you do w/a horse's head in
1. lateral recumbency
2. dorsal recumbecy
1. head slightly raised
2. head up but NOT stretched (could cause laryngeal paralysis)
Equine: w/intra-operative anesthesia, there is often no CV change until when?
the horse moves
Equine: why are opioids not always useful?
they can cause movement even under anesthesia
Equine: which inhalant causes the worst myocardial depression?
halothane
Equine: which inhalant causes the worst vasodilation?
isoflurane
Equine: causes of hypotension during anesthesia
myocardial depression and low HR
vasodilation
Equine: dangers of hypotension
-Severe –-> cardiac arrest
-Moderate and prolonged –-> myopathy
-Contribution to poor gut blood flow and post-op colic
Equine: how to improve hypotension

--do not do what ? unless very very severe
Improve by improving CARDIAC OUTPUT - positive inotropes (ex dobutamine, ephidrine), reduce volatile, give fluids
--do not give drugs to vaso-constrict (e.g. phenylephrine)
Equine: w/inhalational anesthesia, what is commonly quoted as major contributor to mortality
CVS depression
Equine: what is the problem w/blood pressure being used as an indirect indicator of cardiac output during inhalational anesthesia?
is it NOT an indicator
Equine: what are the two most popular inotropes used during inhalational anesthesia
-dobutamine (alpha1 agonist, given by infusion)
-ephedrine (alpha and beta effects, given as bolus)
Equine: problem w/treating hypoxemia during inhalational anesthesia

--possible methods
nothing works!!

--IPPV using 100% oxygen (does not always work)
--bronchodilator (albuterol)
-improve CO (improves oxygen delivery)
Equine: experimental methods for treating hypoxemia during inhalational anesthesia
-use of nitrogen in carrier gas (nitrogen in the skeleton of the lung)
-Positive End Expiratory pressure (‘sighing’)
-pulsed nitric oxide
Equine: T/F hypercapnia is usually a response to hypoxia
False: hypoxic horses usually breath well and are not very hypercarbic

--is it possibly a response to hyperoxia
Equine: why is detection of cardiac arrest difficult w/o electronic monitoring?

--what is the success rate of resuscitation?
bc horses continue breathing for a lone time after the heart stops

--good if it is instituted in time
Equine: possible reasons for cardiac arrest during anesthesia
-High vagal tone (need anti-cholinergic if surgery may cause a vagal reflex)
-Severe hypotension means that heart is inadequately perfused
-Heart almost always stops in asystole
Equine: how to treat a cardiac arrest during anesthesia
-switch off volatile agent
-IPPV with 100% oxygen
-External Cardiac Massage (horse in lateral – front legs forward, jump on heart landing on knees)
Equine: a reversible TIVA includes...
-Benzodiazepine-based agent
-Opioid based agent (Immobilon!)
-Alpha 2 based agent
Equine: 3 propofol-based techniques/combinations of TIVA
-Propofol/ketamine
-Propofol/alpha 2
-Propofol/alpha 2/ketamine
Equine: what do you use to reverse a TIVA of climazolam and ketamine
-which is given at induction?
--which has a higher infusion rate? (mg/kg/hr)
Sarmazenil
-ketamine
--ketamine
Equine: why is propofol unsuitable for induction anesthesia in large horses?
cannot inject enough fast enough
Equine: why would you combine medetomidine w/propofol
medetomidine is an analgesic and hypnotic that has a rapid recovery w/no need for an antagonist
Equine: w/medetomidine/propofol infusions, how do we keep the cardiopulmonary parameters normal?
keep the animal well-oxygenated
Equine: problem w/using Alfaxan in horses
very expensive
Equine: agents commonly used for partial intravenous infusion (PIVA)
lidocaine
ketamine
medetomidine
Equine: IV lidocaine is the idea analgesic for after what sx and why?
ideal analgesic post-colic surgery bc it has a positive effect on gut motility
Equine: nasal swelling during recovery can be reduced by ?
phenylephrine nasal drops
Equine: problems that show during or after anesthesia (mainly after prolonged)
-injury (corneal abrasions, fractures)
-nasal edema and respiratory obstruction
-myopathy
-neurapraxia and neuropathy (facial, femoral)
-pulmonary edema
-myelomalacia
Equine: 2 types of post-anesthetic myopathy
standard and sporadic
Equine: what can standard post-anesthetic myopathy be caused by?
-prolonged recumbency
-poor positioning
-prolonged hypotension
-hypoxaemia
-NO evidence of any relationship to feeding or fitness
Equine: what can sporadic post-anesthetic myopathy be caused by?
unknown, but possibly related to "tied-up" syndrome (many muscles involved, can occur several days post-op)
Equine: what is essential to use when treating post-anesthetic myositis?
fluids bc it is essential to prevent renal damage from free myoglobin
Equine: side effects of Immobilon
-excitement on induction
-tachycardia and hypertension
-severe respiratory depression
-muscle tension
-PRIAPISM
-recycling after antagonist, so may throw excitement stage 6-12 hours after
Equine: what can be used to treat spinal cord malacia?
Immobilon
Equine: problem w/accidental contamination of Immobilon in man

--how do you treat accidental injection?
-it may be absorbed across mucous membranes/through cuts, damaged skin etc
--human antagonist – Naloxone (must be in date)
--if that fails, use diprenorphine
Rum: In which spp is:
1. GA more practical
2. LA +/- sedation more practical
1. goats and sheep
2. cattle
Rum: out of these 5 techniques, which one CANNOT be used for obstetric and laparotomy procedures: epidural, inverted L-block, dorsal paravertebral, lateral paravertebral, line-block
cannot use the line-block
Rum: name 4 local anesthetic techniques
Caudal epidural
Blocks for laparotomy
IV regional analgesia
Cornual blocks (cattle or goats)
Rum: which agents cause hypoxia in ruminants and in which spp is it the worst?
alpha 2 agonists
-sheep
Rum: are really sensitive to what drug?
xylazine
Rum: when can you NOT use xylazine?
pregnancy (it's ecbolic)
Rum: T/F the dose of detomidine in ruminants is similar to that for the horse
true
Rum: caudal epidural anesthesia
1. where do you do it
2. what is it used for?
3. which agents can be used (which is the most common)
4. what do you try to prevent?
5. max recommended volume
1.C1-C2 intercoccygeal space
2. to abolish rectal straining - calving, uterine, vaginal prolapse
3. Lidocaine (most common). xylazine, morphine, procaine in europe
4. limb paralysis
5. 6 - 8 mls
Rum: what is the most commonly used block in practice for laparotomy for any reason?
inverted-L block
Rum: T/F the inverted L-block is less effective than paravertebral but easier
true
Rum: need to make sure you do what w/an inverted L-block?
infiltrate each layer to hit all the nerves
Rum: what are you trying to block w/a paravertebral block?
aiming to block the nerves after they have left the spinal canal (dorsal and ventral branches)
Rum: how to do a dorsal paravertebral block
Needle aimed to hit wing, then ‘walked’ back - pushed through the transverse ligament
--Can go behind each process (hit nerve of segment in front) or go behind and in front of alternate transverse processes
Rum: how much lidocaine is used where in a dorsal paravertebral block?
--15 mls 2%lidocaine below process then 5 mls above as withdraw needle (nerve is above and below the wing)
Rum: dorsal paravertebral block: what nerves does it block and for how long?
blocks T13, L1, L2, L3

--lasts 90 minutes
Rum: what does the lateral paravertebral block and how is it done?
blocks T13, L1, L2

--lateral approach above and below each transverse process of L1, L2, L4
Rum: why do we not like the line block?
-incomplete anaesthesia (especially of the peritoneum - though can re-inject local when reach it)
-incomplete relaxation of abdominal muscle
-distortion of normal tissue
-expensive - large vol of LA used
Rum: what type of anesthesia do you sue for distal limb surgery?

--which limb is it mostly used for?
IV regional anesthesia (digital amputations, deep infections)

--hindlimb
Rum: how do you do it and how much is used?
-use tourniquet and provide supplementary analgesia
use up to 30 mls lidocaine (in adults) w/o adrenaline
Rum: Cornual nerve block
1. what is it used for?
2. which nerve are we blocking?
3. this nerve is found between...
1. dehorning
2. cornual branch of zygomaticotemporal nerve
3. lateral canthus of eye and horn
Rum: Cornual nerve block
1. problem in goats
2. where is this problem in goats found?
3. what else do you use to provide LA?
1. accessory sensory supply (infratrochlear nerve) which is difficult to block completely
2. halfway between medial canthus and horn bud
3. provide additional ring block around base of horn
Rum:
1. what 2 blocks do you use for eye enucleations or ocular sx?
2. which nn are blocked?
3. which agents are used?
4. which of these blocks is safer?
1. Retrobulbar or Peterson's blocks
2. cranial nerves III,IV, V, VI and ciliary ganglion
3. bupivacaine or lidocaine
4. Peterson’s block (though more technically challenging
Rum: T/F the tail vein is a common spot for LA

--T/F the milk vein should only be used when there are no other veins left
false: usually the tail artery

--true
Rum: name the only drugs licensed for use in adult cattle
Xylazine
Detomidine
Rum: Xylazine
1. which route is NOT licensed
2. major concern
3. do not use when? why?
1. IV
2. hypoxia
3. during the last trimester of pregnancy: increases uterine contractions and vascular resistance, abortigenic
Rum: Detomidine in comparison to xylazine in cattle
-Effective sedative - licensed for cattle in Europe
-no dose sensitivity spp difference
-Hypoxia is similar
-Less hypnotic - cow less likely to go down
-Less uterine effects
Rum: what is a useful alternative in pregnant cattle
1. can also be used to ?
2. careful bc ?
ace/morphine
1. enhance sedation
2. regurgitation
Rum: in recumbency, boat and regurgitation can be due to ?
esophageal sphincter being covered with fluid
Rum: potential complications of GA
regurgitation
bloat
salivation
respiratory depression
hypoxemia
Rum: there is a high risk of regurgitation w/what dz?
displaced abomasum
Rum: difference between active and passive regurgitation
active: under light anesthesia
passive: deep anesthesia, position, drug specific, dz specific
Rum: Bloat
1. what is it caused by?
2. what does it contribute to?
1. caused by accumulation of CO2 and methane in the rumen; no eructation while unconscious
2. contributes to hypoventilation
Rum: what do you NOT do when salivation is a complication of anesthesia? why?
Do not administer atropine!

-atropine induces ileus and increases viscidity of saliva --> could lead to respiratory obstruction
Rum: what can cause hypoventliation and/or hypoxemia?
-central depression due to drugs
-V/Q mismatch due to recumbency
-low chest wall and pulmonary compliance
-abd pressure on the diaphragm
-expanding rumen
Rum:
1. how do you premed for GA?
2. best/easiest site for catheter
3. agents used for anesthesia
1. use sedative agents at low doses
2. auricular vein is easiest site for catheter placement (Dr. C says jug v)
3. ketamine/midazolam, thiopentone (Dr. C says xylazine followed by ketamine)
Rum: advantages of ketamine/midazolam induction
-small volume
-minimal cardiovascular depression
-regurgitation prior to intubation rare
-relatively fast recovery
Rum: agents used in triple drip
GGE/ketamine/xylazine
(cattle more sensitive to haemolysis than horses, so 5% GG is preferred in this species)
Rum: what do you HAVE to do even when using the triple drip?
still need to intubate and give oxygen
Rum: positioning for endotracheal tube
always keep head elevated and mouth below poll, so that saliva, regurgitation drains downwards and out
Rum: minimum O2 supply
5 ml/kg/min
Rum:
1. eye signs when anesthesia is light
2. normal HR
3. normal RR
4. best way to measure direct BP
5. tidal volume
6. ETCO2 low or high?
1. eye down when very light
2. HR 45 - 80
3. RR 15 - 30
4. can measure direct BP using auricular artery
5. small tidal volume (4-6 ml/kg)
6. tends to be very high.
Rum:
1. how are they placed during recovery?
2. what do they need during recovery
1. sternal recumbency, well supported
2. supplementary oxygen, maintain ET tube in situ until chewing/ swallowing starts
SmRum: special problems w/small ruminants and anesthesia/sedation
-Goats: sensitivity to local (or just straight overdose)
-Sheep: more likely to get pulmonary edema with xylazine or other alpha 2 agonists
SmRum: in goats, which is better: jugular vein or cephalic?

--in sheep?
jugular

--cephalic bc less moveable skin
SmRum: which drugs do you use for epidural anesthesia and how much?
-lidocaine, morphine, (xylazine)
--5 - 8 mls 2% lidocaine without epinephrine
SmRum: list of sedative agents used
-alpha2 agonists - xylazine, medetomidine
-ace
-morphine, buprenorphine
-diazepam, midazolam
-benzodizepines
SmRum: what do you have to be careful w/when using ace?
regurgitation if recumbent
SmRum: alpha2s
1. careful w/in what spp
2. risks
3. which type of injection is less risky?
1. sheep
2. pulmonary edema and related hypoxaemia
3. less risk with IM injection than IV
SmRum: diazepam or midazolam
1. less ___ than alpha2s
2. how long to they work?
1. less CVS depression
2. short acting (10 mins)
SmRum: more likely to regurgitate when using what type of induction?
mask induction
SmRum: how should they be positioned until intubated?
keep in sternal recumbency
SmRum: when recovery, don't remove ET tube until what?
they can remain in sternal recumbency
Camelids/llamas: why is IV catheterization so hard?
--which v is the best?
---what is a good option for sedation
-veins have valves - difficult to thread a catheterize
-carotid artery lies close to the vein
-thick skin– up to 1 cm in males
--right jugular vein, high up; cephalic or saphenous vein if desperate
---IM injection
Camelids/llamas: tubing it diffucult.
1. what do you need
2. size of tube (length and diameter)
1. laryngoscope and guide-wire (essential!!); desensitize larynx with lidocaine before intubation
2. 35 - 40 cm long , 8-10 mm diameter tube
Camelids/llamas: for sedation, they are less sensitive to ___ than other ruminants
---what may improve sedation and analgesia?
-xylazine
-opioids
Camelids/llamas: prone to what during GA?

--must give what during recovery?
-hypoxemia

--supplementary O2
Baby ruminants (incl creas):
1. how long do you fast them?
2. good sedatives
3. what do you use for mask induction
4. what do you use for short duration sx? (drug and technique)
1. not for long (rumination only begins at 8 - 12 weeks old)
2. diazepam/midazolam are excellent sedatives
3. mask induction ideally with sevoflurane
4. TIVA using xylazine/ketamine
Baby ruminants (incl creas): normal doses and toxic doses of (mg/kg):
1. lidocaine
2. bupivicaine
3. ropivicaine
1. N = 5; T = 10-20
2. N = 2; T = 3.5-4.5
3. N = 1.5; T = 5
Baby ruminants (incl creas): T/F post-op analgesia is generally not given for disbudding of goat kids
--what do you have to remember w/goat kids and NOT cattle?
true

--extra branches
Baby ruminants (incl creas): what drugs are used for disbudding?
procaine and lidocaine
Rum: one thing you have to consider w/post-op analgesia in ruminants that you DON'T have to consider w/horses, dogs, cats, etc...
Food animal and cost limitations
Pig: problem w/IM injection in pigs
drugs often deposited into fat
Pig: 3 things you need to consider about the pig CV when anesthetizing
-small heart relative to body mass
-rapid heart rate
-tachycardia markedly reduces cardiac output
Pig: things that need to be considered about the respiratory system when anesthetizing
-high incidence of rhinitis, pneumonia, pleuritis, ‘shipping fever’
-upper airway easily obstructed
-airway secretions easily obstruct airway
Pig: sites for IM injections in:
1. commercial pigs
2. pet pigs
3. length of needle needed
1. close to the ear base
2. thighs, epaxial muscle
3. use long needle
Pig: where do you give IV injections?
auricular vein (dorsal surface of ear)

-Limb veins OK once asleep
Pig: where do you place an IV catheter

--what do you use to help raise the vein?
dorsal auricular vein

--an elastic band
Pig: sedatives and premeds used in pigs (+ examples)
-butyrophenones (Azaparone, Droperidol)
-acepromazine
-alpha2 agonists (xylazine, medetomidine)
-dissociative agents (ketamine, tiletamine/zolazepam)
-anticholinergics (atropine, glycopyrrolate)
Pig: brand name for azaparone
1. what is it?
2. has similar effects and side effects to what?
3. how is it given? why is it not given another way?
4. short or long acting?
Stresnil
1. butyrophenone
2. similar effects/side-effects to ace
3. IM only; IV causes excitement
4. short acting tranquilliser
Pig: how are alpha2s given?

--the two mostly used alpha2s
in combination w/ketamine (have a very limited effect on their own, but very good w/ketamine)

--xylazine, medetomidine
Pig: name the 3 different xylazine combinations used for introduction and maintenance of GA

--name two agents used alone
-xylazine - tiletamine-ketamine
-xylazine-ketamine - butorphanol
-guaifenesin-ketamine-xylazine
--thiopentone
--propofol
which spp are prone to laryngospasm?

--how do you correct this?
pigs and cats

--lidocaine spray
Pig: possible structural problems w/intubation
-larynx and trachea set at an angle
-soft palate is long and soft
-large ventral saccules
-long narrow trachea
-apical lung lobe has separate bronchus, can be occluded by ET tube
Pig: why do you need to be careful not to obstruct the nostrils?
they are obligate nasal breathers
Pig: which inhalational agents are used with pigs?
all
Pig: which breed does NOT get malignant hyperthermia?
pot-bellied pigs
Pig: why is epidural anesthesia easier than in most spp?

--which drugs do you use?
pigs have an open epidural space

--lidocaine and morphine
Pig: procedure for anesthetizing potbellied pigs
1. intranasal midazolam
2. use long needles
3. always intubate and supplement oxygen
4a. medetomidine plus ketamine im
4b. tiletamine/xylazine
4c. tiletamine/xylazine/ketamine
5. reverse alpha2 agonist at end of procedure
Pig: malignant hyperthermia (MH)
1. what is it
2. what can trigger it (non drugs)
3. which drugs/agents can trigger it
1. genetic disorder associated with defective gene for ryanidine
2. stress, transport, several drugs
3. can be induced by all inhalational agents primarily halothane and succinylcholine)
Pig: CS of malignant hyperthermia
Peracute tachycardia, hypercapnia, muscle rigidity, hyperthermia…death
Pig: how do you detect MH?
-increase in temperature (‘pink’ pigs go very red)
-‘toes’ spread (Increase in jaw tone)
-very rapid respiration.
-increase in ET CO2 (Use up CO2 absorbent)
Pig: tx for MH
-stop inhalant and switch to totally new machine
-non-rebreathing system if there
-rapid body cooling, ice cold fluids
-administer Dantrolene
Pig: what can you give prophylactically for MH?
Dantrolene (oral, as IV is expensive)
OR
a muscle relaxant which works directly on ryanodine receptor to block calcium release
2 things that could cause fire and explosions
Oxygen supports combustion (so DON'T use oil)
Overheated ‘soda lime’
how to prevent sloughing and abscess after SQ thiopentone injection
tx at the time of accidental inj w/large volumes (1 Litre) of saline plus hyaluronidase would prevent this
T/F aim to pass the ET tube before regurgitation takes place
TRUE
regurgitation could cause ___ in rum
esophageal obstruction
in horses w/colic, what do you want to do before anesthetic induction?
empty stomach
how do you treat the inhalation of stomach contents?

--which spp is particularly susceptible
clear airway --> suction --> bronchial lavage --> antibiotics/corticosteroids

--horses (and man)
ABC stands for...
Airway
Breathing
Circulation
how to dx airway obstruction
-type of breathing (effort)
-air movement at nostrils: mouth: ET tube
-movement of rebreathing bag
response to treatment/removal of cause
common causes of obstruction while under anesthesia: non-intubated
Laryngeal obstruction
Soft palate (brachycephalics)
Nasal obstruction
tongue
common causes of obstruction while under anesthesia: intubated
-kinked ET tube
-over-distended cuff
-blocked circuits: faulty valves
-esophageal intubation, endobronchial intubation
what does endobronchial intubation cause

--CS
causes a 'shunt (blood passes through non-aerated lung)

--hypercarbia
--high inspired concentrations of inhalation agent required
esophageal intubation is most likely found in what spp?

--how do you detect it?
cat or very small dog

--Capnogram, limited (but some) movement of rebreathing bag, inhalation agent seems ineffective
one way to secure an airway ONLY in a dog and cat
pull tongue forward, hard
what happens to CO2 and O2 in respiratory arrest?
patient becomes hypercapnic (stops breathing so can't get rid of CO2) and hypoxic (not breathing in O2)
what is different about respiratory inadequacy (than a full arrest)?
oxygen deficiency can be compensated by increasing the inspired oxygen concentration, so the patient may be hypercapnic but not necessarily hypoxic
define: hypoventilation
ventilation inadequate to remove CO2. Thus patient will be hypercarbic (high PaCO2)
define: hypoxemia
low arterial PaO2 with Hb not fully saturated
if it is not caused by hypoventilation, what will hypoxia do?

--what does this cause?
stimulate breathing

--therefore, the hypoxic animal may then hyperventilate
how do you dx hypoventilation?

what will you see?
-capnogram and/or arterial blood gas analysis (not easy w/o these)
-bright pink mucous membranes (hypercarbia)
-cynotic mucous membranes (hypoxia)
how do you dx hypoxemia?
-colour of mucous membranes
-pulse oximeter
(need adequate peripheral circulation and Hb for both!!)
-animal hyperventilating
-may not show under anesthesia
-arterial blood gas analysis
causes of hypoxemia
-low inspired oxygen
-oxygen cylinder running out!
-severe hypoventilation/respiratory arrest
-pulmonary pathology
what is IPPV and what do you have to be careful of?
Intermittent Positive Pressure Ventilation

--blowing up the stomach
agent used to start ventilation in neonates?
--what does it do?
---how is it administered?
----when do you use this in animals besides neonates?
Doxapram
--general CNS stimulation
---IV, via mucous membranes, intra-tracheal
----ONLY if there is no other method of ventilation
for all circulatory emergencies, what do you want to do?
treat the cause
common causes of circulatory failure under anesthesia
-inadequate circulating volume
-inadequate cardiac output
reasons for inadequate circulating volume
Pre-operative hypovolaemia
Blood loss
Vasodilatation from anaesthetic drugs
reasons for inadequate cardiac output
Inadequate circulating volume
Depression by anaesthetic agents
Cardiac rate and rhythm (drug induced bradycardia)
High peripheral resistance
common causes of tachyarrhythmias under anesthesia
-hypercapnia
-hypoxia
-electrolyte imbalances
-adrenaline/epinephrine (halothane sensitizes, acepromazine protects)
common causes of bracyarrhythmias under anesthesia
-vagal reflex
-electrolyte imbalances
-drugs used in anaesthesia (high dose opioids, alpha2 adrenoceptor agonists)
T/F Reflex vagal bradycardia/cardiac arrest under anaesthesia is an "all or nothing" reflex, meaning either no effect or cardiac arrest
true: all or nothing
what are some high risk areas of surgical stimulation of reflex bradycardia/cardiac arrest under anesthesia?
--how do you protect/treat it?
-eye, end of nose, larynx, around vagal trunk high risk
--with anti-cholinergic drugs (atropine, glycopyrollate etc)
problem w/noticing cardiac arrest under anesthesia
animals may breath for some time after the heart stops
resuscitation routine for cardiac arrest under anesthesia
1. tell surgeon, call help
2. check airway, (intubate if not already) stop anesthetic administration, IPPV with O2
3. external cardiac massage - external (judge efficacy), internal (if necessary)
4. remove cause
5. drug/shock therapy to restart heart
resuscitation routine in cardiac arrest under anesthesia in a horse (heart in asystole)
1. stages 1 and 2 as for all animals.
2. external cardiac massage
3. ensure effective circulation prior to drugs
4. ephedrine/atropine IV then continue massage
CPCR stands for:
cerebro-cardiopulmonary resuscitation
Evidence based classification of CPr procedure:
1. Class I
2. Class IIa
3. Class IIb
4. Class III
5. Indeterminate class
1. excellent evidence, definitely helpful
2. good to very good evidence, acceptable, probably helpful, standard of care
3. fair to good evidence, acceptable, possibly helpful, optional or alternative care
4. unacceptable, no proven benefit, may be harmful
5. insufficient evidence, no harm, no benefit.
One important changed made to how CPCR is performed in veterinary medicine
avoid administration of excessive ventilatory rates because this maneuver severely decreases myocardial and cerebral perfusion, decreasing the chance of survival
CPCR: cannot have more than ___ between chest compressions
--how long should they resume between defibrillator shocks?
no > 10sec
-- approx 2 minutes
Define: cardiorespiratory arrest
abrupt, unexpected cessation of spontaneous and effective ventilation and systemic perfusion (circulation)
it is important to differentiate between cardiorespiratory arrest and what other 2 things?
-cardiorespiratory arrest
(note: respiration can continue for some minutes after cardiac arrest)
-respiratory arrest: loss of effective, spontaneous ventilation
pulseless electrical activity (PEA)
things that can cause cardiorespiratory arrest
-vagally mediated cardiac arrest/ vasovagal syncope
-trauma
-systemic and metabolic disease
-respiratory disease
-cardiac disease
-acid-base and electrolyte abnormalities: (hyperkalemia (urethral obstruction, renal failure), hypocalcemia, hypermagnasemia, hypoglycemia
high risk patients intra-operatively
anaesthetic overdose
hypothermia
hypoxia
hypercarbia
hypotension/hypovolaemia
changes in respiratory rate, depth, or pattern can indicate what?
that cardiac arrest has already occurred
will find no palpable pulse if systolic pressure is ?

--will find no heart sounds if systolic pressure is ?
<60mmHg

-- <50mmHg
clinical signs of cardiac arrest
-no palpable pulse or heart sounds
-central eye - pupillary dilation (really shows in the dog)
-absence of observable ventilation
-cyanosis (may be late to show)
-very slow capillary re-fill (get some re-fill from the venous side.)
signs of cardiac arrest (electrical monitoring
-EKG
-direct blood pressure - will still read low, but no pulse pressure
-pulse oximeter - no signal
-no doppler signal
-NIBP fails
-capnograph - low, and falling ET CO2
Problem w/using EKG to determine cardiac arrest

--reason for a capnograph
10% of cardiac arrests are from electromechanical dissasociation (so just bc you have an ECG reading, doesn’t mean it’s alive)
--if you have a decent end tidal CO2, IT’S ALIVE!!
what are the 3 stages of CPR?
-Basic life support
-Advanced life support
-Prolonged life support
the ABCs of Basic life support
A – ASSISTANCE and establish an Airway
B - Breathing support (also Blood)
C - CHEST COMPRESSIONS and Circulatory support
effective CPR requires how many people?
4-5 assistants
first thing you do:
-immediate intubation/tracheostomy
-100% oxygen (turn off anesthetic) --> if no spontaneous ventilation ventilate 10 - 15 times/minute
-continuous with chest compressions (most important !! )
what does the C stand for in the ABCs of basic life support?
Compressions
get your Circulation going!!
Connect ECG
Catheters
Calm
what position should the animal be in for closed chest compressions?

--how are they performed (location, rate, etc)
right lateral recumbency
--4th - 5th intercostal space
--at least 80 - 120/minute
--interpose abdominal compressions
--high ratio of chest compressions:ventilations
--without interruption
what does it mean if the pupils constrict
it means you're winning!!
What is the cardiac pump theory and when is it used?
used in animals <15kg
-Strength of chest compressions is transmitted directly to the heart
-More effective means of generating cardiac output
What is the thoracic pump theory and when is it used?
used in animals >15kg
-Forward flow is achieved through changes in intrathoracic pressure
-Less effective generation of cardiac output
Limitations of closed chest compressions
1. produces ___ of the normal CO
2. cerebral and myocardial flow are ___ pre-arrest values
3. renal and hepatic blood flow during CPR is ____ of pre-arrest values
1. up to 20%
2. less than 5%
3. 1% to 5% of pre-arrest values
During CPR, what determines the efficacy of organ perfusion?
force, rate, and duration of chest compression
All methods will fail if...?
there is no venous return
when should open chest compressions start?
w.i 2-5 minutes of starting CPR
what will PETCO2 monitor during CPR?
non-invasive way of estimating blood flow (and meaningful perfusion) through the lungs
when and animals has a peak ETCO2 of ___ it is unlikely to be resuscitated
1. dog
2. cat
1. < 15 mm Hg
2. < 20 mm Hg
most helpful cranial nerve reflex during CPCR
pupil size
the thing to remember about ECG
it only provides information about electrical activity, not functional output
what are the 4 ECG rhythms that means something during CPCR?
-asystole (flat)
-ventricular tachycardia
-ventricular fibrillation
-electro-mechanical dissociation (beautiful ECG but everything else being measured says no circulation – ex capnograph)
the DEF of Advanced Life Support
D -- Diagnosis and Drugs
E -- Electrocardiography
F -- Fibrillation control
what is the ONLY drug that has received the Class I recommendation for treatment for CPCR?
atropine (for bradycardia)
what is the most common arrest rhythm in dogs?
electromechanical dissociation (though asystole is a close second)
how should we administer drugs during CPR?
intravenous
intra-osseous
intra-tracheal
(intra-cardiac is NOT recommended)
though shock doses of fluids are recommended for CPCR, what do we need to be careful of?
--what type do we want to consider?
they can impair myocardial and cerebral perfusion

--colloids and hypertonic saline
most important drug used in CPR
oxygen!
list of drugs used for CPR
epinephrine
atropine
lidocaine
vasopressin
antagonist drugs
epinephrine aka

-when is it indicated?

--what does it do?
adrenaline

-in almost all cases of cardiac arrest
--acts as a vasopressor and positive chronotrop
contraindications of epinephrine
-ventricular tachycardia & fibrillation
presence of drugs that increase ADRENERGIC drug effects (xylazine, halothane, etc) --> incr ventricular fibrillation
what type of drug is epinephrine?

--what receptors does epinephrine act on during CPCR?
mixed alpha and beta agonist

--alpha, beta1, and beta2
epinephrine: it's effects on:
1. alpha receptors
2. beta1 receptors
3. beta2 receptors
1. vasoconstriction
2. increased contractility
3. bronchodilation, skeletal muscle vasodilation, increased HR
epinephrine: other effects
-Increased myocardial and cerebral perfusion
-Increased arrhythmogenicity
epinephrine:
1. when do alpha effects predominate?
2. when do beta effects predominate?
1. at high doses (vasoconstriction)
2. at low doses (inotropy, chronotropy)
why do we keep doing CPCR when we first give epinephrine?

--benefit and problem w/high dose
need to get the drug to the coronary vessels

--improves cerebral blood flow but incr refibrillation rate and decr survival rate (has been assoc w/myocardial dysfn and neuro outcomes)
adverse effects of epinephrine
-Increased myocardial oxygen demand/ consumption
-Increased lactate production
-Increased intrapulmonary shunting
-Increased likelihood of fibrillation
what kind of drug is atropine and when is it indicated?
-antimuscarinic parasympatholytic drug
--To decr an increased vagal tone
--Bradyarrythmias
Atropine: what types of things is it used for when decr vagal tone?
light anesthetic depth/awake intubation
retching/vomiting
ocular manipulations
concurrent opioid use
Atropine: what types of bradyarrhythmias is it used for?
-Sinus bradycardia
-Sinus arrest, slow pulseless electrical activity
-2nd degree AV block
Vasopressin: when is it indicated and what does it do?
-Ultra-potent vasoconstrictor
-improves cerebral and myocardial blood flow
-particularly indicated in sepsis, systemic inflammatory response syndrome
Vasopressin:
currently recommended to replace or be given adjunct to what in CPCR therapy?
adrenaline
rare cardiac arrhythmia in dogs
ventricular tachycardia
what is the only way to convert a ventricular fibrillation to a perfusing rhythm
defibrillation
CPCR indications for lidocaine
-beneficial for ventricular arrhythmias following resuscitation
-no proof of efficacy w/cardiac arrest
-ventricular tachycardia (if underlying SA nodal rhythm)
-may be an effective “free radical scavenger !!
Ventricular tachycardia
1. if you give a lidocaine bolus and it's effective, what do you do?
2. if a lidocaine bolus is NOT effective, then what do you do?
3. what may replace lidocaine as tha anti-arrhythmic of choice?
1. give lidocaine infusion
2. give procaine IV
3. Amiodarone
reversal agents for different anesthetics:
1. opioids
2. xylazine
3. medetomidine
4. midazolam
1. naloxone
2. yohimbine
3. atipamezol
4. flumazenil
On the antero-lateral aspect of the upper arm, 3 cun inferior to the axillary fold and 6 cun superior to Lu-5, in the depression between the lateral border of the biceps brachii muscle and the shaft of the humerus.
Lu-3
Sky Window
Balances above & below - goiter
Affects Po- sadness, weeping, disorientation, forgetfulness, somnolence, insomnia, delerious speech
Cools, clears, calms (heavenly attributes)

Found to increase oxygen
Enhance athletic performance – needle just prior to event
defibrillation is the only means of what?
converting ventricular fibrillation to a perfusing rhythm
what is mannitol used for in follow-up and post-resuscitation?
to decr the chance of cerebral edema
the GHI of Prolonged Life Support
G -- Gauging a patient's response.
H -- Hopeful measures for the brain
I -- Intensive care
what effects does progesterone during pregnancy have on
1. the MAC of inhalational agents
2. body temperature
3. everything else in the body?
1. decr MAC
2. thermogenic, increases body temperature
3. dilation/relaxation
pregnancy: what do you have to be aware of when giving an epidural?

--effect of pregnancy of CO
distended epidural veins

--incr </= 50% thru incr of stroke volume
pregnancy: respiratory changes
-incr oxygen consumption
-altered sensitivity of chemoreceptors to PaCO2
-↓↓ FRC (fnal residual capacity) and ↓↓ RV (reserve volume)
-reduced oxygen reserves
-incr risk of hypoxia
-incr risk of regurgitation/aspiration
pregnancy: if not doing a C-section, what drug is the worst for sx?
xylazine
C-section: what can happen to the dam when it is in dorsal recumbency w/the heavy pressure of the uterus (before it's taken out)? the uterus can...
-press on lungs - V/Q mismatch - ‘apparent ‘slow uptake of isoflurane
-press on vena cava --> reduced venous return to heart --> low CO --> low arterial BP
C-section: what can help take the pressure of the uterus off the dam in dorsal recumbency?
Use a ‘wedge’ to have dam positioned just ‘off’ the straight
C-section: in healthy animals, what will premed do?

--which 2 types of drugs do you avoid?
reduce anxiety, stress and improve uterine perfusion

--alpha2s and benzodiazepines
C-section: what drugs would you use to premed?
--what would you do if the puppy is respiratory depressed?
---why not benzodiazepines?
-prefer fentanyl or meperidine (low doses)
--antagonize opiate
---slowly eliminated from puppies --> puppy depression
C-section: restrictions for using N2O and why?
-stop immediately after induction bc crosses placental membrane and can cause diffusion hypoxia in baby post-partum
C-section: what's a good injectable induction agent to use?
propofol/etomidate
C-section: what can be done for analgesia?
-pre-emptive administration of NSAIDs
-low dose opioids (delay until babies delivered)
-lumbosacral extradural
C-section: if a drug crosses the blood brain barrier...?
it will cross the placenta
Pyometra: anticipated problems
-SHOCK
-anemia
-hypovolemia, toxemia, septicemia
-glomerulonephritis
-risk of vomiting at induction --> aspiration pneumonia
-reduced FRC
-hypoalbuminemia
-CNS depression
-insulin resistance
What agents would you use for a Caslick's sx on a mare?
ACP plus butorphanol (avoid xylazine)
best agent for mare C-section
romifidine
C-section: in a cow, why do you use a caudal epidural?
so it stops straining
Avian: birds have a high metabolic rate, so that means what about oxygen?
they have limited oxygen reserves
Avian: compare w/mammals
1. stroke volume
2. heart size
3. CO
4. resting MAP
1. higher
2. larger
3. higher
4. higher
Avian: what can disturb the high, efficient CVS

--what can this lead to?
posture and anesthetic agents

--depressed venous return in dorsal recumbency and hypotension
Avian: the cardiorespiratory stress response occurs in what type of birds?
--when can this occur
---what's the problem with it?
diving birds and ducks
--from stress before or during GA
---can cause cardiopulmonary depression and incr anesthetic risk
Avian:
1. how could you diminish the dive response?
2. how could you virtually abolish the dive response?
1. pre-med
2. pre-oxygenate
Avian: name the functional components of ventilation in the avian respiratory system
conduction airways
air sacs
thoracic skeleton
muscles of ventilation
Avian: name the functional components of gas exchange in the avian respiratory system
--what is the basic unit for gas exchange?
the parabronchi
--basic unit for gas exchange is the parabronchus (NOT the alveolus)
Avian: respiratory system: what do fowl have in comparison to all other birds
-All birds have paleopulmonobronchi
-fowl have neopulmonobronchi
Avian: they are missing ___, which makes breathing ___
a diaphragm
--active process (both inspiration and expiration)
Avian: tracheas are long and wide, which is compensated by ?
larger tidal volume and relatively low RR
Avian: you can perform mechanical ventilation thru?
air sac cannulation
Avian: the big thing to remember about the "rigid lung"
it does NOT contribute to gas exchange and does not affect anesthetic gas concentration, but it can be a reservoir
Avian: why is gas exchange more efficient than in mammals?
bc of the countercurrent mechanism between gas and blood flow
Avian: changes in depth of anesthesia occur ___ and hypoxia has a ____ impact than in mammals
faster; larger
Avian: how should doses by calculated?
by body mass index/body surface area rather than gram weight
Avian: dorsal recumbency severely impairs what?
venous return
Avian: premedications... for cage birds
Not always necessary
-but can use benzodiazepines and butorphanol
Avian: Induction of cage birds
1. inhalational vs injectable
2. mask induction and intubation are?
3. what is mandatory?
4. type of system used
1. Inhalationals are better
2. are generally very easy
3. IPPV is mandatory
4. low-resistance non-rebreathing systems
Avian: premedication of ratites (ex ostrichs)
benzodiazepines
butorphanol
medetomidine
Avian: induction of ratites
-IM/IV ketamine and medetomidine
-propofol
Avian: where do you give fluids?
-indwelling IV in the medial metatarsal, jugular, ulnar
-intraosseous in the ulna or tibiotarsus
Avian: when doing analgesia, birds have which type of receptors?

--so which drug should be used?
-kappa instead of mu

--use butorphanol (carpofen and meloxican)
Avian: anesthesia
1. eye position
2. which reflexes do you test?
1. always central
2. pupillary diameter, corneal, PLR, withdrawal (toe pinch/wattle pinch/cloacal pinch)
Reptile: their response to anesthetic drug depends on what?
temperature (they're ectothermic)
Reptile:
1. what type of heart do they have?
2. left atrium empties into ?
3. right atrium empties into ?
1. three-chambered
2. cavum arteriosum
3. cavum venosum
Reptiles: compare total lung volume and gas exchange area w/mammals

--which lung is either vestigial or absent?
total lung volume is larger
gas exchange area is smaller

--left lung
Reptiles: what makes their respiratory system similar to a bird's?
they have no (functional) diaphgram
Reptiles: injection routes
-Hindlimb IM injection
-Coccygeal veins – dorsal and ventral veins
-Cervical sinus on the dorsolateral surface of the neck
Reptiles: which drugs work well?

--why is premed generally a waste of time?
benzodiazepines

--prolonged clearance of parental drugs
Reptiles: choice of drugs for injection induction
propofol, telazol, medetomidine + ketamine
Tiny beasts: metabolic rate in small animals
high
Tiny beasts:
1. why is apnea more rapidly fatal in these guys?
2. problem w/starvation and water deprivation
1. bc they have low reserves
2. can cause hypoglycemia and dehydration
Tiny beasts: what does it mean when you find black/reddish brown discharge around eyes and nose?
non-specific response to stress or illness
Tiny beasts:
1. what can you use for premed? what does it do?
2. which animal can this be ineffective in? so what do you use instead?
1. Atropine - reduces salivation (reduce bronchial secretions); can also use opiods
2. atropine is ineffective in rabbits - use glycopyrrolate
Tiny beasts: which spp is stressed by inhalational induction and what can you do to fix this?
rabbits

--premed w/benzodiazepine/ ACP/ opioid/medetomidine
Tiny beasts: what is the optimal way to induce tiny animals?
induction chamber - administer 100% oxygen for 2-3 minutes, then introduce inhalational agent (sevo or haloflurane - NOT isoflurane)
Tiny beasts:
1. vein used in rabbits; in larger rodents
2. 2 other commonly used injectable sites
1. auricular vein; tail vein
2. Intraperitoneal, IM
Tiny beasts:
1. which drug is ineffective if given alone?
2. Rabbits are more sensitive to what combination?
1. Ketamine (rodents are highly resistant)
2. ketamine/medetomidine/benzodiazepine
Tiny beasts: what two pieces of monitoring equipment should be used?
pulse-ox and doppler
Tiny beasts: what should you supplement post-op?
glucose
Rabbits: there are many protocols. what is one very common one?
Medetomidine + Ketamine + Buprenorphine (or butorphanol) mixed in the same syringe
-given IM of SC
-still must give oxygen
an animal is considered neonatal until:
1. dog and cat
2. foal
1. 6 weeks
2. 1 month
an animal is considered pediatric until:
1. dog and cat
2. foal and ruminant
1. 12 weeks
2. 6 weeks
comparison between pediatric and adult:
1. O2 consumption
2. minute volume and respiratory rate
3. pulmonary reserve
4. uptake of inhalational agent
1. high (2 - 3 x adult)
2. high (high respiratory rate)
3. minimal pulmonary reserve
4. high in comparison
Pediatric: what is the danger in respiratory physiology?
lower FRC and high closing volume --> danger of alveolar collapse
Pediatric: CV system
1. resting CO
2. stroke volume
3. heart rate
4. myocardium
5. what determines CO? why?
1. high
2. low (fixed)
3. relatively high labile HR
4. poorly compliant myocardium
5. heart rate is major determinant of cardiac output since stroke volume is fixed (CO = HR x SV)
Pediatrics: T/F become tachycardic is easy.
False: becoming bradycardic is easy bc parasympathetic dominance --> high resting vagal tone
Pediatrics: explain why distribution and metabolism of agents is different bc of:
1. total protein
2. renal and hepatic fn
1. Low albumin/total protein --> incr free portion of highly bound anesthetic drugs
2. Immature renal and hepatic function --> prolonged clearance and altered excretion
Pediatrics: explain why distribution and metabolism of agents is different bc of:
1. fluid balance and body fat
2. blood-brain barrier
1. --> altered drug distribution
2. may be 5 - 6 x more permeable --> ‘more sensitive’ to anesthetics
Pediatrics: anesthetic requirements in neonates and what happens when they become pediatric?
-LOW in neonates, but then incr rapidly so are high in paediatric patients
fluid requirements in
1. adults
2. pediatrics
3. why are they so different?
1. 40 – 60 ml/kg/day
2. 80 – 100 ml/kg/day
3. higher rate of water turnover in pediatric and thus higher fluid requirements
Pediatrics: any rise in HCT over the first month usually means what?
it is a significant indicator of dehydration
Pediatrics: hypothermia will induce ?
bradycardia
Neonates can rapidly become...
hypothermic, hypoglycaemic, dehydrated, hypoxic, and die’
Pediatrics: what do you need to be careful to maintain when using fluids?
normoglycaemia and normovolaemia
Pediatrics: risk of foal death ____ w/age
decreases
Pediatrics: in foals, when will you see...
1. ruptured bladder present
2. retained meconium present
3. orthopedic growth problems present
1. 0.5-3days
2. 2-3 days
3. 1 week and up
Pediatrics: what is the cardinal rule when anesthetizing a foal?
sedate mom and keep with the foal until anesthetized !!
Pediatrics: foal: what do you use to sedate?
ace IM or romifidine IM and IV
Pediatrics: the renal system in foals is...
fully developed at birth
Pediatrics: problem w/pre-op fasting?

--is it needed?
can cause severe hypoglycemia

--no but if you do it, keep it short
Pediatrics: foal:
1. why are benzodiazepines good to use?
2. which ones?
3. when will they cause excitement?
1. good sedation in neonates
-minimal cardiovascular depression
-some respiratory depression
2. Diazepam or Midazolam (sedation or induction)
3. w/hepatic damage bc they have an extensive hepatic metabolism
Pediatrics: foal: which drugs do you want to avoid bc of their dramatic CV effects? what about these drugs can neonates not cope with?
alpha2 agonists

--bradycardia
Pediatrics: foal: which opioids can be used? what do you have to be careful not to cause?
all

--bradycardia (careful w/dose)
Pediatrics: NSAIDS in foals are commonly given w/?

--what do we have to be careful of?
GI protectants

--toxic effect in foals bc extensive hepatic metabolism
Pediatrics: foal:
1. drug of choice for IV injection
2. which drugs should we avoid? why?
1. Ketamine - NOT protein bound, via sympathetic stimulation --> stimulates CV system incl HR.
2. Thiopental (slow recovery, no fat for redistribution, immature enzymes)
Pediatrics: foal: drug of choice for inhalational anesthesia
sevoflurane
Pediatrics: foal:
in foals less than 2 weeks old, use what induction/maintenance agents?
-Sevoflurane (or iso)
-diazepam/midazolam if needed for intubation
-Sevo or Iso maintenance
-Opioids +/- NSAIDS
Pediatrics: foal:
in foals 2-12 weeks old, use what induction/maintenance agents?
-might premed - acepromazine
-induction:ketamine & diazepam or midazolam (same syryinge)
-nasal tube is can't intubate
Isoflurane or sevoflurane maintenance
-analgesia: opioids +/- NSAIDS w/gastro-protectants
Pediatrics: foal:
in foals over 12 weeks, use what induction/maintenance agents?
Treat as adults!!
ACP
Xylazine
Ketamine/ benzodiazepine
Isoflurane
Pediatrics: in young foals, what happens to the anesthesia?
--why?
tend to get "swinging" anesthesia, from light-deep-light

--low MAC, rapid uptake
--no fat reservoir
Pediatrics: foal: what type of circuit do you use?
small animal circle or large animal circle with reduced carbon dioxide absorbent
Pediatrics: foal: how do you treat hypotension?
the same as you would in adults:
-reduce inhalational agent
-fluid bolus (crystalloid or colloid)
-treat bradycardia (anticholinergics, Atipamezole)
-dobutamine or NE
Pediatrics: puppies/kittens: premed drugs
-benzodiazepines
-opioids w/o bradycardia (ex meperidine)
-tiny doses ACP only in older
-sometimes anticholinergic agents
Pediatrics: pup/kit: induction and maintenance
1. make sure you:
2. what drug for mask induction?
3. what drug for IV induction?
4. advantage of low ketamine dose
5. avoid which drugs?
1. Pre-oxygenate!
2. sevoflurane
3. propofol or etomidate
4. NOT protein bound
5. barbiturates
pediatrics: pup/kit: analgesia
1. avoid which drugs?
2. Carprofen is licensed for what age?
3. Meloxicam is licensed for what age?
4. NSAID licensed for kittens under 12 weeks
1. avoid most NSAIDs
2. puppies > 6 weeks old
3. dogs > 6 months old and calves over 1 week old
4. none
Pediatrics: farm

what drugs are used for disbudding goat kids?
lidocaine, procaine
--iso by mask in food animals
Geriatric: CV consequences of old age
-reduced cardiac reserve
-chronic valvular disease, hypertrophic cardiomyopathy
-incr peripheral vasoconstriction assoc with autonomic inefficiency
-reduced hemopoietic efficacy
Geriatric: respiratory consequences of old age
-reduced efficiency of gas exchange
-impaired respiratory muscle fn
-pulmonary fibrosis
-more dead space
-↑risk of respiratory obstruction
-greater proportion of tidal ventilation at lung volumes below closing volume (air trapping, V/Q mismatching, reduced PaO2 )
Geriatric: organ function consequences of old age
-reduced renal and hepatic reserves
-reduced drug clearance - GFR
-reduced efficacy of fluid and electrolyte loading
-impaired perfusion
-decreased hepatic mass
-decreased hepatic perfusion
-decreased skeletal muscle mass
-increased fat
Geriatric: what happens to MAC of inhaled anesthetics as the animal ages?
progressively decreases by 30% from young adult values with increasing age
Geriatric: minimum reduction of ___ GFR
50%
Geriatric: premed drugs
less sedation is required:
-opioids
-benzodiazepines or very low dose of acepromazine
Geriatric: what do you do to improve ventilatory reserve?
pre-oxygenate for 2-5 minutes
Geriatric: how do you medicate an old horse?
like any adult horse, except for low doses of ace