Vet Anaesthesia

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Purpose of Anaesthesia: 1. Restraint
2. Facilitate examination
3. Permit Surgery
4. Facilitate intensive care
5. Control Pain
6. Control seizures
7. Perform euthanasia
Local regional anaesthesia: Block sensation in peripheral nerves or spinal cord.
Prevents sensation from being registered and does not require that the animal lose consciousness.
General anaesthesia: Disrupts activity by disrupting activity in the cortex, reducing activity in ascending reticular formation of spine and brainstem.
Unconsciousness occurs, muscle relaxation, lowered sensitivity to painful stimuli.
Hypnosis/narcosis: sleep or unconsciousness, no perception of peri-operative period.

Amnesia
Analgesia: absence of obvious responses to noxious surgical insult
Muscle relaxation: total absence of voluntary and involuntary movement
Arreflexia: abolition of all responses to surgery
Dmito O2: the maintenance of O2 delivery to vital tissue
Tranquilliser: agent that affects mood
anxiolytic: agent that reduces anxiety without causing sedation
sedative: agent that causes drowsiness
hypnotic: agent that depresses the CNS and induces sleep at higher doses
neuroleptic: agent that reduces aggression and agitation
Acepromazine: oral bioavailability 20-55%
duration 4-6 hours
onset 20 minutes IM 5 IV
liver metabolism
excreted in urine
0.025-0.1 mg/kg
don't use in stallions/ careful in boxers
Propionylpromazine: Used in Europe
similar to ace
chlorpromazine: less potene
longer duration
unreliable in horses
Promazine: similar to chlorpromazine
better sedation and fewer side effects
Methotrimeprazine: potent analgesic
Promethazine: irritant give deep IM
potent antihistamine
Azaperone (stresnil): sedate and modify behaviour
used in pigs for aggression
Deep IM leave for 20 minutes!
duration 2-3 hours
potentiates anaesthetic agents
slight fall in BP
Fluanisone: with fentanyl = hypnorm
neurolept analgesic in small rodents
Droperidol: potent neuroleptic agent
duration 6-8 hours
potent antiemetic prevent vomiting
opiod fentanyl provides neuroleptanalgesia
Benzodiazepines: potentiation of GABA mediated inhibition
with the use of these drugs inhances activity of GABA
does not work without GABA
primary anxiolytic action
muscle relaxation
anticonvulsant
not good sedation
minimal depression of resp
synergistic with central depressants
Uses of Diazepam: status epilepticus
stimulate appetite
with ketamine in horses and sm. animals for muscle relaxation, anaesthesia
minimal cardiovascular and resp depression
pre anaesthetic med. compromised animals
Midazolam (Hypnovel): water soluble
does not cause thrombophlebitis
IM,IV oral
rapid metabolized and short duration
pharmacological effects similar to diazepam
Climazolam: Europe
maintain anaesthesia in horses in combination with ketamine
Tolezepam: Europe and USA
fixed ratio with the dissociative anaesthetic tiletamine
Benzodiazepine antagonists: no intrinsic efficacy but bind to receptor and prevent interaction between the agonist and receptor
Flumazenil: human medicine
antagonism of diazepam/midazolam sedation in dogs, cattle and sheep
What do Adrenoceptors bind?: catecholamines
Where is norepinephrine released from? Epinephrine?: Norepinephrine is released from nerve terminals and circulating epinephrine is released from adrenal glands
Can norepi/epi cross membranes?: nore/epi are charged molecules that can not cross membranes.
How do norepinephrine and epinephrine work to create changes in the cell?: They work by binding to receptors on the cell membrane, which causes a G protein to react to the receptor and an effector system within the cell.
What are alpha receptors stimulated by? antagonised by?: alpha receptors are stimulated by phenylephrine and antagonised by prozosin
What are alpha 2 receptors stimulated by and antagonised by?: They are stimulated by clonidine and antagonised by yohibine.
What happens when Alpha 2 receptors bind to inhibitory G proteins?: when alpha 2 receptors bind to inhibitory G proteins they inhibit adenylate cyclase therefore decrease the formation of cAMP.
What hapens when alpha 2 agonists bind to G proteins?: The alpha 2 agonist binds a G protein they bind to k channel proteins to cause the cell to become hyperpolarized decreasing excitability of CNS.
When they bind to Ca channels it cause a reduction in Ca influx and reduces NT release.
what does blocking of the presynaptic alpha 2 receptors do?: It blocks the release of Norepi causing an inhibition of adenylate cyclase and a reduction of Ca influx thereby modulating sympathetic outflow fromt he CNS.
What does blocking Alpha 2 receptors post synaptically do?: By blocking alpha 2 receptors post synaptically it causes vasoconstriction of arteries and veins.
What are the three main catagories of Alpha 2 agonists?: Imidazoles
Oxazolines
Phenylethylamines
Which alpha 2 agonist is less selective for alpha 2 receptors than the others?: xylazine
What is classified as the two phases of imidazoles?: Phase 1 - hypertension
Phase 2 Hypotension
What is phase 1 of imidazoline?: hypertension by vasoconstriciton causing an increase in the blood pressure resulting in a vagally mediated relfex of bradycardia
What is phase 2 of imidazoline?: There will be presynaptic inhibition of norep release which will cause a decreae in sympathetic outflow which offsets the vasoconstriction and reduces heart rate.
what is the site that modulates alpha 2 reaction on the autonomic system including the vagus?: nucleus tractus solitarius
What are the major effects of imidazoline?: sedation
analgesia
anaesthetic sparing effect
muscle relaxation
basoconstriction
bradycardia
Why would we want to reframe from using imidazoles in pregnant animals?: causes uterine contraction
Why would we want to be careful using imidazoles in horses?: causes a reduction in GI motility
What rule is important to remember when using xylazine in cattle?: the 24 hour rule
What animals is xylazine licensed for?: cows, horses, cats, dogs, deer and zoo animals
What is xylazine used for?: sedation and muscle relaxation

good pre anaesthetic drug prior to ketamine or barbiturate.

Good analgesic for use in horses with colic but not for surgery.
What are the major differences in Detomidine from xylazine?: -more potent than xylazine
- longer duration of action
-smaller volume
-more ataxia
- may be used in preg animals
-not licensed in cattle
What is the duration of action for xylazine?: IV 5 minute onset and 20 minute duration.
What is the duration of action of detomidine?: 1-2 hourse
What is the duration of action for Romifidine?: 3 hours
What animal is romifidine licensed in?: horse
What are the actions of romifidine?: sedative, analgesic and pre anaesthetic mediation
What are the differences of romifidine from xylazine?: -less ataxia
- longer duration
What animals is medetomidine licensed in?: Dog and cat
What is medetomidine used for?: restraint
sedation
analgesia
pre anaesthetic med
what animals is medetomidine contraindicated in?: animals with cardiovascular and respiratory disease
What are the effects of medetomidine?: restraint
sedation
analgesia
pre anaesthetic med
very potent
profound anaesthetic sparing effect
What is the reversal for medetomidine?: alpha 2 antagonist atipamazole
What is another name for medetomidine?: domitor
What is the difference between medetomidine and dexmedetomidine?: Dexmedetomidine-
- may have antiarrhythmic effect
-shorter acting
- have sudden loss of anaesthetic sparing effect
what is dexmedetomidine licensed in?: dogs and cats
What are the alpha 2 antagonists?: atipamazole
yohimbine
tolazoline
idazoxan
What is pain?: the unpleasant sensory and emotional experience associated with actual or potential tissue damage.
What is analgesia?: the absence of pain in the presence of stimuli
What are the mechanisms of pain?: -C fibers, and A fibers
-nociceptive cell bodies in DRG
-Pain fibers terminate in superficial dorsal horn of SC
-spinothalamic tract to thalamus
Where does pain modulation occur?: int he dorsal horn of spinal cord and the brain
What is the gate control theory of pain?: where the noiciceptive infomation is modulated in the substantia gelatinosa of the dorsal horn and can be stimulated by descending inhibitory neurons or non noiciceptive afferent input.
Where are the descending inhibitory neurons located?: in the periaqueductal grey area of the midbrain and the substantia gelatiosa
what is allodynia?: pain provoked by non noxious stimulus
What is wind up?: the increase of synaptic potential with each stimulus
What do analgesics do?: -act at the site of injury
What are the four things that analgesics do?: -act at the site of injury
-alter nerve conduction
-modify transmission in the dorsal horn
-act on the emotional aspects of pain
What is the active metabolite of morphine?: morphine -6-glucuronid
How are opioids metabolized?: - first pass
- 3-6 hour half life
-conjugated in liver
How are opioids eliminated?: -morphine glucuronides excreted in urine.
- glucuronides hydrolysed in gut
- morphine undgergos enterohepatic circulation
What are the unwanted side effects of opioids?: -sedation
-resp depression
- neg chronotropy except pethidine
-Emesis
-dysphoria
-histamine release (pethidine)
What are the effects of stimulatin of opioid receptors?: - G protein receptors
-inhibit adenylate cyclase
-promote opening of K channels
-inhibit opening of voltage gated calcium channels
Where is the principle site of action of opioids?: the spinal cord by inhibition of transmission of nociceptive impulses and inhibition of substance P
What are the pharmological effects of opoids?: - analgesia
-sedation
-cough suppression
-vomiting
-resp suppression
-pupillary constriction
-decrease GI motility
-histamine release: bronchoconstriction and hypotension
What is morphine? what are the effects?: -scheduled 2 drug
-gold standard
-vomiting
-neg chronotrophe
-resp depression
-decrease GI motility
What is pethidine? What are the effects?: - scheduled 2 opioid
-licensed
spasmolytic
positive chronotrope
histamine release when IV
What is fentanyl? What are the effects?: - scheduled 2 opioid
-unlicensed
-rapid onset
- 15-20 minute duration
- rescue analgesia
What is methadone? What are the effects?: - schedule 2 opioid
- synthetic mu agonist
- moderate pain
-NO EMESIS
What is Buprenorphine? What are the effects?: - schedule 2 opioid
- partial mu agonist/antagonist
- moderate pain
- used for partial reversal of full mu agonist
What is butorphanol? What are the effects?: - licensed
-synthetic partial opioid agonist/antagonist
- mild pain
- potent anti - tussive
What is hypnorm?: fentanyl and fluanisone
What is small animal immobilon?: etorphine and methotrimeprazine
What is large animal immobilon?: etorphine and acepromazine
What are the partial mu agonists?: -buprenorphine
-butorphanol
What are the full mu agonists?: -morphine
-pethidine
-fentanyl
-methadone
What do local anaethetics effect?: reversibly interfere with action potential generation generation and conduction of noxious impulse.
What are the two groups linked by of local anaesthetics?: ester or amide
what are the ester linked local anaesthetics?: procaine and cocaine
What are the amide linked local anaesthetics?: lidocaine and bupivicaine
What are the differences between ester and amide linked local anaesthetics?: - ester linkage is easily broken, less stable
- amides are stored for longer ad are heat stable
-ester metabolism produces para-aminobenzoates (PABA) that cause allergic reactions
What are the two enantomers of bupivicaine? What is the significance?: - levobupivacaine L
-dextrobupivacaine D
- Dextrobupivacaine is more cardiotoxic
Why is the absorption of local anaesthetics impaired in tissue?: - tissue ph is 7.4 and LA's are weak acids. In tissues they are more ionized therefore do not enter the cell readily.
- unionised drugs enter cells readily!
How are esters metabolized?: ester are broken down by plasma esterases to inactive compounds and then excreted by the kidneys
How are amides metabolised?: by hepatic amidases and then excreted by the kidneys.
How do local anesthetics block nerve transmission?: by blocking the transmission of the action potential.
- they block binding too voltage gated Na channels preventing depolarization
How do nerve fibers differ in sensitivity to local anaesthetics?: - small fibers blocked before large
-myelinated fibers blocked before unmyelinated
-fast fibers before c fibers
- pain is blocked before touch
What does use dependent mean in Local anaesthetics?: the block is more effective in fibers which are firing than those that are not.
Why are active channels more easily blocked with LA?: in an active neuron the Na channel is open which allows the LA to enter the nerve. If the Na channel is closed then LA's can not enter the nerve therefore take longer to block.
What are the unwanted side effects with local anaesthetics?: - tremors, convulsion
-resp depression
-reduced myocardial contractility
-vasodilation
- reduce epithelial repair
-tissue irritation
- allergic reaction
-bupivicaine is cardio toxic
What is the difference in lidocaine and mepivicaine?: Mepivicaine
- equivalent potency
-less vasodilation
-Less irritant
-Expensive
-no preservative
Describe Bupivicaine.: - amide linked
-long lasting
-extradural anaesthesia
-cardio toxic
What prolongs the duration of Lidocaine?: adrenaline
What is proxymetacaine used for?: conjunctival sac anaesthesia
- toxic to corneal epithelium
- rapid onset
10-20 minute duration
Describe procaine.: - ester linked
-short duration
-vasoconstriction
-PABA reaction
-add penicillin to reduce pain on inj
What is EMLA used for?: - topical anaesthesia of skin
-used to facilitate venipuncture
- 30-60 minutes before
What are NSAIDs?: Non steroidal anti inflammatories
What are NSAIDs used for?: - potent anti inflammatories to reduce inflammation mediators
What are NMDA receptors?: - found in CNS
- ligand receptor for excitatory AA, glutamate and aspartate
What effects do excitatory amino acids have on pain?: they modulate pain transmission by enhancing pain perception
What do NMDA antagonists do?: they block EAA receptors to reduce modulation and CNS activity.
Describe Ketamine.: - POM
-cyclohexane derivative
-chemical restraint/ dissociative anaesthesia
-visceral and somatic analgesia
-inhibits central sensitization
-bolus or CRI
What are the NMDA antagonists?: -ketamine
-tramadol
-gabapentin
-alpha 2 agonists
What are the effects of Tramadol?: - reduce nociceptive transmission by binding at mu receptors
-inhibit reuptake of serotonin and noradrenaline in the CNS
Which NMDA was originally developed as anti epileptic drug in humans?: gabapentin
What is gabapentin used for?: - stabilizes electrical nerve activity
- used as analgesic
- neuropathic pain in animals and human beings
What are alpha 2 agonists used for?: - visceral analgesia
- profound sedation
What is the difference between pain and nociception?: pain is a conscious experience. nociception describes the process of neruotransmission, from sensory receptors triggered by tissue damage
What are the metabolic effects of pain?: substrate mobilisation, catabolism triggered by stress response and pituitary and adrenal gland hormone secretion
What are the long term negative effects of pain response by metabolic breakdown?: - immunosuppression
-delay wound healing
-poor weight loss
- poor growth
What are the cardiovascular effects of pain?: hypertension and tachycardia
What does poor peri operative pain management lead to?: -poor recover
- increase risk of post op complications
-pathophysiological persistent pain (chronic)
- increase mutilation and wound bitting
What is the physiology of pain transmission?: nociceptive fibres triggered by noxious stimulus, impulses to dorsal horn of spinal cord, Afferent fibres in dorsal root ganglion, info to cerebral cortex, conscious perception
Where are the relay centers in the brain that modulate pain?: - thalamus,
-reticular formation
-pons
-amygdala
What is pathological pain?: pain perceived in the absence of tissue damage, or pain that persists after the noxious stimulus has subsided
What is hyperalgesia?: an exaggerated response to a noxious stimulus
What is peripheral sensitisation?: - sensitisation of the peripheral nociceptors to inflammatory mediators where the threshold is lowered to poduce a greater response to same stimulus
What is central sensitisation?: enhanced excitability of spinal nociceptive neurons
- short lived- changes in NT activity
-long lived - phenotypic changes in central neurons
What are the physiological variables associated with pain?: heart rate, respiratory rate, pupil size, humoral factors
What is the best marker of pain at the present time?: response to analgesia
What are the pharmacological and practical aspects of pain management?: - surgical considerations
- nursing
-alternative therapy
-analgesic agens
What are some alternatives from drug usage to control pain?: - acupuncture
-physiotherapy
-trans cutaneous electric spinal nerve stimulation
-heat and cold therapy - osteopathy
What is multimodal analgesia? What are the advantages?: - simultaneous administration of a combination of analgesic agents with different modes of action and different side effects.
- it may be safer to use multiple drugs than one large dose drug
what is pre emptive analgesia?: analgesic agent prior to noxious stimulation
Why is it more useful to use a full agonist to a partial opioid agonist?: We use opioids to control acute/surgical pain.
-partial agonists have a ceiling effect so it may not be possible to enhance opioid analgesia by increasing the dose.
What drugs should be used for opioid overdose?: naloxone
nalbuphine
How do opioids reduce respiratory depression?: they reduce the responsiveness of the medullary respiratory centre to carbon dioxide.
What are two disadvantages of the fentanyl patch?: -human toxicity
- variation in plasma fentanyl concentrations
How is pethidine metabolized?: methylation
What is the most common side effect of NSAID's?: gastro intestinal ulceration
Why should you not use NSAID's in hypovolaemic patients?: PGE2 is restricted with the use of NSAID's. PGE2 is utilized by the kidney to maintain renal blood flow to prevent neephrotoxicity.
What are some uses of topical techniques for local anesthesia?: - skin for IV placement
-splash blocks on wounds
- insertion of urinary catheters
- conjunctiva and corneal analgesia
-intra synovial application
- interpleural anaesthesia
- intraperitoneeal anaesthesia
What does a mental nerve block desensitise?: anterior mandible
What does a mandibular alveolar nerve block desensitise?: skin, mucosa and teeth of mandible
What does an infraorbital and maxillary nerve block desensitize?: upper lip, nose, upper rostral teeth
What medication is used to reverse medetomidine?: atipamezole
Where does the spinal cord end in adult dogs?: L6
What is the difference in duration from lidocaine to bupivicaine?: Lidocaine has a rapid onset with 10 minutes, and lasts 60-90 minutes.

Bupivicaine has slow onset 30 minutes with long duration 4-6 hours.
What are the side effects of extradural anaesthesia?: - don't use in patients with coagulopathies or skin infections over site
- dural puncture
-hypotension- sympathetic blockade
- coat abnormalities
What is the anatomical site of action of injectable anaesthetics?: brain
What is the site of action of inhaled anaesthetics?: spinal cord
What is the correlation between how lipid soluble a drug is and how potent it is?: when you increase lipid solubility then you increase potency
How is lipid solubility increased in barbiturates?: - increase carbon chain on C5
-branched chains
-double and triple bonds
-replace O on C2 with S
What are the effects of increasing lipid solubility of barbiturates?: - increases potency
- speeds onset of action
- shortens duration
What is a barbiturate?: - derivative of barbituric acid
- sedative at low dose
-anaesthetic at high dose
- many have slow onset and long action
Does unionized drug or ionized drug cross the membranes?: Unionized drug is unbound and can cross the cell membrane to have an effect
Why should be lower the dose of a barbiturate with a vomiting animal?: with a vomiting animal they are hypoproteinemic and therefore there will be less protein for the drug to bind. This will increase the unbound unionized drug in the system and increase the effects.
What is the hangover effect of barbiturates?: this is where the drug is taken up into fats and is metabolized over time after the animal has recovered
Why do thin animals recover slower from barbiturates than fat animals?: Thin animals do now have fat reserves to take up the drug so the drug stays in the system longer providing longer effects
what is a vapor?: a substance that at room temperature and at sea level pressure is a liquid
What is a gas?: a substance that at room temperature and at sea level pressure is a gas
What is the critical temperature?: defined as temperature above which a gas can not be liquefied however much pressure is applied
what is the boiling point?: a temperature at which the gas vapour pressure equal the atomspheric pressure
What is vapor pressure?: the pressure exerted by molecules escaping from the liquid surface to enter the gaseous state
What is vapor pressure dependent on?: temperature
What does vapor pressure indicate?: the ability of a liquid to evaporate
how is vapor pressure related to volatility?: increase VP then increase volatility
What is saturated vapor pressure? what is the significance?: - when there is a dynamic equilibrium
- this indicates the maximum amount of gas that can be put into anaesthetic vapor
What does blood gas coefficient determine?: the speed of induction and recovery
What is the relationship between induction and onset with a high blood gas coefficient?: if there is a high blood:gas coefficient then the gas wants to stay in the blood so there will be a longer induction time and a onset.
What does a low blood:gas coefficient determine?: It is less soluble in the blood so it will leave the blood quickly. There will be fast induction and fast onset.
Which gas has the highest induction time but can not be used as an anesthetic it's self?: N2O
Which gas is most soluble in blood?: methoxyflurane
What is the oil:gas coefficient correlated with?: Potency
- higher the oil solubility the more potent
what is MAC?: MAC = minimum alveolar concentration
- the concentration where 50% of the animals are asleep
Why should us used a level above the MAC for that gas?: because the MAC is only 50% of the population so we want to be a little higher.
what does the potency of a drug depend on?: the ability to cross the membrane
what are the signs of hypercapnia?: - tachypnoea
- peripheral vasodilation
- cardiac arrhythmias
what will an increase in CO2 do to the oxyhb dissociation curve?: shift it to the right
why do animals hypoventilate under anesthesia?: Ventilation is controlled by chemo receptors that require stimulation. In an anesthetized animal chemoreceptor sensitivity is reduced causing them to hypoventilate
What is the purpose of sighing?: to expand atalectic regions of lung
Why are spontaneous efforts to breathe in a animal on a PPV suppressed?: rhymic lung inflation and modest hypocapnia suppresses efforts to breath
What is the thoracolumbar pump mechanism?: - diaphragm moves caudally
-thoracic wall moves outwards
- increased intrathoracic volume
-decrease in pleural pressure
- creating a pressure gradient from abd to right heat that facilitates venous returen and enhances cardiac output

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