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Flashcards in Anaesthesia - SA Deck (94):

desc the basic ASA grading

I - normal healthy
II - mild systemic dz
III - severe systemic dz
IV - severe dz, constant threat to life
V - moribund, expected to die wo sx
E - emergency


what are the basic aims of pre-anaesth assessment

to establish how suitable the patient is
any deviation that the GA will effect or create


should you take pre-op bloods

yes- baseline, defence in court if dies, predict complications, O reassurance, baseline for individual
no - cost, acquiring, are they necessary


what are the recocm for food/water with-holdin

feed wet food - quicker digested
starve 8hrs, withold water when brought in
if starve any more = inc chance of regurg


what considerations need to be made before dosing calculated

weight - obese animals dont need that much
body SA better method
breed - some more sensititive
other dz - eg if hypotensive DONT give ACP


what sedatives/pre-op meds are there

- A2 agonist
- Opioids
- Ketamine
- Alfaxalone
- Azaparone


what is the diff bw sedation and pre-med

premed= calm
sedation = for procedures (eg needs more)


whya re sedative risks high

no airway control
poorer monitoring


desc the perfect sedative

many admin routes
wo SE
quick and good DoA
any spp
reasonable volume


desc features of ACP

ONset - 30m
DoA - 4-8hrs
analgesia? NO
uses - bonfire night (NOT an anxiolytic); horses with pre-med
effects - vasodil (blocked a1 adrenoR) - so keep warm!; reduced sympathetic tone (can help some symp-induced arrhythmias); muscle relaxation; reduces PCV; anti-spasmodic and anti-emetic


desc the features of an A2 agonist

onset - 10m
DoA - short
analgesia? YES - centrally acting, activates desc inhib and good + opioids
uses - sedation (LA are ++ sensitive to touch though, watch out! - hence why w ketamine normally)
effects -
- severe CV: reduced symp tone, vasocon, reflex bradycardia, hypOtension, look grey-ish
- resp: depressed
- other: muscle relaxation; diuresis (consider in blocked cats etc); hyperglycaemia (reduced insulin prod and response); mydriasis; CI - pregn
reversal = atipamezole (antiseden) - NOT iv or crazy cats. reverses analgesia too.


name 4 types of a2 agonists and their basic properties

1. xylazine - fastes/quickest. most relaxation + visceral analgesia. colic +
2. detomidine - horses IM, most potent
3. medetomidine - good sed++
4. romifidine - longest DoA, weakest


what are the basic properties of BZ (benzodiazepines)

examples - Diazepam and midazolam - neither licensed in vet spp
uses - anti-convulsant, sedation (but may cause excitement). co-induction agent (aim to lower other drug doses and utilise the muscle relaxant property)
good bits - minor vasodil (keep warmer), CV or resp depression = ++recom for neonates and geriatric patients and muscle relaxation


desc the basics of opioids

uses - sedative, analgesic
effects - minimal CV depression; sign resp depression tho


name 4 types of opioid

1. buprenorphine - 6hrs DOA, good for sx (feisty cats++)
2. butorphenol - 1-2hrs DOA, best sedation (eg for xray)
3. methadone - 4hrs DOA, quick, good sed + analgesia, not emetic (cats++)
4. morphine - 4hrs DOA, need to be glucorinated (sorry cats)


desc the basic propertes of phencyclidine - ketamine

uses - induction agents + BZ - choice in LA; or in combos (ket, medatom and opioid) - SA, analgesia++

properties - dissociative, painful IM (pH-4)

effect - inc muscle tone, analgesic in v low doses. good for aggressive animals, apneustic breathing (min vol maintained tho), noise hypersensitivity, active CN reflexes (protect cornea)


what are the properties of propofol

DoA - short
uses - induction, maintenance, can titrate up to req effect
effects - CV - depression, hypotension; resp - depression and apnoea. indicated for cerebro-protection ++
properties - IV only as need high conc.
analgesia? NONE
metab by glucorinidation + hydroxylation - can give cats induction but not CRI
SE - heinz-body anaemia (C), CI in pancreatitis


what is a dog and cats circulating volume

d - 90mls
c - 60ml


what is pain

processing and perception of nociception


what is nociception

noxious stimulus received and relayed to CNS, but not cortex


name the 4 types of sensory perception and what sensory receptors sense it in the dermis

- pressure - meissner corpuscle
- vibrations - pacinian corpuscles
- stretch - ruffini endings
- light touch - merkel disls


what is allodynia

pain from light touch


what is hyper-algesia

inc sensitivity to pain


desc the difference bw somatic pain R and visceral pain R

somatic - many, widespread, small and precise
visceral - few each with large area. sensitive to distention, ischaemia or inflm. stimulus proportional to size of area, not severity


what duration classes as chronic pain



what does neuroplasticity mean

CNS and PNS can adapt to a pain event both fct'ally and anatomically. results in allodynia, and hyperalgesia


state the 4 stages of pain signal transmission



what is peripheral sensitisation

+++ inflm mediators, nociceptors threshold is reduced. this signals 'silent/redundant' nociceptors to become active (c-fibres and Ad fibres) since there is apparent tissue injury. Anything that inc cAMP, induces hyperalgesia (bradykinins, SubP - vasodil, NA, aa's)


how do NSAIDs work

MoA - targets transduction (inflm) and modulation (CNS), blocks effect of PG synth due to COX blocked (1 = constitutive; 2 = inducible)


where else is cox2 seen which means its not great to be blocking all the time?

cns, kidney, eye, repro constitutively


name the 2 pain fibres and 1 proprioception fibre

pain - c-fibres; Ad
proprioception = Ab


dec basic pain transmission

PNS --> CNS (either Ad synap in laminae I+V; C synap in lmainae II+III, with interneurones to V)
2nd order go to brain in one of many tracts (spinothalamic etc..) and may have 'inter-neuroned' with a reflex arc
3rd order go to organ to perceive pain, eg cortex


describe what the following process and perceieve:
- thalamus
- cingulate gyrus
- amygdala
- hippocamp
- locus coerulus
- cortex

- RAS - motivation
- thalamus - sensory
- cingulate gyrus - behav
- amygdala - anxiety
- hippocamp - memory
- locus coerulus - behav
- cortex - perception


how are nerve transmissions modulated

amplify or suppress the signal that reaches the SC by:
- inhib neurones
- desc inhib
- gate control
- central sensitisation


what is the majot difference in NT bw inhib and excitatory neurones

inhib - inc Cl- = hyperpol (stim by GABA-a and glycine)
excitat - inc Na+ and Ca++ (stim by glutamate and aspartate)


desc the gate control theory

pain fibres inhibit the inhibitory interneurones )eg they get thru)
mechanoR/proprioceptive fibres stimulate the inhib interneurones and do not go to be transmitted as pain


which tract does pain travel in



which tract does mechanical stim pass in



desc descending inhibition

as sensory stim come into the dorsal h - synapses at opiate-R.
serotonin and NA from the brain descend and inhibit the synapse to continue the transmission of the pain perceptio
all happens in peri-aque-ductal grey


desc some ways that maladaptive pain can ensue

neuropathic - nerve injury leading to ectopic charges, allodynia, hyperalgesia
complex regional - hyperresponsiveness, symp dysfct
mech and proprioceptive sprouting and synapsing in the lamninae II, III..


why is pre-empt analgesia impt

cant develop hyperalgesia


where can pain be targeted:

topical to affect R/free nerve endings
prev activation of silent nociceptors (stop inflm mediators)
specifc targets = PGE2, ATP, Subs P, Histamine, Serotonin, bradykinine


how does paracetamol work

not sure, but stimulates desc inhibitory pathway, inhibit re-uptake of endo-cannabinoids, inhibis PGE2
d++, cats - NO


what is central sensitisation

lots of NTs means that 2ry order neurones are now reactive - causing pain to be felt for a very large, unnecessary area (2ry hyperalg and allodynia)


which R are seen on 2ry O neurone mainly in central sensitisation

- this req both glutamate and glycine to bind
- this is why ketamine/methadone so useful for bad pain - blocks NDMA


what are your drugs of choice for chronic pain

paracet + codeine
NMDA antag (ket, methad, amantadine)
SSRI - amitryptaline
TCA - anti-D


what is the purpose of induction

to induce drugs to cause loss of consciousness


what is the pro/con for inhalation or injectabes

inhalation - IV not req, longer, stressful - bad smell and mask, irritant, pollution
inj - smooth, no pollution, need accurate kg, usually Cv and Resp depressants, good to have IV access, maintainance poss by CRI


what are the differences bw SA and LA and injection speed

SA slow so can titrate to just the right amount
LA (horse) - rapid or might become excitable and dangerous


what is the ideal induction agent

well distributed
high tx index (safe)
smooth action and recovery


where do injectable agents act

Gaba-a R


desc the properties of barbituates

uses - induction, PTS, top-up bolus in LA / SA with high ICP
analgesia? NO
CI - vasodil, CV/resp depression


desc the properties neuro-steroids - alfaxalone

use - induction, maintenance, sedation
properties - muscle relaxation - twitch when recovering; IM or IV, rapidly metabolised so okay for CRI
effects - CV - vasodil and tachycardia; resp - depression
analgesia? NO


what family of drugs does tiletamine belong to, and what are its properties

phencyclidine (ketamines)
uses - wild animal GA
properties - twitches and tremors; longer acting than ketamine; IV or IM
effects - CV - tachycardia, arrhythmias; resp - depression; brain - excitatory, inc ICP and IOP


desc the properties of etomidate

uses - induction (partic if CV dz)
properties - no analgesia, 2 x IV prep, Gaba-a R target, minimal CV or resp depression
effect - muscle stiffness, cerebro-protective, rapidly metabolised BUT suppresses the stress response so dont give CRI or will get addisonian crisis


which animals are better without a cuff on an ETT OR having a low P high vol one (long and thin)

rabbits and cats with entire tracheal rings


what is the bevel and the murphey eyes for

bevel - reduced chance of obstruction
murphy - just in case it does


which are at high risk of laryngeospasm

rabits and cats
sheep and goats


state two methods of intubation for the horse

blind - such long oral cavity and big tongue
naso-tracheal intubation = foals and oral sx


desc the techn with ETTing ruminants

salivate a lot and regurg - so keep head up
blind ETT - need it to be a lateral gag or manual palpation
can use a smaller stomach tube first then put ET over top


what is the problem with ETT pigs

larynx = 90degrees so got to rotate a few times to navigate


how do you know you correctly ETT

simult breathing with res bag
capnograph suggests so
cant feel the oesophagus
feel air coming out of ETT


why does atalectasis occur

poor perfusion of ventilated upper lung fields, and opposite of others = collpase. horses in D-rucumbancy +


why isnt IPPV always a good thing

creating positive p not the 'natural' negative p as pushing the air in, therefore blood not forced into the heart
can causes lung trauma and activate the RAAS
the pressure squashes the CrVC


what is TIVA

total intravenous anaesthesia
(sod inhalation, this is easy)
watch out for cumulative effects


what does MAC stand for

minimal alv conc = 50% of patients dont respond to nox stim. inversely related to potency


desc what low solubility inhalations agents are/do

hard to get into the blood, very easy/quick to leave. suitable for induction as quick recovery


what are the major differences bw sevo and isoflurorane

iso - most resp depression
sevo - v low solubility, only D
both vasodil and have no analgesia


do we use inhalation in horses

not much - they are very sensitive to 'their MAC' levels RE- resp depression - so risky as they wont spontaneously ventilate!


why is nitrous oxide partic bad in ruminants

they are so gassy - and NO wants to get out into being a gas ASAP so can cause bloat/pneumothorax!


what are the 6 most important things for all GAs

1. IV
2. O2 supply
3. ETT
4. monitoring equip
5. recording
6. emergency drugs


what are 3 principle reasons for tachycardia GA

- hypovolaemia - either genuine (from RBCs hiding in the spleen) OR from vasodilator used (ACP)
- too light
- shit analgesia


when measuring the alveolar partial pressures (PaCO2) & end tidal CO2 pressure, what should it be

C+D = 35-45mmHg
H = 60mmHg + (and thats fine..)
if high = hypOvent; low = hypERvent


what should be expected of the BP once a bolus of fluids is given

stress relaxation = BP drops!


name some causes of hypoxaemia

inadeq O2
blocked ETT
circulatory shut down
crap gas exchange (as in atelectic horses..)
inc O2 requirements


what partial p should the pulse oximeter show



if a patient becomes very bradycardic and has been given A2 agonist - what should you do

PARTIALLY reverse it (atipamezol)
swiftly replace - anaglesia, muscle relaxant and sedation!!


what does a chnage in SV indicate about the heart under GA

rhythm changing


what is the best indicateor of good perfusion

mean arterial BP of 80mmHg


when is mm cyanosis visible

at 75% saturation, so use a capnograph too


what are the ideal CNS signs of good GA

no movement
no spinal reflexes remain
muscle relaxed
corneal reflex still present
no PLR or jaw tone


other than hot hands and blankets - how else can animals be kept warm

use co-axial bain
warms inspired flow by the external expired gases


when might an oesophageal stethoscope be useful

when peripheral puse cant be felt and thorax sx


what are the 2 types of indirect blood pressure monitors

doppler - over rtery in paw - listen for rtn of whoosh. only systolic BP
oscillometric - like at home, need larger animals. can do all BPs (diastolic, mean and systolic)


what is direct arterial BP monitoring

gold std
cannulate dorsal metacarpal/tarsal or facial (H) and attach P-transducer. risk of thrombus, haem+ and infection..


what are 3 main ways to ammend hypOtensions

+ve inotropes (best in H)
vasopressors (vasocon)

also try changing position, lighten GA and IPPV (H)


how can central venous pressure be measured and why bother

via jug vein (like pacemaker..) go in to the RA
to assess level of cardiac dx and volaemia


what is the differnece bw capnometry and capnograph

capnometry - no trace, just measures ETCO2 (35-45)
capnograph - traces. can ID rebreathing if doesnt return to 0 at inspiration, hypOvent and if CO2 decreases-v poor perfusion!


roughly - what % of deaths occur in recovery



how common in hypOthermia

30% d and 70% cats


what causes hypothermia

drugs - vasodil
clipping, sx scrub, open body cavity
metal table
if cold - lower MAC required!
muscle twitches +/or shivering uses O2


what is the diff bw seizures and emergence dilirium

seizures are silent, with random movement


how do you reduce the risk of hypoxaemia

only extubate when fully breathing alone
give o2
extend their neck and position well


give some spp examples of recovery issues

D+C - gastric reflux/regurg
C - tracheal rupture or blindness (cerebral ischaemia)
Cattle - regug, bloat
H - colic, myopathy, neuropathy and fracture
P - hyperthermia