Anaesthesia - SA Flashcards
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
hx
what sedatives/pre-op meds are there
- ACP
- A2 agonist
- BZD
- 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
- xylazine - fastes/quickest. most relaxation + visceral analgesia. colic +
- detomidine - horses IM, most potent
- medetomidine - good sed++
- 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
- buprenorphine - 6hrs DOA, good for sx (feisty cats++)
- butorphenol - 1-2hrs DOA, best sedation (eg for xray)
- methadone - 4hrs DOA, quick, good sed + analgesia, not emetic (cats++)
- 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
> 3mths
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
transduction
modification
transmission
perception
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:
- RAS
- 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
spinothalamic
which tract does mechanical stim pass in
dorsal
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
chronic
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
NDMA
- 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
NSAIDs paracet + codeine gabapentine 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
painless well distributed cheap high tx index (safe) smooth action and recovery
where do injectable agents act
Gaba-a R
nACh-R
Glycine-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
visualise 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
- IV
- O2 supply
- ETT
- monitoring equip
- recording
- 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 hypovent circulatory shut down crap gas exchange (as in atelectic horses..) inc O2 requirements
what partial p should the pulse oximeter show
60mmHg+
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 consciousness muscle relaxed amnesia 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
IVFT
+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
40-60%
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
