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VSCI300 MOD > Anaesthesia - SA > Flashcards

Anaesthesia - SA Flashcards

1
Q

desc the basic ASA grading

A 
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
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2
Q

what are the basic aims of pre-anaesth assessment

A

to establish how suitable the patient is

any deviation that the GA will effect or create

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3
Q

should you take pre-op bloods

A

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

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4
Q

what are the recocm for food/water with-holdin

A

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

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5
Q

what considerations need to be made before dosing calculated

A

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

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6
Q

what sedatives/pre-op meds are there

A
  • ACP
  • A2 agonist
  • BZD
  • Opioids
  • Ketamine
  • Alfaxalone
  • Azaparone
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7
Q

what is the diff bw sedation and pre-med

A 
premed= calm
sedation = for procedures (eg needs more)
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8
Q

whya re sedative risks high

A

no airway control

poorer monitoring

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9
Q

desc the perfect sedative

A 
many admin routes
wo SE
quick and good DoA
any spp
reasonable volume
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10
Q

desc features of ACP

A

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

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11
Q

desc the features of an A2 agonist

A

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.

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12
Q

name 4 types of a2 agonists and their basic properties

A
  1. xylazine - fastes/quickest. most relaxation + visceral analgesia. colic +
  2. detomidine - horses IM, most potent
  3. medetomidine - good sed++
  4. romifidine - longest DoA, weakest
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13
Q

what are the basic properties of BZ (benzodiazepines)

A

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

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14
Q

desc the basics of opioids

A

uses - sedative, analgesic

effects - minimal CV depression; sign resp depression tho

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15
Q

name 4 types of opioid

A
  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)
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16
Q

desc the basic propertes of phencyclidine - ketamine

A

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)

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17
Q

what are the properties of propofol

A

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

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18
Q

what is a dog and cats circulating volume

A

d - 90mls

c - 60ml

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19
Q

what is pain

A

processing and perception of nociception

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20
Q

what is nociception

A

noxious stimulus received and relayed to CNS, but not cortex

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21
Q

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

A
  • pressure - meissner corpuscle
  • vibrations - pacinian corpuscles
  • stretch - ruffini endings
  • light touch - merkel disls
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22
Q

what is allodynia

A

pain from light touch

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23
Q

what is hyper-algesia

A

inc sensitivity to pain

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24
Q

desc the difference bw somatic pain R and visceral pain R

A

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

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25
Q

what duration classes as chronic pain

A

> 3mths

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26
Q

what does neuroplasticity mean

A

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

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27
Q

state the 4 stages of pain signal transmission

A

transduction
modification
transmission
perception

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28
Q

what is peripheral sensitisation

A

+++ 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)

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29
Q

how do NSAIDs work

A

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

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30
Q

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

A

cns, kidney, eye, repro constitutively

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31
Q

name the 2 pain fibres and 1 proprioception fibre

A

pain - c-fibres; Ad

proprioception = Ab

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32
Q

dec basic pain transmission

A

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

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33
Q

describe what the following process and perceieve:

  • RAS
  • thalamus
  • cingulate gyrus
  • amygdala
  • hippocamp
  • locus coerulus
  • cortex
A
  • RAS - motivation
  • thalamus - sensory
  • cingulate gyrus - behav
  • amygdala - anxiety
  • hippocamp - memory
  • locus coerulus - behav
  • cortex - perception
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34
Q

how are nerve transmissions modulated

A

amplify or suppress the signal that reaches the SC by:

  • inhib neurones
  • desc inhib
  • gate control
  • central sensitisation
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35
Q

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

A

inhib - inc Cl- = hyperpol (stim by GABA-a and glycine)

excitat - inc Na+ and Ca++ (stim by glutamate and aspartate)

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36
Q

desc the gate control theory

A

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

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37
Q

which tract does pain travel in

A

spinothalamic

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38
Q

which tract does mechanical stim pass in

A

dorsal

39
Q

desc descending inhibition

A

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

40
Q

desc some ways that maladaptive pain can ensue

A

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..

41
Q

why is pre-empt analgesia impt

A

cant develop hyperalgesia

42
Q

where can pain be targeted:

A

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

43
Q

how does paracetamol work

A

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

44
Q

what is central sensitisation

A

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)

45
Q

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

A

NDMA

  • this req both glutamate and glycine to bind
  • this is why ketamine/methadone so useful for bad pain - blocks NDMA
46
Q

what are your drugs of choice for chronic pain

A 
NSAIDs
paracet + codeine
gabapentine
NMDA antag (ket, methad, amantadine)
SSRI - amitryptaline
TCA - anti-D
47
Q

what is the purpose of induction

A

to induce drugs to cause loss of consciousness

48
Q

what is the pro/con for inhalation or injectabes

A

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

49
Q

what are the differences bw SA and LA and injection speed

A

SA slow so can titrate to just the right amount

LA (horse) - rapid or might become excitable and dangerous

50
Q

what is the ideal induction agent

A 
painless
well distributed
cheap
high tx index (safe)
smooth action and recovery
51
Q

where do injectable agents act

A

Gaba-a R
nACh-R
Glycine-R

52
Q

desc the properties of barbituates

A

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

53
Q

desc the properties neuro-steroids - alfaxalone

A

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

54
Q

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

A

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

55
Q

desc the properties of etomidate

A

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

56
Q

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

A

rabbits and cats with entire tracheal rings

57
Q

what is the bevel and the murphey eyes for

A

bevel - reduced chance of obstruction

murphy - just in case it does

58
Q

which are at high risk of laryngeospasm

A

rabits and cats

sheep and goats

59
Q

state two methods of intubation for the horse

A

blind - such long oral cavity and big tongue

naso-tracheal intubation = foals and oral sx

60
Q

desc the techn with ETTing ruminants

A

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

61
Q

what is the problem with ETT pigs

A

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

62
Q

how do you know you correctly ETT

A 
visualise
simult breathing with res bag
capnograph suggests so
cant feel the oesophagus
feel air coming out of ETT
63
Q

why does atalectasis occur

A

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

64
Q

why isnt IPPV always a good thing

A

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

65
Q

what is TIVA

A

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

66
Q

what does MAC stand for

A

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

67
Q

desc what low solubility inhalations agents are/do

A

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

68
Q

what are the major differences bw sevo and isoflurorane

A

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

69
Q

do we use inhalation in horses

A

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

70
Q

why is nitrous oxide partic bad in ruminants

A

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

71
Q

what are the 6 most important things for all GAs

A
  1. IV
  2. O2 supply
  3. ETT
  4. monitoring equip
  5. recording
  6. emergency drugs
72
Q

what are 3 principle reasons for tachycardia GA

A
  • hypovolaemia - either genuine (from RBCs hiding in the spleen) OR from vasodilator used (ACP)
  • too light
  • shit analgesia
73
Q

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

A

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

74
Q

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

A

stress relaxation = BP drops!

75
Q

name some causes of hypoxaemia

A 
inadeq O2
blocked ETT
hypovent
circulatory shut down
crap gas exchange (as in atelectic horses..)
inc O2 requirements
76
Q

what partial p should the pulse oximeter show

A

60mmHg+

77
Q

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

A

PARTIALLY reverse it (atipamezol)

swiftly replace - anaglesia, muscle relaxant and sedation!!

78
Q

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

A

rhythm changing

79
Q

what is the best indicateor of good perfusion

A

mean arterial BP of 80mmHg

80
Q

when is mm cyanosis visible

A

at 75% saturation, so use a capnograph too

81
Q

what are the ideal CNS signs of good GA

A 
no movement
no spinal reflexes remain
consciousness
muscle relaxed
amnesia
corneal reflex still present
no PLR or jaw tone
82
Q

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

A

use co-axial bain

warms inspired flow by the external expired gases

83
Q

when might an oesophageal stethoscope be useful

A

when peripheral puse cant be felt and thorax sx

84
Q

what are the 2 types of indirect blood pressure monitors

A

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)

85
Q

what is direct arterial BP monitoring

A

gold std

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

86
Q

what are 3 main ways to ammend hypOtensions

A

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

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

87
Q

how can central venous pressure be measured and why bother

A

via jug vein (like pacemaker..) go in to the RA

to assess level of cardiac dx and volaemia

88
Q

what is the differnece bw capnometry and capnograph

A

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!

89
Q

roughly - what % of deaths occur in recovery

A

40-60%

90
Q

how common in hypOthermia

A

30% d and 70% cats

91
Q

what causes hypothermia

A 
drugs - vasodil
clipping, sx scrub, open body cavity
metal table
if cold - lower MAC required!
muscle twitches +/or shivering uses O2
92
Q

what is the diff bw seizures and emergence dilirium

A

seizures are silent, with random movement

93
Q

how do you reduce the risk of hypoxaemia

A

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

94
Q

give some spp examples of recovery issues

A

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

VSCI300 MOD (32 decks)

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