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Advanced Clinical Veterinary Nursing > Anaesthesia > Flashcards

Anaesthesia Flashcards

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1
Q

define pain

A

unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage

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2
Q

what is the purpose of pain and when is this not the case?

A

protective unless in chronic pain

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3
Q

define nociception

A

neural process of encoding noxious stimuli

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4
Q

define nociceptive pain

A

pair arising from actual or threatened damage to non-neural tissue due to activation of nociceptors, in normally functioning somatosensory system

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5
Q

define neuropathic pain

A

pain caused by lesion or disease of somatosensory nervous system

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6
Q

define hyperalgesia

A

increased pain from stimulus that normally causes pain

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7
Q

define allodynia

A

pain due to stimulus that normally wouldnt cause pain

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8
Q

where do opioids act?

A

endogenous opioid receptors in the CNS

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9
Q

name full mu agonists (opioids)

A

methadone
fentanyl

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10
Q

name partial mu agonist (opioids)

A

buprenorphine

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11
Q

name mixed agonist-antagonist/k agonist (opioids)

A

butorphanol

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12
Q

name opioid antagonist

A

naloxone

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13
Q

define potency

A

how much of a drug is needed to cause an effect

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14
Q

define effiacy

A

degree of effect a drug can have

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15
Q

which routes can you give opioids in?

A

IV
IM
SC
oral
epidural
spinal
transmucosal

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16
Q

which routes of drug admin are most effective?

A

those that result in the drug being in the blood stream, rather than the GI system or liver

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17
Q

state advantages of IV admin of opioids

A

rapid onset of action
reliable uptake
painless irrespective of volume

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18
Q

state disadvantages of IV admin of opioids

A

need IV access
cant use for pethidine as causes allergic reaction

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19
Q

state advantage of IM opioid admin

A

reliable uptake

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20
Q

state disadvantage of IM opioid admin

A

painful if large volume

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21
Q

state advantage of SC and OTM opioid admin

A

easy to do

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22
Q

state disadvantage of SC opioid admin

A

unreliable uptake

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23
Q

state disadvantage of OTM opioid admin

A

only certain ones licenced
cat and bupe

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24
Q

what are the advantages and disadvantages of transdermal opioid admin?

A

good for chronic use
no products licenced

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25
Q

what are advantages and disadvantages of epidural/spinal opioid admin?

A

effective analgesia intraop
non licenced and hard to do

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26
Q

what are the main uses of opioids?

A

preventative, multi-modal and peri-op analgesia

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27
Q

why are opioids not given for chronic pain?

A

poor oral bioavailability so not in tablet form for veterinary - significant first pass metabolism in liver
sedative effects

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28
Q

why are opioids not ideal for neuropathic pain?

A

damaged nerves release cholecystokinin which antagonises opioids

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29
Q

list pharmacological effects of opioids

A

analgesia
sedation
excitation (especially high dose, pain free animals)
bradycardia (vagal effect, mainly in GA)
nausea and vomiting (more if pain free)
antitussive
decreased GI motility (chronic use)
urinary effects (altered frequency, difficultly urinating)
miosis in dogs
mydriasis in cats

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30
Q

what makes opioids safe drugs?

A

wide dose ranges
side effects relate to potency
side effects less likely when painful
naloxone can be used

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31
Q

name the 3 families of opioid peptides/neurotransmitters

A

beta-endorphin
leucine-enkephalins and methionine-enkephalins
dynorphins

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32
Q

list the types of opioid receptors

A

mu
kappa
delta
NOP

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33
Q

where are opioid receptors found?

A

brain and spinal cord

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34
Q

NOP receptors key info

A

bind to nociceptin
recent discovery so limited knowledge

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35
Q

where are delta receptors found?

A

brain and peripheral sensory neurones

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36
Q

list effects from delta receptors

A

analgesia
anti depressant
convulsant
dependence
respiratory depression

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37
Q

where are kappa and mu receptors found?

A

brain
spinal cord
peripheral sensory neurones

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38
Q

list effects from kappa receptors

A

analgesia
anti-convulsant
depression
hallucination
diuresis (excess urine production)
miosis
dysphoria
neuroprotection
sedation
stress

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39
Q

list effects from mu 1 receptors

A

analgesia
dependence

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40
Q

list effects from mu 2 receptors

A

respiratory depression
miosis
euphoria
reduced Gi motility
dependence

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41
Q

list the function from mu 3 receptors

A

vasodilation

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42
Q

why do full agonists provide the most effective analgesia?

A

bind and activate receptor with maximum response an agonist can cause at the receptor

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43
Q

why do partial agonists provide less analgesia than full?

A

only give partial efficacy even if are bound to all receptors

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44
Q

what affects onset of action of opioids?

A

route of admin
time to receptors
how much drug binding is needed for some effect

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45
Q

when does peak effect occur?

A

when all the drug is on the receptors

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46
Q

what determines how long drug effects last?

A

speed of removal

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47
Q

what measures can increase duration of action?

A

higher dose
adding vasoconstrictors

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48
Q

name ultra-short acting opioid

A

fentanyl

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49
Q

how long do ultra-short acting drugs last and what are they used for?

A

20 minutes
intra-op pain, short term infusions

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50
Q

name short acting opioids

A

butorphanol
pethidine

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51
Q

how long do short acting opioids last and what are they used for?

A

2 hours
pain management, multi-modal analgesia, pre-med and sedation

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52
Q

name medium acting opioids

A

methadone
morphine

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53
Q

how long do medium acting opioids last and what are their uses?

A

2-4 hours
pain management, multi-modal analgesia

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54
Q

name longer acting opioid

A

buprenorphine

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55
Q

how long does longer acting opioids last and whats it used for?

A

6 hours
pain management

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56
Q

what are some opioid misconceptions?

A

cause mania in cats - only in very high doses in pain free animals
cant redose until duration of action up - if effect worn off can redose
respiratory depression - mainly in GA patients but control of airway so not problem
cant combine - work well with NSAIDs, LAs, ketamine, alpha 2s

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57
Q

what drugs would you not combine with opioids?

A

other opioids
tramadol - acts on opioid receptors

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58
Q

list opioids most to least efficacy

A

fentanyl
methadone/morphine
pethidine
buprenorphine
butorphanol

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59
Q

what are side effects to fenanyl?

A

respiratory depression
bradycardia

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60
Q

what are benefits to methadone compared to morphine?

A

less nausea and vomiting
no histamine release if IV admin
minimial CVS and respiratory effects

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61
Q

why should you be careful if giving methadone CRI?

A

accumulative effects

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62
Q

why is pethidine not ideal?

A

short acting
large volume so painful IM
histamine release if IV

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63
Q

what are negatives of buprenorphine?

A

may sting due to preservative
not v effective SC
delayed onset of action

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64
Q

what are negatives of butorphanol?

A

low analgesia effects, is more sedative
short acting
need higher doses than normally given

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65
Q

how do LAs stop pain?

A

enter nerve fibres and bind and block voltage-operated Na channels which blocks nerve conductions

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66
Q

describe how action potentials are generated

A

cell body is depolarised causing more na to move inot cell than k leaving through voltage gated sodium channels
casues mrore voltage gated sodium channels to open and more sodium to move in
ap generated when threshold reached

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67
Q

describe how resting membrane potentials happen

A

more sodium ions outside cell and more potassium ions inside of cell
k leaks out of k leakage channels and na leaks in through na leakage channels
na-k pump moves k back in and na back out

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68
Q

how does repolarisation of cells happen?

A

sodium channels inactivate and k channels open

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69
Q

where are voltage gated sodium channels found?

A

all excitable tissues - muscles and heart

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70
Q

in what order do LAs block things in the body?

A

nociception
proprioception
mechanoreception
motor function

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71
Q

list types of nerves in the body

A

Motor (Aα, Aβ, Aγ)
Sensory (Proprioceptors Aα, Aβ, Mechanoreceptors Aβ, Aδ, Nociceptors Aδ,C)
Autonomic (preganglionic B, postganglionic C)

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72
Q

what features of axons make them more resistant to LAs?

A

larger diameter
more heavily myelinated

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73
Q

why are Aδ and C fibres more suceptible to LAs and what is the result?

A

Aδ - very thin myelination
C - no myelination
nociception blocked first so pain relief without loss of feeling or movement

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74
Q

are LAs acids or bases?

A

weak bases

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75
Q

which form of LA can penetrate nerve cells lipid membranes?

A

uncharged

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76
Q

what determines proportion of uncharged LA?

A

pH
pKa - pKa = pH + log [BH+ ]/[B]
handerson hasslbalch equation - B + H= BH+

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77
Q

describe the effect of onset of LA action at higher pKa

A

at higher pKa (same pH) more of the drug is ionised so onset is slower as less drug is available

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78
Q

how does inflammation affect action of LAs?

A

pH decreases in inflammation so more drug ionised and less available to penetrate nerve fibres so less effective

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79
Q

which drug is an ester (LA)?

A

procaine
no i before caine

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80
Q

list features of ester LAs

A

relatively unstable
rapid breakdown by pseudocholinesterase
PABA formed as hydrolysis product - can cause allergic reaction
short plasma half life

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81
Q

which drugs are amides?

A

lidocaine, bupivacaine
i in name before caine

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82
Q

list features of amide LAs

A

broken down by cytochrome P450 enzymes in liver - drugs affecting this enzyme effect drug breakdown
more stable
biotransformed in liver
longer half life

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83
Q

which drugs increase and decrease breakdown of cytochrome P450 enzyme?

A

increase - barbiturates
decrease - midazolam

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84
Q

list body systems that can be effected by LAs

A

CVS
CNS

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85
Q

list CVS effects from LAs

A

heart pumps less efficiently
hypotension - decresed myocardial contractility, relaxion of smooth vascular muscles, loss of vasomotor sympathetic tone
dysrhythmias - rapid entry to open na channels in systole and remains bound in diastole

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86
Q

list CNS effects from LAs

A

behaviour change
muscle twitching
tremors
tonic-clonic seizures
CNS depression
respiratory depression
death
seen at lower doses

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87
Q

what casues LA toxicity to increase?

A

potency increases
dose increases

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88
Q

what can you do to prevent LA toxicity?

A

not exceed maximum dose
dilute small volumes
accurately draw up
aspirate before injection

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89
Q

how is LA toxicity treated and why?

A

symptomatic as no reversals

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90
Q

when are LAs used?

A

multi-modal analgesia
post-op pain management
desensitisation - IV and intubation

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91
Q

define epidural

A

anaesthetic injected into epidural space

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92
Q

define spinal

A

anaesthetic injected into csf

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93
Q

list LAs from most to least potent

A

bupivacaine
ropivacaine
lidocaine
procaine

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94
Q

how is duration of action of LAs effected?

A

lipid solubility
strength of binding to channels
speed of removal - tissue perfusion, vasoconstriction
metabolism - amide vs ester

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95
Q

what forms can LAs come in?

A

sprays
patches
sterile solutions for injection

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96
Q

why can LAs cause stinging on injection?

A

poorly water soluble so made into salt solution but this lowers pH

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97
Q

why is glucose added to LAs?

A

increase baricity to prevent spreading too high in epidural space

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98
Q

what are the benefits of adrenaline being added to LAs?

A

causes vasoconstriction which reduces systemic absorption, prolongs action and reduces toxicity as less spread

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99
Q

how does plasma protein binding affect LA toxicity?

A

higher binding means lower toxicity as less unbound and active

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100
Q

what alters amount of plasma protein binding in LAs?

A

type of drug
lower pH lowers protien binding

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101
Q

what species is lidocaine licenced for?

A

dogs
cats
horses

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102
Q

state onset and duration of action of lidocaine

A

2-5 minute onset
20-40 minute duration

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103
Q

are bupivacaine and EMLA licenced in veterinary?

A

no

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104
Q

how long is bupivacaine duration of action?

A

6 hours

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105
Q

does lidocaine or bupivacaine have higher cardiotoxicity

A

bupivacaine

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106
Q

what drugs are in emla?

A

lidocaine and prilocaine

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107
Q

how long does emla take to have an effect?

A

30-45 minutes

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108
Q

what blocks are VNs not allowed to perform?

A

anything entering body cavity such as epidural

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109
Q

list side effects of epidural

A

hypotension
hypothermia
urinary retention
infection

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110
Q

when cant you do an epidural?

A

sepsis
skin infection
coagulation issues
hard when obese or pregnant

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111
Q

define local LA

A

blocking around small area

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112
Q

define regional LA

A

blocking larger area

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113
Q

list examples of local/regional LA

A

opthalamic
dental
limb block

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114
Q

list types of infiltration block

A

testicular
ovarian ligament
incisional line block
intraperitoneal

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115
Q

how are infiltration blocks done?

A

in v-shape or inverse pyramid

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116
Q

how do NSAIDs work?

A

inhibits COX which inhibits prostaglandin production (inflammatory mediators)

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117
Q

where do NSAIDs work?

A

periphery, some central

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118
Q

what leads to side effects from NSAID use?

A

relate to protective effects of prostaglandins
how easily NSAIDs can leave the circulation and enter tissues

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119
Q

how do prostaglandins occur in the body (cox-1 and cox-2)?

A

cox-1 - constituative or protective functions
cox-2 - induced by inflammation

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120
Q

which nsaids block both types of cox and which are specific to cox-2?

A

both - aspirin, flunixin
cox-2 - meloxicam, carprofen

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121
Q

which is nsaid selectivity to cox-2 beneficial?

A

reduces side effects

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122
Q

list side effects of nsaid use

A

GI ulceration
renal ischemia
water retention
oedema
hypertension
hepatopathy
CNS signs (cats)
haematostasis

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123
Q

how do nsaids cause GI ulceration?

A

prostaglandins maintain mucosal blood flow, bicarbonate and mucosal secretion and epithelialisation

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124
Q

how do nsaids lead to renal ischemia?

A

prostaglandins protect and maintain renal blood flow in hypotension, regulate GFR, renin release and sodium excretion

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125
Q

list how to minimise nsaid side effects

A

dont exceed dose
only give 1 type of nsaid
dont give with corticosteroids
dont give if hypotensive or dehydrated
give with food
care as more at risk if liver disease, geriatric or previous GI ulcers

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126
Q

what are some signs of nsaid adverse effects?

A

vomiting
diarrhoea
blood in faeces
dullness
anorexia

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127
Q

where are nsaids metabolised?

A

liver

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128
Q

why are nsaids often used in OA management?

A

immediate relief when other measures such as weight loss, diet change, supplements, take time

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129
Q

what is gold standard to do before starting nsaids?

A

clinical exam
biochem
haematology
urinalysis
BP

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130
Q

how should nsaid use be montiored?

A

review 2 weeks after starting
regularly recheck parameters 3-6months or more often

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131
Q

what is meant by NSAID cycling?

A

changing to a different nsaid if having side effects or no longer effective

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132
Q

when can and cant paracetamol be used?

A

instead of nsaid if contraindicated
not in cats as toxic

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133
Q

how is tramodol used and why?

A

in multimodal analgesia as limited efficacy alone

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134
Q

how does gabapentin work?

A

binds voltage gated calcium channels to decrease excitatory neurotransmitter release in spinal cord

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135
Q

when is gabapentin used?

A

manage neuropathic pain?
multimodal analgesia
when nsaids contraindicated

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136
Q

what are negatives of gaba?

A

highly sedative
need to be weaned off

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137
Q

where does tramadol act?

A

centrally

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138
Q

how is amantadine used and why?

A

with other analgesics as is antihyperalgesic
chronic pain

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139
Q

what are downsides to amantadine?

A

takes weeks to see benefit

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140
Q

how is amantadine metabolised?

A

kidneys

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141
Q

what makes pregabalin different to gaba?

A

better oral bioavailability
longer half life
limited evidence

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142
Q

list drug types that can cause muscle relaxation

A

LA
benzodiazepine
alpha 2 agonist
guaiphenesin (horses)
NMB

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143
Q

why is ketamine given with alpha 2 or benzo?

A

ketamine alone causes muscle rigidity

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144
Q

why are NMBs not commonly used for procedures?

A

pre-med, induction and mantainance agents provide generally enough muscle relaxation

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145
Q

where does guaiphenesin/GGE act?

A

centrally on spinal cord, brain stem and subcortical brain

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146
Q

when is GGE used in horses?

A

after ketamine to counteract rigidity
part of triple combo - ket, alpha 2, GGE for GA maintainance

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147
Q

what are the negatives of GGE?

A

no analgesia or anaesthetic properties
causes haemolysis over 10% concentration
causes tissue damage if perivascular

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148
Q

list indications of NMB use

A

relax muscles for surgical use
control ventilation
aid intubation in cats
ophthalmic surgery for central eye
assist joint/fracture reduction
reduce anaesthetic agent needed

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149
Q

do NMBs provide analgesia or anaesthetic?

A

no

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150
Q

describe how the NMJ casues muscle contraction and relaxation

A

acetylcholine is released from nerve endings and binds to post-synaptic nicotinic receptor on muscle cell
muscle contracts when 2 subunits bind
acetylcholinesterase hydrolysed ACh in synaptic cleft for muscle relaxation

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151
Q

what is one thing you must do for patients if using NMB?

A

intubate and IPPV

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152
Q

list in order from most to least sensitive muscles are to NMBs

A

peripheral to central
intercostals and diaphragm last to be effected

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153
Q

name the depolarising muscle relaxant

A

suxamethonium

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154
Q

how does suxamethonium work as a NMB?

A

acts like acetylcholine, diffuses into NMJ and binds to receptors causing initial muscle contraction
not broken down by acetylcholinesterase so needs to diffuse out making longer lasting
broken down by plasma cholinesterase

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155
Q

how long does suxamethonium cause effect in cats and dogs?

A

cats - 3-5 min
dogs - 20 min

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156
Q

what are negatives of suxmthonium?

A

can only give one dose as causes prolonged block
short acting
can trigger malignant hyperthermia
increases serum potassium
care in burn patients

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157
Q

name the 2 most common non-depolarising muscle relaxants

A

atracurium
vecuronium

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158
Q

name less common non-depolarising muscle relaxants

A

rocuronium
mivacurium
pancuronium

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159
Q

how do non-depolarising muscle relaxants work?

A

compete with acetylcholine for post-binding junction sites

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160
Q

what are benefits to non-depolarising muscle relaxants?

A

no initial muscle contraction
can top up with 1/3 initial dose
can antagonise
last upto 40 minutes

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161
Q

which type of muscle relaxant has faster onset of action?

A

depolarising

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162
Q

state features of atracurium

A

bis-isoquinolinium compound
10 isomers but only cisatacurinum is active
some hepatically metabolised, the rest undergoes hoffman elimination (temperature dependent reaction in plasma)
needs slow IV admin to prevent histamine release

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163
Q

state features of vecuronium

A

steroid compound, no corticosteroid effects
no histamine release
40-50% hepatic biotransformation
in powder form, stable 24hrs post reconstitution

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163
Q

list key monitoring considerations during NMB use

A

ventilation
tube patency
thoracic wall movement
ETCO2
SpO2

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164
Q

why is it hard to monitor depth when using MNB?

A

most reflexes lost

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165
Q

list signs of light depth when using NMB

A

tachycardia
hypertension
salivation
lacrimation
vasovagal response - bradycardia, hypotension, pallor
increased ETCO2
pupil dilation

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166
Q

describe how to monitor degree of NMB

A

use peripheral nerve stimulator on ulnar, peroneal or facial nerves
train of 4 - 4 impulses applied to nerve over 2 seconds, twitch strength monitored, the more NMB effect, strength decreases across the 4 until no twitch present

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167
Q

what factors effects duration of NMB action?

A

VA
hypothermia and renal/hepatic insufficiency - reduces metabolism
electrolyte/acid base disturbance
muscle disease - myasthenia gravis
aminoglycoside antibiotics - prolong effect
dose given

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168
Q

when can you antagonise non-depolarising NMB?

A

once 1-2 twitches have returned

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169
Q

name NMB antagonists

A

anticholinesterases - neostigmine and edrophonium

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170
Q

how do NMB antagonists work?

A

interfere with acetylcholinesterases so acetylcholine concentration builds up as not being broken down so more is available to compete with NMB agent to bind and cause muscle contraction

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171
Q

list side effects of antagonising NMBs

A

bradycardia
salivation
bronchospasm
diarrhoea

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172
Q

how can side effects of antagonising NMBs be managed?

A

giving IV anticholinergics with the anticholinesterase

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173
Q

describe how you would recover a patient having given a NMB

A

ventilate until return of spontaneous ventilation
monitor for signs of upper respiratory weakness - URT noise, cyanosis, paradoxical breathing

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174
Q

describe negative pressure ventilation and when its seen

A

spontaneous breathing, most anaesthetics
air drawn in by negative pressure

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175
Q

describe positive pressure ventilation

A

forcing air in, mechanical or manual

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176
Q

list factors that affect and compromise spontaneous ventilation

A

anatomical - airway obstruction, stenotic nares, excess tissue, hypoplastic trachea, obesity
external - ETT size, external restriction
internal - effusions

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177
Q

list indications for assisting ventilation

A

reduced ventilation drive
inability to ventilate effectively

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178
Q

list causes of delayed ventilatory drive

A

anaesthetic drugs
increased ICP
encephalopathy
hypothermia

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179
Q

list causes of inability to ventilate

A

open thoracic cavity
muscle failure - NMB, myasthenia gravis
intercostal or diaphragmatic nerve failure
external factors affecting lung inflation

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180
Q

list parameters to indicate needing to ventilate a patient

A

ventilatory pattern
spirometry/tidal and minute volume
blood gases
ETCO2
pulse ox

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181
Q

what are the advantages of manual ventilation?

A

easy to perform
cheap

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182
Q

what are disadvantages of manual ventilation?

A

operator dependent
poor airway pressure control
each breath can be different
boring and time consuming

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183
Q

what are advantages of mechanical ventilation?

A

hands free anaesthetic
appropriate and consistent gas volumes delivered

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184
Q

what are disadvantages of mechanical ventilation?

A

not always available
expensive
requires skill

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185
Q

describe how ventilation effects patients CO

A

positive pressure forced into lungs which exerts pressure on the vena cava in lung expansion so decreased venous return to the heart

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186
Q

list potential side effects of IPPV

A

decreased CO, VR, SV, pre-load and BP causing renal and hepatic perfusion issues
barotrauma - overexpansion of the lungs
sheer stress effect/volutrauma - lung overdistension
oxygen toxicity

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187
Q

when does oxygen toxicity occur?

A

if on 100% over 6 hours as free radicals form causing damage

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188
Q

what observations do you make to monitor effective ventilation?

A

thoracic movement
abdominal movement
auscultation
capnography
pulse ox
art blood gas - PaO2, PaCO2

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189
Q

what would you do if ETCO2 was high?

A

increase ventilation

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190
Q

what would you do if high PaCO2?

A

increase ventilation

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191
Q

what would you do if low PaO2?

A

increase oxygen

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192
Q

what is a ventilator?

A

machine designed to provide mechanical ventilation to a patient by moving air in and out of the lungs

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193
Q

what are common cases that need ventilating?

A

apnoea
NMBs
thoracotomy
diaphragmatic rupture

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194
Q

list settings on ventilators

A

frequency of breaths
tidal/minute volume
I:E ratio
inspiratory flow rate
PIP
PEEP

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195
Q

define PIP

A

peak inspiratory pressure
highest pressure measured during the respiratory cycle

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196
Q

define PEEP

A

positive end pressure ventilation
pressure applied by ventilator at end of each breath to ensure alveoli are not prone to collapse

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197
Q

what are common settings for PIP and when would they be adjusted?

A

8-12H2O
adapt if open or closed thorax, increase if recruitment

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198
Q

what is meant by cycling in ventilation?

A

change from inspiration to expiration

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199
Q

what is meant by cycling variables in ventilation?

A

how and when ventilator moves from inspiration to expiration

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200
Q

list cycling variables in ventilation

A

pressure
volume
time
flow

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201
Q

describe pressure cycling

A

ventilator delivers inspiratory gas until certain pressure is reached and expiratory stage begins

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202
Q

when would you not use pressure cycling in ventilation?

A

if lung compliance changes such as open chest a much larger volume of gas is needed to trigger pressure causing over inflation of the lungs

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203
Q

describe how volume controlled cycling works

A

tidal volume is set based on 10-15ml/kg
pressure limit determined by case and rate
I:E set
start and check expansion/TV and CO2 to ensure right volumes being delivered

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204
Q

what safety measure is in place in for volume controlled cycling?

A

pressure cut off to avoid over inflation

205
Q

describe how time controlled cycling works

A

switches from inspiration to expiration after certain time based on RR, inspiratory time or I:E ratio

206
Q

how does flow cycling work?

A

ventilator delivers set flow until total volume is delivered

207
Q

what is the difference between assist control and control mode ventilation?

A

assist control - breath initiated with patient
control - breath controlled by machine

208
Q

what is normal I:E ratio and RR as a result?

A

I:E 1:2
RR 20

209
Q

list types of ventilators

A

bag squeezer - ascending, descending, horizontal below
mechanical thumb
intermittent blower
volume divider

210
Q

describe features of bag squeezer vent

A

bellow connected to bag port
sets volume and I:E
pressure gauge
set TV and inspiratory time which works out RR

211
Q

list types of bag squeezer

A

hallowell EMC 2000 - time cycle, pressure limited
JD medical - equine, pressure cycled and pressure limited

212
Q

when is mechanical thumb vent used?

A

in small animals

212
Q

how do intermittent blowers work?

A

divides driving gas into smaller volumes and pushes into patient

213
Q

list types of intermittent blower

A

merlin - microprocessor, can set time, pressure or volume
nuffield - time cycled, set inspiratory time and flow

214
Q

how does minute volume divider work?

A

collects continuous flow of gas into the reservoir and delivers to patient under positive pressure with flow rate being MV divided by RR
has high FGF

215
Q

state type of minute volume divider

A

manley MP3 - has main bellow, volume triggered, can set TV and inspiratory time

216
Q

list patient considerations for those on long term ventilation

A

mouth care - gets very dry
humidify cold and dry gases
ETT care - suction, uncuff and reposition to move pressure in trachea
monitor ventilation
periodic sigh to open end parts of lungs
physiotherapy
turning patient
eye care
manage excretions

217
Q

what is the purpose of blood gas analysis?

A

measure partial pressure of gases in the blood
pH analysis

218
Q

define an acid

A

proton donor

219
Q

define a base

A

proton acceptor

220
Q

what is the equation for pH?

A

pH = -log10[H+]

221
Q

what is normal pH?

A

7.4 in range 7.35-7.45

222
Q

what is the effect of pH being outside normal ranges?

A

enzyme changes which effects metabolism

223
Q

what is the relationship between pH and [H+]?

A

as pH decreases [H+] increases

224
Q

why is pH important in the body?

A

effects rate of enzymatic reactions
impacts physiology

225
Q

how does pH in the body get altered?

A

diseases
drugs
fluids

226
Q

when will pH levels cause death?

A

less than 6.8 or more than 7.6

227
Q

how does the body stay electroneutral?

A

lots of ions present with all charges adding to zero
water generates H+ ions t balance any charge differences

228
Q

define acidaemia

A

pH less than 7.35 in the blood

229
Q

define alkalaemia

A

pH more than 7.45 in the blood

230
Q

how is normal pH maintained?

A

buffers
respiratory system
renal system

231
Q

define a buffer

A

any particle capable of accepting or donating H+ to minimise pH changes
fast acting

232
Q

list buffers

A

bicarbonate
haemoglobin
blood proteins
phosphate
lactate

233
Q

what is the henderson hasselbalch equation?

A

pH = pKa + log10[HCO3-]/[0.3pCO2]

234
Q

what does the henderson hasselbalch equation mean for the body?

A

pH, bicarbonate and PP CO2 determined by metabolic and respiratory components

235
Q

how does respiratory effects change pH?

A

change in PCO2 changes pH

236
Q

how does metabolic effects change pH?

A

change of anything that can affect pH, usually bicarbonate due to buffering other acids

237
Q

what is the relationship of PaCO2 and ventilation?

A

inversely proportional
hyperventilation decreases PaCO2
hypoventilation increases PaCO2

238
Q

what is the equation for bicarbonate acting as a buffer?

A

H2O + CO2 <> H2CO3 <> H+ + HCO3-

239
Q

how does the respiratory system respond in respond in response to pH changes?

A

rapidly changes PaCO2

240
Q

how does the renal system work to maintain pH?

A

major way of excess acid removal
regulation of bicarbonate and ions
slow to work over hours and days

241
Q

define acute respiratory acidosis

A

increased PCO2 from hypoventilation

242
Q

what is the compensatory mechanism for acute respiratory acidosis?

A

increasing bicarbonate

243
Q

what are the compensatory mechanisms for chronic respiratory acidosis?

A

kidneys excrete acid and bicarbonate is retained

244
Q

define respiratory alkalosis

A

fall in PCO2 from hyperventilation

245
Q

what are the compensatory mechanisms for respiratory alkalosis?

A

metabolic compensation with bicarbonate

246
Q

define metabolic acidosis

A

decreased bicarbonate due to loss or consumption by excess acid

247
Q

how is metabolic acidosis compensated?

A

increase ventilation to reduce PCO2

248
Q

define metabolic alkalosis

A

increased bicarbonate due to loss of chlorine ions or albumin

249
Q

how is metabolic alkalosis compensated?

A

decrease ventilation to increase PCO2

250
Q

define base excess

A

amount of acid to titrate 1L of blood to pH 7.4 at 37 degrees and PaCO2 of 40mmHg

251
Q

how does base excess allow identification of pH change?

A

it fixes PaCO2 to 40mmHg so any other pH change is due to metabolic processes

252
Q

what is normal arterial and venous PCO2?

A

arterial - 40mmHg
venous - 44mmHg

253
Q

what is normal bicarbonate levels in the blood?

A

24mmol/l

254
Q

what is normal base excess in the blood?

A

4mmol/l

255
Q

what is normal arterial and venous blood oxygen levels?

A

arterial - 90-100mmHg
venous - 40-50mmHg

256
Q

how does PaO2 and FiO2 link?

A

PaO2 = 5xFiO2

257
Q

define hypoxamia

A

less than 80mmHg (arterial)

258
Q

what would you expect normal PaO2 to be under GA and why?

A

400-500mmHg as you give 100% oxygen

259
Q

what parameters do blood gas machines measure?

A

electrolytes
lactate
haematocrit
glucose
blood gases

260
Q

where should you take samples from for acid-base balance?

A

arterial or venous

261
Q

where should you take samples from for gas exchange?

A

arterial

262
Q

what syringes can be used for blood gas samples?

A

heparinised impermeable glass if storing (on ice)
heparinised plastic if short term

263
Q

describe how to handle samples

A

roll to prevent clotting
discard first drop as likely clotted

264
Q

what can be the consequence if blood gas sample analysis is delayed?

A

gas can diffuse in and out of the sample

265
Q

what is the result of air contamination on blood gas analysis?

A

CO2 low as diffuses out
O2 closer to 150mmHg

266
Q

how does saline contamination occur and what is the effects on blood gas?

A

sampling from catheters
high chloride

267
Q

what is the effect of clotting on blood gases?

A

low PCV
low haematocrit

268
Q

what is the normal anion gap value?

A

15-25mmol/l

269
Q

what causes increased anion gap?

A

lactic acidosis
ketoacidosis

270
Q

what causes decreased anion gap?

A

hypoproteinaemia

271
Q

what doesent effect anion gap?

A

GI bicarbonate loss

272
Q

how are the contents of the intercranial cavity distributed?

A

80% brain
10% CSF
10% blood

273
Q

what can affect the BBB?

A

trauma
inflammation
hypertension

274
Q

why does the brain receive 15% CO?

A

is very highly metabolic

275
Q

why does an increase in CSF or blood increase ICP?

A

the skull cant expand

276
Q

what is normal ICP?

A

5-12mmHg

277
Q

what are clinical signs of raised ICP?

A

papilledema (optic disk swelling)
pulsing of retinal vessels
depression
stupor (unconscious/unresponsive)
coma

278
Q

what are the aims when anaesthetising neuro patients?

A

maintain cerebral blood flow
minimise increases in ICP

279
Q

when does the cushing reflex occur?

A

in response to increased ICP

280
Q

describe the cushings reflex

A

reduced blood flow causes CO2 accumulation which is detected by the brain stem and SNS
responds by increasing MAP
baroreceptors detect this causing reflex bradycardia
apnoea and irregular breathing may be seen

281
Q

what is the purpose of the cushings reflex?

A

decrease ICP by reducing blood entering the brain

282
Q

what are considerations to control ICP?

A

minimise pressure on the neck
no coughing
harness
care on intubation that deep enough
no neck restraint
no jugular samples
no vomiting
no straining to toilet

283
Q

what are general conditions for neurological anaesthesia cases?

A

pre-op assessment - bloods, glucose, electrolytes, PCV
MGCS
stabilise prior to GA
care with drugs
pre-oxygenate
use sevo - iso may slightly increase ICP
BP and capnography monitoring
normocapnia - high CO2 vasodilates
IVFT - careful
mild head elevation for venous drainage
seizure monitoring

284
Q

what are aims when choosing drugs for neuro patients?

A

not increase ICP or change MAP

285
Q

why are opioids a good choice for neurological patients?

A

dont alter CBF or ICP
minimal CV and respiratory depression

286
Q

why is morphine not ideal for neurological patients?

A

can cause vomiting

287
Q

what are the benefits of benzodiazepines in neurological patients?

A

no effects on ICP, respiration or CV system
may reduce anxiety

288
Q

why would you not use ACP in neurological patients?

A

may trigger seizures in patients with intercranial pathology
causes vasodilation leading to hypotension and cerebral vasodilation causing increased ICP

289
Q

why would you not use alpha-2s in neuro patients despite not affecting ICP?

A

cardiopulmonary effects
increases MAP and bradycardia which masks cushings reflex making obs harder
can cause vomiting in cats

290
Q

why may ketamine be used in neuro patients?

A

doesnt effect ICP when combined with other sedatives
possibly neuroprotective and have fewer CV effects and resp effects
reduce ICP when given with propofol

291
Q

what are reasons for GA in neuro patients?

A

imaging
CSF tap
spinal surgery
other treatment

292
Q

what are patient considerations for MRI?

A

position - straight, lots of padding, elevate head
safety - often outside so less access to staff, harder to maintain temperature, no metal, remote monitoring
equipment - very expensive for special MRI safe equipment

293
Q

where are CSF taps normally done?

A

lumbar
cisterna magna

294
Q

what are considerations of cisterna magna positioning?

A

neck needs to be bent chin to chest so ETT may be compromised
may seizure in recovery so keep head elevated

295
Q

what are intubation considerations for neuro patients?

A

laterally intubate
depth adequate for intubation
armoured ETT for cisterna tap

296
Q

how do you manage seizure patients?

A

consider medication - current or starting
treat if will increase ICP
place IV
close monitoring pre- and post-ga - capnograph and BP
seizure plan in place

297
Q

what are considerations for neuromuscular disease patients?

A

pre-disposed to regurg and aspiration
monitor gag reflex
monitor capnography in case need to ventilate due to respiratory muscles affected
rapid intubation and recovery for patent airway

298
Q

what are common GI procedures?

A

abdominal surgery
FB removal
GDV
pre-existing conditions
endoscopy

299
Q

what are considerations for planned GI surgery?

A

stabilise patient - may be anorexic, dehydrated, acid base disturbances
risk of reflux and aspiration
pain
avoid drugs that induce vomiting
pre-oxygenate
elevate head until ETT cuffed
likely hypothermic

300
Q

considerations for emergency GI surgery

A

likely shocked
IV access vital
large volume fluid therapy
stabilise to improve CV and pulmonary function as long as quick
ventricular arrythmia common
decompress stomach if GDV

301
Q

what complications are commonly seen in GDV surgery?

A

ventilation affected due to pressure on the diaphragm from abdomen
electrolyte, acid base and clotting abnormalities
pneumothorax potentially post-op if diaphragm damaged
poor perfusion with good BP

302
Q

why can BP look normal in GDV patients when they are not perfusing well?

A

SVR is increased due to restriction of blood return to the heart which compensates for CO decrease from hypovolaemia and dehydration

303
Q

what are post-op considerations for GDV patients?

A

intensive care needed
analgesia

304
Q

list functions of the liver

A

produce urea, clotting factors and albumin
excretion of billirubin
biotransformation of drugs/toxins
metabolism of protien, carbs and fat
glucose haemostasis - glycogen storage and gluconeogenesis
heat production - high metabolic rate

305
Q

list examples of liver dysfunction

A

porto-systemic shunt
billiary obstruction/trauma
chronic disease
acute failure
neoplasia

306
Q

list signs of hepatic dysfunction

A

ascites/oedema - due to hypoproteinaemia and hypoalbuminaemia
PUPD
anaemia
hypocalcaemia
hypoglycaemia
hypothermia
reduced clotting times
acid base disturbances
jaundice
encephalopathy

307
Q

define hepatic encephalopathy

A

neurological abnormalities occurring due to hepatic disease

308
Q

what is the effect of hepatic encephalopathy on the body?

A

increased toxins and ammonia due to liver not processing them

309
Q

what is stage 1 encephalopathy signs?

A

mild confusion
inappetence
decreased attention
dullness
irritability

310
Q

what are signs of stage 2 encephalopathy?

A

drowsiness
lethargy
personality change
disorientation
apparent blindness

311
Q

what are signs of stage 3 encephalopathy?

A

very drowsy
confusion
uncontrolled behaviour
seizures

312
Q

what are signs of stage 4 encephalopathy?

A

recumbence
unarousable
coma
death

313
Q

how is hepatic encephalopathy treated?

A

reduce ammonia levels in the blood by absorption or reduction
using lactulose, which is transformed by colonic bacteria to organic acids which traps ammonia ions and decreases its absorption

314
Q

how does hepatic dysfunction affect anaesthesia?

A

hypothermia - liver produces lots of heat
hypoglycaemia - altered glycogen processes
low albumin meaning reduced protein binding of drugs - overdose
low albumin reducing oncotic pressure of blood causing oedema
slower biotransformation of bloods - longer drug effects
coagulopathies
electrolyte imbalances - sodium retention and lower potassium

315
Q

list considerations for hepatic patients undergoing GA

A

stabilise
minimal drugs - care with doses
slow titrated induction
analgesia
temperature
BG monitoring
consider coagulopathies

316
Q

what considerations should be in place for managing patients with coagulopathies?

A

peripheral veins
pressure after bloods and IVs
no rough handling
avoid trauma
calm recovery to protect wounds

317
Q

which pre-GA labs are recommended for hepatic patients?

A

liver enzymes
bile acids
clotting factors
urea
plasma protiens
glucose

318
Q

what is an insulinoma?

A

pancreatic islet cell tumour

319
Q

what is the effect of an insulinoma?

A

overproduction of insulin causing hypoglycaemia

320
Q

how is insulinoma treated?

A

prednisolone
diazoxide
glucose
care of other drugs being used
surgery

321
Q

what surgery can be done for insulinoma?

A

laparotomy partial pancreatectomy

322
Q

what are post op considerations for partial pancreatectomy?

A

pancreatitis
pain
hyperglycaemia
possible post-op diabetes
BG monitoring

323
Q

what should you do before anaesthetising a diabetic patient?

A

stabilise

324
Q

list symptoms of diabetes mellitus

A

hyperglycaemia
dehydration
weight loss
fatty liver
ketosis

325
Q

what are considerations for nursing patients with diabetes mellitus?

A

learn normal routine
do first op of the day so can go home and eat
monitor BG
insulin as needed

326
Q

what are good protocols for anaesthetising patients with DM?

A

smooth and fast procedure
titrate short acting drugs to effect
good analgesia
no medetomidine - causes hyperglycaemia
IVFT - add glucose if needed
monitor BG
possible second IV for BG samples

327
Q

what is typical signalment of hyperthyroid patients?

A

old cats
multi-organ dysfunction
highly strung
stress intolerable
thin
PUPD
muscle weakness
HCM

328
Q

what are essential steps before anaesthetising hyperthyroid patients?

A

stabilisation
investigation

329
Q

what are good drug protocols to use for hyperthyroid patients?

A

sedate with opioid +/- ACP - if no heart disease
avoid ketamine - increases myocardial workload and HR
avoid medetomidine - drops CO
IV induction if possible - poor muscle mass makes IM harder

330
Q

what are important GA monitoring for hyperthyroid patients?

A

ECG
IVFT

331
Q

what are considerations for during and after thyroidectomy?

A

monitor BP
little access to head
possible post-op laryngeal paralysis
post-op hypocalcaemia
keep IV in patient

332
Q

what is the typical presentation of canine hypothyroidism?

A

elderly dog
megaoesophagus
decreased GI motility
obesity
lethargy
bradycardia
hypotension
slow drug biotransformation

333
Q

list causes of hyperadrenocorticism

A

pituitary or adrenal tumour causing glucocorticoid excess
iatrogenic

334
Q

list signs of hyperadrenocorticism

A

poor muscle tone
overweight
lethargy
poor thermoregulation
bruising
hypercoagulability increasing risk of thromboembolism
PUPD
Na retention
K excretion
wound infection

335
Q

what is the most important considerations of hypoadrenocorticism?

A

avoid stress as dont have normal stress response
stabilise before GA

336
Q

list types of renal disease

A

AKI
CKD
urinary tract obstruction
bladder, urethra or ureter rupture

337
Q

what are effects of renal disease on GA?

A

hypoproteinaemia - increased free fraction of drug due to reduced protein drug binding, decreased oncotic pressure
uraemia - CNS depression
metabolic acidosis - decreased renal drug excretion, myocardial dysfunction
hyperkalaemia - acute where k+ cant escape, chronic where K+ leaks out
anaemia - compromised oxygen carrying capacity

338
Q

list considerations of renal disease patients for GA

A

pre-op bloods to assess kidney function
pre-op fluids
full clinical exam
avoid stress
drug chosen carefully
close monitoring
feed quickly and get home

339
Q

what should you avoid in choosing drugs for renal patients?

A

drugs that affect CVS, renal function or BP

340
Q

what generally increases risks for dental anaesthesia?

A

monitoring of the head is limited
lots of water increases risk of hypothermia and aspiration
commonly at end of day so staff not as on it
often older patients and underlying conditions

341
Q

list considerations for dental patients

A

pain
haemorrhage - unlikely life threatening
hypothermia
aspiration
long procedures
concurrent disease

342
Q

why shouldn’t you do dentals at the same time as other procedures?

A

bacteria from the mouth get aerosolised

343
Q

what are considerations for geriatrics undergoing anaesthesia?

A

have reduced CV reserve and baroreceptor function - prone to hypotension
reduced functional residual capacity - prone to hypoxia
reduced muscle mass
increased fat tissue
prone to hypothermia
reduced kidney and liver function - effect drugs

344
Q

what are baroreceptors?

A

mechanoreceptors detecting BP
causes changes to peripheral resistance and CO to maintain normal BP

345
Q

what is functional residual capacity?

A

volume remaining in the lungs after normal passive exhalation

346
Q

what are pre-op considerations for dental patients?

A

urine and bloods
diagnostics as needed
full clinical exam
may be anorexic from dental disease
concurrent disease
fluid therapy
meds
breathing system

347
Q

what are peri-op considerations for dental patients?

A

analgesia
MAC sparing to maintain BP
local blocks
cuffed ETT
throat pack
maintain body temperature
care with mouth gags especially cats
eye care
haemorrhage

348
Q

what should you do if dental procedures are likely to take too long?

A

stage them over several

349
Q

what type of analgesia is the only one to truely stop pain?

A

nerve blocks

350
Q

why are nerve blocks used for dentals?

A

fully stop pain
reduce VA requirements
manage post-op pain, improving recovery time

351
Q

what areas does an infraorbital/rostral maxillary block?

A

soft tissues
incisor, canine and premolars

352
Q

where do you perform a infraorbital/rostral block?

A

foramen of the maxilla dorsal to 3rd premolar

353
Q

why do you need to be careful when performing intraorbital/rostral maxillary block, especially in cats, small animals or brachycephalics?

A

foramen is found at the level of the eye

354
Q

what areas does the caudal maxillary nerve block block?

A

all bones of maxilla
soft and hard palettes
soft tissue of the nose, upper lip
all teeth rostral to second molar

355
Q

where do you perform a caudal maxillary block?

A

foramen caudal and central to last maxillary molar

356
Q

what areas does the mandibular nerve block block?

A

all teeth of the lower jaw

357
Q

where do you perform a mandibular nerve block?

A

foramen at the ventral angle of the mandible

358
Q

what is the problem with bilateral mandibular nerve blocks?

A

blocks tongue function which can cause problems in recovery

359
Q

what areas does the mental nerve block block?

A

lower incisors
skin and tissues rostral to foramen

360
Q

where do you perform a mental nerve block?

A

foramen found ventral to rostral root of the second premolars

361
Q

why are mental nerve blocks hard to do in small animals?

A

foramen can be hard to find in small animals

362
Q

describe how we prepare for a dental block

A

sterile needle and syringe
calculate maximum LA dose (across all body)
sterile gloves
record admin of LA

363
Q

what are post-op considerations for dental patients?

A

analgesia
warm and dry
clean face
remove mouth gag
get to eat
manage fluids
clear discharge instructions

364
Q

what are reasons for ocular surgery?

A

cataract surgery
enucleation
eyelid mass removal
entropion
cherry eye
trauma

365
Q

what are considerations for before ocular surgery?

A

very painful
potential eye rupture so care with handling and management
underlying disease - likely to have DM unless trauma case
current meds
which procedure

366
Q

what should you do pre-op for ocular surgery?

A

full exam and history
any indicated tests
pre-med
prep eye - not hibiscrub

367
Q

what are peri-op considerations for ocular surgery?

A

avoid further trauma
preserve sight
care with bair hugger near eye
maintain central eye for intraocular procedures
analgesia
manage IOP
care with occulo-cardiac reflex

368
Q

what is normal IOP pressure?

A

15-20mmHg

369
Q

what determines IOP?

A

balance of aqueous humour production and absorption
pupil size
corneoscleral rigidity
extra ocular muscle tone
globe vascularity

370
Q

what happens in acute increases of IOP?

A

damage to the eye

371
Q

how do you manage IOP?

A

maintain normal CO2
avoid coughing on intubation
no straining to toilet
no vomiting, no emetic drugs
avoid ketamine and others that increase IOP
no neck restraint or pressure
keep head elevated

372
Q

what is the occulo-cardiac reflex?

A

sudden bradycardia associated with pressure on the eye or surrounding structures
caused by stimulation of trigeminal and vagal nerves

373
Q

how do you manage occulo-cephalic reflex?

A

stop any surgical manipulation
administer anticholinergics

374
Q

how do you maintain a central eye in surgery?

A

NMBs

375
Q

what analgesia do you use for ocular surgery?

A

multi-modal and preventative
opioids
nsaids
topical local blocks
retrobulbar block

376
Q

what are post op consideration for ocular surgery?

A

analgesia
buster collar
IVFT
general care
no coughing or vomiting
resedate if not calm in recovery

377
Q

what are reasons for airway surgery?

A

BOAS
bronchoscopy
tracheal stenting
laryngeal paralysis
underlying airway disease in other surgeries

378
Q

when is pharyngostomy intubation used?

A

when oratracheal intubation isnt possible
avoid oral cavity

379
Q

what body systems are affected by BOAS?

A

spinal malformations
airway malformations
skin issues
GI system issues

380
Q

list primary abnormalities of BOAS

A

stenotic nares
abnormal nasal turbinates
elongated and thickened soft palette
tracheal hypoplasia

381
Q

how do BOAS dogs compensate and what are the consequences?

A

harder inspiratory pull causing negative pressure in the throat, neck and chest

382
Q

what are secondary BOAS abnormalities?

A

laryngeal collapse
eversion of laryngeal saccules
reflux
regurg

383
Q

what are considerations for BOAS patients?

A

avoid stress
IV access important
constant supervision once sedated as can obstruct and regurg
temperature monitoring
rapid intubation

384
Q

what are good pre-med protocols for BOAS patients?

A

ideally give IV
IM if too stressful
ACP or alpha-2 with opioid

385
Q

how do you manage BOAS patients airways?

A

pre-oxygenate
range of ETT sizes available
cuff tube
suction ready
head down until airway secured

386
Q

what are peri-op considerations for BOAS patients?

A

manage airway
consider ventilation
monitor capnography - likely chronically hypercapnic
pulse ox
ECG
monitor ventilation
avoid hyperthermia
eye care

387
Q

list post-op considerations for BOAS patients

A

close observation
likely will tolerate ETT for long time, keep until swallowing and airway patent
mild sedation if agitated
manage temperature
oxygen
pulse ox
minimise stress
get home quickly
be ready to re intubate

388
Q

what are the benefits of nebulising for BOAS patients?

A

nebulise adrenaline to open airways

389
Q

why may you not give NSAIDs to BOAS patients until they have recovered?

A

may need to give steroids post op to open airways

390
Q

what is the typical patient with laryngeal paralysis?

A

older overweight dogs
large breeds - Labrador
hot weather
distressed

391
Q

how do laryngeal paralysis patients present?

A

stridor
exercise intolerance
panting
coughing
hoarse bark

392
Q

define stridor

A

high pitched breathing sound resulting from airflow through obstructed airway

393
Q

how do you triage suspected laryngeal paralysis?

A

neuro and clinical exam
keep stress free
cool with fan
oxygen
monitor RR
butorphanol to calm and as antitussive
close observations

394
Q

how is laryngeal paralysis managed?

A

weight loss
exercise restriction
owner education
laryngeal tie back/unilateral arytenoid lateralisation

395
Q

list pre-op considerations for laryngeal tie back

A

likely dyspnoeic
sedation may improve breathing
keep cool and calm
care for regurg and aspiration
oxygen
anti-tussives
assess larynx under light GA
pain

396
Q

list post-op care for laryngeal tie back

A

close observation
aspiration pneumonia big risk
pain
nothing around neck
give wet food elevated
keep calm

397
Q

what are reasons for bronchoscopy?

A

chronic cough
lung infection
feline asthma
parasites
aspiration pneumonia
FB
neoplasia

398
Q

list patient considerations for bronchoscopy

A

poor saturation on room air
care on handling
bronchodilator - terbutaline

399
Q

what are pre-op considerations for bronchoscopy patients?

A

history and exam
assess respiratory compromise
rule out cardiac disease
further testing
bloods
x-rays
oxygen
bronchodilators
steroids
anti-tussives
ketamine and propofol are bronchodilatory

400
Q

what are peri-op considerations for bronchoscopy?

A

ETT may not be able to be maintained
ideally use TIVA due to unpredictable gas flow
if big enough ETT scope may fit down
can give flow by oxygen with u cath next to scope but cant full occlude as air needs to come out
protect airway
keep warm
close monitoring

401
Q

what are potential post-op complications of bronchoscopy?

A

hypoxia
bronchoconstriction
desaturation
reduced lung compliance
laryngeal oedema in cats
airway or lung rupture - FB removal or biopsy

402
Q

what equipment do you prepare for bronchoscopy?

A

pre wash scope to compare with patient sample
sterile saline
collection pots
mouth gag
u cath
syringes
emergency box

403
Q

what are considerations for bronchoscopy procedure?

A

lots of people involved for scope, samples, biopsy, monitoring etc
fast
coupage
easy to go wrong

404
Q

what are recovery considerations for bronchoscopy?

A

risky
animal may cough
constant monitoring
head elevated to prevent occlusion
prepare for complications
pulse ox
oxygen
possible pneumothorax

405
Q

what are potential complications of bronchoscopy?

A

haemorrhage in the airways
desaturation
pneumothorax from damaged bronchi

406
Q

why do you need to ventilate patients after opening the thorax?

A

removes negative pressure in the pleural space

407
Q

describe the effect of opening the thorax on the patient

A

when chest wall expands little or no air enters the lungs as the pressure in the lungs is the same as atmospheric pressure
inadequate ventilation and impaired gas exchange
atelectasis occurs, made worse with pressure on lungs or leak checking

408
Q

define atelectasis

A

lung collapse

409
Q

what are the effects of atelectasis?

A

decreased total lung capacity, vital capacity, functional residual capacity
hypoxemia common

410
Q

what is the purpose of functional residual capacity?

A

helps keep airways open
provide reserve of gas exchange

411
Q

what are considerations for thoracic surgery?

A

painful
cause of chronic post-op pain
sternotomy more painful than lateral thoracotomy, thoracoscopy less
thoracoscopy needs gas in thoracic cavity for vision and access so lungs compromises

412
Q

when should you ventilate abdominal approach thoracic patients?

A

as soon as surgery starts not waiting until enter thorax

413
Q

what causes pain in thoracotomys or sternotomys?

A

skin incision
nerve damage
rib retraction
surgical site inflammation
hyperalgesia

414
Q

why is post-op hypoxaemia common in thoracic surgery patients?

A

pain makes patient unwilling to move chest wall so efficiency of ventilation reduced

415
Q

list respiratory conditions needing thoracic surgery

A

lung lobe torsion
bullae
neoplasia
abscess
FB
pre-existing pneumothorax
hypoventilation
hypoxaemia

416
Q

what are considerations for respiratory thoracic surgery?

A

prone to decomposition
keep calm as possible

417
Q

what are cardiac conditions needing thoracic surgery?

A

PDA/patent ductus arteriosis
persistent right aortic arch/PRAA
pericardectomy
heart surgery

418
Q

list considerations for CV thoracic surgery

A

consider CV changes due to manipulation or primary lesion
bleeding
hypotension in PDA
arrhythmia
regurg in PRAA

419
Q

list other types of thoracic surgeries

A

oesophageal FB
thoracic duct ligation

420
Q

what are considerations for other thoracic surgeries?

A

risk of aspiration
regurg
septic complications

421
Q

list pre-op considerations for thoracic surgery

A

prep but may not have a lot of time
risk of bleeding - type and match
hypotension - fluids and drugs planned
hypoventilation
patient specific considerations
equipment
IPPV
art line
blood gas
close monitoring

422
Q

how do you care for patients pre-ga undergoing thoracic surgery?

A

stabilise where possible - chest drain as needed
pre-oxygenate
keep calm
minimise CVS depression
analgesia
no alpha-2s or ACP
only methadone
possibly inotropes

423
Q

what is etomidate?

A

short acting non-barbituate hypnotic drug used to induce man and continuous infusion
causes minimal cardiopulmonary depression
respiratory effects similar to propofol
unlicenced

424
Q

what are the benefits of fentanyl?

A

potent mac sparing - minimises respiratory and CV depression
can be given bolus or CRI

425
Q

what is the onset time and length of action of fentanyl?

A

onset - 5 minutes
duration of action - 20-40 minutes

426
Q

what can you use to allow one lung ventilation?

A

double lumen tube
endobronchial blocker
can use ETT in one lung intubation

427
Q

what are the negatives of using an ETT for one lung ventilation?

A

may not effectively ventilate the lung
risk of contamination between lungs
hard in big dogs due to tube length

428
Q

when do you perform one lung ventilation?

A

when pathology effects only one lung
improve surgical exposure

429
Q

how does an endobronchial blocker work?

A

blocks one of the bronchioles so only one lung is ventilated

430
Q

what are the downsides of using an endobronchial blocker for one lung ventilation?

A

needs bronchoscope to place
high skill needed
expensive
if over inflate can cause bronchial wall damage, or if moving patient and it dislodges

431
Q

what are the negatives of double lumen tube for one lung ventilation?

A

bulky and hard to place
cant do in big dogs due to tube length as are human tubes

432
Q

what are the advantages of double lumen tubes for one lung ventilation?

A

can be done blind
left and right tubes available

433
Q

what are considerations for ventilating thoracic surgery patients?

A

may need NMB
CVS depression can be caused due to decreased venous return so limit I:E to 1:2
trauma caused by baro/volutrauma so limit pressure and volume on chest
care of re expansion pulmonary oedema at the end of surgery so dont over expand lungs especially if collapsed for a long time

434
Q

what ventilatory measure should you monitor when the chest is open and why?

A

PaCO2
ETCO2 and PaCO2 arent consistent with open thorax causing altered ventilation perfusion relationships

435
Q

what is the best way to measure oxygen in thoracic surgery patients?

A

blood gas and PaO2
SpO2 not ideal

436
Q

why is an art line recommended in thoracic surgery?

A

detect hypoxaemia as procedure can cause significant cardiopulmonary disturbances

437
Q

how do you manage hypoxaemia in thoracic patients?

A

100% FiO2
check ETT patency
ensure optimum CVS
check depth of GA
check circulating blood volume
manually ventilate to decrease aletactasis
alveolar recruitment manaouver
introduce PEEP
reduce VA and introduce mac sparing drugs
re-expand collapsed lungs

438
Q

what is the alveolar recruitment manouvure?

A

30cmH2O airway pressure for a breath hold manually

439
Q

what CVS monitoring is in place for thoracic surgery?

A

ECG
art line
BP

440
Q

what other considerations are needed for thoracic pateints?

A

fluid therapy
hypothermia management

441
Q

what analgesia plan shoudl be in place for thoracic patients?

A

aggressive, local and systemic analgesia
full mu agonsit
epidural morphine
intercostal nerve blocks
LA down chest drain
NSAIDs if good BP

442
Q

describe how you would wean a patient off the ventilator following thoracic surgery

A

alveolar recruitment manouvure for pulmonary re expansion
stop IPPV when chest closed and drained or can breathe
support respiration until breathing
slowly decrease IPPV so PaCO2 gradually rises
decrease analgesia and anaesthetics
reverse NMBs

443
Q

how do you recover patients following thoracic surgery?

A

wean on to room air
monitor pulse ox
supplement oxygen
check chest drain
care for oxygen toxicity
fluids
blood transfusion as needed
monitor PCV
check PCV in chest drain for active bleeding

444
Q

what are considerations for elective ortho cases?

A

likely healthy but may have other risks, underlying conditions or injuries
painful
long time - long procedures, pre-and post- imaging
positioning may effect OA if present

445
Q

describe the positioning of the femoral and sciatic nerve block

A

in line with the wing of the ileum and ischiatic tuberosity

446
Q

list considerations for mandibular fractures

A

pain
other injuries
blood loss
hydration
intubation challenging
possible debris in pharynx
analgesia
surgical access for monitoring
feeding tube post op
fluid therapy

447
Q

describe considerations for pharyngostomy intubation

A

used when cant do oral intubation
care as lots of important structures in area
multiple people to place - one for tube, one to cut, one to position head

448
Q

what are considerations for MRI?

A

no metal
limited monitoring access
noisy
if magnet quenched helium is released which may cause hypoxic environment
cold room
contrast/gadolinium may cause hypotension and GA lightening

449
Q

list considerations for spinal surgery patients

A

care with intubation positioning especially if cervical instability
ventilation may be compromised if tilted down or taped to table
ETT may kink
nasal oedema if lower than body
head access may be restricted
poss haemorrhage
surgery may effect diaphragm innervation
vagal stimulation may cause bradycardia
good analgesia

450
Q

when do 50% of anaesthetic deaths occur?

A

within 3 hours of recovery

451
Q

which animals are higher risk under anaesthetic?

A

cats
sick animals
general over sedation
urgent procedures
old age
brachycephalic and dociocephalic

452
Q

which type of airway management has increased risk in cats?

A

ETT

453
Q

which type of induction has higher risk of mortality?

A

inhalational is 6x more risk than injectable

454
Q

why are veterinary anaesthetics more risky than human?

A

less equipment and training

455
Q

what are some types of anaesthetic accidents?

A

sick patients
equipment failure
inadequate prep
inadequate monitoring

456
Q

define complication

A

event that develops not due to human error

457
Q

define error

A

avoidable event caused by human

458
Q

list some human errors that can occur during anaesthetic

A

drug admin errors
poor clinical assessment
inadequate knowledge of equipment/protocols
poor monitoring
closed APL valve

459
Q

list some types of equipment failure

A

inability to deliver oxygen
lack of oxygen from source
disconnection of oxygen
stuck or missing one way valve
leaks in machine or system
ventilator failure

460
Q

how can you improve anaesthetic safety?

A

checklists to prevent mistakes

461
Q

list complications from IVCs

A

trauma on insertion
poor placement
infection
inflammation of skin
phlebitis/inflammation of vein
dislodged from vein
air embolism
pain

462
Q

how can you prevent IV cath complications?

A

aseptic technique
start low then move up if needed
correct catheter size
good technique
prevent interference
daily observation and dressing changes
regular flushing

463
Q

what are some examples of drug admin errors?

A

wrong decimal place
wrong drug
wrong dose
incorrect route
poor communication

464
Q

how to avoid drug admin errors?

A

check calculation
weigh patient
label drugs
look for likely drug reactions
careful prep of drugs
record drug on chart

465
Q

what should you do in the case of drug errors?

A

tell vet
stop giving
close monitoring
check drug sheet
inform owner
poisons service if needed

466
Q

what are risks for regurg in anaesthesia?

A

induction and recovery
species dependent
drug dependent

467
Q

what can increase risk of GOR?

A

incorrect fasting period
drugs - diazepam, opioids as relax sphincters
abdo pressure
long surgery
abdo surgery
ortho surgery as lots of moving

468
Q

what are possible consequences of GOR?

A

unable to swallow on recovery
distress
vomiting blood tinged fluids
damage to oesophagus

469
Q

how to lower risk of GOR pre-ga?

A

8 hour fasting
identify risky patients
pre-op GI protectants
head up and swift induction
cuffed tube
suction ready

470
Q

how do you respond if a patient has regurged?

A

head down
suction/swab out pharynx
consider omeprazole
record
inform vet

471
Q

what can be consequences of GOR?

A

oesophageal strictures
aspiration

472
Q

what can be causes of corneal ulcers under GA?

A

reduced tear formation due to anaesthesia, sedation and opioids
trauma - heat, face masks, liquids

473
Q

how can you prevent ocular damage in anaesthesia?

A

care with warming devices
careful positioning of patient and face masks
avoid droplets around face
regular ophthalmic treatment

474
Q

how do you manage a patient with an ulcer?

A

pain relief
prevent rubbing or scratching with buster collar
tell vet
eye treatment
find cause
tell owner

474
Q

what is core and peripheral body temperature when concious?

A

core - 37
periphery - 31-35

475
Q

what is core and peripheral body temperature when anaesthetised?

A

core - 36
periphery - 33-35

476
Q

why does core and peripheral temperature vary between conscious and anaesthetised patients?

A

vasoconstricted when conscious and vasodilated when anaesthetised

477
Q

what are the negative consequences of patients becoming hypothermic during anaesthesia?

A

increased mortality especially if sick
arryhtmias - a fib at 30 degrees, v fib at 24-28 degrees
bradycardia
poor coagulation and wound healing
shivering increases oxygen demand in recovery

478
Q

how does patients being hypothermic affect the GA?

A

prolong drugs
decrease renal plasma flow
decrease oxygen delivery
lowered anaesthetic requirements

479
Q

how can you try to prevent hypothermia?

A

insulation
warm from premed
can use HME on breathing system
care with clipping and scrubbing
external heat sources
warm environment
minimise GA time

480
Q

how does HME system work and what are the negatives?

A

warms air, as it bypasses URT when intubated
negatives - expensive, increases drag and deadspace

481
Q

what are the effects of hyperthermia on patients?

A

increased basal metabolic rate
increased oxygen requirement
parenchymal cell damage
over 41 degrees - poss irreversible brain damage
over 43 degrees - death

482
Q

which patients are particularly at risk of becoming hyperthermic?

A

brachycephalics
obese

483
Q

how can you avoid hyperthermia?

A

close observation of warming
dont leave on heat they cant move from
cool if needed - fan, wet towel, cold water lavage

484
Q

list mechanisms of respiratory failure

A

depression of respiratory centres in the brain
impaired thoracic cage movement - sandbags, increased intra-abdominal pressure
impaired lung movement - pleural effusion
airway obstruction

485
Q

what are signs of respiratory obstruction?

A

breed or condition indicators
increased RR
paradoxical ventilation
no air movement
cyanosis
capnograph change
careful obs

486
Q

list causes of apnoea, arrest or cyanosis

A

too light or too deep
respiratory tract obstruction
drug related
post induction
poor oxygen supply
low CO

487
Q

how do you manage post-induction apnoea?

A

wait before venting to allow CO2 to build up to stimulate spontaneous ventilation

488
Q

how do you manage respiratory obstruction?

A

inform vet
suction mouth as needed
straighten neck
check oxygen and equipment
oxygenate
intubate
corticosteroids

489
Q

how do you prepare for BOAS patients likely having difficult airways?

A

pre-oxygenate to give more time to decompensation

490
Q

how do you manage respiratory obstructions when a patient is intubated?

A

check for kinks or obstruction
check tube length
check if damaged
check breathing system and oxygen supply

491
Q

how should you manage apnoea and cyanosis during surgery?

A

confirm heartbeat
check depth
check for obstruction
ensure oxygen 100%
manually ventilate
check chest wall movement
antagonise drugs as needed
turn off VA if leading to CA

492
Q

define cardiac arrest

A

cessation of effective circulation

493
Q

what can cause CA?

A

pre-existing CV disease
drug overdose
hypovolaemia
electrolyte and acid base imbalances
vagal reflex causing bradycardia and CA
respiratory arrest

494
Q

how should CA during GA be managed?

A

call for help
check pulse and HR
start compressions
check ventilation
check depth of GA, turn off VA
give 100% oxygen
manually ventilate
debrief afterwards

495
Q

how should ECGs be used during GA?

A

identifying abnormal
not diagnostic

496
Q

what are the functions of the different types of cells in the heart?

A

myocardial cells - contract
self-excitatory cells - generate impulses in the heart

497
Q

define automaticity

A

cells ability to generate a beat

498
Q

what HR can different areas of the heart generate?

A

SA node - 60-160
AV node, bundle of his - 40-60
purkinjie fibres - 20-40

499
Q

define arrhythmia

A

change in rhythm, rate or origin that differs from normal cardiac cycle

500
Q

what is the significance of arrythmias?

A

most clinically insignificant, some fatal

501
Q

what is a 1st degree block?

A

signal struggles to get through, longer PR interval

502
Q

describe a type 1 2nd degree block

A

progressive lengthening of PR interval until dropped beat as impulse blocked, then back to normal

503
Q

describe type 2 2nd degree block

A

intermittent passage of signal so beat suddenly drops

504
Q

describe 3rd degree block

A

complete heart block, electrical signal cant get past AV node so impulses randomly generated in other parts of the heart causing weak heart beat

505
Q

what is v tach?

A

rapid heart rate caused by abnormal complexes from ventricles

506
Q

what do you do if you notice your patient has arrythmia under anaesthetic?

A

take photo/print ECG
tell vet

507
Q
A

Advanced Clinical Veterinary Nursing (4 decks)

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