Anaesthesia Flashcards
define pain
unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage
what is the purpose of pain and when is this not the case?
protective unless in chronic pain
define nociception
neural process of encoding noxious stimuli
define nociceptive pain
pair arising from actual or threatened damage to non-neural tissue due to activation of nociceptors, in normally functioning somatosensory system
define neuropathic pain
pain caused by lesion or disease of somatosensory nervous system
define hyperalgesia
increased pain from stimulus that normally causes pain
define allodynia
pain due to stimulus that normally wouldnt cause pain
where do opioids act?
endogenous opioid receptors in the CNS
name full mu agonists (opioids)
methadone
fentanyl
name partial mu agonist (opioids)
buprenorphine
name mixed agonist-antagonist/k agonist (opioids)
butorphanol
name opioid antagonist
naloxone
define potency
how much of a drug is needed to cause an effect
define effiacy
degree of effect a drug can have
which routes can you give opioids in?
IV
IM
SC
oral
epidural
spinal
transmucosal
which routes of drug admin are most effective?
those that result in the drug being in the blood stream, rather than the GI system or liver
state advantages of IV admin of opioids
rapid onset of action
reliable uptake
painless irrespective of volume
state disadvantages of IV admin of opioids
need IV access
cant use for pethidine as causes allergic reaction
state advantage of IM opioid admin
reliable uptake
state disadvantage of IM opioid admin
painful if large volume
state advantage of SC and OTM opioid admin
easy to do
state disadvantage of SC opioid admin
unreliable uptake
state disadvantage of OTM opioid admin
only certain ones licenced
cat and bupe
what are the advantages and disadvantages of transdermal opioid admin?
good for chronic use
no products licenced
what are advantages and disadvantages of epidural/spinal opioid admin?
effective analgesia intraop
non licenced and hard to do
what are the main uses of opioids?
preventative, multi-modal and peri-op analgesia
why are opioids not given for chronic pain?
poor oral bioavailability so not in tablet form for veterinary - significant first pass metabolism in liver
sedative effects
why are opioids not ideal for neuropathic pain?
damaged nerves release cholecystokinin which antagonises opioids
list pharmacological effects of opioids
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
what makes opioids safe drugs?
wide dose ranges
side effects relate to potency
side effects less likely when painful
naloxone can be used
name the 3 families of opioid peptides/neurotransmitters
beta-endorphin
leucine-enkephalins and methionine-enkephalins
dynorphins
list the types of opioid receptors
mu
kappa
delta
NOP
where are opioid receptors found?
brain and spinal cord
NOP receptors key info
bind to nociceptin
recent discovery so limited knowledge
where are delta receptors found?
brain and peripheral sensory neurones
list effects from delta receptors
analgesia
anti depressant
convulsant
dependence
respiratory depression
where are kappa and mu receptors found?
brain
spinal cord
peripheral sensory neurones
list effects from kappa receptors
analgesia
anti-convulsant
depression
hallucination
diuresis (excess urine production)
miosis
dysphoria
neuroprotection
sedation
stress
list effects from mu 1 receptors
analgesia
dependence
list effects from mu 2 receptors
respiratory depression
miosis
euphoria
reduced Gi motility
dependence
list the function from mu 3 receptors
vasodilation
why do full agonists provide the most effective analgesia?
bind and activate receptor with maximum response an agonist can cause at the receptor
why do partial agonists provide less analgesia than full?
only give partial efficacy even if are bound to all receptors
what affects onset of action of opioids?
route of admin
time to receptors
how much drug binding is needed for some effect
when does peak effect occur?
when all the drug is on the receptors
what determines how long drug effects last?
speed of removal
what measures can increase duration of action?
higher dose
adding vasoconstrictors
name ultra-short acting opioid
fentanyl
how long do ultra-short acting drugs last and what are they used for?
20 minutes
intra-op pain, short term infusions
name short acting opioids
butorphanol
pethidine
how long do short acting opioids last and what are they used for?
2 hours
pain management, multi-modal analgesia, pre-med and sedation
name medium acting opioids
methadone
morphine
how long do medium acting opioids last and what are their uses?
2-4 hours
pain management, multi-modal analgesia
name longer acting opioid
buprenorphine
how long does longer acting opioids last and whats it used for?
6 hours
pain management
what are some opioid misconceptions?
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
what drugs would you not combine with opioids?
other opioids
tramadol - acts on opioid receptors
list opioids most to least efficacy
fentanyl
methadone/morphine
pethidine
buprenorphine
butorphanol
what are side effects to fenanyl?
respiratory depression
bradycardia
what are benefits to methadone compared to morphine?
less nausea and vomiting
no histamine release if IV admin
minimial CVS and respiratory effects
why should you be careful if giving methadone CRI?
accumulative effects
why is pethidine not ideal?
short acting
large volume so painful IM
histamine release if IV
what are negatives of buprenorphine?
may sting due to preservative
not v effective SC
delayed onset of action
what are negatives of butorphanol?
low analgesia effects, is more sedative
short acting
need higher doses than normally given
how do LAs stop pain?
enter nerve fibres and bind and block voltage-operated Na channels which blocks nerve conductions
describe how action potentials are generated
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
describe how resting membrane potentials happen
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
how does repolarisation of cells happen?
sodium channels inactivate and k channels open
where are voltage gated sodium channels found?
all excitable tissues - muscles and heart
in what order do LAs block things in the body?
nociception
proprioception
mechanoreception
motor function
list types of nerves in the body
Motor (Aα, Aβ, Aγ)
Sensory (Proprioceptors Aα, Aβ, Mechanoreceptors Aβ, Aδ, Nociceptors Aδ,C)
Autonomic (preganglionic B, postganglionic C)
what features of axons make them more resistant to LAs?
larger diameter
more heavily myelinated
why are Aδ and C fibres more suceptible to LAs and what is the result?
Aδ - very thin myelination
C - no myelination
nociception blocked first so pain relief without loss of feeling or movement
are LAs acids or bases?
weak bases
which form of LA can penetrate nerve cells lipid membranes?
uncharged
what determines proportion of uncharged LA?
pH
pKa - pKa = pH + log [BH+ ]/[B]
handerson hasslbalch equation - B + H= BH+
describe the effect of onset of LA action at higher pKa
at higher pKa (same pH) more of the drug is ionised so onset is slower as less drug is available
how does inflammation affect action of LAs?
pH decreases in inflammation so more drug ionised and less available to penetrate nerve fibres so less effective
which drug is an ester (LA)?
procaine
no i before caine
list features of ester LAs
relatively unstable
rapid breakdown by pseudocholinesterase
PABA formed as hydrolysis product - can cause allergic reaction
short plasma half life
which drugs are amides?
lidocaine, bupivacaine
i in name before caine
list features of amide LAs
broken down by cytochrome P450 enzymes in liver - drugs affecting this enzyme effect drug breakdown
more stable
biotransformed in liver
longer half life
which drugs increase and decrease breakdown of cytochrome P450 enzyme?
increase - barbiturates
decrease - midazolam
list body systems that can be effected by LAs
CVS
CNS
list CVS effects from LAs
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
list CNS effects from LAs
behaviour change
muscle twitching
tremors
tonic-clonic seizures
CNS depression
respiratory depression
death
seen at lower doses
what casues LA toxicity to increase?
potency increases
dose increases
what can you do to prevent LA toxicity?
not exceed maximum dose
dilute small volumes
accurately draw up
aspirate before injection
how is LA toxicity treated and why?
symptomatic as no reversals
when are LAs used?
multi-modal analgesia
post-op pain management
desensitisation - IV and intubation
define epidural
anaesthetic injected into epidural space
define spinal
anaesthetic injected into csf
list LAs from most to least potent
bupivacaine
ropivacaine
lidocaine
procaine
how is duration of action of LAs effected?
lipid solubility
strength of binding to channels
speed of removal - tissue perfusion, vasoconstriction
metabolism - amide vs ester
what forms can LAs come in?
sprays
patches
sterile solutions for injection
why can LAs cause stinging on injection?
poorly water soluble so made into salt solution but this lowers pH
why is glucose added to LAs?
increase baricity to prevent spreading too high in epidural space
what are the benefits of adrenaline being added to LAs?
causes vasoconstriction which reduces systemic absorption, prolongs action and reduces toxicity as less spread
how does plasma protein binding affect LA toxicity?
higher binding means lower toxicity as less unbound and active
what alters amount of plasma protein binding in LAs?
type of drug
lower pH lowers protien binding
what species is lidocaine licenced for?
dogs
cats
horses
state onset and duration of action of lidocaine
2-5 minute onset
20-40 minute duration
are bupivacaine and EMLA licenced in veterinary?
no
how long is bupivacaine duration of action?
6 hours
does lidocaine or bupivacaine have higher cardiotoxicity
bupivacaine
what drugs are in emla?
lidocaine and prilocaine
how long does emla take to have an effect?
30-45 minutes
what blocks are VNs not allowed to perform?
anything entering body cavity such as epidural
list side effects of epidural
hypotension
hypothermia
urinary retention
infection
when cant you do an epidural?
sepsis
skin infection
coagulation issues
hard when obese or pregnant
define local LA
blocking around small area
define regional LA
blocking larger area
list examples of local/regional LA
opthalamic
dental
limb block
list types of infiltration block
testicular
ovarian ligament
incisional line block
intraperitoneal
how are infiltration blocks done?
in v-shape or inverse pyramid
how do NSAIDs work?
inhibits COX which inhibits prostaglandin production (inflammatory mediators)
where do NSAIDs work?
periphery, some central
what leads to side effects from NSAID use?
relate to protective effects of prostaglandins
how easily NSAIDs can leave the circulation and enter tissues
how do prostaglandins occur in the body (cox-1 and cox-2)?
cox-1 - constituative or protective functions
cox-2 - induced by inflammation
which nsaids block both types of cox and which are specific to cox-2?
both - aspirin, flunixin
cox-2 - meloxicam, carprofen
which is nsaid selectivity to cox-2 beneficial?
reduces side effects
list side effects of nsaid use
GI ulceration
renal ischemia
water retention
oedema
hypertension
hepatopathy
CNS signs (cats)
haematostasis
how do nsaids cause GI ulceration?
prostaglandins maintain mucosal blood flow, bicarbonate and mucosal secretion and epithelialisation
how do nsaids lead to renal ischemia?
prostaglandins protect and maintain renal blood flow in hypotension, regulate GFR, renin release and sodium excretion
list how to minimise nsaid side effects
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
what are some signs of nsaid adverse effects?
vomiting
diarrhoea
blood in faeces
dullness
anorexia
where are nsaids metabolised?
liver
why are nsaids often used in OA management?
immediate relief when other measures such as weight loss, diet change, supplements, take time
what is gold standard to do before starting nsaids?
clinical exam
biochem
haematology
urinalysis
BP
how should nsaid use be montiored?
review 2 weeks after starting
regularly recheck parameters 3-6months or more often
what is meant by NSAID cycling?
changing to a different nsaid if having side effects or no longer effective
when can and cant paracetamol be used?
instead of nsaid if contraindicated
not in cats as toxic
how is tramodol used and why?
in multimodal analgesia as limited efficacy alone
how does gabapentin work?
binds voltage gated calcium channels to decrease excitatory neurotransmitter release in spinal cord
when is gabapentin used?
manage neuropathic pain?
multimodal analgesia
when nsaids contraindicated
what are negatives of gaba?
highly sedative
need to be weaned off
where does tramadol act?
centrally
how is amantadine used and why?
with other analgesics as is antihyperalgesic
chronic pain
what are downsides to amantadine?
takes weeks to see benefit
how is amantadine metabolised?
kidneys
what makes pregabalin different to gaba?
better oral bioavailability
longer half life
limited evidence
list drug types that can cause muscle relaxation
LA
benzodiazepine
alpha 2 agonist
guaiphenesin (horses)
NMB
why is ketamine given with alpha 2 or benzo?
ketamine alone causes muscle rigidity
why are NMBs not commonly used for procedures?
pre-med, induction and mantainance agents provide generally enough muscle relaxation
where does guaiphenesin/GGE act?
centrally on spinal cord, brain stem and subcortical brain
when is GGE used in horses?
after ketamine to counteract rigidity
part of triple combo - ket, alpha 2, GGE for GA maintainance
what are the negatives of GGE?
no analgesia or anaesthetic properties
causes haemolysis over 10% concentration
causes tissue damage if perivascular
list indications of NMB use
relax muscles for surgical use
control ventilation
aid intubation in cats
ophthalmic surgery for central eye
assist joint/fracture reduction
reduce anaesthetic agent needed
do NMBs provide analgesia or anaesthetic?
no
describe how the NMJ casues muscle contraction and relaxation
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
what is one thing you must do for patients if using NMB?
intubate and IPPV
list in order from most to least sensitive muscles are to NMBs
peripheral to central
intercostals and diaphragm last to be effected
name the depolarising muscle relaxant
suxamethonium
how does suxamethonium work as a NMB?
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
how long does suxamethonium cause effect in cats and dogs?
cats - 3-5 min
dogs - 20 min
what are negatives of suxmthonium?
can only give one dose as causes prolonged block
short acting
can trigger malignant hyperthermia
increases serum potassium
care in burn patients
name the 2 most common non-depolarising muscle relaxants
atracurium
vecuronium
name less common non-depolarising muscle relaxants
rocuronium
mivacurium
pancuronium
how do non-depolarising muscle relaxants work?
compete with acetylcholine for post-binding junction sites
what are benefits to non-depolarising muscle relaxants?
no initial muscle contraction
can top up with 1/3 initial dose
can antagonise
last upto 40 minutes
which type of muscle relaxant has faster onset of action?
depolarising
state features of atracurium
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
state features of vecuronium
steroid compound, no corticosteroid effects
no histamine release
40-50% hepatic biotransformation
in powder form, stable 24hrs post reconstitution
list key monitoring considerations during NMB use
ventilation
tube patency
thoracic wall movement
ETCO2
SpO2
why is it hard to monitor depth when using MNB?
most reflexes lost
list signs of light depth when using NMB
tachycardia
hypertension
salivation
lacrimation
vasovagal response - bradycardia, hypotension, pallor
increased ETCO2
pupil dilation
describe how to monitor degree of NMB
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
what factors effects duration of NMB action?
VA
hypothermia and renal/hepatic insufficiency - reduces metabolism
electrolyte/acid base disturbance
muscle disease - myasthenia gravis
aminoglycoside antibiotics - prolong effect
dose given
when can you antagonise non-depolarising NMB?
once 1-2 twitches have returned
name NMB antagonists
anticholinesterases - neostigmine and edrophonium
how do NMB antagonists work?
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
list side effects of antagonising NMBs
bradycardia
salivation
bronchospasm
diarrhoea
how can side effects of antagonising NMBs be managed?
giving IV anticholinergics with the anticholinesterase
describe how you would recover a patient having given a NMB
ventilate until return of spontaneous ventilation
monitor for signs of upper respiratory weakness - URT noise, cyanosis, paradoxical breathing
describe negative pressure ventilation and when its seen
spontaneous breathing, most anaesthetics
air drawn in by negative pressure
describe positive pressure ventilation
forcing air in, mechanical or manual
list factors that affect and compromise spontaneous ventilation
anatomical - airway obstruction, stenotic nares, excess tissue, hypoplastic trachea, obesity
external - ETT size, external restriction
internal - effusions
list indications for assisting ventilation
reduced ventilation drive
inability to ventilate effectively
list causes of delayed ventilatory drive
anaesthetic drugs
increased ICP
encephalopathy
hypothermia
list causes of inability to ventilate
open thoracic cavity
muscle failure - NMB, myasthenia gravis
intercostal or diaphragmatic nerve failure
external factors affecting lung inflation
list parameters to indicate needing to ventilate a patient
ventilatory pattern
spirometry/tidal and minute volume
blood gases
ETCO2
pulse ox
what are the advantages of manual ventilation?
easy to perform
cheap
what are disadvantages of manual ventilation?
operator dependent
poor airway pressure control
each breath can be different
boring and time consuming
what are advantages of mechanical ventilation?
hands free anaesthetic
appropriate and consistent gas volumes delivered
what are disadvantages of mechanical ventilation?
not always available
expensive
requires skill
describe how ventilation effects patients CO
positive pressure forced into lungs which exerts pressure on the vena cava in lung expansion so decreased venous return to the heart
list potential side effects of IPPV
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
when does oxygen toxicity occur?
if on 100% over 6 hours as free radicals form causing damage
what observations do you make to monitor effective ventilation?
thoracic movement
abdominal movement
auscultation
capnography
pulse ox
art blood gas - PaO2, PaCO2
what would you do if ETCO2 was high?
increase ventilation
what would you do if high PaCO2?
increase ventilation
what would you do if low PaO2?
increase oxygen
what is a ventilator?
machine designed to provide mechanical ventilation to a patient by moving air in and out of the lungs
what are common cases that need ventilating?
apnoea
NMBs
thoracotomy
diaphragmatic rupture
list settings on ventilators
frequency of breaths
tidal/minute volume
I:E ratio
inspiratory flow rate
PIP
PEEP
define PIP
peak inspiratory pressure
highest pressure measured during the respiratory cycle
define PEEP
positive end pressure ventilation
pressure applied by ventilator at end of each breath to ensure alveoli are not prone to collapse
what are common settings for PIP and when would they be adjusted?
8-12H2O
adapt if open or closed thorax, increase if recruitment
what is meant by cycling in ventilation?
change from inspiration to expiration
what is meant by cycling variables in ventilation?
how and when ventilator moves from inspiration to expiration
list cycling variables in ventilation
pressure
volume
time
flow
describe pressure cycling
ventilator delivers inspiratory gas until certain pressure is reached and expiratory stage begins
when would you not use pressure cycling in ventilation?
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
describe how volume controlled cycling works
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
what safety measure is in place in for volume controlled cycling?
pressure cut off to avoid over inflation
describe how time controlled cycling works
switches from inspiration to expiration after certain time based on RR, inspiratory time or I:E ratio
how does flow cycling work?
ventilator delivers set flow until total volume is delivered
what is the difference between assist control and control mode ventilation?
assist control - breath initiated with patient
control - breath controlled by machine
what is normal I:E ratio and RR as a result?
I:E 1:2
RR 20
list types of ventilators
bag squeezer - ascending, descending, horizontal below
mechanical thumb
intermittent blower
volume divider
describe features of bag squeezer vent
bellow connected to bag port
sets volume and I:E
pressure gauge
set TV and inspiratory time which works out RR
list types of bag squeezer
hallowell EMC 2000 - time cycle, pressure limited
JD medical - equine, pressure cycled and pressure limited
when is mechanical thumb vent used?
in small animals
how do intermittent blowers work?
divides driving gas into smaller volumes and pushes into patient
list types of intermittent blower
merlin - microprocessor, can set time, pressure or volume
nuffield - time cycled, set inspiratory time and flow
how does minute volume divider work?
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
state type of minute volume divider
manley MP3 - has main bellow, volume triggered, can set TV and inspiratory time
list patient considerations for those on long term ventilation
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
what is the purpose of blood gas analysis?
measure partial pressure of gases in the blood
pH analysis
define an acid
proton donor
define a base
proton acceptor
what is the equation for pH?
pH = -log10[H+]
what is normal pH?
7.4 in range 7.35-7.45
what is the effect of pH being outside normal ranges?
enzyme changes which effects metabolism
what is the relationship between pH and [H+]?
as pH decreases [H+] increases
why is pH important in the body?
effects rate of enzymatic reactions
impacts physiology
how does pH in the body get altered?
diseases
drugs
fluids
when will pH levels cause death?
less than 6.8 or more than 7.6
how does the body stay electroneutral?
lots of ions present with all charges adding to zero
water generates H+ ions t balance any charge differences
define acidaemia
pH less than 7.35 in the blood
define alkalaemia
pH more than 7.45 in the blood
how is normal pH maintained?
buffers
respiratory system
renal system
define a buffer
any particle capable of accepting or donating H+ to minimise pH changes
fast acting
list buffers
bicarbonate
haemoglobin
blood proteins
phosphate
lactate
what is the henderson hasselbalch equation?
pH = pKa + log10[HCO3-]/[0.3pCO2]
what does the henderson hasselbalch equation mean for the body?
pH, bicarbonate and PP CO2 determined by metabolic and respiratory components
how does respiratory effects change pH?
change in PCO2 changes pH
how does metabolic effects change pH?
change of anything that can affect pH, usually bicarbonate due to buffering other acids
what is the relationship of PaCO2 and ventilation?
inversely proportional
hyperventilation decreases PaCO2
hypoventilation increases PaCO2
what is the equation for bicarbonate acting as a buffer?
H2O + CO2 <> H2CO3 <> H+ + HCO3-
how does the respiratory system respond in respond in response to pH changes?
rapidly changes PaCO2
how does the renal system work to maintain pH?
major way of excess acid removal
regulation of bicarbonate and ions
slow to work over hours and days
define acute respiratory acidosis
increased PCO2 from hypoventilation
what is the compensatory mechanism for acute respiratory acidosis?
increasing bicarbonate
what are the compensatory mechanisms for chronic respiratory acidosis?
kidneys excrete acid and bicarbonate is retained
define respiratory alkalosis
fall in PCO2 from hyperventilation
what are the compensatory mechanisms for respiratory alkalosis?
metabolic compensation with bicarbonate
define metabolic acidosis
decreased bicarbonate due to loss or consumption by excess acid
how is metabolic acidosis compensated?
increase ventilation to reduce PCO2
define metabolic alkalosis
increased bicarbonate due to loss of chlorine ions or albumin
how is metabolic alkalosis compensated?
decrease ventilation to increase PCO2
define base excess
amount of acid to titrate 1L of blood to pH 7.4 at 37 degrees and PaCO2 of 40mmHg
how does base excess allow identification of pH change?
it fixes PaCO2 to 40mmHg so any other pH change is due to metabolic processes
what is normal arterial and venous PCO2?
arterial - 40mmHg
venous - 44mmHg
what is normal bicarbonate levels in the blood?
24mmol/l
what is normal base excess in the blood?
4mmol/l
what is normal arterial and venous blood oxygen levels?
arterial - 90-100mmHg
venous - 40-50mmHg
how does PaO2 and FiO2 link?
PaO2 = 5xFiO2
define hypoxamia
less than 80mmHg (arterial)
what would you expect normal PaO2 to be under GA and why?
400-500mmHg as you give 100% oxygen
what parameters do blood gas machines measure?
electrolytes
lactate
haematocrit
glucose
blood gases
where should you take samples from for acid-base balance?
arterial or venous
where should you take samples from for gas exchange?
arterial
what syringes can be used for blood gas samples?
heparinised impermeable glass if storing (on ice)
heparinised plastic if short term
describe how to handle samples
roll to prevent clotting
discard first drop as likely clotted
what can be the consequence if blood gas sample analysis is delayed?
gas can diffuse in and out of the sample
what is the result of air contamination on blood gas analysis?
CO2 low as diffuses out
O2 closer to 150mmHg
how does saline contamination occur and what is the effects on blood gas?
sampling from catheters
high chloride
what is the effect of clotting on blood gases?
low PCV
low haematocrit
what is the normal anion gap value?
15-25mmol/l
what causes increased anion gap?
lactic acidosis
ketoacidosis
what causes decreased anion gap?
hypoproteinaemia
what doesent effect anion gap?
GI bicarbonate loss
how are the contents of the intercranial cavity distributed?
80% brain
10% CSF
10% blood
what can affect the BBB?
trauma
inflammation
hypertension
why does the brain receive 15% CO?
is very highly metabolic
why does an increase in CSF or blood increase ICP?
the skull cant expand
what is normal ICP?
5-12mmHg
what are clinical signs of raised ICP?
papilledema (optic disk swelling)
pulsing of retinal vessels
depression
stupor (unconscious/unresponsive)
coma
what are the aims when anaesthetising neuro patients?
maintain cerebral blood flow
minimise increases in ICP
when does the cushing reflex occur?
in response to increased ICP
describe the cushings reflex
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
what is the purpose of the cushings reflex?
decrease ICP by reducing blood entering the brain
what are considerations to control ICP?
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
what are general conditions for neurological anaesthesia cases?
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
what are aims when choosing drugs for neuro patients?
not increase ICP or change MAP
why are opioids a good choice for neurological patients?
dont alter CBF or ICP
minimal CV and respiratory depression
why is morphine not ideal for neurological patients?
can cause vomiting
what are the benefits of benzodiazepines in neurological patients?
no effects on ICP, respiration or CV system
may reduce anxiety
why would you not use ACP in neurological patients?
may trigger seizures in patients with intercranial pathology
causes vasodilation leading to hypotension and cerebral vasodilation causing increased ICP
why would you not use alpha-2s in neuro patients despite not affecting ICP?
cardiopulmonary effects
increases MAP and bradycardia which masks cushings reflex making obs harder
can cause vomiting in cats
why may ketamine be used in neuro patients?
doesnt effect ICP when combined with other sedatives
possibly neuroprotective and have fewer CV effects and resp effects
reduce ICP when given with propofol
what are reasons for GA in neuro patients?
imaging
CSF tap
spinal surgery
other treatment
what are patient considerations for MRI?
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
where are CSF taps normally done?
lumbar
cisterna magna
what are considerations of cisterna magna positioning?
neck needs to be bent chin to chest so ETT may be compromised
may seizure in recovery so keep head elevated
what are intubation considerations for neuro patients?
laterally intubate
depth adequate for intubation
armoured ETT for cisterna tap
how do you manage seizure patients?
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
what are considerations for neuromuscular disease patients?
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
what are common GI procedures?
abdominal surgery
FB removal
GDV
pre-existing conditions
endoscopy
what are considerations for planned GI surgery?
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
considerations for emergency GI surgery
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
what complications are commonly seen in GDV surgery?
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
why can BP look normal in GDV patients when they are not perfusing well?
SVR is increased due to restriction of blood return to the heart which compensates for CO decrease from hypovolaemia and dehydration
what are post-op considerations for GDV patients?
intensive care needed
analgesia
list functions of the liver
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
list examples of liver dysfunction
porto-systemic shunt
billiary obstruction/trauma
chronic disease
acute failure
neoplasia
list signs of hepatic dysfunction
ascites/oedema - due to hypoproteinaemia and hypoalbuminaemia
PUPD
anaemia
hypocalcaemia
hypoglycaemia
hypothermia
reduced clotting times
acid base disturbances
jaundice
encephalopathy
define hepatic encephalopathy
neurological abnormalities occurring due to hepatic disease
what is the effect of hepatic encephalopathy on the body?
increased toxins and ammonia due to liver not processing them
what is stage 1 encephalopathy signs?
mild confusion
inappetence
decreased attention
dullness
irritability
what are signs of stage 2 encephalopathy?
drowsiness
lethargy
personality change
disorientation
apparent blindness
what are signs of stage 3 encephalopathy?
very drowsy
confusion
uncontrolled behaviour
seizures
what are signs of stage 4 encephalopathy?
recumbence
unarousable
coma
death
how is hepatic encephalopathy treated?
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
how does hepatic dysfunction affect anaesthesia?
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
list considerations for hepatic patients undergoing GA
stabilise
minimal drugs - care with doses
slow titrated induction
analgesia
temperature
BG monitoring
consider coagulopathies
what considerations should be in place for managing patients with coagulopathies?
peripheral veins
pressure after bloods and IVs
no rough handling
avoid trauma
calm recovery to protect wounds
which pre-GA labs are recommended for hepatic patients?
liver enzymes
bile acids
clotting factors
urea
plasma protiens
glucose
what is an insulinoma?
pancreatic islet cell tumour
what is the effect of an insulinoma?
overproduction of insulin causing hypoglycaemia
how is insulinoma treated?
prednisolone
diazoxide
glucose
care of other drugs being used
surgery
what surgery can be done for insulinoma?
laparotomy partial pancreatectomy
what are post op considerations for partial pancreatectomy?
pancreatitis
pain
hyperglycaemia
possible post-op diabetes
BG monitoring
what should you do before anaesthetising a diabetic patient?
stabilise
list symptoms of diabetes mellitus
hyperglycaemia
dehydration
weight loss
fatty liver
ketosis
what are considerations for nursing patients with diabetes mellitus?
learn normal routine
do first op of the day so can go home and eat
monitor BG
insulin as needed
what are good protocols for anaesthetising patients with DM?
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
what is typical signalment of hyperthyroid patients?
old cats
multi-organ dysfunction
highly strung
stress intolerable
thin
PUPD
muscle weakness
HCM
what are essential steps before anaesthetising hyperthyroid patients?
stabilisation
investigation
what are good drug protocols to use for hyperthyroid patients?
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
what are important GA monitoring for hyperthyroid patients?
ECG
IVFT
what are considerations for during and after thyroidectomy?
monitor BP
little access to head
possible post-op laryngeal paralysis
post-op hypocalcaemia
keep IV in patient
what is the typical presentation of canine hypothyroidism?
elderly dog
megaoesophagus
decreased GI motility
obesity
lethargy
bradycardia
hypotension
slow drug biotransformation
list causes of hyperadrenocorticism
pituitary or adrenal tumour causing glucocorticoid excess
iatrogenic
list signs of hyperadrenocorticism
poor muscle tone
overweight
lethargy
poor thermoregulation
bruising
hypercoagulability increasing risk of thromboembolism
PUPD
Na retention
K excretion
wound infection
what is the most important considerations of hypoadrenocorticism?
avoid stress as dont have normal stress response
stabilise before GA
list types of renal disease
AKI
CKD
urinary tract obstruction
bladder, urethra or ureter rupture
what are effects of renal disease on GA?
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
list considerations of renal disease patients for GA
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
what should you avoid in choosing drugs for renal patients?
drugs that affect CVS, renal function or BP
what generally increases risks for dental anaesthesia?
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
list considerations for dental patients
pain
haemorrhage - unlikely life threatening
hypothermia
aspiration
long procedures
concurrent disease
why shouldn’t you do dentals at the same time as other procedures?
bacteria from the mouth get aerosolised
what are considerations for geriatrics undergoing anaesthesia?
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
what are baroreceptors?
mechanoreceptors detecting BP
causes changes to peripheral resistance and CO to maintain normal BP
what is functional residual capacity?
volume remaining in the lungs after normal passive exhalation
what are pre-op considerations for dental patients?
urine and bloods
diagnostics as needed
full clinical exam
may be anorexic from dental disease
concurrent disease
fluid therapy
meds
breathing system
what are peri-op considerations for dental patients?
analgesia
MAC sparing to maintain BP
local blocks
cuffed ETT
throat pack
maintain body temperature
care with mouth gags especially cats
eye care
haemorrhage
what should you do if dental procedures are likely to take too long?
stage them over several
what type of analgesia is the only one to truely stop pain?
nerve blocks
why are nerve blocks used for dentals?
fully stop pain
reduce VA requirements
manage post-op pain, improving recovery time
what areas does an infraorbital/rostral maxillary block?
soft tissues
incisor, canine and premolars
where do you perform a infraorbital/rostral block?
foramen of the maxilla dorsal to 3rd premolar
why do you need to be careful when performing intraorbital/rostral maxillary block, especially in cats, small animals or brachycephalics?
foramen is found at the level of the eye
what areas does the caudal maxillary nerve block block?
all bones of maxilla
soft and hard palettes
soft tissue of the nose, upper lip
all teeth rostral to second molar
where do you perform a caudal maxillary block?
foramen caudal and central to last maxillary molar
what areas does the mandibular nerve block block?
all teeth of the lower jaw
where do you perform a mandibular nerve block?
foramen at the ventral angle of the mandible
what is the problem with bilateral mandibular nerve blocks?
blocks tongue function which can cause problems in recovery
what areas does the mental nerve block block?
lower incisors
skin and tissues rostral to foramen
where do you perform a mental nerve block?
foramen found ventral to rostral root of the second premolars
why are mental nerve blocks hard to do in small animals?
foramen can be hard to find in small animals
describe how we prepare for a dental block
sterile needle and syringe
calculate maximum LA dose (across all body)
sterile gloves
record admin of LA
what are post-op considerations for dental patients?
analgesia
warm and dry
clean face
remove mouth gag
get to eat
manage fluids
clear discharge instructions
what are reasons for ocular surgery?
cataract surgery
enucleation
eyelid mass removal
entropion
cherry eye
trauma
what are considerations for before ocular surgery?
very painful
potential eye rupture so care with handling and management
underlying disease - likely to have DM unless trauma case
current meds
which procedure
what should you do pre-op for ocular surgery?
full exam and history
any indicated tests
pre-med
prep eye - not hibiscrub
what are peri-op considerations for ocular surgery?
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
what is normal IOP pressure?
15-20mmHg
what determines IOP?
balance of aqueous humour production and absorption
pupil size
corneoscleral rigidity
extra ocular muscle tone
globe vascularity
what happens in acute increases of IOP?
damage to the eye
how do you manage IOP?
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
what is the occulo-cardiac reflex?
sudden bradycardia associated with pressure on the eye or surrounding structures
caused by stimulation of trigeminal and vagal nerves
how do you manage occulo-cephalic reflex?
stop any surgical manipulation
administer anticholinergics
how do you maintain a central eye in surgery?
NMBs
what analgesia do you use for ocular surgery?
multi-modal and preventative
opioids
nsaids
topical local blocks
retrobulbar block
what are post op consideration for ocular surgery?
analgesia
buster collar
IVFT
general care
no coughing or vomiting
resedate if not calm in recovery
what are reasons for airway surgery?
BOAS
bronchoscopy
tracheal stenting
laryngeal paralysis
underlying airway disease in other surgeries
when is pharyngostomy intubation used?
when oratracheal intubation isnt possible
avoid oral cavity
what body systems are affected by BOAS?
spinal malformations
airway malformations
skin issues
GI system issues
list primary abnormalities of BOAS
stenotic nares
abnormal nasal turbinates
elongated and thickened soft palette
tracheal hypoplasia
how do BOAS dogs compensate and what are the consequences?
harder inspiratory pull causing negative pressure in the throat, neck and chest
what are secondary BOAS abnormalities?
laryngeal collapse
eversion of laryngeal saccules
reflux
regurg
what are considerations for BOAS patients?
avoid stress
IV access important
constant supervision once sedated as can obstruct and regurg
temperature monitoring
rapid intubation
what are good pre-med protocols for BOAS patients?
ideally give IV
IM if too stressful
ACP or alpha-2 with opioid
how do you manage BOAS patients airways?
pre-oxygenate
range of ETT sizes available
cuff tube
suction ready
head down until airway secured
what are peri-op considerations for BOAS patients?
manage airway
consider ventilation
monitor capnography - likely chronically hypercapnic
pulse ox
ECG
monitor ventilation
avoid hyperthermia
eye care
list post-op considerations for BOAS patients
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
what are the benefits of nebulising for BOAS patients?
nebulise adrenaline to open airways
why may you not give NSAIDs to BOAS patients until they have recovered?
may need to give steroids post op to open airways
what is the typical patient with laryngeal paralysis?
older overweight dogs
large breeds - Labrador
hot weather
distressed
how do laryngeal paralysis patients present?
stridor
exercise intolerance
panting
coughing
hoarse bark
define stridor
high pitched breathing sound resulting from airflow through obstructed airway
how do you triage suspected laryngeal paralysis?
neuro and clinical exam
keep stress free
cool with fan
oxygen
monitor RR
butorphanol to calm and as antitussive
close observations
how is laryngeal paralysis managed?
weight loss
exercise restriction
owner education
laryngeal tie back/unilateral arytenoid lateralisation
list pre-op considerations for laryngeal tie back
likely dyspnoeic
sedation may improve breathing
keep cool and calm
care for regurg and aspiration
oxygen
anti-tussives
assess larynx under light GA
pain
list post-op care for laryngeal tie back
close observation
aspiration pneumonia big risk
pain
nothing around neck
give wet food elevated
keep calm
what are reasons for bronchoscopy?
chronic cough
lung infection
feline asthma
parasites
aspiration pneumonia
FB
neoplasia
list patient considerations for bronchoscopy
poor saturation on room air
care on handling
bronchodilator - terbutaline
what are pre-op considerations for bronchoscopy patients?
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
what are peri-op considerations for bronchoscopy?
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
what are potential post-op complications of bronchoscopy?
hypoxia
bronchoconstriction
desaturation
reduced lung compliance
laryngeal oedema in cats
airway or lung rupture - FB removal or biopsy
what equipment do you prepare for bronchoscopy?
pre wash scope to compare with patient sample
sterile saline
collection pots
mouth gag
u cath
syringes
emergency box
what are considerations for bronchoscopy procedure?
lots of people involved for scope, samples, biopsy, monitoring etc
fast
coupage
easy to go wrong
what are recovery considerations for bronchoscopy?
risky
animal may cough
constant monitoring
head elevated to prevent occlusion
prepare for complications
pulse ox
oxygen
possible pneumothorax
what are potential complications of bronchoscopy?
haemorrhage in the airways
desaturation
pneumothorax from damaged bronchi
why do you need to ventilate patients after opening the thorax?
removes negative pressure in the pleural space
describe the effect of opening the thorax on the patient
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
define atelectasis
lung collapse
what are the effects of atelectasis?
decreased total lung capacity, vital capacity, functional residual capacity
hypoxemia common
what is the purpose of functional residual capacity?
helps keep airways open
provide reserve of gas exchange
what are considerations for thoracic surgery?
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
when should you ventilate abdominal approach thoracic patients?
as soon as surgery starts not waiting until enter thorax
what causes pain in thoracotomys or sternotomys?
skin incision
nerve damage
rib retraction
surgical site inflammation
hyperalgesia
why is post-op hypoxaemia common in thoracic surgery patients?
pain makes patient unwilling to move chest wall so efficiency of ventilation reduced
list respiratory conditions needing thoracic surgery
lung lobe torsion
bullae
neoplasia
abscess
FB
pre-existing pneumothorax
hypoventilation
hypoxaemia
what are considerations for respiratory thoracic surgery?
prone to decomposition
keep calm as possible
what are cardiac conditions needing thoracic surgery?
PDA/patent ductus arteriosis
persistent right aortic arch/PRAA
pericardectomy
heart surgery
list considerations for CV thoracic surgery
consider CV changes due to manipulation or primary lesion
bleeding
hypotension in PDA
arrhythmia
regurg in PRAA
list other types of thoracic surgeries
oesophageal FB
thoracic duct ligation
what are considerations for other thoracic surgeries?
risk of aspiration
regurg
septic complications
list pre-op considerations for thoracic surgery
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
how do you care for patients pre-ga undergoing thoracic surgery?
stabilise where possible - chest drain as needed
pre-oxygenate
keep calm
minimise CVS depression
analgesia
no alpha-2s or ACP
only methadone
possibly inotropes
what is etomidate?
short acting non-barbituate hypnotic drug used to induce man and continuous infusion
causes minimal cardiopulmonary depression
respiratory effects similar to propofol
unlicenced
what are the benefits of fentanyl?
potent mac sparing - minimises respiratory and CV depression
can be given bolus or CRI
what is the onset time and length of action of fentanyl?
onset - 5 minutes
duration of action - 20-40 minutes
what can you use to allow one lung ventilation?
double lumen tube
endobronchial blocker
can use ETT in one lung intubation
what are the negatives of using an ETT for one lung ventilation?
may not effectively ventilate the lung
risk of contamination between lungs
hard in big dogs due to tube length
when do you perform one lung ventilation?
when pathology effects only one lung
improve surgical exposure
how does an endobronchial blocker work?
blocks one of the bronchioles so only one lung is ventilated
what are the downsides of using an endobronchial blocker for one lung ventilation?
needs bronchoscope to place
high skill needed
expensive
if over inflate can cause bronchial wall damage, or if moving patient and it dislodges
what are the negatives of double lumen tube for one lung ventilation?
bulky and hard to place
cant do in big dogs due to tube length as are human tubes
what are the advantages of double lumen tubes for one lung ventilation?
can be done blind
left and right tubes available
what are considerations for ventilating thoracic surgery patients?
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
what ventilatory measure should you monitor when the chest is open and why?
PaCO2
ETCO2 and PaCO2 arent consistent with open thorax causing altered ventilation perfusion relationships
what is the best way to measure oxygen in thoracic surgery patients?
blood gas and PaO2
SpO2 not ideal
why is an art line recommended in thoracic surgery?
detect hypoxaemia as procedure can cause significant cardiopulmonary disturbances
how do you manage hypoxaemia in thoracic patients?
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
what is the alveolar recruitment manouvure?
30cmH2O airway pressure for a breath hold manually
what CVS monitoring is in place for thoracic surgery?
ECG
art line
BP
what other considerations are needed for thoracic pateints?
fluid therapy
hypothermia management
what analgesia plan shoudl be in place for thoracic patients?
aggressive, local and systemic analgesia
full mu agonsit
epidural morphine
intercostal nerve blocks
LA down chest drain
NSAIDs if good BP
describe how you would wean a patient off the ventilator following thoracic surgery
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
how do you recover patients following thoracic surgery?
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
what are considerations for elective ortho cases?
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
describe the positioning of the femoral and sciatic nerve block
in line with the wing of the ileum and ischiatic tuberosity
list considerations for mandibular fractures
pain
other injuries
blood loss
hydration
intubation challenging
possible debris in pharynx
analgesia
surgical access for monitoring
feeding tube post op
fluid therapy
describe considerations for pharyngostomy intubation
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
what are considerations for MRI?
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
list considerations for spinal surgery patients
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
when do 50% of anaesthetic deaths occur?
within 3 hours of recovery
which animals are higher risk under anaesthetic?
cats
sick animals
general over sedation
urgent procedures
old age
brachycephalic and dociocephalic
which type of airway management has increased risk in cats?
ETT
which type of induction has higher risk of mortality?
inhalational is 6x more risk than injectable
why are veterinary anaesthetics more risky than human?
less equipment and training
what are some types of anaesthetic accidents?
sick patients
equipment failure
inadequate prep
inadequate monitoring
define complication
event that develops not due to human error
define error
avoidable event caused by human
list some human errors that can occur during anaesthetic
drug admin errors
poor clinical assessment
inadequate knowledge of equipment/protocols
poor monitoring
closed APL valve
list some types of equipment failure
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
how can you improve anaesthetic safety?
checklists to prevent mistakes
list complications from IVCs
trauma on insertion
poor placement
infection
inflammation of skin
phlebitis/inflammation of vein
dislodged from vein
air embolism
pain
how can you prevent IV cath complications?
aseptic technique
start low then move up if needed
correct catheter size
good technique
prevent interference
daily observation and dressing changes
regular flushing
what are some examples of drug admin errors?
wrong decimal place
wrong drug
wrong dose
incorrect route
poor communication
how to avoid drug admin errors?
check calculation
weigh patient
label drugs
look for likely drug reactions
careful prep of drugs
record drug on chart
what should you do in the case of drug errors?
tell vet
stop giving
close monitoring
check drug sheet
inform owner
poisons service if needed
what are risks for regurg in anaesthesia?
induction and recovery
species dependent
drug dependent
what can increase risk of GOR?
incorrect fasting period
drugs - diazepam, opioids as relax sphincters
abdo pressure
long surgery
abdo surgery
ortho surgery as lots of moving
what are possible consequences of GOR?
unable to swallow on recovery
distress
vomiting blood tinged fluids
damage to oesophagus
how to lower risk of GOR pre-ga?
8 hour fasting
identify risky patients
pre-op GI protectants
head up and swift induction
cuffed tube
suction ready
how do you respond if a patient has regurged?
head down
suction/swab out pharynx
consider omeprazole
record
inform vet
what can be consequences of GOR?
oesophageal strictures
aspiration
what can be causes of corneal ulcers under GA?
reduced tear formation due to anaesthesia, sedation and opioids
trauma - heat, face masks, liquids
how can you prevent ocular damage in anaesthesia?
care with warming devices
careful positioning of patient and face masks
avoid droplets around face
regular ophthalmic treatment
how do you manage a patient with an ulcer?
pain relief
prevent rubbing or scratching with buster collar
tell vet
eye treatment
find cause
tell owner
what is core and peripheral body temperature when concious?
core - 37
periphery - 31-35
what is core and peripheral body temperature when anaesthetised?
core - 36
periphery - 33-35
why does core and peripheral temperature vary between conscious and anaesthetised patients?
vasoconstricted when conscious and vasodilated when anaesthetised
what are the negative consequences of patients becoming hypothermic during anaesthesia?
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
how does patients being hypothermic affect the GA?
prolong drugs
decrease renal plasma flow
decrease oxygen delivery
lowered anaesthetic requirements
how can you try to prevent hypothermia?
insulation
warm from premed
can use HME on breathing system
care with clipping and scrubbing
external heat sources
warm environment
minimise GA time
how does HME system work and what are the negatives?
warms air, as it bypasses URT when intubated
negatives - expensive, increases drag and deadspace
what are the effects of hyperthermia on patients?
increased basal metabolic rate
increased oxygen requirement
parenchymal cell damage
over 41 degrees - poss irreversible brain damage
over 43 degrees - death
which patients are particularly at risk of becoming hyperthermic?
brachycephalics
obese
how can you avoid hyperthermia?
close observation of warming
dont leave on heat they cant move from
cool if needed - fan, wet towel, cold water lavage
list mechanisms of respiratory failure
depression of respiratory centres in the brain
impaired thoracic cage movement - sandbags, increased intra-abdominal pressure
impaired lung movement - pleural effusion
airway obstruction
what are signs of respiratory obstruction?
breed or condition indicators
increased RR
paradoxical ventilation
no air movement
cyanosis
capnograph change
careful obs
list causes of apnoea, arrest or cyanosis
too light or too deep
respiratory tract obstruction
drug related
post induction
poor oxygen supply
low CO
how do you manage post-induction apnoea?
wait before venting to allow CO2 to build up to stimulate spontaneous ventilation
how do you manage respiratory obstruction?
inform vet
suction mouth as needed
straighten neck
check oxygen and equipment
oxygenate
intubate
corticosteroids
how do you prepare for BOAS patients likely having difficult airways?
pre-oxygenate to give more time to decompensation
how do you manage respiratory obstructions when a patient is intubated?
check for kinks or obstruction
check tube length
check if damaged
check breathing system and oxygen supply
how should you manage apnoea and cyanosis during surgery?
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
define cardiac arrest
cessation of effective circulation
what can cause CA?
pre-existing CV disease
drug overdose
hypovolaemia
electrolyte and acid base imbalances
vagal reflex causing bradycardia and CA
respiratory arrest
how should CA during GA be managed?
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
how should ECGs be used during GA?
identifying abnormal
not diagnostic
what are the functions of the different types of cells in the heart?
myocardial cells - contract
self-excitatory cells - generate impulses in the heart
define automaticity
cells ability to generate a beat
what HR can different areas of the heart generate?
SA node - 60-160
AV node, bundle of his - 40-60
purkinjie fibres - 20-40
define arrhythmia
change in rhythm, rate or origin that differs from normal cardiac cycle
what is the significance of arrythmias?
most clinically insignificant, some fatal
what is a 1st degree block?
signal struggles to get through, longer PR interval
describe a type 1 2nd degree block
progressive lengthening of PR interval until dropped beat as impulse blocked, then back to normal
describe type 2 2nd degree block
intermittent passage of signal so beat suddenly drops
describe 3rd degree block
complete heart block, electrical signal cant get past AV node so impulses randomly generated in other parts of the heart causing weak heart beat
what is v tach?
rapid heart rate caused by abnormal complexes from ventricles
what do you do if you notice your patient has arrythmia under anaesthetic?
take photo/print ECG
tell vet
