Pain Management Flashcards
define pain according to the IASP definition
an unpleasant sensory and emotional experience associated with, or resembling that which is associated with, actual or potential tissue damage
what factors can the experience of pain be influenced by?
biological
psychological
social
define nociception according to the IASP definition
the neural process of encoding noxious stimuli (physiological processes)
what forms may the consequences of encoding of stimuli take?
autonomic
behavioral
is pain sensation implied when nociception occurs?
not necessarily
what is the key difference between nociception and pain?
nociception is the wiring part of the process
pain is how the patient interprets nociception
in two animals injected IM with the same technique are nociception and pain likely to be the same?
nociception is likely to be identical whereas pain, the feeling, interpretation and expression of response to nociceptive stimuli, is not.
define nociceptive pain according to the IASP definition
pain that arises from actual or threatened damage to non-neural tissues and is due to the activation of nociceptors
what is the term nociceptive pain used to describe?
pain occurring with a normally functioning somatosensory nervous system
define neuropathic pain according to the IASP definition
a lesion or disease of the somatosensory nervous system
what is the term neuropathic pain a clinical description of?
a demonstrable lesion or a disease
when is the term lesion used when discussing neuropathic pain?
when diagnostic investigations reveal an abnormality or where there was obvious trauma
when is the term disease commonly used when discussing neuropathic pain?
when the underlying cause of the lesion is known
what is the difference between nociceptive pain and neuropathic pain?
nociceptive pain arises from injury to non-neural tissue, neuropathic pain arises from damage to the somatosensory nervous system
why is it essential to avoid damaging neural tissue during elective surgical procedures?
so that neuropathic pain is is not caused alongside nociceptive
of nociceptive and neuropathic pain, which can be harder to treat?
neuropathic
what do the terms hyperalgesia and allodynia both describe?
changes in nociceptive processing that may occur in patients in an ongoing pain state
define hyperalgesia according to the IASP definition
increased pain from a stimulus that normally provokes pain (increased response at a normal threshold)
give an example of hyperalgesia
pressing on the skin can become painful if enough pressure is applied, however if the skin is bruised the pressure at which pain will be felt is much less (nociceptive threshold is lower)
define allodynia according to the IASP definition
pain due to a stimulus that does not normally produce pain
give an example of allodynia
due to underlying injury/disease a cat now finds being stroked (a non-noxious stimulus) painful
how long does acute pain last for?
a short period of time - minutes and hours to weeks
how long does chronic pain last for?
longer than a few weeks
what may happen if acute pain is not adequately treated?
may lead to a chronic pain state
what may chronic pain arise from?
chronic medical conditions such as osteoarthritis and skin disorders
is chronic pain generally protective or beneficial to the sufferer?
no it is usually detrimental
when may acute pain be productive?
can stop an animal from causing itself further damage
what can untreated or poorly treated pain lead to?
up-regulation of the pain processing system making the pain harder to treat and the establishment of pain states
what can be reduced by untreated or poorly treated chronic pain?
quality of life
why is recognition and quantification of pain so important?
if we cannot recognise pain we are unable to treat it
quantification allows categorisation of pain, assessment and judgements about quality of life to be made
what are the 3 key stages in the quantification of pain?
categorization of pain as absent, mild, moderate, severe
assess treatment efficacy
make judgements about quality of life
what does the categorization of pain as absent, mild, moderate and severe influence?
how we decide to treat the pain
how can treatment efficacy be assessed?
observing weather pain score reduces if a treatment is used
what judgements about quality of life may be made using quantification of pain?
should the animal be treated or is euthanasia a prefurrable option?
what is the key challenge of assessing pain in animals?
they cannot talk
what can be used to assess pain?
behavioural signs
physiological signs
what are the physiological signs associated with pain?
increased HR, blood pressure and body temperature
altered respiration (rate and pattern)
stress hormones increasing
EEG (electroencephalogram) activity
what is a key issue with using physiological signs to indicate pain?
they are non-specific and may increase or decrease along with things other than pain
what stress hormones could be used to indicate pain?
cortisol, noradrenaline and adrenaline
what is the difficulty of using EEG to determine presence of pain?
is this pain or nociception
are behavioural signs of pain species specific?
yes
why may behavioural signs of pain vary between individuals within a species?
depending on temperament or their response to a stressful environment which may cause them to hide pain
why do prey species tend to hide signs of pain?
so they do not stand out to a predator
what are behavioural signs associated with pain specific to?
species
individual
condition
what are the shared behavioural signs associated with pain exhibited by cats and dogs?
hunched appearance 'pain' face lack of grooming inappetance specific signs (e.g. lameness)
what are the behavioural signs associated with pain that are specific to cats?
absence of normal behavioural repertoire hide away at back of cage unwilling to relax fear-aggression resent human contact
what are the behavioural signs associated with pain that are specific to dogs?
positive behavioural signs rather than reduced repertoire
more likely to seek attention
submissive
more likely to vocalize
what are the behavioural signs associated with pain that are specific to rabbits?
immobility profound depression eyes half closed or shut not grooming avoiding attention isolating themselves from other animals bruxism abnormal body position such as a hunched posture and abdominal pressing change in temperament
when is immobility in rabbits particularly acute?
post-op or traumatic pain however they may show this behaviour in unusual environments when there is no pain at all
define bruxism
tooth grinding
what is an essential consideration when handling animals in pain?
prey animals with a strong fight or flight response which means that they can react violently to severe pain
what are the behavioural signs associated with pain that are specific to horses?
low head carriage horse at back of stable vocalisation (groaning or neighing) agitation restlessness weight-shifting tail swishing (with no flies present) lameness limb lifting abnormal distribution of weight 'tucked up' appearance looking at painful body part 'pain face' bruxism sweating muscle fasciculations
what are the main chronic pain indicators in all species?
changes in normal behaviour described by owner (may be put down to animal getting older or slowing down)
unkempt coat if grooming is difficult
loss of body condition/ weight loss due to appetite loss and/or loss of muscle tone if exercising less
slowing down/sleeping more
could also be more restless/fidgety
reluctance to move possibly described as a loss of training (e.g. peeing in the house because they can’t get outside)
difficulty in accessing higher places
what is the NRS?
numerical rating scale which requires patient to assign their pain a score from 1-10
what is VAS?
visual analogue scale which requires patient to make a mark on a line from 1-10 to demonstrate level of pain. The position of the mark on the line is then measured to assign a number
what is SDS?
simple descriptive scale where patients assign themselves a category relating to a description of a pain level that is matched to a number
what can be used to score pain in animal patients?
NRS, VAS or SDS
who awards the scores during pain assessment of animals?
caregiver
what can make pain scoring more accurate?
dynamic interaction with animal rather than just observing
what is an issue with using NRS, VAS or SDS in a veterinary environment?
interobserver variation which can be an issue in a practice where there is likely to be multiple caregivers
what is the purpose of composite pain scales?
over come some of the limitations of the VAS, NRS and SDS
how do composite pain scales work?
multiple items are assessed for each patient and given a score. These are them added to give an overall score
what must happen to composite pain scales in order for them to be useful?
must be validated which requires lots of clinical testing
what is often suggested by composite pain scales?
an intervention level/ score at which the patient should receive an intervention (analgesic medication)
what is the composite pain scale used for dogs?
SF-GCPS: glasgow composite pain scale
what is the SF-GCPS score out of if the dog cannot stand?
20
what is the SF-GCPS score out of if the dog can stand?
24
what is the intervention level of the SF-GCPS?
5/20 or 6/24
what is the drawback of the SF-GCPS?
poor differentiation between sedation and pain which is an issue immediately post-op
what is the composite pain scale used for cats?
CMPS
what is the maximum score of the CMPS?
20
what is the recommended intervention level of the CMPS?
5/20
what is essential to remember when filling in composite pain scores?
follow the order and scores on the sheet
are there composite pain scores for rabbits and horses?
not really at the moment
when may owners be helpful in filling in pain scoring?
to show pain levels over time and levels when not in the veterinary environment. Useful for post-op or chronic pain
what is involved in chronic pain assessment?
can use VAS, NRS, SDS and CPS for a snapshot of pain at a specific time but may want to include other elements such as appetite and sleep over a period of time
are there chronic pain composite pain scores available?
yes, tend to be condition and species specific used to collect data on pain and impact on life functions
with owner pain scoring of chronic pain what are the questions more often about?
quality of life as opposed to specific questions about pain at a single point in time
how does the LOAD questionnaire for OA work?
each of the mobility questions is given a score from 0-4 (not present to most severe). The LOAD score is the sum of the questions
what is another way of monitoring chronic pain?
client specific outcome measures
what is involved with client specific outcome measures?
along with owner 4 or 5 different behaviours are identified that the animal normally performs (or used to)
changes in the frequency of these behaviours or activities are recorded over time (usually from the start of analgesic therapy)
what is a key benefit of client specific outcome measures?
very specific to pet (tailored)
quick to complete
easy to track changes over time
what are the main advantages of owner questionnaires for chronic pain?
allow owner and clinician to see impact of pain on quality of life and the impact of external factors like weather and exercise on pain and quality of life
allows ongoing monitoring and assessment of interventions
what is the benefit of videos as add on or stand alone assessment?
can be shared within the team
behaviour can be shown in the animals natural environment
week on week records can help to detect changes
visible evidence of improvement may improve owner compliance with medication
owner and vet team can see how other factors affect behaviour
any species
why is assessment of health related quality of life useful?
aids decision making about requirement for analgesia or timing of euthanasia
improved patient well-being through holistic/global care
improve continuity of treatment between clinicians or treatment centres
help to build and maintain owner and veterinary professional relationships
what is involved in health-related quality of life assessment?
assessment of quality of life in relation to analgesia and chronic pain
what is preventative anaesthesia?
administration of effective analgesia before, during and after the surgery/procedure, well into the post operative recovery period
what is the aim of preventative analgesia?
prevention of upregulation of the nervous system in the presence of noxious stimuli (e.g. surgery) by administering effective analgesia
what should be seen in response to preventative analgesia?
reduction both in intensity and duration of acute pain and a reduction in persistent (chronic) pain
what is multi-modal analgesia?
using different classes of analgesic agents/techniques to attempt to over come the fact that there is no single analgesic agent that can block all nociceptive/pain pathways
what is a benefit of multi-modal analgesia?
leads to more effective analgesia often with lower doses of analgesic agents
what are the 6 main analgesic agents used in veterinary practice?
opioids NSAIDs local anaesthetics Alpha-2 agonists ketamine others/misc
what is different about alpha 2 agonists and ketamine?
alpha-2 agonists are sedatives which are analgesic
ketamine is an anaesthetic that is analgesic
rather than being only analgesics
what schedule of drugs are full opioid agonists?
schedule 2
give an example of 2 full opioid agonists
methadone and fentanyl
what schedule of controlled drugs are partial opioid agonists?
schedule 3
give an example of 2 partial opioid agonists
buprenorphine and butorphanol
what are the requirements for schedule 2 drugs?
special prescription, storage, destruction and record keeping
what are the requirements for schedule 3 drugs
special prescription and some have special storage requirements (e.g. bupe must be locked away)
where do opioids licensed for cats, dogs and horses act within the body?
endogenous opioid receptors primarily in the brain and spinal cord
what are the 3 key opioid receptors?
delta, kappa and mu
what sorts of agonists may opioids be?
full agonists, partial agonists, mixed agonist antagonist or antagonist
give an example of an opioid mixed agonist-antagonist
butorphanol
give an example of an opioid antagonist
naloxone
which type of receptor agonists are associated with analgesia?
mu
what type of agonists provide the most effective analgesia?
full mu agonists
under what circumstances are opioids used?
acute pain - preventative and part of multi-modal analgesia regimens
define potency
mg/kg of drug required to show effect
define efficacy in terms of drugs
the maximum response possible from a specific drug
why is fentanyl so dangerous?
is highly potent and efficacious - very little required to overdose
how may opioids be administered?
IV oral SC IM buccal
what opioid must not be given IV?
pethidine
what drug may not be so effective when given SC to cats?
buprenorphine
how does buccal administration differ from oral?
buccal requires transmucosal absorption by oral mucous membranes, oral medication is absorbed in the small intestine
why is there poor bio-availability of orally administered opioids?
significant first pass metabolism so they are broken down very quickly and easily by the liver
what does poor bio-availability of opioids mean for chronic pain?
limited role in management of chronic pain
give an example of a short acting mu agonist
fentanyl
when are short acting mu agonists used?
intra-operative and short term infusion
give an example of a long acting full mu agonist
methadone
when are long acting full mu agonists used?
general use for acute and pre, peri and post operative pain
how long do long acting full mu agonists tend to last?
2-4hr
give an example of a partial mu agonist
buprenorphine
when are partial mu agonists often used?
general use for acute and pre, peri and postoperative pain
how long to partial mu agonists last for?
6hrs
give an example of a K agonist and mu receptor
butorphanol
when would a mixed K agonist and mu receptor be used?
general use for acute and pre, peri and postoperative pain
how long do mixed K agonist and mu receptor drugs last for?
2hrs
what are the key side effects of opioid use at clinical doses?
respiratory depression sedation excitation minimal effect on inotropy bradycardia nausea and vomiting antitussive decrease GI motility various effects on urinary system
when are respiratory depression effects most often seen when using opioids?
dose dependent and mostly during anaesthesia
when are sedation side effects seen during opioid use?
species and dose dependant, more sedation seen in dogs
when is excitation often seen as a side effect of opioid use?
at high doses particularly in pain free animals. can cause box walking in horses and excitement in cats
what is inotropy?
force of heart contraction
what causes bradycardia as a side effect when giving opioids?
vagal effect
how can bradycardia as a side effect of opioid use be managed?
use of an anticholinergic such as atropine
when does nausea and vomiting most often occur in patients receiving opioids?
seen in dogs and cats and more common in pain free animals
what is an antitussive effect?
reduction of cough
what effect may opioids have on GI motility?
decrease
how much of an issue is decreased gut motility in dogs and cats?
not too problematic
when is decreased gut motility in opioid use more of an issue?
chronic use
when are side effects of opioids on the urinary system of clinical significance?
not unless administered epidurally
what does NSAID stand for?
non steroidal anti-inflammatory drugs
how do most NSAIDs work?
inhibition of prostaglandin production either through inhibition of COX (cyclo-oxygenase) or LOX (lipoxygenase) enzymes
what are NSAID side effects directly linked to?
protective effects that prostaglandins have on the body
where are NSAIDs metabolised?
the liver
what are NSAIDs effective analgesics for?
acute and chronic pain
when is caution needed when giving NSAIDs?
if administering pre/peri-operatively or if a patient is dehydrated or hypotensive
in what regimens are NSAIDs useful?
multi-modal analgesic
can more than one NSAID be used in a multi-modal analgesic approach?
no - due to side effects
what are the 2 main NSAIDs licensed for use in dogs and cats?
meloxicam
carprophen
who can most NSAIDs be administered to the patient?
injection or oral
what is the main NSAID used in rabbits?
meloxicam
what are the main NSAIDs used in horses?
meloxicam
phenylbutazone
what are the main side effects of NSAID use at clinical doses?
GI ulceration Renal ischaemia Hepatopathy blood clotting CNS effects
when should special care be taken when giving NSAIDs?
those with history of GI ulceration
any patient with reduced drug clearance capacity
during anaesthesia of dogs and cats
why can NSAIDs cause renal ischemia?
during hypotension prostaglandins protect renal blood flow and so this action is blocked by NSAIDs
with what type of NSAIDs is clotting an issue?
the less commonly used non-COX selective NSAIDs
what information should be given to owners about safe use of NSAIDs in dogs and cats?
GI side effects are most common
will present as vomiting and diarrhoea
may see digested blood (coffee grounds)
general malaise
what should owners do if they see any side effects of NSAID use?
discontinue medication immediately and ring the practice
what information should be given to owners about safe use of NSAIDs in horses?
GI side effects most common: GI ulceration presenting as colic, diarrhoea, dehydration and weight loss
renal effects
malaise
when do side effects of NSAIDs most commonly occur in horses?
overdose
chronic administration
weight loss
when are renal effects of NSAIDs more of an issue in the horse?
when dehydrated
what information should be given about safe use of NSAIDs in rabbits?
aware of the fact no NSAIDs are licensed for use in rabbits
GI effects most common
if animal appears unwell (anorexia, bruxism, depression, reluctance to move) owners should discontinue medication and phone practice
when do NSAIDs side effects most commonly occur?
in chronic use
what is the key pharmacology of local anaesthetics?
enter nerve fibre and block voltage gated Na+ channel so blocking nerve conduction
which fibres are preferentially blocked by local anaesthetics?
C fibres and A-delta fibres
what type of blockade is achieved by blocking C and A-delta fibres during local anaesthetic?
nociceptive blockade before proprioceptive, mechanoreceptive and motor blockades
what type of molecules are most local anaesthetics?
weak bases (pKa = 8-9)
what form of the weak base can penetrate lipid membranes and enter the nerve cell?
uncharged form
how does ionisation (pKa) affect onset of local anaesthetic action?
higher pKa will be more ionised in plasma and so have a slower onset of action
what happens to local anaesthetic if the pH of the tissue decreases (e.g. inflammation)?
greater proportion of the drug is ionized and therefore less drug can penetrate the nerve membrane to bind to the sodium channel
where is local anaesthetic less effective?
inflamed tissue
what are the 2 linkages that may be found in different local anaesthetics?
ester
amide
how stable are ester and amide linkages?
ester are relatively unstable
amide are more stable
how rapidly are ester and amide linkages broken down?
ester - rapidly by plasma psudocholinesterase
amide - subject to bio-transformation with conjugation in the liver
how long are ester and amide linkage half-lives?
ester - short local anaesthetic half life
amide - longer plasma half life
how can you tell which local anaesthetic drugs have ester and amide linkages?
ester - no ‘i’ in name before ‘caine’
amide - ‘i’ in name before ‘caine’
what is formed as a byproduct of hydrolysis of ester linkages that can provoke allergic reactions?
PABA
give an example of an ester linkage LA
procaine
give an example of an amide linkage LA
lidocaine
what does the toxicity/side effects of LA depend on?
the dose - safe total dose must never be exceeded
what are the side affects associated with LA?
CNS toxicity
CVS toxicity
what effects are seen with CNS toxicity of LA?
minor behavioral changes
muscle twitching and tremors
tonic-clonic convulsions
CNS depression/ respiratory depression and death
what are the effects seen with CVS toxicity of LA?
hypotension
dysrhythmias
does CNS or CVS toxicity occur at lower doses?
CNS
what is involved in treatment of CNS/CVS side effects of LA?
symptomatic treatment
what animals is lidocaine licensed for?
horses, dogs and cats and is used in rabbits
what is the onset of action of lidocaine?
rapid, 2-5 mins
how long acting is lidocaine?
short - 20-40 mins
what is an advantage of lidocaine over bupivacaine?
lower cardiotoxicity
when are local anaesthetics used?
part of balanced anaesthetics regimen (e.g regional infiltration or epidural under GA)
to provide anaesthesia for standing procedures
post-operative pain relief
desensitisation for procedures (e.g. EMLA)
lameness investigation in horses
what class of drugs does paracetamol fall under?
not an NSAID but can be considered one
what is the mechanism of action of paracetamol?
not fully understood
to what species is paracetamol very toxic?
cats
when is paracetamol useful in dogs?
when NSAIDs are contraindicated
when is paracetamol used in horses?
useful as an adjunctive analgesic in very painful cases and also where NSAIDs are contraindicated
what is the mode of action of tramadol?
multi-modal
mu opioid system, noradrenergic system and serotonergic system
what are the actions of tramadol associated with?
some with tramadol enantiomers and some with its metabolites
what is tramadol used for?
acute and chronic pain conditions
believed to have a wide therapeutic index and lower risk of abuse than opioids
what drug schedule does tramadol fall under?
schedule 3
how should tramadol be administered to dogs?
IV as oral is unlikely to be effective
does current evidence suggest that tramadol should be used alone?
no - should only be used as a co-analgesic
how effective is tramadol in cats?
some analgesic effect given IV, may have effects on chronic pain when given orally
can tramadol be used in horses?
only for laminitis patients that aren’t responding to other analgesics as extended use of opioids can lead to decreased gut motility and risk of impaction/colic
what is the oral bio-availability of tramadol like in horses?
variable
has a short half life
how does gabapentin work?
precise mechanism of action unknown; analgesic action is attributed to binding voltage gated calcium channel
what does binding of gabapentin to voltage gated calcium channels lead to ?
decreased release of excitatory neurotransmitters in the dorsal horn of the spinal chord - reduction in pain sensation in cases of allodynia, hyperalgesia etc
what may gabapentin be used for?
management of neuropathic type pain conditions
what is a major side effect of gabapentin?
sedation
why should liquid solutions containing xylitol be avoided?
due to potential for toxicity as this is a human medication and the sweetner is toxic to veterinary patients
how should gabapentin administration be stopped?
slowly - reduce dose over 1-2 weeks
what is amantadine?
oral NMDA receptor agonist
what is amantadine used for?
antihyperalgesic so should be used alongside an analgesic
how is amantadine excreted?
via kidneys so should be used cautiousl in patients with reduced renal function
when may amantidine be useful?
chronic pain states to reverse or obtund central sensation
how long any it take to see benefit of amantadine therapy?
3-4 weeks
why are animals premedicated prior to anaesthesia?
decreases stress and risk of injury to patients and staff production of balanced anaesthesia provide preventative analgesia assists smooth recovery from anaesthesia reduce side effects of anaesthetic drugs
how can balanced anaesthesia be produced by premedicating animals prior to anaesthetic induction?
reduce dose of induction and maintenance agents
how does premedication reduce the side effects of anaesthetic drugs?
either by giving less or by administering something that counteracts the side effects
what are the 5 main classes of drugs used for premedication?
phenothiazines alpha-2 agonists benzodiazepines butyrophenones opioids
do phenothiazines have sedative and analgesic action?
sedative but not analgesic
do alpha-2 agonists have sedative and analgesic action?
yes
do benzodiazepines have sedative and analgesic action?
sedative but not analgesic
do butyrophenones have sedative and analgesic action?
sedative but not analgesic
do opioids have sedative and analgesic action?
some have sedative action (species dependent) all have analgesic action
what is the mode of action of phenothiazines?
dopamine receptor agonist in the CNS
what is the mode of action of alpha-2 agonists?
alpha-2 adrenergic receptor agonist in the CNS
what is the mode of action of benzodiazepines?
enhance the effect of gamma-aminobutyric acid (GABA) at the GABA-alpha receptor
what is the mode of action of butyrophenones?
dopamine receptor antagonist in the CNS, also interferes with GABA, noradrenaline and serotonin-mediated neuronal activity
what is the vet licenced phenothiazine in the UK?
Acepromazine (ACP)
what are the vet licenced alpha-2 agonist in the UK?
dexmedetomidone and medetomidine are most common
also romifidine and xylazine
what are the vet licenced benzodiazepines in the UK?
diazepam and midazolam
what is the vet licenced butyrophenone in the UK?
Fluanisone - only available in a combination product with fentanyl (Hypnorm)
what are the licenced species for phenothiazines in the UK?
ACP - dog and cat
what are the licensed species of the vet licensed alpha-2 agonists in the UK?
all licensed in dogs and cats
what are the licensed species for veterinary licensed benzodiazepines in the UK?
diazepam in dogs and cats
midazolam in horses
what are the licensed species for veterinary licensed butyrophenones in the UK?
rabbits
what is the advantage of IV premed?
rapid onset of action
predictable effect
what is the advantage of IM premed?
fairly rapid onset of action
predictable effect
what is the advantage of SC premed?
easier to do than IV or IM
what is the advantage of OTM (oral transmucosal) premed?
not useful routinely - can be helpful in special cases (e.g. feral cats)
what is the disadvantage of IV premed?
requires restraint and/or IV catheter placement before anaesthesia
what is the disadvantage of IM premed?
painful
what is the disadvantage of SC premed?
not all drugs are absorbed by this route
can be unpredictable
slower onset than IM
what is the disadvantage of OTM (oral transmucosal) premed?
not all drugs are absorbed by this route
can be unpredictable
slower onset than IM
what are the key clinical effects of ACP (phenothiazine)?
sedation
anxiolytic
what is ACP often used in combination with in premeds?
opioids
what is ACP widely used for in cats and dogs?
sedation for procedures and premedication
what is ACP used for in rabbits?
premedication although not licenced
what is ACP sedation level dependent on?
dose up to plateau dose
how can ACP sedation be improved?
combination with opioid
if animal is left in a quiet environment for 30-40 mins
how effective is SC injection of ACP for sedation?
non-irritant and efficacious, particularly in cats
should the same does of ACP be used for sedation and premedication?
lower doses for premed than for sedation
what are the physiological effects of ACP on the CVS?
peripheral vasodilation
potential to decrease blood pressure particularly in animals with CVS disease or shock
vasodilation also causes fall in body temperature (issue in smaller animals)
minimal effects on respiration
anti-arrythmatic action
what is the time to clinical effect from administration of ACP IV?
10-15 mins (slower than alpha-2 agonists)
when is the clinical effect of ACP seen after IM administration?
30-40 mins
where should animals be left to become sedated with ACP?
quiet area
how long is the duration of action of ACP?
4-6 hours
how is ACP metabolised?
in the liver
in what animals is the action of ACP prolonged?
those with liver diease
how good is the oral bio-availabilty of ACP?
poor
what are the clinical effects of alpha-2 agonists?
sedation
analgesia
muscle relaxation
what is the duration and level of sedation with alpha-2 agonists dependent on?
dose
are alpha-2 agonists potent?
yes - use body surface area rather than weight to calculate dose
what type of drugs are alpha-2 agonists often used with?
opioids
what effect can occur when alpha-2 agonists are combined with other sedatives/analgesics?
additive or synergistic effects
what are the key advantages of alpha-2 agonists?
significant dose reduction for anaesthetic induction and maintenance agents
reversible using antagonist (atipamazole)
what antagonist can be used to reverse alpha-2 agonists?
atipamazole
what are the physiological effects of alpha-2 agonists on the CVS?
bradycardia
reduced cardiac output
second degree AV block
initial rise in BP which will then fall to normal or hypotension
what are the physiological effects of alpha-2 agonists on the respiratory system?
variable between species and individuals within a species
respiratory depression seen in some but not all patients - rate decrease seen but no overall effect on minute volume or blood gases
what can the CVS effects of ACP be managed by?
administration of fluids
what are the physiological effects of alpha-2 agonists on the GI system?
can be emetic in dogs and cats
can depress GI activity and has been reported to cause GI stasis in dogs
why should deep chested dog breeds avoid alpha-2 agonists?
risk of GDV
what are the physiological effects of alpha-2 agonists on animal behaviour?
some temporary behavior and personality changes in dogs and cats (similar to other sedatives)
what are the physiological effects of alpha-2 agonists on the pancreas?
reduced secretion of insulin - may see transient hyperglycaemia which is not harmful to the animal but may mess with blood work
what are the physiological effects of alpha-2 agonists on the renal system?
increase in urine production by a decrease in secretion of vasopressin
what should happen to animals receiving alpha-2 agonists by CRI?
catheterisation
what are the physiological effects of alpha-2 agonists on the uterus?
can affect contractility dependent on dose and concentrations of oestrogen and progesterone
at what life stage should alpha-2 agonists be avoided?
pregnancy - near term due to its effect on uterine contractility and risk of abortion
how long until full clinical effect of alpha-2 agonists after IV administration?
5 minutes
at what time after administration are alpha-2 agonist effects seen?
30 mins
what is the duration of action of alpha-2 agonists if atipamezole isnt used?
2-3 hours
in what animals is the duration of alpha-2 agonists prolonged?
those with liver disease
how are alpha-2 agonists metabolized?
in the liver
what are the clinical effects of benzodiazepines?
minor tranquilisers
muscle relaxation
anticonvulsant
what is sedation with benzodiazapines like in healthy animals?
unreliable and can cause excitement when administered alone
to what animals do benzodiazapines provide good sedation?
the young or sick
what can benzodiazapines be combined with to improve sedation?
opioid, ketamine or alpha-2 agonists
what are benzodiazepines often used for?
adjuncts to anaesthetic induction agents for co-induction
why are benzodiazepines a good choice for unhealthy patients?
they have minimal effects on CVS and respiratory system
what are the effects of benzodiazepines on the CVS?
minimal depression - commonly used with unwell patients or those with CVS disease
what are the effects of benzodiazepines on the respiratory system?
mild, dose dependant respiratory depression
what are the effects of benzodiazepines on the musculoskeletal system?
enhances inhibitory action of GABA (allosteric binding) which prevents muscle contraction
what are benzodiazepines often administered with due to their effects on the musculoskeletal system?
drugs that do not provide muscle relaxations (e.g. ketamine)
why must benzodiazepines be administered slowly IV?
rapidly cross blood brain barrier
when do benzodiazepines have good bio-availability?
when given intranasally
what has been reported rarely in cats following diazepam?
idiosyncratic liver failure
which has a shorter plasma half life out of diazepam and midazolam?
diazepam
how are benzodiazepines metabolised?
liver
what gives diazepam its prolonged effect?
metabolites of diazepam remain active after it is metabolised in the liver
what benzodiazepine can be given by CRI without significant accumulation?
midazolam
what is the benzodiazepine reversal agent?
Flumazenil - expensive!
what can be provided by fentanyl alone?
surgical anaesthesia for minor surgery/diagnostic techniques
what is the duration of sedation/immobilisation associated with fentanyl?
30-60 mins
what is the muscular relaxation like with fentanyl administered alone?
poor
what can provide good muscle relaxation and good surgical anaesthesia if administered alongside fentanyl?
midazolam/diazepam
what respiratory effects may be seen with fentanyl?
moderate to severe respiratory depression
how may depression of the respiratory system by fentanyl be reversed?
reversed or partially reversed by the administration of butorphanol/buprenorphine
how should ASA I and II influence anaesthesia?
standard protocols with routine monitoring
how should ASA III influence anaesthesia?
thorough stabilization should be performed before anaesthesia is attempted. IV catheterisation, fluid therapy and airway protection advised
how should ASA IV and V influence anaesthesia?
as for grade III. Owners should be fully briefed as t additional anaesthetic risk. Doses for CPR should be calculated and first dose drawn up
what is the ASA I and II protocol for dogs and cats?
ACP and opioid
alpha-2 agonist and opioid
what is the ASA I and II protocol for rabbits?
ACP and opioid
alpha-2 agonist and opioid
Fentanyl (Hyponorm) alone or with benzodiazepine
what is the ASA III protocol for dogs?
ACP and opioid
BDZ and opioid
what is the ASA III protocol for cats?
BDZ (midazolam) and ketamine
what is the ASA III protocol for rabbits?
BDZ and opioid
what is the ASA IV and V protocol for dogs, cats and rabbits?
BDZ and opioid
BDZ and ketamine
opioid alone
no premed but need higher doses of induction
how should the sedated/premedicated patient be cared for?
quiet environment observed regularly (with all senses!) ABC monitor temperature, pulse, RR and MM use pulse ox if possible record obs
what can go wrong during sedation/premed?
excitement or excessive sedation
airway obstruction (vomit or anatomical - brachycephallic)
CVS effects up to and including arrest
patient unable to compensate for existing condition/hidden condition is exposed
something odd develops (e.g. gastric dilation)
what parameters should be monitored in the sedated/premedicated patient?
temperature pulse RR MM pulse ox
what is the difference between sedation and premedication?
during sedation the patient is sedated but not anaesthetised, there is no loss of consciousness
premedication is administered before anaesthetic
how do drug doses differ between premedication and sedation?
same drug combinations often used but doses for premedication will be lower than sedation
what is sedation?
patient is not fully awake but is not fully unconscious (anaesthetic)
what is the purpose of sedation?
allows procedures that may/would be impossible in a fully concoius patient
what is the difference in sedation between large and small animals?
in farm animals it is common to perform procedures including invasive surgery using (standing) sedation and LA
very unusual in small animals
when is sedation appropriate in small animal practice?
safe handling of anxious/dangerous/feral animals for procedures that would usually be performed with out sedation (e.g. blood sample)
procedures that are not painful or invasive but require the animal to be still (e.g. radiography)
minor procedures (e.g. wound redressing, de-matting)
why may sedation be safer that full GA for small animals?
theoretically less extreme
why is sedation not necessarily safer than full GA in small animals?
no control over airway
often no option of deepening sedation if it is inadequate for the job without progressing to full GA
staff and patient safety - will sedation do the job (e.g. radiography - will the patient jump off the table)
what methods of sedation are best used in feral/dangerous cases?
IM in crush cage
OTM can be squirted in
what sedation can be reversed?
alpha-2 agonists, opioids and benzodiazepines can all potentially be reversed. usually only alpha-2 agonists reversed. (atipam)
fentanyl
what can be used to reverse sedation with fentanyl?
opioid partial agonist/agonist antagonist/antagonist
define potency
mg/kg of drug required to show effect
