SA Anaesthesia Flashcards
How common is anaesthetic related mortality in healthy dogs, cats, rabbits and horses?
Dogs: 0.05%
Cats: 0.1%
Rabbits: 0.7%
Horses: 1%
What risk factors are there for perianaesthetic mortality?
Pre-existing disease (main one)
Overweight/underweight
Procedure urgency and duration
Emergency procedures
5 day 1 anaesthetic skills?
- Ensure patent airway
- Give oxygen
- Know how to apply IPPV
- IV catheter and giving IV drugs
- Basic CCPR
ASA statuses for anaesthesia?
ASA 1: normal healthy animal
ASA 2: mild systemic disease
ASA 3: moderate systemic disease
ASA 4: severe systemic disease, constant life threat
ASA 5: moribund, not expected to survive following 24h
What are the 3 aims of anaesthesia?
Unconsciousness
Analgesia
Muscle relaxation
Which of the following anaesthetic drugs give analgesia, sedation, unconsciousness and muscle relaxation?
ACP Benzodiazepines A2 agonists Opioids Barbiturates Ketamine Propofol Inhalationals N2O Local anaesthetics
Analgesia: - a2 agonists - opioids - ketamine - N20 - local anaesthetics Sedatives: - ACP - a2 agonists - opioids Unconsciousness: - barbiturates - ketamine - propofol - inhalationals Muscle relaxation: - ACP - benzodiazepines - a2 agonists - barbiturates - propofol - inhalationals
What is balanced anaesthesia? Why used?
Using 2 or more agents to provide anaesthetics
Reduces doses of each drug, reduces side effects and optimises analgesia
Define sedation?
Mental calming/sleeping and disinterest in environment/decreased responsiveness to stimuli
Purpose of a premedication?
Relieve anxiety Smooths induction, maintenance and recovery Anaesthetic sparing effects Pre-emptive analgesia Reduces muscle tone
Uses of sedation?
Premedication
Chemical restraint
Analgesia
Reduce muscle tone
ACP: Type of drug? What used for? What used alongside? How does it work? Does it give analgesia? Onset of action? Duration? Side effects? Patients to be careful with?
Type: Phenothiazine
Action:
- mental calming due to dopamine antagonism
- potentiates CNS depressant effects of other agents
Use:
- commonly used as a premed, often with opioids
- no analgesia
- not reversible
Onset and duration:
- 30-40 mins for mental calming
- 4-6h duration
- unpredictable sedative
Side effects:
- vasodilation and hypotension
- syncope (CV collapse due to hypotension and bradycardia, esp. brachycephalics)
- pharyngeal muscle relaxation (problem in brachycephalics)
- hypothermia
- at high doses, can cause excitation
Be careful with:
- cardiovascularly compromised patients
- brachycephalics
- very excited animals
- paediatric patients (CV effects more risky)
- breeding stallions
- epileptics (may lower seizure threshold)
Azaperone: Type of drug? How it works? When used? When to be careful? Side effects?
Type: butyrophenones Action: - antidopaminergic and anti-adrenergic effects in reticular activating system of CNS Use: - pigs Side effects: - penile prolapse in boars if large doses - hypothermia Be careful with: - brachycephalic pigs
A2 agonists: Uses? How it works? Is there any analgesia or muscle relaxation? Reversible? Side effects? What to be careful with?
Uses: - sedation and premed - predictable, dose dependent sedation How it works: - suppresses activity in reticular activating system - a2 agonism in the locus coeruleus in brainstem - analgesia (shorter duration than the sedation) and muscle relaxation - reversible (atipamezole) Side effects: - initial hypertension and peripheral vasoconstriction -> reflex bradycardia -> relaxation of peripheral vascular tone -> BP stabilises - significant reduction of cardiac output - sinus arrhythmia, SA block, AV block - diuresis - hyperglycaemia - GI effects - sweating - hypoxaemia with high doses - suppression of thermoregulation Care with: - absorbed across mucous membranes - animals with CV disease/compromise - sick/debilitated patients - patients with diabetes mellitus - patients with laryngeal dysfunction - small ruminants
Benzodiazepines: Uses? How it works? Does it give analgesia and muscle relaxation? Side effects? Reversible? Care? Licensed?
Uses: - unreliable sedation in healthy animals - useful in 'at risk' patients - anti-convulsant - often used for induction with other agents Action: - GABA-specific benzodiazepine binding sites in brain and spinal cord - central muscle relaxtation - no analgesia - reversible with flumazenil or surmazenil Side effects: - minimal CV depression - at high doses, midazolam will cause greater CV depression than diazepam - minimal respiratory depression - enhances depression of other drugs Care with: - diazepam binds to some plastics - postural muscle weakness (can't use for large animals as this makes them panic) - care if hepatic disease None licensed
Opioids: Uses? Analgesia? Action? Reversible? Analgesia?
Uses: - potent, effective analgesia - poor sedation (can be used for low level sedation of severely compromised patients) Action: - bind to opioid receptors - reversible Side effects: - resp, GI, CV
Advantages and disadvantages of injectable induction agents?
Advs: - not much equipment needed - generally rapid and smooth - no environmental poolution Disadvs: - can't retrieve - need accurate weight/good estimate - CV and respiratory depression
Propofol: Use? Benefits? Side effects? What to be aware of with cats? When to be careful?
Use: induction Benefits: - rapid and smooth - not often painful - twitching not common Side effects: - vasodilation with no compensatory increase in HR (reduces CO) - post-induction apnoea - negative inotrope Cats: - repeated doses are cumulative (takes a couple of days to remove from body) - potential for Heinz body anaemia (oxidative damage to RBCs) Careful with: - cardiovascularly compromised patients
Why does propofol cause post-induction apnoea? What to do if happens/to compensate?
Increases the level of CO2 allowed before brain signals to breathe (to about 60mmHg)
Can use IPPV
Pre-oxygenate for 5 mins via mask before induction to compensate
Alfaxolone: Use? Side effects? Benefits? When to be careful?
Use: induction
Side effects:
- vasodilation with compensatory increase in HR
- post-induction apnoea (less than propofol)
- less smooth than propofol
- more twitching than propofol (avoid in seizure patients)
Benefits:
- cardiac output maintained better than propofol
- non cumulative in cats
- can give IM or IV
Ketamine: Uses? How it works? Side effects?
Use:
- induction (main induction agent for horses)
- analgesia (can use lower dose alongside propofol/alfaxolone for analgesia)
- often given IM as part of ‘triple combination’ in cats
Action:
- NMDA antagonist
Side effects:
- increases sympathetic tone -> vasoconstriction
- direct negative inotrope (in normal animal, CO stays the same due to opposite effects of vasoconstriction and negative inotropy)
- post-induction apnoea (often breathe again after giving one breath)
- muscle rigidity (use with drug which gives muscle relaxation e.g. benzodiazepine)
- excessive salivation in dogs and cats
- often keep cranial nerve reflexes so hard to tell how asleep
Etomidate: Use? Benefit? Side effects?
Use: - induction - but not often used/available Benefits: - only agent with virtually no CV effects - good for CV compromised patients Side effects: - stops adrenal glands working
Is thiopental used in smallies? Why?
No (just horses as only drug able to use at sensible volume when horse too light on table)
CV effects - arrhythmias etc
Advantages and disadvantages of inhalation agents for induction?
Advs: - doesn't require IV access Disadvs: - prolonged induction time - distress - airway irritation - environmental pollution - requires tight fitting mask or chamber - increased risk of death
Avoid unless have to use!
Sevo better - smells nicer, breathe better, quicker, reduced chance of death
Which is the only induction agent with true analgesia?
Ketamine
Advantages and disadvantages of inhalation agents for maintenance of anaesthesia?
Advs: - also delivers oxygen - can ventilate if required - easy to alter anaesthetic level - easy to remove from animal - low running costs Disadvantages: - expensive equipment - cannot deliver without specialist equipment - must have an airway
Advantages and disadvantages of intravenous agents for maintenance of anaesthesia?
Advs:
- no need for a lot of specialist equipment
- bolus or TIVA
- may be better for some types of problem
Disadvs:
- cumulative effect -> prolonged recovery, slower changes in depth
- doesn’t deliver oxygen
- can’t be easily removed
- drugs can be expensive
What is MAC?
= Minimal alveolar concentration
The alveolar concentration a which 50% of patients will respond to a standard noxious stimulus
Majority of animals should be adequately anaesthetised at 1.2-1.5 x MAC (if need more, likely not enough analgesia or leak)
What affects MAC?
Species Age Hypoxia Profound hypotension Temperature Circulating catecholamines Pregnancy Other drugs
Nitrous oxide: Advs? Disadvs?
Advs: - some analgesia - few CV/resp side effects - cheap Disadvs: - potentially teratogenic - moves into gas filled spaces - can make colic/pneumothorax etc worse (care in ruminants)
Side effects of isoflurane and sevoflurane?
Vasodilation
Respiratory depression
Why monitor anaesthesia?
Maintain physiology Maintain adequate anaesthetic depth Prevent patient suffering from pain Safety to personnel Legal implications
How to monitor the CNS system during anaesthesia?
Palpebral and anal reflexes: brisk -> sluggish -> absent
Eye position: central -> ventral -> central
Pupil: constricted when awake -> dilated -> constricted -> dilated (deep)
Lateral nystagmus = light (or ketamine_
Lacrimation
Changes to autonomic tone:
- sweating
- CV changes
Muscle tone:
- tension in tendon of sternocephalicus
- jaw tone
Movement = very light or about to die (flexor muscles)
How to monitor the CVS during anaesthesia?
Pulse/HR
Pulse quality (subjective)
Feel peripheral pulse for indication of perfusion
Mucuous membrane colour - indicates oxygenation and perfusion
CRT:
- <1s = poor perfusion or hypovolaemia
- >2s = maldistributive shock
Normal HR under anaesthesia for dogs, cats and horses?
Dogs: 50-120
Cats: 60-140
Horses: 24-40
Normal systolic, diastolic and mean BP under anaesthesia for dogs?
Systolic: 80-130
Diastolic: 40-60
Mean: >60
Differences between invasive BP and non invasive BP?
Invasive (IBP):
- continuous readings, have SBP, DBP and MAP
- invasive/risk of infection
- allows arterial blood sampling for blood gases
- more expensive equipment
Non invasive (NIBP):
- intermittent readings, may only get SBP or MAP
- no risk of infection
- need correctly fitting cuffs or inaccurate values
What is pulse oximetry? What level is normal?
Measures % saturation of oxygen of Hb (SpO2)
Also measures pulse
Indirect indication of perfusion (plesthysmograph)
Normal: 97-99%
Be concerned if <95%
Limitation of pulse oximetry?
Affected by: - hypotension/vasoconstriction - bright light - non pigmented mucosa - movement Probe may blanch capillary bed
What is capnography? Normal level? Other uses?
Measures EtCO2 Normal: 35-45mmHg >60 = hypoventilation <35 = hyperventilation Other uses: - checks correct placement of ETT - confirms pulmonary circulation - indicates problems e.g. with breathing system
On which parts of the pain pathway do NSAIDs, opioids, local anaesthetics, NMDA antagonists, Ca channel blockers and tramadol work?
Local anaesthetics just nerve terminal
NMDA antagonists, Ca channel blockers and tramadol: dorsal horn of spinal cord and brainstem-cerebellum
NSAIDs and opiates all 3
NOLANP?
NSAIDs Opioids Local anaesthetics A2 agonists NMDA antagonists Paracetamol
When to not use NSAIDs for short term anaesthetic analgesia?
If think animal may be/become hypotensive (-> reduced renal perfusion)
How do protein binding and vasodilation affect the duration of action of a drug?
Increased protein binding = longer duration
Vasodilation = shorter duration
What increases potency?
Increased lipophilicity
Small size
What toxicities do lidocaine and buipvacanine have?
Lidocaine: - respiratory depression - seizures Bupivacaine: - cardiotoxicity (don't use IV)
Paracetamol: Licensing? Can you use it alongside NSAIDs or steroids? Contraindications?
Licensed in dogs in combination with codeine
Can use with NSAIDs or steroids (despite data sheet)
Not cats!!! Can’t glucoronidate so makes toxic metabolite
Define pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
What are the 4 parts of the pain pathway?
- Transduction by nociceptor: convert stimulus to nerve impulse
- Transmission by sensory nerve fibre: transmit impulse to brain
- Modulation by spinal cord: ensure pain perceived is proportional to stimulus
- Perception by brain: perceive pain in the brain
Differences in speed of primary afferent axon types for pain? Why is there a difference?
Aa AB: fastest Ad: second fastest C: slowest Due to different amounts of myelination (C fibres are unmyelinated, Aa most myelinated)
Difference in myelination, speed, type of pain and which stimuli elicit the pain, between Ad and C fibres?
Ad: - myelinated - fast pain - sharp, brief pain - well localised - elicited by mechanical or thermal stimuli C: - unmyelinated - slow pain - dull, burning, aching, prolonged pain - more diffuse - elicited mainly by chemical stimuli or persisting mechanical/thermal stimuli
What are nociceptors?
Free nerve endings
What are descending inhibitory neurons?
Originate from the brain
Travel down spinal cord
Inhibits pain stimulus arriving at spinal cord
What are ascending spinothalamic tracts?
Transmits pain stimulus to thalamus in brain
Tracts project contralateral and ipsilateral
What are interneurons for in the pain pathway? How does it work?
Site of stimulus modulation
Non noxious stimulus downgrades the pain stimulus
Mediated by Aa/AB fibres (e.g. rubbing arm after knocking elbow)
What 3 abnormal pain states are there?
Peripheral sensitisation (abnormality of pain receptors or primary afferent neurons) Central sensitisation (abnormality of spinal cord - modulation problem) Altered perception in brain
What causes peripheral sensitisation?
Tissue inflammation in a chemical environment
- > chemical nociceptors continuously activated
- > changes to neuron
Why does central sensitisation happen? What does it result in?
Increased pain transmission via spinal cord
Results in animals responding in exaggerated matter to benign stimuli
What are NMDA receptors for?
= ‘gate keepers’ of spinal cord
Only open if glutamate binds and AMPA prod AP
If Mh dislodged from channel
Impact of sensitisation and plasticity?
Causes chronic pain
Outlasts original tissue injury or healing time
Pain lasting >3mo
E.g. dogs with OA or diabetic neuropathy
Fluid compartments?
60% of body is water
- 40%: ICF
- 20% ECF (15% ISF, 5% plasma)
What is the circulationg volume of dogs, cats, horses, rabbits, sheep and cows?
Dogs and horses: 8-9% BW (80-90ml/kg)
Cats, rabbits, sheep and cows: 6-7% BW (60-70ml/kg)
Which osmotic particles are found in the ECF, ICF and intravascular fluid?
ECF: Na+ and Cl-
Intravascular fluid: Na+, Cl- and colloidal proteins
ICF: K+ and proteins
Normal fluid maintenance requirements?
2-3ml/kg/day or 50-75ml/kg/day
Types of fluid loss? What is lost? From where? Effect on PCV and TP or osmotic potential? Examples of causes?
Whole blood: - e.g. haemorrhage - lose everything - intravascular space only - PCV and TP not altered in short term ECF: - e.g. diarrhoea, vomiting, diuresis - lose water, Na+ and Cl- - lost from ECF - osmotic potential of remaining ECF doesn't change, ICF not affected Protein rich ECF: - e.g. effusions, protein losing conditions, exudates - lose water, proteins, Na+ and Cl- - lost from ECF Pure water loss: - e.g. dehydration - lost from all 3 compartments - osmotic potentials all increased but same gradients so remaining water distributed in normal ratios
Aims of fluid therapy?
Replace like with like
Replace the volume lost
Replace the rate of loss
ECF volume replacers: For each litre given, how much remains in intravascular space?
250ml
Examples of ECF volume replacers? Difference between the two?
Hartmann’s:
- contains the ‘bicarbonate sparing’ lactate ion
Normal saline (0.9%):
- not as good as causes metabolic acidosis??
Types of fluids?
ECF volume replacers
Water replacers
Plasma volume expanders
Blood products
Examples of water replacers: differences between the two? What is needed for a water replacer?
Aquapharm 18:
- contains 4% glucose
Aquapharm 6:
- contains 5% dextrose
Normal fluid loss is hypotonic to the ECF and contains more K+
But can’t put a fluid which is too hypotonic into the vascular space as would cause haemolysis
Types of plasma volume expanders? What is important to know?
Colloids:
- large molecules which can’t pass through a healthy vascular endothelium
- so increase the colloidal osmotic pressure to ‘pull’ water in from ISF
Hypertonic saline (7.2%):
- draws water in from ISF
- causes a pulmonary-vagal reflex -> venoconstriction and bypass of pulmonary circulation
Any effect is only transient
Must be used followed by ECF replacers to payback ISF space
Advantages of enteral fluids? Risks of parenteral fluids?
Enteral: - feeds the gut - natural - no need for sterility - owner can do Parenteral: - sterile - air/thrombus embolism - expense - veterinary procedure
How to monitor fluid therapy?
Urine production/SG
Pulse quality
Skin tent
PCV/TP
What are the main 5 peri-anaesthetic/recovery complications to consider?
Hypotension Hypoventilation/hypoxaemia Hypothermia Pain Bradycardia/tachcardia
Why is it so important to maintain a good blood pressure during anaesthesia?
Affects tissue perfusion!! MAP of >60mmHg needed for perfusion of vital organs (brain, heart, kidneys
What defines hypotension under anaesthesia?
MAP <60mmHg
And/or SAP <80mmHg
Causes of hypotension under anaesthesia?
Hypovolaemia: - haemorrhage - pre-exisitng fluid deficits - fluid loss from evaporation - 'third spacing' - inadequate IVFT Vasodilation: - anaesthetic drugs - severe metabolic or respiratory acidosis - endotoxaemia - septicaemia - anaphylactic reaction Decreased CO due to arrhythmias: - bradycardia - AV block, AF, VT Obstruction of venous return: - secondary to IPPV - pericardial effusion, mediastinal tumours, tension pneumothorax, surgical retraction of organs
What to do if hypotension under anaesthesia?
- Check BP device - cuff/tranducer position, repeat measurement
- Anaesthesia level - lighten?
- Fluid bolus
- Positive inotropes (B1 agonist)
- Vasopressors (a1 agonist)
- Positive chronotropes
Consequences of intra-op hypotension?
Poor recovery
Myopathy
Organ injury
Causes of bradycardia under anaesthesia?
Drugs - high doses of mu opioids, a2 agonists High vagal tone Hypothermia CNS disease (increases ICP) Hyperkalaemia
What to do if bradycardia under anaesthesia?
Check if necessary to treat by checking BP
If a2 agonists were used, can use atipamezole
Anticholinergics (atropine vs glycopyrrolate)
Treat underlying cause
Why is tachycardia a worry under anaesthesia? What to do?
Severe tachycardia greatly reduces CO Reduced diastolic filling time and reduced ejection and coronary perfusion time -> myocardial ischaemia
Treat underlying cause of SNS stimulation
Causes of sinus tachycardia under anaesthesia?
SNS stimulation:
- pain
- inadequate anaesthesia
- hyperthermia
- hypotension
- hypovolaemia
- hypoxaemia
- hypercapnia
- hypoglycaemia
What is hypoxaemia?
Abnormally low oxygen content in systemic arterial blood (PaO2)
What values of PaO2 are considered mild, moderate and severe hypoxaemia?
Mild: <80-90mmHg
Moderate: <60-80mmHg
Severe: <60mmHg
What are the general effects of anaesthesia on the respiratory system?
Respiratory centres and chemoreceptors depressed by GA agents and mu opioid agonists -> reduced ventilatory drive
Depressant effects of anaesthetic drugs on the intercostal muscles and diaphragm -> hypoventilation (consequence hypercapnia)
What is the effect of dorsal recumbency or obesity on respiration?
Lung volume at end of expiration (functional reserve capacity, FRC) is reduced
When FRC is close or less than closing capacity, small airways start to close -> atelectasis
How to recognise hypoxaemia in anaesthetised patients? Problem with anaemia?
Arterial blood gases (PaO2) = gold standard
Pulse oximetry
Animal may breathe ‘hard’ (increased respiratory drive)
MM colour:
- cyanosis (>5g/dl of deoxyHb in blood)
- normal Hb is around 15g/dl
- so if animal is anaemic with Hb<5g/dl it can never be cyanotic
- cyanosis late indicator of hypoxaemia
Causes of hypoxaemia under GA?
Inadequate O2 supply:
- empty cylinder
- blocked hosing
Airway obstruction:
- blocked/kinked ETT or respiratory tract (mucus, blood)
Profound hypoventilation -> hypercapnia (opioids, dorsal recumbency)
V/Q mismatch and shunt
Circulatory failure
Poor gas exchange (increased diffusion barrier)
Increased O2 requirements
What to do if SpO2 <95% and clinical?
Check O2 supply and patency of ETT
Give O2/increased inspired O2 % if possible
IPPV:
- increases TV and RR to increase MV and opens up alveoli
- to reduce effects of hypoventilation/hypercapnia on promoting hypoxaemia
- to improve V/Q mismatching
Ventilation manoeuvre: large breath to open up alveoli
B2 agonist (intra-tracheal best)
CV support - fluids, dobutamine
Intra and post-op consequences of hypothermia?
Intra-op:
CV changes:
- bradycardia
- hypotension
- increased blood loss/coagulopathy
- PCV increases (blood more viscous which increases myocardial work)
Respiratory changes:
- hypoventilation with CO2 retention (respiratory acidosis)
- slight left shift of Hb/O2 dissociation curve (impedes tissue oxygen delivery)
- decreases mucociliary activity (inc risk of airway obstruction and infection)
- immunosuppression
CNS depression:
- MAC reduction (beware of deepening anaesthesia)
Post-op:
- slow recovery (slow metabolism/drug elimination)
- shivering once >34C increases metabolic rate and oxygen demand, increases cardiopulmonary work
- delayed wound healing
- increased wound infection
Define anaphylactic reaction and anaphylactoid reaction
Anaphylactic reaction = IgE mediated, requires previous exposure to agent
Anaphylactoid reaction = IgE independent, no immune trigger necessary
What to anaphylactic/oid reactions cause? Clinical signs?
Both cause rapid degranulation of mast cells -> histamine release, PG, LT Clinical signs: - hypotension - tachycardia - arrhythmias - bronchoconstriction - facial/periorbital/sublingual/laryngeal oedema - death
Treatment for anaphylaxis under anaesthesia?
Depends on severity Antihistamines (chlorphenamine) Corticosteroids IVFT Epinephrine CRI Oxygen therapy CPR
Why is the recovery phase of anaesthesia dangerous?
Greatly reduced physiological support (e.g. secure airway, O2, fluids)
Reduced monitoring
Some problems manifest themselves after a delay
What are the 4 most common recovery problems?
Hypothermia (most common)
Emergence delirium
Hypoxaemia
Hypotension/hypertension?
Causes and consequences of hypothermia in recovery?
Causes: - drugs - clipping - surgical spirit - open body cavity Consequences: - reduced MAC requirement - delayed recovery - shivering - problems with wound healing
What is emergence delirium? Prevention/treatment?
State of dissociation of consciousness Patient is incoherent, inconsolable, irritable and uncooperative Self limiting: 5-15 mins Risk of injury to animal and handlers Prevention/treatment: - sedation - physical restraint - reduce stimulation (noise, light) - adequate analgesia
Causes of hypoxaemia in recovery? Clinical signs? Treatment?
Causes: - airway obstruction - inadequate ventilation (painful breathing, still too deeply anaesthetised) - poor gas exchange (pneumonia, congested lungs, atelectasis) Clinical signs: - cyanotic mm - tachpnoea, dyspnoea - stertor, stridor - reduced level of consciousness Treatment: - ensure patent airway - ventilate - oxygen - analgesia - only extubatne when animal can protect its own airway
Specific recovery problems in dogs and cats?
Gastric reflux/regurgitation/aspiration/stricture:
- related to presence of low pH fluid in oesophagus and/or airway
- reflux into oesophagus occurs in 1 in 6 dogs and cats
- repeated anaesthetics, large/giant breeds and barrel chested dogs may increase risk
Tracheal tear/rupture in cats:
- related to over-inflation of ETT cuffs
- predominantly occur in dental cases
- prevent with pharyngeal packing as alternative measure to protect airway
Blindness in cats:
- related to cerebral ischaemia through hypotension or altered blood flow through use of mouth gags
How to reduce recovery problems?
Monitoring
Communication
Anticipation of risks
Rapid recognition and intervention
What is the aim of euthanasia?
To produce irreversible unconsciousness leading to death as safely as possible with the minimum possible pain, distress or anxiety
Methods of euthanasia? How do they work?
Exsanguination:
- results in hypoxic disruption of CNS activity
Anaesthetic overdose:
- chemical CNS depression
- leads to respiratory and cardiac arrest
Electrical stun:
- electrical disruption of CNS function
Bullet, captive bolt, cervical dislocation (often followed by pithing):
- physical destruction of CNS activity
How do ketamine and opioids affect the eyes under anaesthesia?
Ketamine: affects eye position
Opioids: pupil dilation
Opioid options: type of receptor agonist/antagonist, onset and duration?
Butorphanol: - kappa agonist - mu antagonist Buprenorphine: - partial mu agonist - 30 min onset - 6-8h duration Methadone: - full mu agonist - 5 min onset - 4h duration - has some NMDA antagonism so better analgesia Morphine: - full mu agonist - 30 min onset - 4h duration - not licensed in any species Pethidine: - increases HR instead of decreasing so good for young animals
What is intubeaze? Use? How much to use?
Lidocaine to stop larynx spasming?
Respiratory depression if use too much
1 spray enough for 3kg cat
Tramadol: Use? How does it work? How effective? Side effects?
Use:
- chronic pain
Action:
- metabolised to M1 which acts on mu receptors
- no proper evidence for efficacy
- dogs and cats not very good at metabolising it
Side effects:
- increases chance of GI ulceration if combined with NSAID
Not licensed
Supraorbital (frontal) block: blocks which nerve(s)? Desensitises what? What is it useful for?
Blocks:
- branch of ophthalmic division of trigeminal nerve
- may also block medial fibres of the palpebral nerve -> further inhibit motor function to upper eyelid
Desensitises: middle 2/3 of upper eyelid and skin extending to midline
Artery also emerges from foramen
Useful for:
- thorough ophthalmic exam
- sub-palpebral lavage system placement
Infratrochlear block: blocks which nerve(s)? Desensitises what? What to feel for landmark?
Blocks:
- branch of ophthalmic division of trigeminal nerve
Desensitises:
- medial cants of eye and small surrounding area of skin
Palpate small notch on orbital rim as landmark
Zygomatic block: blocks which nerve? Desensitises what?
Blocks:
- branch of maxillary division of trigeminal nerve
Desensitises:
- middle 2/3 of lower eyelid and small area of adjacent skin
Difficult to identify nerve
Lacrimal block: blocks which nerve? Desensitises what? Technique?
Blocks:
- branch of ophthalmic division of trigeminal nerve
Desensitises:
- lateral canthus of eye and adjacent region of skin
Technique:
- difficult to identify nerve
- direct needle s/c along rostromedial border of supraorbital process
What is a ‘diamond’ block?
Complete desensitisation of eyelids (and eye?)
Subraorbital, lacrimal, zygomatic and infratrochlear blocks
(Auriculo)palpebral block: Blocks which nerve? Technique? Desensitises what?
Blocks:
- palpebral branch of facial nerve
Technique:
- nerve palpable sc over dorsal border of zygomatic arch
Desensitises:
- motor function only o orbiculares oculi
- blocking further caudally will affect the ear
What blocks can be used for an enucleation? How much local anaesthetic needed?
Retrobulbar block: - 1 point or 4 point Peterson block: - usually combined with palpebral block to decrease eyelid movement 10-20ml local anaesthetic
Retrobulbar block: Blocks which nerves? Result?
Blocks: - cranial nerves II-VI Result: - sensory and motor block - blindness - some motor function to eyelids may be retained from facial nerve
Complication risks of a retrobulbar block?
Haematoma Intravascular injection Nerve damage Injection into optic nerve sheath -> brain -> seizures Intraocular damage Oculocardiac reflex -> bradycardia
What blocks may be used for the muzzle/dentals?
Infraorbital or maxillary block:
- to block the maxillary branch of the trigeminal nerve
Mental or mandibular block:
- to block the inferior alveolar branch of mandibular division of the trigeminal nerve
Infraorbital block: Blocks which nerve? Desensitises what? Technique?
Blocks:
- maxillary branch of the trigeminal nerve
Desensitises:
- soft tissue only (not teeth), rostral to site of injection
Technique:
- nerve emerges from infraorbital foramen deep to levator labii superiors and elevator nasolabialis muscles
- foramen palpable by displacement of these muscles
How to block the muzzle/lips e.g. for a nose ring in cattle?
Local infiltration of fleshy tissue of nasal septum
Or bilateral infraorbital nerve block
Maxillary block: Blocks which nerve? Desensitises what? Technique?
Blocks:
- maxillary nerve
Desensitises:
- all teeth in maxillary arcade and associated structures including paranasal sinuses and soft tissue
Technique:
- blocks nerve where it enters caudal aspect of infraorbital canal
- risk of hitting maxillary artery
Mental block: blocks which nerve? Desensitises what? Technique?
Blocks:
- inferior alveolar branch of mandibular division of the trigeminal nerve
Desensitises:
- soft tissues rostral to this point (not teeth)
Technique:
- nerve emerges from mental foramen deep to depressor labii inferioris muscle
- foramen palpable by displacing muscle
- inject 2-5ml around foramen
Mandibular block: blocks which nerve? Desensitises what? Technique?
Blocks:
- mandibular nerve
Desensitises:
- all lower teeth and soft tissue structures rostral to site of injection
Technique:
- blocks nerve where it enters mandibular foramen on medial aspect of mandible
- foramen lies at intersection of lines drawn along occlusal surfaces of cheek teeth and vertically from lateral canthus of eye
- need 15cm spinal needle
- approach from ventral or caudal aspect of
mandible
- inject 10-20ml
Auricular block: blocks which nerve(s)? Desensitises what?
Blocks:
- auriculotemporal nerve (branch of mandibular nerve -> trigeminal)
- great auricular nerve (spinal nerves C2-C3)
Desensitises:
- sensory blockade of external ear canal and pinna
What is IVRA? Which drug used? Possible complications?
Intravenous regional anaesthesia
= Anaesthesia of limbs distal to tourniquet
Only lidocaine!
Complications:
- faulty tourniquet -> high systemic plasma levels - toxicity
- ischaemia/reperfusion injury if tourniquet left for too long (max 2h)
Brachial plexus block: Blocks which nerves?
Nerves forming from C6, C7, C8 and T1 Musculocutaneous Axillary Radial Median Ulnar
What is a RUMM block? Blocks where? Technique? Benefit?
Radial, ulnar, median and musculocutaneous
Blocks distal to elbow
Lateral surface -> radial
Medial surface -> ulnar, median, musculocutaneous
No risk of thoracic puncture
Contraindications of an epidural?
Bacterial infection of the skin
Hypovolaemia, hypotension!!
Bleeding disorders
Epidural anaesthesia: What can be injected?
Opioids
A2 agonists
Local anaesthetics
Preservative free drugs should be used
Lumbosacral epidural: landmarks? How to check correct placement?
Landmarks: - wings of ileum - middle finger at L-S space Correct placement: - 'pop' sensation - negative pressure in epidural space - hanging drop technique if in sternal, lack of resistance to injection if in lateral
Intercoccygeal epidural: Technique?
Technique:
- first intercoccygeal space
- sacrococcygeal articulation usually difficult to access
- feel for first obvious articulation
- ‘3 finger’ rule
Caudal epidural: Technique? Blocks where?
Technique: - space between sacrum and Co1 or Co2 Blocks: - perineum - tail - sacrum
How to know if a paravertebral block has worked (cows and horses)?
Spinal curvature and bowing out of flank so blocked side is convex (flank muscle relaxation)
Flank feels warm (vasodilation as sympathetic nerve blocked)
No response to needle prick
Intercostal block: Indications? Technique?
Indications: - lateral thoracotomy - analgesia for rib fractures - chest drain placement Technique: - block 5 intercostal spaces - the one of the incision - 2 in front and 2 behind - inter needle caudal to rib
Components of a breathing system?
Fresh gas inlet
Breathing system tubes
Reservoir bag
Adjustable pressure limiting (APL) valve - connected to scavenging system
Types of anaesthetic scavenging systems?
Passive scavenging:
- waste gases are transferred to a canister containing activated charcoal to absorb inhalation anaesthetic agents
Active scavenging:
- waste gases are actively suctioned away under negative pressure to a remote area
What makes up an exhaled breath?
1/3 is from dead space: high O2, no CO2 (safe to breathe in)
2/3 is from alveoli: less O2, contains CO2 (potentially harmful if breathed in again)
Difference between non-rebreathing and rebreathing circuits?
Non-rebreathing: end tidal CO2 containing gases flushed out of system by fresh gas flowing in
Rebreathing: soda lime absorbs and removes CO2, conserving the remainder of the warm, moist gases for re-use
What are the Mapleson breathing systems? How efficient are they?
A - F (A most efficient, F least efficient)
Mapleson A:
- Magill: fresh gas and exhaled gas through same tube
- Parallel lack: tubes side by side
- Coaxial lack: fresh gas tube inside exhaled gas tube
Mapleson B and C not commonly used
Mapleson D:
- Coaxial Bain: tube within tube (same as coaxial lack except thinner inner fresh gas tube)
- Mini modified parallel Bain system
Mapleson E:
- Ayre’s T piece: fresh gas tube and exhaled gas tube, no reservoir bag or valve, doesn’t go to scavenge
Mapleson F:
- Jackson-Rees modified Ayre’s T-piece: fresh gas tube and exhaled gas tube, reservoir bag added on to exhaled gas tube
Benefit of rebreathing systems? Types?
Need less fresh gas
Circle or to and fro
Circle system: Type of breathing circuit? How do the valves work?
Rebreathing
One way valves means one way flow of gases in circular route
Which breathing system is used for which size patient?
T piece systems: - Ayre's T-piece, Jackson-Rees modified Ayre's T=piece, mini Mapleson D - patients <10kg - mini mapleson D if <5kg (or no valve) Bain: - 10-80kg Small animal circle: - 10-135kg Large animal circle: - >135kg
In Sath, use Mapleson D if <10kg, circle if >10kg?
How big a rebreathing bag do you need?
A capacity of at least twice a normal tidal volume for the animal
What is the inter-granular volume of soda lime? Relevance?
The volume of air gaps between the soda lime granules
Usually about half the canister’s capacity
Ideally should be at least twice the maximum tidal volume for the animal (2-3 x resting TV)
Calculation for tidal volume and respiratory rate? What is minute ventilation?
TV = 10-20ml/kg RR = 10-20brpm Minute ventilation = TV x RR So minute ventilation is 100-400ml/kg/min Go for middle so 200ml/kg/min
How to calculate the fresh gas flow for T piece, modified Bain, Magill and Lack?
T piece and modified Bain: - 2-4 x minute ventilation - = 400-800ml/kg/min Magill and Lack: - 1 x minute ventilation - = 300ml/kg/min
Which non-rebreathing breathing systems are better and worse at IPPV?
T piece and Bain more efficient for IPPV so can halve the fresh gas flow (to 200-400ml/kg/min)
Magill and Lack are less efficient for IPPV so double the fresh gas flow (to 400-800ml/kg/min)
How to calculate the fresh gas flow needed for rebreathing systems?
Metabolic O2 requirement = 4-10ml/kg/min
Larger animals require relatively less as smaller surface area to size (horses closer to 4ml/kg/min, small animals closer to 10ml/kg/min)
Why do we start on a higher fresh gas flow than the required calculation for rebreathing systems?
Accuracy of flow meters and vaporisers:
- not as accurate at O2 flows <500ml/min
Small leaks in breathing system tubing:
- plastic tubes not completely impermeable to gases
Capnography:
- removes around 150ml/min of gas
So times calculation by 2-4 (still more efficient than non re-breathing)
Why is a higher fresh gas flow needed for the first 5-20 mins of an anaesthetic?
For de-nitrogenation
Removes air from the breathing system tubing and the patient’s lungs/body which is around 70% nitrogen
Allows everything to fill with oxygen and inhalation anaesthetic agent
Can turn down to calculated value after this
E.g. on rebreathing system, give minute volume (200ml/g/min) for first 5-10 mins, then reduce to calculated value
How long does a single dose of IV anaesthetic agent work for?
10-20 mins
Factors affecting the choice of an anaesthetic breathing system?
Size of patient
Mode of ventilation (spontaneous or IPPV)
Requirement for economy of O2/inhalational anaesthestic agent
Expected duration of anaesthetic
Requirement for heat and moisture preservation (also depends on size of patient and length of procedure)
Necessity for sterilisation of breathing system afterwards
Requirement for surgical access to mouth/nose etc
Ease of scavenging
What colour are the O2, air, N2O and CO2 cylinders?
O2: white Air: black and white N2O: blue CO2: grey Check expiry
What to check when setting up anaesthetic machine?
Check O2 cylinder expiry before attaching
Check vaporiser is attached and locked in place
Check dial to ensure doesn’t get stuck
Check enough isoflurane
How to do a leak test on a rebreathing circuit?
Always attach scavenger
- Close APL valve
- Finger over T-connector
- Increase fresh gas flow until IPPV bag filled
- Feel pressure in bag and ensure it is not deflating (leak if is)
- Check APL working by opening valve and check bag deflates
How to do a leak test on a non rebreathing circuit?
Attach scavenger Attach black tube to common gas outlet Attach circuit 1. Close APL valve (next to scavenger) 2. Finger over T connecter 3. Pressure gauge - ensure it's at 20 and feel bag 4. Turn O2 off 5. Open valve
What is CPCR? What is ROSC?
Cardio-pulmonary cerebral resuscitation
Return of Spontaneous Circulation
What are the 2 components of CPCR?
Chest compressions:
- cardiac pump theory
- thoracic pump theory
Ventilation:
- preferably simultaneous with chest compressions but needs 2 people
- ideally with ETT and IPPV using pure oxygen and the reservoir bag of a breathing circuit
- can blow down ETT but exhaled air around 15% oxygen
- mouth to snout ventilation if not intubated
What are the two theories for chest compressions for CPCR?
Cardiac pump theory:
- ventricles directly compressed between sternum and spine (dorsal recumbency) or between ribs (lateral recumbency)
- blood forced out of heart to lungs and periphery
- relaxation of ventricles returns blood to heart
Thoracic pump theory:
- intra-thoracic pressure increased
- this compresses the aorta and collapses the vena cava, leading to blood flow out of thorax
- during elastic recoil of the chest, decreased intra-thoracic pressure results in blood flow back into the thorax and lungs
Recumbency and chest compression theory used for: round chested dogs, narrow chested dogs, barrel chested dogs, small dogs with compliant chest/most cats and small dogs with incompliant chest/large cats?
Round chested dogs:
- lateral recumbency
- thoracic pump theory over widest portion of chest
Narrow chested dogs:
- lateral recumbency
- cardiac pump theory directly over heart
Barrel chested dogs:
- dorsal recumbency
- cardiac pump theory directly over heart
Small dogs with compliant chests and most cats:
- lateral recumbency
= cardiac pump theory by wrapping fingers of one hand around sternum at level of heart
Small dogs with incompliant chests and large cats:
- lateral recumbency
- cardiac pump theory directly over heart
Rate for chest compressions for CPCR? How deep?
Minimum of 100-120/min
Up to 150/min likely better
Must be 1/3 - 1/2 the width of the thorax
Full elastic recoil of chest wall should be allowed before the next compression
Rate for ventilation via ETT for CPCR? How much?
10 breaths/min
10ml/kg TV
Short inspiratory time of 1s
Mouth to snout ventilation for CPCR: ratio of chest compressions:ventilation?
30:2
How long should a cycle of CPCR be for? How long to try for?
Uninterrupted cycles of 2 mins
Try for 10 mins - unlikely to resuscitate after that and may have brain damage
What are interposed abdominal compressions for CPCR? Risks?
Application of abdominal pressure during elastic recoil phase of chest compressions
Pressure applied just cranial to umbilicus
Risk of lacerating liver/spleen if not performed carefully?
