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Year 3 > Anaesthesia > Flashcards

Anaesthesia Flashcards

1
Q

Which drug is used to reverse the effects of medetomidine?

A

Atipamezole

Reverses sedation but also analgesia

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2
Q

Which drugs can be used as sedatives?

A

Phenothiazines eg acepromazine (2mg/ml SA)
Alpha 2 agonists eg xylazine, Medetomidine, Dexmedetomidine (SA), Detomidine (LA), Romifidine (horses)
Benzodiazepines eg Diazepam, Midazolam

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3
Q

Which 2 types of drugs are often used in combination for pre-meds?

A

Opioid and sedative (neurolept-analgesia)

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4
Q

Give some examples of opioid analgesic drugs

A 
Methadone
Pethidine 
Butorphanol
Fentanyl
Buprenorphine (Vetergesic)
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5
Q

What are the uses of premedication?

A

Reduce the patient’s fear and anxiety and make animal handling easier/safer for us too
Provide pain relief
Reduce the doses of anaesthetic induction (and maintenance) agents required
Prevent/reduce undesirable events (e.g. drug effects on autonomic activity)
Reduce muscle tone

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6
Q

Give some examples of injectable anaesthetics

A

Propofol
Alfaxalone
Thiopental
Ketamine

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7
Q

Give some examples of inhalational anaesthetics

A 
Halothane 
Isoflurane              
Sevoflurane 
Desflurane 
Nitrous oxide
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8
Q

Why, when intubating a cat, do you spray the larynx with topical local anaesthetic solution?

A

Cats are prone to laryngospasm (where the larynx closes)

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9
Q

When assessing eye position when an animal is under anaesthesia, under which circumstance may eyes often remain central and open?

A

Under ketamine anaesthesia.

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10
Q

How can alpha-2-agonists affect heart ryhthm?

A

Can cause bradyarrythmias (slow, irregular heart rates)

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11
Q

What is a thermistor?

A

Attaches to the endotracheal tube connector.
Detects each exhalation, as the exhaled gases are warmer than the inhaled gases. If you want to be warned when less than 3-4 breaths/minute are detected, then the device can be set to alarm when the breathing rate falls below this. These devices are often called ‘Ap-alerts’ – for ‘Apnoea-alert’.

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12
Q

Brick red mucous membranes indicate what?

A

Septicaemia or endotoxaemia
These animals may also develop haemorrhages (petechiae or ecchymoses) in their mucous membranes too, which is a sign that they are having problems with their blood clotting, and that they are extremely toxic and very poorly.

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13
Q

What is normal capillary refill time?

A

1-2 seconds

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14
Q

What are the 3 components we wish to achieve with general anaesthesia?

A

Unconsciousness
Analgesia
Muscle relaxation

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15
Q

What do pulse oximeters tell us?

A

Pulse rate

Degree of saturation with oxygen of Hb in arterial blood

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16
Q

What saturation values do we expect from an animal under anaesthetic (from pulse oximetry)?

A

96-100%

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17
Q

What value should mean arterial pressure be?

A

70mmHg

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18
Q

Which value of carbon dioxide should there be in the end tidal breath?

A

Should normally be around 5.3% (40mmHg), and should not exceed around 8% (60mmHg)

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19
Q

What is the difference between nociception and pain?

A

Nociception –information regarding a noxious insult relayed from periphery to the central nervous system

Pain – integration and processing of nociceptive input by the brain allowing it to be recognised as pain (implies recognition at the cortical level) (occurs in thalamus)

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20
Q

What is the difference between physiological and pathological pain?

A

Physiological – activation of nociceptors by extremes of temperature, pressure or chemical concentrations. Tends to be transient, localised and protective (Aδ fibre mediated) and linked to withdrawal reflexes and behaviour adaptation
Pathological – associated with actual tissue damage, ongoing noxious input and may produce chronic pain states, hyperalgesia and allodynia (the experience of pain from a non-painful stimulation of the skin eg light touch). Acute pathological pain may be protective, but chronic pain disrupts homeostasis, causes suffering and has a significant impact on animal’s behaviour and quality of life

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21
Q

Where do Aδ fibres synapse?

A

Laminae I and V.

First pain; mechanical and thermal stimuli

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22
Q

Where do C-fibres synapse?

A

Synapse in laminae I and II.
Interneurones connect with lamina V.
Dull persistent pain; chemical, mechanical and thermal stimuli

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23
Q

Where do Aβ fibres synapse?

A

Laminae II, III, IV, V

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24
Q

Local anaesthetics block which channels?

A

Sodium channels

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25
Q

What do 1st order neurones do?

A

Transmit information from periphery to CNS

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26
Q

What do 2nd order neurones do?

A

2 main types:
Interneurones (located within grey matter): excitatory or inhibitory – local processing and modulation of pain signals
Projection neurones ascend spinal cord to higher centres. Involved in reflex aspects of nociception

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27
Q

What do 3rd order neurones do?

A

Processing, integration and recognition of a harmful or painful experience

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28
Q

What is central sensitisation?

A

Increased second order neurone activity due to recruitment and upregulation of post synaptic receptors in response to sustained or massive release of excitatory neurotransmitters

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29
Q

What does central sensitisation result in?

A

Secondary hyperalgesia – spread of area of increased responsiveness to noxious mechanical (not thermal) around site of primary injury

Secondary allodynia – increased perception of innocuous stimuli as painful

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30
Q

Give some examples of drugs which are capable of antagonising NMDA receptors

A 
Ketamine
Amantadine 
N2O
Pethidine 
D-methadone
xenon
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31
Q

What type of receptor is a NMDA receptor?

A

Ionotropic glutamate receptor
Activated when glutamate and glycine bind to it
Allows positively-charged ions through
Important in controlling synaptic plasticity and memory function

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32
Q

What is meant by synaptic plasticity?

A

The ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity

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33
Q

Gabapentin blocks which channels?

A

Calcium

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34
Q

How should alfaxolone be given?

A

im or sc

Injectable anaesthetic

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35
Q

Why might buprenorphine be favourable when choosing an opioid?

A

Only takes 30 mins to act

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36
Q

What is a disadvantage with using NSAIDs?

A

Reduce renal perfusion

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37
Q

What pre-medication would you give a cat in for a spay?

A

Pre-med: Medetomidine (sedative; alpha-2-agonist) with buprenorphine (opioid)
Induction of anaesthesia: propofol iv
Maintenance: Isofluorane

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38
Q

Why should propofol not be used repeatedly in cats?

A

Can cause Heinz body anaemia and prolonged recovery

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39
Q

Give an example of a NMDA antagonist

A

Ketamine

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40
Q

Why is methadone licensed in cats and not morphine?

A 
Faster onset (5 mins compared to half an hour), cats can't metabolise morphine to the active metabolites
Methadone has additional analgesia
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41
Q

What are the advantages of pre-anaesthetic screening?

A 
Predicting potential complications   
Recognising hidden disease  
Owner information  
Ability to alter the anaesthetic protocol to suit the individual  
Can individualise supportive care
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42
Q

Why do we want to withhold food from an animal prior to surgery?

A

Want to reduce abdominal contents:
It puts pressure on the diaphragm
Regurgitation and therefore aspiration risk

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43
Q

Describe the ASA grading system scale for patients prior to anaesthesia

A

I: A normal healthy patient.
II: A patient with mild systemic disease.
III: A patient with severe systemic disease
IV: A patient with severe systemic disease that is a constant threat to life.
V: A moribund patient who is not expected to survive without the operation
E: Emergency

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44
Q

Which sedative should you give to an adult horse? Why not any others? (give examples)

A

Detomidine
Not diazepam: potentially dangerous to use in adult horses-muscle relaxation produced can cause excitement and panic reactions

Not ACP: slow onset with unpredictable results. In an excited animal, collapse from profound hypotension due to ‘adrenaline reversal0 can result

Also, neither diazepam nor ACP provide analgesia

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45
Q

Why should ACP be used with caution in brachycephalic breeds?

A

Increases the risk of respiratory obstruction due to the sedation and muscle relaxation produced (inc pharyngeal muscles).
Brachycephalic breeds have a high resting vagal tone (low heart rate), and ACP causes hypotension (low BP) and bradycardia -> can lead to fainting

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46
Q

If ACP is being used and hypotension becomes a problem, how can you treat it?

A

IV fluids and alpha-1 agonists eg phenylephrine

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47
Q

Should ACP be used in animals with epilepsy?

A

Should be used with caution or avoided.

ACP lowers the seizure threshold in animals with epilepsy.

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48
Q

Explain ‘adrenaline reversal’ with regards to ACP

A

Excited animals have high amount of circulating adrenaline. Adrenaline preferentially produces vasodilation.
ACP blocks alpha-1 activity, so beta-2 activity takes over: arenaline’s beta-2 induced vasodilation can potentiate the alpha-1 blocking effects of ACP, and worsen the vasodilation and hypotension.

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49
Q

Which group of sedatives would you use to sedate a foal and why?
Why not any others? (give examples)

A

Benzodiazepines: CV stability, work well in neonates
Not alpha-2-agonists: profound CV effects may be catastrophic in a compromised neonate
Not ACP: vasodilation accelerates heat loss

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50
Q

Which is the only alpha-2-agonist (sedative) licensed for administration via the IM route?

A

Detomidine

Also the most potent (only a small volume needs to be injected)

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51
Q

How do we prevent the re-breathing of CO2-rich gases in anaesthetic circuits?

A

Soda-lime cannister absorbs CO2 (rebreathing systems)

High fresh gas flows ensures CO2 is flushed out of the system between breaths (non-rebreathing systems)

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52
Q

What is the average breathing rate of cats and dogs?

A

10-20 breaths per minute

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53
Q

What is the average tidal volume for cats and dogs?

A

10-20ml/kg

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54
Q

How do you calculate minute ventilation?

What value is it usually?

A

Breathing rate x tidal volume

200ml/kg/min

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55
Q

With regards to minute ventilation, how much fresh gas flow is required for Mapleson A, D, E and F circuits, during spontaneous breathing?

A

Mapleson A: 1-2 x MV

Mapleson D, E, F: 2-4 x MV

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56
Q

With regards to minute ventilation, how much fresh gas flow is required for Mapleson A, D, E and F circuits, during intermittent positive pressure ventilation?

A

Mapleson A: 2-4 x MV

Mapleson D, E, F: 1-2 x MV

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57
Q

Give 3 problems with the ‘to and fro’ model of rebreathing systems

A

Soda lime dust may be inhaled
Dead space increases as the soda lime exhausts
Channeling can occur-reduces CO2 removal

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58
Q

What are the oxygen requirements for a patient in a rebreathing circuit?

A

4-10ml/kg/min
The bigger the animal, the smaller the value
(4=horse)
(10=dog/cat)

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59
Q

For the first 5-20 mins of use of a rebreathing circuit, it is usual to use high fresh gas flows. What values do we use?

A

Dogs: 2-5 litres/min
Horses: 10 litres/min

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60
Q

As a minimum, the patient should be breathing how much inspired O2 in a rebreathing circuit?

A

33%

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61
Q

Explain diffusion hypoxia in relation to anaesthesia and N2O

A

Nitrous oxide flow should be switched off 10 mins prior to the volatile agent and patient disconnection because:
Due to the insolubility of N2O, any taken up by tissues/blood quickly comes out of solution and enters the alveoli, diluting out the other gases present, including O2. This is called diffusion hypotoxia.

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62
Q

What are the contra-indications of using muscle relaxants during anaesthesia?

A

Inability to judge depth of anaesthesia adequately

Inability to ventilate patients lungs adequately

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63
Q

How do peripherally-acting neuromuscular blocking agents work?

A

Compete with acetylcholine at post-synaptic nicotinic ACh receptors, thus blocking normal neuromuscular transmission

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64
Q

What is the difference between depolarising and non-depolarising peripherally-acting neuromuscular blocking agents?

A

Non-depolarising simply compete with acetylcholine (need to block 75% of receptors).
Depolarising first stimulate post-synaptic receptors, then the ‘block’ follows as the membrane becomes refractory (only needs to interact with 5-20% of receptors).

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65
Q

How can we assess the degree of a neuromuscular block?

A

Apply an electrical stimulus to a superficial nerve supplying a muscle, whose ‘twitch response’ we can observe

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66
Q

How can you reverse a neuromuscular block?

A

Use anti-cholinesterases to increase the amount of ACh available in the synaptic cleft

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67
Q

Which (unwanted) muscarinic effects do you see with the use of anti-cholinesterases used to reverse neuromuscular blocks?

A 
Increased parasympathetic effects:
Bradycardia
Bronchoconstriction
Salivation
Defecation/urination
Miosis (constricted pupils)
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68
Q

What are the sites of action of injectable induction agents?

A

GABA-A receptors

NMDA receptors

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69
Q

Ketamine is contra-indicated in cats with which problems and why?

A

Cats with compromised renal or hepatic function, as ketamine is excreted unchanged in urine
Metabolised in liver

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70
Q

Which injectable anaesthetic agent is best for small animal patients with severe CV disease?

A

Etomidate

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71
Q

How can you facilitate emergency airway access?

A

Urinary catheters through the larynx
Trans-tracheal needle
Tracheostomy

72
Q

Give the effects of anaesthesia on the respiratory system

A

Central respiratory depressant effect (decreases response of chemoreceptors to increased CO2)
Relaxation of respiratory muscles (diaphragm, intercostal muscles)
Relaxation of pharyngeal/laryngeal muscles (upper airway obstruction, unprotected airways)
Dependant lung atelectasis (collapse) (reduced blood gas exchange)

73
Q

Give some common problems with recovery from surgery

A

Hypothermia
Hypotension
Hypoxaemia
Emergence delirium

74
Q

What is MAC?

A

Minimal alveolar concentration
Concentration of the vapour in the lungs required to prevent movement in 50% of subjects in response to surgical (pain) stimulus
Used to compare strengths (potency) of anaesthetic vapours
Lower MAC= more potent

75
Q

What are the consequences of an animal contracting hypothermia after surgery?

A

Reduced MAC requirement (animal becomes more deeply anaesthetised as it gets colder)
Increased risk of arrhythmias
Delayed recovery
Shivering -> increased O2 consumption (problematic if borderline hypoxic)
Problems with wound healing

76
Q

With regards to MAC, how much is required for suitable analgesia?

A

1.2-1.5 x MAC

77
Q

What is Pp?

A

Partial pressure, of an inhalation agent within the brain

78
Q

Regarding inhalation agents, is a high or low blood solubility desirable and why?

A

Low, as induction and recovery and changes in depth are faster, because an agent with low blood solubility will reach high partial pressures in the blood more quickly.

79
Q

What is SVP?

A

Saturated vapour pressure
Pressure exerted by the molecules in the vapour phase in equilibrium with the liquid phase at a given temperature (To)
A liquid with a high SVP is more likely to evaporate at a given temperature

80
Q

What is a problem with the bolus approach of TIVA (total intravenous anaesthesia)?

A

Hard to maintain drug concentration in desired (therapeutic) range and likely to spend more of the time under/ over dosed

81
Q

Compare the pros and cons of continuous infusion vs bolus approach to TIVA

A

CI does not need repeated catheter/ bung/ 3-way tap handling
CI means can attempt to titrate drugs for level of anaesthesia
CI should mean quicker recovery

BUT

CI takes more time to set up
CI costs more in equipment and often in drugs as often make up more than you need
CI has possibility of severe over-dose if using drip bag and giving set and you are not observant

82
Q

Why should you take care when using N2O in ruminants?

A

N2O has a low blood solubility, so will readily move out of the blood into gas-filled spaces (rumen)

83
Q

What is the strongest and longest-lasting opioid?

A

Methadone

84
Q

What is meant by anaesthetic depth?

A

Degree of CNS depression

85
Q

Why do we monitor the patient during anaesthesia?

A

To warn us of any problems with the patients well-being
To warn us of any problems with our anaesthetic equipment
To give us a guide to the patients anaesthetic depth
It’s a legal requirement

86
Q

What kind of things can we measure to give us an idea of anaesthetic depth of a patient?

A

Nervous system: palpebral (blink) reflex, jaw tone, limb withdrawal reflexes
CV and resp systems: HR, RR (and pattern/depth), pulse rate, ECG, blood gas analysis, mm colour, CRT, temperature, urine output
Eye position

87
Q

Where can you feel for a pulse in an anaesthetised animal?

A

Femoral pulses
Carpal arch pulses (below carpus, back of leg, just below ‘stopper pad’)
Dorsal pedal (or metatarsal) pulses (below hock)
Lingual pulse (underside of tongue)

88
Q

White/pale mucous membranes indicate what?

A

Anaemia

Peripheral circulation is constricted (eg after alpha 2 agonists)

89
Q

Blue/ grey/ purple mucous membranes indicate what?

A

Struggling of oxygenate the blood

Problem with resp or cv system

90
Q

What is capnography?

A

The facility to measure the amount of CO2 in the gases breathed in and out of a patient

91
Q

Give some reasons why inspired CO2 may be higher than zero

A

The O2 flow is not fast enough to flush exhaled CO2 from the system (non-rebreathing)
Soda lime is exhausted (rebreathing)
The valves in the anaesthetic breathing system are not functioning correctly, and the animal is re-inhaling exhaled gases

92
Q

What is the ‘end-tidal’ breath?

A

The last part of the exhaled breath

Contains carbon dioxide (and less O2)

93
Q

Chronic pain is defined as pain that persists for how long?

A

Beyond expected time frame (over 3-6 months)

94
Q

What is neuroplasticity?

A

Functional and/ or anatomical adaptation of the nervous system in response to environmental and physiological processes

95
Q

What is hyperalgesia?

A

Exaggerated response to a normally painful stimulus

96
Q

What is allodynia?

A

Normally innocuous stimulus perceives as painful

97
Q

What is multimodal analgesia?

A

Analgesia which affects as many of the Nociception pathway stages as possible eg transduction, transmission, modulation, perception

98
Q

What is transduction?

A

Conversion of applied stimulus (eg thermal, mechanical) into an electrical signal (action potential) by activation of nerve end receptors

99
Q

How do primary hyperalgesia and allodynia occur?

A

Inflammatory mediators and products of cell damage lower nociceptor threshold and recruit silent nociceptors

100
Q

Describe the ‘Gate Control’ theory of pain

A

Stimulation by a non-noxious input will suppress pain

Input from Aδ or C fibres inhibits the inhibitory interneuron, and thus increases the chances that the projection neuron will fire -> pain

Input from Aβ fibres activates the inhibitory interneuron, and so suppress the projection neuron -> no pain

101
Q

What do all alpha-2 agonists have in common?

A

All give analgesia, sedation and muscle relaxation

However, all affect GI motility and have profound CV side effects

102
Q

What types of fluid loss are there?

A

Pure water: dehydration
Water and electrolytes: diuresis, vomiting, diarrhoea
Water, electrolytes and protein: transudates, exudates, effusions, severe enteritis, protein-losing enteropathy, protein-losing nephropathy
Blood: haemorrhage

103
Q

Why will an animal always be hypovolaemic if its dehydrated?

A

Deficit of water meaning they’ve lost water from all body compartments, including intravascular compartment

104
Q

Which anaesthetic systems can be used for patients under 10kg?

A

Ayre’s T piece
Mapleson D
Mini parallel lack
(all non-rebreathing)

105
Q

Which require a higher gas flow: rebreathing or non-rebreathing systems?

A

Non-rebreathing

106
Q

Rebreathing systems are used for patients of which weight?

A

Over 10kg (higher resistance in circuit)

107
Q

How does ACP affect vessels?

A

Causes vasodilation

108
Q

How do alpha 2’s affect vessels?

A

Cause vasoconstriction

109
Q

What is the onset for ACP?

What is the duration of action?

A

Onset: 30 mins
Duration: 4-8 hours

110
Q

Why should you be careful using ACP in anaemic pets?

A

Can reduce PCV by up to 50% (via vasodilation)

111
Q

Give the effects of ACP

A

Vasodilator
Unreliable sedation
No analgesia
Can lower seizure threshold so be careful in epileptic patients
Anti-arrhythmic
Can be associated with syncope with high vagal tone and bradycardia (Boxers)

112
Q

Give the effects of alpha 2’s

A 
CV effects 
Reliable sedation
Analgesia
Initial peripheral vasoconstriction
Reflex bradycardia
Decreased RR
Decreased BP to just below normal
Muscle relaxation
113
Q

Give the effects of benzodiazepines

A

Not licensed for veterinary use
May cause excitement rather than sedation
Anti-convulsant
Often used at induction rather than sedation
Minimal CVS and resp depression (so good for neonates)

114
Q

Give some effects of opiods

A

Give some sedation
Methadone provides the most analgesia, then buprenorphine, then butorphanol
Minimal CVS depression

115
Q

Give some effects of ketamine

A

More often used as an induction agent
Can be used to enhance sedation of other drugs
Increases muscle tone
Analgesia

116
Q

Why should you not use diazepam in adult horses?

A

Muscle relaxation produced can cause excitement and panic reactions
Doesn’t provide analgesia

117
Q

Does informed consent have to be in writing?

A

No

118
Q

Which of the 3 gives the most muscle relaxation in horses: xylazine, romifidine, detomidine

A

Xylazine > detomidine > romifidine

119
Q

Of the alpha 2 agonists used in horses, which is the only one licensed for IM use?

A

Detomididne (is also the most potent)

120
Q

Magill and Lack breathing systems are suitable for patients of what weight?

A

10-50kg

121
Q

Bain breathing systems are suitable for patients of what weight?

A

10-25kg

122
Q

T pieces breathing systems including Mapleson D are suitable for patients of what weight?

A

<10kg

123
Q

What are the 2 main types of rebreathing systems?

A

To and fro

Circle

124
Q

How do peripherally-acting neuromuscular blocking agents work?

A

Compete with acetylycholine at post-synaptic Nicotinic

ACh receptors -> block normal neuromuscular transmission

125
Q

Name 2 barbiturate induction agents

A

Pentobarbital

Thiopental

126
Q

How does thiopental affect the CV system?

A

Arrhythmogenic
Negative inotrope
Vasodilation -> hypotension
Resp depression

127
Q

Is thiopental analgesic?

A

No

128
Q

How is thiopental administered?

A

iv

129
Q

When is thiopental used?

A

Top-up boluses
Induction
(Horses)

130
Q

How does alfaxalone affect the CV system?

A

Vasodilation
Reflex tachycardia
Respiratory and CV depression but not as pronounced as propofol

131
Q

Does alfaxalone provide analgesia?

A

No

132
Q

How is alfaxalone administered?

A

iv or im

133
Q

When is alfaxalone used?

A

Induction and maintenance of anaesthesia in small animals

Sedation

134
Q

How does propofol affect the CV system?

A

Mild negative inotrope
Vasodilation (no reflex tachycardia)
Hypotension
Depression, apnoea

135
Q

Is propofol analgesic?

A

No

136
Q

How is propofol administered?

A

iv

137
Q

How does ketamine affect the CV system?

A

Increased HR, CO, BP

Minimal resp depresion

138
Q

Is ketamine analgesic?

A

Yes

139
Q

Does ketamine provide good muscle relaxation?

A

No -> administer with benzodiazepines

140
Q

How is ketamine administered?

A

iv or im (painful)

141
Q

When is ketamine used?

A

Induction of large and small animals
Co-induction agent in small animals
To provide analgesia intra and post-operatively

142
Q

How can you confirm an ET tube is in the correct place?

A 
Direct visualisation with laryngoscope
Simultaneous movements of thorax and rebreathing bag
Capnograph -> detects exhaled CO2
Detection of air coming out of ET tube
Neck palpation
143
Q

How can you provide emergency airway access?

A

Urinary catheter through larynx
Trans-tracheal needle
Tracheostomy

144
Q

Give the effects of anaesthesia on the respiratory system

A

Central respiratory depression effect
Relaxation of respiratory muscles
Relaxation of pharyngeal/laryngeal muscles
Dependant lung atelectasis

145
Q

Give some negative effects of mechanical ventilation during an anaesthetic

A

Uses positive intrathoracic pressure during inspiration -> decreased venous return to the heart -> decreased CO
May cause lung trauma
Activates RAAS-> increased ADH production -> fluid retention

146
Q

Sevoflurane is licensed in which species?

A

Dogs

147
Q

Give the effects of isoflurane

A

Respiratory depression
Potent vasodilation
No analgesia
Pungent

148
Q

Give the effects of sevoflurane

A 
Quick induction and recovery
Not pungent
Less respiratory depression than isoflurane
Vasodilation 
No analgesia
149
Q

Which is the only inhalation agent to provide analgesia?

A

Nitrous oxide

150
Q

Why is total intravenous anaesthesia normally reserved for shorter procedures?

A

Due to cumulative effects of all injectable agents

151
Q

How far should you insert an oesophageal stethoscope?

A

Inserted down oesophagus until level with the heart

152
Q

How big should the cuff be when measuring indirect blood pressure?

A

40% of circumference of the limb

153
Q

What is the gold standard method for measuring blood pressure?

A 
Direct arterial blood pressure 
Dorsal metatarsal artery (dogs, cats) 
Facial artery (horses)
154
Q

What do you do if a dog or cat is hypotensive during surgery?

A

Reduce anaesthetic depth
Fluids
Positive inotrope

155
Q

What do you do if a horse is hypotensive during surgery?

A 
Reduce anaesthetic depth if possible
Fluids
Assess ventilation
Alter body position if possible
Check acid-base status 
Positive inotrope
156
Q

How do you measure central venous pressure?

A

Jugular catheter

Tip of the catheter lies in the right atrium

157
Q

What does it mean if end-tidal Co2 is too high (>60mmHg) or too low (<20mmHg)?

A 
Too high (>60mmHg): patient is hypoventilating
Too low (<20mmGh): patient is hyperventilating
158
Q

What do you do if a dog or cat is hypoventilating during surgery?

A

Decrease depth of anaesthesia
Start IPPV
May be endobronchial intubation

159
Q

What do you do if a capnograph shows signs of rebreathing?

A

Increase FGF
Change the soda lime cannister
Check the valve

160
Q

What is the ideal value for SpO2 on a pulse oximeter?

A

> 98%

161
Q

Which is the only local anaesthetic licensed for use in food-producing animals?

A

Procaine

162
Q

When would you give systemic lidocaine?

A

Ventricular arrhythmias

163
Q

Which is the most potent local anaesthetic agent?

A

Bupivacaine (but most cardiotoxic)

164
Q

What is the onset of action of bupivacaine?

A

30 mins

165
Q

What is the onset of action of mepivacaine?

A

10 mins

166
Q

Order the following local anaesthetic agents in terms of their duration of action, starting with the shortest:
Procaine, bupivacaine, lidocaine, mepivacaine

A

Procaine (60 mins) < lidocaine (1.5 hrs) < mepivacaine (2 hrs) < bupivacaine (4 hrs)

167
Q

What are the 4 dental local blocks?

A

Maxillary (blocks all upper teeth)
Infraorbital (blocks rostral to 3rd premolar; upper)
Mandibular (blocks all lower teeth)
Mental (blocks rostral to 1st premolar; lower)

168
Q

Where do you block before an enucleation?

A

Ophthalmic nerve

Techniques: retrobulbar, modified Peterson’s block (behind eye)

169
Q

Which nerves do you block when doing an auricular block?

A

Auriculotemporal nerve

Great auricular nerve

170
Q

Which nerves does a RUMM block block?

A

Radial, ulnar, medial, musculocutaneous

Blocks distal to (but not including) the elbow

171
Q

Which local anaesthetic block would you use if you wanted to block the elbow?

A

Axillary brachial plexus block

172
Q

What is a bier block?

A 
Intravenous regional block
Used for eg limb/digit amputation
Blocks limb distal to a tourniquet
Lidocaine only
Anaesthesia lasts until tourniquet is released
173
Q

How long should you keep a tourniquet on for?

A

2 hours max

174
Q

Give some possible complications of a Bier block

A 
Lidocaine toxicity (CNS and CV effects)
Ischaemia if tourniquet left on for too long
175
Q

Where is an epidural carried out in a dog or cat?

A

Between L7 and S1

176
Q

What does an epidural block in a dog or cat?

A

Both HLs and caudal abdomen (up to umbilicus)

177
Q

When is an epidural contra-indicated?

A

Skin infections (could spread to spine)
Coagulopathies (haemorrhage -> spinal cord compression)
Neuro dz
Abnormal anatomy eg pelvic fracture

Year 3 (28 decks)

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