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Fourth Year > Anaesthesia > Flashcards

Anaesthesia Flashcards

1
Q

Uses of regional anaesthesia

A

Standing surgeries in equine -> dentals, urogenital surgery, laparoscopic procesdures, nerve blocks

Standing procedures in bovines -> caesaerian, GI surgery

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2
Q

Stage 1 of anaesthesia

A

Voluntary excitement
Increase HR,RR, salivation
Voiding of faeces + urine
struggling

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3
Q

Second stage anaesthesia

A

Involuntary excitement, cortical depression, narcosis, some reflex struggling, pupils dilate/nystagmus

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4
Q

Stage 3 anaesthesia

A

Surgical

Loss of reflexes
Increased CV/respiratory depression
Increase muscle relaxation

Plane 1 - light
Plane 2 - medium
PLane 3 - deep

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5
Q

Stage 4 anaesthesia

A

Dead

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6
Q

What species is greatest risk? what is the perioperative 7d mortality rate?

A

Horses
1% in healthy horses

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7
Q

Risk factors for perioperative mortality in horses

A

Age, duration of surgery, type, time procedure was undertaken

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8
Q

Level 1 monitoring

A

Observation of reflexes, assessment of muscle tone, respiration
MM colour
HR, rhythm, strength, pulse, CRT
Temperature

The basic requirement for all animals

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9
Q

Level 2 monitoring

A

Routine use recommended for some/all animals

ECG, arterial blood pressure (direct or indirect)
Pulse oximetry
Urine output
Blood glucose
PCV/protein
Capnography

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10
Q

Level 3 monitoring

A

specific patients/issues

Anaesthetic gas monitor
Blood gas machine
Cardaic output
Central venous pressure
Peripheral nerve stimulator

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11
Q

Benefits of premed

A

Relieves anxiety resistance to induction

MAC sparing - less volatile required

Counters vomiting, salivation, bradycardia

Contributes to peri-anaesthetic analgesia

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12
Q

Pre anaesthesia ASA scoring stages

A

I-V, E is emergency surgery

I - fit, healthy
II - mild systemic disease
III - severe systemic disease
IV - Incapacitating disease constant threat to life
V - moribund patient, wont live >24h without surgery

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13
Q

Tranquilizer vs sedative

A

Tranq -> induce feeling of calm
Sedative -> above + reduce response to external stimuli

Analgesia can be feature of some but not all

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14
Q

What are phenothiazines we use in vet?
Mode of action

A

Acepromazine, fluphenazine, perphenazine enanthate

Dopamine antagonist +
a1 adrenergic receptor antagonism -> decreases blood pressure by vasodilation and decreases thermoregulation

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15
Q

Concentrations of ace used

A

2mg/mk
10mg/ml

Small + large animals

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16
Q

Dose rates of ace used
Injection routes

A

Smallies + large -> 0.02-0.05mg/kg
stick to lower end

IV, IM, SC, oral

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17
Q

Clinical aspects of ace

A

Vasodilation/hypotension
Minimal resp depression
Higher dose does not equal higher sedation but = higher side effects
No analgesia
MAC sparing
Antiarrhythmic effects
Antiemetic
Hypothermia
Reduces haematocrit (splenic dilation)

Metabolised in liver - dont use in liver disease

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18
Q

Length of activity of ace

A

4-6h
no reversal

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19
Q

What phenothiazine is good for wildlife?

A

Fluphenazine -> long acting, causes too many side effects in horses

Perphenazine enanthate also

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20
Q

Butyrophenones MOA and drugs used in vet

A

Dopamine antagonist
Potent antiemetic, counter effects of opioids

Limited vet use

Azaperone - pigs
Fluanisone / droperidol - fixed ratios with fentanyl

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21
Q

Benzos MOA and effects

A

Enhance receptor affinity for GABA in the CNS

Sedation, anxiolysis, muscle relaxation, amnesia, anticonvulsant

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22
Q

2 benzos
What are they often used with?

A

Diazepam and midazolam

Ketamine

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23
Q

Diazepam clinical aspects - who can it be used in

A

Poorly water soluble - mixed with ethanol or propylene glycol making it painful IM, better IV

No vasodilation, good CV and respiratory parameters

Unrealiable sole agent for sedation in fit patients (not recommended) -> so used for sick or older patients (ASA 4/5), or foals (0.2mg’kg) to achieve recumbency

Longer acting than midazolam

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24
Q

Midazolam clinical aspects - what is used in horses?

A

Water soluble and tolerated as IM
Shorter acting than diazepam, also metabolised in liver
Unpredictable sole sedative (excitement and agitation in horses)

triple dip formulation in horses with xylazine (alpha 2 agonist) and ketamine

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25
Q

What is zoletil?

A

Zolazepam (benzo) combined with tiletamine (like ketamine but longer acting)

Dogs, cats, wildlife licensed

Not great recoveries after
Given as small volume IM

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26
Q

What is an anticholinergic drug and what is the MOA?

A

Atropine, glycopyrrolate

Blocks acetylcholine (muscarinic receptors) at PS postgangionic nerve endings

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27
Q

What are anticholinergics used for?

A

Treatment of anaesthetic induced bradycardia, excessive salivation and respiratory secretions and blockage of vasovagal reflexes

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28
Q

5 alpha 2 agonists

A

Xylazine - never smallies
Romifidine - horses
Detomidine - horses
Medetomidine - smallies
Dexmedetomidine - smallies

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29
Q

Effects of alpha 2 agonists and MOA

A

Central sedation effects - binding of presynaptic a2 receptors causes negative feedback loop and less norepinephrine released

Analgesia results from binding of receptors centrally and within dorsal horn of spinal cord (pre and post synaptic)

Also have some a1 effects -> medetomidine more of pure a2 agonist, xylazine more a1 effects so more CV effects

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30
Q

CV effects of alpha 2 agonists

A

Peripheral a2 receptors stimulated = Vasoconstriction, hypertension, increased BP detected, increased PS vagal tone, bradycardia, restore BP towards normal

Central a2 receptors stimulated = decreased smpathetic outflow -> bradycardia, BP restores

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31
Q

When can alpha-2 agonists be used as a premed

A

never ASA 3/4/5 or patients with heart problems

only 1/2

due to CV depression

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32
Q

Respiratory effects of alpha 2 agonists

A

Dose and depth related, blood gas normally maintained in healthy patients

Sheep = hypoxia and pulmonary oedema

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33
Q

Other systems affected by alpha 2 agonists apart from CV

A

Uterine stimulation
Reduced renin and insulin
Sedation variable across species and sudden arousal can occur
Can be reversed with atipamezole -> be careful of tachycardia and hypotension

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34
Q

What can we give with alpha 2 agonists to prevent excitement?

A

Opioid

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35
Q

3 effects of opioids

A

Analgesia
anti-tussive
Anti-diarrhoeal

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36
Q

Where are opioid receptors found and how do they work?

A

Brain, spinal cord, chemoreceptor trigger zone, GIT, urinary and synovium

G-protein coupled receptors, closure of Ca gated channels, hyperpolarization and reduced cAMP -> inhibit neurotransmitters

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37
Q

4 full mu agonists

A

Morphine
Fentanyl
Methadone
Remifentanil

More analgesia, but more side effects (resp depression + bradycardia)

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38
Q

What kind of opioid is buprenorphine?

A

Partial u and k agonist with ceiling effects

Used in mild-moderate pain

Can be used to displace some full agonists and decrease potential side effects like resp. depression without losing all analgesia

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39
Q

What kind of opioid is butorphanol?

A

Mixed k agonist and u antagonist
Sedative and mild antitussive effects, minimal analgesia

Used for endoscopy in dogs or to reverse u opioids

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40
Q

What is guaifenesin?

A

Centrally acting muscle relaxant with no analgesia used in triple drips in horses

Replaced by midazolam now

Recumbant dose 100mg/kg

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41
Q

5 injectible induction agents

A

barbiturates
propofol
alfaxalone
ketamine
tiletamine

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42
Q

4 barbiturates and their MOA

A

Phenobarbitol (anticonvulsant)

Pentobarbitol, thiopental and methohexital

GABA receptor

Resp depressants with poor analgesia

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43
Q

Thiopental injection

A

Strong alkaline solution and perivasular injections are irritable + tissue damage - kept with sodium bicarb as its dissociates fast

Diluted to 5% or lower

Cumulative in nature

Fast uptake and action

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44
Q

Thiopental effects

A

Depression of myocardial contractility, increase HR to compensate

Decrease RR

Cerebroprotective properties - CBF and ICP decrease - good choice for seizures

Poor analgesic

Redistribution decreases iwth hypovolaemia and acidaemia, increasing clinical effect

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45
Q

Thiopental dose rate and contraindications

A

7-10mg/kg in premeded dogs
Horses similar

Beware using in. neonates, c sections or sighthounds

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46
Q

Propofol - onset, solubility, licensed in, metabolism

A

Rapid onset
Lipid soluble
Cats and dogs
Liver metabolism

Similar characteristics to thiopentone/tol

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47
Q

Propofol effects and dose rate

A

Dose dependent CV and respiratory depression

Poor analgesia

Alfax better choice for cats - cats take longer to metabolise in liver

unpremicated dogs - 6mg/kg or lower with premed

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48
Q

1 Steroid anaesthetic

A

Alfaxalone

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49
Q

Alfax metabolism, duration of action, dose and injection

A

Rapidly in liver
Short acting
2mg/kg in premed dogs
IV slowly over 1 minute

Cats may need up to 5mg/kg

Can be used as CRI - beware resp depression

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50
Q

Ketamine/tiletamine MOA

A

Non competitive antagonists at NMDA receptor
Prevent glutamate from binding

No interaction at GABA but possible action at opioid receptors and muscarinic

Produces cataleptic (dissociated) state with complete analgesia

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51
Q

Reflexes maintained in ketamine use

A

Pharyngeal, laryngeal
hypertonus present
eyes remain open

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52
Q

Ketamine - onset, metabolism, effects

A

Onset Slower than circulation time
Liver, excreted by kidneys
CV maintained
Indirect sympathomimetic effects (increase HR)
Minimimal Resp depression

Increased CBF and ICP -> avoid in head trauma

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53
Q

Ketamine routes

A

IM, SC

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54
Q

Ketamine/tiletamine needs to be combined with?

A

Benzos or alpha 2 agonists to offset poor muscle relaxation

eg zolatil -> not used in horses as ketamine is preferred due to bad recoveries

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55
Q

Define MAC

A

alveolar concentration required to prevent musclar movement in response to a painful stimulus in 50% of subjects

1.1-1.3 MAC likely to maintain good anaesthesia in most individuals

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56
Q

What is mac reduced by?

A

Other drugs, premed
Age, neonates and oldies
Hypothermia
Pregnancy
Disease processes
Arterial BP <50mmhg
PaO2 <40mmHg
PaCO2 > 95mmHg

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57
Q

Uptake of inhalationals pathway

A

Inspired air -> alveolar air -> blood -> brain

continues until equilibrium reached

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58
Q

What is the blood gas partition coefficient?

A

The ratio of agent in the phases once equilibrium is reached = solubility of given agent

Lower the value, the faster it works (achieves equil faster)

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59
Q

Which inhalational is the fastest?

A

Sevoflurane followed by iso then halothane

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60
Q

5 factors that influence the inspired volatile

A
  1. Concnetration of vaporiser -> increased leads to increased rate of rise in blood, tissue and brain
  2. Oxygen flow rate
  3. Respiratory rate
  4. Cardiac output -> increased slows down process, low cardiac output speeds up process as equilibration happens faster
  5. Lung disease - ventilation perfusion mismatch
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61
Q

Mode of action of inhalationals

A

Not clearly understood

Likely to be multiple sites in brain and spinal cord
Some potentiation of inhibitory GABA receptors likely as well as inhibition of NMDA receptors

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62
Q

What is isoflurane?

A

Halogenated ether, non flammable liquid

Highly volatile and low solubility in blood and tissues - relatively quick inductions and recoveries

Irritant to airways

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63
Q

What does isoflurane cause?

A

Vasodilation, dose dependent depression of CV system, decrease BP

Little cardiac depression, HR maintained
CO and blood flow preserved

Respiratory depression significant

Poor analgesia, moderate muscle relaxation
Less than 1% metabolised

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64
Q

8 things needed for adminstration of inhalationals

A
  1. Oxygen source
  2. Regulator
  3. Flowmeter
  4. Vaporiser
  5. Breathing circuit - rebreathing or non-rebreathing
  6. Rebreathing circuit needs CO2 absorber
  7. Endotracheal tubes
  8. Scavenging system
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65
Q

Advantages of rebreathing system

A

Low O2 flows - reduce waste gases and cost
Flow rates only high enough to meet metabolic demands
Natural humidification of inspired gases reduces heat loss

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66
Q

Disadvantages of rebreathing system

A

Resistance to breathing increases
Circuit conc. slow to change
Expense of absorber

Suits

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67
Q

Advantages of non-rebreathing system

A

Minimal resistance -> due to no valves or CO2 absorber
Rapid changes in circuit concentrations after changing vaporiser settings
No CO2 absorber required decreases costs, dust and interaction with volatile agent
Light weight disposable circuits

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68
Q

Disadvantages of non-rebreathing system

A

Dry and cold gases increases hypothermia
High O2 flow increases wastage, pollution

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69
Q

Minute ventilation required in non-rebreathing system

A

3xMV -> about 500ml/kg/min
3kg cat 1.5L per minute entire way through

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70
Q

What system do animals under 4kg go on?

A

Bain - less resistance than rebreathing circuit

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71
Q

How does rebreathing system work?

A

Circle system with unidirectional / one way valves directing exhaled gas through absorber then back to patient

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72
Q

Advantage of coaxial circuit

A

AKA Universal F

Inspiratory limb on inside of expiratory limb to increase warming

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73
Q

Rebreathing system oxygen flow rate

A

Initial flow rate 100ml/kg/min or 2L/m -> whichever is greatest

Stable maintenance is 10ml/kg/min or minimum or 500ml/min

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74
Q

2 categories of vapourisers

A
  1. Simple uncalibrated -> low resistance in inspiratory limb of circle system
  2. Precision vaporiser -> complex + efficient for temp and fresh gas flow rate to maintain constant rate of anaesthetic (more common)
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75
Q

What do reservoir bags show us?

A

Resp rate not resp flow

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76
Q

Size of rebreathing bag

A

4/5x tidal volume (10ml/kg)

20kg dog - 1L bag
Cats - smallest we have is 500ml

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77
Q

Effect of large reservoir bag

A

to large increases volume of circuit and slows down conc changes and make breathing assessment more difficult

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78
Q

Benefits of endotracheal tubes

A

Maintain airway
Prevent aspiration
Better administration of gases
Controlled ventilation

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79
Q

Appropriate sizes of endotracheal tubes

A

Adult cats 3.5-4mm
Dogs 10-25kg -> 6-10mm

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80
Q

What is. v-gel?

A

goes at back of larynx instead of ET tube for tricky animals

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81
Q

2 types of ET tubes

A
  1. Murphy tubes -> beveled end and side holes, possible cuff
  2. Cole tubes -> no side hole or cuff, abrupt change in diameter, birds and reptiles
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82
Q

3 reasons for fluid therapy

A

Correct deficits
replace ongoing losses
Maintain normal levels

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83
Q

Fluid levels in the body

A

intracellular 2/3
Extracellular 1/3 -> interstitial or plasma

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84
Q

Electrolytes in intracellular and extracellular fluid

A

Intracellular -> potassium
Extracellular -> Na, Cl, bicarbonate

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85
Q

What is osmolality?

A

Number of osmoles per kg of solvent

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86
Q

What is starlings law?

A

What controls fluid movement in and out of blood vessels

Fluids with high oncotic pressure relative to plasma will raise plasma oncotic pressure and capillary hydrostatic pressure

Fluids with low oncotic pressure relative to plasma with lower plasma oncotic pressure and raise capillary hydrostatic pressure

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87
Q

2 factors that retain water in vasculature

A
  1. endothelial integrity (gycocalyx lining)
  2. Albumin
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88
Q

Advantages of oral (enteral) fluids

A

Natural
Allows normal enteric regulation of incoming water, electrolytes and nutrients -> by mucosa of intestine
Feeds GI system mucosa
Doesnt need to be sterile
Large doses intermittently

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89
Q

Disadvantages of oral (enteral) fluids

A

SLow absorption
Not suitable in emergencies
Requires functioning GI system
Some substances destroyed (digested) - proteins, cells, synthetic colloids

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90
Q

Advantages of SC and IP fluids

A

Depot of fluid under skin
Sustained release of electrolytes and fluid
Avoids rapid fluctuations in electrolyte levels
Bypass GI system

Eg - dont want big spike in Ca levels in blood in downer cow

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91
Q

Disadvantages of SC and IP fluids

A

Slow absorption
Not suitable for emergencies
Only simple molecules can be absorbed - water, electrolytes and glucose

Cannot use blood products, nutrients or colloids

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92
Q

IV fluids advantages

A

Direct infusion of fluid into venous blood
Rapid dist. through body

Bypass GI system

Used for emergencies, blood products or when precise control needed

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93
Q

IV fluids disadvantages

A

Sterility essential
Vascular access may be problematic
Changes in blood levels rapid
Bypasses natural regulation of gut

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94
Q

Vascular access

A

Peripheral vein
Large central vein
Bone marrow cavity - intraosseous administration

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95
Q

Oral fluids contain:

A

Water, electrolytes or glucose mix

Or nutrition fluids -> complete nutrition feeds

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96
Q

2 types of IV fluids

A

Crystalloids - small molecules
Colloids - large molecules and cells

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97
Q

What are crystalloid fluids?

A

Water + small molecules that form crystals
Sodium chloride, glucose, other electrolytes

Most common

Can be hypertonic, isotonic or hypotonic

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98
Q

3 types of crystalloid fluids

A

Maintenance

Replacement

Special -> concentrated solutions for special circumstances

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99
Q

Maintenance crystalloid fluid description

A

Hypo or isotonic
Given slowly to meet ongoing needs
Low in sodium, high in glucose

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100
Q

Replacement crystalloid fluids description

A

Iso or hypertonic
Replaces losses
Can be given rapidly
High in sodium = matches that in blood

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101
Q

5 types of replacement crystalloids

A
  1. Hartmans
  2. LRS
  3. 0.9NaCl
  4. Plasma lyte 148
  5. 7% NaCl
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102
Q

Hartmans contents

A

131 Na+ -> high amounts to match body so can give rapidly
5 K+
111 Cl-

Small amount of calcium, then lactate added to balance cations

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103
Q

LRS contents

A

Almost exactly the same as hartmans

130 Na+
4 K+
109 Cl-

Same osmolality and lactate

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104
Q

0.9NaCl contents

A

Higher sodium than others, 154 Na+ and 154Cl-

0 K+
0 lactate

Above phys levels of sodium and chloride = can get hyperchloraemia

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105
Q

Plasma lyte 148 contents

A

lowest chloride of all - 98 Cl-
140 Na+ (higher than hartmans and LRS, less than 0.9)
5 K+
Acetate 27 and gluconate 23 as anions

NO calcium unlike hartmans, so we can give with drugs that have reactions to calcium

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106
Q

7% NaCl contents

A

very hypertonic
1200 Na and 1200 Cl only

Suck fluid out of interstitium into blood stream to increase blood volume rapidly -> 1L in = 5L expansion

have 60 mins before it diffuses out of vasculature again

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107
Q

What is a colloid and what does it do?

A

Large molecule that gets trapped in blood vessels that hold water and increase volume of vessels

more effective blood volume expansion - stays inside vessels where hartmans would diffuse out after an hour

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108
Q

What are natural colloids? 1 example

A

Proteins found in blood eg albumin

They are species specific so must give dog dog albumin

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109
Q

What percentage of plasma protein is albumin?

A

40-60%

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110
Q

What are two available natural colloid fluids?

A

Frozen plasma
Canine albumin (north america)

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111
Q

What are synthetic colloids made from and what are 4 advantages to natural?

A

Starch or gelatine

  1. Long shelf life at room temp
  2. Any species
  3. No disease transmission or transfusion reactions
  4. Cheap compared to plasma

Highly effective blood volume expansion and used in patients where albumin conc. is low

112
Q

Disadvantages of synthetic colloids

A

More expensive than crystalloids
Reduce blood clotting ability
Potential nephrotoxicity - cats more vulnerable

113
Q

4 types of blood products and what they offer

A
  1. Plasma ( contains colloid, clotthing factors + immunoglobulins)
  2. Albumin
  3. Packed red blood cells -> replace lost red cells for oxygen transport
  4. Whole blood -> rbc, plasma + platelets
114
Q

What situation would plasma be used?

A

Animal with coagulopathy and haemorrhage that needs volume and clotting proteins

115
Q

When would packed RBC be used?

A

Cases of anaemia or blood loss

116
Q

What are risks of blood products?

A

Disease
Transfusion reactions

117
Q

What are maintenance fluid losses? what does this cover

A

Urine output
Insensible losses -> evaporative from skin and respiration

2-3ml/kg/h

118
Q

What is the rate of replacement for dehydration?

A

1/2 in first 6h
1/4 in next 6h
1/4 in next 12h

119
Q

What is peri-operative fluid therapy accounting for?

A

Maintenance + losses

Increased evaporation -> dry gas, surgical site open, bypass URT

Urine output -> decreased due to CVS depression or increased due to alpha 2 agonists

Blood loss

120
Q

What is the standard peri-operative fluid therapy rate? What is bolus rate?

A

5ml/kg/h

+/- fluid bolus (hypotension, blood loss) -> 10ml/kg/h

Large open cavity -> 10-30ml/kg/hw

121
Q

Fluid type and rate for 20kg lab OVH

A

5ml/kg/h x 20kg = 100ml/h

Isotonic balanced solution = hartmans

122
Q

Advantages of regional anaesthesia

A

Fast, minimal equipment
Highly effective -> definite removal of pain
Low risk of complications -> not depressing CV system
Standing surgery -> avoid complexities of lying down
Adjunct to general -> reduce side effects of GA

123
Q

MOA of local anaesthesia

A

Blocks sodium channels in sensory nerves preventing signal conduction

Also blocks conduction in -> motor nerves (paralysis), sympathetic nerves (vasodilation), the brain (seizures), myocardium (CVS depression)

124
Q

Which neurons in the brain are most vulnerable to local anaesthesia?

A

Inhibitory neurons -> seizures

125
Q

When does LA toxicity occur?

A

Excess dose - increased systemic absorption
Intra-vascular injection

126
Q

Lignocaine vs bupvacaine -> what actions occur first in toxicity?

A

Lignocaine -> CNS signs seen first (seizure) - cause less cardiovascular depression than other drugs
Bupivacaine -> CVS depression and cardiac arrest occur first

127
Q

Dose lignocaine for sheep/cattle and goats

A

Sheep/cattle -> 10mg/kg

Goats -> 7mg/kg

SC/IM

128
Q

Bupivacaine dose

A

2mg/kg -> more potent and cardiotoxic

129
Q

Lignocaine and bupivacaine onset of action

What 2 factors affect this?

A

Lignocaine -> 5min

Bupivacaine -> up to 20 mins

  1. Proximity to nerve
  2. Concentration
130
Q

Duration of action lignocaine and bupivacaine

A

Lignocaine -> 60-90mins

Bupivacaine -> 180-360mins

131
Q

What affects the DOA of LA?

A

Concentration of LA

132
Q

What affects the rate of systemic absorption of LA? What is added to slow it?

A
  1. The faster it is absorbed into blood and lymphatics the faster it wears off
  2. pH of tissue -> inflammation lowers pH and it wont penetrate nerves as easily

Slow down absorption with adrenaline -> causes localised vasoconstriction, blood flow reduced and less flow taking it out of tissue

133
Q

5 general precautions for LA

A
  1. Avoid intravascular injection
  2. Aseptic technique
  3. Dont inject through infected tissue or tumours (pushes infected cells elsewhere)
  4. Coagulopathy or thrombocytopaenia
  5. Never use adrenaline in ring or digit blocks, use with care in highly vascular areas (can ischaemia digits)
134
Q

4 LA techniques

A
  1. Direct infiltration
  2. Line blocks
  3. Nerve blocks
  4. Intra-articular
135
Q

3 regional anaesthetic techniques

A
  1. Epidural
  2. Para-vertebral -> blocks as they merge in spinal canal
  3. Intravenous regional -> confine LA to part of limb using torniquet

Blocks bundles

136
Q

Key differences between LA and regional anaesthesia

A

local may not block all tissue layers, regional does

Large area and volume for LA, smaller volume of LA for regional

137
Q

What nerves innervate upper eyelid and upper eye muscles?

A

Eyelid -> supraorbital nerve

Upper eye muscles -> motor auriculopalpebral nerve

Block both for surface and conjunctiva block

138
Q

What block needs to be done for enucleation?

A

Retrobulbar block -> block optic nerve and all globe structures by placing needle behind eye

139
Q

What nerve is blocked for dehorning?

A

Cornual nerve

140
Q

Point of injection for dehorning

A

Midway between lateral canthus of the eye and the base of the horn along the zygomatic process on the upper third of the temporal ridge, about 2.5 cm below the base of the horn.

141
Q

Peripheral nerve blocks -> how many points in forelimb and hindlimb?

A

6 point NB in forelimb
4 point NB in hindlimb

Opposite in horses

142
Q

When is a ring block used?

A

When we cant palpate nerves in distal limb, thick skin or animal difficult
Line of LA around limb -> may miss deep structures like bone

143
Q

What is needed for IV regional anaesthesia?

A

Torniquet - left on for max 60-90mins

MUST use lignocaine not bupivacaine

LA stays below torniquet and careful with dose because when torniquet removed it goes systemically

144
Q

How much lignocaine used for IV regional anaesthesia?

A

10-20ml for distal limb of large animal

145
Q

Disadvantages of Infiltration method

A

Direct injection along incision line

Simple but large volume of LA, short DOA, delayed wound healing, no muscle relaxation, deep layers of viscera not blocked

146
Q

Inverted L block disadvantages and dose

A

Essentially a long line block - above and in front of incision

Simple but large LA, no muscle relaxation and deep layers of viscera not blocked

Can use 80-100ml LA

147
Q

Paravertebral RA advantages and disadvantages

A

Advantages -> lower volume of LA, muscle relaxation and deep tissues blocked (including peritoneal lining)

Disadvantages -> more complex, increased difficulty in fat cattle, need long needle (18g 9-15cm)

148
Q

PVRA dorsal approach

A

Inject closer to midline where less likely to have branched
Block last thoracic and first 2 lumbar vertebrae

  1. Nerves run caudally and across TP’s of next vertebrae
  2. 5cm off the midline palpate the TP and drive needle down
  3. Get needle on cranial edge of TP, feel it slip off then penetrate a ligament and come out again
  4. Pull back and inject 10-15ml LA
  5. Bring needle up again to edge of bone and draw back again, inject for upper surface as one branch is above TP and one is underneath

Do not block L5/6 -> innervate hind quarters

149
Q

PVRA dorsal approach in horses

A

Cannot palpate, need ultrasound to visualise bones and arteries

10ml either side of TP

150
Q

PVRA lateral approach

A

Slide needle over and under TP laterally, coming in and out to spread it over TP instead of injecting all in one place

Palpate tips of TP so dont need as long a needle (only need 3-5cm)

Downside -> nerves branch at this point so we can miss and get patchy anaesthetic and poorer muscle relaxation

151
Q

Epidural technique

A

S-CO1 space or Co1-Co2 space
5-10ml volume

Stand behind animal, look at midline and visualise dorsal processes of the spine
Lift tail up and down to feel gaps
Put needle in space perpendicular to midline on the midline
Confirm epidural space by “popping” or hanging drop
Inject 5-10ml LA

Any bigger volume would get motor fibres of hindlimb

152
Q

Epidural precautions

A

Strict aseptic and non-preservative drugs

Don’t use in coagulopathy or thrombocytopaenia, dermatitis near the site or raised ICP

153
Q

What confirms entry in epidural space?

A

Pop
Hanging drop technique -> drop of needle hub sucked in when needle enters
Loss of resistance -> air drop in syringe, apply small back pressure and it will compress if in connective tissue or lose compression in epidural space

154
Q

2 examples of synergistic sedation in cattle

A
  1. Ace + xylazine
  2. Ace or xylazine + butorphanol
155
Q

When can we use drugs off label?

A

For an individually identified animal
Adjust WHP as necessary

156
Q

3 LA used in food animals

A

Lignocaine
Tri-solfen -> lignocaine, bupivacaine, adrenaline and cetrimide
Mepivacaine -> only in horses (not in food animals)

157
Q

Sedatives used in food animals

A

Acepromazine - sheep, goats good, mild to moderate in cattle

Azaperone -> pigs

Xylazine -> pulmonary oedema and hypoxia in sheep, effective in cattle

Diazepam -> good in neonatal calves/lambs, no CVS side effects

158
Q

Acepromazine -> DOA, type of injection, onset of action, side effects

A

Long DOA
Slow onset (20 mins after IV)
Mild to moderate sedation with no analgesia in cattle, heavy sedation in goats
Vasodilation decreases BP
IV, IM, PO

159
Q

Azaperone class, sedation type, side effects

A

Class butyrophenone
Dose dependent sedation
No analgesia
Vasodilation and risk of hypotension more than ace

Most reliable sedative in pigs, only drug registered for pigs

160
Q

Xylazine - sedation quality, route, onset, DOA, side effects

A

Mild to profound sedation + analgesia
IV, IM, mucosal
Rapid onset
Moderate DOA in ruminants
Complex CVS side effects and others
Pulmonary oedema and hypoxaemia in sheep + goats
Contraindicated in last trimester

161
Q

Ketamine -> sedation quality, dose rate

A

3-5mg/kg for general anaesthetic
0.25-0.5mg/kg for sedation

Adjunct to sedations - combined with xylazine

Analgesia at sub-anaesthetic doses
On label for wide range of species

162
Q

Which circuit uses a Co2 absorber?

A

Rebreathing -> remove gases that have been exhaled

163
Q

Advantages of a rebreathing system

A

Low O2 flows -> low cost and less waste gases
Natural humidification of inspired gases reduces heat loss

164
Q

Disadvantages of rebreathing systems

A

Resistance to breathing increases (worse for smallies)
Circuit concentration is slow to changes
Expense of absorber

165
Q

Advantages of non-rebreathing system

A

Minimal resistance
Rapid changes in circuit concentrations after changing vapouriser settings
No Co2 absorber required -> decreases cost

166
Q

Disadvantages of a non-rebreathing system

A

Dry and cold gases increase hypothermia risk
High O2 flows - waste and cost, pollution, cold animals

167
Q

Which circuit is for non-rebreathing?

A

Bain

168
Q

What is the flow rate for spey clinic?

A

500ml/kg/min

(2-3x minute ventilation)

169
Q

What animals use a bain?

A

All cats and dogs under 4kg

170
Q

Flow rates for rebreathing circuit

A

100ml/kg/min or 2L per minute - whichever is greatest to begin with

and then 500ml/min maintenance

171
Q

Bag size

A

kg of dog x 10ml (tidal vol) x 5

20kg dog = 1L bag

172
Q

CO =

A

HR x SV

173
Q

What does BP roughly equate to?

A

CO x systemic vascular resistance

174
Q

Which receptors cause vasoconstriction?

A

alpha 1

175
Q

What is systolic arterial pressure?

A

Determined by SV and arterial compliance
Highest pressure of the cardiac cycle during emptying of the ventricles

normal -> 90-160 in dogs and cats

176
Q

What is diastolic arterial pressure?

A

Determined by circulating blood volume and vasomotor tone
Lowest pressure of cardiac cycle
During filling of ventricles

Normal -> 55-90 (ideally 70-80) in dogs and cats

177
Q

What is mean arterial pressure?

A

Area under curve of systolic and diastolic

MAP -> 60-100mmHg

Below 60 = vital organ perfusion inadequate

178
Q

Reasons for a drop in temp

A

Vasodilation caused by drugs
Inhibition of shivering
Cold tables, clipped areas, skin prep, open abdomen

179
Q

Below what temp do we see effects? What are they?

A

below 36 degrees
Severe hypothermia is <34

Hypothermia reduces MAC, we get bradycardia also and hypoventilation, decreased metabolism

Poor recovering, increased oxygen demand in recovery due to shivering, coagulation issues

180
Q

4 stages of anaesthesia depth

A

I = awake, voluntary excitement, HR + RR up, struggling
II = involuntary excitement, pupils dilate, narcosis, cortical depression
III = surgical anaesthesia (3 planes)

  1. Light - palpebral reflex, lacrimation
  2. Medium - corneal reflex
  3. Deep - losing corneal reflex, eye forward

IV = dead

181
Q

What is level 1 monitoring?

A

Stethoscope
Bag movement - amount/rate
MM colour, refill
Pulses, lingual and pedal
Reflexes
Muscle tone - jaw
Eye position
Bleeding at site

182
Q

Level 2 and 3 monitoring

A

Heart rate monitors, pulse oximetry, BP using doppler or oscillometric
Direct arterial monitors
Capnography
Gas monitors / gas analyser
Blood gas measurements
Thermometers

183
Q

How does pulse oximetry work?

A

Red and infrared light transmitted through thin layer of tissue back to reciever in the probe

Hb bound to O2 absorbs more infrared, unbound Hb absorbs more red light

Ratio of red:infrared light = SpO2

184
Q

What can lead to reduced pulse oximeter readings?

A

Pigment, compression of the area, thickness of tissue, hair

185
Q

What pulse oximeter reading signifies hypoxaemia?

A

60mmHg or SpO2 <90%

186
Q

What is the size of the cuff for doppler?

A

40% of limb circumference
Too wide -> false decrease in BP
Too narrow -> false increase in BP

187
Q

Surgical plane specs for:
Palpebral reflex
Jaw tone
Pupil
Corneal reflex
Anal tone

A

Absent
Loose
Ventral, medial
Present
Absent, lax

188
Q

What is PA?

A

Partial pressure of alveolar gas

189
Q

What is Pa?

A

Partial pressure of arterial gas (gas dissolved in plasma)

190
Q

What is Pv?

A

Partial pressure of venous gas

191
Q

What classifies hypoxia? What are mild symptoms?

A

SpO2 <90%
PaO2 <60mmHg

Tissue damage = muscle, Git, myocardium, kidney CNS

192
Q

Resting oxygen requirements

A

2-3ml/kg/min

193
Q

What 2 things does oxygen uptake depend on?

A

Useable lung SA
Oxygen diffusion gradient

High FiO2 >85% = high diffusion gradient
With FiO2 above air RR can be very low

194
Q

What is atelectasis?

A

Collapsed alveoli (perfused but not ventilated)
Loss of ventilated surface area for gas exchange
Risk of hypoxia despite normal RR and Vt

195
Q

What is hypercapnia?

A

CO2 >45mmHg

Acidosis with pH <7.4

196
Q

What is hypocapnia?

A

CO2 <35mmHg

Alkalosis with pH >7.4

197
Q

How fast do resp. pH occur?

A

Within minutes
Kidneys take days-weeks to correct this

198
Q

What 2 things affect minute ventilation?

A

Respiratory rate
Tidal volume

And PACO2 depends on minute ventilation

199
Q

Will high FiO2 (supplemental oxygen) prevent hypercapnia?

A

No

200
Q

6 reasons for resp. depression

A

Pathology
Airway obstruction - foreign, body fluids, URT swelling
Central resp depression - decreased drive or sensitivity to chemoreceptors, opioids
Muscle relaxation
Atelectasis
Equipment failure

201
Q

Common resp depressant drugs

A

Iso, injectible anaesthetics

Opioids
- Mu agonists like methadone are strong depressants
- Partial and mixed (buprenorphine and butorphanol less)

Ketamine (mild resp depression)

Benzos - mild but synergistic

202
Q

What is peripheral resp. depression?

A

Reduced tidal vol and/or increased atelectasis

Caused by relaxed resp muscles (benzos, anaesthetics, fatigue in animasl with chronic resp disease)

Muscle paralysis -> high epidural and spinal blocks, neuromuscular blockers

203
Q

What is the effect of increased pressure on thorax?

A

More effort to breathe due to more abdominal pressure (on back, pregnant, rib fractures, pneumothorax)

Results in peripheral respiratory compromise

204
Q

Relationship between peak inspiratory pressure and tidal volume

A

Higher PIP = higher Vt
Smaller PIP = smaller Vt

205
Q

What does the arterial blood gas measurement tell us?

A

Gas diffusion across alveolar membrane
Direct, but invasive and intermittent

206
Q

What does oxygen sat tell us?

A

Oxygen binding to haemoglobin

207
Q

What does capnography tell us?

A

Co2 in alveolar gas

208
Q

Normal SpO2

A

97-98%

209
Q

What is end tidal CO2?

A

Last part of each exhale = pure alveolar gas (equilibrated with blood leaving the lung)

210
Q

What does ETCO2 change with?

A

Minute ventilation (if CO and metabolism are constant)

Or if minute ventilation is constant, with CO and metabolism

211
Q

What is normal ETCO2?

A

35-45mmHg

212
Q

Steps to treat resp. depression

A
  1. Decide if hypoxia/hypercapnia or both
  2. Is it breathing and normally?
  3. Obstruction?
  4. If hypoxia -> decrease depth, check function of equipment, start ventilating if not breathing, increase FiO2 if breathing
213
Q

What does hypoventilation always lead to

A

Hypercapnia, may or may not lead to hypoxia

214
Q

Benefits of positive pressure ventilation

A

Control breathing
Maintain MV
Normalise Co2
Overcome atelectasis and high abdominal pressure

215
Q

Risks of positive pressure ventilation

A

Over inflation
Hyperventilation (hypocapnia and alkalosis)
Increased intra-thoracic pressure = decreased venous return, CO and BP + perfusion

Intercostals cause neg pressure to draw air in normally, when we ventilate this does not happen causing the above issues

216
Q

What to monitor when giving pos pressure ventilation

A

Resp rate
Vt
Inspiratory flow
Peak inspiratory pressure

217
Q

Rate for pos pressure ventilation - Tidal volume

A

10-15ml/kg

218
Q

How to minimise damage giving pos pressure ventilation

A

PIP as low as possible with adequate Vt or ETCO2
RR conservative - decrease times pressure is high
Ensure adequate blood vol

219
Q

3 factors affecting stroke volume

A

Preload - blood in ventricle prior to contraction
Strength of contraction
Afterload - resistance to out flow

220
Q

What does the oxygen delivery to organs equal?

A

Cardiac output (Qt) x (O2 per ml of blood)

221
Q

3 things the oxygen delivery to organs is affected by

A

Haemoglobin concentration
SpO2% -> oxygen saturation
Less so plasma oxygen concentration

222
Q

2 primary CVS monitoring machines

A

Pulse oximeter
Blood pressure

223
Q

5 additional CVS monitoring modalities

A

ECG
Central venous pressure (preload)
Cardiac output - invasive
Echocardiography - contractility
Urine output

224
Q

What is CRT measuring?

A

MM perfusion and peripheral blood flow
Sense of vasodilation or constriction

225
Q

What is pulse palpation measuring?

A

Peripheral blood flow - vasomotor tone not blood pressure

226
Q

Normal MAP

A

90-100mmHg

227
Q

Normal DAP

A

70-80mmHg

228
Q

MAP and SAP in hypotension

A

MAP <60mHg
SAP <90mmHg

requires intervention

Doppler gives systolic, oscillometric gives MAP

229
Q

SAP Hypertension

A

> 130-150mmHg

230
Q

How is direct blood pressure measured?

A

Cannula into peripheral artery - highly accurate
Invasive and difficult

231
Q

What parameter does oscillometric measurement read?

A

MAP
Automated regular measurements

232
Q

What parameter does Doppler measurement read?

A

SAP +/- PR
Not automated, longer setup, intermittent readings

233
Q

Factors affecting the accuracy of oscillometric BP readings

A

Cuff size
Position above/below the heart
Regular pulse - may fail in severe bradycardia
Pulse pressure -> may fail if it is weak or severe hypertension
Some patients too small or large

234
Q

What affect does the distance a cuff is above or below the heart have on BP?

A

Above - lower BP
Below - higher BP

235
Q

Advantages of doppler

A

Works with smaller animals, despite poor pulse pressure
Audible continuous pulse signal

236
Q

What does ECG measure?

A

HR and rhythm
Arrythmia diagnosis
Early detection of electrolyte based rhythm disturbances (Ca and K)

No assessment of mechanical function - pulseless electrical activity (cardiac arrest) still gets normal ECG

237
Q

Bradycardia in cats/small dogs, medium dogs and large dogs

A

Small: <100
Medium: <60
Large: <50

238
Q

3 consequences of bradycardia

A

Reduced cardiac output
Hypotension
Organ injury - death

239
Q

Which 2 drug classes causes bradycardia?

A

Alpha 2 agonists and high dose opioids

240
Q

Action steps for bradycardia patient

A
  1. Confirm HR
  2. Assess BP and ECG
  3. Assess anaesthetic depth and drug use

Bradycardia + hypotension = administer anticholinergic (atropine)

Bradycardia + normotension + sinus rhythm and normal peripheral perfusion = HR is adequate and no treatment indicated

241
Q

Tachycardia in cats, small dogs, medium dogs and large dogs

A

Cats: 180-200
small dogs: >160
medium dogs: >100
Large dogs: >80

242
Q

Reasons for tachycardia

A

Too light
Pain
Hypovolaemia or vasodilation
Hypoxia or anaemia
HypoK, HyperCa
Myocardial or electrical issues

243
Q

Consequences of tachycardia

A

Increased myocardial work and O2 demand
Progression to tachyarrhythmia or awareness/movement

244
Q

Tachycardia action steps

A
  1. Confirm HR
  2. Assess anaesthetic depth
  3. Assess BP and ECG - verify sinus tachycardia and not another tachyarrythmia
  4. Increase depth or administer analgesia if too light - increase ISO or opioid, alpha 2
  5. Assess for haemorrhage or hypovolaemia, hypoxia
  6. Consider crystalloid fluid bolus 10-15ml/kg over 10 mins or blood tranfusion
245
Q

types of vagal bradyarrhythmias that are common

A

Sinus arrhythmia, 1st or 2nd degree AV block

Or drug induced - alpha 2 agonists, high dose opioids

246
Q

Hypotension action steps

A
  1. Check patient and heart rate
  2. Check position of equipment - Cuff placement, position to heart, probe position, flush IBP line and check depth - turn down if too deep
  3. No hypovolaemia present - choose MAC sparing and give analgesia and turn down depth. Can give dopamine CRI or atropine (bradycardia) here
  4. Hypovolaemia present = IV fluids. Isotonic crystalloids, colloids, blood products (10ml/kg bolus over 10 mins)

Inotropes, dopamine 5-10ug/kg/min, atropine for bradycardia 0.02-0.04mg/kg IV

247
Q

Clinical signs of intra-operative blood loss

A

Tachycardia
Pale MM and weak pulse
Hypotension (late indicator)

248
Q

Haemorrhage action steps

A

Blood loss >10% of total requires replacement - crystalloids (hartmans) 2-3x blood loss

Transfusion IF -> PCV low, coagulation support needed

Coagulation support: Anti-fibrinolytics (tranexamic acid)
Blood products - FFP or FWP

Monitor PCV and lactate

249
Q

Hypertension SAP and reasons

A

130-150mmHg

Assess depth
Pain/stimulus
Vasoconstriction - alpha 2, vasopressors
Pre-existing disease

250
Q

Hypertension consequences

A

Inadequate depth - awareness and or movement
Mild/moderate = not acute life threatening

251
Q

Risk factors for complications of anaesthesia

A

Brachycephalics
Age, size (draught horses)
ASA classificaion I-V (E)
Use of drugs (ace - dec. BP, xylazine dec HR)
Length of procedure
Staff experience

252
Q

If we have good MAP does this mean we will have good perfusion?

A

No - may have too much vasoconstriction and not enough cardiac output

253
Q

Drugs causing hypotension

A

Premed - ACP, opioids, alpha 2
Volatile anaesthestics
Induction - propofol, alfax
ACE inhibitors

254
Q

Patient causes of hypotension

A

Hypovolaemia
Azotaemia
CNS depression
Sepsis
Haemorrhage
Cardiac disease - decreased contractility, decreased rate
Respiratory - pleural space disease
Allergies - histamine release due to med reaction

255
Q

4 causes of heat loss

A

Convection - heat transfer to water or air moving past the animal

Conduction - heat transfer across a surface

Radiation - exchange of heat between body and objects not in contact

Evaporation - moisture in contact with skin dissipates into air

256
Q

Phases of heat loss

A

Phase 1 -> First hour. Initial rapid decrease in core temperature

Phase 2 -> 2-3 hours. Slow, linear reduction in core temperature due to heat loss exceeding production

Phase 3 -> 3-4 hours. Body temp reaches a plateau where loss=production

257
Q

Control of thermoregulation

A
  • Hypothalamus
    • Thermoreceptors throughout the body afferent input to CNS
    • Efferent response instigated as required
    • Threshold range very narrow -> 0.2 degrees
258
Q

Reasons for perioperative hypothermia

A

Inhibition of thermoregulation
Vasodilators
Inability to initiate voluntary behaviour changes

259
Q

When does the biggest drop in temp occur?

A

First hour of anaesthesia

260
Q

Patients most at risk of hypothermia

A

Small animals
Neonates
Cachetic
Debilitated
Immobile animals

261
Q

Hypothermia results in:

A

Impaired CV function, bradycardia + arrythmias

Hypoventilation + hypoxia - shivering in recovery

Decreased metabolism of drugs -> Decreases MAC

Increased delayed healing

Coagulopathies and platelet dysfunction

262
Q

Prevention of hypothermia

A

Prewarm 30mins prior to surgery
Insulate table - minimise conductive heat loss
Turn off AC - minimise convective heat loss, use warm fluids
Foil wrap - minimise radiation

Minimise evaporation -> low flow anaesthesia, rebreathing circuit, faster surgery

Heaters in recovery, heated IV fluids (38.9-39), bear huggers`

263
Q

Causes of hyperthermia

A

Certain drug interactions - ketamine, tiletamine, opioids in cats

Malignant hyperthermia - humans and pigs. Inherited and triggered by inhalationals and succinylcholine. Releases Ca from sarcoplasmic reticulum of skeletal muscle to increase muscle contraction and cell metabolism

264
Q

Aetiology of arrythmias

A

Imbalance of PNS/SNS tone
Atropine, alpha-2, ketamine, opioids

Electrolyte imbalances - hyperkal, hypokal

Cardiac disease, critically ill animals

265
Q

Treatment of ventricular fibrillation and pulseless ventricular tachycardia

A

Defibrillation and CPR

266
Q

Treatment of asystole and pulseless electrical activity

A

CPR

267
Q

Aetiology of cardiopulmonary arrest

A

Resp or cardiac insufficiency -> low O2 -> brain/heart dysfunction

Many causes -> hypoxaemia, hypoventilation, hypotension, hypovolaemia, arrythmia, hypothermia, drug OD

268
Q

Warning signs of cardiac arrest

A

Gradually increasing or decreasing HR, pupil size, irregular or gasping breathing patterns, gradually decreasing ETCO2

269
Q

Diagnosis of cardiac arrest

A

Loss of palpable pulse or lack of heart sounds on ausculation and apnoea

270
Q

Regurgitation causes in anaesthesia

A

Change in body position, drugs, change in sphincter tone

Species and breed - brachycephalics more likely

Pre-existing GIT disease, incraesed age, increased time under GA, larger size, change in body position

271
Q

Consequences of vomiting

A

Oesophagitis
ASpiration

272
Q

Prevention of regurgitation

A

Cuffed ET tube
Appropriate fasting - dogs 12h, water 2h
Positioning
Morphine increases risk

Prophylactic GIT medications - high dose metoclopramide to increase lower oesophageal tone

273
Q

Causes of hypoventilation

A

Recumbency, atelectasis, distended abdominal viscera, body composition
Thoracic trauma
Airway obstruction

Results in = HYPERCAPNIA

274
Q

Hypercapnia can result in:

A

Tachychardia and increased BP
Or sometimes hypotension

Controlled ventilation required

275
Q

Hypoxaemia causes and signs

A

Low inspired O2
Hypoventilation
Venous admixture

Signs -> cyanotic MM, increased RR, HR, BP, low SPO2

tissue damage

276
Q

Aetiology of venous admixture

A

Anatomic shunts
Diffusion defects
ventilation perfusion mismatch
Atelectasis - compression of lungs by viscera, recumbency

277
Q

Treatment of venous admixture

A

Mechanical ventilation, drugs (salbutamol), position change

Fourth Year (8 decks)

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