Preanaesthetic Assessment and Premedication. Intravenous and Inhalant Anaesthetics. Flashcards

1
Q

What are the overall statistics for anaesthetic related deaths in:
1.Dogs
2.Cats
3. Rabbits
4. Horses

A
  1. 1 in 601 (0.17%)
  2. 1 in 419 (0.24%)
  3. 1 in 72 (1.39%)
  4. 1.9 % within 7 days of GA
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2
Q

What are the statistics for anaesthetic related deaths in Healthy:
1. Dogs
2. Cats
3. Rabbits
4.Horses

A
  1. 0.05% (1 in 1849)
  2. 1 in 895 0.11%
  3. 0.73% 1 in 137
  4. 1 in 100
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3
Q

What are the statistics for anaesthetic related deaths in unwell:
1.Dogs
2.Cats
3.Rabbits
4. Horse

A
  1. 1.33% 1 in 75
  2. 1.4% 1 in 71
  3. 7.37% 1 in 14
  4. Up to 8%
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4
Q

What factors increase the risk of anaesthetic death?

A
  • Illness/co-morbidities
  • Age
  • over/underweight
  • emergency or complex procedures
  • ET intubation in cats
  • fluid overload (in cats)
  • manual ventilation
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5
Q

What factors decrease anaesthetic death?

A
  • pre-anaesthetic physical exam
  • pre-medication with dom/ACP
  • IV placement
  • Monitoring HR BP SPO2 temp ECG
  • Recording observations
  • close observation during recovery
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6
Q

What about a neonate could affect its anaesthetic?

A
  • Poorly development renal/hepatic function
  • Immature CVS
  • Prone to hypothermia
  • Prone to hypoglycaemia
  • Drug distribution and effects may vary
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7
Q

What physical checks should be done on a patient, upon arrival in the practice?

A

PR, pulse quality, RR, MMcolour and CRT, HR and ausc of chest (pulse deficits, lung sounds, arrythmias, murmurs), temperature, ocuclar or nasal discharge, Venous access - any issues?, peripheral lymph nodes, abdo palpation, any current pain?

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8
Q

What would an ASA 1 indicate?

A

A normal healthy animal

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9
Q

What would an ASA 2 indicate?

A

An animal with mild systemic disease which is compensating well

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10
Q

What would an ASA 3 indicate?

A

An animal with severe systemic disease which is not compensating fully

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11
Q

What would an ASA 4 indicate?

A

An animal that has severe uncompensated systemic disease which is a constant threat to their life.

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12
Q

What would an ASA 5 indicate?

A

A moribund patient which is not going to survive 24 hours without surgery

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13
Q

How long should water be witheld for in healthy animals

A

RIght up until pre-med

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14
Q

How long should food be witheld in healthy animals?

A

4-6 hours

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15
Q

What exceptions are there to the usual fasting rules

A

Younger animals dont need as long a fast as at risk of hypoglyceamia
Neonates or less than 8w or 2kg should not be fasted for more than 1-2 hours.
Food is not witheld in rabbits due to risk of hypoglycaemia and gut stasis.

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16
Q

What is the anaesthetic triad?

A

Narcosis, muscle relaxation and analgesia

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17
Q

What is the difference between pharmacokinetics and pharmacodynamics?

A

Pharmacokinestics is what the body does to the drug. It describes absrorption, distributoin, metabolism and elimination.

Pharmacodynamics is what the drug does to the body.

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18
Q

Describe what step is missed in IV route of drug administration?

A

Absorption. The drug goes straight into systemic circulatioand causes a rapid rise in plasma concentration.

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19
Q

What is bioavailibility?

A

The fraction of a dose that reaches the systemic circulation after administration, compared to the same dose given by IV route.

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20
Q

What affects bioavailibility?

A

-Properties of the drug
- Formulation of drug
- route of administration and site
- indiviual patient state

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21
Q

What are 5 factors that influence drug distribution

A
  • Protein binding
  • Tissue binding
  • Organ blood flow
  • Membrane permeability
  • Drug solubility
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22
Q

What is the main plasma protein that binds drugs?

A

Albumin

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23
Q

What effect would hypoalbuminaemia have on administration of a drug?

A

Reduction in plasma proteins that can bind with drugs therefore increasing the ‘free’ fraction of drug, increasing its effect and possibly causing overdose.

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24
Q

Why are most drugs not easily filtered by the kidney?

A

Most drugs are lipophillic and highly plasma protein bound so are not easily filtered by the kidney.

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25
Q

What type of molecule does the kidney easily excrete?

A

Polar, water-soluble compounds

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26
Q

What is the main organ of metabolism ? Describe the phases of drug metabolism within it.

A

Liver
Phase 1 - reactions covert drug to polar metabolite
Phase 2 - reactions involve conjugation with substrates and consumptoin of energy

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27
Q

What do opioids and alpha-2 drugs act on in the body?

A

Receptors

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28
Q

Define Affinity

A

How well a drug binds to its receptor

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29
Q

Define Intrinsic activity or efficacy

A

The magnitude of effect once the drug is bound

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30
Q

Define POtency

A

Dose of drug reqiured to produce a response

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31
Q

Define a full agonist

A

Can generate a maximal response after binding to its receptor

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32
Q

Define Partial agonist

A

Doesnt produce maximal effect, even when dose is increased

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33
Q

Describe how an antagonist works

A

Has affinity for the receptor but doesnt produce an effect once its bound . However it can block the effect of an agonist

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34
Q

What is therapeutic index

A

The maximum non toxic dose tot eh minimum effective dose

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35
Q

What are the aims of pre-medication?

A
  • Calm the animal through anxiolysis
  • allow patietn handling
  • perioperative analgesia
  • contribute to balanced anaesthesia
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36
Q

What is a synergistic effect?

A

A syngergist effect occurs when the interaction between 2 or more drugs causes the total effect of the drugs to be greater than the sum of the individual effects of each drug on their own

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37
Q

How does stress affect a pre-med?

A

Stress can result in high levels of circulating catecholamines which can interfere with sedative effects

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38
Q

Describe the drug selection cascade

A
  1. A veterinary medicine authorised for use in another species or by a different route in the same species
  2. A medicine authorised for human use
  3. A medicine made up at that time as a one off by a vet
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39
Q

Describe the characteristics of ACP

A
  • phenothiazine
  • dopamine receptor antagonist
  • mild-mod, long-lasting sedation
  • plateau effect seen at 0.05mg/kg
  • 15-30 minute onset
  • approx 6h duration
  • metabolised by liver and cannot be antagonised
  • anti-histamine
  • anti-arrythmic and vasodilator (as is an alpha 1 antagonist
  • reduces PCV by up tp 20%
  • anti-emetic
    -‘fainting’ in boxers?
  • avoid in brachy as prolongs recovery
  • lowers seizure threshold
    -MAC sparing
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40
Q

Describe the characteristics of alpha 2 adrenoreceptor agonists

A
  • unpredictable in aggressive/excited dogs as high levels of adrenaline can compete with drug molecules at adrenoreceptors
  • Onset of action within 5 minutes IV 15-20 mins IM
  • Metabolised by the liver
  • Reduce hepatic blood flow
  • Can be reversed by atipamezole
  • Intial vasoconstriction, reflex bradycardia and reduce CO.
  • Can cause first or second degree AV block
  • Good muscle relaxant
  • Can cause vomitting, reduce GI motility, reduce ADH and renin which increases urine production, reduces insulin secretion resulting in hyperglycaemia.
    -MAC sparing
41
Q

Describe the characteristics of Ketamine

A
  • NMDA antagonist
  • Can cause muscle rigisity and excitement if used alone
  • Schedule 2 CD
  • Metabolised by the liver and the active metabolite nor-ketamine is excreted by the kidneys.
  • Onset of action approx 3-10minutes
  • Effects last 30-45 minutes
  • causes myocardial depression
  • catelcholamine release which produces positive chronotropic effects
  • can increase intra-ocular and intra-cranial pressures.
  • better somatic (tissues, bone, skin) analgesia than visceral (organs).
42
Q

Describe the characteristics of Benzodiazepines

A
  • metabolised in the liver
  • GABA agonists
  • Midazolam water soluble, administered IM IV and produces inactive metabolites
  • Diazepam painful on injection, can cause thrombophlebitis, has active metabolites.
43
Q

What can diazepam cause in cats?

A

Idiosyncratic hepatic necrosis

44
Q

Where is Acetylcholine found?

A

Neurotransmitter found in brain, spinal cord, peripheral nerves and some other cells including RBCs

45
Q

Where is Noradrenaline found and what receptors does it act on?

A

Many tissues of body including brain and sympathetic ganglia and acts on alpha and beta adrenoreceptors

45
Q

What receptors does Acetylcholine act on?

A

Muscarinic (from post-ganglionic parasympathetic fibres) and nicotinic (from motor nerve fibres)

46
Q

What is glutamate found and what receptors does it act on?

A

It is the principle excitatory neurotransmitter in the vertebrate central nervous system and acts on AMPA, NMDA, metabotropic glutamate and kainate receptors

47
Q

Where is gamma amino butyric acid (GABA) neurotransmitter found?

A

It is the principle inhibitory neurotransmitter in the adult CNS and acts on the GABA receptor to decrease excitability of neurons

48
Q

What type of neurotransmitter is histamine?

A

Widely distributed affferent neurotransmitter involved in itch and pain senses

49
Q

What is the role of dopamine?

A

Precursor of noradrenaline, involved in the control of movement and behaviour

50
Q

Where is adrenaline produced in the body? What receptors does it act on and what are the effects?

A

Produced by adrenal glands and neurones in the medulla oblongata. Acts on alpha and beta adrenoreceptors and increases CO. Increases muscle blood flow, increases blood glucose and dilate pupils (fight or flight).

51
Q

Where does serotonin act and what effect does it have?

A

Acts on 5HT receptors to regulate sensory pathways and control mood.

52
Q

In basic terms describe the pharmokinetics of an IV drug injected

A

After injection, the plasma concentration of the IV agent increases rapidly to a maximum value. It is then redistributed to the tissues and is metabolised and elminiated.

53
Q

Define Volume of distribution

A

A theoretical concept linking dose given to plasma concentration
Vd = dose / plasma concentration

54
Q

Define Clearance

A

The volume of plasma that the drug is removed from over time.

55
Q

Define Half Life

A

The time taken for the plasma concentration to fall by 50%.

56
Q

What is the Context Sensitive half time?

A

The time taken for the plasma concentration of a drug that has been being maintained at a constant plasma level to fall by 50%. And the context relates to the duration of the infusion.

57
Q

Describe the ideal injectable anaesthetic

A
  • rapid onset
  • non-irritant
  • minimal cardiopulmonary effects
  • rapidly metabolised and eliminated
  • non-cumulative
  • good analgesia
  • good muscle relaxation
58
Q

Describe how propofol and alfaxan actually work

A

They are agonists at the GABA receptor. Once bound, they increase the frequency or duration of GABA dependent chloride channel opening. The increase in chloride conductance causes hyperpolarisation and neuronal inhibition.

59
Q

Describe how ketamine works

A

NMDA antagonists and antagonises the excitatory neurotransmitter glutamate at NMDA receptors in the CNS.

60
Q

List the key features of Propofol

A
  • phenol
  • GABA agonist
  • Rapid onset of action
  • IV
  • Rapidly metabolised in liver and eliminated
  • Non-cumulative in dogs
  • Commonly causes apnoea
  • Causes myocardial depression and peripheral vasodilation
  • no analgesia
  • non-irritant if accidentally injected peri-vascularly.
  • Highly plasma protein bound (96-98%)
61
Q

Why is metabolism of propofol slower in cats than dogs?

A

Thye lack the glucuronidation pathway in liver.

62
Q

What caution should be taken when using propofol in cats?

A

Cumulative.
Avoid consecutive days use. Can cause oxidative damage to RBCs (heinz body formation) seen after 3 days.

63
Q

How is water insoluble alfaxan made water soluble for use as an injectable?

A

Sits inside a sugar ring called cyclodextrin. Inside is hydrophobic and outside is water soluble.

64
Q

List the key features of Alfaxalone

A
  • steriod anaesthetic
  • high therapeutic index
  • non-irritant
  • IV
  • rapid onset
  • non-cumulative
  • hepatic metabolism and elimination
  • some resp depression
  • preserves baro-receptor tone - HR increases in respose to reduced BP
  • no analgesia
  • plasma protein bindin approx 20%
65
Q

List the key features of Ketamine

A
  • IV or IM, SC or transmucosal
  • can cause excitement in busy environment
  • metabolised by liver - active metabolite is norketamine
  • plasma protein binding 50%
  • sympathetic stimulation and maintians CVS and rep function
  • increases myocardial workload ( care with hypertrophic cardiomyopathy cases)
  • analgesia
  • slow onset
  • non-cumulative
  • may increase IOP and ICP
66
Q

Define MAC

A

Minimum alveolar concentration.
The alveolar concentration of inhalant anasesthetic agent required to prevent purposeful movement in response to noxious stimuli in 50% of patients

67
Q

What decreases MAC in practice?

A
  • sedatives
  • analgesics
  • co-administered anaesthetic agents e.g. midazolam
  • Hypothermia (decreased metabolic rate)
68
Q

What increases MAC in practice?

A
  • Increased metabolic rate (hyperthermia, young animals, hyperthyroidism)
  • Concurrent administration of catecholamines and sympathomimetics e.g. ephidrine.
69
Q

What determines the effect of a volatile agent in that patient?

A

The partial pressure of the volatile agent in the brain.

70
Q

What is a partition coefficient?

A

Describes the ratio of the concentration of a compound in two solvents at equilibrium (equal volume, pressure and temperature).

71
Q

What is a blood gas solubility co-efficient?

A

Describes the solubility of a gas in the blood. Agents with a low blood-gas solubility exert a high partial pressure. Therefore a rapid induction and recovery will occur. The more soluble the agent, the more agent is needed to increase its partial pressure int he alveoli.

72
Q

What determines the potency of an inhalational agent? How is the potency measured?

A

Its lipid solubility, ability to cross the blood brain barrier and into the lipid tissues of the brain.
Measured it’s oil-gas partition coefficient.

73
Q

What are 3 theories for how inhalational anaesthetics work?

A
  • disruption of the cell membrane lipid bilayer
  • binding to proteins on ion channels and inhibiting synaptic transmission
  • direct effects on specific receptors such as GABA NMDA etc
74
Q

Describe the Meyer-Overton Hypothesis

A

Describes a link between the oil-gas partition coefficient of an agent and its potency.
The molecules of the inhalational anaesthetics dissolve in the lipid bilayer of cell membranes within the brain and when this happens in sufficient amounts, a state of unconsciousness (anaesthesia) is induced.

75
Q

Describe the factors that influence speed of uptake of inhaant anaesthetic agents

A
  1. Inspired concentration (i.e. the percentage on the vaporiser). The higher this is, the higher the partial pressure of the agent in the lungs and faster onset.
  2. Alveolar Ventilation - increases AV increases the partial pressure of the agent in the alveoli, increasing the rate of uptake.
  3. CO. with low CO the uptake of the anasthetic agent fromt he alveoli to the pulmonary circulation is low so the partial pressure in the alveoli rises radipdly.
  4. Blood Gas Partition Coefficient. Anaesthetics with a low blood gas solubility coefficient produce rapid onset of anaesthesia.
76
Q

What is the percentage of hepatic metabolism in sevoflurane and isoflurane

A

Sevo - 2-5%
Iso 0.2%

77
Q

List the properties of an ideal inhalant anaesthetic agent

A
  • non-irritant to mucous membranes
  • minimal effects of cardiorespiratory system
  • low blood gas solubility - rapid uptake and elimination
  • minimal metabolism
  • non-toxic
  • non-flammable and chemically stable
  • easily vaporised
  • good analgesia and muscle relaxation
  • minimal environmental effect
78
Q

What is the MAC and blood gas solubility of isoflurane

A

dog 1.3- cat 1.6%
BGS 1.4

79
Q

What are the dose-dependent side effects of isoflurane?

A
  • hypotension due to myocardial depression (contractility) and peripheral vasodilation
  • Hypoventilation due to respiratory depression
  • Bronchodilation
  • irritant
80
Q

What is the MAC and blood gas solubility of sevoflurane

A

2.1-2.6%
BGS 0.7

81
Q

What are the dose-dependant side effects of sevoflurane?

A
  • hypotension due to myocardial depression (contractility) and peripheral vasodilation
  • May have less effect on cerebral blood flow and sometimes called ‘neuroprotectant’.
82
Q

What is the MAC and BGS of desflurane and what percentage is metabolised in the liver?

A

MAC 7.6-9.8%
BGS 0.45
liver metabolism 0.02%

83
Q

What are the concerns with using desflurane

A
  • hard to vapourise safely as boiling point close to room temp
  • very irritant to mucous membranes
    -can cause airway hyperreactivity
  • hypotension, but minimal effect on resp system
  • risk of ‘sympathetic storm’ where increase HR BP and RAA system
84
Q

What is the MAC, BGS of halothane?

A

MAC 0.8-1.1%
BGS 2.5

85
Q

What does heating ammonium nitrate to 250 degrees celcius do?

A

Produced NO

86
Q

What is the MAC , BGS of NO

A

More than 100% (so cannot be used alone)
BGS approx 0.45

87
Q

What are the concerns with using NO ?

A
  • environmental impact
  • very insoluble and diffuses into air filled cavities in body (should be avoid in those with risk of pneumothorax etc.)
  • Administered with O2 so reduced FiO2
  • Makes the alveoli smaller and therefore increases partial pressure and uptake of inhalational agent
  • Can cause diffusion hypoxia at the end of surgery of not supplemented o2
88
Q

List the inhalational agents from highest BGS to lowest

A

Halothane, isoflurane, sevoflurane, NO and desflurane same.

89
Q

List the inhalational agents from highest MAC to lowest

A

NO, Desflurane, Sevoflurane, Isoflurane, Halothane

90
Q

What are the 3 most common side effects of inhalational anaesthesia?

A

Hypotension, Respiratory depression, cerebral metabolism

91
Q

Why should we be careful when using iso or sevo with neuro patients?

A

They decrease cerebral metabolism and therefore oxygen consumption through cerebral vasodilation - resulting in an increase in cerebral blood flow

92
Q

What are the main concerns with inhalational induction of anaesthesia?

A
  • pollution
  • irritant
  • obstruct view of face
  • aspiration/regurgitation/obstruction
93
Q

What patients are more suceptible to hpothermia under GA?

A

Small patients due to their increased surface area:volume ratio
Patients with low metabolic rate (e.g. hypothyroid).

94
Q

What effects does hypothermia haev on the rest of the anaesthetic?

A
  • Lower anaesthetic requirement (with each decrease in degree C, the MAC decreases by 5%)
  • Shivering can increase oxygen requirements by 400%
  • Prolonged duration of aciton of drugs
  • Bradycardia that is often unresponsive to antimuscarinics.
  • Cardiac arrythmias
  • impaired coagulation and wound healing
  • Decreased enzyme activity
  • Decreased renal plasma flow
95
Q

How can hypothermia be minimised

A

-Minimising clipping, avoid excessive wetting during prep and warm water.
- Use of heating methods
- Warm environment
- Warm IV fluids
- Re-breathing systems and moisture exchangers

96
Q

What temperature should active warming be stopped in hypothermic patients?

A

37 degrees

97
Q

Why must care be taken when warming hypothermic patients?

A

Heating peripheral tissues can cause vasodilation and worsen hypotension