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Anaesthetics > Introduction > Flashcards

Introduction Flashcards

1
Q

What are the 4 main objectives of anaesthesia?

A
  1. To work with zero morbidity and mortality
  2. Make patient unaware of surgery and recover pain free
  3. Make some surgery posisble and all surgery as easy as possible
  4. To support psychological function and counter adverse effects of surgery
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2
Q

What are 7 differences between sleep and anaesthesia?

A
  1. Respond to pain in sleep, not in anaesthesia
  2. Move around in sleep vs. no movement in anaesthesia
  3. Can dream in sleep but not anaesthesia
  4. Maintain your airway in sleep (snoring/apnoea if not fully maintained), but lose this in anaesthesia
  5. Normal breathing in sleep, depressed ventilation and altered CO2 response in anaesthsia
  6. Can swallow in sleep, reduced swallowing under anaesthesia (pharyngeal secretions sometimes build up)
  7. Sleep EEG and anaesthesia EEG are very different
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3
Q

What are the 3 components of general anaesthesia?

A
  1. Hypnosis - ‘sleep’, lack of awareness
  2. Muscular relaxation - preventing movement in response to surgery
  3. Analgesia - obtund painful stimuli (note - can’t be in pain if anaesthetised but can respond - use analgesics to block response)
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4
Q

What is meant by a ‘balanced anaesthesia’?

A

Traditional name fo the combination of drugs: anaesthetic, aanlgesic and a if needed a muscle relaxant (this combo is given in addition to the large dose of IV or inhalational anaesthetic)

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5
Q

What are the 2 key things needed to achieve the components of anaesthesia?

A
  1. Sufficiently large dose of intravenous or inhalational anaesthetic
  2. Using a combination of drugs:
  • anaesthetic at much lower dose
  • analgesic
  • muscle relaxant if needed
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6
Q

What are 2 broad approaches to anaesthesia?

A
  1. Single agent anaesthesia
  2. Balanced technique
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7
Q

What is the advantage of single-agent anaesthesia?

A

Very simple, only one delivery system needed

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8
Q

What is the key disadvantage of single-agent anaesthesia?

A

As such a large amount of one drug is needed, it can lead to respiratory and cardiac depression - “not taking the drug well” e.g. chloroform and ether in the past, can lead to death due to profound respiratory and cardiovascular depression

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9
Q

In modern times, what is single-agent anaesthesia used for?

A

Now used for short procedures only, e.g. resetting a wrist fracture: single shot of IV agent, IV agent infusion or inhaled in oxygen

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10
Q

What are 2 benefits of the balanced technique of anaesthesia?

A
  1. Each component contributes its effects
  2. Side effects are reduced
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11
Q

What is a key disadvantage of the balanced technique of anaesthesia? Give 3 examples.

A

Requires attention to detail

  1. Too little anaesthetic agent = awareness
  2. Too little analgesia = excess reponse to noxious stimuli
  3. Too little relaxant = unwanted movement, or unwanted muscle tone - e.g. makes abdominal surgery different
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12
Q

What are 2 steps to general anaesthesia and how can they each be achieved?

A
  1. Induction: can be induced by intravenous or inhalational agents
  2. Maintenance: can be maintained by intravenous or inhalational agents
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13
Q

What are 2 ways that general anaesthetics can be combined with other drugs?

A
  1. Can be combined with analgesics and muscle relaxants as in balanced anaesthesia
  2. Combined with local or regional anaesthesia
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14
Q

What are 2 states of patient care that general anaesthesia can be administered in?

A
  1. Patient breathing spontaneously OR
  2. ventilation provided artificially
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15
Q

What is sedation?

A

Form of semi-hyponosis in which the patient is rousable, can talk, but may have no memory of events (e.g. midazolam especially good at blocking memory)

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16
Q

Why is it important that a sedated patient is able to talk?

A

Means you must be able to maintain your airway

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17
Q

Where does sedation turn into anaesthesia and why is it important?

A

Some deep sedation may be like anaesthesia, need to think about maintenance of airway in these patients

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18
Q

What are the 2 types of local anaesthesia?

A
  1. Topical e.g. cream
  2. Infiltration e.g. before putting in venflon, dentist
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19
Q

What are 5 types of regional anaesthesia?

A
  1. Peripheral nerve block
  2. Ganglion/ plexus block
  3. Epidural
  4. Spinal
  5. Intravenous regional
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20
Q

What 2 types of anaesthesia are being increasingly combined?

A

General and regional anaesthesia

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21
Q

How does general anaesthesia act on the body’s response to pain?

A

Prevents pain that is generated from being interpreted as pain by the central nervous system; doesn’t stop transmission of painful stimuli from the source of pain

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22
Q

How do local and regional anaesthesia act with regards to pain?

A

Prevent transmission of a painful stimulus reaching the central nervous system

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23
Q

Why might local anaesthesia be combined with general anaesthesia or sedation on some occasions?

A
  • When combined with general anaesthesia, local anaesthesia used as the analgesic part of balanced anaesthesia
  • When combined with sedation, can take advantage of the benefits of both approaches
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24
Q

What is the chemical structure of most local anaesthetics?

A
  • Most have a lipid soluble, hydrophobic aromatic group and a charged, hydrophili amide group and a charged, hydrophilic amide group.
  • There is an amide or ester bond between groups
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25
Q

What are 3 examples of amide-bonded local anaesthetics?

A
  1. Lignocaine
  2. Bupivacaine
  3. Prilocaine
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26
Q

What are 2 examples of ester-bonded local anaesthetics?

A
  1. Cocaine
  2. Amethocaine (used topically as lozenges)
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27
Q

What does the metabolism of ester-bonded LAs result in?

A

The production of para-aminobenzoate (PABA) = associated with reasonably high incidence of allergic reactions

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28
Q

How do local anaesthetic agents work?

A
  • Inhibit sodium influx through sodium-specific ion channels int he neuronal cell membrane (voltage-gated sodium channels)
  • Are weak bases (B), usually available as hydrochloride solutions
  • At physiologic pH, both the ionised (BH+) and unionised forms (B) of the molecule exist; only the ionised form is able to block sodium channels
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29
Q

Why is pH important in the way local anaesthetic agents work?

A

pH is important in determining the ratio fo ionised to unionised forms of the LA molecules, as they’re an acid-based compound; only the unionised form diffuses readily across cell membranes

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30
Q

In what form is the LA agent given?

A

Weak base injected as a hydrochloride salt in an acid solution - tertiary amine group becomes quarternary and suitable for injection i.e. dissolves in solution

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31
Q

What happens once an LA agent has been injected?

A

pH increases (due to higher pH of the tissues, which is usually 7.4) and the drug dissociates, the degree of which depends on pKa, and free base is released

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32
Q

What happens once the LA agent has been injected and it has dissociated?

A

Lipid soluble free base (B), i.e. the unionised form, enters the axon. Inside the axon, pH is lower/more acidic, and re-ionisation takes place. The re-ionised portion enters the Na+ channels and blocks them, preventing depolarisation

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33
Q

Give the 5 steps to summarise how LA agents work.

A
  1. Weak base exists as hydrochloride salt in acid solution
  2. Injected and dissociates to B and BH+
  3. Unionised, free base form B crosses neuron cell membrane and enters axon
  4. Re-associates in axon due to lower pH
  5. Re-ionised portion enters Na+ channels and blocks them
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34
Q

By which route should local anaesthetic never be given?

A

Intravenously

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35
Q

How safe are local anaesthetic agents generally?

A

In right dosage and properly injected, they are very safe

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36
Q

What negative effects can occur as a result of local anaesthetics if injected IV, with increasing concentration?

A
  • 4mg/ml: light headedness, tinnitus, circumoral and tongue numbness
  • 6mg/ml: visual disturbances
  • 8mg/ml: muscular twitching
  • 10mg/ml: convulsions
  • 12mg/ml: unconsciousness
  • 15mg/ml: coma
  • 20mg/ml: respiratory arrest
  • 26mg/ml: cardiovascular collapse
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37
Q

What are the maximum safe doses of a) bupivacaine b) lignocaine and c) prilocaine?

A

Bupivacaine: 2mg/kg

Lignocaine: 3mg/kg

Prilocaine: 6mg/kg

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38
Q

What is the ratio of cardiovascular collapse : convulsion for bupivacaine vs lignocaine and what does this mean?

A

The ratio os 4 for bupivacaine, 7 for lignocaine; therefore lignocaine less likely to cause seizures than bupivacaine, bupivacaine carries higher risk if injected by accident (lower number = more cardiotoxic)

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39
Q

What are the 2 routes of administration of local anaesthetics?

A
  1. Topical application
  2. Local infiltration
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40
Q

What are 4 examples of local anaesthetics given via topical application?

A
  1. Eutectic mixture of local anaesthetic (EMLA) cream, lignocaine 2.5% and prilocaine 2.5% in an emulsion
  2. Amethocaine cream/ gel
  3. Lignocaine spray (10%) - sometimes used for vocal cords, strong
  4. Benzocaine lozenges - for back of throat
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41
Q

What are 2 types of local infiltration that can be done with local anaesthetics?

A
  1. Field block
  2. Wound infiltration
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42
Q

What are 4 examples of local infiltration used to give local anaesthetic?

A
  1. Cannulae
  2. Sutures
  3. Inguinal hernia - done using field block
  4. Post-operative pain relief - using wound infiltration
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43
Q

What is local anaesthetic used in wound infiltration often given with, and what should you be careful of?

A

adrenaline, to reduce absorption of drug (so it’s longer lasting): have to be careful of the total dose, however

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44
Q

At what level would regional spinal anaesthesia by put in, in an adult for transurethral resection of the prostate?

A

L3-L4, sometimes L2-L3

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45
Q

What is the advantage of putting the spinal anaesthesia at the level of L3-4?

A

The spinal cord is finished her so no risk of puncturing

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46
Q

What kind of needle is used to insert spinal anaesthesia (type of regional)?

A

25-27g needle i.e. very fine

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47
Q

What is the aim when inserting the needle to administer spinal anaesthesia?

A

Aiming to pass thorugh all layers of the dura into the CSF, which can be determined by CSF leaking back through the needle

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48
Q

How much drug and what types can be injected during spinal anaesthesia?

A

Small volumes of drugs, often bupivacaine and occasionally other types

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49
Q

How quikly does it take for spinal anaesthesia to work and what should be the effect?

A

Rapid onset if in the right place; total block: sensory and muscle block

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50
Q

What type of block is produced by spinal anaesthesia?

A

Total block: sensory and muscle

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51
Q

What can be added to spinal anaesthesia?

A

Opioids e.g. fentanyl (done by some anaesthetists)

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52
Q

In which specialty is epidural anaesthesia very popular?

A

Obstetrics

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53
Q

How is epidural anaesthesia given?

A
  • Tuohy needle (pronounced too-ee) used through the ligaments int he back until there’s loss of resistance, into the epidural “space”, an area with fat and some vessels.
  • Feel a loss of resistance, pop through the ligamentum flavum and can start to inject fluid.
  • Pass catheter through after putting the needle in
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54
Q

At what level can epidural anaesthesia be given?

A

Commonly L2-3 or 3-4 for lower limb surgery in adults, or lower thoracic; occasionally cervical

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55
Q

How much anaesthetic drug can be given during an epidural?

A

Large volumes of drug

56
Q

How can epidurals be given in children?

A

Through the sacral hiatus into the caudal epidural space

57
Q

What are 4 differences between spinal and epidural types of regional anaesthesia?

A
  1. Spinal is a single injection but epidural has a catheter sitting in one spot so larger volumes of drug can be given, and can last longer
  2. In spinal, a hole is made in the dura and drug is injected. In epidural, the drug is delivered outside the dura
  3. Epidural can be given anywhere along vertebral column but spinal more common below L2 to avoid piercing spinal cord
  4. Larger needle required for epidural
58
Q

What is a nerve block (type of regional anaesthesia?

A

Local anaesthetic is inject close to a nerve/ nerves

59
Q

What is important to avoid when delivering a nerve block?

A

Avoid vessels - don’t want intra-arterial or intravenous injection

60
Q

What dosage of anaesthetic may be required for a nerve block?

A

Up to 30ml required, very close to maximum dose

61
Q

What are the 2 types of nerve block and examples of each?

A
  1. Single nerve: femoral (lower limb), intercostal, dental
  2. Multiple nerves: ankle block - multiple nerves to the ankle blocked, brachial plexus - upper limb
62
Q

What is the name of the common intravenous regional anaesthetic that used to be given?

A

Biers block: done for fractured wrist

63
Q

How is a Biers block performed?

A
  • Arm exsanguinated - lift it up, special double tourniquet used,
  • Tourniquet blown up above arterial pressure so no blood flows into the forearm.
  • Large volume of prilocaine given intravenously (no longer bupivacaine, dangerous).
  • Cuff up >20 minutes.
64
Q

How can a Biers block/ intravenous regional anaesthetic be hazardous?

A

If cuff comes down too early, can get severe toxic side effects

65
Q

Why has the Biers block technique fallen into disuse?

A

unpleasant if you have a broken wrist

66
Q

What sort of standards apply when administering local anaesthesia?

A

The same standards of pre-operative assessment as for general anaesthesia

67
Q

What sort of things does the selection of LA technique depend on?

A

The operation, the patient, the surgeon, the anaesthetist and their interactions; most surgeons find it easier if patinet under LA than GA

68
Q

What should be given and offered to a patient before receiving local anaesthesia?

A

Full explanation of what to expect, should normally be offered sedation (apart from C section)

69
Q

During which procedure is the patient not offered sedation with their LA/ regional anaesthesia?

A

C-section - mother is intentionally fully awake

70
Q

What element of preparing for surgery is essential for anaesthetic and surgical success?

A

Time spent positioning the patient

71
Q

What should be remembered when giving local or regional anaesthesia?

A

Time must be allowed for the block to work

72
Q

What preparations should be made in case local anaesthesia is unsuccessful?

A

a plan B e.g. cancel and come back on another day; if urgen,t may need to convert to GA (difficult if not planned)

73
Q

What must be available for a patient with a plan for continuing analgesia in the post-operative period?

A

Proper recovery facilities, as often become hypotensive, paralysed, unable to pass urine - can be significant physiological disturbances

74
Q

What are 5 absolute contraindications to local anaesthesia?

A
  1. Patient unwilling or unable to give consent
  2. Surgeon unhappy with conditions provided under local anaesthesia
  3. Absence of operating room staff who understand the implications of operating under local anaesthesia - not right staff/equipment to help you
  4. Anticoagulation or coagulopathy
  5. Infection at the site of injection
75
Q

What is a relative contraindication to local anaesthesia?

A

Existing or suspected neurological deficit e.g. rare complication of epidural is an epidural haematoma which produces prolonged paraesthesia and occasionally prolonged paralyses → is a relative CI because you must be able to detect whether an epidural haematoma has occurred

76
Q

What type of chemical is lidocaine?

A

amide

77
Q

What 2 uses does lidocaine have?

A

local anaesthetic and less commonly used antiarrhythmic (affects sodium channels in the axon)

78
Q

How is lidocaine metabolised/ transported/ excreted?

A

Hepatic metabolism, protein bound, renally excreted

79
Q

What key thing can cause lidocaine toxicity and what 2 states can increase this risk?

A
  • Toxicity due to IV or excess administration
  • Increased risk if liver dysfunction or low protein states
80
Q

What can cause lidocaine to detach from protein binding?

A

Acidosis

81
Q

How can local anaesthetic toxicity be treated?

A

IV 20% lipid emulsion

82
Q

What are 3 drug interactions of lidocaine?

A
  1. Beta blockers
  2. Ciprofloxacin
  3. Phenytoin
83
Q

What are 2 features of lidocaine toxicity?

A
  • Initial CNS over-activity, then depression as lidocaine initially blocks inhibitory pathways, then block both inhibitory and activating pathways
  • Cardiac arrhythmias
84
Q

How can increased doses of lidocaine be given?

A

combined with adrenaline, to limit systemic absorption

85
Q

In what form does pure cocaine usually exist, and how is it supplied for LA purposes?

A
  • As a salt, usually cocaine hydrochloride
  • Supplied for LA purposes as a paste
86
Q

What are the 2 concentrations that cocaine is supplied in?

A

4% and 10%

87
Q

How can cocaine be applied?

A

Topically to nasal mucosa

88
Q

What are the actions of cocaine?

A

Lipophilic so crosses blood-brain barrier, rapid onset of action –> LA effects, additional advantage of causing marked vasoconstriction

89
Q

What are systemic effects of cocaine?

A

Cardiac arrhythmias and tachycardia

90
Q

When is cocaine used as a LA?

A

limited use in ENT surgery (rarely in mainstream surgical practice)

91
Q

What is lidocaine also known as?

A

lignocaine (they’re the same thing)

92
Q

What is the mechanism of action of bupivacaine?

A

Binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarisation

93
Q

How does the duration of action of bupivacaine compare to lignocaine, and what can it therefore be used for?

A

bupivacaine has much longer duration of action than lignocaine; bupivacaine can be used for topical wound infiltration at end of surgery with long duration analgesic effect

94
Q

What procedures is bupivacaine contra-indicated in and why?

A

regional blockage, because it is cardiotoxic so CI-ed in case tourniquet fails

95
Q

What is the less cardiotoxic form of bupivacaine and what else does it result in?

A

levobupivacaine (chirocaine) - also causes less vasodilation

96
Q

What is the key adverse effect of bupivacaine?

A

cardiotoxic

97
Q

What is prilocaine the LA of choice for and why?

A

IV regional anaesthesia e.g. Biers block, because it is far less cardiotoxic

98
Q

What can reduce the efficacy of local anaesthetic agents and why?

A

acidic tissues e.g. where an abscess is present, because all LAs dissociate in tissues which contributes to therapeutic effect, but acidic tissues shift the dissociation constant

99
Q

What is the guide plain dose of lignocaine?

A

3mg/kg

100
Q

What is the guide plain dose of bupivacaine?

A

2mg/kg

101
Q

What is the guide plain dose of prilocaine?

A

6mg/kg

102
Q

What is the guide dose of lignocaine with adrenaline?

A

7mg/kg

103
Q

What is the guide dose of bupivacaine with adrenaline?

A

2mg/kg

104
Q

What is the guide dose of prilocaine with adrenaline?

A

9mg/kg

105
Q

What 3 things do actual doses of LAs depend on, meaning the guide doses are subject to change?

A
  1. site of administration
  2. tissue vascularity
  3. co-morbidities
106
Q

What is the maximum total local anaesthetic dose of 1% lignocaine plain based on ideal body weight?

A

3mg/kg –> 200mg (20ml)

107
Q

What is the maximum total local anaesthetic dose of 1% lignocaine with adrenaline based on ideal body weight?

A

7mg/kg –> 500mg (50ml)

108
Q

What is the maximum total dose of bupivacaine 0.5% based on ideal body weight?

A

2mg/kg –> 150mg (30ml)

109
Q

What are 2 benefits of mixing LA with adrenaline?

A
  1. prolongs duration of action at site of injection due to vasoconstriction
  2. permits usage of higher doses and reduces systemic absorption
110
Q

In which 2 groups of patients is adding adrenaline to LAs contraindicated?

A
  1. patients taking MAOIs
  2. patients taking tricyclic anti-depressants
111
Q

What is the toxicity of bupivacaine related to, and why does this preclude the addition of adrenaline?

A

toxicity is related to protein binding; addition of adrenaline doesn’t permit increases in the total dose of bupivacaine i.e. doesn’t reduce protein binding, in contrast to lignocaine where it reduces toxicity through vasoconstriction

112
Q

What are the 2 key groups of muscle relaxants aka neuromuscular blocking drugs and what category do 4 examples fall into?

A
  • Depolarising: suxamethonium
  • Non-depolarising: atracurium, vecuronium, pancuronium
113
Q

What is the mechanism of action of suxamethonium?

A

inhibits action of acetylcholine at the neuromuscular junction; degraded by plasma cholinesterase and acetylcholinesterase

114
Q

Which has both the fastest onset and shortest duration of all the muscle relaxants?

A

Suxamethonium

115
Q

What effect does suxamethonium have?

A

Produces generalised muscular contraction prior to paralysis

116
Q

What are 3 adverse effects of suxamethonium?

A
  1. hyperkalaemia
  2. malignant hyperthermia
  3. lack of acetylcholinesterase
117
Q

What is the usual duration of action of atracurium?

A

30-45 minutes

118
Q

What are 3 side effects of atracurium?

A

Generalised histamine release on administration may produce:

  1. facial flushing
  2. tachycardia
  3. hypotension
119
Q

How is atracurium excreted?

A

Not excreted by liver or kidney, broken down in tissues by hydrolysis

120
Q

Which drug can reverse atracurium?

A

Neostigmine

121
Q

What is the usual duration of action of vecuronium?

A

approx. 30-40 minutes

122
Q

How is vecuronium degraded and what effect can organ dysfunction have?

A

Degraded by liver and kidney, effects prolonged in organ dysfunction

123
Q

Which drugs can reverse the effects of vecuronium?

A

neostigmine

124
Q

What is the time of onset of action of pancuronium?

A

2-3 minutes

125
Q

What is the duration of action of pancuronium?

A

up to 2 hours

126
Q

How can the effects of pancuronium be partially reversed?

A

with drugs such as neostigmine

127
Q

What is the mechanism of action of depolarising neuromuscular blocking drugs?

A

binds to nicotinic acetylcholine receptors resulting in persistent depolarisation of the motor end plate

128
Q

What are 2 adverse effects of depolarising neuromuscular blocking drugs?

A
  1. malignant hyperthermia
  2. hyperkalaemia (normally transient)
129
Q

What visible side effect might suxamethonium cause?

A

fasciculations

130
Q

Which is the muscle relaxant of choice for rapid sequence induction for intubation?

A

suxamethonium (depolarising)

131
Q

What are 2 key examples of when suxamethonium (aka succinylcholine) is contraindicated?

A

penetrating eye injuries or acute angle closure glaucoma - increases intra-ocular presure

132
Q

What is the mechanism of action of non-depolarising neuromuscular blocking drugs?

A

competitive antagonist of nicotinic acetylcholine receptors

133
Q

What are 4 examples of non-depolarising neuromuscular blockers?

A

tubcurarine, atracurium, pancuronium, vecuronium

134
Q

What is a key adverse effect of non-depolarising muscle relaxants?

A

hypotension

135
Q

What drug can bring about the reversal of non-depolarising neuromuscular blocking drugs?

A

Acetylcholinesterase inhibitors e.g. neostigmine

Anaesthetics (11 decks)

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