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Block 3 > Anaesthesia > Flashcards

Anaesthesia Flashcards

1
Q

What are the 3A’s that make up a normal state of consciousness?

A

Alertness
Attention
Awareness

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2
Q

What is the most commonly used scale for measuring consciousness in the clinic?

A

Glasgow Coma Scale (GCS)

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3
Q

What are the main effects of anaesthetics?

A
  1. Unconsciousness via action on reticular formation + ARAS
  2. Loss of reflexes via affecting sensory input to reflex arc
  3. Analgesia via reduced transmission of conscious sensation
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4
Q

What are the 2 main groups of anaesthetic agents?

A
  1. General (IV e.g. Propofol OR inhalation e.g. isofluorane)

2. Local (same as general but administered in lower doses to affect small localised areas)

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5
Q

What do local anaesthetics drugs names often end in?

A

‘…caine’

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6
Q

What are the 2 groups of local anaesthetics?

A
  1. Amino esters: mainly metabolised in plasma - T1/2 ~ 3mins (rapid hydrolysis by plasma esterases)
  2. Amino amides: mainly metabolised in liver - T1/2 ~ 3hrs
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7
Q

How do local anaesthetics work?

A

Na channel block which dampens down neuronal activity reducing sensory transmission to cortex by:

  • Directly entering channel when open (use-dependence)
  • Accessing channel by crossing axonal membrane + binding from inside
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8
Q

Why do local anaesthetics tend not to work when tissues are inflamed?

A

Their ability to work is pH-dependent and inflammatory soup in damaged tissue is generally acidic which makes them ionise and reduces their ability to cross neuronal membrane to attach to Na channels

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9
Q

What types of fibres do local anaesthetics work best on?

A

Smaller un-, lightly OR unmyelinated autonomic nociceptive sensory fibres (Aδ + C) as access to Na channels via membrane is easier and there is a larger surface/volume ratio to act on

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10
Q

When selecting a local anaesthetic what 3 factors should you take into account?

A
  1. Agent with low irritant effect + toxicity
  2. Rapid onset of action
  3. Half-life to allow adequate time to do procedure
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11
Q

What are the 3 most commonly used agents?

A
  1. Lidocaine (amide) e.g. local infiltration, regional IV anaesthesia, nerve block, dental + topical
  2. Bupivacaine (amide) e.g. local infiltration, regional IV anaesthesia, peripheral nerve block, epidural or sympathetic block
  3. Benzocaine (ester) e.g. throat lozenges
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12
Q

What is the benefit of using levobupivacaine than bupivacaine?

A

Less cardiotoxic as it is the L-isomer version of it

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13
Q

What is the benefit of using tetracaine?

A

Topical application

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14
Q

What are the main side effects of local anaesthetics?

A

Local irritation/inflammation (exacerbated by local vasoconstrictors which can lead to local ischaemia e.g. in fingers)

Tissue damage in traumatic administration

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15
Q

What are the rare systemic side effects of local anaesthesia generally caused by over-administration?

A
  • CVD changes due to local vasodilation or cardiotoxicity through binding in heart
  • CNS changes e.g. light-headedness, sedation or loss of consciousness
  • Anaphylaxis (only with ester drugs)
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16
Q

What do general anaesthetics do than local anaesthetics dont?

A

Induce an altered state of consciousness and loss of memory for what happens under its influence

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17
Q

What is the process of general anaesthesia?

A
  1. Premedication (BZD)
  2. Induction
  3. Muscle relaxation (NMB) + intubation
  4. Maintenance
  5. Analgesia
  6. Reversal of NMB (chemically) + anaesthesia(redistribution, metabolic breakdown or exhalation) to return conciousness
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18
Q

Why do you give premedication before general anaesthesia?

A

To reduce anxiety and to help with memory loss

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19
Q

When would you want to relax muscles in general anaesthesia?

A

Long surgical procedures
Abdominal surgery
Thoracic surgery
Mechanical ventilation during NMB block

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20
Q

What are inhalational anaesthetics?

A

Potent agents that are simple gases (nitrous oxide) or volatile liquids readily mixed with O2 for administration having low blood solubility enabling rapid induction + recovery with fewer lingering effects (blood levels can be quickly adjusted)

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21
Q

How much oxygen does inhalational anaesthetics contain?

A

Min 25% O2 to prevent hypoxia

Increased to over 30% with nitrous oxide

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22
Q

What volatile liquids are used as inhalational anaesthetics?

A

Sevoflurane
Isoflurane
Desflurance

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23
Q

What is the advantage of using nitrous oxide as an inhalational anaesthetic?

A

Provides some analgesia so use in combination can mean reduction in required doses of other drugs

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24
Q

What are the 4 factors that determine depth and speed of recovery from inhalational agents?

A
  1. Rate of alveolar absorption
  2. Speed of equilibration
  3. Relative concentrations at equilibrium
  4. CO
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25
Q

What is the activity of an inhalational agent linked to?

A

Blood:gas partition coefficient and oil:gas partition coefficient indicating solubility (blood gas) and relationship between [inhaled agent] and that in fat (brain/lipid membranes) respectively

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26
Q

How do you calculate the potency of an inhalational anaesthetic?

A

Minimum alveolar concentration (MAC) = EC50 = required to immobilise 50% of patients during noxious stimulation (skin incision)

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27
Q

What is the most famous theory explaining mechanism of action of inhalational anaesthetics?

A

Meyer-Overton theory: correlation between lipid solubility of agents and MAC stating that anaesthesia occurred when a sufficient no. of molecules had accumulated in lipid cell membrane irrespective of drug type but does not take into account protein/receptor interactions, 2nd messenger pathways interaction + hydrophilic effect

28
Q

What are the side effects of inhalational anaesthetics?

A

Reduce activity throughout body via depression of CO + BP

Respiratory depression via brainstem centre

Irritation of resp. tract can cause bronchospasm + laryngospasm

29
Q

When should you not use sevoflurance or desflurane?

A

In children due to resp. tract irritation + increased secretions

30
Q

What is the mechanism of action of IV anaesthetics?

A

Supress consciousness through reduction of CNS activity e.g. Thiopental/Midazolam increase GABA receptor activity + Ketamine blocks NMDA receptors

31
Q

What are the side effects of IV anaesthetics?

A

Decreased cardiac contractility
Respiratory depression in OD
Decreased CNS function
Reduced sympathetic activity

32
Q

Why are Ketamine and Midazolam the best IV anaesthetics?

A

Do not have respiratory or CVD effects like others (although slower acting)

33
Q

Why are IV opioids used?

A

Provide analgesia helping to reduce dose of anaesthetic required through sedative effect and their effects on CV and respiratory system can counter effects of invasive treatments reducing HR, BP + resp. rate increases caused by stress

34
Q

What types of IV opioids are often used?

A

Fast-acting that are effective with 1-2 minutes of administration e.g. Fentanyl

35
Q

Why should care be taken when administering IV opioids?

A

Marked respiratory depression can occur

36
Q

When are epidural anaesthetics used?

A

Lower GU, Obs & Gyn and lower limb orthopaedic work

also pain control

37
Q

What do epidural injections use?

A

Local or general anaesthetics with sedatives to remove sensation and analgesics to block pain sensation specifically

38
Q

Why do epidurals have more effect on sensory rather than motor function?

A

Sensory neurons more sensitive to local anaesthetics than motor neurons - linked to myelination and ease of entry of anaesthetic

39
Q

__ sensation generally not as affected by epidural as other sensations.

A

Cold

40
Q

What effect do epidurals have on labour?

A

Changes duration of stages increasing stage 2 significantly

41
Q

Why might adrenaline be given with epidural anaesthetics?

A

Prolong duration of block, decrease bleeding and toxicity

42
Q

Describe the levels of the Bromage scale used for epidural blocks.

A
  1. Complete block = patient unable to moves knees or feet
  2. Almost complete block = patient demonstrates ability to flex knees but ability to flex feet
  3. Partial block = patient can partially flex knees + resist gravity + has feet movements
  4. No block = patient can flex knees + feet fully
43
Q

What are neuromuscular blockers (NMB)?

A

Block activity at NMJ

44
Q

What are the 2 groups of neuromuscular blockers (NMBs)?

A
  1. Depolarising/agonist/non-competitive e.g. Suxamethonium (IV ester) + anticholinesterases (e.g. Neostigmine)
  2. Non-depolarising/competitive/antagonist NMB
45
Q

What do depolarising neuromuscular blockers (NMBs) do?

A

Bind ACh receptor causing prolonged depolarisation (fasciculations = post-operative muscle pain) + then block site desensitizing receptor and preventing further depolarisation and muscle contraction

46
Q

How do anticholinesterases work?

A

Increase levels of ACh in junctional cleft by blocking acetylcholinesterace (AchE) breakdown of ACh causing muscle paralysis by overloading system activating all ACh receptors at max leaving no room for additional movement like depolarizing NMBs

47
Q

What else are anticholinesterases used for?

A

To counteract ACh depletion in Mysathenia Gravis counteracting muscle fatigue associated with disorder

48
Q

What are the problems wit acetylcholinesterases?

A

Effect on ANS increasing PNS muscarinic activity causing bradycardia, increased secretion and increased peristalsis(give with atropine prior to/with reversing agent to counteract these effects)

49
Q

How do non-depolarising neuromuscular blockers (NMBs) work?

A

Compete with ACh to bind ACh receptor preventing depolarising blocking ACh effects

Also act presynaptically to reduce Ca entry reducing release of transmitter from presynaptic vesicles

50
Q

What is the pros and cons of non-depolarising neuromuscular blockers (NMBs)?

A

Pros:

  • None cross BBB so no effect on CNS,
  • Water-soluble with no accumulation so more suitable for long-term use than depolarizing NMBs

Cons:

  • Slower onset time than depolarising NMBs
  • Inhalational anaesthetics increase effects
51
Q

Gives examples of non-depolarising neuromuscular blockers (NMBs).

A

Atracurium

Vecuronium (active metabolite may cause residual paralysis)

52
Q

How do you reverse neuromuscular blockers (NMBs)?

A
  1. Anticholinesterase e.g. Neostigmine (in non-depolarizing NMBs but prolong effects in depolarizing NMBs)
  2. Selective relaxant binding agent Sugammadex (in depolarizing NMBs, not non-depolarizing)
53
Q

How does Sugammadex work?

A

Forms complex with NMB drug encapsulating it to inactivate it preventing it from working at NMJ

54
Q

What are the 3 main scales to determine and maintain correct levels of sedation?

A
  1. The Ramsay Scale
  2. The Richmond Agitation Sedation Scale (RASS)
  3. The Riker Sedation Agitation Scale (ASAS)
55
Q

What is the Ramsay scale?

A

6-point scale covering a range of arousal levels: want level 2 (calm, orientated and co-operative) for minor surgical procedures e.g. shoulder/joint reduction

56
Q

Where is the glabellar tap performed?

A

Between eyebrows and above nose eliciting a blink reflex or rapid eye opening in sedated patients

57
Q

What is the Richmond Agitation Sedation Scale (RASS)?

A

Validated, reliable 10 point scale used to assess levels of sedation most commonly in ICU for patients with mechanical ventilation, to ensure appropriate levels of sedation are being maintained -broader scale than the Ramsay ranging from combative to coma - want level 0 (alert + calm) for minor surgical procedures

58
Q

What is the Riker Sedation Agitation Scale (ASAS)?

A

Validated, reliable scale that uses 7 points to assess levels of sedation comparable to the Richmond scale and can be used as an alternative that avoids the terminology used by the ASA to describe sedation, making it clearer to use - want a score of 4 (calm, easily arousable + co-operative) for minor surgical procedures

59
Q

In order of increasing pupil size, what different levels of anaesthesia will each show?

A
  1. Surgical anaesthesia (light)
  2. Analgesia
  3. Surgical anaesthesia (deep)
  4. OD
60
Q

How can you tell during a surgical procedure that a patient is anaesthetized if there pupils are of a normal size?

A

Reduced corneal and pupil reflexes

61
Q

Why are IV anaesthetics generally not used alone for long-term anaesthesia?

A

Accumulation effects and slow redistribution (Propofol is the exception)

62
Q

What painkiller should you avoid pre and post surgery?

A

NSAIDs as they may increase bleeding

63
Q

What other adjuncts can be given with anaesthesia?

A

Antimuscarinics to reduce secretions and with NMB + Propofol to reduce bradycardia

Adrenergics to improve anaesthetic performance reducing bradycardia and increasing resp. rate

Antihistamines to reduce gastric secretions/increase pH

64
Q

What is dexmedetomidine?

A

Selective alpha2-adrenoceptor agonist licensed for intensive care use when patients need to maintain verbal response

Presynaptic: inhibits NA release terminating propagation of pain signals
Postsynaptic: inhibits sympathetic activity, decreasing BP + HR

65
Q

What is Entonox?

A

Gas used for light sedation that is a 50:50 mix of N2O and O2

Block 3 (40 decks)

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