General Anaesthetics Flashcards

1
Q

What are the two broad types of anaesthesia

A
  1. General anaesthesia - makes patient unconscious
  2. Local/regional - blocks feeling to localised region e.g. limb
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2
Q

Fasting before GA
1. Purpose
2. When is the patient at highest risk of aspiration
3. Major causes of morbidity/mortality in anaesthetics
4. Fasting time-frames

A
  1. empty stomach = reduced risk of reflux = reduced risk of aspiration pneumonitis
  2. Before and during intubation, and when they are extubated (once the endotracheal tube is correctly fitted, the airway is blocked and protected from aspiration)
  3. Aspiration pneumonitis and pneumonia
  4. 6 hours of no food or feeds before the operation
    2 hours of no clear fluids (fully “nil by mouth”)

Emergency –> RSI (rapid-sequence induction)

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3
Q

Preoxygenation
1. What is it
2. What physiological measure of spirometry is it relevant to

A
  1. Before GA, patient on 100% O2 –> O2 reserve for period between loss of consciousness and intubation + ventilation.

Emergency –> may be skipped

  1. Functional reserve capacity - the volume remaining in the lungs after a normal, passive exhalation
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4
Q

Premedication
1. Purpose
2. Examples (BOA)

A
  1. relaxation, reduce anxiety, reduce pain and make intubation easier

Benzodiazepines (e.g., midazolam) –> muscle relaxation + reduce anxiety (also causes amnesia)

Opiates (e.g., fentanyl or alfentanyl) –> reduce pain and reduce the hypertensive response to the laryngoscope

Alpha-2-adrenergic agonists (e.g., clonidine), which can help with sedation and pain

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5
Q

Rapid Sequence Induction/Intubation (RSI)
1. What is it
2. Why is it higher risk than normal intubation
3. What are its uses non-emergency
4. What is the single highest risk of RSI
5. How can you reduce the risk of 4.

A
  1. Gain airway control quickly and safely in emergency scenario using an ET tube as soon as possible after induction (patient unconscious)
    • No fasting
    • No pre-planning e.g. difficult airway

3.GORD or pregnancy

  1. Aspiration

5.
1. more upright bed
2. Cricoid pressure?

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6
Q

Hypnotic agents
1. What is their use
2. How can they be delivered to the patient

A
  1. Make patient unconscious
  2. IV or inhaled
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7
Q

What is the triad of general anaesthesia (HMA)

A

Hypnosis
Muscle relaxation
Analgesia

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8
Q

Examples of IV hypnotic agents (PKTE)

A

Propofol (the most commonly used)
Ketamine
Thiopental sodium (less common)
Etomidate (rarely used)

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9
Q

Examples of inhaled hypnotic agents (SDI fluranes + NO)

A

Sevoflurane (the most commonly used)
Desflurane (less favourable as bad for the environment)
Isoflurane (very rarely used)
Nitrous oxide (combined with other anaesthetic medications – may be used for gas induction in children)

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10
Q
  1. What characteristic do sevoflurane, desflurane and isoflurane share in common?
  2. What device is used to deliver these agents?
A
  1. All are volatile anaesthetic agents i.e. liquid at room temperature and need to be vaporised into a gas to be inhaled.
  2. Vaporiser (liquid poured into and turned to vapour mixed with air –> conc can be altered to control depth of anaesthesia)
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11
Q

Which agent is usually given first (IV or inhaled)?
1. Why
2. What is TIVA?

A

IV to induce, inhaled to maintain
1. IV acts quicker, while inhaled must diffuse across lung tissue until ideal concentration is reached
2. TIVA = Total intravenous anaesthesia i.e. IV used throughout (easier wake up)

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12
Q

Muscle relaxants (Neuromuscular blockers)
1. MoA
2. Types
3. How to reverse

A
  1. Block nicotinic N1 receptors in neuromuscular junctions, preventing skeletal muscle stimulation –> relax and paralyse muscle –> intubation is easier
  2. Depolarising - suxamethonium
    Non-depolarising - Rocuronium, atracurium
  3. Cholinesterase inhibitors e.g. neostigmine
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13
Q

What is Sugammadex

A

Used specifically to reverse the effects of certain non-depolarising muscle relaxants (rocuronium and vecuronium)

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14
Q

Adverse effects of volatile anaesthetic agents

A
  • Myocardial depression
  • Malignant hyperthermia
  • Halothane (not commonly used now) is hepatotoxic
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15
Q

Adverse effects of nitrous oxide

A

May diffuse into gas-filled body compartments → increase in pressure → avoid in pneumothorax

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16
Q

Mechanism of action of propofol, thiopental sodium and etomidate

A

Potentiate GABAa

17
Q

MoA of ketamine

A

NMDA antagonist

18
Q

Adverse effects of propofol

A
  • Pain on injection (TRPA1 activation)
  • Hypotension
19
Q

Adverse effects of thiopental sodium

A
  • Laryngospasm
  • Unsuitable for maintenance –> metabolites build up quickly
20
Q

Adverse effects of etomidate

A
  • Unsuitable fo rmaintenance –> primary adrenal suppression (reversible binding to 11 β-hydroxylase)
  • Myoclonus
  • Common post-op N&V
21
Q

Adverse effects of ketamine

A
  • Disorientation
  • Hallucinations
22
Q

Advantages of propofol

A
  • Rapid onset of anaesthesia
  • Suitable for maintenance –> rapidly metabolised with no build-up
  • Anti-emetic
23
Q

Advantages of thiopental sodium

A

Extremely rapid onset of action making it the agent of choice for rapid sequence of induction

24
Q

Analgesia: most commonly used in anaesthetics

A

Fentanyl
Alfentanil
Remifentanil
Morphine

25
Q

Key considerations for emergence
1. TOF
2. Sites of stimulation
3. What happens when relaxant has worn off

A
  1. Train-of-four (TOF) stimulation, nerve stimulation four consecutive times
    - muscle contraction strong –> worn off
    - gets weaker with additional stimulation –> not fully worn off –> “awareness under anaesthesia” if woken early
  2. A. ulnar nerve at the wrist, watching for thumb movement (twitches)
    B. facial nerve (movement in the orbiculares oculi muscle at the eye)
  3. Stop inhaled anaesthetic, patient will regain consciousness, extubated at the point where they are breathing for themselves.
26
Q

Risks of GA

A

Common: sore throat and PONV
Significant:
- Accidental awareness (waking during the anaesthetic)
- Aspiration
- Dental injury, mainly when the laryngoscope is used for intubation
- Anaphylaxis
- Cardiovascular events (e.g., myocardial infarction, stroke and arrhythmias)
- Malignant hyperthermia (rare)
- Death

27
Q

Malignant Hyperthermia: what is it

A
  1. rare but potentially fatal hypermetabolic response to anaesthesia
28
Q

Malignant hyperthermia: anaesthetic agents that are at higher risk of causing it

A
  1. Volatile + suxamethonium
29
Q

Malignant hyperthermia: genetic mutations + pattern of inheritance

A
  1. RYR1 (mostly) and CACNA1S mutations increase risk of MH –> autosomal dominat
30
Q

Malignant hyperthermia: presentation

A
  • Increased body temperature (hyperthermia)
  • Increased carbon dioxide production
  • Tachycardia
  • Muscle rigidity
  • Acidosis
  • Hyperkalaemia
31
Q

Malignant hyperthermia: treatment

A

Dantrolene - interrupts the muscle rigidity and hypermetabolism by interfering with the movement of calcium ions in skeletal muscle.