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HNNS > HNS20 General Anaesthetics > Flashcards

HNS20 General Anaesthetics Flashcards

1
Q

Modern general anaesthetics

A

Only IV / Inhalation

—> NO oral preparation

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2
Q

Anaesthesia vs Analgesia

A

Anaesthesia: Absence of ALL sensations
—> general anaesthesia (GA): ALL sensations including consciousness
—> regional anaesthesia (RA) (e.g. nerve block): consciousness preserved

Analgesia: Absence of pain

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3
Q

Multiple ways of stopping pain

A
  1. Local anaesthetic
    - block pain signal transduction (block Na channel)
  2. Opioid
    - modify pain signals
  3. General anaesthetic
    - shut off brain
    - even though pain signals generated, conducted, but NOT interpreted
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4
Q

Modern balanced anaesthesia

A

3 targets:

  1. Unconsciousness (by GA)
  2. Analgesic (by opioid / LA)
  3. Muscle relaxation (by neuromuscular blocker)
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5
Q

Action of inhaled anaesthetics

A

MOA still not fully understood
—> till today NO antidote to GA
—> patient only wake up after body metabolise and excrete GA

Only thing known (part of mechanism):
- bind to GABA receptor (ligand-gated Cl channel) —> Cl channel open —> hyperpolarisation

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6
Q

Pharmacokinetics of GA

A

Narrow therapeutic window

  • ED95 = LD05
  • ED50 close to LD50
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7
Q

Potential danger of unconsciousness

A
  1. Airway obstruction (tongue fall back to touch posterior pharyngeal wall)
  2. Aspiration (due to vomit go into lung + loss of protective airway reflexes) —> aspiration pneumonitis
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8
Q

Intravenous GA

A

Must have following properties:

  • ***Lipid-soluble (diffuse BBB to gain access to brain)
  • ***Less context-sensitive (i.e. not accumulate)
  1. Thiopentone (thiopental)
    - not commonly used now
  2. Propofol
  3. Ketamine
  4. Etomidate
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9
Q

Pharmacokinetics of Thiopentone

A
  • Ampule form (also contain NaHCO3 powder)
    —> reconstitute with water —> alkaline solution —> thiopentone in ionised state
    —> injected into body (pH 7.4) —> becomes unionised —> rapid conversion to highly lipid-soluble form
    —> readily crosses BBB
  • Terminal t1/2: 12 hrs (i.e. takes 36 hours to leave body, does NOT mean patient wakes up after 36 hours, ∵ redistribution of thiopentone)
  • Redistribution of thiopentone in body: from CNS (site of action) to other parts (muscles, fat) —> ∴ patient wake up before terminal t1/2
  • Significance of redistribution: accumulation of drug in body (muscles / fat) —> longer context-sensitive half-time —> ∴ thiopentone not used repeatedly / continuous infusion (only used at initial stage: Anaesthetic induction), use other substance subsequently (如果唔係有排都唔醒)
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10
Q

Pharmacodynamics of Thiopentone

A
  1. ↓ vascular resistance (vasodilatation)
  2. ↓ cardiac contractility
  3. ***↓ arterial pressure
    —> reflex ↑ HR
  4. ***↓↓ respiration
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11
Q

Pharmacokinetics of Propofol

A
  • very lipid soluble
  • cannot be dissolved in water
  • Terminal t1/2: 4.8 hrs
  • accumulate much less extent —> much ***less context-sensitive —> good for IV infusion (no need to replace with something else after induction)
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12
Q

Target Controlled Infusion (TCI)

A

Input target plasma concentration to computer
—> computer calculate dosing rate accounting for accumulation, patient factors, pharmacokinetic variations etc.
—> can achieve precise level of sleep in patient (sedation / drowsiness / sleep / anaesthesia)

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13
Q

Pharmacodynamics of Propofol

A
  1. ***↓↓ vascular resistance (vasodilatation)
  2. ↓ cardiac contractility
  3. ***↓↓ arterial pressure —> Not desirable in patients with active bleeding (low BP)
  4. ***↓↓ respiration
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14
Q

Pharmacokinetics of Ketamine

A

Fairly similar to other IV GA

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15
Q

Pharmacodynamics of Ketamine

A

**No CVS depression, BUT cause **hallucination, nightmares

  1. ***↑ vascular resistance (vasoconstriction)
  2. ↑ cardiac contractility
  3. ***↑ arterial pressure —> good for patients with active bleeding, but undesirable for patients with IHD, hypertension
  4. ↓ respiration
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16
Q

Pharmacokinetics of Etomidate

A

Fairly similar to other IV GA

17
Q

Pharmacodynamics of Etomidate

A

CVS stable, BUT causes **CNS excitation, a lot of **N+V

  1. NO change vascular resistance (vasoconstriction)
  2. NO change HR
  3. NO change cardiac contractility
  4. NO change arterial pressure —> good for ***cardiac anaesthesia patients who cannot tolerate hypertension / hypotension
  5. ↓ respiration
18
Q

Inhaled GA

A 
Volatile liquids (NOT gas)
—> Vaporisers
—> deliver a known concentration of GA vapour through intubation (endotracheal tube)
  • 1st ever inhaled GA: Ether

6 drug:

  1. Isoflurane
  2. Desflurane
  3. Sevoflurane
  4. Enflurane (NOT used anymore)
  5. Halothane (NOT used anymore)
  6. Nitrous oxides (rarely used)
19
Q

Vaporisers

A 
Carrier gas (oxygen-air mixture)
—> vaporising chamber OR bypass channel (controllable by dial)
—> one exit
20
Q

Minimum alveolar concentration (MAC)

A

Alveolar concentration of inhaled agent which prevents movement in response to a standard painful stimulation in 50% of subjects
—> Potency measure
—> NOT a fixed number
—> depends on patients’ age (children have ***higher MAC value —> harder to anaesthetised)

General number:

  1. Isoflurane: 1.15 vol%
  2. Desflurane: 7 vol%
  3. Sevoflurane: 2.05 vol%

How to measure alveolar conc of inhaled GA:
- Use concentration in mouth

21
Q

MAC and Oil:gas partition coefficient

A

Measure of ***lipid solubility

Higher oil:gas partition coefficient —> more lipid soluble —> Lower MAC

Meyer-Overton correlation (log MAC vs log O:G) —> Negative linear relationship

22
Q

Blood:gas partition coefficient

A

Predict ***pharmacokinetic properties of inhaled GA
—> Determine speed of Wash-in effect (how quickly Fa approaches Fi)
—> higher blood:gas partition coefficient —> slower wash-in

Fa: alveolar concentration
Fi: inhaled concentration

23
Q

Wash-in effect: Fa / Fi

A

Fa: alveolar conc
Fi: inhaled conc

Faster to reach 1 —> goes into alveoli more quickly / build up of GA in alveoli —> faster onset

Affected by:

  1. Drug itself (Blood:gas partition coefficient: higher —> slower wash-in) (∵ carried away quickly, take longer time to build up in alveoli —> slower onset)
  2. Ventilation rate (higher rate —> faster wash-in)
  3. Cardiac output (higher CO —> slower wash-in) (∵ carried away quickly, take longer time to build up in alveoli —> slower onset)
24
Q

Metabolism %

A

Inhaled GA metabolised to very little extent (a few %)
—> Not really metabolised
—> patient awake not by breaking down GA
—> excreted through ***elimination
1. Lungs (via concentration gradient with blood: Blood has higher concentration after vaporiser switched off)
2. Kidney unchanged

25
Q

Pharmacodynamics of Inhaled GA

A

Similar to Thiopentone and Propofol

  1. ↓ CO
  2. ↓ Vascular resistance
  3. ↓ Arterial pressure
    —> reflex ↑ HR
26
Q

Factor important when considering GA in clinical perspective

A

Co-morbidities (e.g. heart disease)

27
Q

Summary of choice of IV GA

A
  1. Thiopentone
    - longer context-sensitive half-time
    —> ∴ thiopentone not used repeatedly / continuous infusion (only used at initial stage: Anaesthetic induction), use other substance subsequently
  2. Propofol
    - much ***less context-sensitive —> good for IV infusion
    - ↓↓ arterial pressure —> Not desirable in patients with active bleeding (low BP)
  3. Ketamine
    - No CVS depression, BUT cause ***hallucination, nightmares
    - ↑ arterial pressure —> good for patients with active bleeding, but undesirable for patients with IHD, hypertension
  4. Etomidate
    - CNS excitation, a lot of N+V
    - for cardiac anaesthesia patients who cannot tolerate hypertension / hypotension

HNNS (58 decks)

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