Anaesthetics Flashcards

1
Q

How can the different types of anaesthetics be split?

A
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2
Q

What is concious sedation?

A

Use of small amounts of anaesthetic/ benzodiazepines to produce a ‘sleep like’ state

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3
Q

What are the 4 stages of Guedel’s signs?

A

Typical course of conciousness:

Stage 1: analgesia and conciousness

Stage 2: unconcious, breathing erratic, delirium could occur leading to excitment phase (paradoxical excitment)

Stage 3: Surgical anaestheisa, with 4 levels describing increasing depth until breathing is weak

Stage 4: Respiratory paralysis and death

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4
Q

How is potency measured in aneasthesia?

A

MAC - Minimum Alevolar Concentration

[alveolar] at 1 atm at which 50% of subjects fail to move to a surgical stimulus

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5
Q

What happens when MAC is at eqilibrium?

A

At equilibrium [alveolar] = [spinal cord]

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6
Q

What factors affect solubility (partition co-efficients) of anaesthesia?

A

Blood: Gas partition (in the blood)

  • low value fast induction and fast recovery

Oil:Gast partition (fat)

  • determines potency and slow accumulation due to partition in fat
  • high potencu= high fat solubility
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7
Q

What factors will affect MAC?

A
  • Age (High in infancts, low in elderly)
  • Hyperthermia (increased), hypothermia (decreased)
  • Pregnancy (increased)
  • Alcholism (increased)
  • Central stimulants (increased)
  • Other anaesthetics and sedatives (decreased)
  • Opiods (decreased)
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8
Q

Why are volatile anaesthetics typically mixed with nitrous oxide

A
  • NO reduces the amount of anaesthesia needed
  • Therefore, decreases side effects
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9
Q

How do most anaesthetics interact with the GABAA receptor?

A
  • GABAA is a major inhibitory transmitter
  • Ligand gated Cl- channel
  • Most anaesthetics potentiate GABA mediated Cl- conductance
  • Cause neuronal hyperpolarisation to depress CNS activity
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10
Q

Which anaesthetics do not target the GABAA receptor?

Which receptor do they target instead?

A
  • Xe
  • N2O
  • Ketamine

Target the NMDA receptor blockin excitation

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11
Q

Explain what happens to the brain circuitry when targetted with anaesthetics?

A
  • Reticular formation depressed. Connectivity lost
    • usually causes increased arousal
  • Thalamus transmits and modifies sensory information
  • Hippocampus depressed (memory)
  • Brainstem depressed (repiratory and CVS)
  • Spincal cord depressed (dorsal horn) and motor neuronal activity
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12
Q

Name some of the main intravenous anaesthetics and their speed of onset?

A
  • Propofol (rapid)
  • Barbituates (rapid)
  • Ketamine (slower)
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13
Q

What is TIVA?

A

Total IntraVenous Anaesthesia

Anaesthesia given by an infusion pump, no volatile gas required → benefical if doing surgery on airways/face

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14
Q

How are IV anaesthetics Rx’d?

A

Usually given as a bolus then infused at a set rate calculated by PK

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15
Q

When would you use local and regional anaesthesia?

A
  • Dentistry
  • Obstetrics
  • Regional surgery
  • Post op- (wound pain)
  • Chronic pain management
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16
Q

Name some local anaesthetics

A
  • Lidocaine
  • Bupivacaine
  • Ropivacaine
  • Procaine
17
Q

How to local anaesthetics work?

A
  • Bind to the inside of voltage gated Na+ channel
  • Need to become charged to pass through
  • Block is use dependant → higher firing = more effective block
  • Blocks small myelinated afferent nerves preferentially
18
Q

What are some of the main side effects of general anaesthesia?

A
  • PONV - post operative nausea and vomiting
  • CVS- hypotension
  • POCD- post operative cognitive dysfunction
  • Chest infection