inhaled anaesthetics, IV anaesthetics Flashcards

1
Q

3 components to balanced anaesthetics

A
  1. hypnosis/amnesia = IV or volatile agent
  2. autonomic areflexia = opioids
  3. immobility = muscle relaxant
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2
Q

mechanisms of anaesthetic uptake

A

Pi = PA = Pa = Pbr

beginning gases are breathed in and at the end breathed out

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3
Q

relationship between dosage and solubitilty

A

solubility (=oil:gas partition coefficient)

the more soluble the less dose required in a patient

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4
Q

how do volatile agents work?

A

increasingly likely that it works through GABA modulation in the brain and glycine modulation in the spinal cord

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5
Q

describe MAC

A

minimum alveolar concentration producing immobility on standard surgical stimulus in 50% of patients

  • a means of describing dose and potency referenced to a standard clinical effect
  • NOT a target

(way of describing dose to a standard clinical effect)

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6
Q

what causes the MAC dose-response curve to move

A

the use of other drugs

e.g. fentanyl (opioid) moves the curve to the left

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7
Q

what increases MAC

A
  • young age
  • hyperthermia
  • hyperthyroid
  • drugs
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8
Q

what decreases MAC

A
  • old age
  • hypothermia
  • hypothyroid
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9
Q

how is dosing titrated

A

controlled inhaled fraction of vapour on a vapourizer

measured by level in exhaled gas

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10
Q

does setting 6% on the vapourizer mean the patient has an alveolar concentration of 6%

A

no, because fraction of drug in the alveolar is determined by the fraction of drug you inspire and the minute volume. At the same time, blood is taking it away around the body

  • monitored by ‘end tidal’ agent

(dose titration higher at the beginning)

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11
Q

what do these anaesthetics do to the CNS

A
  • hypnosis, immobility (along with NMBA), amnesia
  • decrease CMRO2 (cerebral metabolic rate of oxygen)
  • dose dependent increase CBF & ICP
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12
Q

what do these anaesthetics do to the CVS

A
  • peripheral vasodilation, lower BP
  • HR unchanged
  • modern agents do not affect SV greatly
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13
Q

what do these anaesthetics do to the respiratory system

A
  • respiratory depressant
    (impair response to hypoxia and CO2)
  • bronchodilation
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14
Q

nitrous oxide

A
  • odourless non-flammable gas
  • low potency
  • rapid onset
  • analgesic

(potential adverse effects e.g. nausea & vomiting)

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15
Q

chemical structure of modern agents

A

methyl ethyl ethers

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16
Q

isoflurane

A
  • relative cardiovascular stability
17
Q

sevoflurance

A
  • good for gas inductions (children)

- reaction with CO absorber-nephrotoxic by-product (kidney patients)

18
Q

desflurane

A
  • rapid onset and offset

- good for long cases

19
Q

types of intravenous agents

A
  • barbiturates (e.g. thiopentone)
  • phenols (e.g. propofol)
  • imidazoles (e.g. etomidate)
  • phencyclidine derivates (e.g. ketamine)
  • benzodiazepine (e.g. midazolam)
20
Q

mechanisms of action for IV agents (include exception)

A

(like inhalation agents)

enhance GABA transmission (prolong Cl- current)
- hyperpolarisation

ketamine = antagonises NMDA receptor

- suppress excitation
- analgesic effect
21
Q

pharmacokinetics of IV agents

A
  • highly lipid soluble & cross BBB
  • offset after a single IV dose is therefore primarily due to redistribution
  • metabolism is much slower for most agents (not ketamine)
22
Q

thipoentone

A
  • very rapid onset (10 seconds)
  • often used in emergency Caesarian
  • rapid offset by redistribution
  • slow clearance
  • metabolized in liver
  • some decrease in PVR & BP (careful in shocked patients)
  • repsiratory depression & loss of airway reflexes
23
Q

propofol

A
  • moderately rapid onset
  • rapid offset by redistribution
  • fast clearance (can be used for maintenance)
  • metabolised in liver
  • significant decrease in PVR & BP
  • respiratory depression & loss of airway reflexes
24
Q

propofol vs thiopentone

A
  • propofol is now the preferred ‘standard’ IV anaesthetic
  • wears off quicker
  • metabolised faster
  • good for day surgery

however both cause CVS instability

25
Q

Etomidate

A
  • remarkable CV stability
  • less respiratory depression
  • rapid clearance & good recovery profile

but:
-adrenocortical inhibition (loss of stress hormone production for healing/recovery)

26
Q

ketamine

A
  • analgesic
  • CVS stimulant (good in shocked patient)
  • preserves airway reflexes and respiratory drive (e.g. will still cough)
  • increases CMRO2, CBF & ICP (not good for neurosurgey)
  • dissociative state, emergence slower and complicated by dysphoria
27
Q

total intravenous anaesthesia and when its used

A
  • when we dont want to give a volatile agent
  • avoids inhalation route/complications of vapours
  • but expensive and no monitoring agent
  • e.g. a pateint who sufferes from post-operative nausea and vomiting (as all volatile agents produce this) TIVA can be given
28
Q

inhaled anaesthetics work by:

A

modulating the action of GABA in the brain and glycine in the spinal cord