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PPT Phase II > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What are the 6 stages of typical general anaesthetic?

A
  1. premedication
  2. induction
  3. muscle relaxation and intubation
  4. maintenance of anaesthesia
  5. analgesia
  6. reversal
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2
Q

what are the 4 clinical stages of anaesthesia using inhalational anaesthetics?

A

stage I - analgesia
stage II - excitation
stage III - surgical anaesthesia
stage IV - medullary depression

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3
Q

name 3 drugs that enhance activity at GABAa receptors

A

etodimate, propofol, thiopental

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4
Q

name 3 effects of etodimate, propofol, thiopental

A

potent amnesics
potent sedatives
weak muscle relaxants

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5
Q

what receptors do nitrous oxide and ketamine work on

A

inhibit glutamate NMDA receptors. inhibit ACh nicotinic receptors, open two-pore K+ channels

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6
Q

what are the actions of nitrous oxide and ketamine?

A

potent analgesics,
weak sedatives,
weak muscle relaxants

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7
Q

what receptors do sevoflurane, isoflurane and desflurane work on?

A 
enhance activity at GABAa,
enhance activity at glycine receptors,
inhibit glutamate NMDA receptors
inhibit ACh nicotinic receptors,
open two-pore K+ channels
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8
Q

what are the actions of sevoflurane, isoflurane, desflurane

A

potent amnesics,
potent sedatives,
potent muscle relaxants

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9
Q

name 4 factors that affect inhalation anaesthetics

A
  1. absorption across alveolar membranes
  2. solubility of the anaesthetic in the blood
  3. cardiac output - circulation time
  4. relative concentration of the anaesthetic in the brain and blood at equilibrium
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10
Q

what is minimum alveolar concentration a measure of?

A

potency

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11
Q

what is blood:gas partition coefficient a measure of?

A

the solubility in the blood.

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12
Q

what is the blood:gas partition coefficient used for?

A

determines the rate of induction and revocery of inhalational anaesthesia

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13
Q

what does a low blood:gas partition coefficient mean in terms of induction and recovery

A

faster induction and recovery

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14
Q

what does the Meyer-Overton correlation show in terms of the oil:gas partition coefficient?

A

it shows that the potency of an anaesthetic can be predicted from its lipid solubility

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15
Q

nitrous oxide is not sufficiently potent to be used alone so why is it used?

A

in a combination of drugs to allow a reduction in dosage.
used for maintenance aneasthesia.
used in sub-anaesthetic concentrations for analgesia - eg. entonox (50:50 mixture wth O2)

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16
Q

what makes up entonox?

A

50:50 mixture of nitrous oxide and oxygen

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17
Q

what is the major route of elimination of inhalational anaesthetics?

A

via the airways in expired air

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18
Q

name 4 factors that influence elimination rate of inhalation anaesthetics

A
  1. ventilation rate
  2. blood:gas partition coefficient
  3. duration of inhalation
  4. extent of tissue equilibration
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19
Q

name 4 unwanted cardiovascular effects of inhalational anaesthetics

A

myocardial depression,
vasodilatation,
hypotension,
bradycardia/reflex tachycardia

20
Q

name 2 unwanted CNS effects of inhalational anaesthetics

A

increase cerebral blood flow and ICP,

decreased cerebral vascular resistance

21
Q

name 2 general unwanted effects of inhalational anaesthetics

A 
postoperative nausea and vomiting (PONV),
malignant hyperthermia (rare)
22
Q

what stage of anaesthesia are IV anaesthetics used for?

A

rapid induction

23
Q

name 4 examples of IV anaesthetics

A
  1. etomidate
  2. ketamine
  3. propofol
  4. thiopental
24
Q

where does metabolism of thiopental occur?

A

liver

25
Q

why can propofol be used as a continuous infusion for total IV anaesthesia or for sedation of adults in ICU/

A

because it does not accumulate

26
Q

what order kinetics is propofol metabolised by?

A

first order kinetics

27
Q

what order kinetics is thiopental metabolised by?

A

zero-order kinetics

28
Q

what is the benefit of using propofol over thiopental as an induction agent?

A

more rapid recovery and less hangover effect.

29
Q

what patients might etomidate be preferred to be used for rapid induction?

A

pts who are in shock as it is believed to have less effects on the CVS

30
Q

why can etomidate not be used as a continuous infusion?

A

toxicity on adrenals and adrenocortical suppression

31
Q

what is the MOA of ketamine?

A

blocks activation of NMDA receptor

32
Q

what is meant by the ‘dissociative anaesthesia’ produced by ketamine?

A

where there is marked sensory loss and analgesia, as well as amnesia, without complete loss of consciousness.

33
Q

why is ketamine useful for accident and emergency situations or low-technology healthcare situations?

A

IM administration is possible and it does not reduce BP or HR.

34
Q

neuromuscular blocking drugs block transmission through the neuromuscular junction at what receptors?

A

nicotinic receptors

35
Q

what is the role of neuromuscular blockadge?

A

decreases skeletal muscle tone

36
Q

name a non-depolarising neuromuscular blockade agent (6)

A 
prototype = curare,
atracurium,
cisatracurium,
mivacurium,
pancuronium,
rocuronium,
vercuronium
37
Q

name a depolarising neuromuscular blockade drug

A

prototype = succinylcholine,

suxamethonium

38
Q

name 3 uses of neuromuscular blockers

A

endotracheal intubation,
surgical procedures,
Intensive care

39
Q

how does suxamethonium need to be given?

A

IV - as it does not cross blood brain barrier

40
Q

what is the onset and duration of action of suxamethonium

A

onset of aciton within 1min.

duration of action 3-12mins

41
Q

why do you get muscle fasciculation with suxamethonium?

A

because you initially get depolarisation of motor endplates prior to blockade

42
Q

you need to be aware of a genetic deficiency of what that occurs in about 1 in 2000-3000 individuals that results in a very prolonged paralysis in pts given suxamethonium

A

pseudocholinesterase deficiency

43
Q

what can reverse non-depolarising agent neuromusclar block?

A

anticholinesterases e.g. neostigmine

44
Q

when reversing non-depolarising blockers with an anticholinesterase (e.g. neostigmine), what is given immediately before and why?

A

anti-muscarinic (e.g. atropine or glycopyrrolate) to prevent bradycardia or excessive salivation

45
Q

what opiates can be used as analgesia adjuncts

A

fentanyl, alfentanyl

PPT Phase II (37 decks)

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