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ANAESTHETICS & PERI-OPERATIVE MEDICINE > 2: Anaesthetic Drugs > Flashcards

2: Anaesthetic Drugs Flashcards

1
Q

what are the different types of anaesthetic techniques

A

general - inhalation and intravenous
local - regional

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2
Q

give some practical uses of anaesthesia

A

premedication
induction
- IV maintenance
- IV and/or inhalation

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3
Q

give 4 examples of intravenous anesthetics

A

propofol (rapid)
barbituates (rapid)
etomidate
ketamine (slower)

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4
Q

what is conscious sedation

A

is the use of small amounts of anaesthetic or benzodiazepines to produce a sleep like state

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5
Q

describe the process of administering anaesthesia in 7 steps

A
  1. premedication
  2. induction - Iv/inhalation
  3. intraoperative analgesia
  4. muscle paralysis
  5. maintenance
  6. reversal of muscle paralysis
  7. provision for PONV
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6
Q

what are the stages of Guedel’s signs for anaesthesia

A

stage 1 : analgesia and consciousness
stage 2 : unconscious, breathing erratic, excitement phase
stage 3 : surgical anaesthesia, increasing depth until breathing weak
stage 4 : respiratory paralysis and death

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7
Q

what is anaesthesia a combination of (4 - DAHM!)

A
  • Depression of spinal reflexes
  • Analgesia
  • Hypnosis
  • Muscle paralysis
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8
Q

how do you determine the volatile anaesthetic potency

A

minimum alveolar concentration

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9
Q

what is the anatomical substrate for MAC

A

spinal cord

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10
Q

What is MAC (minimum alveolar concentration)

A

[alveolar] at 1 atm at which 50% of subjects fail to move to surgical stimulus (unpremediated breathing air)
at equilibrium [alveolar] = [spinal cord]

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11
Q

explain how partition coefficients (solubility) affect the induction and recovery of general anaesthesia

A
  • blood : gas partition (in the blood) - low value fast induction and recovery e.g. desflurane
  • oil : gas partition (in fat) - determines potency and slow accumulation due to partition into fat e.g. halothane
  • greater ability to travel in fat, the higher the potency but the anaesthetic can accumulate in fat so can take patient a long time to wake up
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12
Q

give 5 factors that would increase MAC

A

age (high in infants low in elderly)
hyperthermia
pregnancy
alcoholism
central stimulants

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13
Q

give 3 factors that would decrease MAC

A

age
other anaesthetics and sedatives
opioids

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14
Q

give 4 examples of inhalational anaesthetics

A

nitrous oxide
xenon
chloroform
cyclopropane

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15
Q

what is the role of GABA receptors in general anaesthesia

A

GABAa receptors are a critical target and act as a major inhibitory transmitter for CL- conductance via LGIC
- all anaesthetics (except for Xe, N20 and ketamine) potentiate GABAa mediated Cl- conductance to depress CNS activity

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16
Q

what is the relationship between anaesthetic potency, lipid solubility and GABAa activity

A

potency correlates with lipid solubility and GABAa activity

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17
Q

which 3 anaesthetics do not potentiate GABAa as their mode of action

A

Xe
N2O
ketamine

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18
Q

what are the 3 main effects from anaesthetics potentiating GABA

A

anxiolysis
sedation
anaesthesia

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19
Q

how do anaesthetics modulate the consciousness of the brain

A

modulate the balance between excitation (glutamate) and inhibition (GABA)

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20
Q

what are the effects of general anaesthesia on the brain circuity

A
  • reticular formation (hindbrain, midbrain and thalamus) depressed and connectivity lost
  • hippocampus depressed (memory)
  • brainstem depressed (resp and CVS)
  • spinal cord - depress dorsal horn (analgesia) and motor neuronal activity (MAC)
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21
Q

what can be used as a sole anaesthetic in TIVA (total intravenous anaesthesia)

A

propofol (rapid)
barbituates (rapid)
ketamine (slower)

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22
Q

what is involved in regional anaesthesia

A

involves selectively anaesthetising a part of the body
- blocks a nerve and hence the patient remains awake
- uses local anaesthetic or an opioid
- extradural/intrathecal/combined (labour)

23
Q

give 4 examples of local anesthetics

A
  • lidocaine
  • bupivacaine
  • ropivacaine
  • procaine
24
Q

what is the lipid solubility of local anasthetics

A

higher
- greater potency

25
Q

what is the dissociation constant characteristic of local anaesthetics

A

lower pKa (more unionised) = faster onset

26
Q

what is the chemical link and protein binding duration for local anaesthetics

A
  • metabolism higher
  • protein binding - higher for longer duration
27
Q

give 4 examples of nerves blocked in regional anaesthesia in the upper extemitiy

A
  • interscalene nerve
  • supraclavicular nerve
  • infraclavicular nerve
  • axillary nerve
28
Q

give 4 examples of nerves blocked in the regional anaesthesia in the lower extremity

A

femoral nerve
sciatic nerve
popliteal
saphenous

29
Q

which local anaesthetic is used for wound analgesia

A

bupivacaine

30
Q

what is the mechanism of action of wound analgesia

A

block small myelinated (afferent) nerves in preference hence nociceptive and symp block
- cocaine archetypal
- esters - short acting
- amides - longer acting
- adrenaline inc duration

31
Q

what are the side effects of general anaesthesia (4)

A

PONV - post operative nausea + vomiting (opioids)
CVS - hypotension
POCD (post operative cognitive dysfunction )
chest infection

32
Q

identify 5 examples of where local and regional anaesthesia are used

A

dentistry
obstetrics
regional surgery (patient awake)
post-op (wound pain)
chronic pain management

33
Q

what are the side effects of local and regional anaesthesia

A

depends on the agent used and usually result from systemic spread
- locals are Na+ channel blockers so cardiovascular toxicity

34
Q

what is intravenous anaesthetic potency

A

plasma concentration to achieve a specific end point (e.g. loss of eyelash reflex)
- for induction in mixed anaesthesia - bolus til end point then swtich to volatile
- TIVA uses a defined PK based algorithm to infuse at a rate to maintain set point but pre-ceded by a bolus

35
Q

why are nitrous oxides often added to other volatile agents

A

reduced dosing

36
Q

what is the meyer-overton hypothesis

A

anaesthetic potency correlates to its lipid solubility and GABAa activity

37
Q

what are the molecular-cellular targets of general anaesthesia

A

GABAa and NMDA glutamate receptors

38
Q

what are the target sites of main IV anaesthetics

A
  • ketamine NMDA
  • barbituates and propfol GABAa
39
Q

compare the potecy, speed, metabolism and duration of local anaesthetics

A
  • compared to procaine, bupivacaine is more potent with a longer duration of action
  • procaine is ester metabolised and has a slower onset time but not much in it
40
Q

what are the phases of general anaesthesia

A
  1. pre-assessment
  2. preparation
  3. induction
  4. maintenance
  5. emergence
  6. recovery
  7. follow-up
41
Q

give an examples of a depolarising muscle relaxant

A

succinylcholine - used in rapid sequence inductions
- binds to NAChR resulting in persistent depolarisation of the motor end plate

42
Q

give an example of a non-depolarising muscle relaxant

A

atracurium, rocuronium
- competitive antagonist of nAChR

43
Q

compare when endotracheal vs laryngeal airways are used

A
  • endotracheal usually for emergencies and pt w ‘full stomach’, major surgery, long duration surgery
  • laryngeal mask/iGel used for elective, well fasted pt, short duration surgery
44
Q

what are the components of maintenance of GA (4)

A
  • IV (TIVA e.g. propofol), inhalational (volatiles)
  • fluid management
  • other essential drugs e.g. abx, insulin, etc
  • drugs to prevent PONV, post op pain, etc
45
Q

what are the different ways in which a patient is ‘woken up’ after GA (5)

A
  • wears off: e.g. suxamethonium, mivacurium which is metabolised by enzymes in our body after one-off use
  • withdraw: stops maintenance IV drugs and volatiles
  • reverse: antagonising non-depolarising muscle relaxants e.g. neostigmine+glycopyrrolate
  • antagonise: e.g. opiates, BZDs use antagonists e.g. flumazenil, naloxone
  • stimulate: not used often but resp stimulants e.g. doxapram
46
Q

what are the components of recovery of a pt following anaesthesia

A

■ Monitoring- (EWS chart, fluid balance, etc.)
■ Airway (ability to maintain airway without support)
■ Side effects of GA drugs
- Sedation
- PONV
- Shivering
■ Side effects of Regional anaesthesia
- Monitoring sensory and motor block levels
- Hypotension
■ Observing for Surgical complications
- Bleeding
- Vascular supply
■ Post operative pain management
■ “fit for ward” tests.

47
Q

what are the advantages of using ketamine to induce anaesthesia

A
  • good choice for haemodynamically unstable patients
  • preserves BP and does not cause cardiosuppression
48
Q

what alterations need to be made for a patient taking prednisolone before surgery

A

hydrocortisone supplementation
- needed to prevent Addisonian crisis as long term steroids cause the adrenals to be suppressed and not produce enough cortisol

49
Q

when are neuromuscular blocking drugs used

A

as adjuncts to anaesthetic agents as they cause muscle paralysis which is a necessary prerequisite for mechanical ventilation

50
Q

in what conditions are non-depolarising anaesthetic agents contraindicated and why

A

myasthenia gravis
- pt w this conditions have fewer nicotinic receptors due to autoimmune mediated destruction so they are more sensitive to non-depolarising blockade which is how these agents work

51
Q

give a contraindication of succinylcholine

A

penetrating eye injuries or acute angle glaucoma as ↑ intraocular pressure

52
Q

why is thiopental useful

A

lowers intracranial pressure so useful in head trauma

53
Q

what might the use of the non depolarising neuromuscular blocker cause and how is this reversed

A
  • generalised histamine release on administration may produce facial flushing, tachycardia and hypotension
  • reversed by Neostigmine

*Neostigmine also reverses Vecuronium, Pancuronium

ANAESTHETICS & PERI-OPERATIVE MEDICINE (5 decks)

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