Case 10 - Yaffas Flashcards

1
Q

what is general anaesthesia

A

this is a medically induced coma and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents

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2
Q

what are the purposes of general anaesthesia

A

Analgesia – loss of response to pain
Amnesia – loss of memory
Immobility – loss of motor reflexes
Unconsciousness – loss of consciousness
Skeletal Muscle Relaxation

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3
Q

what is the theory of general anaesthetic action

A

alter neurone function by interacting directly with a small number of ion channels.

upon activation, channels change the electrical excitability of neurones by controlling the flow of depolarising (excitatory) and hyper polarising (inhibitory) ions across the cell membrane via an ion channel that is integral wtith the receptor that senses the initial signal

general anaesthetics primarily act by either enhancing inhibitory signals or by blocking excitatory signals

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4
Q

what is the pre anaesthetic evaluation key factors

A

patient’s age, body mass index, medical and surgical history, current medications and fasting time.

also an evaluation of the patients airway, involving inspection of the mouth opening and visualisation of the soft tissues of the pharynx is required.

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5
Q

does consent have to be obtained

A

yes

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6
Q

what is monitored during GA

A

ECG – this may also help identify early signs of heart ischaemia.
Blood pressure – can be invasive or non-invasive.
Oxygen saturation – pulse oximetry – allows early detection of a fall in a patient’s haemoglobin saturation with oxygen (hypoxaemia).
End tidal CO2 – carbon dioxide measurement (capnography).
Inspired oxygen – low oxygen alarm.
Inspired agent concentration
Neuromuscular blockade
Airway pressures and flows
Temperature – to discern hypothermia or fever.
Depth of anaesthesia

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7
Q

what are the three stages of anaesthesia

A

induction
maintenance
reversal

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8
Q

what is the excitement stage

A

there is an excitement stage that occurs after induction and before maintenance. this is marked by excited and delirious activity - there may be an irregular heart rate and breathing rate

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9
Q

what is included in the induction stage

A

anaesthetic agents may be administered by various routes, including inhalation, injection, oral or rectal.

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10
Q

the stages of intravenous induction

A

bolus of drug injected
travels to the brain
highly lipid soluble
rapidly enters the brain
onset is in one arm - brain time
initial recovery by redistribution
ultimate recovery by elimination

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11
Q

what happens once drugs are in the circulatory system

A

they are transported to their biochemical sites of action in the central and autonomic nervous systems, where they exert their pharmacologic effect

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12
Q

what are the stages of inhalation induction

A

vapour breathed in via lungs
enters the blood
travels to the brain
highly lipid soluble
enters the brain
initial recovery by exhalation
ultimate recovery by exhalation
minimal amounts are metabolised

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13
Q

is the onset of anaesthesia faster with IV or inhalation

A

faster with IV, taking about 10-20 seconds to induce total unconsciousness

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14
Q

what are commonly used IV induction agents

A

propofol, sodium thiopentone, etomidate and ketamine.

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15
Q

when may an inhalation induction be chosen

A

where IV access is difficult to obtain, where difficulty maintaining the airway is anticipated or due to the patient preference e.,g children

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16
Q

what is the duration of action of IV drugs

A

5-10 minutes, after which time spontaneous recovery of consciousness will occur

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17
Q

how is anaesthesia prolonged

A

for the reuquired duration, anaesthesia must be maintained.

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18
Q

how is maintenance achievee

A

allowing the patient to breathe a carefully controlled mixture of:
oxygen
nitrous oxide
isoflurane (volatile anaesthetic agent)

this can also be achieved by having a carefully controlling continuous infusion propofol through an IV catheter

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19
Q

what are inhaled agent usually supplemented by

A

intravenous anaesthetics, such as opioids (usuallyfentanyl or morphine) and sedative-hypnotics (usually propofol).

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20
Q

when does recovery of consciousness occur

A

when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes, depending upon the duration of surgery)

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21
Q

what is an integral part of modern anaesthesia

A

paralysis or temporary muscle relaxation with a neuromuscular blocker

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22
Q

what does muscular relaxation allow

A

surgery within major body cavities e.g abdomen and thorax, without the need for very deep anaesthesia, and is also used to facilitate endotracheal intubation

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23
Q

what does acetylcholine do

A

causes muscle to contract when it is released from nerve endings

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24
Q

what do muscle relaxants do

A

prevent acetylcholine from attaching to its receptor

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25
Q

examples of muscle relaxants

A

E.g. atracurium, succinylcholine (suxamethonium), tubocurarine (curare), rocuronium, vecuronium.

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26
Q

what happens when paralysis of the muscles of respiration occurs

A

requires artificial respiration

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27
Q

how are the airway usually protected

A

by an endotracheal tube

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28
Q

how are the effects of muscle relaxants revered at the terminations of surgery

A

by acetylcholinesterase drugs

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29
Q

with the loss of consciousness, what else is there a loss of

A

Protective airway reflexes (such as coughing)
Airway patency (airway obstruction)
Regular pattern due to the effect of anaesthetics, opioids, or muscle relaxants.

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30
Q

what is used to reverse the muscle relaxants (drugs used)

A

(neostigmine + glycopyrrolate).

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31
Q

what is spontaneous respiration

A

normal negative pressure breathing

supine position and V/Q matching

respiratory depression - increase in CO2 - hypercapnia

hypoxic on room air

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32
Q

what is positive pressure ventilation

A

inspiration is now positive pressure

expiration is passive

needs a tracheal tube

increased indcidence of chest infection

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33
Q

what are the cardiovascular consequences of anaesthesia

A

Decreased venous return
Decreased cardiac output
Decreased force of contraction
Increase in arrhythmia potential
Vasodilation
Change in regional flow patterns

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34
Q

what are the CNS consequences of anaesthesia

A

Unconsciousness
Depression of cerebral metabolism
Dreaming
Awareness
Specific EEG changes
Possible long-term effects

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35
Q

what happens with agents with high lipid solubility

A

they accumulate gradually in body fat and may produce a prolonged hangover. if used for a long operation.

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36
Q

why does this happen

A

because of the low blood flow to adipose tissue meaning it can take hours for the drug to enter and leave the fat

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37
Q

what is monitored and assessed during post operative recovery

A

oxygenation
pain control
fluid balance
postoperative nausea and vomiting
cardiovascular stability
conscious level
urine output

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38
Q

what is early postoperative management

A

‘recovery’

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39
Q

what is late post operative recovery

A

wound infection
DVT
chest infection
surgical problems

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40
Q

what is the risk due to anaesthesia alone

A

less than 1 in 500,000

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41
Q

what is used for rapid induction

A

an IV anaesthetic

42
Q

what is an example of an IV anaesthetic

A

propofol

43
Q

what is used to maintain anaesthesia during surgery

A

an inhalation anaesthetic - isoflurane

44
Q

what is the perioperative analgesic

A

an opioid for example fentanyl

45
Q

what produces adequate muscle relaxation

A

a neuromuscular blocking agent - example is atracurium

46
Q

what is an example of another muscle relaxant

A

suxamethonium

47
Q

what is used to prevent or treat bradycardia or to reduce bronchial and salivary secretions

A

a muscarinic antagonist for example atropine or glycopyrrolate

48
Q

what is used toward the end of the procure to reverse neuromuscular blockade and for postoperative pain relief

A

an anticholinesterase agent for example neostigmine is used to reverse neuromuscular blockade

opioid or NSAID used for post op pain

49
Q

what does such combinations of drugs result in

A

much faster induction and recovery, avoiding long periods of semiconsciousness and it enable surgery to be carried out with less undesirable cardiorespiratory depression

50
Q

diagram of GA etc. please learn this off as a summary

A
51
Q

where do anaesthetic agents act

A

GABA A receptors
two pore domain K+ channels
NMDA receptors
glycine, nicotinic and 5HT receptors

52
Q

what are GABA A receptors

A

ligand gated ion channels (inotropic receptors)

they are Cl- channels and most abundant fast inhibitory neurotransmitter in the CNS

53
Q

where do almost all anaesthetics potentiate the action of GABA

A

at the GABA A receptor

54
Q

what do they do at the GABA A receptor

A

they have a positive modulation of the inhibitory function of GABA by causing an increased influx in Cl- ions into the postsynaptic neurone

55
Q

what type of GABA A receptors do anaesthetics work on

A

extrasynaptic receptors

56
Q

what are two pore domain K+ channels

A

leak channels

57
Q

what do inhalation inducing agents do to these channels

A

directly activate these channels, causing hyperpolarisation, thus reducing membrane excitability

this may contribute to the analgesic hypnotic and immobilising effects of these agents

58
Q

what are these channels not affected by

A

intravenous inducing agents

59
Q

what are the effects of anaesthetic and their aims

A

enhance tonic inhibition (through enhancing actions of GABA)

reduce excitation (opening K+ channels - hyperpolarisation)

inhibit excitatory synaptic transmission (by depressing transmitter release and inhibiting ligand gated ion channels)

60
Q

where are the most sensitive brain regions

A

midbrain reticular formation, thalamic sensory relay nuclei and parts of cortex

inhibiton of these regions results in unconsciousness and analgesia

61
Q

what can volatile anaesthetics cause

A

inhibitions at the spinal level, producing a loss of reflex responses to painful stimuli

62
Q

do anaesthetics cause short term amnesia

A

yes

63
Q

how do anaesthetics cause death

A

by loss of cardiovascular reflexes and respiratory paralysis

64
Q

what are inhalation anaesthetics

A

small, lipid-soluble molecules that readily cross alveolar membrane

65
Q

what determines the overall kinetic behaviour of an anaesthetic

A

the rates of delivery of drug to and from the lungs, via the inspired air and bloodstream

66
Q

what are the properties of anaesthesia that determines the speed of induction and recovery

A

blood:gass partition coefficient (solubility in blood) - speed of induction / recovery

oil:gas partition coefficient (solubility in fat) - potency

67
Q

what are the physiological factors that determine the speed of induction and recovery

A

alveolar ventilation rate

cardiac output

68
Q

what is anaesthetic potency expressed as

A

the minimal alveolar concentration (MAC)

69
Q

what is the MAC

A

the concentration of vapour in the lungs that ids needed to prevent movement (motor response) in 50% of patients in response to surgical (pain-incision) stimulus

70
Q

how does the potency of a drug increase

A

with increasing lipid solubility (the higher lipid solubility is the lower the MAC)

71
Q

what is propofol

A

is an IV anaesthetic agent used for induction of general anaesthesia

72
Q

what is it used for

A

to induce unconsciousness after which anaesthesia may be minted using a combination of mediations

73
Q

wha is the onset and distribution of propofol

A

rapid onset of action - 30seconds
rapid rate of distribution

74
Q

why is there a rapid recovery with propofol

A

rapidly metabolised to inactive metabolites

75
Q

what is the volume of distribution of propofol

A

60L/kg

76
Q

what is the mechanism of action of propofol

A

positive modulation of inhibitory function of GABA through GABA A receptor

77
Q

what are the major side effects of propofol

A

Hypotension and bradycardia
Respiratory depression
Pain with injection
Involuntary movement and adrenocortical suppression
Nausea and vomiting

78
Q

what can propofol also be given as

A

a continuous infusioon to maintain surgical anaesthesia without the need for any inhalation agent

79
Q

what is isoflurane

A

the most widely used volatile anaesthetic - inhalation inducing agent - used for maintenance of general anaesthesia

80
Q

what is isoflurane always administered with

A

oxygen or nitric oxide

81
Q

what is the mechanism of action of isoflurane

A

likely binds to GABA, glutamates (NMDA) and glycine receptors , but has different effects on each receptor

82
Q

what are the major side effects of isolfurane

A

hypotension
coronary vasodilator
respiratory suppression

83
Q

what is fentanyl

A

a potent narcotic analgesic

84
Q

relationship between fentanyl and morphine

A

similar actions but with a more rapid onset and shorter duration fo action

85
Q

what is the dose of fentanyl given

A

0.05mg/mL IV

86
Q

what is the mechanism of action of fentanyl

A

strong agonist at the U-opioid receptor

upon binding, it inhibits adenylate cyclase, which causes an inhibition in the release of nociceptive substances such as substance P, GABA, dopamine etc

87
Q

how do neuromuscular blocking drugs work

A

work postsynaptically either:
- blocking Ach receptors
- activating Ach receptors and thus causing persistent depolarisation

88
Q

which is the only drug used clinically that is not non -depolarising

A

suxamethonium

89
Q

what is the mechanism of action of non depolarising neuromuscular blocking agents

A

non-depolarising blocking agents all act as competitive antagonists at the ACh receptors of the motor endplate

non-depolarising blocking agents also block facilitatory presynaptic auto receptors and thus inhibit the release of ACh during repetitive stimulation of the motor nerve

90
Q

what are the pharmokinetics of non depolarising neuromuscular blocking agents

A

most of the non-depolarising blocking agents are metabolised by the liver or excreted unchanged in the urine, exceptions being atracurium which hydrolyses spontaneously in plasma

91
Q

what are the effects of non-depolarising blocking drugs

A

motor paralyiss - help facilitate endotracheal intubation

92
Q

what are the major side effects of non-depolarising neuromusclar blocking agents

A

hypotension
bronchospasm - histamine release
ganglion block

93
Q

what is atracurium

A

a non-depolarising neuromuscular blocking agent - muscle relaxant

94
Q

what is the duration of action of atracurium and why is this an advantage

A

it has a short duration - this has a clinical advantage because of the decreased cardiovascular effects and decreased dependency on good kidney function

95
Q

what are the optimum conditions for atracurium

A

low pH (acidosis) and high temperature

96
Q

what is reduced due to repsiratory acidosis

A

elimination

97
Q

what is suxamethonium

A

a depolarising neuromuscular blocking agent - muscle relaxant

98
Q

what is the duration of action of suxamethonium

A

lasts between 3-5 minutes

99
Q

what is the mechanism of action of suzamethonium

A

Persistent” depolarisation of neuromuscular junction.
It is caused by mimicking the effect of Ach but without being rapidly hydrolysed by acetylcholinesterase.
The constant depolarisation leads to desensitisation.
Suxamethonium is hydrolysed by plasma cholinesterase (butyrylcholinesterase (BuChE)).

100
Q

what re the major side effects of suxamethonium

A

bradycardia and hyperjalemia
increased intraocular pressure
postoperative pain