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Semester 3 > Case 10 - Yaffas > Flashcards

Case 10 - Yaffas Flashcards

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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
examples of muscle relaxants
E.g. atracurium, succinylcholine (suxamethonium), tubocurarine (curare), rocuronium, vecuronium.
26
what happens when paralysis of the muscles of respiration occurs
requires artificial respiration
27
how are the airway usually protected
by an endotracheal tube
28
how are the effects of muscle relaxants revered at the terminations of surgery
by acetylcholinesterase drugs
29
with the loss of consciousness, what else is there a loss of
Protective airway reflexes (such as coughing) Airway patency (airway obstruction) Regular pattern due to the effect of anaesthetics, opioids, or muscle relaxants.
30
what is used to reverse the muscle relaxants (drugs used)
(neostigmine + glycopyrrolate).
31
what is spontaneous respiration
normal negative pressure breathing supine position and V/Q matching respiratory depression - increase in CO2 - hypercapnia hypoxic on room air
32
what is positive pressure ventilation
inspiration is now positive pressure expiration is passive needs a tracheal tube increased indcidence of chest infection
33
what are the cardiovascular consequences of anaesthesia
Decreased venous return Decreased cardiac output Decreased force of contraction Increase in arrhythmia potential Vasodilation Change in regional flow patterns
34
what are the CNS consequences of anaesthesia
Unconsciousness Depression of cerebral metabolism Dreaming Awareness Specific EEG changes Possible long-term effects
35
what happens with agents with high lipid solubility
they accumulate gradually in body fat and may produce a prolonged hangover. if used for a long operation.
36
why does this happen
because of the low blood flow to adipose tissue meaning it can take hours for the drug to enter and leave the fat
37
what is monitored and assessed during post operative recovery
oxygenation pain control fluid balance postoperative nausea and vomiting cardiovascular stability conscious level urine output
38
what is early postoperative management
'recovery'
39
what is late post operative recovery
wound infection DVT chest infection surgical problems
40
what is the risk due to anaesthesia alone
less than 1 in 500,000
41
what is used for rapid induction
an IV anaesthetic
42
what is an example of an IV anaesthetic
propofol
43
what is used to maintain anaesthesia during surgery
an inhalation anaesthetic - isoflurane
44
what is the perioperative analgesic
an opioid for example fentanyl
45
what produces adequate muscle relaxation
a neuromuscular blocking agent - example is atracurium
46
what is an example of another muscle relaxant
suxamethonium
47
what is used to prevent or treat bradycardia or to reduce bronchial and salivary secretions
a muscarinic antagonist for example atropine or glycopyrrolate
48
what is used toward the end of the procure to reverse neuromuscular blockade and for postoperative pain relief
an anticholinesterase agent for example neostigmine is used to reverse neuromuscular blockade opioid or NSAID used for post op pain
49
what does such combinations of drugs result in
much faster induction and recovery, avoiding long periods of semiconsciousness and it enable surgery to be carried out with less undesirable cardiorespiratory depression
50
diagram of GA etc. please learn this off as a summary
51
where do anaesthetic agents act
GABA A receptors two pore domain K+ channels NMDA receptors glycine, nicotinic and 5HT receptors
52
what are GABA A receptors
ligand gated ion channels (inotropic receptors) they are Cl- channels and most abundant fast inhibitory neurotransmitter in the CNS
53
where do almost all anaesthetics potentiate the action of GABA
at the GABA A receptor
54
what do they do at the GABA A receptor
they have a positive modulation of the inhibitory function of GABA by causing an increased influx in Cl- ions into the postsynaptic neurone
55
what type of GABA A receptors do anaesthetics work on
extrasynaptic receptors
56
what are two pore domain K+ channels
leak channels
57
what do inhalation inducing agents do to these channels
directly activate these channels, causing hyperpolarisation, thus reducing membrane excitability this may contribute to the analgesic hypnotic and immobilising effects of these agents
58
what are these channels not affected by
intravenous inducing agents
59
what are the effects of anaesthetic and their aims
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
where are the most sensitive brain regions
midbrain reticular formation, thalamic sensory relay nuclei and parts of cortex inhibiton of these regions results in unconsciousness and analgesia
61
what can volatile anaesthetics cause
inhibitions at the spinal level, producing a loss of reflex responses to painful stimuli
62
do anaesthetics cause short term amnesia
yes
63
how do anaesthetics cause death
by loss of cardiovascular reflexes and respiratory paralysis
64
what are inhalation anaesthetics
small, lipid-soluble molecules that readily cross alveolar membrane
65
what determines the overall kinetic behaviour of an anaesthetic
the rates of delivery of drug to and from the lungs, via the inspired air and bloodstream
66
what are the properties of anaesthesia that determines the speed of induction and recovery
blood:gass partition coefficient (solubility in blood) - speed of induction / recovery oil:gas partition coefficient (solubility in fat) - potency
67
what are the physiological factors that determine the speed of induction and recovery
alveolar ventilation rate cardiac output
68
what is anaesthetic potency expressed as
the minimal alveolar concentration (MAC)
69
what is the MAC
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
how does the potency of a drug increase
with increasing lipid solubility (the higher lipid solubility is the lower the MAC)
71
what is propofol
is an IV anaesthetic agent used for induction of general anaesthesia
72
what is it used for
to induce unconsciousness after which anaesthesia may be minted using a combination of mediations
73
wha is the onset and distribution of propofol
rapid onset of action - 30seconds rapid rate of distribution
74
why is there a rapid recovery with propofol
rapidly metabolised to inactive metabolites
75
what is the volume of distribution of propofol
60L/kg
76
what is the mechanism of action of propofol
positive modulation of inhibitory function of GABA through GABA A receptor
77
what are the major side effects of propofol
Hypotension and bradycardia Respiratory depression Pain with injection Involuntary movement and adrenocortical suppression Nausea and vomiting
78
what can propofol also be given as
a continuous infusioon to maintain surgical anaesthesia without the need for any inhalation agent
79
what is isoflurane
the most widely used volatile anaesthetic - inhalation inducing agent - used for maintenance of general anaesthesia
80
what is isoflurane always administered with
oxygen or nitric oxide
81
what is the mechanism of action of isoflurane
likely binds to GABA, glutamates (NMDA) and glycine receptors , but has different effects on each receptor
82
what are the major side effects of isolfurane
hypotension coronary vasodilator respiratory suppression
83
what is fentanyl
a potent narcotic analgesic
84
relationship between fentanyl and morphine
similar actions but with a more rapid onset and shorter duration fo action
85
what is the dose of fentanyl given
0.05mg/mL IV
86
what is the mechanism of action of fentanyl
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
how do neuromuscular blocking drugs work
work postsynaptically either: - blocking Ach receptors - activating Ach receptors and thus causing persistent depolarisation
88
which is the only drug used clinically that is not non -depolarising
suxamethonium
89
what is the mechanism of action of non depolarising neuromuscular blocking agents
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
what are the pharmokinetics of non depolarising neuromuscular blocking agents
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
what are the effects of non-depolarising blocking drugs
motor paralyiss - help facilitate endotracheal intubation
92
what are the major side effects of non-depolarising neuromusclar blocking agents
hypotension bronchospasm - histamine release ganglion block
93
what is atracurium
a non-depolarising neuromuscular blocking agent - muscle relaxant
94
what is the duration of action of atracurium and why is this an advantage
it has a short duration - this has a clinical advantage because of the decreased cardiovascular effects and decreased dependency on good kidney function
95
what are the optimum conditions for atracurium
low pH (acidosis) and high temperature
96
what is reduced due to repsiratory acidosis
elimination
97
what is suxamethonium
a depolarising neuromuscular blocking agent - muscle relaxant
98
what is the duration of action of suxamethonium
lasts between 3-5 minutes
99
what is the mechanism of action of suzamethonium
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
what re the major side effects of suxamethonium
bradycardia and hyperjalemia increased intraocular pressure postoperative pain

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