Case 10 - Yaffas Flashcards
what is general anaesthesia
this is a medically induced coma and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents
what are the purposes of general anaesthesia
Analgesia – loss of response to pain
Amnesia – loss of memory
Immobility – loss of motor reflexes
Unconsciousness – loss of consciousness
Skeletal Muscle Relaxation
what is the theory of general anaesthetic action
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
what is the pre anaesthetic evaluation key factors
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.
does consent have to be obtained
yes
what is monitored during GA
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
what are the three stages of anaesthesia
induction
maintenance
reversal
what is the excitement stage
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
what is included in the induction stage
anaesthetic agents may be administered by various routes, including inhalation, injection, oral or rectal.
the stages of intravenous induction
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
what happens once drugs are in the circulatory system
they are transported to their biochemical sites of action in the central and autonomic nervous systems, where they exert their pharmacologic effect
what are the stages of inhalation induction
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
is the onset of anaesthesia faster with IV or inhalation
faster with IV, taking about 10-20 seconds to induce total unconsciousness
what are commonly used IV induction agents
propofol, sodium thiopentone, etomidate and ketamine.
when may an inhalation induction be chosen
where IV access is difficult to obtain, where difficulty maintaining the airway is anticipated or due to the patient preference e.,g children
what is the duration of action of IV drugs
5-10 minutes, after which time spontaneous recovery of consciousness will occur
how is anaesthesia prolonged
for the reuquired duration, anaesthesia must be maintained.
how is maintenance achievee
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
what are inhaled agent usually supplemented by
intravenous anaesthetics, such as opioids (usuallyfentanyl or morphine) and sedative-hypnotics (usually propofol).
when does recovery of consciousness occur
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)
what is an integral part of modern anaesthesia
paralysis or temporary muscle relaxation with a neuromuscular blocker
what does muscular relaxation allow
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
what does acetylcholine do
causes muscle to contract when it is released from nerve endings
what do muscle relaxants do
prevent acetylcholine from attaching to its receptor
examples of muscle relaxants
E.g. atracurium, succinylcholine (suxamethonium), tubocurarine (curare), rocuronium, vecuronium.
what happens when paralysis of the muscles of respiration occurs
requires artificial respiration
how are the airway usually protected
by an endotracheal tube
how are the effects of muscle relaxants revered at the terminations of surgery
by acetylcholinesterase drugs
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.
what is used to reverse the muscle relaxants (drugs used)
(neostigmine + glycopyrrolate).
what is spontaneous respiration
normal negative pressure breathing
supine position and V/Q matching
respiratory depression - increase in CO2 - hypercapnia
hypoxic on room air
what is positive pressure ventilation
inspiration is now positive pressure
expiration is passive
needs a tracheal tube
increased indcidence of chest infection
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
what are the CNS consequences of anaesthesia
Unconsciousness
Depression of cerebral metabolism
Dreaming
Awareness
Specific EEG changes
Possible long-term effects
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.
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
what is monitored and assessed during post operative recovery
oxygenation
pain control
fluid balance
postoperative nausea and vomiting
cardiovascular stability
conscious level
urine output
what is early postoperative management
‘recovery’
what is late post operative recovery
wound infection
DVT
chest infection
surgical problems
what is the risk due to anaesthesia alone
less than 1 in 500,000
what is used for rapid induction
an IV anaesthetic
what is an example of an IV anaesthetic
propofol
what is used to maintain anaesthesia during surgery
an inhalation anaesthetic - isoflurane
what is the perioperative analgesic
an opioid for example fentanyl
what produces adequate muscle relaxation
a neuromuscular blocking agent - example is atracurium
what is an example of another muscle relaxant
suxamethonium
what is used to prevent or treat bradycardia or to reduce bronchial and salivary secretions
a muscarinic antagonist for example atropine or glycopyrrolate
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
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
diagram of GA etc. please learn this off as a summary
where do anaesthetic agents act
GABA A receptors
two pore domain K+ channels
NMDA receptors
glycine, nicotinic and 5HT receptors
what are GABA A receptors
ligand gated ion channels (inotropic receptors)
they are Cl- channels and most abundant fast inhibitory neurotransmitter in the CNS
where do almost all anaesthetics potentiate the action of GABA
at the GABA A receptor
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
what type of GABA A receptors do anaesthetics work on
extrasynaptic receptors
what are two pore domain K+ channels
leak channels
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
what are these channels not affected by
intravenous inducing agents
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)
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
what can volatile anaesthetics cause
inhibitions at the spinal level, producing a loss of reflex responses to painful stimuli
do anaesthetics cause short term amnesia
yes
how do anaesthetics cause death
by loss of cardiovascular reflexes and respiratory paralysis
what are inhalation anaesthetics
small, lipid-soluble molecules that readily cross alveolar membrane
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
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
what are the physiological factors that determine the speed of induction and recovery
alveolar ventilation rate
cardiac output
what is anaesthetic potency expressed as
the minimal alveolar concentration (MAC)
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
how does the potency of a drug increase
with increasing lipid solubility (the higher lipid solubility is the lower the MAC)
what is propofol
is an IV anaesthetic agent used for induction of general anaesthesia
what is it used for
to induce unconsciousness after which anaesthesia may be minted using a combination of mediations
wha is the onset and distribution of propofol
rapid onset of action - 30seconds
rapid rate of distribution
why is there a rapid recovery with propofol
rapidly metabolised to inactive metabolites
what is the volume of distribution of propofol
60L/kg
what is the mechanism of action of propofol
positive modulation of inhibitory function of GABA through GABA A receptor
what are the major side effects of propofol
Hypotension and bradycardia
Respiratory depression
Pain with injection
Involuntary movement and adrenocortical suppression
Nausea and vomiting
what can propofol also be given as
a continuous infusioon to maintain surgical anaesthesia without the need for any inhalation agent
what is isoflurane
the most widely used volatile anaesthetic - inhalation inducing agent - used for maintenance of general anaesthesia
what is isoflurane always administered with
oxygen or nitric oxide
what is the mechanism of action of isoflurane
likely binds to GABA, glutamates (NMDA) and glycine receptors , but has different effects on each receptor
what are the major side effects of isolfurane
hypotension
coronary vasodilator
respiratory suppression
what is fentanyl
a potent narcotic analgesic
relationship between fentanyl and morphine
similar actions but with a more rapid onset and shorter duration fo action
what is the dose of fentanyl given
0.05mg/mL IV
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
how do neuromuscular blocking drugs work
work postsynaptically either:
- blocking Ach receptors
- activating Ach receptors and thus causing persistent depolarisation
which is the only drug used clinically that is not non -depolarising
suxamethonium
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
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
what are the effects of non-depolarising blocking drugs
motor paralyiss - help facilitate endotracheal intubation
what are the major side effects of non-depolarising neuromusclar blocking agents
hypotension
bronchospasm - histamine release
ganglion block
what is atracurium
a non-depolarising neuromuscular blocking agent - muscle relaxant
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
what are the optimum conditions for atracurium
low pH (acidosis) and high temperature
what is reduced due to repsiratory acidosis
elimination
what is suxamethonium
a depolarising neuromuscular blocking agent - muscle relaxant
what is the duration of action of suxamethonium
lasts between 3-5 minutes
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)).
what re the major side effects of suxamethonium
bradycardia and hyperjalemia
increased intraocular pressure
postoperative pain
