L25: Anaesthesia Flashcards
2 ways GA is given
- intravenous
- inhaled
2 types of local anaesthetic agent
esters
amides
2 types of neuromuscular blocking drugs
depolarising
non-depolarising
analgesia=
opioids
3 commonly used inhalational GA
- nitrous oxide
- isoflurane
- sevoflurane
4 intravenous GAs
- propofol
- sodium thiopentone
- etomidate
- ketamine
what may effect how potent a GA is
lipid solubility (the more soluble= more potent)
MAC=
minimal alveolar concentration of specified substance
what do GAs work on
potentiate GABAa receptors
which GABA receptor subunit do intravenous GAs work on
beta subunit
how does increasing levels of GABA work
GABA is inhibitory neurotransmitter so potentiating it will induce a decreased level of consciousness
3 desirable effects of anaesthesia
- unconsciousness
- loss of reflexes
- analgesia
most important brain area for unconsciousness
reticular formation
side effects of anaesthesia (3)
- decreased cardiac contractility
- sympathetic inhibition
- respiratory depression
What is a volatile substance
one that is very close to boiling point -quickly turns into gaseous state
in which patients does inhaled GA work fast
kids- as they breath more
in which patients does GA work slower
anyone with impaired breathing - e.g COPD
are inhaled drugs metabolised
no
what metabolises intravenous drugs
liver
which form of GA is faster onset
intravenous
what are IV drugs dependant on for onset
cardiac output (need to be carried from blood stream to brain)
what time do all IV drugs work in
one arm-brain circulation time
what makes you wake up with IV drugs
when the drugs are redistributed around the body (not metabolised till after this)
what determines when the Inhalation drugs stop working
how quickly you breath of the gases
what do local anaesthetics do
block voltage sensitive Na+ channels
where are voltage sensitive Na+ channels found
on all peripheral and central nerves
what pH are all local anaesthetics
weak bases
which tissues do local anaesthetics work worse in
acidic tissues (e.g absess)
A fibres=
large diameter, myelinated
B fibres
small diameter, myelinated
C fibres=
small diameter
unmyelinated
which fibres are first affected by local anaesthetic
C-fibres
what C-fibres are first effected
postganglionic autonomic fibres
what does blocking of the Na channels in postganglionic autonomic neurons do
- vasodilation
- warm dry feet
- systemic hypotension
second C-fibres to be affected
sensory fibres
what fibres are the final ones to be anaesthetised
alpha fibres
what are alpha fibres
motor
antagonist neuromuscular drugs=
- non-depolarising
- competitive
e.g of 3 non-depolarising neuromuscular blocking drugs
- atracurium
- rocuronium
- vecuronium
agonist neuromuscular drugs=
- depolarising
- non-competitive
e.g of agonist neuromuscular blocking drugs
suxamethonium
reversal agent for neuromuscular blocking drugs
anticholinesterase
MOA of nondepolarizing muscle relaxants
they bind to the ACh receptors but are unable to induce ion channel openings preventing ACh binding
MOA of depolarizig muscle relaxants
bind to ACh receptors causing an action potential but aren’t broken down meaning extended depolarization so the end plate can’t repolarize
how do anticholinesterases reverse the effects
by inhibiting cholinesterase so it can’t break down ACh increaseing conc of ACh
e.g of 2 anticholinesterases
- pyridostigmie
- Neostigmine
what happens first with suxamethonium
muscle fasciculations (and then relaxation)
how long does suxamthonium last
-short acting normally
side effects of anticholinesterases
- increase parasympathetic increased:
- saliva
- bronchial secretions
- GI
what needs to be taken with anticholinesterases to counteract the side effects
atropine
what new drugs can be used instead of anticholinesterase
cyclodextrin
how many stages of anaesthesia
4
what stage 1 also called
induction
what is stage 1 between
initial administration and loss of consciousness
what is stage 2 also known as
excitement stage
what is stage 2
period following loss of consciousness marked by excited and delirious activity
what may happen in stage 2
- respirations and heart rate may become irregular
- may be uncontrolled movement, vomiting, pupillary dilation
why are rapidly acting drugs used to minimise stage 2
as the combination of spastic movements, vomiting and irregular respirations may lead to airway compromise
what happens in stage 3
- the skeletal muscles relax, vomiting stops and respiratory depression occurs
- eye movement slow then stop
what stage are patients ready for surgery
stage 3
what is stage 4
overdose stage- where too much medication has been given relative to the amount of surgical stimulation
reliable clinical signs to use in anaesthetics (5)
- muscle tone
- light reflex
- eyelid reflex
- lacrimation
- eye position
