PPT Flashcards
MOA of local anaesthetics?
they block the voltage-dependant Na+ channels that depolarise the neutron
ore than 90% of channels must be affected to stop nerve conduction
which drugs are most likely to cause malignant hyperthermia?
volatile anaetshetics
suxamethonium
CI to suxamethonium?
penetrating eye injuries or acute narrow angle glaucoma, as suxamethonium increases intra-ocular pressure
moa of depolarising vs non-depolarising neuromuscular blocking drugs
depolairisng: Binds to nicotinic acetylcholine receptors resulting in persistent depolarization of the motor end plate
non-depolarising: Competitive antagonist of nicotinic acetylcholine receptors
what factors influence LA action?
local concentration of LA
size of nerve fibre
nerve myelination
length of nerve exposed to LA
which nerve fibres transmit pain?
myelinated A delta and small non-myelinated C fires
why is ketamine often used as an induction agent in emergency surgeries?
as it doesn’t drop the bp
LA action of myelinated and non-myelinated nerves?
myelinated - LA penentrates at nodes of Ranvier and must block at least 3 consecutive nodes
unmyelinated nerves must be blocked over a sufficient length and around the full circumference of the nerve
which neuromuscular blocking drug causes muscle fasciculations?
suxamethonium
what is the potency of a LA directly related to?
its lipid solubility
do LAs exist as acids or bases?
weak bases
what is pKa? what is it for lidocaine?
the pH at which the ionised and non-ionised forms are equal
7.8
what happens when the pKa of a LA = the physiological PH?
there will be a higher concentration of non-ionised base and a faster onset
in which form is the water solubility of local anaesthetics greatest?
in the ionised form (this is why injectable preparations are formulated as hydrochloride salts with a pH of 5-6 as it keeps the LA in its ionised form)
what are the implications of LAs with high pKa?
a larger proportion of the drug will be more ionised at physiological pH = less molecules in non-ionised state = less lipophilic = so speed of onset is slower BUT once inside a higher proportion of LA is in the ionised state = produce a more effective blockade
what does use-dependance mean?
the more channels that are opened, the greater the block becomes
common LAs?
lidocaine
bupivacaine
tetracaine
prilocaine
max concentration of a topical anaesthesia?
up to 10%
what can LA be mixed with in peripheral nerve blocks to increase speed of onset and duration of action?
Bicarbonate for speed
epinephrine for duration
how much LA is given in a spinal?
1.5-2.5ml
where is a spinal anaesthetic inserted?
between L3 and L4
why can adrenaline be given alongside a LA?
as most LAs cause vasodilation so adrenaline causes vasoconstriction to reduce their removal
what does the spread of the LA within the subarachnoid space in a spinal depend on?
density of sollution
posture of person during the first 10-15 mins
what are the amide-linked drugs?
lidocaine
prilocaine
bupivacaine
etidocaine
mepivacaine
ropivacaine
what are the ester-linked drugs?
tetracaine
choroprocaine
cocaine
procaine
how are ester-linked LAs metabolised?
rapidly hydrolysed by plasma cholinesterase = short half life
how are amide-linked LAs metabolised?
metabolised in the liver by N-dealkylation
metabolites are often pharmacologically active
Local SE of LA?
irritation and inflammation
ischaemia from use of vasoconstrictor agents
systemic SE of LA?
myocardial depression
vasodilation
hypotension
arrhythmias
agitation
confusion
tremors
convulsions
respiratory depression
how is LA toxicity treated?
with IV 20% lipid emulsion
drug interactions for lidocaine?
Beta blockers, ciprofloxacin, phenytoin
dose of lidocaine without and with adrenaline?
3 and 7
dose of bupivicaine with and without adrenaline?
2and 2
dose of prilocaine without and with adrenaline?
6 and 9
when is adding adrenaline to LA CI?
in pts taking MAOIs or TCAs
which has a longer duration of action bupivicaine or lidocaine?
bupivicaine (has a higher pKa)
4 stages of anaesthesia?
analgesia
excitation
surgical anaesthesia
medullary depression
MOA of etomidate?
binds to GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
MOA of propofol?
positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors.
MOA of thiopental?
binds to GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
MOA of NO?
Exact mechanism of action unknown. May act via a combination of NDMA, nACh, 5-HT3, GABAA and glycine receptors
MOA of ketamine?
interacts with NMDA, opioid, monoaminergic, muscarinic and voltage sensitive Ca ion channels
MOA of sevoflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
MOA of isoflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
MOA of desflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
what factors affect inhalation anaesthesia?
Absorption across alveolar membranes
Solubility of the anaesthetic in the blood
Cardiac output – circulation time
Relative concentration of the anaesthetic in the brain and blood at equilibrium
what is MAC?
a measure of potency. its the minimum concentration at which 50% of th population will fail to respond to a single noxious stimuli e.g. first surgical skin incision
what is the Meyer-Overton correlation for anaesthetics?
a graph showing the MAC against the olive oil:gas partition coefficient
it shows tan the lower the blood:gas ratio the more GA will arrive at the brain i.e. the higher the MAC
what Is the blood:gas partition coefficient?
a measure of solubility of GA in the blood
it determines the rate of induction and recovery of inhalation anaesthesia
the higher the blood: gas coefficient the slower the induction and recovery i.e. the lower the MAC
the potency of an anaesthetic increases as its solubility in oil increases
which innhalational anaesthetic agents have the highest blood: gas partition coefficients?
isoflurane and halothane (this means they have the lowest MAC - halothane is no longer used in the UK)
what is NO used for?
it is not sufficiently potent to be used alone
Is used part of a combination of drugs to allow a significant reduction in dosage (with other inhalational anaesthetics or intravenous anaesthetics)
used for maintenance of anaesthesia or In sub-anaesthetic concentrations for analgesia – e.g. Entonox® – 50:50 mixture with oxygen
MAC of NO?
105%
what factors influence elimination of inhalational anaesthetics?
ventilation rate
bod:gas partition coefficient
duration of inhalation
extent of tissue equilibration
examples of IV anaesthetics?
etomidate
ketamine
propofol
thiopental
why has propofol largely replaced thiopental as an induction agent?
more rapid recovery and less hangover effect
why is etomidate not used as a continuous infusion?
due to toxicity on adrenals and adenocortical suppression
what is dissociative anaesthesia nd what causes it?
ketamine
marked sensory loss and analgesia with amnesia but without complete loss of consciousess
the analgesia outlasts the anaesthesia
examples of non-depolarising neuromuscular blockers?
atracurium
cisatracurium
mivacurium
pancuronium
rocuronium
vecuronium
adverse effects of depolarising neuromuscular blocking drugs?
malignant hyperthermia
hypekalaemia
examples of depolarising neuromuscular blockers?
suxamethonium
what is an important but rare adverse event with suxamethonium?
a very prolonged paralysis occurs in 1 in 2000 people who have a genetic deficiency of pseudocholinesterase
reversal agent for non-depolarising neuromuscular blockers? what is given with it?
neostigmine (not with depolarising neuromuscular blockers!)
and an antimuscarinic such as atropine or glycopyrrolate is given immediately before to prevent bradycardia or excessive salivation
universal donor blood?
O neg
monitoring when giving blood transfusion?
observations at 0, 15, 30 mins and then hourly and then again on completion
1 unit should increase Hb by xg/L
10
when is a platelet transfusion indicated?
if plt <10
if <30 with grade 2 clinically significant bleeding
<100 with grade 3/4 bleeding
50-100 if having invasive procedure
daily requirements of water, Na+, K+, Cl-. glucose?
water 25-30mls/kg
Na+ 1 mmol/kg
K+ 1 mmol/kg
Cl- 1 mmol/kg
glucose 50-100g
what does adrenaline interact with?
amitryptiline
beta blockers
MAOI
