NS 43 - anaesthesia

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(Neuroscience ) JC3 Fichas sobre NS 43 - anaesthesia, creado por Erica Lai el 30/11/2018.
Erica Lai
Fichas por Erica Lai, actualizado hace más de 1 año
Erica Lai
Creado por Erica Lai hace casi 6 años
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decrease in anaesthetic mortality because of (5) better knowledge newer drugs more training better equipment closer monitoring
propofol from egg phosphatide/soya oil/glycerol induces anaesthesia - produces unconsciousness within one arm-brain circulation time rapidly passes from blood to brain because it is highly lipid soluble quality of recovery is good and quick (within 5 mins following bolus induction dose)
C/I of propofol airway obstruction haemodynamic compromise epilepsy (because it causes activation of EEG and may be associated with seizures)
propofol S/Es hypotension (especially in elderly - use reduced dose in them) respiratory depression pain on injection (mix with lignocaine) propofol infusion syndrome (fatal metabolic acidosis)
propofol metabolism glucuronidation in the liver elimination: t 1/2 = 3 - 4.8 hours 0.3% of drug excreted unchanged
how would you obtain minimum desired blood circulation of propofol targeted continuous infusion (TCI)
Thiopentone (sodium thiopentone) is an ultra-short acting barbiturate produces unconscious within one arm-brain circulation time recovery within 5-7 mins but there is significant 'hangover' effect 80% bind to plasma proteins metabolised in the liver 10-15% of drug metabolised per hour elimination: t 1/2 is 11 hours
thiopentone indications in adults, elderly, paeds adults: 3-5 mg/kg elderly: 1.5-2.5 mg/kh paeds: 5-7 mg/kg
barbiturate coma for raised ICP barbiturates have a neuroprotective effect by reducing the brain's oxygen consumption rate used in severe head injuries
thiopentone C/I airway obstruction haemodynamic compromise (shock, CCF) porphyria
list 4 general anaesthetic IV agents propofol tiopentone ketamine etomidate
volatile agents are used for maintenance of anaesthesia
why aren't volatile agents typically used to induce anaesthesia? because they are much slower and have a high incidence of coughing/breath-holding/movements
administration of volatile agents gas delivery
sevoflurane volatile agent, inhaled relatively high MAC - need more agent to maintain anaesthesia clean profile, rapid uptake and recovery low solubility in blood
MAC minimum alveolar concentration MAC at eqm at 1 atmospheric P, which produces immobility in 50% of subjects exposed to a standard noxious stimulus
ED50 median effective dose (50% of people have therapeutic effect)
TD50 median toxic dose dose at which toxicity occurs in 50% of cases
LD50 medianlethal dose dose at which death occurs in 50% of cases
stages of anaesthesia (4) stage analgesia stage of delirium (should be minimised) stage of surgical anaesthesia stage of medullary depression
awareness during procedures caused by inadequate anaesthesia in a patient who is immobilised by muscle relaxants 1:10,000 super scary stuff - very traumatic
2 classes of muscle relaxants competitive neuromuscular blockers non-competitive neuromuscular blockers
indications (uses) of muscle relaxants (3) tracheal intubation abdominal / thoracic surgery permit 'light' anaesthesia during surgery
risks of using muscle relaxants (2) awareness (during procedure the scary thing) residual muscle weakness post-op
reversal of muscle relaxants non-competitive nm blockers can't be reversed but suxamethonium is short-acting competitive nm blockers are reversed by AChE inhibitors - act to increase ACh levels (neostigmine is commonly used)
what are opiates used for intra-operatively? to suppress the reflex response to pain
examples of opiates used fentanyl remifentanil morphine
local anaesthetics - 4 types local infiltration nerve blocks plexus blocks spinal block
MOA of local anaesthetics reversible depression of nerve conduction when applied to the nerve fibre inhibition of Na channels
local anaesthetic with amide linkage (3) where are they metabolised? lignocaine mepivacaine bupivacaine liver
local anaesthetic with ester linkages where are they metabolised? procaine chlorprocain tetracaine in plasma by pseudocholinesterase
lignocaine available as 0.5, 1.0, 2.0, (5.0) % dose 3 mg/kg (or 7mg/kg with adrenaline) metabolised in the liver t 1/2 = 1.5 hours (this is increased in people with heart failure/liver disease)
bupivacane available as 0.25, 0.5, 0.75 % dose 2 mg/kg t 1/2 = 3 hours
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