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| Frage | Antworten |
| 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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