General Anaesthetics Flashcards
What are the 6 stages of typical general anaesthetic?
- premedication
- induction
- muscle relaxation and intubation
- maintenance of anaesthesia
- analgesia
- reversal
what are the 4 clinical stages of anaesthesia using inhalational anaesthetics?
stage I - analgesia
stage II - excitation
stage III - surgical anaesthesia
stage IV - medullary depression
name 3 drugs that enhance activity at GABAa receptors
etodimate, propofol, thiopental
name 3 effects of etodimate, propofol, thiopental
potent amnesics
potent sedatives
weak muscle relaxants
what receptors do nitrous oxide and ketamine work on
inhibit glutamate NMDA receptors. inhibit ACh nicotinic receptors, open two-pore K+ channels
what are the actions of nitrous oxide and ketamine?
potent analgesics,
weak sedatives,
weak muscle relaxants
what receptors do sevoflurane, isoflurane and desflurane work on?
enhance activity at GABAa, enhance activity at glycine receptors, inhibit glutamate NMDA receptors inhibit ACh nicotinic receptors, open two-pore K+ channels
what are the actions of sevoflurane, isoflurane, desflurane
potent amnesics,
potent sedatives,
potent muscle relaxants
name 4 factors that affect inhalation anaesthetics
- 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 minimum alveolar concentration a measure of?
potency
what is blood:gas partition coefficient a measure of?
the solubility in the blood.
what is the blood:gas partition coefficient used for?
determines the rate of induction and revocery of inhalational anaesthesia
what does a low blood:gas partition coefficient mean in terms of induction and recovery
faster induction and recovery
what does the Meyer-Overton correlation show in terms of the oil:gas partition coefficient?
it shows that the potency of an anaesthetic can be predicted from its lipid solubility
nitrous oxide is not sufficiently potent to be used alone so why is it used?
in a combination of drugs to allow a reduction in dosage.
used for maintenance aneasthesia.
used in sub-anaesthetic concentrations for analgesia - eg. entonox (50:50 mixture wth O2)
what makes up entonox?
50:50 mixture of nitrous oxide and oxygen
what is the major route of elimination of inhalational anaesthetics?
via the airways in expired air
name 4 factors that influence elimination rate of inhalation anaesthetics
- ventilation rate
- blood:gas partition coefficient
- duration of inhalation
- extent of tissue equilibration
name 4 unwanted cardiovascular effects of inhalational anaesthetics
myocardial depression,
vasodilatation,
hypotension,
bradycardia/reflex tachycardia
name 2 unwanted CNS effects of inhalational anaesthetics
increase cerebral blood flow and ICP,
decreased cerebral vascular resistance
name 2 general unwanted effects of inhalational anaesthetics
postoperative nausea and vomiting (PONV), malignant hyperthermia (rare)
what stage of anaesthesia are IV anaesthetics used for?
rapid induction
name 4 examples of IV anaesthetics
- etomidate
- ketamine
- propofol
- thiopental
where does metabolism of thiopental occur?
liver
why can propofol be used as a continuous infusion for total IV anaesthesia or for sedation of adults in ICU/
because it does not accumulate
what order kinetics is propofol metabolised by?
first order kinetics
what order kinetics is thiopental metabolised by?
zero-order kinetics
what is the benefit of using propofol over thiopental as an induction agent?
more rapid recovery and less hangover effect.
what patients might etomidate be preferred to be used for rapid induction?
pts who are in shock as it is believed to have less effects on the CVS
why can etomidate not be used as a continuous infusion?
toxicity on adrenals and adrenocortical suppression
what is the MOA of ketamine?
blocks activation of NMDA receptor
what is meant by the ‘dissociative anaesthesia’ produced by ketamine?
where there is marked sensory loss and analgesia, as well as amnesia, without complete loss of consciousness.
why is ketamine useful for accident and emergency situations or low-technology healthcare situations?
IM administration is possible and it does not reduce BP or HR.
neuromuscular blocking drugs block transmission through the neuromuscular junction at what receptors?
nicotinic receptors
what is the role of neuromuscular blockadge?
decreases skeletal muscle tone
name a non-depolarising neuromuscular blockade agent (6)
prototype = curare, atracurium, cisatracurium, mivacurium, pancuronium, rocuronium, vercuronium
name a depolarising neuromuscular blockade drug
prototype = succinylcholine,
suxamethonium
name 3 uses of neuromuscular blockers
endotracheal intubation,
surgical procedures,
Intensive care
how does suxamethonium need to be given?
IV - as it does not cross blood brain barrier
what is the onset and duration of action of suxamethonium
onset of aciton within 1min.
duration of action 3-12mins
why do you get muscle fasciculation with suxamethonium?
because you initially get depolarisation of motor endplates prior to blockade
you need to be aware of a genetic deficiency of what that occurs in about 1 in 2000-3000 individuals that results in a very prolonged paralysis in pts given suxamethonium
pseudocholinesterase deficiency
what can reverse non-depolarising agent neuromusclar block?
anticholinesterases e.g. neostigmine
when reversing non-depolarising blockers with an anticholinesterase (e.g. neostigmine), what is given immediately before and why?
anti-muscarinic (e.g. atropine or glycopyrrolate) to prevent bradycardia or excessive salivation
what opiates can be used as analgesia adjuncts
fentanyl, alfentanyl
