anaesthetics Flashcards
what is a general anaesthetic
act on the brain to produce a loss of sensation - small lipid soluble molecules that pass the BBB, affects synaptic transmission and neuronal excitability
what is local anaesthetics
block local nerve trunks
what is the reticular formation
complex network of neurons in the brainstem connecting to the hypothalamus, cerebellum and cerebral cortex - arouses cerebral cortex to wakefulness - inhibition causes unconsciousness
what are the 4 stages of anaesthesia
- cortical inhibition - minor procedures
- excitation/inhibition of cortical neurons - delirium and involuntary movements
- surgical anaesthesia - 4 planes - gradual loss of respiratory function and muscle tone
- overdose - resp and circulatory paralysis - death
what anaesthetics can be used at induction
ketamine
thiopental
propofol
etomidate
what are the pharmacokinetics of thiopental
areas receiving high levels of cardiac output will immediately get high levels of anaesthetic - hours after receiving the drug it is still in fatty tissue - hangover
saturation kinetics - large doses can accumulate and lead to CV/resp depression
what are the pharmacokinetics of propofol
rapid onset and rate of distribution - rapidly cleared so no hangover but hard to maintain levels
ketamine kinetics
increased BP and HR, no effect on RR
slower onset than propofol and thiopental
which inhaled anaesthetics can be used for maintenance
o Halothane
o Isoflurane
o Sevoflurane
o NO
o Desflurane
which 2 equilibrium events must occur for an inhaled anaesthetic to be effective
blood - gas
oil - gas
what is the blood - gas coefficient and how does it work
Concentration of anaesthetic in the brain mimics that in arterial blood
how do low solubility drugs affect the blood - gas coefficient
NO - low partial pressure in alveoli, slow blood absorption - eventual equilibrium
how do high solubility drugs affect the blood - gas coefficient
halothane/ether
rapid dissolution into the blood, low alveolar concentration so takes longer to equilibrate
what is the oil gas coefficient
transfer of anaesthetic between blood and tissue- majority ends up in fat so can take hours
what is halothanes oil-gas coefficient
very high - very fat soluble, more fat the patient has the slower the recovery
what two factors affect the rate of induction and recovery when using inhaled anaesthetics
- alveolar ventilation rate - greater vol of air in - faster equilibrium
- cardiac output - reduced alveolar perfusion = reduced absorption so faster induction
what is the MAC
minimal alveolar concentration required to abolish response to surgical incision in 50% of subjects
what are the three proposed targets of anaesthetic
GABAa
glutamate receptors
voltage gated sodium, potassium and calcium channels
how do anaesthetics work at GABAa receptors
enhance the effect of GABA on GABAaR
binds to hydrophobic pockets
how do anaesthetics work at glutamate receptors
decreases activity (NO- blocks channel pore )
xenon and isoflurane inhibit NMDAR by competing with glycine for its regulatory site
how do general anaesthetics work at Voltage gated sodium, potassium and calcium channels
activated by low concentrations of volatile and gaseous anaesthetic to reduce membrane excitability - no response to IV