Anaesthesia Flashcards
(32 cards)
Give 3 examples of inhalational anaesthetic agents
Give 2 IV
Inhalational: - Nitrous oxide - Isoflurane - Sevoflurane IV: - Propofol - Ketamine
What is the general theory behind anaesthesia?
Principal anaesthetic agent plus adjuvant drugs
What is regional anaesthesia?
Affects larger regions of the body by blocking transmission between that region and the spinal cord
What is local anaesthesia?
Affects small region via peripheral nerve block
Where does general anaesthesia act in terms of anatomical locations?
- Reticular activating system
- Brainstem
- Spinal cord
List 4 molecular targets of anaesthetic agents
- GABA chloride channels
- Glycine chloride channels
- Nicotinic ACh receptors
- NMDA receptors
What is the mechanism of action of Propofol?
Binding to which other channel works exactly the same way?
Acts via GABA chloride channels - bind to channel and increase its sensitivity to GABA - in turn increases chloride currents so cell is hyperpolarised - less excitable
Glycine chloride channels
What is the theory behind targeting nicotinic ACh receptors in anaesthesia?
Inhibiting nACh receptors reduces excitatory currents - contributes to amnesia and analgesia
What is the mechanism of action of nitrous oxide and ketamine?
Bind to glutamate NMDA receptors, which reduces calcium currents and therefore reduces neurotransmission
In terms of pharmacodynamics, what is the mechanism of action of anaesthetic agents which bind to inhibitory ligand-gated channels (GABA/glycine)?
(Mention potency and efficacy)
They are positive allosteric modulators - they decrease the EC50, meaning less GABA/glycine needs to bind in order to exert the same level of effect
Therefore there is increased ligand potency and efficacy
In terms of pharmacodynamics, what is the mechanism of action of anaesthetic agents which bind to excitatory ligand-gated ion channels?
(Mention potency and efficacy)
Non-competitive allosteric antagonism -
once agent binds, receptor is inactivated. Therefore fewer receptors available for binding, so decreased efficacy.
BUT affinity for the unbound receptors is still just as high - no change in potency.
Therefore potency (i.e. EC50) is unchanged but efficacy decreases
How are the inhalational anaesthetic agents administered?
Volatile liquids at room temperature - vaporised and mixed with “carrier” of O2/air/nitrous oxide
Breathed in via mask
What is the MAC?
Minimum alveolar concentration - alveolar concentration at which 50% of patients fail to move to a surgical stimulus
How is MAC linked to potency?
The lower the MAC, the more potent the agent is -
MAC is related to lipid solubility, and the higher the lipid solubility, the more potent the anaesthetic
What is the normal MAC dose needed?
1.2 - 1.5
How could you reduce the MAC needed?
Give a MAC-sparing drug alongside the inhalational such as nitrous oxide or fentanyl
Give 4 factors that affect MAC
Age - MAC needed decreases with age
Temperature - increases with temp
Pregnancy - increases MAC needed
Other anaesthetics/sedatives/opioids - decrease MAC needed
How are inhalational agents absorbed?
Pass down concentration gradient from alveoli into bloodstream
What determines the absorption of inhalational anaesthetic agents?
Blood:gas coefficient - describes volume of gas in litres that can dissolve in 1L of blood
What does a high blood:gas coefficient signify?
Agent will enter blood more readily
What does the tissue: blood coefficient signify?
Specific uptake capacity of certain tissues for each agent - i.e. how readily anaesthetic will move from blood into that tissue
How are inhalational agents eliminated?
Basically reverse of absorption and distribution:
- Anaesthetic withdrawn slowly
- Blood conc drops so agent moves from tissues into venous blood, then removed at alveoli unchanged
Why might a patient take quite a while to recover from a GA?
Drug continues to circulate - may get reabsorbed into arterial blood when it reaches lungs
Which tissue takes longest for inhalational anaesthetics to clear from?
Fat - highly lipophilic
