L22: General Anaesthetics Flashcards
What is the triad of general anaesthesia
Need unconsciousness
Need for analgesia- pain relief
Need for muscle relaxation for loss of reflexes
what is the lipid theory of anaesthesia about
The concentration of agent required to immobilise tadpoles is inversely proportional to lipid:water partition coefficient. This means that a low concentration of GA agent is required if its lipid soluble.
How do general anaesthetic action work through
Depressing CNS activity
What is the anaesthetic concentration in the cell membrane for any agent to show an effect
0.05m
What has to happen to the volume of lipid for anaesthesia to occur
Expand by 0.4%
What is the protein theory for general anaesthetics about
Lipid solubility is required to access/target the proteins (ion channels/receptors)
What is the cut off phenomenon
As the chain length of the GA increases lipid solubility increases so potency (ability to bind to receptor) increases however after a certain length the potency stops as the size of the GA is important because it has to fit somewhere
What is steroselectivity of GA about
Potency is preserved with protein binding as GA bind to hydrophobic pockets within the cell membrane of proteins
What are the 2 main targets of ion channels/receptors for inhaled GA
- GABAa receptors
- potassium channels
When GABAa receptors are activated which neurotransmitter is released
GABAa
What type of neurotransmitter is GABAa
Inhibitory neurotransmitters
What does GABAa do to the cns
Depression
What does potassium channel activation lead to
Hyperpolarization
What does hyperpolarization lead to in the cns
Depression
What channels are inhibited with GA
Excitatory channels of:
NMDA
5HT
ACH nicotinic
Why does the CNS become depressed
Due to decrease in neurotransmitter release and transmission
What structure is suppressed that leads to unconsciousness
Reticular formation in the midbrain
Which structure is suppressed that causes analgesia
Thalamus
What structure is suppressed that causes loss of reflexes
Spinal cord
What happens at a low concentration of anaesthetics
No one can form memory
What happens with a small increase in anaesthetic concentration
Consciousness decreases
What happens with a higher concentration of anaesthesia
Loss of motor reflexes i.e movement
What happens at the highest concentration of anaesthesia
Inhibition of the cardiovascular respiratory response which can lead to death
What is the therapeutic window between suppressing movement and inhibiting the cardiovascular respiratory response like
Narrow
What are the 4 stages of anaesthesia
1) analgesia
2) delirium
3) surgical anaesthesia
4) medullary paralysis
What occurs in the analgesia stage
Drowsiness
Reflexes intact
Still concisous
Pain is still felt
What happens in the delirium stage
Excitement
Delirium
Incoherent speech
Unresponsive only to non-painful stimuli
What phase can occur during the delirium stage
Dangerous phase
What does the dangerous phase involve
Cardiac arrthymias
Vomiting
Chocking
What occurs in the surgical anaesthesia stage
Patient is:
- unresponsive to painful stimulus
- Regular breathing
- muscle relaxation
What occurs in the medically paralysis stage
Pupillary dilation
Respiration and circulation declines
EEG waves
Death
Why can the medically paralysis stage occur
Due to overdose
What are the 2 characteristic that make a good general anaesthetics
Potent
Fast acting
What is potency measured by
MAC (minimal alveolar concentration)
What is MAC
Concentration of anaesthetics in the alveoli required to produce immobility in 50% of patients when exposed to noxious stimulus
What is MAC inversely proportionate to
The lipid solubility
What does it mean if MAC is inversely proportionate to lipid solubility
If the GA has a high lipid solubility less concentration of MAC is required to produce anaesthesia
What is fast acting about
Speed of induction
Why do we want a fast acting ga
When we go through the delirium stage if a dangerous phase occurs it will allow a faster recovery
Where does GA work in the body
Brain
What are the 2 ways to increase transfer of GA to the alveoli
- Increase the anaesthetic conc in gas as you are breathing in
- increase the rate and depth of breathing as you are getting the agent into your body faster
What are the way in which you can increase the speed of induction from transfer to blood to the brain
- give a relatively blood insoluble gas so the blood saturates quickly and agent transfers to brain faster i.e a lower blood:gas partition coefficient
- higher cardiac output means faster transfer
What are the factors that can increase/decrease the speed of induction of GA from blood to tissue
- obese patients will have higher adipose tissue which has a high capacity for GA, therefore this will slow down the speed of induction
- lean tissue mass has a higher blood flow so this will allow a faster transfer
What are the 2 ways in which we can eliminate GA
- breathe it back out via the lungs
- metabolism of GA
What is a balanced anaesthesia
Using a combination of different drugs for optimal clinical effect with lowest risk
When is intravenous anaesthesia used
For short proceeds or for induction of anaesthesia so you can maintain the rest by inhalation
What receptors does intravenous anaesthesia work on
GABAa receptros
NMDA receptors antagonist
What are the 3 broad adjuvants i.e add ons to anesthesia that are used
1) pre medication
2) muscle relaxants
3) anti-emetics
What types of drugs are used as pre-medications
Benzodiazepines
Opioids
Anti muscarinics
What are benzodiazepines used for
Sedation
Reduce anxiety
Amnesia
What are opioids used for
Pain relief
What are anti muscarinics used for
Facilitate intubation and ventilation by relaxing smooth muscle
Why are muscle relaxants used
To relax deep abdominal, tracheal, diaphragm muscles without the need for deeper anaesthesia so you can use a reduced dose of GA and prevent overdose
What are the types of drugs used as muscle relaxants
Benzodiazepines
Neruomuscular blockers
Why are anti-emetics used
To decrease peri-operative nausea and vomiting
Give an example of a anti-emetic
Metocloprimide
