Anaesthetics Flashcards
Name the inhalational and IV agents
Inhalational:
- nitrous oxide
- isoflurane
- (desflurane)
- (sevoflurane)
IV
- propofol
- ketamine
What are the effects of anaesthesia?
Sedation up to unconsciousness Amnesia Muscular relaxation Reflex suppression and immobilisation Anxiolysis Analgesia
How does general anaesthesia work (generally)
Reversible inhibit sensory. motor and sympathetic nerve transmission in the CNS to produce unconsciousness and absence of sensation
Which parts mediate the different effects of anaesthesia?
Immobilisation - spinal cord
Inhalation anaesthetics work at
- the thalamus - unconsiousness
- the hippocampus - amnesia
What is important to predict potency?
Lipid solubility - affects their ability to dissolve and enter cell membranes
What is potency?
The concentration of a drug needed to attain 50% of it’s maximal effect
What are the two main excitatory and inhibitory neurones needed in consciousness
Excitatory: glutamate
Inhibitory: GABA
Mechanism of action of propofol?
Agonises GABA, increases the sensitivity
This increases Cl- influx, hyperpolarising the neurone, decreasing its excitability
Stops depolarisations that would cause pain and increased consciouness etc.
What are the effects of propofol?
Potentiating GABA causes
- anxiolysis
- sedation
- anaesthesia
What is the effect of potentiating glycine (inhibitory neurotransmitter)
Signalling inhibitory neurotransmission in the spinal cord and brainstem
Reduces response to noxious stimuli
What is the effect of inhalational anaesthetics binding to and inhibiting nicotinic ACh receptors?
No Na+ influx
Less depolarisation so less excitation
-analgesia and amnesia (not sedation)
Which neurotransmitter acts on NMDA receptors?
Glutamate
Which anaesthetics exert their effects on NMDA receptors?
Nitorus oxide
Ketamine
What do nitrous oxide and ketamine do at NMDA receptors?
They bind to NMDA LGIC receptors to reduce Ca2+ influx
Less excitation
Which are the only anaesthetics not to potentiate GABA?
Xenon
Nitrous oxide
Ketamine
What are inhaled agents combined with before being inhaled?
Oxygen, air and often nitrous oxide
What is the definition of MAC?
Minimum alveolar concentration
-the percentage of inhaled anaesthetic that abolishes response to surgical incision in 50% of patients
What does it mean if an inhaled agent has a low MAC?
It is more potent - MAC relates to its lipid solubilty
What are standard MAC doses given to patients?
1.2-1.5
What can reduce the MAC?
When a drug is given in combination with other agents such as nitrous oxide or fentanyl (opiate)
What is the blood-gas co-efficient?
The degree of absorption across the alveoli into the blood - this has a direct effect on the concentration of drug that reaches target sites in the CNS
Describes the volume of gas in litres that can dissolve in 1L of blood
What does it mean if a drug has a high blood gas co-efficient?
The more readily it will enter the blood
What does distribution of anaesthetics depend on?
The relative blood supply to each organ or tissue
The specific tissue uptake capacity for the anaesthetic
What does the tissue-blood partition co-efficient determine?
How readily the anaesthetic will move from the blood to a specific tissue type
How are inhaled agents eliminated?
As conc in the blood drops, the anaesthetic moves out of the cell membranes, into venous blood, back to alveolus to be eliminated unchanged
Eliminated from well-perfused tissues first (brain, kidneys), then muscle, then fat
Fat and muscle can be large reservoirs, and as it diffuses out of these compartments, can enter the CNS, affecting consciousness
What is the duration of recovery from inhaled agents proportional to?
Length of procedure
Degree of loading of muscle and fat compartments
Why are IV anaesthetics combined with inhaled ones?
Reduces time taken to reach anaesthetic depth sufficient for surgery
Bypasses the excitement/aggression of stage II
Protein binding of inhaled and IV agents?
Inhaled - low
IV - high (98%)
Distribution of IV agents?
Rapidly to the CNS (well perfused)
Drug redistributes throughout the circulation into muscle and fat - large capacity for lipophilic drugs
Metabolism and elimination of IV agents (propofol)
Hepatic and extra-hepatic conjugation
Half-life around 2 hours
ADRs of general anaesthesia?
Post-operative nausea and vomiting (opioids)
CVS - hypotension
Post-operative cognitive dysfunction - increases with age
Chest infection
ADRs of local anaesthetics?
Can block heart depolarisation
Anaphylaxis
Uses of benzodiazepines in general anaesthesia?
Low dose a few hours before surgery - anxiolytic
High dose - sedation for short procedures
Uses of propofol?
Rapid IV induction of anaesthesia
Uses of nitrous oxide?
Contributes to analgesia via NMDA receptors
Reduces the effective MAC of flurane
Minimises recovery time
Uses of opiates (and which ones) in anaesthetics?
Morphine and fentanyl
Produce analgesia
Fentanyl more potent than morphine
Induces analgesia almost immediately
Finer control of analgesic effect in surgery
Reduce MAC
Reduce risk of CVS depression by flurane
What are the two classes of drugs that abolish reflexes and induce muscle relaxation?
Competitive nicotinic ACh receptor antagonists
- tubocurarine
- pancuronium
Nicotinic ACh receptor depolarising agonists
-succinylcholine
Flurane also potentiates neuromuscular relaxation
What are the different depths of anaesthesia?
1: Analgesia - due to effects on spinothalamic tract
2: Excitement - delirium and aggressive behaviour, now uncommon due to propofol
3: Surgical anaesthesia - CNS depression, muscles relaxed
4: Death - due to medullary depression leading resp and cardiac arrest
