Flashcards in 8.2 Anaesthetics Deck (30):
What are the types of anaesthetics?
What are the types of general anaethetics?
Examples of volatiles?
How do volatiles work?
A gas is passed over a filament where the volatile is turned into its gaseous form and breathed in via a ventilator
Advantages to Volatiles?
Easily turned on/off
Add a MAC sparing gas to reduce side effects
How do you measure the potency of volatiles?
Minimum Alveolar Concentration required for 50% of patients to be anaesthatised at that concentration (no response to surgical stimuli)
At equilibrium, it is equal to the spinal cord concentration, therefore CNS
Predicted by lipid solubility --> how well they can cross a membrane
What are the stages of anaesthetising a patient?
1) Give them a relaxing agent - premedicate
3) Maintain state - muscle relaxant, analgesia (opioid)
4) Recovery - undo state, give analgesia
Stages of Falling Under Anaesthesia... (4)
3) Surgical Anaethesia
4) Respiratory Paralysis
How do anaesthetics act on the CNS?
Where does it act?
Analgesia - dorsal horn
Muscle Relaxant - SC
Depress Reflexes - SC
Hypnosis - thalamus and the RAS
Resp/CVS Depression - Brainstem
(Amnesia - Hippocampus)
What increases MAC?
What decreases MAC?
What affects Volatiles' Pharmacokinetics?
A: MAC and Blood:Gas Coefficient
D: Organ perfusion, Tissue Uptake Capacity
E: Blood:Gas Coefficient, Oil:Gas Coefficient
What are some IV general anaesthetics?
When do you use IV general anaesthetics?
For induction or can do for whole operation (TIVA)
Bypasses the excitation stage of falling under
Pharmacokinetics ADME of IV General Anaesthetics?
A: Rapidly to CNS
D: Rapidly redistributed to tissues with higher capacity for Lipophilic drugs,
D/M: Protein Bound
E: Hepatic and Renal Conjugation
How do you measure potency of IV?
The plasma concentration to get to a certain endpoint, e.g. no eyelash reflex
Normally you switch to volatiles at this point
How do anaethetics work? Targets...
Inhibit excitatory neurones: Glutamate
Excite Inhibitory neurones: GABA and Glycine
How does it affect GABA and Glycine Receptors?
What do they normally do?
What effect do they have of pharmacodynamics?
Positive Allosteric Regulation
Bind externally to Cl- pore
Increases sensitivity to GABA, so increases Cl intracellularly to hyperpolarise, sends fewer signals
They increase efficacy and potency
Which anaesthetics act on GABA?
All of them except Ketamine, N2O, Xenon
Which excitatory neurones are effected?
By which anaesthetics?
NMDA and nACh receptors
Non competitive allosteric antagonist (decrease efficacy but not potency/affinity)
NMDA- Inhibit them to glutamate, decrease the Ca2+ current
nACh - decrease Na+ currents
nACh- contributes to analgesia/amnesia but not sedation
Ketamine and N20
When do we use local anaesthetics?
Chronic Pain Management
What is the difference between local and regional anaesthetics?
Local - used against specific peripheral nerves to give a specific loss of sensation
Regional - "block" used to prevent pain signals to a specific organ/limb, uses a local anaethetic and an opioid
What are some local anaesthetics?
How do local anasthetics work?
Reduce Na+ channels to prevent nerve transmission
so prefers small myelinated nerves
Use-dependent, block the active pain signalling molecules
Properties of Local anaesthetics?
Ring and amine structure
Bound by amide or ester bond (ester shorter t1/2)
What can you use to prolong local anaethesia?
General ADRs of Anaesthetics?
Depression of Resp/CVS
Post-Op Cognitive dysfunction
An ADR of N20?
Can expand the airways and cavities which causes diffusion hypoxia
ADRs of Local Anaesthetics?
Due to systemic spread