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Welcome back to the tasty morsels of critical care podcast.
This is a mammoth topic that listening to 5 mins of me rambling will in no way seriously prepare you to either practice clinically or write a semi coherent exam answer. That being said here we go.
In terms of reasons to sedate someone in the ICU the following would seem a reasonable selection of reasons
- as treatment for disease process (eg seizures, alcohol withdrawal)
- to facilitate tolerance of ICU therapies (eg ventilation)
- to reduce O2 consumption (eg brain injury or sepsis)
- use as palliation
In terms of assessing sedation I think most of us are beholden to the Richmond Agitation Sedation Scale. I think it’s useful to give a target as it is a moderately objective and reproducible scale but I should be honest and say I rarely prescribe it.
Oh’s manual quotes a number of potential strategies for sedation.
- goal directed (eg sedate to a RASS)
- sedate with daily interruptions
- something called analgosedation where you always target pain first, and analgesia only if needed
- patient controlled sedation (which sounds a little too close to Michael Jackson’s strategy for my liking)
In terms of agents we have a veritable cornucopia of agents to play with of which I’m just going to give you a buzz word or useful fact or two to go with each agent.
The GABA-A receptor agonists
- GABA is an inhibitory neurotransmitter. If you agonise it then you inhibit neurotransmission and the brain slows down and you get sleepy.
In terms of choices of GABA agonists we have
- Benzos
- these bind to the gamma sub unit of the GABA-A receptor
- Propofol
- this binds to the beta sub unit of the GABA-A receptor and causes a conformational change on the chloride receptor.
- there is rapid hepatic and extra hepatic conjugation and any metabolites are inactive hence its attraction as an on/off agent
- finally the lipid carrier is a source of calories that usually your dietician will remember to take into account in their assessment. Which is important cause there’s no chance I’m ever going to remember to do that.
NMDA receptor antagonist
- basically ketamine
- unique dissociative anaesthesia which I’ve previously heard described as disconnecting the thalami from the cortex thus allowing some kind of consciousness without awareness of many of the sensory inputs. This may be entirely inaccurate but conceptually I found it useful.
Major tranquilisers
- haloperidol/droperidol (butyrophenones)
- phenothiazines (chlorpromazine)
- these target a range of receptors include dopaminergic, serotonin and cholinergic
- main advantage is lack of respiratory depression and the lack of increased mortality that seems to be associated with benzo use in delirium.
Alpha 2 agonists
- clonidine and dexmetetomidine are the options here
- dex is highly selective sedation and analgesia
- can be extubated with infusion running, personally seems particularly helpful in transitioning the young male intoxicated head injured patient back to the real world.
- hypotension and brady the main concern