Characteristic bold claim from Marc .

C-19 has encouaged me to use Thio again, with the benefit of pEEG (and a bit of geekiness) I thought I'd have a look at this.

This might be an interesting thread or turn into a new induction technique by itself. https://twitter.com/quartered_onion/status/1260129838758801408

Given a potential shortage of Propofol and Roc, I’ve reverted back to volatile anaesthesia. Hopefully temporarily. Fewer planes in the sky will offset my increased carbon footprint . Maintaining skills is good. TST here we come…!

I do like a bit of pEEG for all my anaesthetics. Odd that we routinely monitor every surrogate of anaesthetic effect - but not the target organ of our core drugs. I wonder if we're unique in that regard. We’ve been evaluating the #narcotrend so consumables are pennies (No COI).

So, with that in mind, what does a TST RSI look like? (with a bit of Alf - I’m a big boy now…). This is reflects experience so far.

This this the awake EEG. Lovely fine, low amplitude B-waves. Correctly classified Stage A whilst preoxygenating
Don't look at the rest yet…

Around 50 seconds post Alf 1mg, a pre-calculated "sleep*” dose (475mg) STP and 150mg sux.

Lovely big delta waves and some theta. This is consistent with unconsciousness. pEEG classified as D2 - seems appropirate. Young patient so Burst Supp. less likely.

[sleep ≠ anaesthesia!]

Straight forward Glidescope DVM intubation - no strong left arm needed! ETCO2 and onto Sevo (start at 8%). Look at the Beta - arousal! EEG now showing loss of delta activity, and increased beta. This is sedation - not anaesthesia! Seen this several times with STP... why?

Now; cortical arousal doesn't indicate AAGA per se. There's suggestion that new memory formation takes >30 seconds of “conciousness". Dutton et al did some brave work - try getting this through ethics now…

Even positive isolated forearm doesn't equate to consciousness... but it’s clear that movement is a valuable warning of an inadequate anaesthetic state. From Jamie Sleigh:

Musings to continue when the kids are asleep! (Physiological sleep rather than pharmacological!)

The process of induction requires a brain state change from awake - overcoming neural inertia - to anaesthetised (dynamically related to the stimulus applied to the patient. It's often forgotten that intubation is the most stimulating thing…

…yet less noxious stimuli are clinically acceptable end-points for LoC (mOAA/S - below) although papers choose inconsistant points. (define "mild prodding”…)

Back to Thio and cortical arousal… you'd think this would be a keenly researched area. I'm always mindful that there is always a bigger geek :) One has to look back in time a little.

20 patients; equipotent induction dose of Thio http://6mg.kg  vs Prop http://3mg.kg  - 50% N2O / Vec http://0.2mg.kg . EEG recording, intubation at 3 mins post induction; thick line is Thio…

Sustained rise in beta oscillations and drop in delta - that's beta arousal! Up to 1000% and sustained to minute 5. Just like I saw in the relative band frequency pics!

Why… . It's down to nociception (we know propofol has an analgesic effect…). Anaesthesia is a triad after all - the classic opiate-free RSI would be a beta-arousal nightmare @Rollo002 can you see where this is heading...

NAP5 noted an increased incidence of AAGA in RSI with STP - 8.21 RSI over represented… 8.22 "more 2/3rds of patients received opioids during RSI, but of AAGA cases involving RSI, only 1/3 received opioids.”

STP's lack of anti-nociception creates cortical beta arousal apparent on EEG; withholding opioids likely exacerbates this (what does it do for ICP/CBF…?). Does anyone still teach the "classic RSI”?

Sie et al used the BIS and showed the same thing - sustained rise with STP (lots of beta oscillations trigger the BetaRatio algorithm and generate values >60).

Especiallly for @rollo and @dmlevy - an Obs twist. Superb work from Park et al, who have a digital anaesthetic system which records everything… :) LSCS under GA with thio vs propofol - the pEEG gap is visible (cortical arousal again!) https://www.nature.com/articles/s41598-020-62999-5

And if you like a DSA trace (and who doesn’t…?) if there’s more sea than sky the brain is aroused… (electrophysiologically speaking!)

And all that is going on BEFORE the vapour has reached a useful ET concentration (which is a myth to bust another day!). So “The Gap" isn't just induction agent effect decay and rise in ETAA, but (with STP) all that AND cortical arousal!

So I'm not sure I agree with @quartered_onion this time - STP is not a superior induction agent; creating conditions of cortical arousal and a electrophysiological gap which relies on ETAA equilibrium to fill (slower than you'd like when watch the EEG!)

What is the solution…?

via continuous target controlled infusion with pEEG monitoring ;) Which you'd guess I'd say.

Hope that was of some vague interest. C-19 has given many challenges to many people in many ways and we've all changed the way we do things. I've enjoyed questioning what I've noticed so far with this (temporary) change in part of our practice -life long learning!