The EACTAIC Education Committee has organised the seminar episode in collaboration with the OLV Aalst – Belgium.
The OLV Aalst – Belgium supported this seminar episode.
What’s in it for me?
After participating in this webinar, you will better understand:
that processed EEG is much more than an indexed value.
the spectrograms associated with intravenous and volatile based anesthesia.
how to adjust the anesthetic management based on processed EEG.
to identify the key elements of processed EEG associated with postoperative outcome.
and appreciate the complementary use of cerebral oximetry and processed EEG.
the complementary role of the newer oximetry modalities in the diagnosis of brain desaturation.
how to develop an approach in the presence of abnormal cerebral oximetry and processed EEG.
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IMPORTANT: If you do not receive your link 48 hours after the registration, please contact eactaic@iameetings.sg Registrations will be accepted until 17.25 of the 7th of November. All the registrations sent after that time, will not be accepted.
Talk: The Take the Home Message and Closing Speaker: Stefaan Bouchez, Aalst, Belgium, Mohamed El Tahan, Mansoura, Egypt https://youtu.be/sruWjwi4cAs
Brown: We don't have adequate information from clinical trials yet. Clinical trials are one thing, the science behind is another. There's tremendous information from the EEG which can guide anesthetic management in terms of improved outcome. We need to continue to use EEG to refine our anesthetic management. As EEG doesn't tell you everything about the brain,therefore the complementary use of oximetry is recommended. Denault: Will be hard to find a monitor that changes mortality. However both burst supression that occur in up to 30% of our patients and rarely awareness is definitively an objective. Reducing costs of anesthesia by avoiding excessive Rx and their side effect is also a consequence of pEEG monitoring
I agree. When you look at the EEG you'll be able to find that spike rates are turned off while with ketamine, the spike rates ressemble the awake state. Looking at the EEG of ketamine, you'll be able to detetct an alteration in spake rate pattern. This cannot be appreciated in the value of the depth of anesthesia number. So do not solely rely on the index value but learn to use the EEG.
First, I do not like the term 'depth of anesthesia'. We need to talk of unconsciousness in stead of DOA. When looking at the median frequencies when using ketamine, you'll notice a repettiive increase and decrease in these frequencies. This doesn't mean that the patient is waking up but this reflects the intrinsic (frequency) pattern of ketamine. We have to learn how these patterns relate to the drugs we're using.
Eventuelly but lets start with something simple
Retrospective study before and after, at that point we did not have any algorythm except reducing anesthesia when burst supression was present
Eventuelly but lets start with something simple
Difficult to use NIRS as a stroke monitor because the monitored region is so small. However in carotid endarterectomy, the loss or significant reduction of a signal is higly suggestive of future stroke if uncorrected
We stop. Antegrade perfusion goal it to provide perfusion to the brain but when there is no electrical activity and burst supression, what would be the end point of anesthesia?
yes. Try to rely on the the measurement of the EEG.
yes, both anesthetics as analgesics.
Very useful to detect abnormal perfusion and also to monitor emboli
Up to 34°C, you'll notice an increase in the depth of anesthesie with lower values of DOA. You can try to avoid burst suppression by lowering the anesthetics. Don't be afraid to do so as you're measuring the effect. In very old and fragile patients, often burst suppression does occur more often. Also here you can decrease anesthetic depth even further. Make sure indeed that the indices of oxygen delivery remain normal as you've stated as burst suppression may occur in states of poor oxygen delivery and severe hypotension. There's no lower limet of anesthetic depth. Each patient is different and depending on age you'll find dfiiferent values. In this setting the use of the sepctrogram can be valuable. Denault: As temperature go domn, burst suppression will appear. As long as brain saturation remain normal, it means that it is well tolerated.
We don't have experience with TCD but I'm sure this has a value in experienced hands. Useful to detect embili and/or changes in perfusion. The latter for example may lead to altered managemend of flow and pressure during CPB. FYI a recent case report where they've used a robot TCD. https://issuu.com/bibapublishing/docs/vn_novasignal_a4_advertorial_1.6
Maybe this would introduce a new era of neuromonitoring but on this moment, we need to encourage people to use the current technology and even more important, teach them. Neuromonitoring should become standard in cardiovascular anesthesia like other ASA monitoring. I think you mention a good point but at this time, this will be too early. Just as a notice: know that the alpha waves seen during anesthesia at the front, are present occipital just before the induction of anesthesia. The alpha wave travels from the back to the front and vice versa during emergence. So the EEG is not the same in every region...so indeed a huge learning curve will be needed.
