UNCOOL (updated on 29th January)

This post is a doozy, you will need to get your noodle into high gear as we will be delving into 4 publications on or related to the subject of NDEs during HCA (hypothermic circulatory arrest). Before we start, can I ask you a small favour. This blog costs money to create, and time to write. If you have been coming here for a while and enjoy reading what I write, then I would be grateful if you “bought me a coffee” (if you are rich, you can buy more than 1!). This site is trustworthy and used by media creators around the world to get appreciation for creators like me. You will need a credit card, provide the number, expiry, CVV number AND your zip code – the details are not passed on to me or held on the Buymeacoffee site (BTW it’s easy to forget the ZIP code which tripped me up when I tried it out for the first time today, you need to scroll across the details box). If I get lots of support it may motivate me to write more!

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Now to the blog. So this is not a great news blog for those longing for that illusive scientifically verified OBE, and may be bad news for Parnia’s HCA study, but there is a caveat with that.

So to the first paper (big shout out to Constiproute for alerting me to this one – how did I miss it!!):

Does Hypothermic Circulatory Arrest for Aortic Surgery Trigger Near-Death Experience? Incidence of Near-Death Experiences after Aortic Surgeries Performed under Hypothermic Circulatory Arrest

Ref: Manduit et al; Aorta (Stamford). 2021 Apr; 9(2):76-82. doi: 10.1055/s-0041-1725091

Brief summary of design, methods and results:

Design: It was a prospective study looking at consecutive patients who underwent thoracic aortic surgery between July 2018 and September 2019. Procedures without HCA were included to constitute a control group. The primary outcome was the incidence of NDE assessed with the Greyson NDE scale during the immediate postoperative course, via a standardized interview.

Results: None of the patients reported any recollection from their period of unconsciousness. There was no NDE experiencer in the study cohort.

This makes AWARE II look like a resounding success! The authors sound slightly bitter in their summary of the results, as far is it possible to sound bitter in a clinical study publication.

Firstly let’s get into the weeds. This is a well designed prospective controlled study which makes it a very credible study.

The procedure basically requires cooling the body to 21-28^oC by using a bypass technique that cools the blood, and once this temperature is achieved circulation is halted. At this temp many of the metabolic processes that occur within cells are slowed to the extent that damage will not occur, particular to brain tissue. However, after 30 minutes things may get more dangerous and another technique is initiated that restores flow of fluid to the brain. Here are the numbers recruited.:

Overall ( n  = 101)		HCA group ( n  = 67)		Control group ( n  = 34)

All patients survived, and while it is not stated (something the editors or reviewers should have picked up) I assume that all were interviewed. Given data from previous NDE studies looking at CA survivors, you would expect about 6 reports of NDEs from the HCA group given that they were in circulatory arrest. However there were none.

In the lengthy discussion section a number of factors were listed as potential confounders which might have caused this lack of NDEs. Here they are verbatim:

• The hypnotic agents and analgesics used during general anesthesia may induce retrograde amnesia, or merely prevent NDE, although some NDE during anesthesia have previously been described. 
• The potential influence of modified neurotransmitter release and systemic inflammatory response induced by the CPB, along with the varying degrees of ischemia/reperfusion during aortic surgery, should also be taken into consideration. 
• The duration of unconsciousness in our study (14.4 hours on average), inherent to the prolonged general anesthesia, might prevent the patient from remembering NDE events. Furthermore, the time between awakening from anesthesia and the patient’s interviews might have been too long.
• The number of patients included in our study might also be too limited to evidence NDE, although the incidence rates reported among cardiac arrest survivors suggest that such cohort size should be adequate.
• The level of hypothermia and the optional use of adjunctive cerebral perfusion during circulatory arrest might also play a crucial part. 

The first 4 are self explanatory. The issue of being under sedation prior to CA is something that I think is potentially relevant. Does the consiousness need to be consious when CA occurs for an NDE to occur? Not convinced personally since I can recall of NDEs that have been reported when patients were under anesthesia, had a CA during a procedure and consiousness started at that point with the NDE ensuing. Moreover we have the cases from the HCA study in Montreal (the original COOL study) led by Mario Beauregard. I will return to that in a moment.

It is the fifth point that interests me and two papers that are cited in the section of the discussion that delves into this.

Electroencephalography During Hemiarch Replacement With Moderate Hypothermic Circulatory Arrest by Keenan et al in 2016

and

Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials by Stecker et al in 2001

To summarize the key points, with the application of cerebral perfusion (used in both studies), the EEG does not in general become silent until the body has reached a temperature of 16^oC. Below about 24^oC it goes into burst suppression, during which consiousness is not possible. This is the status usually encountered during anesthesia.

In summary there are 3 states and outcomes to consider:

1. Temp >16^oC no circulation (artificial or natural) = isoelectric EEG or clinical brain death in under a minute.
2. Temp >16^oC with some kind of circulation, either natural or artificial = EEG activity of some kind.
3. Temp <16^oC with or without circulation = no EEG activity and clinical brain death.

Now I will discuss the Beauregard study from Montreal. The details were published in a journal as a letter which does not require peer review. It was more hypothesis generating than anything, and was supposed to be the launch pad for a larger scale prospective study, but it never happened. Anyway, here is a link to the letter:

Conscious mental activity during a deep hypothermic cardiocirculatory arrest? Beauregard et al 2011

In summary, it was a retrospective study looking at cases between 2005-2010 in which 33 patients underwent DHCA ( deep hypothermnic circulatory arrest), and were interviewed afterwards. 3 reported consious recollections, and one had an OBE, the details of which were later confirmed to be accurate. Given it was retrospective and in such a small cohort, the evidence is a little sketchy (unless you add it to the mountain of other evidence), however this is what has inspired further study. So there is one huge question to ask, why did Beauregard’s study have NDEs and Manduit’s not?

It is noteworthy that when looking at Keenan’s paper, the methods for HCA appeared to change around 2010-2013, with cooling often going to 21-28^oC, whereas during DHCA conducted prior to 2010, it appears the body may have been cooled to 16^oC or lower.

This may be the key difference between Beauregard’s (recruited 2005-2010) study and Manduit’s (recruited 2018-2019). However, given that in Manduit’s study only 31% of patients had ancilliary cerebral perfusion, therefore 69% would have had isolectric EEG (although they did not measure this), I am not sure this would make any difference in terms of potential for NDEs.

However, this is potentially hypothesis generating regarding the interation between consiousness and the brain in a dualist understanding of our existence, and which I will delve into during the discussion or in another post because I think this is enough for now.

Finally, this has implications for Parnia’s HCA study. Is he using DHCA cooling to 16^oC, or MHCA (moderate HCA) and only going to 21-28^oC. Is there cerebral perfusion? The answers could effect the outcome.

Wow, my brain is overheating – definitely not 16 or even 21-28^oC…it is smoking!

Please review the papers yourselves and see if I am adding 2 and 2 and getting 762, but I think I may be right on this.

Finally, surely after that, you want to buy me a coffee

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