May 08 2008
MIRACLE MAX: See, there’s a big difference between mostly dead, and all dead. Now, mostly dead: he’s slightly alive. All dead, well, with all dead, there’s usually only one thing that you can do.
INIGO: What’s that?
MIRACLE MAX: Go through his clothes and look for loose change.
— The Princess Bride
Can you trust anyone when they purport to tell you what the medical literature says? No. As an example we will use the issue of near death experiences, or NDE’s.
We will avoid the obvious paradox in this entry, sort of the ‘everything I say is a lie paradox’ that will cause computers in the Federation to shut down.
Why am I going to comment on this issue? Well, this months Skeptic has a back and forth between Michael Shermer and Deepak Chopra about life after death.
No. I am not going to comment on whether there is life after death. I am more interested in life during life, thank you very much. I’ll let the afterlife take care of itself.
But in their point counterpoint, they both refer to a Lancet article about NDE’s and it then begs the question:
Does anyone actually read or understand the literature they quote ?
This is a small point, but I went and read, really read, the December 1 Lancet, “Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands.” You can read it too, if you want to follow along at home.
I read the article with the bias of a practicing physician who spends all his time in an acute care hospital and has been involved with many cardiac arrests over the years. I haven’t caused them, by the way, I have just helped out with their care in one way or the other.
Both sides in this article say the patients were dead, or nearly dead. Or close enough for an organ harvest. Read the paper. I don’t think so.
In the article they “defined clinical death as a period of unconsciousness caused by insufficient blood supply to the brain because of inadequate blood circulation, breathing, or both. If, in this situation, CPR is not started within 5–10 min, irreparable damage is done to the brain and the patient will die.”
Every patient in this study had CPR; most within 10 minutes of their arrest. Everyone had blood delivered to their brain. That is the point of CPR: to provide sufficient blood to the brain and other organs.
It is, as an aside, why the conclusion of the study in the discussion is flawed “If purely physiological factors resulting from cerebral anoxia caused NDE, most of our patients should have had this experience.” Good CPR does not lead to cerebral anoxia Most patients in this study did not have an NDE because they had CPR, so they had blood and oxygen delivered to the brain so they could not have an anoxia mediated NDE.
So the real question is whether patients who had brain anoxia had an NDE, and there is no way to determine that in this paper. CPR by its self is not a good surrogate for cerebral anoxia.
Having a cardiac arrest and being promptly coded does not mean there is insufficient blood and oxygen being supplied to the brain.
CPR has variable efficacy, depending on the both the patient and the experience of the provider. Most of us who have had to be involved with a code know, for example, the horrible sensation of all the ribs cracking when you start CPR on a frail old lady and knowing that the CPR is probably not going to be effective.
AS a result of variable CPR, the time it takes the brain to become anoxic is variable. And you would be surprised at how little oxygen people can tolerate with no discernible dysfunction in their cognition, although you might not want them flying your 747. People come into the hospital all the time with with the amount of oxygen in their blood decreased by 30,40, 50% and can walk and talk.
The point is that during a resuscitated cardiac arrest the ability of the brain to get oxygen can be quite variable and if the CPR is done effectively, the brain gets enough oxygen that it is not damaged.
By the definitions of the paper, nobody experienced clinical death. No doctor would ever declare a patient in the middle of a code 99 dead, much less brain dead.
Picky picky, I know, but having your heart stop for 2 to 10 minutes and being promptly resuscitated doesn’t make you “clinically dead”. It only means your heart isn’t beating and you may not be consciousness. Although the discussion states they were”clinically dead”, it takes a lot more than a short course of no heart beat to be dead in this this day and age. But it sure sounds impressive. So when Dr. Shermer quotes the article as saying the patients were “clinically dead”, they weren’t. They were cardiac arrest patients who all received prompt resuscitation. They were “clinically dead” only if nothing was done to them, which is probably not going to pass the hospital ethics committee.
And that brings up the question as to when you are dead. Dying is a continuum. If your heart doesn’t beat for 15 minutes, you are a goner.
10 minutes? not so much.
5? you will be OK.
1 minute? 30 patients in the study had a deliberate cardiac arrest in the cath lab that lasted less than one minute. Were they dead?
Point is that declaring someone dead if their heart isn’t beating is not so simple and in this study you were dead if you had no pulse and were unconscious. Not a good definition. But good for making a splash.
Was Superman really dead when he was beaten to death by Doomsday? No. He met the criteria of the paper, but he came back.
How about Westley when he was cast into the pit of despair and hooked up to The Machine? Dead? I think not.
That’s the issue, they say the patients were DEAD. But they look at “Near Death” experiences. Were they mostly dead? Completely dead?
All these people had change in their pockets when they left the hospital; they were not dead.
The only case I know where someone was truly dead and mouldering in their grave and came back with a good description of a NDE, or in this case a DE, was Buffy Summers.
But I digress.
The other way you can declare people dead is brain dead, again, not so easy to do. There are many criteria for brain death:
The patient has to have no clinical evidence of brain function by physical examination, including no response to pain and a variety of nerve reflexes that do not work: cranial nerve, pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, and no spontaneous respirations.
They have to be off all drugs that mimic brain death for several days and they cannot have metabolic conditions that mimic death. It is important to distinguish between brain death and states that mimic brain death and most of the patients received either a benzo (valium like drugs) and/or a narcotic.
It’s nice to have flat line EEG’s as well, usually two at least 24 hours apart.
And the patient has to drive 45 in the left lane of the freeway with the left turn signal on. That example is not really considered brain dead. But it should be. There are a lot of people I think I should be able to declare brain dead. But I digress. Again.
Being declared brain dead is a time consuming and detailed procedure, as it should be. This will become important in a moment.
Dr. Shermer at least quotes the paper that the patients were ‘clinically dead” using the papers own flawed definitions. But as we have seen their definition of being clinically dead is an artifice used for the paper but of no clinical or physiological relevance. Dr. Chopra, as best I can tell, just makes stuff up. He states, and the emphasis is his “when there was no measurable activity in the brain, when they were in fact brain dead.”
Nowhere, and I mean nowhere, in the Lancet article do they mention whether, besides being unconscious, neurologic function was assessed and the clinical diagnosis of brain dead was determined.
Brain dead, as we saw, is a condition not made at the time of an arrest but a diagnosis that takes time and the patient has to meet multiple criteria before being declared brain dead. They were unconscious for a short period of time after a cardiac arrest, and that is not the same as no measurable brain activity or being brain dead.
None, that’s none, zero zilch, nada, zippo, empty set, of these patients in this study were brain dead. If they had been brain dead they would have been organ donors then buried, not interviewed. They were unconscious for mostly short periods of time, a state that, if the same as being brain dead, means many college students are dead Saturday nights.
In the discussion of the paper the authors state ”Also, in cardiac arrest the EEG usually becomes flat in most cases within about 10 s from onset of syncope’
They reference an annals of internal medicine article as well as one in the journal Anesthesiology where they put EEG monitors on patients in who were having defibrilators implanted. One of the side effects of having a defibrilator placed is that your heart is often stopped for a period of time or you have a heart rhythm induced called ventricular tachycardia, that is usually fatal but can, to a small degree, perfuse the brain.
That quote is not true. I pulled the articles and read them.
What they showed was slowing, attenuation and other changes, but only a minority of patients had a flat line and it took longer than 10 seconds.
The curious thing was that even a little blood flow in some patients was enough to keep EEG’s normal
To quote the annals “Electroencephalographic changes were variable. Background slowing was usually followed by relative loss of electrocerebral activity. ”
Big difference between that and saying everyone flat lines in 10 seconds.
How long does it take to flat line? If there is zero perfusion, the best I can figure out in talking with the experts around my hospital is more like 20 seconds. That’s with NO perfusion. And the EEG experts tell me that the sensitivity of an EEG for function is more like a one megapixel camera than a 5 megapixel. The brain probably doesn’t start to die until several minutes goes by. In my state an EEG is considered so insensitive it does not have to be included as part of the criteria for determining if someone is brain dead, although we get it anyway, a flat line EEG is only part of the mix.
So there is flat line EEG that occurs acutely when the brain is not getting oxygen and there is the flat line that occurs when the brain is dead and an EEG cannot distinguish between them, only the person at the bedside can do that.
So the quote “in cardiac arrest the EEG usually becomes flat in most cases within about 10 s
from onset of syncope” by the authors of the Lancet article is not supported by the literature they reference.
So that brings up several options. 1) They cannot read. 2) They can read, but they cannot understand. 3) They can read and understand but they can’t write a coherent sentence or 4) They are deliberately making stuff up to bolster their position knowing that few will look up their references.
In medicine and in the medical literature, either you have integrity all the time in everything or everything you do is suspect. That one lie, I mean line, in the article, being so counter to the substance of the articles referenced, means to my mind that the whole article is suspect. You judge a man by the company he keeps.
Dr. Chopra’s analysis that they were flat line and brain dead suffers from the same problems as the authors of the Lancet article. It simply isn’t supported by the particulars of the literature he quotes. So in my mind, Dr. Chopra’s writing has the same options: 1) He can’t read, or doesn’t read, the literature he quotes. 2) He can read, but he cannot understand what he read. 3) He can read and understand but he can’t write a coherent sentence or 4) He are deliberately making stuff up to bolster his position.
I have not read the rest of Dr. Chopra’s oeuvre, so I do not have the information at hand to be able to distinguish which of the above options represents his modus operandi.
Both authors quoted the article correctly as to number of NDE. It depended on how an NDE was defined, hence saying 12% (Shermer) or 18% (Chopra) of patients had an NDE is correct. It depends on how many criteria you include as part of your NDE as an NDE is defined two different ways in the paper,
Also, if you read the discussion, you will find that the authors suspect a selection bias in their study and offer a ‘real’ rate of 10% for NDE, or only 5% of patients if based on the number of resuscitations, as more CPR’s lead to more NDE’s. They also admit in the discussion that their broad definition of NDE’s makes their percentage higher as it is more inclusive. It’s all in how you define NDE.
Dr. Shermer has the intellectual honesty to at least delineate which criteria he used from the study for his percentage. Dr Chopra doesn’t bother to explain why there are two different percentages of NDE in the study, choosing to present the alternative percentage as if Dr. Shermer were misquoting, rather than selectively quoting, the study.
“(The actual figure was 18%, by the way).” I love the snarky way this is said.
On his website Dr. Chopra puts MD after his name, and based on his reading and analysis of the paper, I am suspicious that the MD represents an homage to Maryland. Perhaps he has an affiliation with U of M. Go terrapins. Or has an affinity for Baltimore. I am hence forth to be known as Mark Crislip, OR as I like Oregon so much. But if MD means medical doctor, then he should know better.
If I had a medical student on service do such a sloppy analysis of a paper and make up the conclusions, they would be hard pressed to pass their rotation.
It is doubly ironic as Dr. Chopra refers to Dr. Shermer as having “slipshod reasoning” and ‘misrepresents and distorts… Rupert Sheldrake” and saying “skepticism is only credible when it is not being devious.” Holy Pots, kettles and blackness, Batman.
The only thing this article can say is who in this study population had an NDE and what constituted an NDE.
Nothing can be said as to what causes an NDE, except with the caveat that to quote from the accompanying commentary.
“The investigators report that, at the 2-year follow-up, four of 37 patients contacted to act as controls (i.e., people who had not initially reported an NDE) reported that they had had one. Although these patients represent fewer than 1% of the total sample, they represent over 10% of the 37 patients interviewed with a view to acting as controls. If this subsample is at all representative, it implies that around 30 patients from the sample of 282 who initially denied an NDE would, if they had survived for another 2 years, be claiming that they had had one. ”
Some of the NDE’s were, it seems, implanted memories.
The discussion also greatly exaggerates the conclusions that can be drawn from their data.
“We did not show that psychological, neurophysiological, or physiological factors caused these experiences after cardiac arrest.”
Of course not, as set up the study could not have any reliable data as to causation of NDE’s.
“NDE pushes at the limits of medical ideas about the range of human consciousness and the mind-brain relation.”
I do not see this conclusion from the data in this article. Upon close reading I think the only thing this paper is qualified to determine is a description of who get NDE’s and what patients report. As to etiology of NDE’s, much less mind brain relation, it can say nothing. Their reach exceeds their grasp.
I am not saying NDE don’t happen, and I am certainly not going to disagree with the idea that nearly dying is transformative. It is. It is probably why real NDE have greater effects than lab induced NDE. The knowledge that you are really truly mortal is life altering. Cancer survivors can have the same epiphany with out the cardiac arrest
The devil is in the details. As is so often the case, when you go back and read the original paper and its references, what the paper says and what the paper is purported to say often turn out to be two very different things.
In the end the point counterpoint on the NDE’s was, to my mind, done between two people who may not have really understand the literature, one honestly, the other maybe not so much.
Take home message:
Read the original literature. Remember that what a paper says and what people say it says are not the same thing.
Trust no one. But me. References follow. Now you can read them yourself. Let me know if I got it wrong.
Skeptic. Vol 13, #4. The Great Afterlife Debate. Page 52 – 57.
Electrocerebral accompaniments of syncope associated with malignant ventricular
arrhythmia’s. Ann Intern Med. 1988 Jun;108(6):791-6. PubMed ID: 3369769.
Electroencephalographic changes during brief cardiac arrest in humans. Anesthesiology1990;73:821–25. PubMed ID: 2240671.
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