George Floyd WAS Murdered, by Derek Chauvin and His Cohorts — Part One
Leonard R. Jaffee, Copyright © 2021, all rights reserved
A. Splitting This Article Into Two Parts
As this article neared completion, Substack’s software generated the notice that the draft bore “Unsaved Changes.” In writing an earlier piece I posted at Substack (at my Substack site), I learned:
(a) that if I post (publish) a draft at Substck when the “Unsaved Changes” notice appears, the posted (published) text will be either incomplete or wrong;
(b) that the trouble can be too many instances of boldface or italic font or too many URL hyperlinks or too many instances of use of the “Preserve whitespace” function, rather than a draft length greater than Substack permits (and apparently Substack permits very long articles, like the first article I published at Substack).
So, I spent about 13 hours on cutting back boldfaces, italics, and uses of the “Preserve whitespace” function; and I struggled to shorten the text and endnotes. My effort failed. (Once, my entire article vanished, and I was condemned to re-start from scratch.)
I perceived that I might cure the problem by splitting the article into two parts. Apparently (at this moment), the strategy has succeeded.
As this piece’s title indicates, this text and its endnotes constitute Part One. Its main thrust is examination of the question of whether George Floyd’s pre-existing condition was the “proximate cause” of his death — whether his death was not legally attributable to the neck/dorsal-thorax compression holds Chauvin and two other policemen applied to Floyd
(a) because only Floyd’s pre-existing condition explained Floyd’s death or
(b) because the police are not culpable since their compression holds alone would not have killed Floyd or they (the policemen) could not have foreseen that Floyd’s special condition rendered their (the policemen’s) compression holds lethal
This part’s (Part One’s) emphases (though not exclusive considerations) are matters of, e.g., medicine. forensic pathology, biochemistry, pharmacology, and even physics, rather than matters of law, though legal matters must necessarily inform the extralegal considerations.
Part Two’s emphasis is the law — legal rules and judicial precedents pertinent to determining the legal significancies of the conduct of George Floyd and the conduct of Derek Chauvin and his cohorts and the extralegal matters treated in this Part (Part One).
B. Why the Endnotes?
This article’s endnotes supply substantive supplementation of this article’s text — not mere citations of sources. So, the reader must read the endnotes along with the text.
Why do I not include the endnotes’ material directly in the text? Some text passages serve as quasi-abstracts of essences of issues or factual matters the beg substantial elaboration with, e.g., minutiae of evidence or history or logic or legal reasoning or……. Rather than burden the text’s flow of essences and render the text clumsy, I provide the minutiae in endnotes. Also, I consign to endnotes matters that are a bit tangential but bear useful significance or illumination.
C. Limitation of Availability of the Record of the Prosecution and Judicial Proceedings and Testimonies Involved
Though I am a long-time law-professor and have litigated, in this instance I do not have access to the all the legal records of the George Floyd murder case. My access is little greater than that of an average non-lawyer, and far lesser than a that enjoyed by seasoned journalist employed by a newspaper, news service (like Reuters), or TV network or cable news entity.
So, often I am forced to discuss what the prosecution or defense might do or have done or what a witness (expert or nonexpert) might say or have said. Given what I have been able to learn of the lawyering of the prosecution, I perceive that a necessarily frequent, oft-critical consideration is what the prosecution might, or ought to, have done.
About 6 Months ago, I volunteered (gratis) formal, detailed. written legal/forensic-medical advice to the Minnesota Attorney General. I have not seen that his office has used very much of that advice.
A. Four Legal Principles You Must Accept to Judge The Case Legitimately
Whatever your view of the Derek Chauvin trial, you must appreciate four, intimately-related legal principles that govern the matter of whether Chauvin (and three fellow police) murdered George Floyd. You may decry one or more of the four principles. But they have been law for more than a century. And they did not become law because of racial or pro-police bias, but reflected English and American socioeconomic/legal philosophy manifested in cases where race or pro-police bias could not have been an influence. Killer and victim were White; and police were not involved.
The first principle is best-shown by a hypothetical case oft-used in law school criminal law classes: A woman leaps from the roof of a 12-floor building. As she passed by a large open window of the building’s 6th floor, a man shoots the falling woman with a shotgun, The shot kills the woman instantly. The man’s act was murder — despite one might expect that the woman would have died seconds later, when, or shortly after, her body hit the ground.
The principle is that a killing is a homicide even if an independent, supervening event might or would have killed the victim a millisecond later.
[Part One endnote 1 ]
The second principle has been dubbed the “eggshell skull” rule: A wrongdoer takes her victim as she finds him; so, if the victim is peculiarly susceptible to serious physical injury because of a special infirmity and the wrongdoer’s act would not harm the victim had the victim not suffered such infirmity, still the wrongdoer is liable for what harm the victim suffers because of the wrongdoer’s act.
The third principle is that a homicide defendant is guilty if his unlawful act was a “proximate cause” of the victim’s death. “Proximate cause” is a cause that, in a direct sequence, unbroken by a new independent, supervening cause, produces the victim’s death and without which cause the death would not have occurred. The concept “a proximate cause” does not equal “the cause” — i.e., “proximate cause” is not the only or the sole direct cause.
The fourth principle is that a wrongdoer is legally responsible for the foreseeable proximate harm of his act — for the harm that the wrongdoer ought to have foreseen if he knew, or could and ought to have known, that his action could cause the harm it produced. The here-pertinent corollary is that if the wrongdoer disregards the foreseeability of the harm her act could cause, she is legally responsible for the harm her act actually produces.
Those principles govern, at least ultimately, virtually every aspect of George Floyd murder case. Later below, this article elucidates those principles’ ingredients, origins, premises, and mechanisms of application.
Derek Chauvin’s main defense is that his conduct was not a “proximate cause” of George Floyd’s death — that Floyd’s pre-existing imminently fatal condition killed Floyd, that even if Floyd died from asphyxiation, the sole, independent cause was a lethal overdose of fentanyl and methamphetamine, the lethality of which was worsened by Floyd’s pre-existing cardiovascular disease rather than Chauvin’s pressing his knee on Floyd’s neck for more than 9 minutes, including more than 3 minutes after Floyd fell unconscious.
[Part One endnote 2 ]
For Chauvin, the fatal problem is that (as appears below) quantitatively/qualitatively overwhelming, compelling evidence indicates that Floyd’s pre-existing condition was not imminently fatal — that Floyd would have survived longer than the duration of Chauvin’s kneeling on Floyd’s neck, that even if Floyd’s pre-existing condition could have caused Floyd’s death in the very near future following the time-span during which Chauvin knelt on Floyd’s neck, still, Floyd would not have died soon as he did had Chauvin not knelt on his neck.
Worse (as appears below): Chauvin’s pre-existing-condition-defense clashes with the legal principle that the wrongdoer takes his victim as he finds him — the “eggshell skull” rule that the wrongdoer is not excused by the victim’s peculiar frailty that the wrongdoer did not anticipate or account, a frailty without which the wrongdoer’s act would not have harmed the victim as the victim was harmed, in Floyd’s case, caused death.
Worse still: Even if Chauvin’s knee-on-neck restraint might not have killed Floyd had Floyd been healthy, still Chauvin knew Floyd’s condition was relatively fragile. Therefore, Chauvin ought to have apprehended the substantial chance that the neck-restraint would kill Floyd.
Much worse: Chauvin continued to kneel on Floyd’s neck more than 3 minutes after Floyd became patently unconscious and apparently lacked pulse — so that the knee-on-neck restraint’s manifest lethality was blatantly foreseeable.
Hugely worse (as also appears below): Chauvin had notice of Floyd’s pre-existing condition and, therefore, ought to have foreseen that his (Chauvin’s) knee-on-neck restraint-hold threatened Floyd’s death.
B. Disclosure of My “Biases”
I am not Black. My body does not bear a single Black gene, not one gene peculiar to a Black “race.” My ethnicity is Magyar and Estonian.
[Part One endnote 3 ]
I dislike Black “culture” (all but some old-time ragtime and blues, which I might appreciate for about 20 minutes once in year or two). Even do I despise much of Black “culture” — like rap, hip hop, Ebonics, the sword & shield of Black “victimhood,” using foul language as excessive punctuation, the demanding and using of special, unearned advantages (e.g., of affirmative action), marring of NFL football with idiotic, sometime lewd, end-zone antics, producing children to collect welfare money, destroying inner cities with drug-”culture” and gang-warfare.......
[Part One endnote 4 ]
I oppose the Back Lives Matter movement. It manifests psychopathic enjoyment of irrational oppression and insane, causeless vengeance imposed on premise of race. Worse: it evinces contemnible, grotesque stupidity.
And George Floyd was disgusting trash, garbage. His life contributed no benefit to anyone, even to Floyd, himself; and surely he burdened many whose lives his touched.
[Part One endnote 5 ]
So, why do I write and publish this article? Two reasons:
(1) I am morally certain — beyond doubt — that two or three arresting officers murdered Mr. Floyd and a third or fourth “aided and abetted” that murder. Though Floyd was trash, the law entitled him to live — not to suffer the murderous abuse the arresting officers committed against him.
(2) If George Floyd’s murderers and their accomplice are acquitted or suffer sorely inadequate plea-bargained sentences, then (a) police will continue to feel entitled to abuse police-power and use excessive force in detaining Blacks and Whites, Asians, and others and (b) the United States will experience a nationwide bloody uprising never experienced since the Civil War.
The matter is not the lives of Blacks. The matters are: (1) the life and liberty of every person, irrespective of “race” and (2) abuse of power of “law-enforcement” agencies and of police and other “law-enforcement” officers. The second matter is but one aspect of the manifest psychopathy of most of the world’s governments, surely the federal government of the United States and most U.S. state and local governments.
[Part One endnote 6 ]
Though George Floyd was scum, he was a 5th amendment and 14th amendment human person. He was entitled to due process of law, not extrajudicial summary execution by a cop. Despite Floyd was rubbish, he did nothing that could support a court’s sentencing him to death. A rational, civil society accords due process even to the meanest, vilest of its members.
[Part One endnote 7 ]
C. My Credentials
I am a law professor — appointed assistant professor of law in 1972, tenured associate professor of law in 1976, tenured full professor of law from 1978 to 31 December 1997, professor of law emeritus since 1 January 1998.
Among the law-subjects I have taught, several relate to considerations involved in the George Floyd murder case: (a) criminal law, (b) evidence, (c) constitutional law, (d) civil procedure, (e) conflict of laws, (f) federal courts, (g) remedies, (h) law and statistics, (i) legal method, (j) jurisprudence (the philosophy of law).
I have rendered legal consultation to federal, state, and local government agencies and to numerous law firms. My law-firm consultations have addressed, inter alia, matters of criminal law, tort law, criminal procedure, evidence law, constitutional law, civil procedure (which applies to aspects of criminal procedure), statistics and law (pertinent to the medical/forensic aspect of the Floyd murder case), law and medicine, and habeas corpus and other forms of post-conviction relief (a field that requires the lawyer be expert in all fields listed above in this paragraph).
I have written published works pertinent to all the problems of the George Floyd murder case. My publications address matters of law (including, e.g., criminal law, criminal trial procedure, and rules of evidence), math, statistics, medical forensics, probability calculus, formal and mathematical logic, linguistics, and philosophy.
Since 1995, I have been a physician. I practice a form of alternative medicine that, though not allopathic, requires that I be expert in the fields necessary to competent allopathic practice. My medical knowledge is vital to my appreciation of the problems of the George Floyd murder case, because the principal defense is that a drug overdose, not the arresting police’s conduct, killed Mr. Floyd.
III. THE ASSISTANT HENNEPIN COUNTY ATTORNEYS’ INTERVIEW OF THE HENNEPIN COUNTY MEDICAL EXAMINER AND SUNDRY FORENSIC MEDICINE MATTERS
Before the Minnesota Attorney General’s Office took over the prosecution of the case, the trial judge, Peter A. Cahill, disqualified the Hennepin County attorney, Mike Freeman, and three of his Assistant County Attorneys, because of the quality of two Assistant County Attorneys’ pretrial Interview of Hennepin County Medical Examiner [hereinafter “ME”], who issued the official Report of the autopsy of George Floyd and a Press Release that stated the ME’s determination that Floyd’s death was caused by homicide.
Addressing the quality of the Assistant County Attorneys’ Interview of the ME, Judge Cahill rendered this gross understatement: “I think it [the Interview] was sloppy....”
During the Assistant County Attorneys’ Interview of the ME [hereinafter “ME Interview”], the lead interviewer was Assistant County Attorney Amy Sweasy. Ms. Sweasy made Notes of the Interview [hereinafter “ME Interview Notes” or “the Notes”]. She filed the Notes in the court. The Notes provide the defendants substantial, but illegitimate, showing of reasonable doubt. And the defense has made use of that provision.
George Floyd died 25 May 2020. One must be astounded by the Assistant County Attorneys’ interviewing the ME just six days after Mr. Floyd died, five days after the day of Mr. Floyd’s autopsy, and one day before the ME signed his Autopsy Report. I have found no evidence that either interviewing Assistant County Attorney has had any medical training. One must wonder whether the ME-interviewing Assistant County Attorneys designed to weaken the State’s case — intended to provide exculpatory evidence to the defense.
(a) Forensic Issues the ME-Interview Notes Threaten and (b) Related Prosecution Problems and Likely Defense-Ploys
A. The Notes
In the above-referenced court-filed Notes, the following text appears [the initials “AB” = Dr. Andrew Baker, ME]:
AB walked us down the list of substances for which NMS labs tested. Those values he highlighted were: 4ANPP – a precursor and metabolite of fentanyl present in Mr. Floyd's blood. Methamphetamine – 19 ng/mL which he described as “very near the low end” and “a stimulant hard on the heart.” Fentanyl – 11. He said, “that's pretty high.” This level of fentanyl can cause pulmonary edema. Mr. Floyd's lungs were 2-3x their normal weight at autopsy. That is a fatal level of fentanyl under normal circumstances. Norfentanyl – 5.6 a metabolite of fentanyl. Mr. Floyd's urine was tested for 4 things and are redundant, given the blood analysis. AB said, “the only thing that matters is what's in his blood.” AB said that if Mr. Floyd had been found dead in his home (or anywhere else) and there were no other contributing factors he would conclude that it was an overdose death.
B. Medical/Forensic Matters the Prosecution Must Attend
Norfentanyl is an inactive metabolite of fentanyl. The norfentanyl level could not have affected Floyd in any way. Its significance is only that the norfentanyl level implies the existence of some previous level of fentanyl. I have no information respecting whether the ME stated that norfentanyl is utterly inactive (as it is) or stated anything concerning the previous fentanyl level the norfentanyl level implied.
I have searched, long and rigorously, the medical, pharmaceutical, and forensic pathology literature and have found no source that suggests a time-2 norfentanyl quantity can indicate reliably, or usefully, a time-1 level of fentanyl. Fentanyl metabolizes near-exclusively in the liver and is excreted with urine and fecal matter. But liver, kidney, colon, and related endocrine and neural functions vary widely person-to-person and circumstance-to-circumstance (even within minutes, even seconds) — too widely to permit deducing previous fentanyl level from current norfentanyl level.
2. Serum Fentanyl Concentration
The Notes erred significantly with its “Fentanyl – 11” language. That language begs the question “11” what? “11” per what measure of concentration found in what of Floyd’s body — muscle tissue, lung tissue, liver tissue, urine, blood? The Notes assert that the ME said “that's pretty high” — apparently (per the Note’s seeming implication) referencing “Fentanyl – 11,” hence, creating significant ambiguity: again, “11" what?
But suppose the ME referenced the fentanyl concentration found, antemortem, in Floyd’s blood — the serum fentanyl level. That supposition consists with the a statement the Notes attribute to the ME: “the only thing that matters is what's in his blood.” Still, the language “Fentanyl – 11” begs the question “11” what — 11: ng/dL, or ng/mL, or ng/L, or......?
Yet suppose the ME intended to reference the serum fentanyl level measure indicated in the ME’s Autopsy Report. Then the measure is ng/mL, hence (per that Report) serum fentanyl 11 ng/mL.
But the Notes’ ME-attributed statement “that's pretty high” is very questionable as is the Notes’ ME-attributed (but not quoted) proposition “if Mr. Floyd had been found dead in his home (or anywhere else) and there were no other contributing factors he [the ME] would conclude that it was an overdose death.”
The ME-interviewing Assistant County Attorneys committed grave error by not challenging the ME’s propositions, an error near certainly explained by the Assistant County Attorneys’ not having researched the pertinent medical matters. Had they done the research, they might have learned that the ME at best mis-spoke if, actually, he stated (a) that “if Mr. Floyd had been found dead in his home (or anywhere else) and there were no other contributing factors he would conclude that it was an overdose death” and (b) that serum fentanyl 11 ng/mL concentration is “pretty high.” [See also infra § III.4, “George Floyd’s Serum Fentanyl Concentration and His Lungs.”]
An 11 ng/mL serum fentanyl level is not possibly a presumptive lethal level. The notes’ statement “Fentanyl – 11” is a “fatal level under normal circumstances” is medical nonsense — even if “Fentanyl – 11” equals 11 ng/mL serum fentanyl concentration.
In a study of patients admitted to a hospital partly because of medical conditions possibly caused at least partly by serum fentanyl concentrations, the studying medical experts noted the therapeutic, toxic, and lethal serum concentrations of sundry drugs found in the patients, and the experts observed:
The therapeutic (TL) and toxic (TX) serum levels…are: fentanyl TL = 1-2 ng/mL, TX = 2-20 ng/mL, lethal >20 ng/mL…. [“>20 ng/mL” means “greater than 20 ng/mL.”]
Mark E. Sutter, MD, Roy R. Gerona, PhD, M. Thais Davis, MD, Bailey M. Roche, MD, Daniel K. Colby, MD, James A. Chenoweth, MD, Axel J. Adams, BS, Kelly P. Owen, MD, Jonathan B. Ford, MD, Hugh B. Black, MD, and Timothy E. Albertson, MD, PhD, Fatal Fentanyl: One Pill Can Kill, Academic Emergency Medicine 2017 2017; 24:106–113 [hereinafter “Fatal Fentanyl”] at p.110, in the Key of Table 2 (© 2016 by Society for Academic Emergency Medicine).
Fatal Fentanyl was a study of 18 patients who presented with “exaggerated opioid toxicity.” Toxicology testing and analyses were performed on serum, urine, and surrendered pills. Fatal Fentanyl at p.106.
Apparently, the 18 studied patients were admitted to one California hospital’s emergency department: “...our institution cared for 18 patients with symptoms of an exaggerated opioid overdose.” Fatal Fentanyl at 107 [emphasis added]. The institution may have been the Department of Emergency Medicine, University of California, Davis, since that institution is the first noted in the credits footnote set at Fatal Fentanyl p.106.
The patients were treated thus:
Five patients underwent cardiopulmonary resuscitation, one required extracorporeal life support, three required intubation, and two received bag-valve-mask ventilation. One patient had recurrence of toxicity after 8 hours after naloxone discontinuation. Seventeen of 18 patients required boluses of naloxone, and four required prolonged naloxone infusions (26–39 hours). All 18 patients tested positive for fentanyl in the serum. Quantitative assays conducted in 13 of the sera revealed fentanyl concentrations of 7.9 to 162 ng/mL (mean = 52.9 ng/mL).
Fatal Fentanyl at 106.
One patient died — patient # 10 . See Fatal Fentanyl Table 1 (id. at p.108). But the study’s report does not indicate the serum fentanyl quantity found in that patient. See Fatal Fentanyl Table 1 (id. at p.108) and id. Table 2 (id. at pp.109-110).
Still, all other patients survived. And several had serum fentanyl levels very markedly higher than the 11 ng/mL serum fentanyl the Medical Examiner reported found in George Floyd.
One patient’s serum fentanyl level was 162.3 ng/mL, another’s 123.1 ng/mL, a third’s 65.9 ng/mL, a fourth’s 64.3 ng/mL, a fifth’s 53.3 ng/mL, a sixth’s 51.3 ng/mL, a seventh’s 39.4 ng/mL, an eighth’s 36.3, a ninth’s 27.0 ng/mL, a tenth’s 22.7 ng/mL,, an eleventh’s 17.0 ng/mL, and a twelfth’s 16.5 ng/mL — all markedly higher than George Floyd’s 11 ng/mL, and several many times higher. Fatal Fentanyl Table 2.
So, one patient’s serum fentanyl level was 14.75 times higher than Floyd’s. Another’s was 11.19 times higher. Four others’ were more than 4.6 times higher. Another four others were more than 2 times higher. Fatal Fentanyl Table 2 (pp.109-110). And all those patients survived.
True: the survivors received treatment that was, or may have been, necessary to their survivals. But some survived for hours before blood samples were taken. Hence, some survived a substantial time before receiving treatment. Fatal Fentanyl Table 2 (id. at pp.109-110), including Table 2's Key (id. p.110). And, the 17 surviving patients had hospital stays of a substantial number of hours — a range of 4 hours, 7 minutes to 296 hours 5 minutes.
[Part One endnote 8 ]
Patient # 13's serum fentanyl concentration was 64.3 ng/mL. Patient # 13's blood bore also:
Hydrocodone ....... 18.6 ng/mL
Oxycodone ...…..... concentration not noted
Promethazine ....... 3.1 ng/mL
Promethazine [trade name Phenergan] is an antihistamine-like drug that blocks effects of histamines naturally occurring in humans. Promethazine is used to treat (a) certain allergy-symptoms, e.g., hives, itchy rashes, runny nose or sneezing, itchy or watery eyes, (b) motion sickness, nausea, vomiting, post-surgical pain, and (c) insomnia.
Promethazine is contraindicated for treatment of lower respiratory tract infections (pneumonia) or asthma. Fentanyl can cause pulmonary inflamation or pulmonary edema. Promethazine can, near-certainly would, exacerbate fentanyl-caused pulmonary inflamation or pulmonary edema.
Promethazine use, alone, can be lethal: A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with promethazine.
A Promethazine/hydrocodone combinination has been found to contribute to drug-explained death. Example: A patient was treated with Hydromorphone, Prochlorperazine, Pantoprazole, and Promethazine [aka “Phenergan”]. He was discharged without a workup that might have ruled out potentially fatal cardiac or respiratory disease. Three days later, the patient was found dead in his home. Death-contributing chemistry included lethal combination of Phenergan [Promethazine], Hydrocodone, and Diphenhydramine. See also, e.g., here.
Recall that patient # 13's serum hydrocodone concentration was 18.6 ng/mL. Using promethazine and hydrocodone together may increase side-effects such as dizziness, drowsiness, confusion, difficulty concentrating. Some people, especially the elderly, may also experience impairment of thinking, judgment, and motor coordination.
Central nervous system or respiratory-system-depressant effects may be additively or synergistically increased in patients taking multiple drugs that cause these effects. Cf., e.g., this text — which considered, e.g., a promethazine/hydrocodone interaction.
Last year (2016) in Massachusetts, for example, three quarters of the state’s fatalities from unintentional overdose had fentanyl in their system—this is up from 57 percent in 2015. Regrettably, this trend is spreading across our nation. At the same time in San Francisco, two patients at the Contra Costa Regional Medical Center emergency department (ED) were seen for severe nausea, vomiting, central nervous system depression, and respiratory depression, just 30 minutes after ingesting what they believed was Norco, a prescription opioid pain medication that contains hydrocodone and acetaminophen that they bought from a friend. Analysis of the drug and specimens from the patient’s revealed that the pills were in fact counterfeit, containing dangerously high levels of fentanyl and a highly sedating phenothiazine called Promethazine (trade name Phenergan).
A fentanyl/hydrocodone combination can be lethal. See J. Kuhlman, Rebecca McCaulley, Tara J. Valouch, and George S. Behonick, Fentanyl Use, Misuse, and Abuse: A Summary of 23 Postmortem Cases, Journal of Analytical Toxicology, Vol. 27, October 2003, at Table I case 1 and at Table II cases 14, 15, and 16. To view this article, first open the web-page linked here, then click on the “button” that bears the words “[PDF] academic.oup.com” and the above-cited article will appear in PDF format. See also Fatal Fentanyl and this source.
But, despite patient # 13's blood bore (a) 64.3 ng/mL fentanyl (5.85 times the 11 ng/mL fentanyl concentration found in George Floyd’s blood) and also patient # 13's blood bore (b) 18.6 ng/mL hydrocodone and (c) 3.1 ng/mL promethazine, patient # 13 survived. Other patients survived despite serum fentanyl concentration markedly higher than Floyd’s and despite having notable serum-concentrations of cocktails of potentially lethal drugs, like hydrocodone and promethazine. See Fatal Fentanyl Table 2 (at pp. 109-110).
No rebuttal can obtain from the fact that Fatal Fentanyl patients were treated with the antidote Naloxone.
Some patients survived for hours before blood samples were taken — hence they survived a substantial time before receiving treatment. Fatal Fentanyl Table 2 (id. at pp.109-110), including Table 2's Key (id. p.110). And, the 17 surviving patients had substantial hospital-stays — a range of 4.12 hours to 296.08 hours (12.34 days).
[See also Part One endnote 8]
The record does not indicate that Floyd was critically at risk — hopelessly moribund, at the brink of death — before Chauvin and his cohorts applied compression holds to Floyd’s neck and dorsal thorax. No defense evidence shows Floyd was critially at risk. No such evidence exists; and sound evidence shows well that Floyd was not at risk. Compare, e.g., this and this and this and this and this.
But suppose, for argument, that, visibly and audibly, Floyd had been seriously at risk 15 seconds before the police began applying neck and dorsal thorax compressions. Still the Fatal Fentanyl record indicates strongly that Floyd would have survived had the police not applied those compressions but called paramedics and merely kept Floyd handcuffed and sitting (as he had been sitting) until paramedics arrived and transported Floyd to an emergency room (with a police officer guarding Floyd). Police department policy and protocol supported, even indicated, such arrest-procedure. Compare this and this and this and this.
More important, even if Floyd had been moribund, Chauvin and his cohorts are liable for murdering Floyd because of the law’s eggshell skull rule and the law’s rule that a killing is a homicide even if an independent, supervening event might or would have killed the victim a millisecond later. See both (a) this Part’s (Part One’s) § II.A (sub-§ A of this Part’s PREFACE) and (b) George Floyd WAS Murdered, by Derek Chauvin and His Cohorts — Part Two.
A few other studies — all postmortem — assert that even a 3.0 ng/mL serum fentanyl concentration can kill. But most such studies’ conclusions are invalid. For purpose of establishing a mean lethal serum fentanyl level, such studies are at best unreliable, because they beg the question whether the deceased subjects would or could have survived, or survived longer, in different circumstances, especially circumstances not including comorbidities or interactions of fentanyl and other-drugs.
Often such studies’ statistical analyses are questionable at best. One reason is that they tend not to address the medians and modes of skewed curves. Suppose the mean is ≈3.0 ng/mL but the results are markedly skewed so that the mode is, say, 13.0 ng/mL and the mode or median is significantly less than two standard deviations from the mean. Then the mean is not a valid, reliable predictor of lethality.
The Chauvin Defense may adduce sources like G L Henderson, Fentanyl-related deaths: demographics, circumstances, and toxicology of 112 cases, J Forensic Sci. 1991 Mar;36(2):422-33. One can perceive such sources’ invalidity merely by comparing available serum fentanyl concentration data of Fatal Fentanyl, supra.
In Fatal Fentanyl, the stated serum fentanyl ng/mL concentrations were: 162.3, 123.1, 65.9, 64.3, 53.3, 51.3, 39.4, 27.0, 22.7, 17.0, 16.5, 7.9. Suppose: (a) the two outlier amounts (162.3 & 123.1) are not present, and (b) all concentration-amounts, except the 16.5 amount, are rounded off, but the 39.4 & 27.0 quantities are instead (after rounding-off) 39.0 each. Then the data are: 66, 64, 53, 51, 39, 39, 23, 17, 16.5, 8.0. Hence:
The median and mode are identical. Thus, the median/mode — 39 ng/mL — predicts lethality better than does the mean (37.65 ng/mL). Now, lower all quantities, and make the mean ≈3.0, thus: 11.6, 11.6, 4.1, 2.0, 1.1, 0.8, 0.7, 0.5, 0.3, 0.2.
[Part One endnote 9
The mode is 0.6 ng/mL higher than George Floyd’s 11.0 ng/mL serum fentanyl concentration. And such possibility fits medical reality — as proved by Fatal Fentanyl, supra, where among survivors, all but one had a serum fentanyl concentration very markedly greater than 11.0 ng/mL.
Fatal Fentanyl is far from the only study that shows an 11 ng/mL serum fentanyl concentration survivable. Another example is Teri L. Martin, Karen L. Woodall, and Barry A. McLeHan, Fentanyl-Related Deaths in Ontario, Canada: Toxicological Findings and Circumstances of Death in 112 Cases (2002-2004), J. of Analytical Toxicology, Vol. 30, October 2006 [hereinafter “Fentanyl-Related Deaths”].
That study presents several charts showing serum fentanyl concentrations of deceaseds. [One study question was whether fentanyl explained the deceaseds’ deaths. That question was confounded by the deceaseds’ having serum concentrations of other drugs (opioids, amphetamines.....).]
In one chart, the serum fentanyl concentrations — stated as μg/L [which equals ng/mL] — were: 4.8, 6.1, 6.2, 6.7, 7, 8, 9, 9.1, 9.2, 10, 10, 10, 11, 11, 11, 12, 12, 12, 13, 13, 14, 14, 15, 15, 17, 18, 34, 40, 71, 97, 119. Fentanyl-Related Deaths at Table II (p.605). The mean concentration was 20.81. The median was 12.0. The curve was tri-modal — 10, 11, 12 — but since three other concentrations were double (13,13,14,14, 15,15) and the outlier extremes (97, 119) were far from the three modes, the modes were not good predictors.
Both the mean (20.81) and median (12.0) were higher than George Floyd’s 11 ng/mL serum fentanyl concentration — the 20.81 mean virtually twice Floyd’s serum concentration. But such does not render strong proof that Floyd’s serum concentration was non-lethal (that it could not explain Floyd’s death). The subjects were dead when their blood was tested — hence one cannot deduce, securely, whether a slightly lesser fentanyl concentration would not have killed them or whether fentanyl alone caused their deaths.
Still, the study’s facts indicate clearly that many, most, or all deceaseds did not use fentanyl per prescription. That indication follows from the fact that (likely except in the case of a 4-years-old subject) the fentanyl administration-means were not those a physician would prescribe. Apparently (likely except a 4-years-old subject), the deceaseds used: intravenous injection of patch contents; oral transmucosa abuse (8-10); rectal insertion; and volatilization and inhalation of fentanyl patches.” Fentanyl-Related Deaths p.603 (Abstract) & p.603 (col.2). And, the study-conductors appear to treat near-all cases as cases of drug-abuse.
Therefore, one can deduce that most or many study-subjects were relatively long-term illicit fentanyl-users. Hence, one can deduce near-securely that most or many subjects had built up fentanyl-tolerance, so that likely a 11 ng/mL serum fentanyl concentration would not have killed them. That deduction obtains reinforcement from this study statement:
There were 54 cases in which death was attributed solely to fentanyl intoxication; the mean blood concentration was 25 μg/L (range: 3.0-383 μg/L). This concentration range overlapped with blood fentanyl concentrations measured among cases where the presence of the drug was considered incidental. For example, a mean blood concentration of 12 μg/L was observed among 12 cases of natural death (range: 2.7-33 μg/L).
Fentanyl-Related Deaths p.603 (Abstract). That language implies: (a) that the study-conductors determined or concluded previously that the usual or average lethal serum fentanyl concentration is 25 μg/L [which equals 25 ng/mL]; (b) that even a 12 μg/L [which equals 12 ng/mL] is presumptively not a fatal serum concentration — even that a 33 μg/L [which equals 33 ng/mL] concentration may not be lethal.
[Part One endnote 10
Equally important: In the George Floyd murder case, the matter — the legal matter — is not whether the alleged victim’s 11 ng/mL serum fentanyl concentration would have been fatal eventually had the police not applied neck and dorsal thorax compressions. The matter [see Part Two of this article] is whether the neck and dorsal thorax compressions hastened the alleged victim’s death.
[Part One endnote 11
3. Fentanyl, Amphetamines, and Drug-tolerance
Another matter is drug-tolerance, which the ME’s supposed Interview statements do not account.
Commonly, a opioid-user’s system withstands more of a specific opioid as the user continues to use the drug. Concomitantly, the user “needs” more of the drug to obtain the “pleasant” effect he desires; and he takes, and his system can withstand, higher doses. Studies address this matter and show that a long-time user can survive doses markedly higher than a supposed mean lethal dose. Such tolerance obtains with fentanyl use quite as it does with use of other opioids.
According to well known evidence — evidence surely the state possesses — George Floyd used opioids for a substantial time before the day of his arrest and death. Likely the opioids included fentanyl. Therefore, likely George Floyd had developed fentanyl tolerance that rendered his time-of-arrest ≈11 ng/mL serum fentanyl concentration clearly non-lethal.
That serum fentanyl concentration was likely toxic despite Floyd’s fentanyl tolerance and may have enhanced the life-threatening effect of the neck and dorsal thorax compressions the arresting police applied. But Floyd’s apparent pre-compression-hold-suffering condition did not suggest the fentanyl concentration, itself, would have killed him had the police not applied neck and dorsal thorax compressions to him. See this and this and this and this [and Dr. Michael Baden the video included there] and this and this and this.
The medical/pharmacological literature (e.g., Fatal Fenantyl and Fentanyl-Related Deaths) and Floyd’s history suggest that Floyd was able to tolerate (survive with) the 11 ng/mL serum fentanyl concentration the autopsy found. Essentially the same observation applies to the matter of Floyd’s serum amphetamine concentration.
4. George Floyd’s Serum Fentanyl Concentration and His Lungs
The Notes state: “Fentanyl - 11. He [the ME] said, “that's pretty high. This level of fentanyl can cause pulmonary edema. Mr. Floyd's lungs were 2-3x their normal weight at autopsy.”
Assume that “Fentanyl - 11” means “11 ng/mL serum fentanyl concentration.” The assertion “Floyd's lungs were 2-3x their normal weight at autopsy” is incompetent.
The Medical Examiner had no basis of knowing the “normal” weight of Floyd’s lungs. Nothing suggests that the Medical Examiner [“ME”] had ever examined, or even ever encountered, Floyd before the ME autopsied Floyd’s corpse.
A particular human’s lungs weigh what they weigh because of, e.g., the particular human’s anatomy, body weight, health, ethnicity, physical-activity-history....... Medicine can establish an average lung weight of a normal human adult male. But no “normal” lung-weight exists. See, e.g., this source:
The weight of the lungs was found to be 442.0 ± 152.3 g left lung and 504.6 ± 174.6 g right lung in the male population.... The percent body weight of the lungs in males was 0.76% for the left lung and 0.86% for the right.....
Neither a competent Medical Examiner or competent pathologist nor any other competent physician would say Floyd’s lungs were “2-3x their normal weight.”
The statement “Fentanyl – 11” is a “fatal level under normal circumstances” is medical nonsense. Does “normal” refer to the norm of use, the norm of users, the norm of health measured by what standard (??), the norm of conditions in which the fentanyl is introduced, by what means — injection, pill, snorting, anal-insertion, patch.......?
A competent physician would address a population or sub-population’s “average” or “mean” — not a “normal.” What is “normal” lethality of fentanyl intake? An absurd question.
What was George Floyd’s “normal”? Does “mean” apply sensibly to an erratic, cardiovascularly-compromised individual human who uses numerous variously dangerous drugs?
Does not “normal” require comparison of the actual circumstances of Floyd’s death — the neck-press compression/occlusion of carotid arteries and jugular veins, the dorsal thorax compression..…..and what Floyd had to eat or drink or whether he slept much or at all the night before or whether he engaged in sexual conduct recently or….…?
One might need to search for eternity to find even one valid, reliable, substantial study of the mean death-rate among large, cardiovascularly-compromised men who have 11 ng/mL serum fentanyl concentrations and small serum concentrations of methamphetamine and cannabinoid(s) and are forced to a front-down prone position on street pavement and suffer posterior handcuffing and more than 9 minutes of neck/dorsal-thorax compressions applied by knees of two or three adult male police — applied even for more than 3 minutes after the study-subjects become unconscious.
Directly, the dorsal thorax compression impaired the function of Floyd’s diaphragm. Indirectly, the neck-compression/blood-vessel-occlusion weakened further the function of Floyd’s diaphragm, eventually stiffened his diaphragm, because both neck and dorsal thorax compressions caused brain hypoxia and brain hypercapnia. The neck-and-dorsal-thorax-compression effects impaired the lungs’ capacity of evacuating not only oxygen and carbon dioxide (and other gases), but also blood and other fluids.
Suppose that (postmortem) Floyd’s lungs did weigh markedly more than the average weight of lungs of a “normal” male human of Floyd’s size, age, ethnicity, and general health-condition. Then the obvious, evidence-based (not hypothetical) cause was the compression of Floyd’s lungs, diaphragm, and neck (carotid arteries & jugular veins).
Very likely, the lung/diaphragm (dorsal thorax) and neck (carotid-artery/jugular-vein) compressions/occlusions caused a condition akin to bloody pleural effusion — pathologically great accumulation of pulmonary blood, lymph, and pulmonary extravascular lung-water. That condition could have occurred
(a) partly because of the dorsal thorax compression’s impairment of diaphragm-function and lung-function,
(b) partly because of the diaphragm-function-impairing effects of brain hypoxia and brain hypercapnia, and
(c) partly because the brain hypoxia and brain hypercapnia slowed and weakened the heart’s electromechanical pump (before the brain hypoxia/hypercapnia caused asphyxia that resulted in cardiopulmonary arrest).
(a) adds insignificance to the ME’s statement “Floyd’s lungs were “2-3x their normal weight”
(b) supports the prosecution, and
(c) undermines the defense very markedly.
Floyd was not exhibiting any symptom of potentially lethal fentanyl overdose until after he suffered 4 or 5 minutes of the police’s more-than-9-minutes-long application of two asphyxia-death-threatening compression-holds. Compare this and this and this and this and this.
So, if (postmortem) Floyd’s lungs weighed markedly more than the “average weight” of lungs of a “normal” male human of Floyd’s size, age, ethnicity, and general health-condition, quite possibly, if not likely, the cause was not drug-overdose, but the combined neck and dorsal thorax compressions applied by Officer Chauvin and two other arresting police. Also, the assertion “Mr. Floyd's lungs were 2-3x their normal weight” [my emphasis] is medically, forensically, empirically incompetent; and if the ME actually uttered exactly such assertion (unmodified), the ME erred (perhaps just slipped).
[Part One endnote 12
5. Effect of Serum Concentrations of Cannabinoids
The autopsy report’s “Blood drug and novel psychoactive substances screens” include this finding: “11-Hydroxy Delta-9 THC 1.2 ng/mL; Delta-9 Carboxy THC 42 ng/mL; Delta-9 THC 2.9 ng/mL.” All those substances are compounds or metabolites of one or more cannabinoids. Autopsy Report p.2. Floyd’s urine was “presumptive positive for cannabinoids.” Id. Cannabinoids tend to mitigate slightly or not potentiate adverse fentanyl effects. See here and here and here and here.
The defense may, likely will, argue that Floyd died not because of police conduct but because of Floyd’s combined serum fentanyl and serum methamphetamine. That argument ought to fail for reasons outlined here: See also Part Two of this article and compare this and this and this and this and this and this.
Such defense argument ought fail also partly because of the effect of interaction of cannabinoids and amphetamines, including methamphetamine — which interaction mitigates the Floyd-case-pertinent adverse effects of methamphetamine, e.g., methamphetamine’s brain-damage effect. Compare this an this and this and this.
The autopsy report’s cannabinoid compounds/metabolites finding either reinforces or cannot undermine the conclusion that Floyd’s serum fentanyl and amphetamine concentrations did not render Floyd moribund when police began applying neck and dorsal thorax compressions to Floyd.
6. Excited Delirium and Positional Asphyxia
In Asia Takeuchi, MD, Terence L. Ahern, BA, and Sean O. Henderson, MD, Excited Delirium, West J Emerg Med. 2011 Feb; 12(1): 77-83, [hereinafter “Excited Delirium”], the authors state:
Excited delirium (EXD), first described in the mid 1800's, has been referred to by many other names Bell's mania, lethal catatonia, acute exhaustive mania and agitated delirium.1 Regardless of the label used, all accounts describe almost the exact same sequence of events: delirium with agitation (fear, panic, shouting, violence and hyperactivity), sudden cessation of struggle, respiratory arrest and death.
Excited Delirium, in its “INTRODUCTION.”
Online journals have pressed the argument that George Floyd died not because of police conduct, but because he suffered drug-induced — especially fentanyl-overdose-induced — excited delirium. See, e.g., this medically, forensically, statistically, and legally incompetent, bigotry-biased article.
The police body-cam record transcript hereinafter “Body-camTranscript”] bears some evidence of Floyd’s panicking during his arrest. But Floyd’s panic appears to relate to his previous police contact, his criminal conviction experience, the circumstances of his arrest, and the conduct of the police who arrested him — not to drugs present in his system at the time of his arrest. See again the seven sources linked in the immediately preceding paragraph.
The Body-cam Transcript indicates that often Floyd said “I can’t breathe.” Body-camTranscript at lines 244, 258, 261, 277, 284, 288, 292, 324, 335, 347, 356, 362, 366, 372, 288. But [see id. line 284 et seq.] apparently the police had begun applying compression-holds (neck-compression, dorsal-thorax-compression) when Floyd began repeating very frequently his claim “I can’t breathe.” From that time on, Floyd’s panic resulted from actual life-threatening (and unlawful and unconstitutional) police-conduct.
[Part One endnote 13 ]
Very likely also Floyd’s panic obtained from fear of suffering another felony conviction as a three-time loser. Floyd seems to have suffered nine criminal prosecutions, six for felonies — all in Texas.
I have not researched whether in all nine cases, Floyd suffered conviction — though I have read sundry internet “reports” that suggest he suffered felony convictions at least two times. [See also endnote 5.] I have not researched the matter of whether Minnesota law may count sister-state-rendered convictions in determining whether to enhance a sentence. Those matters bear little if any relevance respecting Floyd’s state-of-mind, which is the critically pertinent issue vis-a-vis whether Floyd was suffering excited delirium during his arrest.
The question is whether Floyd believed, or likely would have believed, and feared, that another felony conviction would put in prison for “life-without-parole” or for a very long term. Alone, such fear could explain Floyd’s panic.
Several times Floyd said “mama, mama,” or “mama, mama, mama, mama.” Body-cam Transcript at, e.g., lines 296, 300, 304. And Floyd said: “I can't believe this man. Mom, I love you. I love you” [id. line 316] and “Tell my kids I love them. I'm dead” [id. line 320]. Earlier he said his mother had just died: “I just lost my mom, man.” [Id. line 12.] And at other times he indicated he feared his arrest would lead to his death. Numerous times, Floyd begged the police not to shoot him. [Id. at lines 4, 8, 20.]
Among others of Floyd’s displays of serious fear and anxiety, Floyd’s shooting-fear [“Don’t shoot me”] prompts this colloquy of Officer Lane and Shawanda Renee Hill, apparently another occupant of the car in which Floyd sat when the police approached him to take him into custody:
Lane: Why's he getting all squirrelly and not showing us his hands, and just being all weird like that? Shawanda Renee Hill: I have no clue, because he's been shot before. Lane: Well get that, but still when officers say, "Get out of the car." Is he drunk, is he on something? Shawanda Renee Hill: No, he got a thing going on , I'm telling you about the police. Lane: What does that mean? Shawanda Renee Hill: He have problems all the time when they come, especially when that man put that gun like that. It's been one.
Body-cam Transcript at lines 60-72. That colloquy reinforces the inference that Floyd’s behavior did not reflect excited delirium, but rational (if perhaps unusually extreme) fear of police and possible prosecution and the possibility that his arrest would lead to his death or very long loss of liberty — fear the effects of which were exacerbated by distress associated with recent “loss” of his mother. Compare again this and this and this and this and this and this and this.
One may question even the theory of excited delirium — as yet only a theory. The theory is not generally accepted in the relevant scientific community or communities. The theory’s proponents do not quite accord concerning the constituents of indication of excited delirium’s presence. And the article Excited Delirium (supra) depends significantly on another article the essential thesis of which is patently invalid, at least vis-a-vis the George Floyd murder case.
Excited Delirium asserts: “The positional asphyxia theory has been refuted.” Positional asphyxia is a fact, not a theory; and it has not been refuted.
Positional asphyxia involves causing a subject to suffer asphyxia by placing the subject in a body-position that stresses specially the subject’s pulmonary/cardiovascular system, thence the subject’s brain-function, and thence stresses further the subject’s pulmonary/cardiovascular system, sometimes fatally. See, e.g., Positional Asphyxia-Sudden Death, National Institute of Justice Program, U.S. Department of Justice, Office of Justice Programs, National Institute of Justice (June 1995).
To support its assertion that positional asphyxia has been refuted, Excited Delirium cited “Chan et al.” The pertinent “Chan et al” article is T. C. Chan, MD, T. Neuman, MD, J. Clausen, MD, J. Eisele, MD, and G. M. Vilke, MD, Weight Force During Prone Restraint and Respiratory Function, Am J Forensic Med Pathol 25(3):185-189, Sept 2004 [hereinafter “Weight Force”].
Weight Force’s key assertion is this: Even if a healthy, 18 to 45 years old male subject is placed in front-down prone position while he is handcuffed behind his back and has his ankles handcuffed together and drawn up near his wrists by means of a restraining cuff device — a restraint position called “hobble,” “hogtie, or PMRP” — and then the subject has 50 pounds of “weight force” (two 25-pound sandbags) placed on his back between his scapulas, still the subject will not suffer asphyxia. The 50-lb-weighted hogtie [hobble or PMRP] restraint appears thus:
Images copied from Weight Force p.186.
The assertion does not — cannot — account the actual experience of a person who suffers the kinds of compression restraints applied to George Floyd.
Officer Chauvin kneeled on George Floyd’s neck and bobbed up and down while he (Chauvin) kneeled so. Some evidence indicates that Officer Chauvin weighed about 154 to 167 pounds. Compare this and this.
Because of the position Chauvin held while he kneeled on Floyd and because of Chauvin’s mass, the force of gravity, and intentional pressure Chauvin applied, Chauvin imposed on Floyd’s neck a force and weight much greater than the dead-weight two 25-lb sandbags could apply between two scapulae. And with his bobbing motion, Chauvin added to the weight-force pressed on Floyd’s neck.
So, the neck-compression effect was much greater than 50-lb sandbag pressure placed between scapulas. And the neck-compression was much more life-threatening because imposed, much directly, on soft tissue and carotid arteries and jugular veins of the neck. At the side of the neck, the carotid arteries and jugular veins are partly unprotected by bone or muscle. But between the scapulae, the back is constructed of hard muscle, ribs, and spine that protect the heart and lungs from direct effect of weights of foreign objects.
Two policemen applied substantial pressure to Floyd’s dorsal thorax while Officer Chauvin applied compression to Floyd’s neck. That dorsal thorax pressure was (a) substantially greater than the pressure applied between the scapula in the Weight Force experiment and (b) applied directly to the area of Floyd’s lower lungs and diaphragm.
The neck-and-dorsal-thorax compressions’ synergistic effect was much more life-threatening than could be the dead weight of two 25-lb sandbags laid between scapulae of a healthy male adult — not only because of the weight difference (50 pounds versus more than 200 pounds)
[Part One endnote 14 ] and the intentional force the police applied, but also because the neck/dorsal-thorax compressions were applied to an unhealthy male whose cardiopulmonary and central nervous system functions were somewhat compromised by drugs.
So, even if (although dubious) Weight Force could enjoy some degree of validity and reliability for cases involving the kind of restraint and weight-pressure involved in Weight Force, still Weight Force’s thesis is utterly inapplicable to the George Floyd murder case.
The same is true of Excited Delirium.
Assume, for sake of argument, that a fentanyl “overdose” or a combined fentanyl/methamphetamine “overdose” can cause fatal “excited delirium.” Disregard the critical question of the meaning of “overdose” — a term that must be modified by adjectives accounting many pertinent innate individual differences and many discrete internal and external individual environmental forces (e.g., the person’s age, sex, general health, comorbidities, drug-tolerances......). Still, in George Floyd’s case, the death-causing sine qua non of moribundity was the conduct of police.
[Part One endnote 15
7. Absence of Evidence of Hypoxic Ischemic Brain Injury
Respecting the condition of Floyd’s brain, the Autopsy Report states, inter alia, this [at p.9 & p.12]:
The basal ganglia, brainstem, cerebellum, and arterial systems are free of injury or other abnormalities. * * * Sections of hippocampus, cerebellum, cerebral cortex, and midbrain show the expected microscopic architecture, without hypoxicischemic [sic], reactive, neoplastic, or inflammatory changes.
The defense may argue that those Autopsy Report observations belie the claim that neck/dorsal-thorax compressions killed Floyd by occluding a carotid artery or jugular vein and compressing his diaphragm and lower lungs, hence asphyxiating Floyd by causing brain hypoxia, brain hypercapnia, and impairment of the lungs’ capacity of evacuating oxygen and carbon dioxide (and other gases). The argument would be that had carotid artery or jugular vein occlusion occurred and caused brain hypoxia and brain hypercapnia, the autopsy would have disclosed hypoxic ischemic brain injury.
Hypoxic ischemic brain injury? If the brain has insufficient oxygen because insufficient oxygen-bearing blood reaches the brain or not enough carbon dioxide exits the brain or both, brain blood vessels or other brain tissue may suffer injury. See, e.g., this. The defense may assert that always hypoxic ischemic brain injury occurs near-instantly after the brain begins to suffer hypoxia. Such assertion is false.
No brain-injury — not even a very slight ischemic brain injury — necessarily follows from asphyxia-causing compression of carotid artery or jugular vein or from dorsal thorax compression.
In Floyd’s case, only jugular-vein-occlusion may have caused asphyxia by causing pathological cranial carbon dioxide retention (brain hypercapnia), which is less likely to cause ischemic brain-injury.
Asphyxia biochemical/physiological mechanics can be largely, though not only, local to the lungs, thence the heart — by means of impairment of pulmonary management of oxygen/carbon-dioxide transfer and obstruction of heart/lung blood-exchange.
The carotid artery and jugular vein can be compressed, hence occluded, and simultaneously the dorsal thorax can be compressed and thence the lungs occluded and diaphragm disabled more than enough to cause asphyxia without causing brain injury.
In Floyd’s case, rapid-occurring asphyxia can have induced death too quickly to permit brain-injury. In condition of normothermia, within 20 seconds of cranial blood flow interruption, the brain’s electrical activity may begin to disappear, probably (but not surely) per failure of high-energy metabolism. Often (but not always) within 5 minutes, high-energy phosphate levels may have nearly disappeared — thus ATP depletion. Serious cell-electrolyte-balance-disturbance may begin.
But, most often, ischemic brain-tissue injury requires occurrence of still other, different pathologic biochemical/physiological events, which require more time. The other events may involve, e.g., pathologic alterations of calcium, sodium, and phosphorous distributions/exchanges and eventual consequent mitochondrial sequestration, thence calcium-overloading of mitochondria and diminished oxidative-phosphorylation-capacity.
Elevated intracellular Ca++ will activate membrane phospholipases and protein kinases, thence production of free fatty acids [hereinafter “FFA’s”], thence membrane-degradation caused by phospholipases and advanced reduction of calcium-pumping efficiency, which produces further calcium-overload and intracellular calcium-regulation-failure, which occurs during an ischemic episode. And, most often, FFAs bear other cell-membrane-degrading effects.
Officer Chauvin and two other policemen applied their compression-holds for around 9 minutes. Floyd fell unconscious 4 to 5 (no more than 6) minutes after the neck-and-dorsal-thorax compression applications began. Floyd became fully limp, quite apparently dead, at some point from one to two minutes after he became unconscious.
See this (especially, but not only, at time 14:44 to the end) and this testimony, which indicates that Floyd had suffered cardiac arrest for 30 minutes before the attending Emergency Room physician tried to resuscitate Floyd. And compare testimony of a Fire Department captain who stated (see video at time 11:43 to end) that when paramedics attended Floyd, Floyd was unresponsive to CPR procedures that included a medical devices that pumped air into Floyd’s lungs and functioned to force heartbeat — that Floyd was apparently dead.
The asphyxiation process could not have begun immediately upon initiation of neck-compression and dorsal-thorax-compression. Yet, the asphyxiation-process may have been complete within 4 or 5 minutes (not more than 6 minutes) after the start of neck/dorsal-thorax compression. (a) See the sundry videos of the Floyd-arrest/killing events; also (b) compare, e.g., this and this.
A likely 4 to 5 minute (less than 6-minute) pre-asphyxia time-lapse was likely too brief to permit onset of ischemic brain-tissue-injury. Brain-ischemia-causation/ischemic brain-tissue-injury can require notably more than 6 minutes. That causation’s mechanisms (or processes) may (though need not necessarily) involve operations of number or element-details-proliferation greater than outlined above — e.g., the following:
(1) ATP-driven membrane pump causes active extrusion of calcium from cells (2) cell-membrane calcium/sodium exchange driven by intracellular-to-extracellular concentration-differential of Na+ resulting from the cell membranes’ Na+ – K+ pump (3) ATP-driven process of sequestration of intracellular calcium in endoplasmic reticulum (4) intracellular calcium-accumulation driven by oxidation-dependent calcium sequestration inside mitochondria (a)(ii) High-energy cellular compound loss thence Na+ – K+ gradient-loss eliminates three of the four mechanisms of cellular calcium homeostasis. That effect causes massive, rapid calcium-influx into cells. Then mitochondrial sequestration causes calcium overloading of mitochondria and diminished capacity of oxidative phosphorylation. Elevated intracellular Ca++ activates membrane phospholipases and protein kinases. One vital consequence is production of FFA’s, including the potent prostaglandin inducer, arachidonic acid [hereinafter “AA”]. Phospholipases-caused membrane degradation may (very often does) damage membrane integrity, and that effect reduces further the efficiency of calcium pumping and leads to further calcium overload and failure of regulation of intracellular calcium levels. (b) FFAs cause other membrane-degradative effects. FFA-release-produced AA causes biochemical cascade ending with thromboxane and leukotriene production. Both compounds are intense tissue-irritants which can cause platelet-aggregation, clotting, vasospasm, and edema, which can increase the compromising of restoration adequate cerebral perfusion. (c)(i) Lactic acidosis also may participate in causation of ischemic-tissue-injury — though lactic acidosis is not a necessary culprit. Lactic acidosis does contribute to the pathophysiology of ischemia. Above threshold level of 18 - 25 micromol/g, lactate can cause irreversible neuronal injury. (c)(ii) Lactic-acidosis-caused pH decrease may injure and inactivate mitochondria. Lactic acidosis can cause degradation of NADH [which is necessary to ATP synthesis]; and lactic acidosis may also interfere with recovery of ATP levels. Lactic acidosis may increase iron decompartmentalization, thence induce or increase free-radical-mediated injury.
Those mechanisms’ number and complexity can require notable time to develop and cause detectible injury. Therefore, ischemic-brain-tissue-injury may not occur until passage of more than 6 or 7 minutes.
[Part One endnote 16
Hence, ischemic-brain-tissue-injury likely did not occur in Floyd, because, apparently, Floyd died about 4 or 5 minutes (certainly not 6 minutes) after police began applying their compression techniques. Compare the sundry videos of the Floyd-arrest and killing events and, e.g., (1) this and (2) this, especially, but not only, at time 14:44 to end.
The preceding ischemic-brain-tissue-injury-mechanism details do not exhaust the field. But they suffice to show the possibility, even significant probability, that Floyd’s brain did not suffer detectible ischemic injury.
Another consideration is that the Autopsy Report did not indicate, expressly, that the ME dissected and examined interiors of the brain’s blood vessels, which often are victims — even first victims — of hypoxic ischemic injury.
[Part One endnote 17 ] Hence, Floyd’s brain may have suffered some hypoxic ischemic brain injury despite not observed by the Autopsy Report.
See also this, which reinforces the inference that Floyd suffered brain brain-hypoxia/brain-hypercapnia notwithstanding ischemic brain injury despite the autopsy report did not state that ischemic brain injury was detected.
8. The Autopsy Report’s Cause-of-Death Statement
The Autopsy Report [hereinafter “AR”] stated that the cause-of-death was “cardiopulmonary arrest complicating law enforcement Subdual, restraint, and neck compression.” [Top of page 1 of AR.] Several sources have misread or misrepresented that AR language, as if that language means that the cause-of-death was cardiopulmonary arrest rather than the compression-restraints police applied to Floyd’s neck and dorsal thorax. Cardiopulmonary arrest was not the cause-of-death, but the end death-event.
To apprehend correctly AR’s statement of cause-of-death, one must parse that statement carefully vis-a-vis pertinent professional usage.
The term “subdual” is both noun and adjective; its nominative denotation is “an act that subdues or seeks to subdue;” and its adjectival denotation indicates that the modified nominative denotes a thing that bears the quality of subduing or of seeking to or being capable of subduing. In the Report, the term is nominative — a “subdual,” which is an act of subduing.
The term restraint is a nominative denoting an act or event that involves or achieves the precluding of movement or free movement of the thing that is the object of the act or event. Since “Subdual” and “restraint” are separated by a comma and since a comma and the conjunction “and” separate “restraint” from “neck compression,” “restraint” denotes an independent event or independent determination — particularly, a determination that, inter alia, a “restraint” was involved in causing death.
The term “neck-compression” denotes constricting pressure applied to the neck. “Compression “ is not mere pressure, but pressure that constricts (like the pressure a python applies to its prey’s breathing apparatus).
In the AR’s cause-of-death language, the term “complicating” denotes “enhancing” — enhancing the effect of (a) the subdual, (b) the restraint, and (c) the neck-and-dorsal-thorax compressions. Such “complicating” signification is rather common in law and also in medicine. See, e.g., Brackett v. Peters, 11 F.3d 78 (7th Cir. 1993), at p.82, where, in a discussion of felony murder, the court states:
No intent to kill…is required; and though the Illinois cases do require that death be a “foreseeable” consequence of the felony…; all they [Illinois cases] mean is that the death must be caused by the felony; for remember that “cause” in law means not just but-for cause but also an enhancement of the likelihood (what in law is often called “foreseeability”) that the [lethal] class of events would occur.
[Case-cites omitted and ellipsis & emphasis added]. Cf. infra under heading “10. Eggshell Skull Rule, Foreseeability, and Enhanced Foreseeability.”
So, AR’s cause-of-death statement does not mean
(a) that Floyd suffered cardiopulmonary arrest and also subdual, restraint, and neck/dorsal-thorax compressions
(b) that Floyd suffered cardiopulmonary arrest and then subdual, restraint, and neck/dorsal-thorax compressions
Rather, the AR’s cause-of-death statement means that cardiopulmonary arrest “enhanced” the life-threatening effect(s) (e.g., brain-hypoxia, brain-hypercapnia, and unconsciousness) of the subdual, restraint, and neck/dorsal-thorax compressions.
Cardiopulmonary arrest “enhanced” the life-threatening effect of the “law enforcement Subdual, restraint, and neck compression” because cardiopulmonary arrest is death if, as in Floyd’s case, it is permanent, not very fleeting or reversed. Compare this (especially, but not only, at time 14.44 to end) and this (especially, but not only, from time 2:17 to time 2:27) and this (especially, but not only, at time 11:43 to end).
Testifying at Chauvin’s trial, Dr. Lindsey Thomas, Forensic Pathologist, interpreted the AR’s cause-of death statement essentially as I have indicated above — though Dr. Thomas did not parse the AR cause-of-death statement’s grammar/syntax or interpret its diction quite linguistically. See also this video of the opinion of Dr. Mike Hansen, especially at time 11:44 to the end.
The ME’s Press Release renders the preceding AR language-construction linguistically/grammatically, medically, and legally quite correct. The Press Release concluded that Floyd’s death was “homicide.”
If cardiopulmonary arrest were the (only) cause-of-death, Floyd’s death would not be homicide. Though not a necessary consideration, a pertinent (and arguably judicially noticeable) empirical fact is that very, very few (if any) humans die simply and only because of sudden auto-induced total cessation of heart-and-lung function (i.e., with zero involvement of any other causative agent or event).
But those are only medical and AR-interpretation considerations. One must appreciate that, in law, the death-cause matter is a matter of “proximate cause.” In Floyd’s case, the core legal issue is the “proximate cause” of Floyd’s death.
“Proximate cause” is a cause that, in a direct sequence, unbroken by a new independent cause, produces the death and without which the death would not have occurred. The concept “a proximate cause” does not equal “the cause” — i.e., “proximate cause” is not the one and only cause. As observed by the court in Brackett v. Peters, 11 F.3d 78 (7th Cir. 1993) [cited & quoted supra], “proximate cause” is “not just but-for cause but also an enhancement of the likelihood (...“foreseeability”) that the [lethal] class of events would occur.” [Emphasis added here.]
Also, recall: Fatal Fentanyl (supra) at p.110, in the Key of Table 2: “The therapeutic (TL) and toxic (TX) serum levels…are: fentanyl TL = 1-2 ng/mL, TX = 2-20 ng/mL, lethal > 20 ng/mL…..” [The term “> 20 ng/mL” means “greater than 20 ng/mL.” ]
If Floyd’s serum fentanyl concentration (itself or together with methamphetamine) produced symptoms and those symptoms eventually could have been fatal, such fact would not be evidence that a drug overdose was the proximate cause of Floyd’s death. It would be evidence that arresting police murdered Floyd.
In the body-cam record’s transcript — see Part One endnote 10 (supra) & Body-cam Transcript (supra) — much evidence shows that the arresting police noticed Floyd’s displaying symptoms that could indicate a possibly lethal drug overdose. See Body-cam Transcript at, e.g., lines 60-77, 86-89, 255-261, 362-409. Especially, but not only, at id. lines 379-409, such evidence is striking:
Lane (a policeman): We found a weed pipe on him ,there might be something else, there might be like PCP or something. Is that the shaking of the eyes right is PCP? George Floyd: My knee, my neck. Lane: Where their eyes like shake back and forth really fast? George Floyd: I’m through, through. I'm claustrophobic. My stomach hurts. My neck hurts. Everything hurts. I need some water or something, please. Please. I can't breathe officer. Chauvin: Then stop talking, stop yelling. George Floyd: You're going to kill me, man. Chauvin: Then stop talking, stop yelling, it takes a heck of a lot of oxygen to talk. George Floyd: Come-on, man. Oh, oh. crosstalk. I cannot breathe. I cannot breathe. Ah! They'll kill me. They'll kill me. I can't breathe. I can't breathe! *** Lane: Should we roll him on his side ? Chauvin: No, he's staying put where we got him . Lane: Okay. just worry about the excited delirium or whatever. Chauvin: Well that's why we got the ambulance coming.
So, the arresting police ought to have foreseen that they ought merely have kept Floyd handcuffed and confined while he was standing or sitting on the ground — without applying neck/dorsal-thorax compressions to Floyd — until an ambulance arrived. They ought to have foreseen that if (as apparently they thought possible) Floyd was drug-overdosed, such compression-holds would either kill Floyd directly or hasten his death.
[Part One endnote 18 ]
Despite foreseeability that such neck/dorsal-thorax compressions would augment a chance of fatal asphyxiation of a man who may have taken high doses of possibly lethal drugs, the police enhanced the likelihood of such fatal asphyxiation [cf. Brackett v. Peters, supra]. That enhancement created a condition without which Floyd would not have died when he did. [Again cf. Brackett v. Peters, supra.]
So, the arresting policemen’s neck/dorsal-thorax compressions constituted the legal proximate cause — and the medical direct cause (see supra this section) — of Floyd’s death. These matters are developed further in Part Two of this article.
9. The Toxicology Report Appended to the Autopsy Report
I expect the defense has tried or will try to make much of the toxicology report [hereinafter “TR”] that the ME appended to the AR — because TR asserted (wrongly) that “In fatalities from [sic] fentanyl, blood concentrations are variable and have been reported as low as 3 ng/mL.” Comment 9 of TR’s “Reference Comments.”
[Part One endnote 19
I expect the defense has pressed or will press TR’s “3 ng/mL” assertion together with the ME-interviewing Assistant County Attorneys’ Notes’ medically and legally incompetent assertion: “Fentanyl – 11. He [the ME] said, ‘that's pretty high.” .... That is a fatal level of fentanyl under normal circumstances.”
TR was produced and signed by Daniel S. Isenschmid, Ph.D., F-ABFT. Dr. Isenschmid, Ph.D., F-ABFT is not a physician. As appears below, Dr. Isenschmid’s language “In fatalities from [sic] fentanyl, blood concentrations…have been reported as low as 3 ng/mL” is not evidence admissible in a criminal trial (or even a civil trial).
In TR Reference Comment 9, Dr. Isenschmid’s language “In fatalities from fentanyl…have been reported” is at best ambiguous.
Because Dr. Isenschmid is not a physician and did not cite even one actual case in which death occurred quite and only because of intake of fentanyl producing a 3 ng/mL serum fentanyl concentration, a fact-finder must question, sternly, whether “fatalities from fentanyl” excludes the possibility of a comorbidity’s or comorbidities’ contributing to the fentanyl-involved deaths.
Just as very, very few (if any) humans die simply and only because of sudden auto-induced total cessation of heart-and-lung function (i.e., with zero involvement of any other causative agent or event), so also, few humans die simply and only because of intake of some quantity of fentanyl or any other opioid (i.e., with zero involvement of any other causative agent or event).
Dr. Isenschmid’s “low as 3.0 ng/mL” serum-fentanyl-caused-death “reports” are highly suspect. Dr. Isenschmid did not cite any such reports. He did not specify the allege reports’ pathology-bases or show that the alleged reports’ reflected performance of all necessary pathology-investigations.
Also, many medical-test laboratories [hereinafter “lab” or “labs”] operate in the U.S. Each lab has its own “normal,” “low,” and “high” “reference”-ranges respecting every chemical substance respecting which it runs quantity-tests. Lab-to-lab, ranges vary, sometimes markedly. Example: LabCorp’s free triiodothyronine [“free T3”] “normal” range is 2.0-4.4 pg/mL; but Quest Diagnostics “normal” range” is 2.3-4.2 pg/mL. The difference can be significant vis-a-vis the patient’s reverse-T3, thyroxin [“T4”], and thyroid stimulating hormone [“TSH”] levels.
Labs obtain their reference-ranges much from “reports” of serum, urine, mucous, or solid-tissue levels of the substances that are subjects of tests; but many such reports are not verified scientifically valid and reliable. Too many lab results are false (false counts, false positives, false negatives, erroneous test-procedure applications......).
Only a properly conducted immensely thorough, peer-reviewed and empirically sound forensic pathologist’s antemortem analysis could, possibly, be a scientifically trustworthy basis of a conclusion that, alone (without presence of any possible comorbidity), some certain serum fentanyl quantity — per TR’s assertion, 3 ng/mL — caused a closely ensuing death.
“Empirically sound”? If valid, reliable scientific studies produced results that impeach such forensic pathologist’s analysis, then a related autopsy report must be treated as questionable — despite the report obtained support of a peer review.
Then, too, TR Reference Comment 9 includes this language:
It is reported that patients lost consciousness at mean plasma levels of fentanyl of 34 ng/mL when infused with 75 mcg/Kg over a 15 min period; peak plasma levels averaged 50 ng/mL.
So, per TR Comment 9, a patient can survive 50 ng/mL or greater plasma concentration of fentanyl. That inference follows from TR Comment 9' statement that “patients lost consciousness” after peak plasma levels that averaged 50 ng/mL and TR Comment 9's failing to state that all such patients either did not regain consciousness but died or regained consciousness and then died.
Now the matter of the admissibility of the TR attached to the AR — a matter of scientific or statistical validity and reliability, not just judicial policy.
The TR’s “as low as 3 ng/mL” statement would not be admissible in the defendant policemen’s criminal trial.
Like all other Anglo-American jurisdictions, Minnesota has a hearsay evidence rule — that if a statement is made outside a judicial trial in which a party seeks to introduce that extrajudicial statement as proof of what the statement says, the statement is inadmissible unless it fits a certain exception the law deems trustworthy enough to deserve admission as independent evidence. Minnesota’s root hearsay rule consists of two interrelated rules, Minnesota Court Rules: Evidence Rules 801 and 802.
[You can read the official Minnesota evidence rules here, where you can confirm the evidence rule statements I put in this paragraph and below.
Minnesota’s hearsay rule permits, per exception, admission of certain “public records and reports.”
Unless the information’s sources or circumstances indicate lack of trustworthiness, a court may admit into evidence “records, reports, statements, or data compilations, in any form, of public offices or agencies, setting forth...matters observed pursuant to duty imposed by law as to which matters there was a duty to report, excluding, however, in criminal cases and petty misdemeanors matters observed by police officers and other law enforcement personnel....” Minnesota Court Rules: Evidence Rule 803(8)
But the report must be that of “public officers or [public] agencies. Dr. Isenschmid is not a public officer, surely not a public agency. He was an employee of a private, independent firm, “NMS Labs.”
Is Dr. Isenschmid’s report an admissible hearsay rule exception because the Hennepin County Medical Examiner used it? No: It is not the Medical Examiner’s record, report, statement, or data compilation setting forth matters the ME observed.
The TR’s statement is hearsay within hearsay — double hearsay — hence deemed specially lacking trustworthiness unless “each part of the combined statements conforms with an exception to the hearsay rule.” Minnesota Court Rules: Evidence Rule 805.
The TR’s “fatalities...have been reported [caused by serum fentanyl concentrations]...low as 3 ng/mL” statement is inadmissible hearsay for the same reason that makes the TR itself inadmissible hearsay. Also, who or what “reported” the fatalities? What methods were used? Were comorbidities ruled out validly, reliably?
But suppose (as is near-absolutely certain) the ME testifies, first for the prosecution. Then Minnesota Court Rules: Evidence Rule 703 would govern:
(a) The facts or data in the particular case upon which an expert bases an opinion or inference may be those perceived by or made known to the expert at or before the hearing. If of a type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject, the facts or data need not be admissible in evidence.
(b) Underlying expert data must be independently admissible in order to be received upon direct examination; provided that when good cause is shown in civil cases and the underlying data is particularly trustworthy, the court may admit the data under this rule for the limited purpose of showing the basis for the expert’s opinion. Nothing in this rule restricts admissibility of underlying expert data when inquired into on cross-examination.
If the case were not a criminal case, then, during a direct examination (not cross-examination), the ME could reference the TR. I am not privy to a complete recording of the ME’s testimony. As I observed at the start of this article
] I have only snippets like this and this and this. But, I should hope that the prosecution did not, and will not, ask a question that could lead the ME to address TR’s “as low as 3 ng/mL” assertion. The “as low as 3 ng/mL” assertion would require the prosecution to disprove a matter that would unduly and unfairly prejudice the state’s case. See Minnesota Court Rules: Evidence Rule 403.
Also, TR’s “as low as 3 ng/mL” assertion would need to be proved to be a “type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject.” That proof would be very difficult if not impossible. More important: The “expert data must be independently admissible...to be received upon direct examination,” and the data are not independently admissible since they are inadmissible hearsay. Compare Rule 703(a), Rule 703(b)’s first sentence and Rules 801, 802, 803(8), & 805.
But the conclusively controlling matter is: TR (including its “as low as 3 ng/mL” assertion) could not be admissible in direct examination, because the case is a criminal trial: “...when good cause is shown in civil cases and the underlying data is particularly trustworthy, the court may admit the data under this rule for the limited purpose of showing the basis for the expert’s opinion.” Rule 703(b), 1st sentence.
During cross-examination, defense counsel may inquire into TR — to impeach the ME or his direct examination testimony supporting the ME’s ruling that Floyd’s death was homicide. But though “Nothing in this rule [Rule 703 (quoted above)] restricts admissibility of underlying expert data when inquired into on cross-examination, other Rules do restrict such data’s admissibility — Rules 403, 801, 802, 803(8). Those other rules would render very difficult defense counsel’s convincing the judge to allow admission of TR’s “as low as 3 ng/mL” assertion.
Beyond the above-presented reasons why TR’s “as low as 3 ng/mL” assertion would not be admissible, an immensely critical reason obtains in pertinent medical science literature and the opinions of medical experts of medical fields specially pertinent to the drug issues of Floyd’s case — earlier in this Part (Part One) of this article, this article showed very abundantly.
The ME’s Press Release concluded that Floyd’s death was “homicide.” AR confirms the ME’s Press Release. See supra § III.8 “The Autopsy Report’s Cause-of-Death Statement.” If fentanyl were the cause-of-death, Floyd’s death would not be homicide. AR and the ME’s Press Release would not rule Floyd’s death homicide if the ME believed fentanyl was, or could have been, the sole, direct cause-of-death.
AR seems to suggest that Floyd died about a half-hour after Floyd was removed from the arrest-scene. AR asserts: “Toxicology...testing performed on antemortem blood specimens collected 5/25/20 at 9:00 p.m. at HHC and on postmortem urine....” [AR p.2.] But even if Floyd was alive when he was removed from the arrest scene (a matter that is debatable, see below), the police compression-restraints were the legal proximate cause of Floyd’s death.
The compression-restraints would have been the legal proximate cause of Floyd’s death even if Floyd lived hours after being removed from the arrest scene or if a panicked Floyd resisted, mindlessly, a medical attempt of resuscitating him or if he refused certain resuscitation means because he was a Jehovah’s Witness. See Part Two of this article.
Floyd was pronounced dead at 9:25 PM. But, according to rule, or negligently, paramedics or emergency room physicians, technicians, or nurses may consider pre-official-death-pronouncement tests technically “antemortem,” because
(a) they are using heroic measures to resuscitate the patient who has not been officially pronounced dead or
(b) the paramedic or emergency room protocol may be that a patient is not “dead” until he is formally, officially, pronounced dead. Arrest scene videos and the police body-cam record show that paramedics tried to resuscitate Floyd.
If not the paramedics, emergency room staff would have drawn blood near-immediately during resuscitation efforts. The police body-cam record (supra) and sundry arrest videos suggest, strongly — arguably prove — that Floyd died at the arrest scene. On premise of several videos of Floyd’s arrest and other evidence including that derived from Emergency Room examination of Floyd, a forensic pathologist my conclude Floyd died at the arrest scene.
[Part One endnote 20 ]
Floyd’s actual time-of-death — whether he died at the arrest scene — can be important. If actually the blood-draw occurred after Floyd was dead, Floyd’s (postmortem) serum fentanyl level would not be reliable evidence of whether fentanyl overdose (perhaps together with “excited delirium”) was the direct and sole cause of Floyd’s death.
In Chauvin’s trial, the court heard testimony of the he Emergency Room physician who attempted to resuscitate Floyd after paramedics took Floyd to hospital. That physician testified that he did not find evidence that Floyd had suffered excited delirium but that the evidence indicated hypoxia had caused cardiac arrest. The same physician testified also that Floyd had suffered cardiac arrest for 30 minutes or more. [See again Part One endnote 20.]
Only if one knows in advance of death a patient’s serum fentanyl concentration (or the serum concentration of any other oft-lethal drug) can one deduce whether the drug’s serum concentration level was the direct, and only, cause of the patient’s death. In a case like Floyd’s, forensic medical science cannot work, reliably, in reverse. If, somehow, a pathologist rules out any cause of death other than drug overdose, still the pathologist offers no more than an assertion of a probability that only a drug “overdose” was the direct cause of death. The assertion would beg two related questions:
(a) Was the drug’s serum concentration level an “overdose”? That is a very muscular question because (as this article shows above) the literature does not — cannot — set a certainly lethal serum concentration level.
(b) Could some comorbidity’s presence have evaded the pathologist’s investigation? Pathology is an inexact science. It depends much on judgment that, in turn, depends on imperfect-knowledge, imperfect-experience, imperfect evidence, and a partly-emotional sense of what feels ethically or morally defensible. Medical science — hence pathology — is still just learning what ingredients constitute medical “reality,” including the “reality” of what constitutes this or that “disease” and its “cause(s).” Cf. the immense and shifting ignorance that infests the whole field of Covid-19 [and vis-a-vis the Covid-19 matter, compare Part Two endnote 9 & related Part Two text.]
Ultimately, TR’s “as low as 3 ng/mL” assertion impeaches itself with its own terms: The phrase “as low as 3 ng/mL” begs an intractable question: What is the upper limit of non-lethal serum concentration? Again see, e.g., Fatal Fentanyl (supra) at id. p.110, in the Key of Table 2: “The therapeutic (TL) and toxic (TX) serum levels…are: fentanyl TL = 1-2 ng/mL, TX = 2-20 ng/mL, lethal >20 ng/mL....” [The term “>20 ng/mL” means “greater than 20 ng/mL.”]
Recall that in the Fatal Fentanyl study (supra), one surviving patient’s serum fentanyl concentration was 162.3 ng/mL, another’s was 123.1 ng/mL, third’s was 65.9 ng/mL, a fourth’s was 64.3 ng/mL, a fifth’s was 53.3 ng/mL, a sixth’s 51.3 ng/mL, a seventh’s 39.4 ng/mL, an eighth’s 36.3, a ninth’s 27.0 ng/mL, a tenth’s 22.7 ng/mL, an eleventh’s 17.0 ng/mL, and a twelfth’s 16.5 ng/mL — all markedly higher than George Floyd’s 11 ng/mL, and several many times higher. See Fatal Fentanyl Table 2 (pp.109-110).
So, zero evidence suffices to support even a rebuttable presumption that Floyd died because of drug abuse or even drug abuse compounded by cardiovascular weakness. But much strong evidence indicates powerfully — even proves conclusively — that Floyd would not have died when he did because of serum concentration of fentanyl and other drugs or because of cardiovascular weakness or both.
See also this, which reinforces the rest of the above-discussed evidence that shows the cause-of-death was asphyxiation caused by brain-hypoxia/brain-hypercapnia caused by the neck/dorsa-thorax compression-holds the police applied to Floyd.
The remaining matters are near-exclusively matters of law and of evidence of the conduct of Chauvin and his cohorts. Those matters are addressed in Part Two of this article.
Actually, the woman might not have perished had the man not shot her. Suppose the woman thrust her body outward with great force, so that her fall would end at the nearest lane of the four-lane street below — not on a sidewalk. A millisecond before the victim’s body reached the building’s third floor, a farmer stopped his large pickup truck in that nearest lane of the street. The truck was hauling a long, open trailer filled high with hay. The victim’s body fell onto the hay. Had she not suffered the shotgun blast, she would have survived. Later below, this article presents judicial judgments holding that, in some circumstances, a homicidal act renders the wrongdoer legally liable despite the victim (a) died a substantial time after the wrongdoer’s homicidal act occurred and (b) died partly, or even directly, because of the victim’s own supervening conduct. Such judgments are explained partly by the second, third, and fourth principles, which, partly, explain each other and also the first principle.
Chauvin has tried to defend with the argument that he did not kneel on Floyd’s neck, but on Floyd’s shoulder. That defense is clearly untenable, as will appear below.
My father’s grandfather was an Estonian born into Greek Orthodox Christianity. In his early adulthood, he converted to Judaism and took a Jewish name. My father did not practice Judaism (though he pressed me unsuccessfully to undergo bar mitzvah), but he (my father) immersed himself in Theosophy (thence also Hinduism, and Buddhism). I am an atheist who despises all religion, even personal moral codes, even the quasi-religion the superego imposes on near-all humans. My mother was Greek Orthodox Christian but never tried to impose her religion on me.
In 1946, just 15 days after my 6th birthday, my parents shunted my sister and me to an orphanage run by Roman Catholic nuns. The orphanage “society” was brutal. A Black inmate, an 8-year-old boy, became my protector, voluntarily, even as if by instinct. I shall never forget his goodness. See my short story “DIAMOND STREET: A True Story.” In 1962, I lived in a slum apartment of a Philadelphia section called Powelton Village. I had a Black roommate, Jim Bullock. Jim held a BA degree and attended graduate school. We became close friends. Once, after Jim and I had drunk a bit too much booze, Jim asked me whether I thought he was my friend. I said: “Sure.” Jim disagreed. “You can’t be my friend ‘til you admit to yourself that your heart recoils against me, even from my smell, because I’m Black and you’re White.” Jim insisted nature made all creatures gravitate away from others who are different and toward those who are “the same.” I could be his friend only if I accepted that fact-of-nature and found a rational, honest means of rising above it. Jim was right. And we did become true friends. We are fools if we deny our natural aversion to the different and inclination toward the same. We are fools if we feel guilt merely because we tend away from the different. But we are worse fools if we dislike others merely because they are different. I feel just one empathic obligation: that I not hurt or disparage another merely because he is not like me. We must feel free to enjoy our tastes, guiltlessly — but not to damage or contemn others merely because of our tastes.
Compare endnote 4, supra. I appreciate the Blacks who contribute utility to society or, at least, are not burdens or crass annoyances. I concede, painfully, that too many non-Blacks— rich, middle class, and poor — also are garbage: criminal (whether caught or not), empathy-and-conscience deficient, takers who produce little or nothing beneficial to others, blithely ignorant but troublously opinionated, inelegant and rude....... But the matter is George Floyd — neither any non-Black or any other Black. Floyd was prosecuted, or at least arrested and charged, nine times, for felonies at least six times, one time for robbing a pregnant woman and pointing a pistol at her belly or joining in an armed robbery of a woman whom the robbers pistol-whipped in the presence of her children — and for which crime Floyd was sentenced to a prison term. Floyd was arrested or charged at least 19 times during his adulthood. Some woke apologists claim Floyd was fundamentally good and had big dreams. But for most of his adult life, Floyd dealt and used drugs and engaged also in other criminal conduct; and if he had “big dreams,” the dreams never manifested as contributions to society, rather than as social costs.
“Law-enforcement” agencies and their officers abuse Whites, Asians, and other non-Blacks quite frequently enough. I have been a victim of such abuse, as have numerous of my friends, both Black and non-Black. Though serious physical abuses enjoy widely felt infamy, other, non-physical abuses injure lives and individual liberty more often and too frequently render much worse effects. One heinous example is our society’s Covid-19 lock-downs and mask/social-distancing mandates that have devastated our society economically, psychologically, and educationally — for zero scientific reason, but contrary to all pertinent scientific indications. [See also Part Two endnote 9, which debunks reliance on the utterly unreliable PCR test, which has formed much of the false premise of the phony Covid-19 pandemic.] A related example is the Democrats’ using Covid-19 to distort the process and outcome of the 2020 elections.
I used the language "5th amendment and 14th amendment human person" [emphasis added here] because a corporation can be a 5th amendment or 14th amendment “person.” Though Floyd was judged to have committed at least one felony, he was never alleged to have committed a capital offense [see supra endnote 5]. Hence I wrote that Floyd “did nothing that could support a court’s sentencing him to death.” “A rational, civil society accords due process even to the meanest, vilest of its members”? Even a serial child-rapist/murderer is entitled to due process of law — before and during his murder trial and after being adjudged a serial child-rapist/murderer.
Fatal Fentanyl Table 1 (p.108). The full range was [listed by patient number]: 296h 5m 69h 1m 8 h 22 m 21h 11m 41h 33m 6h 40m 67h 33m 10h 54m 16h 30m 5h 42m 12m death 10h 49m 31h 55m 4h 7m 6h 40m 43h 21m 8h 9m 4h 13m
A low-fentanyl-tolerance individual may not survive even a 0.2 ng/mL serum fentanyl concentration if, e.g., his blood bore also high concentrations of other opioids and amphetamines and promethazine and he suffered several comorbidities (e.g., renal disease, diabetes, cardiovascular disease, acute hepatitis, and influenza......).
In its Table IV (p.607), Fentanyl-Related Deaths maps out cases in which the deceased’s fentanyl administration was intravenous. Serum fentanyl concentrations were [measured as μg/L (= ng/mL)]: 3, 7, 8, 8, 9, 18, 21, 21, 22, 28, 34, 40, 91, 383 — mean 49.5, median 21, σ = 94.9298613262, s = 98.513372774383. The curve was bimodal — 8, 21. Since (a) the median equaled one mode (21), (b) another mode was greatly lower than the mean, and (c) the median, mean/median difference, and one mode were significantly less even than one standard deviation from the mean, the median, 21 [= mode 21], not the mean (49.5), was the most reliable predictor, and nearly twice Floyd’s 11 ng/mL serum fentanyl concentration. No evidence suggests the means of fentanyl-administration George Floyd used. Floyd may have said [per transcript of a body-cam record (see infra endnote 13)] that he was hooping (which, apparently, is a gutter slang term meaning inserting anally). But Floyd did not say he had administered fentanyl anally. And no evidence either precludes or indicates consideration of the prospect that Floyd administered fentanyl intravenously. Floyd’s criminal record includes conviction for possession with intent to deliver cocaine. See endnote 5 and this source. But very few cocaine-users inject that substance. And I have found no information that Floyd possessed, distributed, or used heroin or any illicit drug typically administered intravenously. Intravenously-administered fentanyl is deadlier than orally or dermal-patch delivered administered or inhaled fentanyl. If the fentanyl dose is a constant, intravenous delivery will shock the system most, because it drives the entire dose instantly into the bloodstream. This much is clear. Whatever Floyd’s administration-means, minutes after paramedics took him from the arrest scene, his serum fentanyl concentration was 4.5 times less than the mean and about half the median of the Fentanyl-Related Deaths cases in which fentanyl was delivered intravenously and about half the mean serum fentanyl concentration found in most of the other Fentanyl-Related Deaths subjects. See supra — discussion of Fatal Fentanyl.
The ME Interview Notes asserted that the ME said “Fentanyl – 11. He said, ‘that's pretty high.’ This level of fentanyl can cause pulmonary edema. Mr. Floyd's lungs were 2-3x their normal weight at autopsy. That is a fatal level of fentanyl under normal circumstances.” Then the Notes asserted also that the ME said “if Floyd had been found had been found dead in his home (or anywhere else) and there were no other contributing factors he would conclude that it was an overdose death” Who, actually, used the exact language “if Floyd had been found dead in his home (or anywhere else) and there were no other contributing factors he would conclude that it was an overdose death”? The Medical Examiner, or an Assistant County Attorney? Does “normal” require comparison of the actual circumstances of Floyd’s death — the neck-press/dorsal-thorax compressions police applied to Floyd? What is the meaning of “under normal circumstances” or of “contributing factors”? In the actual case, were the “circumstances” “normal”? Were “contributing factors” present? The police applied neck/dorsal-thorax compression-holds to a man showing symptoms of possible serious physiological stress. The police applied the compression-holds for more than 9 minutes, even more than 3 minutes after Floyd became unconscious. The neck-compression must have caused brain-hypoxia and brain-hypercapnia. The dorsal thorax compression exacerbated that neck-compression effect. The brain cannot survive hypoxia and hypercapnia for more than ≈2 minutes. Diaphragm/lung occlusion will diminish, possibly stop, the brain’s oxygen-supply and expulsion of carbon dioxide from the brain. Cf., e.g., this and this [and Dr. Michael Baden the video included there] and this and this and see this matter’s further discussion occurring below. Found “dead in his home”? Suppose; (a) Floyd had not died at the arrest-scene or very shortly after at an emergency room, but, resuscitated, was released after a judge found lack of “probable cause” of arrest and (b) Floyd returned to his residence and soon died. [In testimony, the ME explained that the Floyd death special circumstances were the neck/dorsal-thorax compressions the police applied to Floyd and that those circumstances supervened over any influence of Floyd's serum concentrations of fentanyl or other drugs. See here. Cf. the sources linked two paragraphs above in this endnote.] All the video evidence and other related evidence (including numerous expert opinions) show that Floyd never exhibited any symptom of possible moribundity — e.g., unconsciousness — until after he suffered 4 to 5 minutes of the police’s 9-minutes-long application of two asphyxia-death-threatening compression-holds. The law would render the compression-hold-applying police guilty of murder or other homicide. See infra Part One endnote 13 & infra § III.8 “The Autopsy Report’s Cause-of-Death Statement” & Part Two of this article. The ME-interviewing Assistant County Attorneys ought to have examined the ME concerning such matters.
Two related matters are “excited delirium” and positional asphyxia — discussed below, under heading 6 “Excited Delirium and Positional Asphyxia.” Likely the defense will claim both that Floyd was suffering excited delirium caused by serum fentanyl/amphetamine concentration and that the excited delirium — not neck-and-dorsal-thorax compression — caused him to suffer asphyxia and cardiopulmonary arrest. Likely the defense will add that positional asphyxia is a myth. The defense may use sources like these: (1) Asia Takeuchi, MD, Terence L. Ahern, BA, and Sean O. Henderson, MD, Excited Delirium, West J Emerg Med. 2011 Feb; 12(1): 77-83. (2) Theodore C. Chan, MD, Tom Neuman, MD, Jack Clausen, MD, John Eisele, MD, and Gary M. Vilke, MD, Weight Force During Prone Restraint and Respiratory Function, Am J Forensic Med Pathol 25(3):185-189, September 2004.
RE: the police conduct’s unlawfulness and unconstitutionality, see Part Two of this article. RE: Floyd’s drug-use and his panic: Floyd said he had been “hooping.” Kueng (a policeman): You got foam around your mouth, too? George Floyd: Yes, I was just hooping earlier. Body-cam Transcript at lines 86-89. Likely, Floyd used the term “hooping” as a gutter slang word that denotes intaking a drug by inserting it in the anus. So, Floyd’s statement may prove that Floyd had engaged in drug abuse not long before the start of the policemen’s arresting him. The defense has tried to make a point of Officer Kueng’s assertion that Floyd had “foam around [Floyd’s] mouth. But (a) Kueng’s assertion is dubious [see below, this note], and (b) Floyd’s drug-abuse is not, itself, an issue, since the autopsy report includes a tox screen that shows Floyd’s blood bore 11 ng/mL fentanyl, 19 ng/mL methamphetamine, and sundry cannabinoid compounds or metabolites (11-Hydroxy Delta-9 THC 1.2 ng/mL; Delta-9 Carboxy THC 42 ng/mL; Delta-9 THC 2.9 ng/mL). Floyd’s “hooping” statement is, however, relevant to prove that the arresting police ought to have foreseen that their compression holds would kill Floyd. Still, an interesting question is whether Floyd had “foam around [his] mouth” (if he did) because of his intaking a drug. A frothy whitish substance can form at the lips because of dryness after hard work or other physical stress or for other nonpathological causes — rather than because of a seizure or intake of fenantyl or some other opioid or amphetamine or methamphetamine or another such drug. Floyd was stressed for reason other than intake of drugs. Nothing indicates he had eaten or ingested liquids recently. So, the “foam” (if it was “foam”) might have resulted from influences other than drugs. And a drug-abuse cause is not deducible from Floyd’s having said “Yes, I was just hooping earlier” immediately after Officer Kueng uttered the apparent question “You got foam around your mouth, too?” Since Floyd was panicking, we cannot presume that his “hooping” statement responded to Officer Kueng’s question. Even must we question whether the Body-cam Transcript reports truth with its language that Floyd said “Yes [emphasis mine], I was just hooping earlier.” Except in Floyd’s putative “hooping” statement, throughout the Transcript and in the audible portions of all the available online-published videos of the Floyd’s arrest, Floyd’s language is not formal or that of a well educated, “proper” person, but a rather poorly educated, very informal ghetto Black, who would not have used the term “Yes” — especially in the context of his stressful arrest. And why “just hooping”? Does that phrase fit an event of taking a drug by anal insertion, rather than shooting hoops (playing basketball)? Floyd was a serious, nearly professional, basketball player earlier in his life. So, Floyd may have meant that he had been doing a bit of “shooting hoops” not long earlier — activity that could explain the presence a frothy whitish substance around his mouth, especially vis-a-vis the added stress of the arrest.
Chauvin weighed 154 to 167 lbs (see supra). One or two other policemen pressed some or all of their weight to Floyd’s dorsal thorax. Suppose the two other policemen weighed only 140 pounds each (rather light weight for adult males). Then, even if each such other policeman pressed only half his weight onto Floyd’s dorsal thorax, the total dorsal-thorax-applied weight would have been 140 lbs. [Videos show two policemen pressing at Floyd’s dorsal thorax area.] During Chauvin’s trial, the defense showed part of a video of the events that led to Floyd’s death. Defense counsel urged that the video showed Chauvin’s having kneeled on Floyd’s shoulder, not on Floyd’s neck. Defense counsel pressed a witness to agree that Chauvin was kneeling only on Floyd’s shoulder. During brief stretches of at least one of the several videos showing the Floyd murder events, the camera angle and the participants’ body-movements rendered the images ambiguous. But other videos showed clearly that Chavin knelt on Floyd’s neck, e.g., this. And in Chauvin’s trial, quite enough police testified that Chauvin knelt on Floyd’s neck with deadly force that violated Minneapolis police department rules or norms. See, e.g., this and this and this and this. No video suggests Chauvin knelt exactly on Floyd’s shoulder. Sometimes, briefly, Chauvin’s left knee’s right-lateral extreme touched a tip or edge of Floyd’s scapula. But even then, the knee’s forward (distal) portion remained on Floyd’s neck, still pressing into the trough where neck meets clavicle and clavicle curves down and fore toward the sternum and cervical spine — still pressing Floyd's neck, still compressing Floyd’s carotid artery or jugular vein or both. Throughout the 9-plus minutes of Chauvin’s kneeling on Floyd’s neck, Chauvin’s knee pressed Floyd’s neck enough to occlude Floyd’s carotid artery or jugular vein or both.
See infra § III.8 “The Autopsy Report’s Cause-of-Death Statement” and supra Part One endnote 13 & related text. And see Part Two of this article. The ME’s report states that the autopsy blood screen showed presence of fentanyl [and fentanyl metabolites norfentanyl and 4-ANPP (despropionyl fentanyl)] and also methamphetamine, and that the urine screen results were presumptively positive for amphetamines and “fentanyl/metabolite.” Amphetamines and fentanyl can interact to cause serotonin syndrome. See, e.g., this and this and this. And cf. this and this. Serotonin syndrome may involve confusion, extreme changes of blood pressure, increased heart rate, shivering, shaking, blurred vision, muscle spasms, tremor, or physical incoordination— or a combination of such symptoms. See, e.g., this and this and this and this. Such symptoms are consistent with Floyd’s appearing destabilized — stumbling, lurching, having uneven gait, falling, panicking, fearing dypsnea....... But per observation of a video record of the events that led to Floyd’s death and the contents of autopsy reports and the ME’s press release, forensic pathologist Dr. Judy Melinek opined that Floyd did not appear to be suffering excited delirium or agitation leading to sudden death. Other experts have reached the same conclusion. Compare this and this and this and this and this and this; and see this testimony of the Emergency Room physician who tried to resuscitate Floyd when paramedics took Floyd to hospital — testimony that the evidence contraindicate a finding that Floyd had suffered excited delirium.
Additionally to the sources put in the text of this section — § III.7 “Absence of Evidence of Hypoxic Ischemic Brain Injury?” — the following sources render support of this section’s observations and conclusions. Most below-listed sources are not available online except (a) for a fee or (b) to medical-science professionals who have paid subscriptions to the publishing journals. * Ames A III, et al., Cerebral ischemia II. The no-reflow phenomenon, Amer J Pathol 1968;52:437-53 * Biros MH, Dimlich RW, Barsan WG, Post-insult treatment of ischemia-induced cerebral lactic acidosis in the rat, Ann Emerg Med 1985;15:397-404 * Blaustein MP, Ratzlaff R, Kendrick N, The regulation of intracellular calcium in presynaptic nerve terminals, Proc NY Acad Sci 1978;307:195-212 * Carafoli E, Crompton M, The Regulation of Intracellular Calcium, Curr. Topics Memb. Transport, 1978;10:151-216. * Farber JL, Chien KR, Mittnacht S, The pathogenesis of irreversible cell injury in ischemia, Amer J Pathol 1981;102:271-81 * Hertz L, Features of astrocyte function apparently involved in the response of central nervous tissue to ischemia-hypoxia, J Cereb Blood Flow Metab 1981;1:143-53. * Heuser D, Guggenberger H, Ionic changes in brain ischemia and alterations produced by drugs, Br J Anesth 1985;57:23 * Kalimo H, Rhencrona S, Soderfeldt, et al, Brain lactic acidosis and ischemic cell damage, Histopathology. J Cereb Blood Flow Metab 1981;1:313-27 * Kaplan J, Dimlich RVW, Biros MH, Hesges J, Mechanisms of Ischemic cerebral injury, Resuscitation 1987;15:149-169 * Lowry OH, Passonneau JV, Rock MK, The stability of pyridine nucleotides, J Bio Chem 1961;236:2756-59 * Mitchell P, Moyle J, Chemiosmotic hypothesis of oxidative phosphorylation, Nature 1967;213:137-139 * Mullane KM, Salmon JA, Kraemer R, Leukocyte derived metabolites of arachidonic acid in ischemia-induced myocardial injury, Fed Proc 1987;46:2422-33. * Raichle ME, The pathophysiology of brain ischemia, Ann Neurol 1983;13:2-10 * Reichelt KL, The chemical basis for the intolerance of the brain to anoxia, Acta Anesthesiol Scand 1978; Suppl. 29:35-46 * Rhenchrona S, Brain acidosis, Ann Emerg Med 1985;14:770-76 * Rhenchrona S, Rosen I, Siesjo B, Brain lactic acidosis and ischemic cell damage: I. Biochemistry and neurophysiology, J Cereb Blood Flow Metab 1981;1:297-311 * Rhencrona S, Rosen I, Smith ML, Effect of different degrees of brain ischemia and tissue lactic acidosis on the short-term recovery of neurophysiologic and metabolic variables, Exp Neurol 1985:87:458-73 * Siesjo BK, Bendek G, Koide T, et al., Influence of acidosis on lipid peroxidation of brain tissues in vitro, J Cereb Blood Flow Metab 1985;5:253-58 * Siesjo BK, Cell damage in the brain: a speculative synthesis. J Cereb Blood Flow Metab 1981;1:155-85. * White BC, Wiegenstein JG, Winegar CD, Brain ischemia and anoxia: Mechanisms of injury, J Amer Med Assoc 1984;251:1586-90 * Wolfe LS, Eicosanoids: prostaglandins, thromboxanes, leukotrienes and other derivatives of carbon-20 unsaturated fatty acids, J Neurochem 1982;38:1-14.
See, e.g., this source — under its heading “Mild to Moderate Asphyxia: Intraventricular Hemorrhage”: “It is believed that hypoxia-ischemia initially causes damage to the endothelial cells of the germinal matrix capillaries, resulting in loss of normal capillary integrity.” [Emphasis added here.]
But see supra endnote 15 & generally supra §§ II.2 (“Serum Fentanyl Concentration”) through II.6 (“Excited Delirium and Positional Asphyxia”). Cf. infra under heading “EGGSHELL SKULL RULE, FORESEEABILITY, AND ENHANCED FORESEEABILITY.
Reference Comments’ Comment 9 bears this text: Fentanyl (Duragesic®; Sublimaze®) - Hospital Blood: Fentanyl is a DEA Schedule II synthetic morphine substitute anesthetic/analgesic. It is reported to be 80 to 200 times as potent as morphine and has a rapid onset of action as well as addictive properties. It is reported that patients lost consciousness at mean plasma levels of fentanyl of 34 ng/mL when infused with 75 mcg/Kg over a 15 min period; peak plasma levels averaged 50 ng/mL. After application of a fentanyl transdermal preparation (patch), serum fentanyl concentrations are reported to be in the following ranges within 24 hours: 25 mcg/hour patch: 0.3 - 1.2 ng/mL 50 mcg/hour patch: 0.6 - 1.8 ng/mL 75 mcg/hour patch: 1.1 - 2.6 ng/mL 100 mcg/hour patch: 1.9 - 3.8 ng/mL Following removal of the patch, serum fentanyl concentrations are reported to decrease with a mean elimination half-life of 17 hours (range, 13 to 22 hours). The mean peak plasma serum fentanyl concentration in adults given an 800 mcg oral transmucosal fentanyl preparation over 15 minutes is reported at 2.1 ng/mL (range, 1.4 - 3.0 ng/mL) at approximately 0.4 hours. Signs associated with fentanyl toxicity include severe respiratory depression, seizures, hypotension, coma and death. In fatalities from fentanyl, blood concentrations are variable and have been reported as low as 3 ng/mL. Substance(s) known to interfere with the identity and/or quantity of the reported result: 4-methylphenethyl acetyl fentanyl