George Floyd's Death - Response to Comments

Many commenters to my last post offerred up alternative explanations to my conclusion as to the cause of Mr. Floyd's death. Let's go through them.

In my previous post on the George Floyd case, I presented both a truncated version of the reasoning and evidence supporting my legal expert opinion report as well as the official eleven-page legal, written testimony that I submitted to the lawyers who retained me in his civil case.

Based on the number and content of comments to my post, I discovered several areas which continue to lead to confusion and questions and alternative hypotheses. Some were a surprise to me and some were not. For instance, it is unsurprising that the case of Mr. Floyd continues to elicit strong emotions and strong beliefs and that the shortened version of my official testimony was insufficient (few read the longer version and many appear to have skimmed or superficially thought through the shortened version).

Although I do not really want to delve into the case of Mr. Floyd further because I do not believe that countering data can change belief systems (nor do we need to flame more emotions or division/polarization). However, I will make a final attempt to address the data underpinning alternative conclusions to mine. Plus, many of us “medical dissidents” in Covid have been crying out with authorities for public debates of the available evidence underlying early treatments, vaccines, lockdowns, and masks. None were granted.

So, although not a “true” debate, what I am doing is consistent with what academics do to critique and counter scientific papers in journals - they send their critique as a “Letter to the Editor” of the journal who published the paper, and the authors are required to offer a defense of their data, analysis, and conclusions in regards to the specific critique offerred.

One critique from commenters is that Mr. Floyd was heard saying “I can’t breathe” well before he was put into prone restraint and thus his inability to breathe was caused by something other than prone restraint, like opiate intoxication, heart attack, methamphetamine use etc. This argument was best articulated in an article sent to me written by former Federal and State Prosecutor George Parry. He is also the Chief of the Police Brutality/Misconduct Unit of the Philadelphia District Attorney’s Office, which investigated and prosecuted use of deadly force by police.

In the above article, Parry’s marshaling and interpretation of the evidence led him to conclude that Mr. Floyd died of an opiate overdose. Unfortunately, Mr. Parry exhibited no knowledge of the various types and presentations of acute respiratory failure which I believe is required to make an assessment of his death. That is why a pulmonologist and ICU specialist was retained and not a lawyer. .

Now, what makes a clinical expert in medicine is not just medical knowledge, but rather the development of deep powers of “pattern recognition” which can only be acquired over years in the evaluation and treatment of thousands of patients. There are several discrete categories of respiratory failure with a large number of inciting causes. I have seen and treated all, thus I am highly familiar with their presentations, trajectories, treatments, and prognoses.

To wit, I worked for years in the ICU and pulmonary wards at a busy hospital in Manhattan at the equivalent of more than 2.0 FTE per year. The reason for this is that other intensivists kept leaving and recruiting knew ones took a long time so we were always running a deficit in the number of intensivists to take care of the large volume of patients. As a result, I was treating and billing for so many patient hours that at one point the hospital administration became concerned it would trigger an audit for fraud (know that as an employee of the hospital I saw a small fraction of the billings generated). What I am trying to say is that I was evaluating and treating patients in acute respiratory failure for years (and giving lectures on causes and treatments for years).

The important facts overlooked by many is that when someone is in a life threatening, severe form of acute “hypoxic” pulmonary pathology, they exhibit severely increased “work of breathing” as evidenced by rapid breathing, use of accessory muscles, exaggerated respiratory efforts, over-expansion of chest, nasal flaring, sweating etc. They often can barely speak. Although they might be able to say “I can’t breathe,” they certainly cannot speak full sentences. I observed no such signs of hypoxic respiratory failure in the multiple videos of the arrest episode.

Further, in his article, Parry provides the transcript of the conversation Mr. Floyd was having with the officers before and during their first attempt to place him in the police car. The most important parts that I focused on in that transcript were fundamentally different than Parry’s. Although Floyd said he couldn’t breathe he also repeatedly said he was claustrophobic but the important point is that he was capable of having a prolonged conversation.

For instance, read this exchange between Officer Keung, Lane and Floyd:

Floyd: I can’t breathe.

Kueng: You’re fine, you’re talking fine.

Lane: Your talken (sic), Deep breath.

Note that both Keung and Lane are making observations on his respiratory function and status - Keung rightly remarks that he is able to speak normally and Lane even encourages him to take a deep breath (patients in respiratory distress or failure do not need to be told this - it is automatic. That is instead something often recommended to people in panic or distress.

Next, Floyd starts talking to Chauvin, and he starts to complains of a number of other random symptoms:

Floyd: I’m through, I’m 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.

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.

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. Oh!

Chauvin literally has to tell him to “stop talking” because “it takes a lot of oxygen to talk.” True. Again, patients in respiratory failure do not need to be told to stop talking. The respiratory deficit prevents them from doing so.

Further, the autopsy findings of his lungs were consistent with autopsy findings in patients post CPR such that the medical examiner did not even include it in his summary of significant findings even though they were described as edematous and congested. He also remarked on other areas of the lung:

No mass lesions or areas of consolidation are present. The pulmonary vascular tree is free of thromboemboli. The tracheobronchial tree is free of blood, edema fluid, or foreign material.

In terms of the autopsy findings in his heart:

Cross sections of the vessels show multifocal atherosclerosis, with 75% proximal and 75% midnarrowing of the left anterior descending coronary artery; 75% proximal narrowing of the 1st diagonal branch of the left anterior descending coronary artery; 25% proximal narrowing of the circumflex coronary artery; and 90% proximal narrowing of the right coronary artery. The myocardium is homogeneous, redbrown, and firm.

The bolded finding is the most important finding (which many commenters overlooked) and indicates that, although he had significant atherosclerotic heart disease (welcome to America), no areas of scar or tissue damage were found indicating a heart attack.

Ok, so the above should address all the comments suggesting he died of a heart attack from his atherosclerosis and/or methamphetamine use given that heart attacks would also typically present as hypoxic respiratory failure. One commenter even argued that Floyd died of “negative pressure pulmonary edema” - a rare form of hypoxic respiratory failure which can also very very rarely be caused by opiates.

Now, the other main category of respiratory failure is called hypercapneic respiratory failure. This occurs when a patient is unable to take in a sufficient volume of air with each breath and/or their breathing rate slows such that not enough air is exchanged and carbon dioxide rises in the blood, rendering them unconscious.

Opiate overdoses are one of the most common causes of hypercapneic respiratory failure and lead to unconsciousness. Prone restraint is also a cause of hypercapneic respiratory failure and leads to unconsciousness. So, which did he die of?

Autopsy won’t really help here given that transient external compressive forces like in prone restraint as well as opiate overdose will not show evidence of acute pathologic changes in the lung or windpipe. From this review paper on prone cardiac arrest:

Autopsy examinations in arrest-related deaths may be unrevealing. Luke and Reay stated that deaths in-custody often demonstrate little pathologic evidence of the cause of death and there are no diagnostic markers of asphyxial deaths [35].

So, how can we differentiate between opiate overdose and prone-induced cardiac arrest? Again, from my prior post, patients dying of an opiate overdose do not say “I can’t breathe.” Why? Because before they stop breathing they first become lethargic in a highly pleasurable state, then progress to unconsciousness and then they stop breathing (this can happen very fast with IV administration of opiates).

What must also be recognized is that in patients suffering from terminal breathlessness from lung pathology, administering opiates in therapeutic palliative doses is a standard treatment to blunts feelings of “dyspnea” (i.e. the sensation of difficulty breathing). Thus, someone high on opiates should not be feeling or complaining of breathlessness.

Thus it is contradictory of Mr. Parry to emphasize that Mr. Floyd was awake, speaking full sentences, and complaining of numerous symptoms including “I can’t breathe” while also concluding he died of a fentanyl overdose. It defies physiologic and pharmacologic reasoning. Thus, given the findings on autopsy, along with Floyd’s behavior and speech and history of claustrophobia, the most rational explanation for why he complained that he couldn’t breathe during the earlier episode was from anxiety/panic at being placed in the police car with claustrophobia. In fact, anxiety/panic is one of the most common causes of dyspnea when the lungs and heart are normal.

That is why both the first medical examiner and the 2nd opinion medical examiner, the plaintiff medical expert in the civil case (me), the plaintiff medical expert in the criminal case (Dr. Martin Tobin) as well as a jury all found that asphyxiation was the cause of death.

Another argument that Parry makes to conclude fentanyl was the cause of his death is based on the measured level of fentanyl in his blood. From my post yesterday,

“..in order to properly interpret the levels found, one must first recognize that chronic opiate users, which Mr. Floyd was, can and do often develop significant levels of physiologic tolerance to opiates. Thus the absolute level measured in a chronic user is not accurately predictive of the degree of intoxication or death. However, I agree that if Mr. Floyd’s level was found in an opiate-naive user, it would almost certainly predict unconsciousness and/or risk of death.”

My favorite argument is when people pointed out that on his death certificate, Floyd was determined to have died of “CARDIOPULMONARY ARREST.” Just so you know, this is the condition of death and is what everybody “dies” from. So much so that it is often unnecessary and redundant to put it on a death certificate. The most important part of a death certificate is the proximate cause contributing to “cardiopulmonary arrest” and not the final arrest state (i.e. death).

Finally, one of Parry’s most compelling arguments is that the medical examiners reached their initial conclusions prior to the toxicology report being made available. This is presented as damning evidence of some sort of malfeasance.

I do not feel this is as significant a finding as Parry because the relevance of his toxicology findings is mitigated by the extensive clinical/observational data from a highly videotaped arrest episode showing Floyd walking, talking, resisting officers and complaining of claustrophobia, difficulty breathing, and multiple other symptoms. None of that behavior supports a finding of severe opiate intoxication which is why they did not conclude that was the primary cause of death. I am sure he was high though, just like millions of people every day who do not die of their drug use.

Thus the absolute level of fentanyl in his blood did not alter their conclusions even after becoming known.

Another argument by commenters was that I, as a plaintiff’s witness, was biased towards arriving at my conclusion. Arguing lack of bias to me is impossible, so all I can offer is that I have done plaintiffs work before and on two occasions I arrived at a conclusion that did not support a finding of malpractice of the accused physician. I was quickly dropped from the case both times. Note that was after being paid for my review work. Thus payment is not predicated on my conclusion.

Another argument by commenters was that his methamphetamine use killed, presumably via an “excited delirium.” From this review paper:

In 2020, Strömmer et al. comprehensively reviewed the literature and concluded that restraint was the common denominator for virtually all fatalities and found “no existing evidence that indicates that [excited delirium] is inherently lethal in the absence of aggressive restraint” [39].

Another argument made by commenters is that Parry states that prone restraint is included as a tactic in the police manual. Not true. Instead, Parry is referring to the use of a neck restraint technique involving compressing the neck with an arm or leg, which he then argues is equivalent to placing a knee on the neck in prone position. The manual nor Parry mention that the neck restraint should not be combined with another officers two knees on his back and one holding down his legs.

And yes, prone restraint deaths are rare but not zero. Citing papers that found no deaths in thousands of prone restraints ignores the factors which are required to cause death, such as the duration of the restraint and multiple forces. In fact the dangers of prone restraint are well known such that many agencies have restricted or prohibited the use of prone restraints, especially for extended periods, and have emphasized alternative, less risky methods of control. From this excellent review paper by Weedn et al:

Social scientists and prosecutors have typically investigated deaths during police encounters by use-of- force analyses [4], but such analyses are not scientific or medical determinations of whether or not the police intervention caused the death. The Bureau of Justice Statistics (BJS) collects data on arrest-related deaths from law enforcement agencies that are more specific to cause of death determinations pursuant to the Death in Custody Reporting Act of 2013 (DCRA). BJS recently reported that of the 70% of the cases in which the manner of death was classified as homicide [5]:

• In 19.9%, the police fought or struggled with decedents.

• In 7.6%, the police physically restrained decedents.

• In 12.3%, the police restrained decedents with equipment.

• In 6.2%, decedents were placed in the prone position.

However, due to non-uniform, non-detailed, and possibly biased reporting, we do not have good statistics on the frequency, manner, or duration of prone positioning, use of restraints, the underlying health of the subjects in these police encounters, or other factors that should be analyzed to understand these deaths.

Lastly, in a truly odd coincidence, I happen to have met someone that I consider one of the world experts in the physiology and risks of prone restraint (a co-author of the above paper), albeit this happened long after the Floyd case. His name is Dr. Alon Steinberg and he happens to be the husband of my friend, colleague, and well-known fellow Covid “dissident,” Dr. Sabine Hazan (who is also a gastroenterologist and microbiome expert who has researched and published on a number of Covid topics).

Turns out we both have daughters who are sophomores at the same University. We met up for a drink at parents weekend when I learned he had published his comprehensive review below:

Interestingly, we also had a debate as to the physiologic cause of death in prolonged prone restraints. Although I believed that it is largely the resulting hypoventilation which leads to increased CO2, he instead argues that it is not only from hypoventilation but likely more so from diminished cardiac output via external compression as well as metabolic acidosis from both overexertion and poor perfusion. Although illuminating, the underlying relative contributions of the pathologic consequences of prone restraint does not alter the finding that prone restraint can lead to an arrest.

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P.S I just want to say thanks to all my subscribers, especially the paid ones! Your financial support is greatly appreciated as it allows me to devote what is often large amount of time I spend researching and writing my posts, so again, thanks. - Pierre

P.P.S - Proud to report that my book is gaining Best Seller status on Amazon in several countries and is climbing up the U.S Amazon rankings… Link: