George Floyd Did Not Die Of a Fentanyl Overdose

Although the American public is lied to about nearly everything at this point, the cause of Floyd's death is not one of them. I should know as I was the medical expert who testified in his civil case.

Recently, Tucker Carlson, who I consider to be a highly skilled, professional, and widely respected journalist, reported that the public was lied to about the cause of George Floyd's death and that he actually died of an opiate overdose. He is apparently basing this reporting on the opinion of the Hennepin County Prosecutor Amy Sweasy who claims that Dr. Andrew Baker, the medical examiner who performed Floyd’s autopsy, withheld Floyd’s true cause of death for fear of public retaliation.

As the pulmonologist expert witness retained in the civil case, I was provided access to all of the medical evidence. I spent dozens of hours reviewing video footage, ambulance records, medical records, toxicology reports and autopsy findings. I want Mr. Carlson to understand why my interpretation of all of the available evidence (still) strongly leads to the opposite conclusion of what the medical examiner is apparently now saying. I want to state at the outset that the medical examiner’s opinion then, as well as now, did not influence my conclusion so his changing of his interpretation has little relevance.

I am curious as to whether Mr. Carlson will correct his reporting if indeed he agrees with my below interpretation as an independant medical expert.

Before I go any further, a disclaimer: I recognize that the George Floyd case is a highly divisive and emotionally charged one for countless Americans. Many are profoundly saddened and outraged over the circumstances of his death; others are convinced he died of a drug overdose or believe he deserves little sympathy given his criminal background. Plenty are angered by the often supportive media coverage of the subsequent and sometimes violent Black Lives Matter movement protests.

So let me be clear: I am not a lawyer, a prosecutor or a judge. I am not a political scientist, or a sociologist, or a psychologist. I was not asked to deliver a moral or character assessment of Mr. Floyd. I have never met a saint, although I have known a few people that I feel come close. I never met Mr. Floyd. I was simply asked for my expert opinion as a lung and ICU specialist as to the proximate cause of his death based on all the available evidence, of which there was an extensive amount. It was an important task and one I felt confident I was expertly suited to perform.

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Know that I have for years done expert witness reviews of medical malpractice cases as I find the work both interesting and challenging. The lawyers I worked for had consistently rated my work highly thus I was consulted often. The firm representing Mr. Floyd’s family in their wrongful death lawsuit interviewed me within days of his death and I was quickly retained (as an aside, this was 5 months before I became an expert in the use of ivermectin in Covid and was subsequently punished professionally for my resulting advocacy of the medicine). Had Mr. Floyd’s death occurred after that point, I am sure I would never have been retained.

The official expert testimony I submitted (found at the end of this post) is a lengthy and comprehensively detailed document which I’m honored to say my mentor Paul Mayo called, "a master class in pulmonary physiology."

My report concluded that George Floyd didn’t die from (just) a knee on the neck nor were the drugs found in his system a major contributor. Just as with the response to the Covid pandemic, I think it is important to understand exactly what happened to Mr. Floyd so that it never happens again.

For those not interested in reading the lengthy report, I will instead focus on clarifying what I think are the two most critical misinterpretations of the available evidence that I have seen on social media and in certain press outlets.

1. That Mr. Floyd died of an opiate overdose due to severely elevated levels of fentanyl measured in his bloodstream as documented in his toxicology report.

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.

Much more important than the level of opiates found in his blood is that clinically, throughout the videotaped arrest, Mr. Floyd was conscious and able to walk and communicate clearly. Due to his known claustrophobia, he was even able to struggle with officers on two separate occasions as they tried to force him into the back of a police car. His awake and physically active state was observed up until he was placed into prone restraint for many minutes. Also, when he was first placed in prone restraint, he was clearly awake, in distress, and begging to have the pressure of the officers bodies be removed from his back and neck.

The physical and cognitive abilities exhibited by Mr. Floyd are completely inconsistent with someone severely intoxicated with an opiate. In opiate intoxication, patients are lethargic, minimally arousable, and/or exhibit slowed breathing.

As a pulmonologist expert in physical examination, I did not observe shallow or slowed breathing until he was put into prone restraint (i.e. face and chest down on a hard surface). Recall that properly trained police officers are taught to never restrain a suspect in this position, because it is well known to cause death due to the inability of a suspect to sufficiently breathe. So, although he was probably somewhat high given the fentanyl found in his system, it was not severe clinically nor did it appear life-threatening.

Third, opiate overdoses occur within seconds to minutes of IV administration and the first physiologic effect is loss of consciousness prior to breathing then slowing and the heart then stopping minutes later (in massive IV overdoses, the first two can occur simultaneously and quickly). Thus, the prolonged time between when he would have last had access to IV opiates and when he stopped breathing in prone restraint was far too prolonged to blame on an IV opiate overdose. But what about if he had swallowed a bunch of pills containing opiates as the officers were approaching just prior to the arrest?

Certainly, if it was a really large amount of pills or a very high dosage form, this could lead to an overdose, but again, the absorption of oral opiates is much much slower and, if that was occurring, would have led to a slowly progressive intoxication evidenced by gradually diminishing consciousness and clarity, loss of muscle tone/activity, and slowed breathing. Although not directly relevant nor did it figure into my conclusion, I was provided no evidence of him having overdosed in the past.

But let’s just say, for the sake of argument, that the opiates he allegedly took prior to arrest just started to enter his bloodstream during the same time period he was put into prone restraint. A couple of problems with making this argument. First, I found no report of any witness or police officer who described him swallowing pills. That supposedly happened in a prior arrest in 2019 but was not documented in the 2020 arrest. From a media report, he had “foam” around his mouth and “semi-chewed pills” were allegedly found in his car but again, even if it were true, from the above, he was not initially severely intoxicated.

Second, know that prone restraint causes carbon dioxide (CO2) to slowly rise in the suspect’s blood as a result of their inability to inhale and exhale sufficiently, a condition called “CO2 narcosis.” C02 narcosis, as the name suggests, presents identically to opiate intoxication with increasing lethargy evolving into unconsciousness, slowed breathing, and then cardiac arrest.

Thus, in order to say that he died of an opiate overdose, you have to believe that it is more likely that his (supposedly) slowly rising opiate absorption reached a critical level at the same time that he was many minutes into a breath-restricting and C02 narcosis-causing prone restraint position. This is so improbable as to be near impossible. In medical malpractice causation, the evidence standard for cause is that which is “more likely than not.” The problem with this argument is that patients whose respiratory drive is being suppressed by opiates… never complain of it (Mr. Floyd was crying “I can’t breathe” repeatedly - with each plea ignored). In contrast, opiate overdose victims first descend into a sleep-like, highly pleasurable state, and then progress into unconscious, their breathing slows, stops, and they arrest.

But there’s more to disprove opiate overdose than a compelling probability assessment.

So lets entertain this hypothesis even further. Let’s again entertain that the (allegedly) rising oral opiate absorption hit a critical level causing gradual unconsciousness perfectly timed in the middle of a prolonged, three officer-weight bearing prone restraint episode.

Here is where you need to know that in one of the videos, there is a bystander who claimed he had specific training which led him to shout at the officers, over and over, “get off his neck man, you ain’t supposed to do that, get off his neck, get off his neck, he can’t breathe” which, after Mr. Floyd lost consciousness, changed to “check his pulse, check his pulse, he ain’t breathing, check his pulse, he is dead man.”

They did not take their weight off of Mr. Floyd, either at the time or for many minutes after. This is important because opiate overdoses are easily treatable as long as you can support breathing. For instance, I have taken care of many many dozens of opiate overdoses in the ICU. As long as the unconscious overdose patient is found with a pulse or pulse can be restored with CPR, all they need is a breathing tube and mechanical ventilator support until the opiate wears off. I cannot tell you how many young overdose victims I admitted on a ventilator. The majority would wake up hours later when the opiates wore off and then were quickly discharged alive from the ICU.

Certainly an uncomfortable minority never woke up due to anoxic brain injury from being in cardiac arrest for too long prior to successful CPR. However, in Floyd’s case, that would not and should not have happened because 4 police officers trained in CPR were present at the scene and could have identified pulselessness quickly (they were being begged to do so by bystanders). So, they were right there when he lapsed into unconsciousness, and thus they could have rapidly taken their body weight off of him, identified pulselessness, and initiated CPR.

But that didn’t happen until many minutes later when an ambulance paramedic showed up on the scene and tapped Officer Chauvin’s shoulder to get him to release his knee from the neck of the lifeless Mr. Floyd (I should point out that even the paramedic did not immediately check the pulse of unconscious Mr. Floyd, which to me as an intensivist, violated medical standards).

Thus, and I don’t want to litigate this, but I believe that based on the above actions, the crime would still have been homicide/unintentional murder/3rd degree murder based on the use of an aggressive and life-threatening prone restraint along with their indifference to Mr. Floyd’s unconscious and limp body. Lastly, all of the toxicology data and medical record data were presented and argued in the criminal case, and a jury of his peers found Chauvin guilty of same.

2. The second misinterpreted piece of evidence is that that no damage or fracture to his trachea (windpipe) was found on autopsy thus he did not die of asphyxiation.

What you need to know is that the windpipe is only half made of cartilage/bone. The posterior half is actually made of soft tissue. Windpipes can thus be occluded easily, either with hands around the neck via strangling, or just pressure from a knee. The trachea does not have to fracture to be occluded. Heck, when I was doing bronchoscopy and my scope was in the trachea, if the patient responded with a vigorous cough, the trachea would occlude transiently due to thoracic pressure “ballooning” the posterior membranous wall to contact the anterior wall and occlude. But that occurs transiently and is of no significant consequence. So, fracture of the trachea is not required for prolonged occlusion to have occurred.

Further, it is my opinion that Mr. Floyd did not die of asphyxiation solely due to the pressure on Mr. Floyd’s neck from Officer Chauvin’s knee. Had this been the sole cause, total occlusion of the trachea via external forces would have rendered communication impossible. When Chauvin’s knee was initially placed on Mr. Floyd’s neck, he could phonate (i,.e. make sounds) given that he was recorded pleading with the officers to “get off” of him and then later, just before he became unconscious, he began calling out for his mother. This is impossible with an occluded trachea. It is also impossible in severe opiate intoxication.

Instead, my conclusion was that Mr. Floyd died by the combined forces of three officers bearing weight on his thoracic cage (upper back, lower back, and neck/throat) against a concrete surface, rendering him unable to take in sufficient oxygen or expel sufficient carbon dioxide with each breath. It is a rapidly and extremely distressing sensation to not be able to take in a sufficient volume of air with each breath. Just think back to the last overly vigorous bear hug you received and how quickly you became uncomfortable and sought release.

Ultimately, it was my determination that Mr. Floyd was slowly suffocated as a result of the combined weight of multiple officers on this thoracic cage and windpipe after being placed in the prone position. It was a severely distressing way to die.

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P.S My official submitted report follows but I first 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

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GEORGE FLOYD EXPERT OPINION REPORT

June 9, 2020

Dear Ms. Roman (not the attorneys name):

You have asked me to review materials and offer expert opinions concerning the cause of death of Mr. George Floyd during his videotaped apprehension and arrest which occurred on May 25, 2020, in Minneapolis, MN.

I am a physician licensed by the States of Wisconsin and Illinois.  I am a graduate of St. George’s University School of Medicine and I completed an Internal Medicine Residency at Columbia University’s St. Luke’s-Roosevelt Internal Medicine Residency Program in New York City followed by a Pulmonary Disease and Critical Care Medicine Fellowship at The Albert Einstein School of Medicine’s Beth Israel Medical Center in Manhattan. I am Board Certified in Internal Medicine, Pulmonary Diseases, and Critical Care Medicine. I have evaluated and treated a large number of patients over the past 15 years who have presented with a myriad of respiratory ailments with a large proportion of those patients having suffered acute respiratory failure in the ICU or on the hospital wards at multiple medical centers that I have worked at. Further, I had a large pulmonary and bronchoscopy practice for almost a decade in New York City where I performed numerous interventional and diagnostic procedures in the airway and thoracic cavity. I have also served as the Program Director of a large fellowship training program at Beth Israel Medical Center in New York City for a period of 3 years prior to being recruited by the University of Wisconsin where I then served as the Chief of the Critical Care Service and the Medical Director of the Trauma and Life Support Center for the past 5 years. I am also known as one of the pioneers and world experts in critical care ultrasonography, a skill set which has led to me becoming the senior editor of the best-selling textbook “Point of Care Ultrasound” which is in its 2nd edition and has been translated into 6 languages.

My expert opinions are based upon my skill, education, training, and experience, and my knowledge of the medical and scientific literature.  I have also considered the following materials in forming my opinions in this matter:

1.    Code of Conduct, City of Minneapolis – Dated May 25, 2020

2.    Use of Force, Minneapolismn.org, 5/26/20

3.    911 Call Transcript, Redacted, FOIA, 111725.pdf

4.    Hennepin CME Autopsy 2020-3700 (Floyd) -111817

5.    EMT Report -111711.pdf

6.    Hennepin CME Summary Autopsy Findings

7.    Videos

a.    Watch A Minute-To-Minute Breakdown Leading Up To George Floyd's Deadly Arrest | NBC News NOW

b.    Full video of 2 officers murder George Floyd

c.     Facebook posted video of George Floyd Arrest https://www.facebook.com/NIT2019/videos/255189079067424

d.    How George Floyd Was Killed in Police Custody | Visual Investigationse.    Presentation of preliminary independent autopsy findings

I have found with a reasonable degree of medical certainty that George Floyd died from asphyxiation as the direct result of the use of excessive restraining force by at least 3 of the police officers who participated in restraining Mr. Floyd. The forces that caused his asphyxiation (defined as “the state or process of being deprived of oxygen, which can result in unconsciousness or death; suffocation) resulted from the simultaneous application of near full body weight pressure by two grown men of unknown weight, with one who applied pressure with both knees on his back and one with his knee on his neck/spine while he lay prone on the ground in handcuffs, with the third officer restraining the movement of his legs such that Mr. Floyd could not change this threatened position.

The foundation of this expert opinion will be detailed in the summary of the evidence along with a review of respiratory system structure and function that follows. I will state at the outset that, based on the evidence presented, I am unable to determine precisely the relative contribution of each of the injurious forces that I have identified as it is my opinion that Mr. Floyd’s asphyxiation resulted from multiple, simultaneous injurious forces which limited his ability to take in sufficient volumes of air which led to him being deprived of sufficient oxygen to sustain his life. The simultaneous forces, combined with a disadvantageous mechanical respiratory position to support breathing are as follows; 1) excessive weight pressure on neck/upper back by Officer Chauvin which limited the superior expansion of the thorax during compromised positioning while also partially or completely occluding the upper airway “windpipe”, 2) excessive body weight pressure on lower/mid back by Officer Keung whose knees were positioned on top of Mr. Floyd and which limited diaphragmatic displacement to an extent which prevented sufficient inhaled air flow and volume, and 3) the prone positioning of Mr. Floyd on the ground which subsequently compressed his chest, limiting thoracic cage expansion which would allow for sufficient inhaled air flow and volume, and 4) the immobilization of Mr. Floyd’s legs by Officer Lane, preventing him from adjusting his body position in any manner which could relieve him of the aforementioned injurious restricting forces on his ventilatory ability.

Evidence

FORCE 1: As seen on the above listed videos taken from the sidewalk side of the police vehicle, and based on identification taken from a review of newspaper reports, Officer Chauvin can be seen applying pressure using his knee positioned on the upper neck and back of Mr. Floyd for a continuous period of approximately 10 minutes and 32 seconds.

FORCE 2: Officer Keung can be seen, during a shorter video taken from the street side of the car, with his 2 knees elevated off the street and placed on what appears to be the mid-lower back of Mr. Floyd. Given the limited duration of this video, I am unable to determine the length of time that Officer Keung’s body weight pressure was placed on Mr. Floyd’s mid-lower back beyond the time duration of this video.

FORCE 3: Officer Lane is positioned closest to Mr. Floyd’s feet with Officer’s Lanes arms extended over what appear to be the position of Mr. Floyd’s legs, thus rendering them immobile. The immobility of his legs further restricted Mr. Floyd’s ability to shift body position so as to relieve the injurious restricting ventilatory forces above.

MALPOSITION: Throughout both videos taken from street and sidewalk side of the car, Mr. Floyd can be seen in; 1) prone position and, 2) with his hands pulled behind him in a handcuff position preventing him from relieving the pressure on his chest or modifying his position so as to augment his breathing capacity.

Overview of the Critical Structures and Functions of the Respiratory System

In order to understand how the above forces and malposition led to the asphyxiation of Mr. Floyd, several concepts must be understood in order to understand the minimum amount of breathing (i.e. “minimum minute ventilation”) required to sustain life and how the above forces and malposition rendered Mr. Floyd unable to achieve this “minimum minute ventilation” so as to prevent his cardiac arrest/death.

Oxygen gas, present in atmospheric air, is required by all the cells in the body in order to create and use the energy to maintain each individual cell’s structure and function. These life sustaining oxygen molecules are absorbed by the air sacs in the lungs and then are transferred to the red blood cells circulating through the lung capillaries to then be pumped by the heart through the blood vessels of the body so that the oxygen molecules they carry can be delivered to each organ/cell. However, if these cells and/or organs are deprived of sufficient oxygen/energy, they begin to lose function, structural integrity, and if deprived of sufficient oxygen over a prolonged period, the cells and/or organs will sustain irreversible damage and cell/organ death.

Oxygen delivery is dependent on 2 main physiologic functions; 1) cardiac output, i.e. sufficient circulating blood flow per minute such that oxygen carrying red blood cells can “deliver” oxygen to each cell, with cardiac output dependent on the “pump function” of the heart, i.e. the heart must be able to receive sufficient oxygen to contract and forcefully eject enough blood flow throughout the circulation and 2) minute ventilation, i.e. the sufficient intake (inhalation) of a sufficient volume of fresh oxygen gas to be absorbed by these red blood cells while also transferring the carbon dioxide gas content from the blood to the open lung units in order to be able to exhale this gas into the atmosphere (carbon dioxide being the waste product of energy metabolism of the body).

Minute ventilation is defined by the volume of air inhaled/exhaled with each breath (i.e. “tidal volume”) multiplied by the rate at which this volume is exchanged per minute (i.e. “respiratory rate”).

Minute ventilation (MV) varies with the amount of energy being consumed which is dependent on the amount of activity being performed. For instance, at rest, an adult male will breathe, on average, approximately 12 times per minute and take in about 500 milliliters of air with each breath, thus the MV of an adult human at rest is approximately 6 liters per minute to support the energy required of a body at rest.  During light, moderate, and extreme exercise in highly trained male athletes, MV can be increased to approximately 12, 60, and up to 180 liters per minute respectively. Note that MV can only increase via 2 factors; 1) the “tidal volume” of each breath is increased by expanding the volume of the thoracic cage via; contraction of the diaphragmatic muscle which pulls the diaphragm lower into the abdominal cavity, contraction of the intercostal muscles which spread the ribs further apart, and contraction of multiple accessory muscles in the neck, chest and spine which extend the height of the thorax, and/or, 2) increasing the respiratory rate up to 40-50 times per minute at peak exercise.

Conversely, the minimum minute ventilation required to sustain life is the MV at which both oxygen and carbon dioxide levels remain in the normal range.

Hypoventilation is the condition where the MV is decreased such that carbon dioxide levels rise above normal and oxygen levels fall below normal, with the former becoming abnormal prior to the latter. Mild hypoventilation which causes slight abnormal fluctuations in oxygen or carbon dioxide levels are generally well-tolerated, especially if this hypoventilation occurs gradually over time, for example in morbid obesity, the slow and persistent accumulation of adipose tissue surrounding the thoracic cage and abdomen causes progressively worsening hypoventilation over months to years and is generally well tolerated. However, if acute, severe, or prolonged enough, both oxygen and carbon dioxide levels will become rapidly and severely abnormal. If hypoventilation is severe enough, patients will first lose consciousness due to the high carbon dioxide levels (a condition called “CO2 narcosis” given that high Co2 levels produce unconsciousness), and if MV persists at this low level, oxygen levels will then start to decrease to such an extent that the cells in the heart begin to lose energy/function, causing the heart as a whole to cease function, leading to a state of cardiac arrest/death.   

It is my opinion that Mr. Floyd suffered cardiac arrest as a result of prolonged hypoventilation, i.e. he was unable to inhale enough oxygen and exhale enough carbon dioxide such that he lost consciousness and then suffered cardiac arrest.

Causes of Hypoventilation

In order to achieve sufficient minute ventilation (MV) to sustain life, three factors must be present, which I have traditionally taught as the “three A’s” of breathing; 1) an “airway”, i.e. a windpipe that is patent/open to allow air to flow down through the airways to the lung tissues, 2) “ability” – i.e. both an intact neurologic respiratory drive combined with sufficient strength of the respiratory muscles to contract, along with sufficient “space” for the thoracic cavity to expand in size, thus creating a “vacuum” for fresh air to flow in on a pressure gradient from the atmosphere into the lungs, and 3) “area” – sufficient surface area of viable lung tissue so that oxygen can be absorbed from the inhaled air into the bloodstream while carbon dioxide can pass from the bloodstream into the inhaled air volume to then be expelled into the atmosphere during exhalation.

If any limitations in the above factors are present, hypoventilation will result, generally from three causes; 1) a reduced tidal volume (reduced volume of an inhaled breath),  2) a reduced respiratory rate, or 3) insufficient viable lung surface area, a cause only seen in acute and chronic lung conditions such as pneumonia, pulmonary edema, asthma, emphysema, pulmonary embolism etc.

I found no evidence that Mr. Floyd’s respiratory drive (rate) was significantly suppressed, despite the fact he had opiates in his bloodstream, an agent known to suppress respiratory rate. His intact respiratory rate is evidenced by observing him in the minutes prior to and at the beginning of the restraint by the officers whereby he was able to walk, sit, stand, answer questions, and cry out for help. It is clear from these observations that the opiates in his bloodstream at the time were not of sufficient concentration to suppress his respiratory rate.

I find no evidence, based on the reported autopsy results, that Mr. Floyd, despite his history of smoking and of a recent Covid-19 infection, had a chronic or acute lung disease which would lead to loss of sufficient lung tissue surface area that would lead to the degree of hypoventilation that would cause a cardiac arrest.

Therefore, given no evidence of either 1) a suppressed respiratory rate or 2) an acute or chronic lung disease, it is my opinion that Mr. Floyd died from 3) hypoventilation secondary to an insufficient volume of air with each breath, preventing him from exhaling sufficient carbon dioxide and inhaling sufficient oxygen to sustain life. The evidence for this is as follows:

1)    His complaints of “I can’t breathe” very soon after being restrained in a prone position with the weight of two grown men on his mid and upper back/neck. In my opinion, the fact that he was able to form words at that point in his prolonged restraint, leads to the following conclusion;

a.     Mr. Floyd, at least initially, was drawing enough air to “phonate” or “make sounds/speech”, (sounds are made on exhalation and require a sufficient volume of inhaled air to create sufficient exhaled flow through the vocal cords). The only conclusion I can draw from the fact that he was heard to phonate early on in the videos of his prolonged restraint is that “complete occlusion” of his airway was not occurring at that time because, if it had occurred, by definition, no sounds could have been produced by Mr. Floyd.

b.    Although his ability at the time to speak indicates that at least some air flow in and out of his airways/lungs was occurring, it is my opinion that this amount of airflow and inhaled volume was insufficient to sustain life if not reversed in minutes. I base this assertion on the fact that Mr. Floyd immediately communicated “I can’t breathe” indicating that he was suffering from a sensation termed “dyspnea” defined as “the sensation of difficulty breathing” which arises whenever airflow or air volume entering the chest is decreased to the point where gas exchange is compromised, a state immediately sensed by the nervous system, and is a well-described and uniquely distressing sensation (see below). 

c.     Thus, it is my belief, at least initially, that the force of Officer Chauvin’s knee on Mr. Floyd’s neck did not lead to complete collapse of his upper airway/windpipe but rather caused at least some “narrowing” given his diminished, but not absent, ability to phonate. It is my opinion that the most injurious impact of the officers weight on the knee placed over Mr. Floyds cervical spine/upper back was that it led to restriction of the respiratory accessory muscles of the neck such that it prevented him from drawing in sufficient air to counteract the pressure on his thoracic cage from Officer Keung (explained in detail below under “Compensatory Mechanisms of the Respiratory System).

d.    Although complete compression of the airway, by definition, was not present while Mr. Floyd was able to speak, there were prolonged periods in the video where no speech was heard and thus I cannot rule out the possibility that with subtle changes in neck position or weight directed by Officer Chauvin’s knee over Mr. Floyd’s neck that complete compression and lack of airflow occurred for transient or prolonged periods. Further, it is my opinion that, despite the fact that the autopsy reported no fracture or injury to the cartilaginous structures of the trachea (“windpipe”), the absence of such an injury does not in any way exclude the possibility that the airway was completely compressed at some point. The reason for this possibility is that only half the circumference of the windpipe is made of cartilage, i.e. the anterior trachea. The posterior trachea is “membranous” and is composed of soft tissue/mucosa and can easily be displaced/compressed such that it can oppose the anterior trachea thus leading to complete occlusion of the windpipe, either transiently through benign forces such as a vigorous cough or from sustained life threatening forces such as external body weight pressure applied over a knee to the cervical vertebrae which would then cause the vertebrae to compress the windpipe just anterior to it. In conclusion, the windpipe can be completely occluded without causing permanent damage to the tracheal rings.

DYSPNEA (“I can’t breathe”)

“Dyspnea” is a medical term defined as “the sensation of difficulty breathing” and most commonly occurs when the amount of muscle work required to draw in a sufficient volume of air is increased due to some “load” which restricts either airflow through the windpipe, ability of the lung to inflate, ability of the lung tissue to absorb sufficient oxygen with each breath, or the ability of the chest wall to expand to draw in a sufficient volume of air into the lung/chest. Many acute and chronic lung conditions cause this sensation, such as asthma where the airways are constricted and thus it requires increased, exaggerated muscular effort to inhale and exhale each breath through “smaller” airways, or pulmonary edema whereby water fills many lung units causing the lungs to become heavier and partially collapse, thus inflating them with each breath requires an increased and exaggerated effort.

It must be recognized that humans are exquisitely sensitive to any force that impairs our ability to breathe, and this “extreme sensitivity” likely developed as an evolutionary adaptation to promote our survival given that its intent is to immediately alert us to and reflexively correct via compensatory respiratory mechanisms (see below) any force which threatens or impairs our ability to sustain breathing. This is reflected by the fact that our thoracic cage (chest) is one of the most highly innervated parts of the body. Millions of nerves course over the skin and alongside the ribs of the thoracic cage. There are two types of nerves; “afferent” and “efferent” nerves. The former send “sensory” information to the brain, such as touch/movement, pain, temperature, and vibration thus allowing humans to constantly be aware of the amount of chest expansion or “stretch” that is occurring with each breath.

Efferent nerves conduct information from the brain to the muscles to direct muscle effort/movement. The normal amount of effort applied to a breath and the resulting amount of chest expansion that is sensed is generally perfectly matched and thus normal breathing is typically unconscious/not sensed. In other words, the unconscious automatic impulses sent from the brain to our respiratory muscles/diaphragms lead to volumes of air inspired which are perceived as “satisfying” or “non-distressing”, i.e. they are not perceived as insufficient but as adequate/normal, and thus are generally imperceptible. However, as soon as any force is applied such that it limits the ability of our chest to expand or “stretch” sufficiently with a normal or even increased respiratory effort, this immediately results in the sensation of “dyspnea”, or “inability to achieve a “satisfying” or sufficient volume of air intake, which, when severe and/or acutely severe, is known to be one of the more distressing sensations one can experience and can immediately create a superimposed sense of “panic”. Some examples of this sensation are when an over-exuberant or prolonged “bear hug” may be applied by a friend or family member and one feels immediately that “they cannot breathe”, a situation which is generally quickly reversed/decompressed upon release of the “hug” such that this distressing sensation is typically short-lived. Another example would be when a group of children (or adults) are wrestling or playing in a pile and the child/adult on the bottom of the pile suddenly experiences the cumulative weight of their playmates on their chest or back such that their normal or even exaggerated respiratory effort leads to the highly distressing, noxious, fearful feeling of insufficient air flow/chest expansion such that they immediately cry out “get off, I can’t breathe”.

Knowing the forces, diseases, situations, and positions that can restrict breathing, it is my opinion, that as soon as Mr. Floyd was placed prone on the ground and the weight of the two officers knees were applied to upper back/neck and mid-lower back, he immediately suffered acute, severe “dyspnea”, i.e. a sensation of difficulty breathing due to the resulting “restriction” of his ability to expand his chest preventing him from inhaling a sufficient “tidal volume” or a “satisfying breath.” This led to his immediate exclamation of “I can’t breathe”. In essence, he immediately sensed that the volume of air entering his chest was insufficient to maintain normal oxygen and carbon dioxide concentrations in the blood. It is my opinion that the severe and prolonged “hypoventilation” caused by the weight of the officers on his chest and shoulders/neck led to his loss of consciousness due to progressively increasing blood carbon dioxide levels followed by a cardiac arrest secondary to his progressively decreasing blood oxygen levels due to his inability to take in a sufficient volume of air to be able to absorb sufficient oxygen or expel sufficient carbon dioxide. In treating acute and chronic respiratory failure throughout my career, it should be recognized that this symptom/condition is one of the most distressing/noxious/panic inducing symptoms a human can suffer.

Respiratory System Compensation to Inspiratory or Ventilatory Deficits

Another important concept to understand are the compensatory abilities of the respiratory system that counteract limitations or restrictions in ventilatory function. Examples are as follows:

1)    INCREASING RESPIRATORY RATE: When we have insufficient ability to take in a large enough breath due to thoracic wall restriction, we typically compensate by increasing the respiratory rate, in this way sufficient minute ventilation can still be achieved, as per formula above. However, this compensatory mechanism fails if the volume of air inhaled with each breath is smaller than the volume of air in the windpipe and bronchi, a.k.a. smaller than the “dead space volume” (i.e. the volume of air that enters the thoracic cavity but does not come into contact with the lung tissue and thus the oxygen in this volume of air cannot be absorbed into the blood). This volume of air is equivalent to the air volume in the mouth/nose/trachea/proximal bronchi and is about 150ml in an adult male – i.e. any volume of air lower than this amount does not participate in gas exchange and thus cannot be compensated for by increasing the respiratory rate). It is my opinion that the volume of air entering Mr. Floyd’s lung was smaller than his dead space volume thus, his increased respiratory rate was unable to compensate for such a severely reduced tidal volume, again a condition which is immediately experienced as severely distressing or panic-inducing.

2)    INCREASING TIDAL VOLUME VIA USE OF ACCESSORY MUSCLES:

a.    If there is restriction to airflow through the windpipe or restriction to the descent of the diaphragms or a person suffers from a condition which limits lung inflation, the “accessory muscles of respiration” are recruited as follows:

   i. Diaphragm – the first response to an inspiratory load or restriction is to increase the rate and depth of descent of the diaphragm above normal “excursion” such that air flow rate and thoracic air volume is increased. It is my opinion that, in Mr. Floyds case, the ability of his diaphragm to descend further than normal, or even to descend the normal distance/excursion was impaired by two factors; 1) prone positioning on the ground which placed his body weight over his abdomen which compressed the abdominal contents such that they are displaced upwards against the diaphragm and thus limited the  descent of the diaphragm and 2) this upward displacement of abdominal contents/intestines against the diaphragm was further increased due to the added external weight of Officer Keung over Mr. Floyd’s mid back and consequently his abdomen.

ii.     Intercostal muscles – typically, when we make an exaggerated respiratory effort, the space between the ribs expand and the chest wall cavity/volume increases. When we exert increased respiratory effort using the intercostal muscles which run between the individual ribs, such expansion can be increased further. In Mr. Floyd’s case, the pressure on his back/abdomen and neck/shoulders by the two officers rendered the intercostal muscle contraction insufficient to overcome such severe restriction of the chest wall.

iii.     Accessory muscles of the neck/back/chest – after diaphragmatic effort, use of the accessory muscles are the next most powerful compensatory mechanism that humans employ to augment tidal volume or overcome an inspiratory resistance/load. These muscles include the sternocleidomastoid, spinal, neck and chest muscles. When these muscles are recruited/engaged, they serve to expand the thoracic cavity not only by expansion outwards such as with the intercostal muscles between the ribs, but by raising the thoracic cavity superiorly or “upwards.” It is my opinion that the knee of Officer Chauvin on Mr. Floyd’s neck/spine, rather than cutting off airflow at the windpipe, more than likely caused asphyxia/hypoventilation by limiting the neck/spine accessory muscles to achieve sufficient chest expansion to counteract the limitation produced by his prone position combined with the force of Officer #2’s weight on his chest/abdomen.

I have also identified a separate set of actions which caused Mr. Floyd further harm by making it less likely that cardiopulmonary resuscitation (CPR) could be successful which limited his ability to survive. These separate injurious actions were committed by the emergency medical personnel who appeared on the scene in the videos and were as follows:

1)    One emergency medical technician/paramedic clearly checks Mr. Floyd’s pulse at 11:50 of the youtube video entitled “Full Video of 2 officers murder George Floyd”. Although a determination of the presence or absence of a pulse is not audible on the video, it is my opinion that Mr. Floyd was pulseless at that time. If true, as an expert in the performance and training of CPR, it is my opinion that, in the setting of detecting the absence of a pulse of a patient who does not meet exclusion criteria for CPR delivery, chest compressions should immediately be initiated by the first trained bystander or personnel present.

2)    Instead of initiating immediate CPR on Mr. Floyd by; 1) directing Officer Chauvin to release his restraining knee pressure, 2) rolling Mr. Floyd supine and 3) beginning chest compressions, the medical technician/paramedic instead leaves to go to the ambulance to prepare a stretcher and transfer board/sheet. The period of time until the stretcher can be seen is 39 seconds later at 12:29 of the video, with the 39 second period beginning being from the first detection of an absent pulse. Further, it is not until 12:44, a full 54 seconds from absent pulse detection that the medical technician/paramedic directs Officer Chauvin to remove his knee so they can begin the process of transferring Mr. Floyd to a stretcher and into the ambulance. The last time Mr. Floyd can be seen on the video was at 13:29, and at that time, there is no evidence that CPR had been initiated on Mr. Floyd who had then been pulseless a minimum of one minute and 39 seconds since the initial pulse check.

3)    This delay towards attempting to restore circulation via chest compressions or other interventions that make up ACLS (advanced cardiac life support) prolonged the “no flow” period after circulatory arrest which severely limited Mr. Floyd’s chances of achieving successful “recovery of spontaneous circulation” (ROSC). Such an unnecessarily prolonged period of “no flow” clearly added further cellular and organ damage to the prior period of lack of blood flow to Mr. Floyd’s vital organs, namely his heart and brain.

In summary, the prolonged, simultaneously applied restraining forces by Minneapolis Police Officers Chauvin, Keung, and Lane on critical parts of Mr. Floyd’s respiratory and musculoskeletal system while he was in a handcuffed, prone position on the ground led to severe hypoventilation which caused a life-threatening elevation in blood carbon dioxide levels rendering him unconscious, which was then followed by a progressive and severe decrease in blood oxygen levels which directly caused his cardiac arrest and death. Further, the failure of emergency medical personnel to initiate CPR on Mr. Floyd immediately upon discovering he was pulseless led to an additional significant decrease in Mr. Floyd’s chances of achieving ROSC from the CPR that was eventually initiated in the ambulance.

The opinions in this report are expressed to a reasonable degree of medical certainty.

I reserve my right to amend or supplement my opinions based on any additional information that may become available to me.

Yours sincerely,

Pierre Kory, MD, MPA

June 9, 2020

Associate Professor of Medicine

Chief of the Critical Care Service

Medical Director of the Trauma and Life Support Center

Division of Allergy, Pulmonary and Critical Care

University of Wisconsin School of Medicine and Public Health

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