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Taser Death Expert Report, Zipes, 2011

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I, Douglas P. Zipes, M.D., declare under penalty of perjury pursuant to the
laws of the United States as follows:

I am an electrophysiologist, a sub-specialist within cardiology who

focuses on the electrical impulses that regulate the heart rhythm. I am submitting this
expert report pursuant to Federal Rule of Civil Procedure 26(a)(2)(B) in the matter of
Rich v. TASER International, Inc. After setting forth my credentials, I explain my
opinion that, to a high degree of medical certainty, the electrical impulses from a
Model X26 electrical control device (ECD) manufactured by defendant TASER
International, Inc., (TASER) caused the cardiac arrest, and therefore the death, of 33year-old Ryan Rich, M.D., on January 4, 2008.

I also address the inadequacies of TASER’s pre-release testing, and

therefore the recklessness with which it marketed products for law enforcement
officials to use on human beings.

Finally, I explain my opinion that TASER’s representations of safety

made to the involved police agency and officer prior to this incident were not correct,
that the risk of causing cardiac arrest was well known prior to this incident, and that
the risk could have been minimized had TASER issued proper warnings and training
materials rather than false and exaggerated representations of cardiac safety.

Note that many items of fact about TASER products and discussions of

many of the publications were presented to two other courts. The first was in a

declaration I signed January 29, 2010, filed with a successful opposition to a motion
for summary judgment in the matter of Butler v. TASER International, Inc., California
Superior Court for the County of Santa Cruz Case No. CV161436, and the second on
October 28, 2010 filed in the matter of Fontenot v. TASER International, Inc., W.D.N.C.
Case No. 10-CV-125, and have not been changed substantially in this report. I also
filed a report raising many of these same issues in Williams v. TASER International, Inc.,
N.D. Ga. Case No. 06-CV-0051. Of course the unique facts of this case are
My Credentials for Offering This Expert Report

I received my Bachelor of Arts degree cum laude from Dartmouth

College in 1961, and my medical degree (M.D.) cum laude from Harvard Medical
School in 1964. I performed post-graduate training in internal medicine (1964-1966)
and cardiology (1966-1968) at Duke University Medical Center, Durham, North
Carolina. From 1968-1970, I was in the United States Navy and discharged with a
Letter of Commendation at the rank of Lieutenant Commander. I joined Indiana
University School of Medicine as an Assistant Professor of Medicine in 1970, and
became Professor of Medicine in 1976. I also became Professor of Pharmacology and
Toxicology in 1993. In 1994, I became Distinguished Professor, the university’s
highest professorial category for academic accomplishment. In 1995, I became
Director of the Division of Cardiology at the Krannert Institute of Cardiology, a post
I held until 2004, when I became Emeritus. I continue to see patients and consult

with many physicians on difficult patient problems. I attend conferences, teach and
interact with members of the Division, and house staff. (Attached hereto, as Exhibit
A, is a copy of my curriculum vitae.)

My principal areas of research and clinical activities focus on cardiac

electrophysiology (heart rhythm problems). However, I also take care of patients with
the entire spectrum of cardiac diseases, including hypertension, heart failure,
atherosclerosis, acute and chronic myocardial infarction (MI), lipid abnormalities,
heart muscle abnormalities, thromboembolic problems, and adult congenital heart

I have published over 800 medical articles and 21 textbooks. I am the

co-editor of Zipes/Jalife Cardiac Electrophysiology, From Cell to Bedside (2009, fifth edition)
and a co-editor of Braunwald’s Heart Disease, a Textbook of Cardiovascular Medicine (2011,
ninth edition). Each is regarded as the authoritative text in heart rhythm disorders and
in general cardiology, respectively. I am co-author of Clinical Arrhythmology and
Electrophysiology that was published in November 2008.

I am a member of numerous societies, including the American Society

for Clinical Investigation and the Association of American Physicians, both of which
have very stringent acceptance qualifications. I am past president of the Association
of University Cardiologists and of the Cardiac Electrophysiology Society. I have
consulted for, and been on review committees of, the Veterans Administration, the
American Heart Association (AHA), and the National Heart, Lung, and Blood

Institute (NHLBI) of the National Institutes of Health (NIH).

For the Heart Rhythm Society (HRS), which is the largest group of heart

rhythm experts in the world, I was a founding member in 1980, served in many roles,
and became President 1989-1990. I am the founding Editor-in-Chief of the HRS
journal (see below).

For the American Board of Internal Medicine (ABIM) (the organization

that writes all of the examinations for medicine and the sub-specialties which a
physician must pass to call himself/herself Board Certified), I was Chair of the
Clinical Cardiac Electrophysiology Test Committee which wrote the first (and
subsequent two) examinations in clinical cardiac electrophysiology; Chair of the
Subspecialty Board on Cardiovascular Disease, which wrote the examinations dealing
with all of cardiology; Chair of the Committee on Subspecialty Internal Medicine
(dealing with issues of all of internal medicine); and ultimately Chair of the entire
ABIM (2002-2003).

For the American College of Cardiology (ACC) (35,000 cardiology

members worldwide), I have held multiple roles since 1975, becoming a member of
the Board of Trustees (1992-1997 and again 1999-2005); Chair of the Nominating
Committee on two separate occasions; Chair of the Development Committee; Vice
President, President-Elect; and then President (2001-2002). I became a Master of the
ACC in 2002 (highest membership category). I was Co-Chair of the ACC/AHA/
European Society of Cardiology (ESC)/HRS Ventricular Arrhythmia and Sudden

Cardiac Death Guideline Committee, which wrote the guidelines on how to care for
patients with heart rhythm problems. I was also a member of the Ethics Committee
and chaired the Task Force on Legal Expert Testimony. In 2009, I received an ACC
Presidential Citation for organizing and chairing the first International Cardiovascular
Conference: Focus on the Middle East, which brought together cardiologists from
each of the Middle Eastern countries for two days of education and interaction. The
second one was held in March 2010, and was attended by over 500 cardiologists. The
third symposium was held April 2, 2011, attended by over 350 cardiologists. I
received an award from the Iran Cardiac Society when I lectured in Tehran November
2008, and I gave the Plenary Lecture for the Saudi Cardiac Society in February 2010
and for the Qatar Cardiac Society in April 2010.

I am a member of the editorial boards of more than 15 cardiology

journals; and have reviewed articles for other general medical journals, such as the
New England Journal of Medicine (NEJM) and Journal of the American Medical Association. I
have been Editor-in-Chief of Progress in Cardiology, and Founding Editor-in-Chief of
Contemporary Treatments in Cardiovascular Disease and Cardiology in Review. I was the
Founding Editor-in Chief of the Journal of Cardiovascular Electrophysiology (1989-2004),
and in 2004, I became Founding Editor-in-Chief of the journal, HeartRhythm, which is
the official journal of the HRS and has become the number one specialty cardiology
journal in the world.

I have received many awards, but will mention only a few. From the

AHA I received the Distinguished Achievement Award (1989), the Herrick Award
(1997), and the Cor Vitae Award (2004). These awards have been for distinguished
contributions to our knowledge base of clinical cardiology and patient care. I have
received the Distinguished Scientist Award from the HRS (1995) and from the ACC
(1996), for research contributions to both basic and clinical cardiology. On June 2,
2004, the Honorable Baron P. Hill, United States House of Representatives, read a
tribute about me into the Congressional Record. After my tenure as Division Chief,
the following were endowed: the Medtronic Zipes Chair in Cardiology, and the Joan
and Douglas Zipes Visiting Professorship at Indiana University School of Medicine;
the Douglas P. Zipes, M.D., Lectureship given annually at the HRS Sessions; and the
Douglas P. Zipes, M.D., Distinguished Young Scientist Award given annually at the
ACC Scientific Sessions. In 2007 I was made an honorary foreign member of the
Argentine Society of Cardiology, and received the Distinguished Alumnus Award
from the Duke University Medical Center. In May, 2010, I was inducted as an
honorary member in the Hungarian Society of Cardiology. In September, 2010, I
received the President’s Medal from Indiana University, the University’s highest
award. In April 2011, I became a Master of the American College of Physicians
(membership 130,000 internists, internal medicine subspecialists, medical students,
residents, and fellows), which according to their website, is given to “highly
distinguished physicians, selected from among Fellows, who have achieved recognition in medicine by
exhibiting preeminence in practice or medical research, holding positions of high honor, or making

significant contributions to medical science or the art of medicine.”

I am a Fellow of the: AHA, HRS, European Society of Cardiology,

Master of the American College of Physicians and of the American College of
Cardiology, and honorary fellow of the: Argentine Society of Cardiology, the
Hungarian Society of Cardiology, and of the Cardiac Society of Australia and New
Zealand. I am Board Certified in Internal Medicine and Cardiovascular Diseases and
was Board Certified (until 2005) in Clinical Cardiac Electrophysiology, which I let
lapse because I no longer perform invasive procedures.

I was a consultant for Medtronic from 1975 to 2010, and am the

inventor of the implantable cardioverter, which is part of the implantable cardioverter
defibrillator manufactured by Medtronic and other device companies, the usual device
implanted in high risk patients. All royalties for that invention were assigned to
Medtronic and I have received none. I have written on warnings about side effects of
implantable devices and drugs and their ability to cause cardiac arrhythmias. Warnings
are included in a number of manuscripts I have published.

I have been retained as an expert witness and have testified in deposition

and court on multiple occasions both for plaintiffs and defendants. A list of my
testimony is attached as Exhibit B, and my fee schedule as Exhibit C. Three of those
cases involved a cardiac arrest, in my opinion, caused by electronic shocks
administered by a TASER product: Williams v. TASER International, Inc., Butler v.
TASER International, Inc, and Fontenot v. TASER International, Inc. I prepared an expert

report or declaration and sat for a deposition in all cases. I understand that Williams
was resolved, confidentially and Butler for $2.85 million. Fontenot is pending.

Based on my work in Williams (later reaffirmed in Butler and Fontenot), I

became concerned that TASER was misrepresenting that there are no cardiac risks
posed by its ECDs. Accordingly, I delivered a PowerPoint presentation on those
risks at the May 2009 HRS meeting in Boston. A copy is attached as Exhibit D.

The PowerPoint presentation was delivered as part of a formal, invited,

scheduled debate with a distinguished colleague, Patrick J. Tchou, M.D., who headed
the Section of Electrophysiology and Cardiac Pacing in the Robert and Suzanne
Tomsich Department of Cardiovascular Medicine at Cleveland Clinic in Cleveland,
Ohio, from 1994 to 2006, and is currently a practicing staff physician there
concentrating on treatment of cardiac arrhythmias, especially those of complex
origins. At the end of my presentation, Mark W. Kroll, Ph.D., an electrical engineer
and the head of the TASER Scientific and Medical Advisory Board, who was in the
audience -- Dr. Kroll sold TASER stock options for $4 million and makes more than
$100,000 annually for part-time TASER work, according to his deposition
testimony -- spoke in opposition to my remarks. Further, I told an official of TASER,
I now understand him to be Tom Smith, who was also in the audience, that TASER
needed to issue a warning to indicate its products might cause cardiac effects. We had
sharp disagreements, and I left more concerned than ever about the undisclosed
cardiac dangers of ECDs. After the debate finished, the moderator polled the

audience and found that more than 90 percent of the audience supported my side of
the debate that TASER ECD shocks could produce ventricular fibrillation. (TASER
issued its first warnings to avoid chest shocks about four months later, on September
30, 2009.)

I exchanged emails with Dr. Tchou after the debate to arrange for us to

continue our debate in the pages of HeartRhythm. The exchange is attached hereto as
Exhibit E as an email string, and should be read from the bottom. I suggested to Dr.
Tchou that “I would write ‘Taser shocks can cause ventricular fibrillation,’ while you
would write ‘Taser shocks do not cause ventricular fibrillation.’” Dr. Tchou
responded, “I appreciate the invitation. But, the line is drawn too far to one side for
me to truly defend that position very well. From the very beginning, as we obtained
our data from our animal study, I had advised TASER that the possibility of inducing
ventricular arrhythmias is there and at the minimum we cannot categorically say that
this is not possible.”

The list of materials I reviewed in connection with this case, including

some of those I reviewed for Williams, Butler and Fontenot, are attached as an
addendum to this report. In addition to the materials listed, as an ongoing part of my
practice, I continually review scientific literature about materials potentially relevant to
my experience in the areas of cardiology, medicine, and electrophysiology. Being
essentially infinitely voluminous, I obviously cannot identify all such materials in this
case. For practical reasons, I referenced herein those materials which most directly

support my opinions.

This information forms the basis of my findings and analyses and

permits me to arrive at my opinions. I understand that discovery is ongoing, and
should additional information become available, I reserve the right to review that
information as well as my analysis and findings. I just received the important
deposition transcripts of Trooper Lazoff and Dr. Morris. I expect to receive TASER’s
expert witness reports shortly and address the issues stated in them in my deposition
testimony and, if necessary, prepare a supplemental report.
Summary of the Incident Involving Ryan Rich, MD

I have reviewed available statements, interviews and medical records, as

listed in this report, and understand the general facts of this incident to be as follows.

On January 4, 2008, at about 1:00 p.m., Nevada State Trooper Loren

Lazoff observed a black pickup truck traveling southbound on I-15 strike the rear of a
semi-trailer, then hit a van, crossing three lanes of traffic, and then crash into the
center barrier wall twice and stop with its left front wheels halfway up the barrier.
The trooper approached the passenger door and knocked. The driver, Dr. Ryan Rich,
just stared at him, then turned and looked straight ahead. He was wearing hospital
scrubs. The trooper knocked again, and saw no response. The trooper knocked again
and commanded Dr. Rich to open the door. Dr. Rich turned and stared at him.
Trooper Lazoff went back to his car and retrieved his baton. He knocked again,
asking that Dr. Rich open the door, and again Dr. Rich just turned his head and

stared. Trooper Lazoff used the baton to break the passenger window, reached in,
unlocked the door, turned off the ignition and tried to put the gear in park. He was
unable to remove the key. He noted an empty pill bottle on the seat. (It had contained
gabapentin, an anti-seizure medication.) There was no smell of alcohol. Dr. Rich was
not saying anything.
24) Responding to the commands of Trooper Lazoff, Dr. Rich crawled to the
passenger side and Trooper Lazoff cuffed his left wrist. Dr. Rich pulled back in
response to the cuffing, pulling Trooper Lazoff, who was holding the handcuffs, into
the cab. Trooper Lazoff then pulled Dr. Rich out of the cab. Dr. Morris describes Dr.
Rich as being in a “stupor.” According to Dr. Morris, Dr. Rich was standing by his
truck for some time, but kept trying to wander away, potentially into traffic.
According to Trooper Lazoff, however, while Dr. Rich was standing up, “crab
walking” according to the deposition testimony, Trooper Lazoff drew his TASER
Model X-26 and shot Dr. Rich in the chest at a range of 4 to 5 feet. Trooper Lazoff,
as TASER instructed, aimed for “center body mass.” Trooper Lazoff noted that one
probe was near the heart. He did not see the other one. The shock seemed to have
the intended effect and Dr. Rich fell backwards. The dataport shows the cycle to have
lasted 9 seconds. Trooper Lazoff was able to pull Dr. Rich by the right arm to a safer
position on the shoulder, towards the rear of the pickup truck. As Trooper Lazoff
was trying to complete handcuffing, he thought Dr. Rich might be reaching for the
probes, so he shocked Dr. Rich with a second cycle. The dataport shows 9 seconds

between the first two cycles. Dr. Rich stood up and was shocked a third time. The
trooper felt the shocks from the wires and turned off the device. That apparently
happened twice. The Trooper then cycled the device a fifth time. Apparently Dr.
Rich was lying on his chest at this point. According to the dataport and Trooper
Lazoff’s deposition testimony, he cycled the device another six times in probe mode.
The discharges appeared to be constricting Dr. Rich’s body.
25) During the initial tasings, a passerby, Dr. Craig Morris, a facial surgeon,
stopped to help. Trooper Lazoff drive-stunned Dr. Rich, but with the cartridge still in
place. Trooper Lazoff believes that the first drive stun was for the full five seconds,
but the second one was pulled off Dr. Rich prematurely, meaning that most of the
current went through the probes. Trooper Lazoff testified that on this last discharge,
the X26 continued to cycle while out of contact with Dr. Rich. With Dr. Morris’
assistance, Trooper Lazoff was able to handcuff Dr. Rich within a few seconds of the
final discharge. As the trooper stood up, Dr. Rich was on his chest, with his face
turned away. Neither Trooper Lazoff nor Dr. Morris checked Dr. Rich’s eyes,
whether he was breathing or checked his pulse.
26) Because of ongoing transmission problems with his hand-held radio,
Trooper Lazoff had to walk back to his vehicle to use the radio there to inform
dispatch what had happened and to advise them to send the medical team, routine for
TASER uses.
27) Dr. Morris indicates he looked back at Dr. Rich about 30 seconds later and

noted that the suspect was turning blue (cyanotic). He told the trooper and they ran
back to find that Dr. Rich was not breathing. They turned Dr. Rich on his back and
began CPR, with his hands still cuffed behind him. They state that Dr. Rich might
have intermittently breathed on his own, but they felt no pulse and continued CPR
until emergency personnel arrived.
28) In his statement at the Coroner’s Inquest, Dr. Morris states initially that he
thinks Dr. Rich was tased four times but later states he thinks it was five times over a
period of four or five minutes (we know it was 13 times over 3 minutes from the
dataport, see below). In his voluntary statement in an interview with M. Weidmann
on 1/4/08, Dr. Morris states that after cuffing Dr. Rich’s breathing appeared normal
(specifically, not “unbelievably fast”) despite his having actively resisting being
handcuffed at the time they left him. Dr. Morris says he followed the officer to his
vehicle, turned to look at the driver about 20-30 seconds later and saw that Dr. Rich
wasn’t moving. Dr. Morris walked back to the driver who looked pale, asked him if
he was okay. Dr. Rich didn’t respond and his eyes didn’t focus. Dr. Morris went
back to the officer, told him about the driver, and they both walked back to the Dr.
Rich and his face was “pretty much gray”.
29) Dr. Morris listened to the man’s chest but states, “It was so loud, I couldn’t
really hear whether he was breathing or not because of the…the traffic.” He then
states, “I could hear that his heart was beating but I could not hear any air going in
and out…” And then he says that Trooper Lazoff could not feel a pulse and so they

initiated CPR, Dr. Morris providing breathing support and Trooper Lazoff pumping
on his chest.
30) The discrepancies are obvious. The traffic was making so much noise Dr.
Morris couldn’t hear breath sounds but he reports he could hear heart beats with his
ear on Dr. Rich’s chest through the scrub shirt Dr. Rich was wearing (since there is no
indication he took off Dr. Rich’s shirt), during a tumultuous time period. Further, he
heard heart beats at a time when the trooper could feel no pulse. Finally, the events
indicate that Dr. Rich was having cardiac arrest and not likely to have an audible heart
beat. We know that Dr. Morris was mistaken in his recollection of the number of
TASER shocks during the press of the events (noted above), and he was likely also
mistaken about his recollection of Dr. Rich’s normal breathing (when he left him) and
hearing heart beats (when he returned), despite being a physician, albeit a facial
surgeon. In is deposition, Dr. Morris states that, “…the noise from the traffic was so
heavy I couldn’t hear anything, I couldn’t hear whether his heart was beating or
whether he was breathing...”
31) More likely than not, Dr. Rich developed cardiac arrest at the time he no
longer resisted being handcuffed, when they left him to walk to the trooper’s vehicle.
The ECG recorded from the defibrillator pads at Spring Valley Hospital January 4,
2008, shows electrical activity consistent with very fine ventricular fibrillation at the
end of the strip labeled 14:49:35 and in the strip labeled 14:49:55. Probable monitor
strips labeled Acuity begin at 14:02:42 are consistent with asystole. Since he is

pronounced dead at 13:53:00, the timing of the strips recorded from the defibrillator
pads are most likely not synchronized with the timing of the other recordings and
were probably recorded earlier. So, it is likely he developed ventricular fibrillation as
the rhythm causing cardiac arrest, which progressed to low amplitude VF (called fine
VF) and then asystole as the lack of cardiac perfusion progressed.
32) The time line given is that Trooper Lazoff initiates a traffic stop of Dr.
Rich at 13:00:50. At 13:09:25, he requests EMTs, which is presumably after he has
just applied the ECD. At 13:10:51 Lazoff advises dispatch Rich is unresponsive,
presumably after Dr. Morris brought Dr. Rich’s unresponsive state to his attention.
At 13:16:36, the fire truck arrives. At 13:21:00, American Medical Response arrives.
At 13:32:00 Dr. Rich is transported to the hospital, arriving at 13:40:00. He is
pronounced dead at 13:53:00.
33) The dataport of the TASER indicated that the trigger was pulled 13 times,
1 time for 9 sec, 1 time for 2 sec, 4 times for 4 sec and 7 times for 5 seconds, for a
total activation time of 62 seconds delivered over slightly less than 3 minutes. The
first 52 seconds were delivered solely in the probe mode (by the report from the
trooper), with 13:03:38 being the end of first cycle, and a portion of the last 5 second
deployment was delivered through the probes and in the drive stun mode to Dr.
Rich’s right leg, with the last cycle ending at 13:06:29.
34) While the LVMP Homicide Report states there is no way to determine
how many electrical cycles Dr. Rich actually received, the LVMP Homicide Report

also indicates that, “Upon arrival on scene Ell’s crew witnessed an NHP officer
attempting chest compressions and another attempting to provide respiration's via a
BVM on a male pt that was in the supine position handcuffed with the pt's hands to
his back. Pt also appeared to be extremely cyanotic to his face and head. Ell's crew also
noticed what appeared to be 2 sets of tazer barbs attached to the pt.” (italics mine). Therefore,
it is apparent that the TASER barbs were attached to Dr. Rich’s chest for all 13
discharges, for a total of 62 seconds delivered over a period of less than 180
seconds. As I understand Trooper Lazoff’s testimony, probably no more than 6 or 7
seconds were delivered by drive stun.
35) Autopsy revealed cause of death to be “due to seizure disorder with other
conditions including restraining procedures” by Piotr A. Kubiczek, M.D.Medical
Examiner. There was abnormal brain anatomy with neuronal dropout, diffuse
neuronal heterotopias, and other changes consistent with a lifelong seizure disorder.
Many blunt force injuries and abrasions were noted, including burn marks on the
buttocks consistent with the drive stuns. One punctate wound was noted in the left
upper and another left lower chest, consistent with chest barbs from the TASER X26. The depth of penetration was not determined. Heart weighed 470 gms, stated by
the medical examiner to be mildly enlarged. I disagree. According to Kitzman et al.
(Mayo Clin Proc 63:137, 1988) normal heart weight for an adult male weighing 220
pounds ranges between 296 and 516 grams. Based on height of 6’2’’, the normal
range is 247-492 grams, but Kitzman et al. indicate that heart size correlates better

with body weight, which should be used, rather than height, when available. The RV
wall measured 0.3 cm thick and the LV wall 1.9 cm. According to Kitzman et al,
normal RV wall thickness is .38-.4 cm and LV between 1.23 and 1.5 cm, so the LV
wall could be considered slightly thickened. There was 10-20% narrowing of the left
anterior descending coronary artery. Cardiac histology was normal. Gabapentin
31micrograms/ml (Neurontin, non-narcotic medication being taken for a seizure
disorder, and for back pain) was noted in the blood, which was negative for alcohol
and other drugs. In patients with normal renal function, the maximum serum
concentration is 25 micrograms/ml with the FDA approved dosing (Blum Clin
Pharmacol Thera 56:154, 1994; Bookwalter Pharmacotherapy 25:1817, 2005). An
average starting dose is 300 mg three times daily with doses increasing to 600 or 800
mg three times daily. Dr. Rich was prescribed 800 mg four times daily.

At the coroner’s inquest April 18, 2008, Dr. Kubiczek indicated the

cause of death was a seizure disorder with other contributing factors including
restraining procedure and manner of death was homicide. He said there was no
scientific evidence that an electronic control device can contribute to death, which is
not correct. Such evidence exists in the peer-reviewed literature. He did not know
whether a TASER application over the heart had any bearing. It is well established in
the peer-reviewed literature that trans-cardiac vectors over the chest pose the highest
risk of cardiac capture. He stated the evidence indicated Dr. Rich was tased four or
five times, when the dataport shows 13 cycles. In his deposition, he states that Dr.

Rich developed an arrhythmia from the seizure disorder and cannot state that it was
the TASER because there is no scientific basis to support that conclusion. Dr.
Kubiczek’s deposition on 3/24/11 affirms that he knows nothing about the scientific
literature that demonstrates how ECD devices can produce sudden death.
Mechanisms Producing Ventricular Fibrillation

It is important to understand the cardiac mechanisms involved in this

incident. Ventricular fibrillation (VF) is a highly disorganized heart rhythm
(fibrillation) of the bottom chambers (ventricles) discharging at rates of 400-600
times/min. Such a rate is too fast for the ventricles to pump blood effectively to the
brain and other organs. VF results in unconsciousness in 10-20 seconds and
irreversible brain damage or death in 5-8 minutes unless the VF is terminated by an
electrical shock from a defibrillator. VF is the mechanism of Rich’s cardiac arrest and
subsequent death. Ventricular tachycardia (VT) is a more organized heart rhythm at
slower rates (100-250/min) that can progress to VF. There are many causes of
VT/VF but in the present context, I will consider two: ischemic and electrical.

Ischemia, or reduced/lack of blood flow, can result when the blood

pressure falls to low levels, such as can occur during very rapid ventricular rates.
Cardiac ischemia, when the heart muscle is deprived of normal blood flow, creates an
electrophysiologically unstable ventricle prone to developing VF. In the TASER
studies on pigs by Lakkireddy and Tchou et al., and Nanthakumar et al, the rapid
ventricular rates following “capture” (see below) of the heart by the TASER ECD

pulses caused very low blood pressures that undoubtedly resulted in degrees of
cardiac ischemia during the duration of the ECD cycle. Long ECD cycles or repeated
short cycles with little recovery time in between could result in cardiac ischemia
sufficient to cause VF.

Recently, Kroll et al. published (32nd Annual International Conference

of the IEEE EMBS Buenos Aires, Argentina, August 31-September 4, 2010) “A
Novel Mechanism for Electrical Currents Inducing Ventricular Fibrillation: The
Three-Fold Way to Fibrillation,” claiming to “present new data showing a 3rd
mechanism of inducing VF which involves the steps of delivering sufficient current to
cause high-rate cardiac capture, causing cardiac output collapse, leading to ischemia,
for sufficiently long duration, which then lowers the VFT (VF threshold) to the level
of the current, which finally results in VF.” I had indicated this mechanism in my
February 19, 2009 expert report on Butler v. TASER International, as explained above,
based on well-established physiological principles known for some time. Kroll et al.
state that “There is some existing support for this hypothesis in scattered data in the
existing literature.” This is not a new mechanism anymore than adding an
intervention such as a drug or coronary occlusion to the rapid pacing would constitute
a new mechanism. It is pacing induced VF modulated by another event, in this
instance, ischemia.

The paper by Kroll et al. hypothesizes that rapid pacing-induced

ischemia leading to VF takes a minimum of 90 seconds to occur. Therefore, the

authors claim that rapid pacing-induced VF, such as might be delivered from a
TASER ECD shock, occurs either in the first 4-5 seconds or after 90 seconds, with
no VF possible in between the two times. I disagree. My conclusion is that VF can
occur at virtually any time during an ECD cycle if there is cardiac capture.

Besides resting on faulty reasoning, the Kroll et al. study on which that

conclusion is based has multiple, serious scientific flaws that invalidate that
conclusion. First, the only figure purporting to show data from the study (figure 4)
exhibits results from only 5 seconds of rapid pacing (not differing periods up to 90
seconds); second, the blood pressure channel has no calibration and shows a return of
blood pressure midway, which the authors explain as a skeletal muscle contraction
effect, which would be unlikely in an anesthetized animal and could represent
transient loss of pacing capture that would blunt the ischemia by allowing transient
coronary blood flow; third, they state that heart contraction and capture by TASER
was monitored by echo but give no examples, so there is no proof of cardiac capture
at the asserted rates; fourth, there is no example of 90 seconds of pacing-induced
ischemia leading to VF, their main conclusion; fifth, there are no endpoints showing
actual attainment of ischemia, such as reduced pH or elevated potassium, known
ischemic end products, important since there can be degrees of ischemia (it is not a
binary end point, present or not), and the cycle length chosen may have been
insufficient to provoke a significant degree of ischemia; sixth, there are no statistics to
prove that the results were statistically significant, i.e., p<.05; and finally, the only

“data” given are not data at all but merely statements labeled “new data” at the
bottom of table 3, without actually showing any data. In that regard, it would be
highly unlikely that 4 of 6 animals all developed VF at 90 sec of pacing exposure, as
stated. The paper was published as part of an IEEE conference in Buenos Aires and
whether it was subjected to the usual review process is not indicated.

Further, even if the authors’ conclusions were supported by data and

tenable, the alleged ischemia attained would be induced in supine, anesthetized,
ventilated pigs with presumably normal hearts at alleged paced rates of 228 beats per
minute. Anesthesia can act as an antiarrhythmic intervention. This animal
experiment is a far cry from rapid pacing in an upright, agitated human being under
severe sympathetic stress, such as Ryan Rich, when the effects of ischemia would be
far more pronounced. Further, the heart might be captured at a faster rate due to the
sympathetic effects that shorten ventricular refractoriness (see below). Finally, some
individuals have underlying heart disease such as coronary obstructions, left
ventricular hypertrophy, or other problems, which would exaggerate the effects of
rapid pacing and shorten the time to VF. (I see no indication of any of these
conditions in Ryan Rich, however.)

Direct electrical stimulation of the ventricles can cause VF in at least two

ways. First, electrical stimulation during the vulnerable period of the T-wave (a 30-40
ms time interval during ventricular recovery from the preceding beat when the heart is
potentially unstable – its timing is during the peak of the T-wave in the ECG) can

provoke VF. The electrical stimulus required to do this is fairly large – about 1 joule –
requiring current 3-4 times that necessary for “capture.” Such T-wave stimulation is
done routinely in the electrophysiology lab to provoke VF in patients and test the
ability of an implanted cardioverter-defibrillator (ICD) to recognize the VF and
defibrillate it.

The second mechanism is by ventricular capture at rapid rates. The

ventricles can be stimulated directly by an electrical pulse of 0.5 milliseconds (msec)
duration and 0.8-1.0 volts, or about 2 mA, delivered over an electrode on or in the
heart. When the heart depolarizes in response to that electrical stimulus, it is said to
be “captured” by the stimulus. The heart also can be captured by an electrical pulse
delivered across the chest wall, which requires more electricity, in the range of 50-80
mA. However, that threshold is modulated by the stimulation site and type of
electrodes, type of shock, sex, torso and body mass, cardiac and non-cardiac diseases,
drugs such as cocaine and alcohol, medications, and the adrenergic (excited) state of
the individual. An adrenergic state means more catecholamines (naturally produced
stimulant chemicals like adrenaline and noradrenaline) are in the blood, which can
facilitate the initiation of VF by electrical stimuli. In fact, in the evaluation of patients
with VT in whom we are unable to induce the VT during an electrophysiologic study
(that involves electrically stimulating the heart at fast or premature intervals), we
routinely infuse a catecholamine IV to facilitate induction of the VT. With electrical
stimuli delivered over electrodes on/in the heart or on the chest wall, when the rate of

capture of the heart by the stimuli exceeds around 250-300/min, the organized
ventricular electrical activity can become disrupted, the contractions can become
disorganized and VT/VF can result, causing a cardiac arrest such as that suffered by
Ryan Rich.

Electrical current from a TASER X26 application that captures the heart

could result in VF at virtually any time during the pulsing shock delivery. The shocks
just need to produce a sufficiently rapid ventricular rate to disorganize the electrical
activity of the ventricles, which can happen at any time during the ventricular capture.
It does not have to be within the first 5 seconds or after 90 seconds for the following
reasons. The X26 delivers 19 pulses per second (52.6 msec intervals), which is a rate
of 1140 beats per minute (BPM) with each pulse 100 microseconds in duration,
delivering a peak amperage of 3-4 amps and a total charge of about 100
microcoulombs. The ventricles of the heart have a period after being stimulated
called the ventricular effective refractory period (VERP) during which they will not
respond to another stimulus at all (absolute VERP) or only respond to a larger
stimulus (relative VERP). It is a “rest period” during which the heart prepares for the
next contraction and is one of nature’s ways to protect the heart from beating too
rapidly. The VERP protects quite well most of the time, as, for example, with
ordinary pacemakers. However, extraordinary pacing exposures such as with a
TASER ECD shock can disrupt that safety feature. Human VERP normally ranges
between 200-250 msec. So, assuming a VERP of 250 ms, the maximum rate of

pacing capture will be 4/sec or 240 BPM (60,000 msec in one minute divided by 250
ms = 240BPM). Accordingly, a TASER ECD shock stimulating at 1140 BPM will
result in roughly a 5:1 capture, i.e., one ventricular response to every 5 stimuli, which
is what Kroll et al. report in the pig study noted above and is close to what Cao et al.
found in the patient with a pacemaker receiving a TASER ECD shock. Importantly,
however, heart rate modulates the VERP, so the faster the heart rate, the shorter the
VERP. Catecholamines from sympathetic discharge also shorten the VERP. I would
expect that Dr. Rich had a significant sympathetic discharge of catecholamines from
the pain of the probe deployments and drive stunning.

Therefore, the following scenario can occur: an individual receives

shocks from a TASER X26 which, depending on his VERP, can result in an initial
heart rate of 240 BPM. However, that increased heart rate, along with sympathetic
discharge from the pain and excitement that causes the release of catecholamines,
shortens the VERP to 200 ms so the capture rate can increase to, say, 300 BPM. That
new rate can further shorten the VERP, which will increase the heart rate still further,
often with irregular captures (the capture ratio does not necessarily remain constant)
that add to the disorganization of the heart beat, until a rate results that is sufficient to
produce VF. A ventricular capture can also occur during the T wave to cause VF due
to a ventricular beat falling in the vulnerable period of the T wave. Clearly, the onset
of VF can occur any time along the continuum of capture from the TASER shock.

The process described above is well illustrated in the Nanthakumar et al

paper, cited below. Figure 2 shows cardiac capture by the TASER X26 in a 3:1 ratio,
at a rate of about 375 BPM, but no VF. The rhythm and blood pressure return to
normal when the TASER shock is stopped. In figure 3, after epinephrine (adrenaline,
a catecholamine) given at 0.5microgm/kg/IV (the anesthetized animal feels no pain
and is not agitated so the clinical scenario of a human being feeling pain in the field is
replicated by administration of a catecholamine IV), the capture ratio spontaneously
decreases from 3:1 to 2:1 (rate about 550 BPM) that results in VF. Importantly, in
that figure, the VF starts more than 20 seconds after the beginning of the TASER
ECD shock, clearly in contrast to the statements by Kroll et al. In addition, the
TASER ECD shock initiated rapid VT, which degenerated to VF about 7 seconds
after the TASER ECD shock was stopped. Thus, VF can occur many seconds
after the beginning of the TASER ECD shock and even after cessation of the TASER
ECD shock, if the latter has induced VT. Here, that helps explain any breathing by
Dr. Rich shortly after the final ECD discharge.

A final important point to emphasize is that the TASER ECD shock can

initially induce polymorphic ventricular tachycardia (VT) that can gradually transform
to VF, as seen in fig 3. Depending on its rate, it is possible for the polymorphic VT
to generate some organized cardiac contractions that can maintain some blood flow
(and a palpable pulse) for a variable period of time before total collapse of the
circulation. That too helps explain any apparent breathing of Dr. Rich after the final
ECD discharge. Moreover, continued or repeated application of the TASER ECD

shock during the polymorphic VT can increase the ventricular disorganization and
help transform the VT into VF.

A fundamental problem with the conclusions from the paper by Kroll et

al is that they fail to account for the complexities and variables of human heart
function. We start here in Ryan Rich with a cardiac collapse that is virtually
simultaneous with the electrical discharge in an individual with no known heart
disease. The mechanisms for the ECD shocks to have caused this cardiac arrest are
well established in the medical literature, and there is no other plausible explanation
for the cardiac arrest at that moment. Without an actual ECG recording, there may be
some question about the precise time and manner in which Ryan Rich’s heart rhythm
went from a normal sinus rhythm to deadly VF under the effect of the ECD shocks
of January 4, 2008; however, there is no doubt that is what occurred.

Therefore, to a high degree of medical certainty, the shocks from the

TASER X26 through these mechanisms caused Ryan Rich’s heart to go into VF,
either directly or through a transformation of VT into VF, and therefore caused the
tragic, untimely death of this 33-year-old physician on January 4, 2008.

TASER’s documents and the peer reviewed literature indicate that ECD

technology was developed in the 1970s as a law enforcement tool. The original
systems were lower power, generally around seven watts. They were nevertheless
associated with a number of in-custody deaths according to a retrospective study by

Kornblum (cited in the addendum). The mechanisms of death in those cases were
unclear, but at least one was attributed in part to the ECD current.

According to “Medical Safety Information” issued in approximately

2000 with the initial sales of TASER’s first high-power ECD, the 26-watt Model M26
ADVANCED TASER, TASER CEO Rick Smith developed a stronger current to
replace the 7-watt system by shocking an anesthetized animal with increasing power,
until at four times the previous level “the muscles of the body went into a complete,
uncontrollable contraction.”

The “Medical Safety Information” document describes TASER’s

pre-release animal testing as follows:
“During these tests, two leading experts in cardiac safety tested
the ADVANCED TASER under extreme circumstances to evaluate if
the system could pose a medical threat. Under none of the applications
simulating potential real world use of the weapon was a dangerous
interaction found. Not only did the researchers test the ADVANCED
TASER by placing the probes on the surface of the chest in the
locations which are known to have the greatest probability of cardiac
interference, they used hypodermic needles inserted into the chest to
directly stimulate the surface of the heart. They used drugs such as
epinephrine, Ketamine, and isoproterenol to see if the ADVANCED
TASER would have an effect on a person under the influence of drugs

known to sensitize the heart to stimulation. They even simultaneously
applied the shock from two ADVANCED TASERS (over 52 Watts of
power) directly to the chest regions where the cardiac affect [sic] would
be greatest. Even under these extreme circumstances, they were unable
to cause a dangerous cardiac fibrillation. Over the course of three days
of testing, in 192 discharges of the ADVANCED TASER, these
researchers administered over 14,000 of the 26 Watt ADVANCED
TASER Wave pulses to five animals all of which are significantly smaller
(and hence more susceptible to electrical fibrillation) than humans. Two
leading experts in cardiac safety, purposefully attempting to cause
fibrillation by using drugs, implanted needles to the surface of the
heart, and even simultaneously applying two ADVANCED
TASERS to the chest were unable to cause fibrillation with the
(Bold in original.) No such studies were peer-reviewed and published at that time,
however. (The first peer-reviewed “ADVANCED TASER” (26-Watt) study would
not be published until five years later.) Moreover, these claims were contradicted by
later independent studies demonstrating consistent cardiac capture and episodic
fibrillation in test animals, some of which were published prior to the Ryan Rich
incident in this report.

TASER’S initial animal studies to determine the safety of its higher

power ECDs were inadequate. The design of the Model M26 waveform, according to
Dr. Stratbucker’s deposition taken June 10, 2010, was based on the concept that a
short pulse or train of short pulses, despite high amplitude, cannot capture the heart
because of the long cardiac refractory period, and the electrical energy transmitted to
the heart is therefore safe. Apparently, on January 11, 1996, he used a custom device
on one anesthetized 18.2 kg Hampshire shoat pig more than 48 times to establish
safety and efficacy of custom designed ECD delivering current via darts in the skin at
the suprasternal notch and umbilicus. The pig was not intubated and he did not
monitor metabolic response, blood gases, etc. He only studied strain gauges for
muscle responses in the extremities. He allowed the pig to wake up, recover, and the
pig was re-tested a few days later. He states that the pig did not show any cardiac
ectopy (i.e., premature beats) or myocardial injury. The experiments resulted in
increases in the capacitor that caused more muscle disruption and culminated in
electrical characteristics of the waveform for the M26 in beginning of 1998, which
went to market late 1999. VF never occurred in the one pig, and capture was not
measured. Importantly, Dr. Stratbucker tested an M26 strength current at only 2-2 ½
pulses/sec (pps; 400 msec intervals) with a duration of 13 microseconds. In fact, the
M26 delivers 15-19 pps (66.7-52.6 msec intervals) of 40 microseconds duration with
peak current of 15-17 amps.

Later, Dr. Stratbucker produced VF in one dog using an off-the-shelf

Model M26 TASER delivering the stimuli over a catheter in the heart. This result,

which contradicted his hypothesis that the ECD cannot capture the heart because of
the long cardiac refractory period, was never reported.

These results are troubling from several points. First, studying one pig

shocked 48 times is very different than studying 48 pigs shocked one time, since that
one pig may not be representative of all pigs, and other pigs may not have been
equally resistant to the shocks. Second, the electrical characteristics of the device,
particularly in terms of pulses per second and duration, were not similar to the actual
M26. Finally, not reporting that one dog developed VF when exposed to the Model
M26 discharge, albeit via a catheter in the heart, was unacceptable because it showed
that under certain circumstances the Model M26 can cause VF in a mammalian heart.
This is especially true because that finding squarely contradicts the statement in the
“Medical Information” at page 9 that “the short pulse duration of stun guns have very
little effect on heart operation which uses much longer electrical pulses.” Regardless,
the statement that trains of short duration pulses would not cause VF is erroneous.

Dr. Stratbucker et al. performed tests with a device capable of increased

current he called a “Super-TASER.” (PACE 2005; Suppl 1:S284) Rick Smith refers to
the devise as a “scalable TASER,” a more accurate description. 9 pigs were subjected
to five second discharges. The results suggested a safety index for stored charge
ranging from 15X to 42X as weight increased from 30 to 117Kg. He stated that the
typical TASER product therefore had a safety margin of at least 100 times and that
the short pulse has little effects on the heart. In a January 6, 2000 letter Dr.

Stratbucker stated he did studies with Dr. McDaniel on an off-the-shelf M26 after the
M26 was being marketed. He attached TASER darts to 5 dogs and fired the M26 for
10 seconds, he thinks. This was published as an abstract (ref 9 in the PACE article).
He states that these devices do not cause serious cardiac rhythm abnormalities in the
otherwise normal heart.

Dr. Stratbucker states in his deposition of June 10, 2010, that the

observation of TASER capture in the Lakkireddy study is a “trivial artifact” and that
“everybody’s known since time began that you can put a hundred amps in there on a
defibrillator pulse and – and – and not make somebody fibrillate. You get plenty of
capture, but – but it doesn’t fibrillate you.” For reasons I explain above, this is an
erroneous conclusion.

The TASER “Medical Safety Information” document also refers to

“human subject studies,” but these are simply anecdotal accounts of various
volunteers being subjected to short duration (.5- to a few full 5-second) exposures,
many through alligator clips and other forms of electrodes. There was no
physiological monitoring or data reported. Referring to these as “human subject
studies” is highly misleading.

In 2003 TASER developed the X26, which is smaller and lighter than

the M26. While similar in most other respects, the X26 uses less power and pulses a
lower current (3-5 amp versus 15-17 amp) but longer (100 microseconds versus 40
microseconds) “waveform.” The total charge delivered per pulse is about the same,

100 microculombs. This is the device that was used on Ryan Rich, January 4, 2008.

The Model X26 “Operating Manual” makes the following

representations regarding safety:

“Aim for the center of the back or the chest of the subject.”


“In animal testing, the X26 was found to have a safety margin of 20

times (the X26 was 1/20th of the danger level).”

“The TASER X26 was tested extensively on both animals and human

volunteers and has been found to cause no dangerous cardiac or other effects.

“Further, the TASER output will not damage an implanted pacemaker.”

Pacemakers are designed to withstand the pulses of electrical defibrillators
hundreds of times stronger than TASER pulses.”

In its original owner’s manual and in the training versions I reviewed,

TASER relied on research performed for the M26 to apply to the X26 as well.
Independent testing, however, revealed that the X26’s longer waveform translates into
a higher capacity for cardiac capture than the M26. (Nanthankumar, 2006).
Police Department Training

Training Version 10 (issued June 2003) and Version 11 (issued January

2004) contain PowerPoint presentations for the instructor courses which made the
following representations regarding cardiac safety:

Slide 19 (Ver. 10) and Slide 21 (Ver. 11) state “It’s not the volts, it’s the

amps that are dangerous,” and then represents the devices to be “Low

Amperage,” stating “Both the M26 and X26 are less than 0.004 amps (very low
amperage).” “High Voltage + High Power + Low Amperage = Safe &
Effective weapon.” In fact the peak amperage (a relevant measure for cardiac
safety) of the M26 is 15-17 amps, and the peak amperage of the X26 is 3-5
amps. The amount of total current delivered is similar because the X26 pulse
lasts longer. (See Braidwood Testimony of J. Patrick Reilly, May 5, 2008).

Slide 22 (Ver. 10) states “TASER tests have found: - No effect on heart

rhythms” when “tested on animals.”

Slide 23 (Ver. 10) states “Heart rate unchanged during TASER X26

stimulation directly through [the] chest, across the heart.” The “Instructor’s
Note” states that the representation is based on “a blood pressure reading from
an anesthetized pig. The X26 was applied across the chest with the two probes
in a ‘worst case’ scenario (the points most likely to stimulate the heart). Note
that the heart beat continues normally. The small fluctuations in blood
pressure are the result of skeletal muscle contractions that add fluctuations to
blood pressure. It is important to note that the heart rate does not change at
all. This is important because it shows that the level of the X26 stimulation is
below the threshold to pace the heart.”

Slide 25 (Ver. 10) and Slide 31 (Ver. 11) state, “Using ‘worst case’

scenarios, two cardiac safety experts found no interference by the M26 with the
heart rhythms.”


Slide 29 (Ver. 11) states, “Extensive animal testing has shown no effect

on heart rhythms or blood pressure.”
Instructing police officers with such information presents the conclusion that TASER
ECD administration cannot cause cardiac arrest. The Ryan Rich case, among other
incidents and studies – some of which occurred prior to the Ryan Rich incident –
show that not to be the case.

Further, the TASER “Command Demonstration” PowerPoint Version

12 (released November 2004) included the following representations relating to
cardiac safety:

Slide 3 states “X/M26 will not cause heart or pacemaker failure.”


Slide 14 states, “Extensive animal testing has shown effect on heart

rhythms or blood pressure to be insignificant.”

Slide 18 states, “The ADVANCED TASER M26 was applied directly to

the chest of experimental animals without causing heart failure during tests at
the University of Missouri,” “Using ‘worst case’ scenarios, cardiac safety
experts found no induction by the M26 weapon of abnormal heart rhythms,”
and “No arrhythmia provocation occurred even when the animals were given
the stimulant drugs epinephrine and isoproterenol, agents that make the heart
more susceptible to electrical stimulation.”

Version 13 (released May 1, 2006), which Trooper Lazoff was most

likely trained on, contains the following representations in its “X26 User’s Course”:


Slide 18 states, “Low average current: M26 & X26 < 0.004 A.”


Slide 21 states, “TASER devices operate at low average currents

(0.0021 - 0.0036 A).” For the reasons stated above, these numbers are very
misleading as the peak current is the relevant measure for cardiac safety, and
the peaks range from 3 to 17 amps. (See Braidwood Testimony of J. Patrick
Reilly, May 5, 2008)

Slide 26 states, “TASER Devices are among the most extensively studied

non-lethal weapons,” clearly implying that the devices have been determined to
be cardiac safe. At the time, however, there were only a few peer-reviewed
publications available (including a case report published in the New England
Journal of Medicine warning that the product appeared to have caused ventricular
fibrillation in a 14-year-old youth), and several warned about cardiac risks, two
specifying increased risk of cardiac capture specifically from shots to the chest.
TASER’s own study had warned that chest shots should be avoided. Yet the
Version 13 User Course illustrated shots to the chest, Slides 11 and 68, and
instructed in Slide 67 to “Aim like a standard firearm at center of mass”
without warning that chest shots significantly increase the risk of cardiac arrest.

Slide 29 states, “Animal testing has shown insignificant effects on heart

rhythms or blood pressure.”

Slide 30 states, “The ADVANCED TASER M26 was applied directly to

the chest of experimental animals without causing heart failure during tests at

the University of Missouri,” and “Using “worst case” scenarios, cardiac safety
experts found no induction by the M26 of abnormal heart rhythms.” These
were based on a TASER funded study, but by the time Version 13 was
released, a more recent TASER-funded study had demonstrated that the X26
captured heart rhythms when probes were stuck into the chests of test animals,
and an electrophysiologist involved in that study had warned TASER that chest
shots should be avoided.

TASER Training Version 14, issued during 2007, which Trooper Lazoff

also was trained on, is very similar to Version 13, and has misrepresentations about
the power of the TASER current, for example Slide 33 claiming it to be many times
smaller than the amount of current required to power a Christmas tree light, when in
fact it is many times higher. Slide 33 states that “Animal testing has shown
insignificant effects on heart rhythms or blood pressure,” when in fact TASER had
the results of the study by Nanthakumar, et al., showing the induction of ventricular
fibrillation. Slide 35 refers to test results from the Model M26 that “No arrhythmia
provocation occurred even when animals were given stimulant drugs epinephrine and
isoproterenol, which make the heart more susceptible to electrical stimulation.” At the
time TASER had test results from Nanthakumar, et al., and Dennis, et al.,
demonstrating the induction of VF with off the shelf Model X26s. Slide 144 instructs
users to aim at “center of mass,” in other words, the chest, slide 145 illustrates the
whole body as “effective target zones,” and Slide 147 instructs to aim at the “open

front of unzipped jacket.” Because he was TASER certified instructor, I understand
that Trooper Lazoff would be familiar with Versions 13 and 14, and would therefore
believe based on TASER’s instructions that TASER ECDs posed no increased risk of
cardiac arrest when shot directly into the chest of individuals. As I explain, however,
this belief is not supported by the medical and scientific evidence available to TASER
at the time it issued Training Versions 13 and 14.
Documented Risks of TASER ECDs Prior to the Rich Incident

I have not seen evidence that was peer-reviewed and published prior to

2005 to substantiate TASER’s representations of cardiac safety, and based on my
knowledge of electrophysiology these representations are inconsistent with what one
might expect when electric shocks of the magnitude delivered by TASER ECDs are
delivered over darts to the chest. Starting in 2005, however, documentation of the
TASER ECD’s cardiac risks began appearing in reputable medical journals.

Kim and Franklin reported in The New England Journal of Medicine

(353:958, September 1, 2005), Ventricular Fibrillation After Stun Gun Discharge, that
an adolescent subdued with a TASER ECD collapsed. “Paramedics found the
adolescent to be in ventricular fibrillation” and began performing cardiopulmonary
resuscitation within two minutes after the collapse. Four shocks and drug
administration restored a perfusing rhythm and the adolescent made a nearly
complete recovery, discharged from the hospital several days later. (The authors
published the electrocardiogram showing ventricular fibrillation being terminated after

a 360 joule defibrillation shock. Although that happened, the strip published was not
the final shock, but one depicting an earlier shock converting VF into an
idioventricular rhythm. That mix-up has no effect on the conclusions.) TASER
criticized this publication, claiming in an open letter (around October 2005) signed by
Drs. Rick Luceri, Hugh Calkins, and Mark Kroll, and a published letter to the editor
of the J Amer Coll Cardiol (49:732, 2007), that the paramedics did not in fact find the
adolescent collapsed or in ventricular fibrillation, as reported, but that the collapse
occurred in an ambulance some 23 minutes after the TASER administration.
Deposition testimony by a paramedic on the scene, Jill Hutchinson, however,
substantiates the conclusions of the article. Specifically, the 14-year-old individual
immediately lost consciousness at the time of ECD shock, initially had a pulse and
appeared to be breathing, but two minutes after collapse had an ECG recorded by the
paramedics that showed VF, thus refuting the arguments made by TASER. In his
deposition, Dr. Kroll blames the difference between the time recorded by the TASER
and actual time for the mistake. The ECGs published in the NEJM were the first two
recorded, showing VF and termination of VF by a 360 J shock (cropped, and actually
200 J). The VF recurred and required three further defibrillations and the young boy
required multiple medications to be resuscitated. Fellow TASER Scientific and
Medical Advisory Board member Dr. Charles Swerdlow refused to sign the letter,
according to the deposition of Dr. Kroll September 29, 2010, because he was not
being paid a high enough retainer to allow TASER to publically use his name. Dr.

Swerdlow, when I told him of that statement, disagreed with Dr. Kroll’s explanation
(see attached email, Exhibit F).

TASER funded a pig study by Lakkireddy, et al., accepted March 20,

2006, entitled Effects of Cocaine Intoxication on the Threshold for Stun Gun
Induction of Ventricular Fibrillation (Journal of the American College of Cardiology Vol. 48,
No. 4, 2006). Dr. Tchou participated in this study, and it is referenced in Exhibit E,
our email exchange. Darts were placed in various positions on anesthetized pigs and
five-second shocks were delivered using a “Super-TASER” modified to deliver both a
standard Model X26 charge as well as increased charges. The study described the
relationship between cardiac capture and the location of the darts on the chest,
describing darts to the chest as more likely to cause capture, with one dart at the
sternal notch and the other on the left side at the “point of maximum cardiac impulse
(PMI),” referred to in the study as “Position A,” being most likely of all the positions
tested to capture the heart.

The authors found that standard X26 discharges at “Position A” resulted

in “ventricular capture ratios ranging from 6:1 through 3:1,” and that “VF was
consistently inducible whenever the ventricular capture ratio was [less than or equal
to] 2:1. The authors write that their “study is the first to describe capture of
ventricular myocardium during application of [ECD] pulses.” The authors state the
following in their discussion:
“Extending animal data to human beings should always be done

with caution. However, pigs frequently have been used in fibrillation and
defibrillation threshold studies with the results generalized to humans.
The results of our study and the few prior animal studies would suggest
that [ECD] discharge at the standard 5-s application is unlikely to cause
life-threatening arrhythmias, at least in the normal heart. Our data
regarding myocardial capture, however, suggest the potential for
induction of ventricular tachycardia in subjects with substrate for
ventricular tachycardia, especially if one of the electrodes were to come
within a few centimeters of the myocardium, with the other positioned
to direct the current toward the heart. In humans, the anterior apical
right ventricular myocardium is closest to the chest wall. Positioning of
an electrode in a small, thin human in the region of the left nipple with
the other electrode near the sternal notch may simulate our Position A
and could potentially achieve comparable proximities of electrodes to
the heart. Avoidance of this position would greatly reduce any concern
for induction of ventricular arrhythmias.”

Although TASER funded this study and therefore must have known of

this finding in early 2006, at the latest, (one participant, Dr. Tchou, told me: “From
the very beginning, as we obtained our data from our animal study, I had advised
TASER that the possibility of inducing ventricular arrhythmias is there.” Exhibit E),
TASER took no steps to warn its users that avoiding shots to the chest “would greatly

reduce any concern for induction of ventricular arrhythmias.” In fact, no such
warning was issued by TASER until September 30, 2009, 21 months after the incident
involving Ryan Rich. Instead, TASER continued to misrepresent the cardiac safety of
its products in its training and promotional literature.

As noted above, Ryan Rich had one dart embedded just above and one

dart just below the left nipple, thus encompassing the heart in an electrical vector
similar to the ideal position established by the Lakkireddy study. There are three
important limitations to the Lakkireddy study, which suggest that the study may have
understated the cardiac risks to human beings. First, the test animals were
anesthetized, which as I mentioned above can suppress development of arrhythmias.
Second, also because the test animals were anesthetized, they did not experience the
pain felt by human subjects when shocked by X26s. Pain causes the body to release
catecholamines (substances like adrenaline) and, as noted above, create an adrenergic
state and stimulate the heart, making it more subject to arrhythmia. Third, shocks
were administered for only one five-second cycle, yet the X26 is designed to deliver
multiple and prolonged cycles. The probability of capture degenerating into VT or VF
increases with increased duration of capture time. As mentioned above, Dr. Rich
received multiple cycles over a 3-minute period.

An animal study by Nanthakumar, et al. (Journal of American College of

Cardiology, accepted February 7, 2006), Cardiac Electrophysiological Consequences of
Neuromuscular Incapacitating Device Discharges, reported on 150 discharges in six

pigs using both the Model X26 and the Model M26. The results were first reported as
a poster abstract on May 19, 2006 at the Heart Rhythm Society meeting in Boston
(Heart Rhythm vol 3: (1S) p. S237, 2006). The first copies of the abstract article were
mailed early that May. Dr. Nanthakumar told me that Dr. Kroll, the head of TASER’s
Scientific and Medical Advisory Board, attended the presentation and spoke against it,
much as he did with me following my presentation three years later. This appears to
me, however, to be a thorough and well designed study by independent researchers,
and its findings are entitled to great weight.

The authors note that, while surface ECG monitoring has been done in

healthy human volunteers before and after delivery of energy from ECDs, there had
been no intracardiac monitoring to eliminate electromagnetic interference produced
by the ECD, causing electrical artifact to be recorded by the ECG. Such artifact
would make interpretation of true cardiac activity difficult or impossible from a
standard ECG. They used an intracardiac recording (electrode recording from inside a
chamber of the heart) approach in this study, a technique too invasive to use on
human volunteer test subjects.

Out of 41 Model M26 discharges delivered to the chest with an interdart

distance of 26-30 cm, 22, or 53.66% resulted in stimulation of the myocardium
(cardiac capture). All but one of 53 Model X26 discharges (98.11%) did so, suggesting
that the longer Model X26 waveform is significantly more likely to result in cardiac
capture, even at about one-fourth the peak amperage of the M26. None of 56

non-thoracic discharges from either device stimulated the myocardium, again
demonstrating the high correlation between darts in the chest, close to the heart, and
potential arrhythmias.

The cardiac capture from electrical stimulation at high rates persisted

during the discharge, and as soon as the discharge ceased there was resumption of
normal electrical rhythm. Importantly, however, the blood pressure fell to very low
values during the rapid stimulation. During epinephrine (adrenaline) infusion (a
catecholamine) to simulate the agitated stress state of an individual experiencing pain
or resisting restraint, one ECD administration resulted in non-sustained ventricular
tachycardia that spontaneously reverted to sinus rhythm, while another produced
ventricular fibrillation and cardiac arrest. These findings demonstrate that the
possibility exists of TASER ECDs – the Model X26 more than the Model M26 –
inducing serious ventricular arrhythmias during discharge in structurally normal
hearts, especially during the intense catecholamine release that accompanies the stress
of the situation and the pain of the ECD discharge.

The authors designed the study to portray the worst case scenario and

noted that general anesthesia – a requirement for the humane treatment of test
animals – may have increased the threshold for arrhythmia induction, in other words
made it more difficult to induce an arrhythmia. While objections have been raised
about using the pig as an animal model, in the Lakkireddy study noted above and
financed by TASER, they state, “However, pigs frequently have been used in

fibrillation and defibrillation threshold studies with the results generalized to
humans.” It is important to note that all the pre-release TASER ECD testing that
could be remotely considered “scientific” rather than anecdotal was performed on
pigs and dogs, rather than human beings.

The results of this study also support my opinion that VF can occur at

any time during a TASER shock that captures the myocardium, as elaborated above.

I have been provided a written Version 13 certification test and answer

key often administered to officers for TASER certification. The test was written after
TASER knew the results of the Lakkireddy and Nanthakumar studies, almost two
years before Ryan Rich’s death. The supposedly correct answer given for Question 24
is that the TASER X26 affects the “sensory and motor nervous systems,” but not the
“cardiac system.” For Question No. 1, “When deploying probes, the TASER should
generally be aimed at?” the answer given is “center of body mass,” in other words the
chest. Yet TASER knew at that time Model X26 administrations near the heart risked
cardiac capture and therefore cardiac arrest.

Additional animal studies continued to confirm cardiac capture and

incidents of VF. Of particular interest were a series of tests performed by independent
researchers at a Chicago institution. Dennis, et al (Journal of Trauma 2007; 63:581)
Acute Effects of Taser X26 Discharges in a Swine Model), performed a study in
which anesthetized pigs were exposed to two 40-second discharges from a TASER
Model X26 separated by a 10-second pause. One of the pigs in the test group

developed ventricular tachycardia progressing to ventricular fibrillation after the ECD
discharge. Three pigs showed capture with rapid (approximate rate 300/min)
contractions seen on echo during the shock, and stopping when the shock stopped.
Two pigs in the control group prior to being euthanized underwent a left anterior
thoracotomy to view the heart during ECD administration to the chest. They both
showed visual cardiac capture by the ECD shock. Immediately after exposure, one pig
developed ventricular tachycardia progressing to fatal ventricular fibrillation (a video
clip of the heart of the open chest pig clearly shows the onset of ventricular
fibrillation). The surviving animals in the test group showed a significant increase in
heart rate and significant hypotension. In their second study, published August 2007,
the researchers injected test animals with a paralyzing agent and were still able to
induce cardiac capture with a standard Model X26 in all eight animals tested, causing
one to experience ventricular fibrillation. In their third study, published December
2008, the researchers induced VF in two of four animals with a 10-second Model X26
discharge to a spot on the left upper chest, again near one of Ryan Rich dart wounds.
They found the cardiac effects of the Model X26 highly dependent on transcardiac
vectors of the probes as well as the configuration of the positive and negative darts.

In a study funded by TASER (two of the authors, Dr. Dawes and Dr.

Ho, serve as medical consultants to TASER and are stockholders, and Dr. Ho serves
as the Medical Director of TASER) Dawes et al (Effect of an Electronic Control
Device Exposure Academic Emergency Medicine 2010; 17:436-443) studied 16 Dorset

sheep exposed to none or incremental doses of methamphetamine and, 30 min later,
to 5, 15, 30, or 40 sec of TASER Model X26 intermittent shocks with darts inserted
9mm deep at the sternal notch and cardiac apex. Cardiac motion was determined by
thoracotomy and echocardiography. Certain animals had supraventricular
dysrhythmias after ECD exposure and one had 6-8 beat multifocal VT, while the
larger animals had only sinus tachycardia. Three of the smaller animals demonstrated
cardiac capture during ECD exposure, while two of the larger control animals did
also. No animal developed VF. Once again, in a study funded by TASER and
conducted by TASER consultants, the Model X26 demonstrated the capability to
capture the heart at rapid rates, which, in a field situation, could lead to VF, and
certainly did in the Ryan Rich case.

In a modeling study (Sun, et al., Estimating the probability that the Taser

directly causes human ventricular fibrillation J Med Engineering and Technology
2010,1-14), the authors “estimated mean probability of human VF was 0.001 for data
from a pig having a chest wall resected to the ribs and 0.000006 for data from a pig
with no resection when inserting a blunt probe. The VF probability for a given dart
location decreased with the dart-to-heart horizontal distance (radius) on the skin
surface.” While these data are interesting, there is no way a modeling study can
replicate the clinical scenario that occurred to Ryan Rich while being shocked for 62
seconds. The authors themselves cite many limitations to their intellectual exercise.
And even if that estimate were possible, the first estimate of 0.001 means that one

individual in a thousand would develop VF while being tasered, which may be
consistent with what is actually experienced, though numbers of total TASER
applications and the incidence of VF, particularly the latter, may not be completely

On September 30, 2009, TASER issued new warnings about the risk of

VF and the importance of avoiding shocks to the chest. Recent TASER training
materials have cited a risk of ventricular fibrillation of 1:100,000 TASER ECD
applications. In fact, if one considers only TASER ECD applications where the darts
were impaled in the anterior chest, since darts in other positions would not be
expected to produce VF, the odds of a TASER shock inducing VF with that dart
configuration are probably significantly higher, as Dr. Kroll testified at his deposition.

There have been some human tests, mostly TASER funded, and I do

not cite these. They do not, in my professional opinion, eliminate the concerns raised
by the animal studies. The basic limitation with the human studies is ethical. Any
human testing must be designed with safety parameters to avoid VF induction, which
eliminates the sort of testing done on pigs, where fibrillation thresholds can be
determined. Moreover, human testing on volunteers cannot replicate the “real life”
situation experienced by individuals involuntarily receiving repeated Model X26
shocks in the chaos of a field setting.

A recent TASER-funded human study (with two authors, Drs. Ho and

Dawes, serving as expert medical consultants to TASER, International for public

speaking purposes and litigation involving corporate product, and who own personal
shares of stock in the company), by Ho, et al. (Human Cardiovascular Effects of a
New Conducted Electrical Weapon Forensic Science International (2010,
doi:10.1016/j.forsciint.2010.05.003) on normal human volunteers tested a new
generation TASER ECD with different circuit and multiple cartridges that can be
discharged simultaneously. They used echo monitoring and demonstrated “an
apparent brief episode of cardiac capture” at a rate of 240 beats/min during the 10
second TASER ECD shock. It was “assumed to be electrical capture by the device,”
according to the authors, thus substantiating the capability of TASER-induced cardiac
capture, albeit with a newer device, in humans. One probe was in the center of the
chest and the second on the right groin area. The study was stopped and a
re-designed TASER ECD was allegedly substituted, which showed sinus rhythm in 27
of 42 subjects, while “the rhythms of the remaining subjects were unable to be
determined due to subject movement during exposure, however, the maximal rate in
any of the subjects exposed to the (new) device was 162 bpm.” Naturally, that does
NOT exclude TASER-induced capture at a rate slower than 240/min. While neither
of these devices was used on Ryan Rich, the importance of this study is that, even
with the new (presumably, improved) TASER ECD, cardiac capture was verified by
experts in TASER’s own company. If it is true that, “The cardiac safety profile of the
NGCEW (new electronic control) device appears similar to previous CEW devices
when used in multiple probe application formats as intended,” this is hardly

reassurance that TASER ECDs do not produce VF.

However, there are human data that support the conclusion that TASER

ECDs cause cardiac capture and even VF. Cao, et al (Journal of Cardiovascular
Electrophysiology 18:876, 2007), published “Taser-Induced Rapid Ventricular Myocardial
Capture Demonstrated by Pacemaker Intracardiac Electrograms.” This is a very
important case report of a 53-year old male with a dual-chamber pacemaker implanted
subcutaneously beneath the left clavicle (Medtronic Kappa) who received ECD
shocks while in a prison, with two barbs delivered with a Model X26. The man was
struck on the right chest and did not suffer any immediate observable adverse events.
During pacemaker evaluation, however, there were two ventricular high rate episodes
that corresponded to the exact time of the Model X26 shocks. I am aware that the
pacemaker leads may have provided a pathway for the Model X26 shocks to reach the
heart, but nevertheless, the study shows clear cardiac capture from Model X26 shocks
in the field.
Selected Clinical Cases of TASER Related Sudden Cardiac Death

I personally examined the case history of Greshmond Gray, a 25-year

old male who was shocked three times – sixteen seconds, five seconds and five
seconds – in La Grange, Georgia, on November 2, 2004, by a TASER ECD. He
became non-responsive coincident with the TASER ECD application. An ambulance
was called and CPR initiated. There was an automatic external defibrillator (AED)
available. Prompt application of the AED showed an initial rhythm of ventricular

fibrillation. 200 joules were delivered followed by asystole and then a wide-complex
rhythm followed by redevelopment of ventricular fibrillation. A second AED shock
of 200 joules was followed by asystole and another wide-complex rhythm. Mr. Gray
could not be resuscitated. The officers testified that it was a very short period of time
between the last ECD shock, recognizing that Mr. Gray was unresponsive, obtaining
an AED from the police car, and giving the first AED shock. One officer believes this
occurred in minutes and certainly less than five minutes. The AED was analyzing for
a second shock when the EMTs first arrived.

The autopsy indicated that Mr. Gray had two puncture sites on the

medial left upper chest at the base of the neck and midline lower chest/upper
abdomen, similar to the ideal “Position A” noted in the Lakkireddy study. Heart
weight was 410 grams (normal) with normal coronary arteries, normal cardiac
chambers and normal cardiac valves. Toxicology found marijuana metabolite in the
blood and 0.145 percent blood alcohol. I concluded to a reasonable degree of medical
certainty that because Mr. Gray developed ventricular fibrillation closely following the
ECD administrations directly to the chest, and there was no other explanation for the
cardiac arrest at that moment of TASER ECD application, the TASER ECD caused
his sudden death due to ventricular fibrillation.

I used this case to support my opinion in Williams v. TASER International,

Inc. Charles D. Swerdlow, M.D., a colleague who was a defense expert for TASER at
the time as well as a member of TASER’s Scientific and Medical Advisory Board

(now no longer consulting for TASER to my understanding), subsequently presented
on this case, along with others, at our 2009 Heart Rhythm Society meeting in Boston,
and then published “Presenting Rhythm in Sudden Deaths Temporally Proximate to
Discharge of TASER Conducted Electrical Weapons” (May 2009). Although he did
not identify the case by name, he described the Greshmond Gray case as follows:
“For subject 1, who collapsed immediately . . . , neither drugs nor cardiac disease can
be implicated; both the time course and the electrode location are consistent with
electrically induced VF,” and “To the best of our knowledge, this is the first reported
fatality suggestive of [ECD]- induced VF.”



Additional cases exist which demonstrate that shocks to the chest by a

TASER ECD can cause sudden death due to ventricular fibrillation. The case of
Butler v. TASER International, Inc., for which I gave a deposition on February 22, 2009,
involved a 48-year-old man who received 3 shocks from a Model X26 TASER for 5,
8, and 5 seconds over about 30 seconds, and became limp without pulse or
respirations. An ECG recorded VF shortly thereafter. He was resuscitated but with
brain damage. Darryl Turner was a 17-year old who, on March 20, 2008, received a
37-second shock from a TASER X-26 directly to his chest that produced
simultaneous cardiac arrest and death. I prepared an expert report very similar to this
one and gave a deposition in that matter as well. Robert Mitchell was a 16-year-old
boy who received a single TASER shock in the chest, collapsed more or less
immediately and presented with VF, according to the reports available to me. I have
seen the autopsy reports and EMS records, including rhythm strips, for this incident.
While the autopsy indicates he had arrhythmogenic right ventricular cardiomyopathy,
if indeed he did have that, it does not exclude a TASER ECD shock from inducing
VT-VF. The ECG strips during resuscitation show an irregular VT. He was not
resuscitated and died. Rory McKenzie was a 25-year-old male who collapsed about 2
min after receiving TASER shocks from two TASERS simultaneously, was found to
be in VF 10-12 minutes later and could not be resuscitated. Autopsy showed no
significant heart disease. Derek Jones was a 20 year-old male who collapsed due to
VF immediately after a TASER shock to his chest and could not be defibrillated. He

had a normal heart at autopsy. Toxicology showed ethanol 0.22%, THC carboxylic
acid, but no other drugs. Additional cases no doubt exist, but to my knowledge
havenot been systematically collected and analyzed.
Statement of Opinions

I was asked to evaluate the available records and information concerning

the cardiac arrest of Ryan Rich following thirteen cycles of TASER Model X26
electronic control device shocks for a total of 62 seconds in about 3 minutes, to
determine whether such data were sufficient to make a finding of causality, whether
TASER provided appropriate warnings to law enforcement about the cardiac risks of
the product, and whether TASER’s representations about its product’s safety were
truthful in light of the known or knowable scientific evidence. My opinions stated
above and that follow are expressed to a reasonable degree of medical certainty, based
on my education, clinical practice, research, training, experience, literature review,
document review, and generally accepted principles of medicine and clinical science.

A TASER Model X26 discharge can cause cardiac arrest by capturing

the cardiac rhythm at very rapid rates and precipitating ventricular tachycardia or
ventricular fibrillation, as shown in animal testing and human reports. The temporal
relationship of Ryan Rich’s collapse to the Model X26 shocks in the absence of any
equally plausible alternative explanation for his heart to develop cardiac arrest at that
precise moment demonstrates that the ECD’s electrical current directly caused Dr.
Rich’s cardiac arrest. His only health problem was epilepsy; there was no family

history of heart disease, nor were there confounding issues such as drugs. I do not
think he had an enlarged heart, based on the data from the Mayo Clinic paper and his
body weight of 220 pounds. The LV wall measurement is probably in error and
included papillary muscle. It is therefore my opinion to a high degree of medical
certainty that Ryan Rich developed ventricular fibrillation as a result of the X26
shocks that he received, which led directly to his death, and that there was no other
cause of death.
92) Because the TASER barbs remained attached to his chest after the initial
ECD applications in the probe mode (see paragraph 34 above) and the TASER
cartridge remained in place, according to the statement given by Trooper Lazoff,
current delivered during the drive stun mode also was distributed to his heart. While
the exact amount of current obviously was not measured, and some may have
“leaked” off, particularly during the first drive-stun application to his legs, the almost
“perfect” probe position for cardiac capture on Dr. Rich’s chest, based on the animal
work, may have facilitated pacing of the heart even with somewhat reduced current
during the drive stun applications
93) In my opinion, the cardiac arrest began when Ryan Rich no longer resisted
handcuffing. The trooper and physician left Dr. Rich to walk to the trooper’s vehicle
at that time. I find it hard to believe Dr. Morris’s statements that Dr. Rich’s breathing
was normal at that time, i.e., not even accelerated due to the fighting. In fact, “normal
breathing” under such conditions would itself be abnormal. I suspect Dr. Morris did

not take accurate notice, since he believed there was no reason to do so. Further, if
Dr. Rich was breathing, it may have appeared more or less “normal” in the early
throes of a ventricular tachycardia. The lethal rhythm can remain somewhat
organized and produce a blood pressure and pulse for several seconds early on, as I
have explained above (see paragraphs 45-48), so there may have been no noticeable
respiratory effects while they were taking leave of him. The 20-30 second walk to the
trooper’s vehicle would be the minimum length of time for someone in cardiac arrest
to become obviously cyanotic, which is around when Dr. Morris turns and notices
this change in Dr. Rich’s appearance.

While Ryan Rich apparently did have epilepsy, and may have been in a

post ictal state from a seizure at the time of his erratic driving, that event played no
direct role in causing his death, as I understand Dr. Engel explains in his report. It is
just as likely that the gabapentin at high doses contributed to a confusional state and
the erratic driving, but as with the epilepsy, played no direct role in causing death.

Alternative causes of Ryan Rich’s cardiac arrest are excluded, including

excited delirium and sudden unexplained death in epilepsy (SUDEP). The former has
been reported as death associated with an extremely agitated and irrational state,
usually compounded by physical restraint. Many of the individuals dying with this
alleged diagnosis have taken stimulant drugs such as PCP, methamphetamine and
cocaine, or suffered from severe mental illness, and were restrained with hands bound
behind them, legs shackled, and held down on the floor in a prone position (on their

chests). Drug toxicity and/or postural hypoxia/anoxia have been appropriately
suggested as contributing to death in many of these individuals. The elevated
catecholamines resulting from such restraint and attempts to break free facilitate the
ability of a TASER shock, such as that from an ECD, to precipitate ventricular
tachycardia or fibrillation, as found by Nanthakumar (above). Ryan Rich did not
exhibit these characteristics, and cannot be said to have been suffering from “excited
delirium.” The diagnosis of “excited delirium” is not recognized by the American
Medical Association as a medical or psychiatric condition but is recognized by
National Association of Medical Examiners. It is possible that “excited delirium” is a
form of takotsubo syndrome (Wittstein et al: Neurohumoral features of myocardial
stunning due to sudden emotional stress. N Engl J Med. 2005 Feb 10;352(6):539-48),
which might be a cause of some in-custody deaths. However, it would be extremely
unlikely for Ryan Rich’s cardiac arrest to occur virtually immediately during/following
the X26 shock and be due to takotsubo syndrome.

SUDEP usually occurs during sleep or rest, is often associated with

hypoventilation, and excessive seizure activity (Langan J Neurol Neurosurg Psychiatry
68:211, 2000; Lhatoo Ann Neurol 68:787, 2010; Bateman Epilepsia 51:916, 2010;
Nilsson Lancet 13:353, 1999; Opeskin Seizure 12:456, 2003; Tomson Epilepsia 46
suppl 11:54, 2005). Most importantly, Ryan Rich was alive and resisting being
handcuffed prior to application of the TASER shocks and long after what might have
been a seizure. I understand that Dr. Engel addresses this issue in more detail in his


The medical hazard of ECD shocks resulting in cardiac arrest was

foreseeable prior to January 2008 and appropriate testing should have been done to
investigate this possibility before placing these products on the market. Delivering 1or 2-second shocks in areas remote from the heart (for example, the back) in humans
while recording an ECG recording is totally inappropriate and in no way would
exclude the possibility of ECD-induced ventricular tachycardia or ventricular
fibrillation from occurring. Even testing 5-,10- or 15- second cycles over the anterior
chest of volunteers does not replicate real-life field conditions. At the least, testing
should have been done in an appropriate animal model with infused catecholamines
to simulate an agitated state, drugs, and various cardiac pathologies such as coronary
artery disease and old myocardial infarction. Further, since the devices are designed to
deliver repeated and prolonged cycles, such animal testing should have employed
multiple, repeated and prolonged shocks. However, noted above, recent testing in
humans has demonstrated that a TASER shock can capture the heart at fast heart
rates of 240 BPM.

It is not open and obvious to the lay or average law enforcement user

that such adverse effects as ventricular tachycardia and fibrillation could occur from
ECD use. TASER has trained and instructed law enforcement individuals that its
device was safe and posed no cardiac risk, even when shot into the chest and cycled
multiple times. TASER’s representations and claims that are detailed above were not,

and are not, scientifically or medically supported. The representations which TASER
made were either false or misleading in that TASER improperly downplayed potential
dangers that were not adequately understood and overplayed its safety claims and

It was not until September 30, 2009, that TASER first warned law

enforcement to avoid shocking individuals like Ryan Rich in the chest. Based on the
medical evidence that TASER should have had from the outset, and that it in fact did
have no later than the spring of 2006 – almost two years before this incident – this
warning should have been provided to law enforcement long before Trooper Lazoff
fired darts from his Model X26 into Ryan Rich’s chest. I note that Trooper Lazoff
testified that now knowing of the cardiac risk he would never use a TASER except in
the most extreme circumstances: “I'd have to, you know, really be getting my
ass kicked to even, you know, think about it again.”
100) Prior to the incident involving Ryan Rich, the failure of TASER to
conduct reasonable testing regarding the cardiac risks of its electronic control device,
the failure to adequately warn of the known and knowable cardiac risks of the
product, and the misrepresentations and misleading statements it made to law
enforcement regarding medical and cardiac safety of the device, were actions in
conscious disregard of the safety of the persons on whom this device was intended by
TASER to be used, and were a substantial factor in the ventricular fibrillation, cardiac
arrest and ultimate death which Ryan Rich suffered.

101) This product is not regulated by the FDA or Bureau of Alcohol,
Tobacco and Firearms. There is no similar regulatory process to determine the
accurate warning regarding known and unknown risks. Accordingly, it is particularly
incumbent upon the manufacturer of this device to perform adequate testing and
issue appropriate warnings.
I declare under penalty of perjury pursuant to the laws of the United
States that the foregoing is true and correct. Executed this 25th day of April 2011, at
Carmel, Indiana.

Douglas P. Zipes, M.D


Addendum List of Case Materials Reviewed
I reviewed the following documents which relate particularly to the
circumstances of the cardiac arrest sustained by Ryan Rich, MD, January 4, 2008:
AMR (EMT) Records;
Autopsy Photos;
Autopsy Report;
Betty Ford Center Drug Treatment Records;
Clark County Coroner’s exam and case notes;
Clark County Coroner’s Inquest transcript;
Clark County Coroner’s Report of Investigation;
Clark County Coroner’s Toxicology Report;
Dataport download for X26 used in incident;
Death Certificate - State of Nevada;
Deposition transcript of Melanie Hunsaker (sister of Ryan
Deposition transcript of Nick Jensen (step-father of Rylee);
Deposition transcript of Rylee Jensen (minor daughter of
Ryan Rich);
Deposition transcript of Tanya Jensen(ex-wife of Ryan
Deposition transcript of Leslie Johnson (sister of Ryan
Deposition transcript of Dr. Craig Morris

Deposition transcript of Criss Rich (mother of Ryan Rich);
Deposition transcript of Greg Rich (brother of Ryan Rich);
Deposition transcript of Randy Rich (father of Ryan Rich);
Dr. Thalgott medical records (orthopedist);
Joan McCraw medical records (neuropsychology nurse
LVMP Incident report;
LVMP Homicide Investigation Report;
LVMP scene photos;
Neuropathology report;
NHP Traffic Collision Report;
Pain Institute of Nevada medical records;
Renaissance Ranch Drug Treatment records;
Spring Valley Hospital medical records;
Deposition transcript of Officer Loren Lazoff
Valley Hospital medical records;
Witness statements (individuals involved in traffic accidents
with Dr. Rich immediately preceding his altercation with
Officer Lazoff).

I have reviewed the following peer-reviewed and other medical and scientific
articles which deal specifically with the effects of TASER products or a related ECD

device, or a specific physiological process related thereto.

January 1987, Ordog, Gary J., M.D., et al, Electronic Gun (Taser)


March 1991, Kornblum, Ronald N., M.D., and Reddy, Sara K., M.D.,

Effects of Taser in Fatalities Involving Police Confrontation;

January 2005, Wayne C. McDaniel, Robert A. Stratbucker, Max

Nerheim, James E. Brewer, Cardiac Safety of Neuromuscular Incapacitating
Defensive Devices;

2005, Kim PJ, Franklin WH, Ventricular fibrillation after stun-gun

discharge and reply by Kroll, et al.;

November 14, 2005, James R. Jauchem, Clifford J. Sherry, David A.

Fines, Michael C. Cook, Acidosis, lactate, electrolytes, muscle enzymes, and
other factors in the blood of Sus scrofa following repeated TASER exposures;

February 7, 2006, Kumaraswamy Nanthakumar MD, Ian M. Billingsley

MD, Stephane Masse MASC, Paul Dorian MD, Douglas Cameron MD, Vijay
S. Chauhan MD, Eugene Downar MD, Elias Sevaptsidis DEC, Cardiac
Electrophysiological Consequences of Neuromuscular Incapacitating Device

January 6, 2006, Jeffrey D. Ho MD, James R. Miner MD, Dhanunjaya R.

Lakireddy MD, Laura L. Bultman MD, William G. Heegaard MD, MPH,
Cardiovascular and Physiologic Effects of Conducted Electrical Weapon

Discharge in Resting Adults;

March 20, 2006, Dhanunjaya Lakkireddy MD, Donald Wallick PHD,

Kay Ryschon MS, Mina K. Chung MD, FACC, Jagdish Butany MD, David
Martin MD, Walid Saliba MD, FACC, William Kowalewski BS, Andrea Natale
MD, FACC, Patrick J. Tchou MD, FACC, Effects of Cocaine Intoxication on
the Threshold for Stun Gun Induction of Ventricular Fibrillation;

March 16, 2006, Raymond E. Ideker MD, PhD, Derek J. Dosdall PhD,

Can the Direct Cardiac Effects of the Electric Pulses Generated by the TASER
X26 Cause Immediate or Delayed Sudden Cardiac Arrest in Normal Adults?;

May 20, 2006, Jared Strote MD, MS, TASER Use in Restraint-related


November 17, 2006, Jeffrey D. Ho MD, Donald M. Dawes MD, Laura

L. Bultman MD, Jenny L. Thacker MD, Lisa D. Skinner MD, Jennifer M. Bahr
MD, Mark A. Johnson BS, James R. Miner MD, Respiratory Effect of
Prolonged Electrical Weapon Application on Human Volunteers;

April 4, 2007, Andrew J. Dennis DO, Daniel J. Valentino MD, Robert J.

Walter PhD, Kimberly K. Nagy MD, Jerry Winners BS, Faran Bokhari MD,
Dorion E. Wiley MD, Kimberly T. Joseph MD, Roxanne R. Roberts MD,
Acute Effects of TASER X26 Discharges in a Swine Model;

2006, J G Webster, J A Will, H Sun, J-Y Wu, A P O’Rourke, S M

Huebner, P S Rahko, Can Tasers® directly cause ventricular fibrillation?;


August 14, 2007, Theodore C. Chan MD, Saul D. Levine MD, James V.

Dunford MD, Tom Neuman MD, Gary M. Vilke MD, Serum Troponin I
Measurement of Subjects Exposed to the Taser X-26;

May 2, 2007, Michael Cao MD, Jerold S. Shinbane MD, Jeffery M.

Gillberg MS, Leslie A. Saxon MD, Taser-Induced Rapid Ventricular Myocardial
Capture Demonstrated by Pacemaker Intracardiac Electrograms;

May 4, 2007, Gary M. Vilke MD, Christian M. Sloane MD, Katie D.

Bouton BS, Fred W. Kolkhorst PhD, Saul D. Levine MD, Tom S. Neuman
MD, Edward M. Castillo PhD, MPH, Theodore C. Chan MD, Physiological
Effects of a Conducted Electrical Weapon on Human Subjects;

December 17, 2008, Jiun-Yan Wu, Hongyu Sun, Ann P. O’Rourke,

Shane M. Huebner, Peter S. Rahko, James A. Will, John G. Webster, Taser
Blunt Probe Dart-To-Heart Distance Causing Ventricular Fibrillation in Pigs;

June 11, 2007, Sloane CM, Chan TC, Vilke GM, Thoracic spine

compression fracture after TASER activation;

June 10, 2007, James R. Jauchem, Michael C. Cook, Charles W. Beason,

Blood factors of Sus scrofa following a series of three TASER electronic
control device exposures;

November 22, 2008, Charles W. Beason MS, James R. Jauchem PhD, C.

D. Clark III BS, James E. Parker MS, David A. Fines BS, Pulse Variations of a
Conducted Energy Weapon (Similar to the TASER X26 Device): Effects on

Muscle Contraction and Threshold for Ventricular Fibrillation;

August 27, 2007, Robert J. Walter PhD, Andrew J. Dennis DO, Daniel J.

Valentino MD, Bosko Margeta MD, Kinberly K. Nagy MD, Faran Bokhari
MD, Dorion E. Wiley MD, Kinberly T. Joseph MD, Roxanne R. Roberts MD,
TASER X26 Discharges in Swine Produce Potentially Fatal Ventricular

December 7, 2007, Dhanunjaya Lakkireddy, MD, Donald Wallick Atul

Verma MD, Kay Ryschon MS, William Kowalewski BS, Oussama Wazni MD,
Jagdish Butany MD, David Martin MD, Patrick J. Tchou MD, Cardiac Effects
of Electrical Stun Guns: Does Position of Barbs Contact Make a Difference?;

November 28, 2008, Jeffrey D. Ho MD, William G. Heegaard MD,

Donald M. Dawes MD, Sridhar Natarajan MD, Robert F. Reardon MD, James
R. Miner MD, Unexpected Arrest-Related Deaths in America: 12 Months of
Open Source Surveillance;

March 6, 2008, Jeffrey D. Ho MD, Donald M. Dawes MD, Laura L.

Bultman MD, Ronald M. Moscati MD, Timothy A. Janchar MD, James R.
Miner MD, Prolonged TASER use on exhausted humans does not worsen
markers of acidosis;

2007, Gary M. Vilke, Theodore C. Chan, Less lethal technology: medical


2007, Amada O. Esquivel MS, Elizabeth J. Dawe DVM, Javier A,

Sala-Mercado MD, PHD, Robert L. Hammond PHD, Cynthia A. Bir PHD,
The Physiologic Effects of a Conducted Electrical Weapon in Swine;

April 26, 2008, Jeffrey D. Ho MD, Donald M. Dawes MO, Robert F.

Reardon MD, Anne L. Lapine MD, Benjamin J. Dolan BS, Erik J. Lundin BS,
James R. Miner MD, Echocardiographic Evaluation of a TASER-X26
Application in the Ideal Human Cardiac Axis;

May 1, 2008, Kumaraswamy Nanthakumar MD, Stephane Massé PEng

MASc, Karthikeyan Umapathy PhD, Paul Dorian MD, Elias Sevaptsidis
Menashe Waxman MD, Cardiac stimulation with high voltage discharge from
stun guns;

September 23, 2008, D. Dawes, J. Hob, J. Miner, The neuroendocrine

effects of the TASER X26: A brief report;

February 3, 2009, Florin Despa, Suki Basati, Zhen-Du Zhang, John

D’Andrea, J. Patrick Reilly, Elena N. Bodnar, Raphael C. Lee, Electromuscular
Incapacitation Results From Stimulation of Spinal Reflexes;

November 25, 2008, Robert J. Walter PhD, Andrew J. Dennis DO,

Daniel J. Valentino MD, Bosko Margeta MD, Kinberly K. Nagy MD, Faran
Bokhari MD, Dorion E. Wiley MD, Kinberly T. Joseph MD, Roxanne R.
Roberts MD, Safety and Injury Profile of Conducted Electrical Weapons Used
by Law Enforcement Officers Against Criminal Suspects;

November 18, 2008, Byron K. Lee MD, Eric Vittinghoff PhD, Dean

Whiteman BS, Minna Parka, Linda L. Lau BS, Zian H. Tseng MD, Relation of
Taser (Electrical Stun Gun) Deployment to Increase in In-Custody Sudden

February 27, 2009, Charles D. Swerdlow MD, Michael C. Fishbein MD,

Linda Chaman MPH, Dhanunjaya R. Lakkireddy MD, Patrick Tchou MD,
Presenting Rhythm in Sudden Deaths Temporally Proximate to Discharge of
TASER Conducted Electrical Weapons;

August 26, 2008, Daniel J. Valentino MD, Robert J. Walter PhD,

Andrew J. Dennis DO, Bosko Margeta MD, Frederic Starr MD, Kimberly K.
Nagy MD, Faran Bokhari MD, Dorion E. Wiley MD, Kimberly T. Joseph MD,
Roxanne R. Roberts MD, Taser X26 Discharges in Swine: Ventricular Rhythm
Capture is Dependent on Discharge Vector;

April 12, 2009, Gary M. Vilke MD, Christian M. Sloane MD, Amanda

Suffecool, Fred W. Kolkhorst PhD, Tom S. Neuman MD, Edward M. Castillo
PhD, MPH, Theodore C. Chan MD, Physiologic Effects of the TASER After

May 22, 2009, Jeffrey D. Ho, Donald M. Dawes, Jon B. Cole, Julie C.

Hottinge, Kenneth G. Overton, James R. Miner, Lactate and pH evaluation in
exhausted humans with prolonged TASER X26 exposure or continued

May 20, 2009, Megan Robb, Benjamin Close, Jeremy Furyk, Peter

Aitken, Review article: Emergency department implications of the TASER;

2009, Evan S. Schwarz MD, Successful resuscitation of a patient in

asystole after a TASER injury using a hypothermia protocol;

2009, Jared Strote, MD, MS, Mimi Walsh, PhD, Matthew Angelidis, MD,

Amaya Basta, BA, and H. Range Hutson, MD, Conducted Electrical Weapon
Use by Law Enforcement: An Evaluation of Safety and Injury;

2010, Donald M. Dawes MD, Jeffrey D. Ho MD, Robert F. Reardon

MD, James R. Miner MD, Echocardiographic evaluation of TASER X26 probe
deployment into the chests of human volunteers; and

2010, Donald M. Dawes MD, Jeffrey D. Ho MD, Mark W. Kroll, Ph.D,

James R. Miner MD, Electrical Characteristics of an Electronic Control Device
Under a Physiologic Load: A Brief Report.

2005, Wittstein et al., Neurohumoral features of myocardial stunning due

to sudden emotional stress, N Engl J Med. 2005 Feb 10; 352(6):539-48

Human cardiovascular effects of a new generation conducted electrical

weapon, Jeffrey D. Ho, Donald M. Dawes, Robert F. Reardon, Seth R. Strote,
Sebastian N. Kunz, Rebecca S. Nelson, Erik J. Lundin, Benjamin S. Orozco,
James R. Miner, Forensic Science International (2010)

A Novel Mechanism for Electrical Currents Inducing Ventricular

Fibrillation: The Three-Fold Way to Fibrillation Mark W. Kroll, PhD, Senior
Member IEEE; Dorin Panescu, PhD, Senior Member IEEE; Andrew F. Hinz,

BS; Dhanunjaya Lakkireddy, MD., 32nd Annual International Conference of
the IEEE EMBS Buenos Aires, Argentina, August 31 - September 4, 2010

Multi-Organ Effects of Conducted Electrical Weapons (CEW) – A

Review Mazda Biria MD, Sudharani Bommana M.Phil, Mark Kroll Ph.D,
Dorin Panescu Ph.D, Dhanunjaya Lakkireddy MD, 32nd Annual International
Conference of the IEEE EMBS Buenos Aires, Argentina, August
31 - September 4, 2010.

Spear et al (Amer J Cardiol 32:814, 1973)


Fisher et al. (J Interv Card Electrophysiol 1:15; 1997)


Fisher et al. Broad applicability of ultra rapid train stimulation as a rapid

alternative to conventional programmed electrical stimulation. PACE 26:518,
I have reviewed the following deposition transcripts by TASER officials and
Taken in Turner v. TASER Interantional:

Robert Stratbucker, M.D. (June 10, 2010)


Magne Nerheim (June 16, 2010)


Mark Kroll, Ph.D. (September 29, 2010)

Taken in Butler v. TASER International

Ashley Alward, DVM (March 1, 2010)


Hugh Calkins, M.D. (February 1, 2010)


Richard Guilbault (January 14, 2010)


Andrew Hinz (March 1, 2010)


Jeffrey Ho, M.D. (March 3, 2010)


Jay Schapira, M.D. (March 5, 2010)


Rick Smith (February 25, 2010)


Stephen Tuttle (October 29, 2009)


Charles Swerdlow, M.D. (March 2, 2010)


Tom Smith (October 28, 2010)


Gary Vilke, M.D. (January 20, 2010)

I have reviewed the following additional materials which related directly or
indirectly to TASER products and other ECDs:

TASER training discs versions 8-17;


TASER “Medical Safety Information” for the “Advanced TASER M26”;


TASER Training Bulletin and Revised Warnings September 30, 2009;


TASER Training Bulletin and Revised Warnings October 15, 2009;


TASER X26 Operating Manual


TASER v. Ruggieri Case Expert Reports for Drs. Tchou, Ideker & Kroll;


TASER Basic Electric Characteristics Sheet;


“Human Effectiveness and Risk Characterization of the Electromuscular

Incapacitation Device - A Limited Analysis of the TASER Part I - Technical
Report,” The Joint Non-Lethal Weapons Human Effects Center of Excellence

(HECOE), March 2005;

“Human Effectiveness and Risk Characterization of the Electromuscular

Incapacitation Device - A Limited Analysis of the TASER Part
II - Appendices,” The Joint Non-Lethal Weapons Human Effects Center of
Excellence, March 2005;

“Whether TASER is Safe to Use on U.S. Army Military and Civilian

Personnel During Training,” Department of Army, February 2005.

“Bradford Non-Lethal Weapons Research Project,” Davison, N. and

Lever, N., Centre for Conflict Resolution Department of Peace Studies.
Research Report No. 8, March 2006;

“Human Effects Advisory Panel Report of Findings: Sticky Shocker

Assessment,” Keeny, John M., et al (Penn State Applied Research Laboratory),
July 1999.

“Effectiveness & Health of Electro-Muscular Incapacitating Devices,”

Jauchem, J., Air Force Research Laboratory, 16 November 2004;

“TASER’s Research Compendium & Sudden In-Custody Death

Research CD and index, 5th Edition and 6th Edition;

Report of Braidwood Inquiry, particularly Executive Summary and Part

9 (medical risks);

Braidwood Testimony of Zian Tseng, M.D., May 9, 2008;


PowerPoint by Zian Tseng, M.D., delivered at Braidwood Inquiry;


Braidwood Testimony of J. Patrick Reilly, May 5, 2008;


Braidwood PowerPoint Presentation: Estimation of TASER Current

Flow and Effects on Human Body, Dorin Panescu, Ph.D.

Greshmond Gray materials;


Steven Butler case file and materials;


Robert Mitchell Materials (EMS report, including rhythm strips, and


Frederick Williams Materials;


Declaration of Charles Swerdlow, M.D., in Silva v. County of Los Angeles.


Darryl Turner case file and materials