93
Being arrested is a highly emotional event and can
result in a fatal, adrenergically supercharged physiological
state.1
The exertion of arrest-related struggle is
several-fold greater than that seen with normal exercise
and leads to numerous extreme metabolic and electrolytic
derangements, including elevated levels of lactate, CO2
,
potassium, creatine kinase, and myoglobin.2
Only 1.6% of
US law-enforcement interactions involve the use or threats
of force, and annually there are ≈700 000 cases in which
force is used or threatened.3
There are ≈700 arrest-related
deaths per year in the United States, yielding a mortality
rate of ≈1 in 1000 for a law-enforcement interaction associated
with force.4
Response by Zipes on p 100
The electronic control device (ECD) has gained widespread
acceptance as the force option for law enforcement because of
its dramatic reduction in both suspect and officer injury. At the
same time, advocacy groups post statements on the Internet
listing the hundreds of arrest-related deaths after ECD use
with the implication that the ECD involvement was causal.
Studies covering a total of >48 000 forceful arrests have consistently
found suspect injury rate reductions of ≈65%.5,6
Of
the 250 000 annual ECD field uses in the United States, only
1 in 4000 is involved in an arrest-related death. This reduction
in fatality rate is consistent with published data showing that
5.4% of ECD uses “clearly prevented the use of lethal force
by police.”7
Of the >3 million total ECD applications, there have been
12 published case reports suggesting a potential cardiac arrest
link, giving an incidence of 4×10−6
per application.8–13
In most
cases, those authors did not consider important factors that are
now better understood. These include separating postural from
cardiovascular collapse, the latency of electrically induced ventricular
fibrillation (VF), the presence of significant cardiac
pathology, failure of prompt defibrillation, the duration of documented
breathing, the distance of the ECD electrode from the
heart, and the stability of electrically induced VF. We have thoroughly
investigated these cases as either TASER scientific advisors
or expert witnesses. The goal of this article is to resolve the
confusion about these cases by introducing more complete data
and by using a consistent case-report scoring methodology.
Methods
Understanding the Confounders
Postural Versus Cardiovascular Collapse
In the normal course of life, an exertional postural collapse is, correctly,
often associated with a cardiac arrest. However, it is sometimes
forgotten that the ECD design goal is to cause a postural collapse to
stop aggression. A sternal rub response is often blunted by the presence
of alcohol, illegal drugs, psychotic break, and endorphins from
the struggle. Hence, nonresponsiveness is also more difficult to evaluate
in the law-enforcement scenario.
(Circulation. 2014;129:93-100)
© 2014 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.113.004401
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
From the University of Minnesota, Minneapolis (M.W.K.); University of Kansas Hospital, Kansas City (D.R.L.); Harvard University, Boston, MA
(J.R.S.); and Holy Cross Hospital, Ft. Lauderdale, FL (R.M.L.).
This article is Part I of a 2-part article. Part II appears on p 101.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.
113.004401/-/DC1.
Correspondence to Mark W. Kroll, PhD, FACC, FHRS, Box 23, Crystal Bay, MN 55323, E-mail mark@kroll.name
Can TASER Electronic Control
Devices Cause Cardiac Arrest?
TASER Electronic Control Devices and Cardiac Arrests:
Coincidental or Causal?
Mark W. Kroll, PhD; Dhanunjaya R. Lakkireddy, MD; James R. Stone, MD, PhD; Richard M. Luceri, MD
Controversies in
Cardiovascular Medicine
94  Circulation  January 7, 2014
Latency and Temporality
Another common error is the assumption that a cardiac arrest minutes
after an electric exposure is temporally related to that exposure. Because
most illnesses have latency periods measured in days, not seconds, it is
common for even physicians to significantly overestimate the latency
period for electrocution.8,13
However, these latency periods are well
established and are summarized in the online-only Data Supplement.
Some of the cited case studies confuse loss of consciousness minutes
later as “precisely” temporal to an alleged electrocution.13,14
Loss of
consciousness actually occurs 13±4 seconds after electrically induced
VF.15
It has also been suggested that an increased latency (of, say, 60
seconds) might be due to the induction of a ventricular tachycardia
(VT) and that this would allow the detection of an intercurrent pulse.13
This intermediate VT induction hypothesis is problematic for the 5
basic reasons discussed in the online-only Data Supplement.
Confusing Electrically Induced VF With Ischemically
Induced VF
Ischemically induced VF is more difficult to defibrillate than electrically
induced VF, which is reliably reversed with defibrillation.16
With
any chest compressions, defibrillation has a 90% success rate after 10
minutes of electrically induced VF with ≤3 shocks.17
Hence, the failure
of prompt defibrillation tends to exculpate an electric cause for VF.
Misappropriating Normal Clinical Judgment to a
Violent Arrest
A cardiologist seeing a patient in the clinic typically has a respectful,
cooperative, and peaceful subject. The subject of a violent
law-enforcement encounter is often antisocial, defiant, violent, intoxicated,
or schizophrenic. The rate of mortality during a clinic visit
is essentially zero, whereas that of a violent arrest is 1 in 1000. As
mentioned above, sudden falls and nonresponsiveness have different
positive predictive values in an arrest compared with in the clinic. The
use of subjective “clinical impression” is a major cause of erroneous
case reports involving arrest-related deaths.
Postulated Diagnosis of Exclusion
Another common error is to blame the ECD because other typical
causes of death (eg, a drug overdose) are not present. This is erroneous
for 3 reasons:
1.	Arrest-related death is a well-recognized syndrome often with
no clear single pathological mechanism.18,19
2.	 The majority of arrest-related deaths do not involve an ECD.19,20
3.	The battery-operated ECD satisfies all relevant safety standards,
including those for electric fences, and thus its inclusion
should be questioned and its exclusion favored.21,22
Procedure
We searched for published case studies reporting a cardiac arrest after
an ECD application and found 12 such incidents.8–13
We obtained autopsy reports, emergency medical services run
sheets, law-enforcement records, medical records, and deposition
transcripts. We then used objective electronic records such as the
ECD download (with clock drift correction), radio logs, 9-1-1 dispatch
records, and audio and video recordings to build detailed timelines
of each incident. All such data were released by the subject or
family as part of litigation. In the majority (6 of 9) of fatal cases
(cases 6 and 8 through 12), myocardial tissue was analyzed by a cardiac
pathologist (J.R.S.).
It has been suggested that case reports of adverse reactions can be
analyzed most objectively by the use of a Naranjo-style algorithm.23
Such
a methodology assigns points for each of a set of predictors to provide a
consistent framework across all cases. We scored the cases by the criteria
listed in Table 1. If a criterion favored ECD-induced cardiac arrest, it was
scored as +1; if not it was scored as −1. If the value for the criterion was
unknown or inapplicable, it was scored as 0. The range of possible scores
was from −7 (probably not ­ECD-induced) to +7 (probable).
A presenting cardiac rhythm of VF (or an automated external defibrillator
finding of a shockable rhythm) was scored as +1 because
asystole and pulseless electric activity are not inducible with electric
stimulation.24
Asystole is rarely confused by emergency medical
services personnel—and very rarely if multiple leads are used.25
Electrically induced VF has not been seen (in published studies)
to deteriorate to asystole in swine in <20 minutes, and the median
time for deterioration is 34 minutes.26
Asystole and pulseless electric
activity were scored as −1. For the 5 non-VF cases, the time from
cardiac arrest to rhythm documentation was 6.3±3.7 minutes (range,
3.0–12.5), thus making deterioration from VF unlikely.
We used a liberal 8-mm criterion for the dart-to-heart distance because
this was the maximum reported in swine for inducingVF (mean, 5.8±2.1
mm).27
The Ideker group (Walcott, Kroll, Ideker, manuscript under
review) has shown that swine are 3 times as sensitive to electric currents
for the induction of VF as humans. This suggests a 3.1±1.1-mm distance
in humans even with high catecholamine levels28,29
(see the ­online-only
Data Supplement for details). The dart-to-heart distance was calculated
from autopsy reports, photographs, or cardiac magnetic resonance imaging.
If it was unknown, it was scored as 0.
The presence of a pulse after the ECD application was scored as
−1. Although false-negative pulse findings are common, false positives
are not.30
In 2 cases (Z0 and Z3), there were contradictory pulse
findings; hence, this was scored as 0.
Loss of normal breathing in <1 minute and loss of agonal breathing
in <6 minutes after the ECD application were scored as +1.31,32
After
a cardiac arrest, normal breathing ceases in 12 to 60 seconds.31,32
However, some subjects will also have agonal breathing for a maximum
total of 6 minutes.33
Successful prompt defibrillation (with ≤3 shocks) was scored as
+1.17
Findings of significant cardiac pathology or long QT (Z1) were
scored as −1.
We also elected to include the medical examiner findings.
Although not specialists in bioelectricity or electrophysiology,
medical examiners tend to investigate arrest-related deaths carefully
and have no financial bias. If the autopsy report blamed the
ECD as a primary cause of death, this was scored as +1. If there
was no autopsy (nonfatal case) or if the report stated that the ECD
could not be eliminated, this was scored as 0; otherwise, it was
scored as −1.
Table 1.  Diagnostic Criteria for an Electrically Induced
Cardiac Arrest by an ECD
Item Cutoff Value Notes
Presenting rhythm VF Asystole and PEA are not inducible
with electric stimulation
Dart-to-heart distance 8 mm The critical dart-to-heart distance is
5.8±2.1 mm in swine
Documented pulse After ECD
Cessation of normal
breathing
60 s Agonal breathing to 6 min
Success of prompt
defibrillation attempts
10 min Electrically induced VF is defibrillated
with a 90% success rate at 10 min
with any chest compressions
Cardiac pathology Severe long QT included
Medical examiner finding Did the medical examiner find the
ECD to be the primary cause of
death?
ECD indicates electronic control device; PEA, pulseless electric activity; and
VF, ventricular fibrillation.
Kroll et al   TASER Devices and Cardiac Arrests   95
We did not score the presence of prescribed or illegal drugs
because that was covered somewhat in the autopsy findings. We
also did not score the duration of ECD application because no cases
had durations long enough (>90 seconds) for a reduction in the VF
threshold.34
Results
The results are summarized in Table 2. With 1 exception (case
8), all subjects had at least 1 probe (or drive-stun electrode)
embedded in or in contact with the anterior thorax. The distances
of the closest electrode to the ventricular epicardium
are given in Table 2 in the dart-to-heart distance column.
Case 1 (K.F.)
The oldest case (K.F.) was reported as follows8
: “An adolescent
was subdued with a TASER stun gun and subsequently
collapsed. Paramedics found the adolescent to be in ventricular
fibrillation and began performing cardiopulmonary resuscitation
within two minutes after the collapse.”
The violent psychiatric subject, a ward of the state, had a psychotic
episode, punched through a glass door, and gave himself
significant lacerations requiring emergency care. Paramedics
and police were called. The subject refused medical care and
jumped at a police officer, who then used an ECD to successfully
Table 2.  Case Study Summary
Case Author
Age,
y/Race
Total
Score Death
Presenting
Rhythm
Dart-to-
Heart
Distance,
mm
Pulse
Found
Breathing,
min
Failure of
Defibrillation
Medical
Examiner
Agreement
Cardiac
Pathology
Medical Examiner’s
Primary COD Notes
1 K.F. 14/Black −2 N VF UNK Y 4 Y NA UNK NA Required 4 shocks
for defibrillation
2 S.N. 18/White −3 N A 60 Y 6 NA NA None NA
3 S.F. 25/Black −2 Y VF >20 N UNK Y N Hypertrophy,
fibrosis
Physiological stress of
a physical altercation,
including use of ECD,
and underlying heart
disease
4 Z0 31/Black −4 Y A No probes UNK 3.5 Y N None on
autopsy
Undetermined Varying reports on
pulse
5 Z1 48/White −1 N VF No
penetration
N UNK Y NA Long QT NA Officer did not
look for breathing,
just noted
nonresponsiveness
6 Z2 17/Black −3 Y VF Right side N 4 Y N HCM* Agitation and stress;
ECD listed as only
adding stress
Video shows
subject walking
during ECD
application
7 Z3 17/Black −2 Y VF 50 UNK 4 Y N None on
autopsy
Uncertain COD with
acute alcohol toxicity
contributing
8 Z4 24/White −5 Y VF Probes
missed
Y 9 Y N LM* Acute alcohol
intoxication, recent
physical exertion
9 Z5 33/White −4 Y A 70 Y 6 N N ARVC*/
normal
Seizure disorder
10 Z6 24/Black −6 Y A/PEA 36 Y 5 Y UNK LM* Nebulous autopsy
report; could not rule
out excited delirium
or ECD in deposition
11 Z7 16/Black −3 Y VF 55 N See text Y N ARVC* ARVC with ECD being
contributory
Agonal breathing
at 8 min
12 Z8 23/White −7 Y A 50 Y 13 Y N LM* Arrhythmia caused
by epinephrine surge
and respiratory issues
related to struggle.
Medical examiner
reported interstitial
fibrosis
A indicates asystole; ARVC, arrhythmogenic right ventricular cardiomyopathy; COD, cause of death; ECD, electronic control device; HCM, hypertrophic cardiomyopathy;
LM, lymphocyctic myocarditis; PEA, pulseless electric activity; UNK, unknown; and VF, ventricular fibrillation.
*Represents findings of a cardiac pathologist (J.R.S.).
96  Circulation  January 7, 2014
control him. The subject had effective loss of muscle tone and
collapsed to the ground. This was misinterpreted as cardiovascular
collapse in the case report. The subject was handcuffed to
the paramedics’ gurney and then stopped responding to communication.
Whether he was faking or had fainted is not clear.
Paramedics checked his pulse and respiration with a 15-second
vitals check and recorded them as normal, with “breathing properly,”
respirations of 16 per minute, and a pulse of 100 bpm.
The subject was taken via elevator to the ground floor and
placed in the ambulance for treatment of his lacerations, where
a second vitals check was taken. Vitals again were found to be
normal. Spontaneous VF followed, and the subject was defibrillated
with 4 shocks after atropine, epinephrine, and chest compressions
for postshock asystole. The delay to VF is an issue of
controversy, lacking objective electronic records, but was clearly
>2 minutes because of the number of intervening activities.
The cardiac rhythm strip shown in the letter (ostensibly
demonstrating a return to sinus rhythm by a defibrillation
shock) was cropped after what were actually 3 premature
ventricular contractions followed by asystole, as shown in
Figure 1. This report has been questioned elsewhere.35
Case 2 (S.N.)
This case was published twice by members of the same emergency
department with contradictory statements.9,10
The ­alcoholand
tetrahydrocannabinol-inebriated subject presented with
asystole ≈6 minutes after his ECD application, which is consistent
with his extreme blood alcohol concentration at 80% of the
mean lethal level.36
His mother was present throughout the incident
(in her kitchen); thus, it is unlikely that the officers merely
ignored any earlier loss of breathing or cyanosis. The asystole
was later converted to VF with epinephrine, atropine, and chest
compressions, whereupon he was defibrillated. The first publication
correctly identified a presenting rhythm of asystole (consistent
with its emergency medical services documentation in 3
leads).9
The second publication incorrectly claimed it was VF.10
Case 3 (S.F.)
This case came out of a retrospective review of 200
­ECD-involved arrest-related deaths from 2001 to 2008 with
a methodical analysis of the 58 cases in which the presenting
rhythm was ascertainable.11
The authors (including D.R.L.)
concluded that “only one death was suggestive of electrically
induced VF.” However, the probes landed in the electrically
insulating sternum; thus, the dart-to-heart electric path distance
was >20 mm. The subject also failed prompt defibrillation
from an automated external defibrillator in the squad car.
The medical examiner noted cardiac hypertrophy and fibrosis.
The autopsy report had findings of ethanol and tetrahydrocannabinol
metabolite and noted a history of cocaine abuse.
Case 4 (Z0)
This case was presented in a conference debate and represents
the only case suggesting that either a TASER model M26
ECD or a drive stun (direct contact without probes) could
have caused a cardiac arrest.12
Swine studies have not found
VF inductions with drive stuns.37
Even in probe mode with
electrodes near the heart, the M26 ECD has not induced VF in
small swine with epinephrine infusion because of its low net
charge and high-frequency oscillations.38
The presenter of case
Z0 did not discuss or include this case in his later case series.13
Case 5 (Z1)
The subject was a long-time alcoholic who had hypokalemia,
hypomagnesemia, hypocalcemia, acquired QT prolongation (he
was taking olanzapine for his schizophrenia), and tetrahydrocannabinol
and alcohol intoxication (blood alcohol concentration,
0.35%, which is at the mean lethal level).36
During his hospital
recovery, his QT was 540 to 560 milliseconds. No ECD probes
penetrated his skin, but some control was achieved by arcing
through his shirt. There was no evidence of cardiac effects during
the first 2 ECD applications, so it is unlikely that the third (with
probes in the same locations) would have caused a cardiac arrest.39
Case 6 (Z2)
The incident was recorded on a store security video. The individual
walked around during a 37-second ECD application (to
his right chest), which is not consistent with hemodynamically
unstable high-rate cardiac capture or VF. The probes penetrated
only to a depth of 3 mm. Only a partial drug screen was performed
despite the subject having 3 baggies of drugs in his
socks. A cardiac pathologist (J.R.S.) diagnosed hypertrophic
cardiomyopathy, but the published account states that a “plaintiff
pathologist” found a normal heart.13
Court records show that
Figure 1. Actual strip of first shock in
case 1 (K.F.) showing 3 premature ventricular
contractions after shock followed
by asystole.
Kroll et al   TASER Devices and Cardiac Arrests   97
the plaintiff pathologist was a person with an MD degree but no
medical license and no board certifications.40
This person testified
that he has never called himself a pathologist, is not a forensic
pathologist, and is not a cardiovascular pathologist.40
Case 7 (Z3)
The young subject was intoxicated with a blood alcohol level
of 0.22% after binging on caffeinated alcoholic beverages now
withdrawn from the market. The autopsy also found tetrahydrocannabinol
metabolite. The subject had a radial and carotid
pulse and was breathing for 4 minutes after the ECD application.
Case 8 (Z4)
The officer attempted to use an ECD to control an unsteady,
extremely intoxicated man (blood alcohol concentration, 0.34%)
but missed with the ECD probes, perhaps because the individual
passed out and fell at the same time. This is clearly demonstrated
by several items of objective evidence. The ECD probe
has a channel near the back where it receives the wire much like
the eye of a needle. Because the wire is only knotted, not soldered,
there is substantial internal splatter, which is easily seen
on scanning electron microscopy when the current is passed.
The absence of such splatter demonstrated that no electric current
was passed (Figure 2). In addition, a wire was broken, and
microscopic analysis showed no arcing at the break (Figure 3),
which again demonstrates that no current was passed. The ECD
had a video camera, and this also showed that no probes contacted
the subject’s chest (see the online-only Data Supplement).
A police officer and a licensed emergency medical technician
on scene verified a pulse and respirations for 9 minutes
after the postural collapse.41
A cardiac pathologist (J.R.S.)
found lymphocytic myocarditis, but the published account
states that a plaintiff pathologist found no specific pathol-
ogy.13
The court records show that the plaintiff pathologist is
not board certified in pathology and lists himself as a general
practitioner in state licensing records.42
Case 9 (Z5)
A trooper used his ECD to prevent a 100-kg (220-lb) postictal
hit-and-run driver from running into freeway traffic. The case
series report states that there were 62 seconds of ECD shocks,
but this is based on the “trigger pull” record of the weapon and
does not represent actual seconds of current delivery.13
There
appears to have been an initial delivery of 14 seconds of current
to the subject’s chest with no cardiovascular effect because
the subject kept struggling for several minutes. The trooper
was then unable to gain control, but a citizen driving by, who
happened to be a physician, stopped and helped the trooper
with the physical struggle to control the subject. There were 9
nonproductive trigger pulls (probably resulting from “sympathetic”
trigger-finger contractions during the struggle) because
a wire had broken when the subject rolled on the pavement.
(Broken wires were found at the site.) This was followed by 2
drive stuns to the leg. The probe closest to the heart was lodged
in the left shirt pocket and probably did not penetrate the skin.
The presenting rhythm was reported in the case series as
fine VF/asystole. In fact, the firefighters’ LifePak defibrillator
found only asystole as the rhythm ≈5.5 minutes after the
radio call was made reporting that the subject was nonresponsive.
An ambulance crew arriving shortly later also found only
asystole. The emergency department also recorded only asystole;
their first strip is shown in Figure 4. The only reported
rhythm in this incident was asystole.
One of us (J.R.S.) diagnosed arrhythmogenic right ventricular
cardiomyopathy, but the subject’s family retained a cardiac
pathologist who reported a normal heart. Thus, this case
was scored as 0 for cardiac pathology. The medical examiner
ruled that the cause of death was seizure disorder.
Case 10 (Z6)
The presenting rhythm was reported as VT/VF.13
The defibrillator
annotated “VFIB/VTACH” at a point (Figure 5). The
Philips device classifies a wide-complex rhythm >120 bpm
lasting >4 seconds as VT/VF; thus, the VT annotation is suspect.
Post hoc frequency spectrum analysis suggests that this
tracing represents a 129-bpm cardiopulmonary resuscitation
artifact; there were intercurrent chest compressions. Before
Figure 2. Scanning electron microscopy of the electronic control
device probe-wire passage for case 8 (Z4) showing no arcing
splatter. Only machining marks and nonconductive contamination
(bright areas) are shown.
Figure 3. Microscopic image of a broken wire for case 8 (Z4)
showing no arcing.
98  Circulation  January 7, 2014
and after this tracing, there were “pads off” warnings and
clear tracings of loose-electrode noise (see strips 1 and 3 in
the online-only Data Supplement). Spectrum analysis suggests
that these strips represented noise on top of probable asystole,
not VF.43
Case 11 (Z7)
The subject ran from police for 265 meters and went up and
down stairs before being subdued by an ECD. About a minute
later, he was nonresponsive, but cardiopulmonary resuscitation
briefly restored breathing and a carotid pulse. Emergency
medical services noted agonal breathing (2 breaths per minute)
at 8 minutes after the ECD application. Defibrillation (4
shocks) resulted in both asystole and VF. The autopsy report
noted arrhythmogenic right ventricular cardiomyopathy and
tetrahydrocannabinol metabolite.
Case 12 (Z8)
The case report stated that the subject was “said to be breath-
ing.”13
In fact, a police dashboard camera video recording
shows breathing at 14 breaths per minute until ≈13 minutes
after the ECD discharge, which clearly eliminates agonal
breathing.32,33
The medical examiner found that the sternum was between
the ECD probe and the heart, thus precluding a sufficiently
short current path for VF induction.
Summary of Results
The mean totaled score for this study cohort was −3.5±1.8
(range, −7 to −1). There were no positive scores.
Many of the case reports confused a postural collapse or syncope
with a cardiac arrest, which is problematic because several
cases involved extreme alcohol intoxication. In 9 cases, there
was no consideration of the time to breathing cessation, which
is critical because the mean time was 6.1±3.1 minutes compared
with the maximum of 60 seconds (P<0.0001 by t test) for
normal breathing after a cardiac arrest.31,32
There was typically
no mention (9 cases) of the failure of prompt defibrillation as
indicating a nonelectric source for the cardiac arrest.16,17
Almost all cases (11 of 12) ignored the critical ­dart-to-heart
distance, which is well established in the literature for the
induction of VF.27
The unsupported implied inclusion criterion
of any chest ECD exposure (regardless of the dart-to-heart distance)
was surprising in view of the negative epidemiological
association found between ECD chest exposures and mor-
tality.44,45
Bozeman et al44
reported that 49% (424 of 874) of
probe-mode cases involved a probe in the chest (not to be
confused with the much smaller percentage of total probes
found in the chest). White et al45
found that only 36% (57 of
158) of ECD-involved arrest-related deaths had a chest probe
(P=0.004 by χ2
), thus disproving the hypothesis that an application
anywhere on the chest presents a risk of VF.
A surprising finding was that none of the fatal case-report
authors gave any weight to the opinions of the medical examiners
(7 were board certified in forensic pathology, 1 was certified
in pathology, and 1 had training but no certifications). In
8 of those cases, the medical examiner did not list the ECD as
a primary cause of death; a single case (Z6) had a nebulous
autopsy report. Is the implication that forensic pathologists are
truly unqualified to rule on cases of possible electrocution?
Discussion
The main findings of the study are as follows:
1.	The demonstrated incidence of ECD-induced cardiac
arrest is extremely low, if not zero.
2.	Conclusions of a connection between ECD use and
cardiac arrest are speculative at best.
3.	The role of several non-ECD confounding factors
explaining cardiac arrests are not accounted for in published
case reports.
Although controversial case reports may generate useful
discussion, they bring with them a great deal of personal interpretation
and speculation by their authors. They need to be
Figure 4. First recorded rhythm strip in
the emergency department for case 9
(Z5).
Figure 5. Strip 2 showing 129-bpm cardiopulmonary resuscitation
artifact (on pads) incorrectly interpreted as ventricular tachycardia
in case 10 (Z6).
Kroll et al   TASER Devices and Cardiac Arrests   99
ratified by properly conducted studies for these hypotheses to
become scientific facts. It is sobering to see that some of these
published cases omitted dispositive facts (eg, documented later
pulse, videotaped breathing 13 minutes later, and hard forensic
evidence of missed probes). This is, however, consistent with
the observation that adverse-event case reports are often poorly
peer reviewed and may contribute more harm than good.23
Our scored analysis suggests that the authors of these case
reports have not met their evidence burden because none of
the cases had a positive score. Even if one would disagree with
a given criterion, it would not change (with a single exception)
the results to positive scores. Except for Swerdlow et al,11
no
authors described a systematic methodology to select cases
and to maximize objectivity.
A key finding was that the majority (7 of 9) of fatal cases had
significant cardiomyopathies; myocarditis was the most common.
The lymphocytic myocarditis in these cases was characterized
by multiple areas of infiltration by lymphocytes with
injury to the cardiac muscle, as shown in Figure 6. The mean
age of our cases was 24.2±9.6 years, which overlaps military
training. Among the fatal cases, the incidence of myocarditis (3
of 9) was similar to that in case series of military recruit training
sudden deaths. Amital et al46
had 14 of 104 cases (P=NS by χ2
),
and Phillips et al47
had 8 of 53 cases (P=NS) with myocarditis.
Althoughtherehavebeensuggestionsthata­law-enforcement
officer armed with an ECD must have an automated external
defibrillator readily available, there was no incident in which
an automated external defibrillator was, without advanced cardiac
life support measures, successful in resuscitating a sub-
ject.8
On the contrary, the failure of prompt defibrillation was
a hallmark of these cases.
Current ECDs satisfy all relevant electric safety standards,
including those for electric fences.21,22
Human echocardiographic
studies have not found cardiac capture with precordial
electrodes with any commercially available ECD.48–50
These
data suggest that the threshold of factual evidence for blaming
a cardiac arrest on an ECD should be set very high. The published
case reports have not met that threshold.
Conclusion
A Naranjo-style case report scoring demonstrates the unreliability
of case reports in identifying an ECD as the cause of
cardiac arrests. This is consistent with the fact that existing
ECDs satisfy all relevant electric safety standards, thus making
electrocution extremely unlikely.
Disclosures
All authors have been expert witnesses for TASER International, Inc,
which also provided funding for this work. Drs Kroll and Luceri are
members of the TASER International, Inc Scientific and Medical
Advisory Board. Dr Kroll is a member of their corporate board.
References
	1.	 Martinez-Selles M. Sudden death in young males after police detention:
a new syndrome of possible cardiovascular origin. Rev Esp Cardiol,
2009;62:101–102.
	 2.	 Hick JL, Smith SW, Lynch MT. Metabolic acidosis in restraint-associated
cardiac arrest: a case series. Acad Emerg Med. 1999;6:239–243.
	 3.	 Hickman MJ, PiqueroAR, Garner JH. Toward a national estimate of police
use of nonlethal force. Criminology & Public Policy. 2008;7:563–604.
	4.	Mumola C. Arrest-related deaths in the United States, 2003–2006.
Washington, DC: Bureau of Justice Statistics; 2011. Bureau of Justice
Statistics Special Report.
	5.	MacDonald JM, Kaminski RJ, Smith MR. The effect of less-lethal
weapons on injuries in police use-of-force events. Am J Public Health.
2009;99:2268–2274.
	 6.	 TaylorB,WoodsD,KubuB,KoperC,TegelerB,CheneyJ,MartinezM,Cronin
J, Kappelman K. Comparing safety outcomes in police ­use-of-force cases for
law enforcement agencies that have deployed conducted energy devices and
a matched comparison group that have not: a quasi-experimental evaluation.
Police Executive Research Forum. 2009. http://www.policeforum.org/library/
use-of-force/CED%20outcomes.pdf.Accessed December 18, 2013.
	7.	 Eastman AL, Metzger JC, Pepe PE, Benitez FL, Decker J, Rinnert KJ,
Field CA, Friese RS. Conductive electrical devices: a prospective,
­population-based study of the medical safety of law enforcement use.
J Trauma. 2008;64:1567–1572.
	8.	 Kim PJ, Franklin WH. Ventricular fibrillation after stun-gun discharge.
N Engl J Med. 2005;353:958–959.
	 9.	 Schwarz ES, Barra M, Liao MM. Successful resuscitation of a patient in
asystole after a TASER injury using a hypothermia protocol. Am J Emerg
Med. 2009;27:515.e1–515.e2.
	10.	 Naunheim RS, Treaster M, Aubin C. Ventricular fibrillation in a man shot
with a Taser. Emerg Med J. 2010;27:645–646.
	11.	Swerdlow CD, Fishbein MC, Chaman L, Lakkireddy DR, Tchou P.
Presenting rhythm in sudden deaths temporally proximate to discharge of
TASER conducted electrical weapons. Acad Emerg Med. 2009;16:726–739.
	12.	 Zipes D. Are you tasing me? TASERs can cause fatal [ventricular tachy]
arrhythmias: HRS debate. 2010. http://www.heartrhythmondemand.org/.
Accessed January 15, 2010.
	13.	 Zipes DP. Sudden cardiac arrest and death following application of shocks
fromaTASERelectroniccontroldevice. Circulation.2012;125:2417–2422.
	14.	 Zipes DP. Response to letters regarding article, “sudden cardiac arrest and
death following application of shocks from a TASER electronic control
device.” Circulation. 2013;127:e261–e262.
	15.	Lukl J, Marek D, Bulava A, Fedorco M, Schneiderka P, Táborsky M,
ZapletalováJ.Prolongedburstasanewmethodfor­cardioverter-defibrillator
testing. Europace. 2013;15:55–59.
	16.	Niemann JT, Rosborough JP, Youngquist S, Thomas J, Lewis RJ. Is all
ventricular fibrillation the same? A comparison of ischemically induced
with electrically induced ventricular fibrillation in a porcine cardiac arrest
and resuscitation model. Crit Care Med. 2007;35:1356–1361.
	17.	 Kroll MW, Fish RM, Calkins H, Halperin H, Lakkireddy D, Panescu D.
Defibrillation success rates for electrically-induced fibrillation: hair of the
dog. Conf Proc IEEE Eng Med Biol Soc. 2012;2012:689–693.
Figure 6. Histological image of a hematoxylin and ­eosin–stained
slide of the heart from case 10 (Z6) showing lymphocytic
myocarditis.
100  Circulation  January 7, 2014
	18.	Pollanen MS, Chiasson DA, Cairns JT, Young JG. Unexpected death
related to restraint for excited delirium: a retrospective study of deaths in
police custody and in the community. CMAJ. 1998;158:1603–1607.
	19.	 Southall P, Grant J, Fowler D, Scott S. Police custody deaths in Maryland,
USA: an examination of 45 cases. J Forensic Leg Med. 2008;15:227–230.
	20.	 Ho JD, Heegaard WG, Dawes DM, Natarajan S, Reardon RF, Miner JR.
Unexpected arrest-related deaths in America: 12 months of open source
surveillance. West J Emerg Med. 2009;10:68–73.
	21.	Nimunkar AJ, Webster JG. Safety of pulsed electric devices. Physiol
Meas. 2009;30:101–114.
	22.	 Panescu D, Nerheim M, Kroll M. Electrical safety of conducted electrical
weapons relative to requirements of relevant electrical standards. Conf
Proc IEEE Eng Med Biol Soc. 2013;2013:5342–5347.
	23.	 Karch SB. Peer review and the process of publishing of adverse drug event
reports. J Forensic Leg Med. 2007;14:79–84.
	24.	 Zima E, Gergely M, Soós P, Gellér LA, Nemes A, Acsády G, Merkely B.
The effect of induction method on defibrillation threshold and ventricular
fibrillation cycle length. J Cardiovasc Electrophysiol. 2006;17:377–381.
	25.	 Cummins RO, Austin D Jr. The frequency of “occult” ventricular fibrillation
masquerading as a flat line in prehospital cardiac arrest. Ann Emerg
Med. 1988;17:813–817.
	26.	 Kroll MW, Walcott GP, Ideker RE, Graham MA, Calkins H, Lakkireddy
D, Luceri RM, Panescu D. The stability of electrically induced ventricular
fibrillation. Conf Proc IEEE Eng Med Biol Soc. 2012;2012:6377–6381.
	27.	 Wu JY, Sun H, O’Rourke AP, Huebner SM, Rahko PS, Will JA, Webster
JG. Taser blunt probe dart-to-heart distance causing ventricular fibrillation
in pigs. IEEE Trans Biomed Eng. 2008;55:2768–2771.
	28.	 Han J, Garciadejalon P, Moe GK.Adrenergic effects on ventricular vulnerability.
Circ Res. 1964;14:516–524.
	29.	 Papp JG, Szekeres L. Analysis of the mechanism of adrenergic actions on
ventricular vulnerability. Eur J Pharmacol. 1968;3:15–26.
	30.	Eberle B, Dick WF, Schneider T, Wisser G, Doetsch S, Tzanova I.
Checking the carotid pulse check: diagnostic accuracy of first responders
in patients with and without a pulse. Resuscitation. 1996;33:107–116.
	31.	 Haouzi P, Ahmadpour N, Bell HJ, Artman S, Banchs J, Samii S, Gonzalez
M, Gleeson K. Breathing patterns during cardiac arrest. J Appl Physiol
(1985). 2010;109:405–411.
	32.	Zuercher M, Ewy GA, Otto CW, Hilwig RW, Bobrow BJ, Clark L,
Chikani V, Sanders AB, Berg RA, Kern KB. Gasping in response to basic
resuscitation efforts: observation in a swine model of cardiac arrest. Crit
Care Res Pract. 2010;10:1–7.
	33.	 ClarkJJ,LarsenMP,CulleyLL,GravesJR,EisenbergMS.Incidenceofagonal
respirations in sudden cardiac arrest. Ann Emerg Med. 1992;21:1464–1467.
	34.	 Kroll MW, Panescu D, Hinz AF, Lakkireddy D. A novel mechanism for
electrical currents inducing ventricular fibrillation: the three-fold way to
fibrillation. Conf Proc IEEE Eng Med Biol Soc. 2010;2010:1990–1996.
	35.	 Roberts J. Medical effects of TASERs. Emerg Med News. 2008;30:12–15.
	36.	 Heatley MK, Crane J. The blood alcohol concentration at post-mortem in
175 fatal cases of alcohol intoxication. Med Sci Law. 1990;30:101–105.
	37.	Valentino DJ, Walter RJ, Nagy K, Dennis AJ, Winners J, Bokhari F,
Wiley D, Joseph KT, Roberts R. Repeated thoracic discharges from a stun
device. J Trauma. 2007;62:1134–1142.
	38.	 Nanthakumar K, Billingsley IM, Masse S, Dorian P, Cameron D, Chauhan
VS, Downar E, Sevaptsidis E. Cardiac electrophysiological consequences
of neuromuscular incapacitating device discharges. J Am Coll Cardiol.
2006;48:798–804.
	39.	 Ho JD, Dawes DM. Letter by Ho and Dawes regarding article, “sudden
cardiac arrest and death following application of shocks from a TASER
electronic control device.” Circulation. 2013;127:e259.
	40.	Maron BJ. Testimony in Fontenot v TASER. US District Court for the
Western District of North Carolina; 3:10-cv-125:43–47 (2011).
	41.	Heegaard WG, Halperin HR, Luceri R. Letter by Heegaard et al
regarding article, “sudden cardiac arrest and death following application
of shocks from a TASER electronic control device.” Circulation.
2013;127:e260.
	42.	 Ugwu OR. Deposition testimony in Piskura v TASER. US District Court
for the Southern District of Ohio; 1:2010CV00248:8–10 (2010).
	43.	 Clayton RH, Murray A, Campbell RW. Analysis of the body surface ECG
measured in independent leads during ventricular fibrillation in humans.
Pacing Clin Electrophysiol. 1995;18:1876–1881.
	44.	 Bozeman WP, Teacher E, Winslow JE. Transcardiac conducted electrical
weapon (TASER) probe deployments: incidence and outcomes. J Emerg
Med. 2012;43:970–975.
	45.	 White MD, Ready J, Riggs C, Dawes DM, HinzA, Ho JD.An ­incident-level
profile of TASER device deployments in arrest-related deaths. Police Q.
2012;16:85–112.
	46.	 Amital H, Glikson M, Burstein M, Afek A, Sinnreich R, Weiss Y, Israeli
V. Clinical characteristics of unexpected death among young enlisted military
personnel: results of a three-decade retrospective surveillance. Chest.
2004;126:528–533.
	47.	Phillips M, Robinowitz M, Higgins JR, Boran KJ, Reed T, Virmani R.
Sudden cardiac death in Air Force recruits: a 20-year review. JAMA.
1986;256:2696–2699.
	48.	 Dawes DM, Ho JD, Reardon RF, Miner JR. Echocardiographic evaluation
of TASER X26 probe deployment into the chests of human volunteers.
Am J Emerg Med. 2010;28:49–55.
	49.	 Ho JD, Dawes DM, Reardon RF, Lapine AL, Dolan BJ, Lundin EJ, Miner
JR. Echocardiographic evaluation of a TASER-X26 application in the
ideal human cardiac axis. Acad Emerg Med. 2008;15:838–844.
	50.	 Ho JD, Dawes DM, Reardon RF, Strote SR, Kunz SN, Nelson RS, Lundin
EJ, Orozco BS, Miner JR. Human cardiovascular effects of a new generation
conducted electrical weapon. Forensic Sci Int. 2011;204:50–57.
Response to Kroll et al
Douglas P. Zipes, MD
TASERS can cause cardiac arrest. My assignment was to validate this assertion, not to litigate these cases in Circulation.
The courts are doing that. Kroll et al’s case summaries attempt to try the cases but contain many misleading statements.
For example, Kroll et al state that case Z1 had electrolyte abnormalities and long QT. True, but only after 3 TASER shocks,
5 automated external defibrillation attempts, and intravenous drugs and during profound cerebral hypoxia. Other assertions
must be countered. Kroll et al stress an “8-mm criterion for the dart-to-heart distance” for TASER-induced VF to occur.
False. This is based on 1 pig study in which a blunt dart was advanced through the anterior chest wall of 5 intubated pigs premedicated
with tiletamine (a dissociative anesthetic) and isoflurane “to induce a surgical plane of anesthesia.” Pigs received
current from the X26 TASER lasting “≈5 seconds.” Cardiac capture could not be determined because no ECG recording was
done during the shock, only after stimulation to “check if the heart was beating normally.” Dart-to-heart distances >8 mm
have clearly caused cardiac capture in humans and produced VF in animals (see my article and the figures for cases Z3,
Z7, and Z8). Kroll et al assert, “Failure of prompt defibrillation tends to exculpate an electric cause for VF.” False. TASERinduced
VF lasting 8 to 10 minutes can require repeated defibrillation and resuscitation attempts, especially if underlying
heart disease is present. Unfounded entries invalidate the use of any scoring system. Other misleading or erroneous assertions
by Kroll et al will be addressed in future venues.