Controversies in
Cardiovascular Medicine
Can TASER Electronic Control
Devices Cause Cardiac Arrest?
TASER Electronic Control Devices Can Cause
Cardiac Arrest in Humans
Douglas P. Zipes, MD

T

he TASER X26 electronic control device (ECD) is a
handgun-shaped device that uses compressed nitrogen to
fire darts ranging from 9 to 14 mm in length that impale the
clothes or skin of an individual up to a distance of 35 ft. Wires
connect the darts to the device. The TASER X26 functions as
a constant current generator and delivers an initial 50 000-V to
begin an arcing shock (the actual voltage delivered to the body
is in the range of 1400–2520 V), followed by electric pulses
of 105- to 155-microsecond duration, at a frequency of ≈19
Hz (≈1140 times per minute), and 80- to 125-microcoulomb
delivered charge.1 A single trigger pull discharges a 5-second
cycle that can be shortened by a safety switch to deactivate the
device or prolonged if the trigger pull is held. The trigger can
be activated multiple times. The X26 data port stores the time
and date of use and number and duration of trigger pulls. If
effective, the shock elicits neuromuscular inhibition, allowing
law enforcement to gain control of a suspect (see www.youtube.com/watch?v=ACUjnJBHIZc for a TASER demonstration). The device can also be applied in a “drive-stun” mode
by directly pressing the X26 ECD against the skin to achieve
pain compliance without neuromuscular inhibition. The
TASER X26 is the most widely sold ECD. Called a less lethal
or nonlethal weapon because it is supposed to be deployed
to temporarily incapacitate, not to kill the subject, the X26 is
not considered a firearm and therefore is not regulated by the
Bureau of Alcohol, Tobacco, Firearms and Explosives.

Response by Kroll et al on p 111

Purpose
The purpose of this article is to present information to support the
conclusion that the TASER X26 ECD can cause cardiac arrest in
humans. As noted in an earlier article,2 the purpose is not to offer
an opinion about whether the use of TASER or any other ECD
product is appropriate because I think that decision belongs to
trained law-enforcement professionals, not physicians.

Background
A previous publication2 presented 8 cases of sudden cardiac
arrest that, in my opinion, resulted from delivery of electric
impulses generated by a TASER X26 ECD. None had manifest cardiovascular symptoms, although several had n­on–
cardiac-related medical problems, including alcohol abuse,
attention deficit disorder, mental confusion that was possibly
postictal from a seizure, and depression/schizophrenia. At
autopsy, several were alleged to have had underlying heart
disease (Table). All had rapid loss of consciousness after
X26 deployment and ECD shocks via 1 or more darts in the
anterior chest (Figures 1 and 2). Selected ECGs recorded at
various time intervals during resuscitation attempts showed
ventricular tachycardia (VT)/ventricular fibrillation (VF) in 5,
a shockable rhythm by an automated external defibrillator in

The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
From the Indiana University School of Medicine, Indianapolis.
This article is Part II of a 2-part article. Part I appears on p 93.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.
113.005504/-/DC1.
Correspondence to Douglas P. Zipes, MD, Distinguished Professor, Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N
Capitol Ave, Indianapolis, IN 46202. E-mail dzipes@iu.edu
(Circulation. 2014;129:101-111)
© 2014 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org

DOI: 10.1161/CIRCULATIONAHA.113.005504

101

102  Circulation  January 7, 2014

Table. 

Summary of the 8 Cases Reported as Having Cardiac Arrest After X26 Administration

Case Age, y

Height/
Weight, lb

Length
of ECD
Shock(s), s

Response to
ECD Shock

Time to Initial
ECG After
ECD Shock, min

Initial
Recorded
Rhythm

Drug Screen

Cardiac
Findings at Autopsy

BAC 0.35
Survived
g/100 mL; THC with memory
present
impairment; normal
echocardiogram

Comments

1

48

6 ft 0 in/155 5, 8, 5

LOC toward
end of last ECD
cycle

Several

VT/VF

2

17

5 ft 7 in/170

37, 5

LOC toward end
of a 37-s cycle

>4.5

VF

3

17

5 ft 8 in/115

5

ILOC

>5

VF

4

24

5 ft 10 in/176

11

ILOC

≈10

AED: “shockable
rhythm”;
asystole after
shock; no
recordings
available

BAC 0.319
g/100 mL

400 g; plaintiff
pathologist: no
specific pathology;
defense pathologist:
lymphocytic
myocarditis

Said to be breathing initially
with a weak radial pulse;
resuscitated in hospital;
life support withdrawn
after 3 d because of anoxic
encephalopathy

5

33

6 ft 2 in/220

13 shocks LOC toward the
totaling 62 s end of multiple
in <3 min
shocks

≈13

Fine VF vs
asystole

Gabapentin
31 μg/mL

470 g; 10%–
20% narrowing of
the LAD; normal
histology

Gabapentin taken for seizure
disorder

6

24

5 ft 6 in/144

49, 5

LOC toward end
of 49-s shock

≈10

VT/VF

Negative

7

16

5 ft 3 in/130

5

ILOC

≈10

VT/VF

THC

8

23

5 ft 9 in/173 21, 7, 3

LOC toward end
of 21-s shock

≈30

Asystole

BAC 0.111
g/100 mL

Negative

410 g; focal
atherosclerosis;
plaintiff pathologist:
normal; defense
pathologist: HCM

5 AED shocks, intravenous
epinephrine, and lidocaine
eventually restored a perfusing
rhythm
3 defibrillating shocks and
an additional 3 shocks from
a second AED at least 9 min
after the collapse failed to
resuscitate

270 g; normal heart Asystole developed after the
BAC 0.25
AED shock and then PEA;
g/100 mL; THC
present
subsequently, VF recurred
and a second AED shock was
delivered, followed by asystole/
PEA; could not be resuscitated

366.7 g; normal
Said to be breathing initially;
gross and
could not be resuscitated
microscopic findings
380 g; medical
6 AED shocks for VT/VF
examiner diagnosis: resulted in asystole/PEA; could
right ventricular
not be resuscitated
cardiomyopathy,
disputed by
plaintiff’s expert
400 g; mild
interstitial fibrosis
of compact
atrioventricular
node; interstitial
fibrosis, atrophy,
and vacuolization
of penetrating and
branching bundle

Said to be breathing with
pulse initially; could not
be resuscitated; cardiac
pathologist could not determine
whether changes contributed
to death

AED indicates automated external defibrillator; BAC, blood alcohol concentration; ECD, electronic control device; HCM, hypertrophic cardiomyopathy; ILOC, immediate
loss of consciousness during/after initial shock; LAD, left anterior descending coronary artery; LOC, loss of consciousness during/after initial shock; PEA, pulseless
electric activity; THC, tetrahydrocannabinol, positive screen for marijuana; VF, ventricular fibrillation; and VT, ventricular tachycardia. Heart weight is given in grams.
Gabapentin is Neurontin.
Reproduced from Zipes DP. Sudden cardiac arrest and death following application of shocks from a TASER electronic control device. Circulation. 2012;125:2417–2422.2

1 (no ECG recording), fine VF/asystole in 1, and asystole in 1
(Figure 3). The last 2 cases had significant time delays from
X26 deployment and loss of consciousness until ECGs were
recorded (Figures 4 and 5). Only 1 of 8 was resuscitated but
with residual anoxic cognitive impairment.

In an accompanying editorial, Myerburg et al3 stated that
the article established “proof of concept” and that the information in at least 2 of the cases lent “…credence to the likelihood of an association that is strong enough to demonstrate a
­cause-and-effect relationship.”

Zipes   TASER Devices and Cardiac Arrests   103

Figure 1. Picture at autopsy of case 3 with TASER X26 barbs still
in place (circles). The heart at autopsy was normal.

After publication, 3 Letters to the Editor by physicians having TASER relationships disputed aspects of single cases but
not the overall concept of TASER-induced VF. As I concluded
in my response to those letters,4 “…the published body of evidence now makes it perfectly clear that a TASER X26 ECD
shock can induce VF in humans, transforming the argument
from if it can happen to how often it happens.”
Cases 7 and 8 from the original article2 are expanded here to
demonstrate causality and to make several points.

Case 7
A 16-year-old black boy (body mass index [BMI] 23 kg/m2)
with attention deficit disorder and asthma but without previous cardiac history or symptoms of heart disease ran ≈290 yd
to an abandoned house. Confronted by police, possibly sweating, he received a 5-second chest shot with a TASER X26
from 3 to 4 ft away, immediately dropped to the ground, and
was unconscious and unresponsive. One officer noted transient moaning and an apparent seizure ≈30 seconds after the
shock and found no carotid pulsations or respirations. After 1
to 1½ minutes of cardiopulmonary resuscitation [CPR], the
officer noted a carotid pulse and spontaneous respirations that

Figure 2. Left, Picture of 12.2- and 13.2-mm TASER X26 darts
used in case 7 after removal from the skin. Right, Picture of
TASER X26 dart marks (circles) above and below the left nipple
of case 7. The head is at the top.

Figure 3. Selected ECGs recorded during resuscitation attempts
in 7 of the 8 cases. Reproduced from Zipes. Sudden cardiac
arrest and death following application of shocks from a TASER
electronic control device. Circulation. 2012;125:2417–2422.2

lasted ≈15 seconds before ceasing spontaneously, and CPR
was resumed. The first recorded ECG ≈8 minutes after the
X26 shock showed VF. He was then defibrillated 4 times at
300 J and once or possibly twice at 360 J. He could not be
resuscitated and was pronounced dead after transportation to
the hospital. Autopsy showed 2 skin marks separated by 5¼
inches, consistent with TASER dart marks, 3 inches above and
2 inches below the left nipple (Figure 2 right). Dart length
was 12.2 and 13.2 mm (Figure 2, left). The heart was slightly
enlarged at 380 g, and the subject was diagnosed as having
arrhythmogenic right ventricular cardiomyopathy (ARVC)
by the forensic pathologist/medical examiner, who stated it
was unknown whether the “taser [sic] device resulted in a
direct effect on the heart or whether it served to exacerbate an

Figure 4. Case 8: still frames taken from video by police camera
before and after TASER X26 administration. Initially, the man struggled with police (left). Off camera, he received X26 shocks of 21-,
7-, and 3-second duration and was then brought back into the video
field by police (right). He was nonresponsive and gasping for breath,
most likely agonal breathing. Note head at bottom of frame when he
was unconscious, likely due to ventricular fibrillation. For full video,
see Movie I in the online-only Data Supplement.

104  Circulation  January 7, 2014

to his death. Blood alcohol level was 0.111 g/100 mL. The
X26 deployment occurred between the left and right panels of
Figure 4 and first and second parts of the video (see Movie I
in the online-only Data Supplement). Scarring, if it played a
direct role, would have had to trigger cardiac arrest precisely
when the X26 shock was delivered. In my opinion, it is more
probable that the X26 shock induced cardiac arrest and sudden
death, and the scarring may have facilitated VF induction.

A More Recent Case

Figure 5. Top, ECG during resuscitation attempt. Bottom,
Picture of case 8 at autopsy showing TASER X26 barb marks
(circles).

arrhythmia….” A second pathologist agreed with the diagnosis
of ARVC and stated that the “TASER ECD played no significant role in his death.” Another forensic pathologist detected
“no convincing morphologic finding that can be construed as
evidence of a preexisting abnormality of his heart” and indicated that the individual “...died as a result of an electric injury
brought about by direct discharge of the Electronic Control
Device….” Still another found that he did not have ARVC
and that cause of death was a “cardiac dysrhythmia associated with the use of an electronic control device…a TASER.”
Marijuana was the only drug found. He had been prescribed
atomoxetine for attention deficit disorder, but its role, if any, is
uncertain. Regardless of whether this young man had ARVC,
he sustained a 5-second X26 chest shock with extra penetration darts near his heart (Figure 2), immediately lost consciousness, was noted to have VF ≈8 minutes later, and could
not be resuscitated. If the alleged ARVC played a direct role,
it would have had to trigger VF precisely when the X26 shock
was delivered. In my opinion, it is more probable that the X26
shock caused the VF and subsequent death, and if the alleged
ARVC was actually present, it facilitated VF induction.

Case 8
The police video (Figure 4 and Movie I in the online-only Data
Supplement.) for this case helps establish causality. A 23-yearold white man (BMI, 25.5 kg/m2) with no history of heart disease or cardiac symptoms struggled briefly with police officers
after a traffic stop. He moved out of camera range for several
minutes and received 3 X26 shocks of 21, 7, and 3 seconds.
One police officer said the young man fell face forward after
the first shock and was given a second shock because he could
not or would not remove 1 of his hands from beneath his chest
to be handcuffed. He was then carried back into camera range
and propped curbside by police (Figure 4). Police officers said
he initially was breathing and had a pulse. Despite CPR, an
ECG recorded many minutes later documented asystole. At
autopsy (Figure 5), cardiac scarring was noted (Table), but the
cardiac pathologist could not state whether that contributed

Since publication,2 new cases have materialized, one of which is
presented here because the police video again makes a compelling case of causality. A 50-year-old woman (BMI, 17.1 kg/m2)
with no manifest heart disease received a reported 3 X26 shocks
to the left chest, with darts just above and below the left breast
(based on dart marks noted subsequently). After the third X26
trigger pull reported by 1 officer, she immediately lost consciousness (video link of the X26 application can be found at
http://www.youtube.com/watch?v=b6dHpt6c6zM) and started
seizing. CPR was begun 6 minutes later, and an automated
external defibrillator was applied 12 minutes after the X26
shock. After a shock for VF, she had return of sinus rhythm,
breathed on her own, and survived, apparently with some
memory deficit. Her drug screen was positive for cannabinoids
but otherwise negative. Echocardiography shortly after resuscitation showed left ventricular end-diastolic dimension of 5.4
cm, estimated ejection fraction of 40%, mild to moderate mitral
regurgitation with annular calcification, and mild to moderate
tricuspid regurgitation consistent with myxomatous degeneration. Subsequent echocardiography showed normal LV size and
systolic function, EF 55% to 60%, with thickened mitral and
aortic valves, indicating most of the changes were likely related
to the cardiac arrest. As in the 2 cases discussed above, this individual was fully active and conscious until receiving the X26
shock and then had a cardiac arrest caused by VF. If underlying
heart disease played a direct role, it would have had to trigger
VF precisely during the X26 shock. In my opinion, it is more
probable that the X26 shock induced cardiac arrest and that any
underlying cardiac pathology facilitated VF induction.

Incidence
The issue of how often cardiac arrest happens noted in my
letter above is critical to establish the degree of risk. Amnesty
International noted 334 deaths after an ECD shock between
2001 and 2008,5 which increased recently to 544.6 Although
all in-custody deaths after ECD shocks are not likely a
direct result of the shock, a number probably are. TASER
International addressed that probability by revising their warnings from “aim at target: center of mass or legs” and “aiming
at open front of unzipped jacket” before September 20097 to
“when possible, avoiding chest shots…” after that date.8 More
recently, they noted that “heart rate, rhythm, capture” can
occur and that “capture” and “cardiac arrest” can contribute to
arrest-related death in physiologically or metabolically compromised persons.9

Zipes   TASER Devices and Cardiac Arrests   105

TASER counsel indicated that the risk of an ECD causing
cardiac arrest was on the order of 1:100 000 applications.10
Given an estimated 3 million TASER ECD applications,10 this
would compute to ≈30 deaths. However, the actual incidence of
cardiac capture and cardiac arrest, and therefore the risk for this
to occur, cannot be determined accurately for several reasons.
First, as noted below, in the 2 instances of documented TASER
ECD cardiac capture in humans, the individuals were totally
asymptomatic during the 5- and 10-second exposure cycles.
Thus, it is possible that transient cardiac capture occurs in the
field but goes unnoticed if it does not result in cardiac arrest.
The second reason is the lack of accurate numbers to calculate incidence because no mandatory reporting exists in
the United States. A bill requiring such reporting, for which
I gave supporting testimony, was recently defeated by the
Connecticut legislature (CGA H.B. No. 6628; 2013). The
total number of TASER deployments is irrelevant because
how often an individual is shot in the buttocks, abdomen,
extremities, or back is of no cardiac concern. The number of
chest shots is the important metric. One study11 found that
of 813 probe deployments, 21.9% had anterior chest placements. Obtaining an accurate estimate of incidence of death,
and therefore risk from the TASER, would require an accurate estimate of the total number of deaths (numerator), a
potentially underreported value, and the total number of chest
shots (denominator), which is unknown. A recent article in the
British newspaper The Guardian reported that of 884 TASER
deployments from 18 of 45 UK forces since 2009, which was
when TASER’s warnings about avoiding chest shots were
published,8 518 (59%) of all shots have hit the chest area.12

Animal Research
The most compelling evidence to prove the assertion made in the
title of this article would be to record the development of VT/
VF from a human during an X26 shock. This is very difficult
for 2 reasons: The individual would require a cardiac recording
device already in place during the shock, and the electric interference from the X26 could make any ECG recording unreadable. Therefore, animal studies become a necessary substitute.

A study in 200613 demonstrated that 5-second shocks from
the equivalent of a standard TASER X26 ECD delivered via
9-mm darts inserted in various chest positions of anesthetized
pigs caused cardiac capture, documented by an intracavitary
right ventricular recording electrode. Dart vectors influenced
capture. A position more likely to cause capture was from the
sternal notch to the cardiac apex, resulting in ventricular capture ratios ranging from 6:1 to 3:1 (190–380 bpm). No VF
occurred with normal output, but an increase in ECD power
decreased the capture ratio, and VF consistently resulted when
the ventricular capture ratio was ≤2:1. The authors noted that
the data suggested
…the potential for induction of ventricular tachycardia in subjects with substrate for ventricular tachycardia….Avoidance of this position would greatly reduce
any concern for induction of ventricular arrhythmias.13
A second study using an off-the-shelf TASER X26 with
a right ventricular recording lead showed that 52 of 53 discharges (98.11%) to the porcine chest caused cardiac capture,
whereas 0 of 56 nonthoracic discharges stimulated the heart.14
As with the prior study,13 blood pressures fell to very low
values at rapid capture rates. During epinephrine infusion to
increase the spontaneous heart rate 50% to simulate the agitated stress state of an individual experiencing pain or resisting restraint, 13 of 16 TASER X26 discharges caused cardiac
capture, 1 caused nonsustained ventricular tachycardia that
spontaneously reverted to sinus rhythm, and 1 caused VT that
evolved to VF and cardiac arrest (Figure 6).
In a series of 3 studies using 12-mm darts, investigators
exposed pigs to two 40-second discharges from a TASER X26
ECD separated by a 10-second pause with ventilation between
shocks. Five minutes after the shocks, pigs were profoundly
acidotic with pH values of 6.86. One pig developed 3 minutes of sustained, monomorphic VT after the ECD discharge
before finally progressing to VF (Figure 7).15 After a left anterior thoracotomy to video the heart during the ECD shock,
another pig developed VT proceeding to VF (http://www.
youtube.com/watch?v=PxcXwk4UHm4). The second study16
showed that succinylcholine eliminated the acidosis after the
Figure 6. A, Recordings during X26-induced
ventricular fibrillation (VF) in a pig while infusing
epinephrine. B, Expanded time scale. The arrowheads at left depict a 3:1 response to the X26
discharge that progressed to a 2:1 response (right),
which resulted in (C) rapid ventricular tachycardia
(VT), degenerating into polymorphic VT and VF.
Recordings are surface ECG lead 1, intracardiac
electrograms from the coronary sinus (CS) and
the right ventricular (RV) apex, and blood pressure
(BP) from a Millar catheter in the descending aorta.
Reproduced from Reference 14 with permission
from the publisher. Nanthakumar K, Billingsley
IM, Masse S, Dorian P, Cameron D, Chauhan VS,
Downar ED, Sevaptsidis E. Cardiac electrophysiological consequences of neuromuscular incapacitating device discharges. J Am Coll Cardiol.
2006;48:798–804. Copyright © 2006, Elsevier.

106  Circulation  January 7, 2014

Figure 7. ECGs from a pig taken before (A) and after (B and C)
TASER X26 discharge. An initial stable monomorphic ventricular
tachycardia was induced after the X26 shock and remained for
≈3 minutes before evolving to ventricular fibrillation. Reproduced
from Reference 15 with permission from the publisher. Dennis
AJ, Valentino DJ, Walter RJ, Nagy KK, Winners J, Bokhari F,
Wiley DE, Joseph KT, Roberts RR. Acute effects of Taser X26
discharges in a swine model. J Trauma. 2007;63:581–590.
Copyright © 2007 Lippincott Williams & Wilkins, Inc.

X26 shock. One pig developed VF after a single 40-second
ECD discharge. In the third study,17 a 10-second TASER
X26 discharge induced cardiac capture in 23 of 27 attempts
over transcardiac vectors and induced VF in 2 of 4 animals.
Nonsustained VT occurred after discharge in the remaining
animals. The authors stated:
If our data can be translated to humans, then ventricular rhythm may be captured and postdischarge dysrhythmias or VF may occur. Such transcardiac vectors
should be avoided when possible and the potential for
deterioration of the cardiac rhythm to VF in the field
should be considered….Users should be trained to
recognize the possible cardiac effects and be prepared
to use automated external defibrillators and cardiopulmonary resuscitation maneuvers when needed.17
Recent reanalysis18 of data from the earlier study14 demonstrated that the average time for cardiac capture was 121 milliseconds (2 impulses from the stun gun), whereas 14 of 38
discharges (37%) captured the heart with the first impulse. The
capture rate during discharge accelerated from 4:1 to 3:1 in
7 cases and from 3:1 to 2:1 in 2 cases in an average time of
3.6 seconds. Nonsustained VT followed 4 discharges. Both
direct and indirect (via retrograde conduction from captured
ventricular beats) atrial capture could occur,19 and this caused
an atrial arrhythmia on 1 occasion. These observations provide
support for a 5-second shock being capable of inducing VF and
the development of atrial fibrillation after a TASER shock.20

Drive-Stun Capture
Two porcine studies documented cardiac capture after X26 exposure in a drive-stun mode with probes taped to the skin between
the suprasternal notch and point of maximal impulse21 or 1 dart
on the right chest and the other over the left upper abdomen.17 In

the latter study, darts held ½ in away from the skin by insulating foam blocks were still capable of producing cardiac capture.
TASER International states that the high voltage used allows
1 probe to arc through a cumulative 2 in of clothing and not
have to physically penetrate the body to have an effect (TASER
Instructor Certification Course V-13, May 1, 2006, slide 35).
Thus, much like transthoracic cardiac pacing used emergently to treat bradyarrhythmias in humans,22 pulses from the
TASER X26 ECD emit sufficient electric charge to produce
transthoracic cardiac capture despite high skin resistance.
Because of this, drive-stun application should be capable of
causing cardiac capture and VF in humans and was the focus
of previous litigation (Williams versus TASER International,
Inc; US District Court for the Northern District of Georgia;
case No. 06-cv-00051 RWS; filed January 9, 2006). Darts that
penetrate the high skin resistance should, in all likelihood,
cause cardiac capture even more easily.

Mechanism of Cardiac Arrest
The porcine studies show that the mechanism by which the
X26 provokes cardiac arrest is by capturing the heart and
increasing its rate to values too rapid for maintenance of organized electric activity, resulting in VT/VF (Figures 6 and 7).
Runaway pacemakers years ago produced the same phenomenon,23 as does rapid pacing during electrophysiological studies. Thus, it should come as no surprise that transcutaneous
rapid pacing from an X26 can accomplish the same thing.
Ischemia from very low blood pressure could contribute to
developing VF. A stimulated ventricular complex falling in
the vulnerable period of the previous beat could theoretically
induce VT/VF as well. Importantly, animal data (Figures 6
and 7) show that VT can precede the development of VF by
seconds to minutes.14,15 Therefore, after an X26 shock, an individual could have a palpable pulse for a variable time interval
before lapsing into pulseless VT/VF.

Dart-to-Heart Distance
As with all cardiac stimulation, the distance between the
stimulating electrodes and the myocardium is critical. When
fired, the 2 TASER darts spread at an 8° angle, separating
by ≈1 ft for every 7 ft of travel,1 so the distance between 2
impaled darts can be fairly great. According to 1 study, 15 cm
was the ideal spread distance for cardiac capture.21 Although
nonphysiological porcine studies have suggested that dart-toheart distances of 4 to 17 mm are required to produce VF,24,25
TASER ECD shocks with 1 dart in the right chest and the
second in the abdomen or right groin, distances exceeding 4
to 17 mm, have been shown to capture the heart in intact pigs17
and humans.26 Rahko,27 evaluating skin-to-heart distance by
echocardiography, stated, “An EMD dart penetrating the skin
directly over the heart might put individuals at risk for ventricular fibrillation” and noted that the skin-to-heart distance
correlated with BMI. Using the porcine finding24 of 26-mm
skin-to-heart distance as a threshold value for individuals

Zipes   TASER Devices and Cardiac Arrests   107

potentially vulnerable to X26-induced VF, he found that 79%
of nonobese individuals with BMIs <25 kg/m2 were at risk.
In addition to anatomy, body position can influence
­skin-to-heart distance and therefore dart-to-heart distance. For
example, changing positions from upright to prone can shorten the
anterior chest-to-heart distance by almost 1 cm (H. Feigenbaum,
MD, personal communication, 2013) and facilitate cardiac capture by darts in the anterior chest. Falling prone could drive the
darts deeper into the skin. Lying on one’s left side brings the heart
so close to the chest wall that the apical impulse lies virtually just
beneath the skin and is visibly seen and palpated. A dart over the
apical impulse would be only a few millimeters from the heart.
An enlarged heart could shorten skin-to-heart and therefore dartto-heart distance. In addition, a state of excitation, for example,
adrenaline released during an agitated state of fight or flight, can
make the heart more susceptible to cardiac stimulation, which
can facilitate capture or VF induction14 (Figure 6). Because of
these variables and the effect of the vector encompassed by the
2 darts,13,14,17 in my opinion, no absolute number exists beyond
which chest darts could not capture the heart in a particular individual. Darts closest to the cardiac silhouette would pose the
greatest risk for cardiac capture and therefore VF induction.

Clinical Research
Multiple clinical studies of varying shock durations, placements, and measurements have not been reported to induce VF.
However, because of ethical considerations to protect the volunteers from risk, none of these trials can replicate the actual
clinical situation experienced by stressed individuals involuntarily receiving chest ECD shocks in the chaos of a field setting, especially if the shocks are repeated or lengthy. Moscati
et al28 tested supine individuals with 15-second TASER X26
shocks over “leads placed on the right upper chest and right
upper abdomen” after alcohol ingestion and found a decrease
in pH and bicarbonate and an increase in lactate after alcohol ingestion, with a further increase in lactate (mean, 4.19
mmol/L) and decrease in pH (mean, 7.31) after X26 exposure.
No VF resulted. Dawes et al29 studied volunteers with 15-second TASER X26 shocks without probe penetration by taping
the conducting wires to the right upper chest and the right upper
abdominal quadrant. Core body temperature did not change,
and no VF resulted. One subject was excluded because of a
history of coronary artery disease with 2 cardiac stents and frequent atrial and ventricular extrasystoles immediately before
testing. Apparently, the authors recognized that this individual would be at risk for developing VF. Dawes et al30 tested
5-second TASER X26 shocks delivered to 10 supine subjects
(median BMI, 27.5 kg/m2) over implanted chest darts (length
not given) during echocardiographic monitoring. Heart rates
before (mean, 91.0 bpm), during (mean, 95.8 bpm), and after
(mean, 85.7 bpm) shocks did not show capture. The relatively
slow mean heart rates are inconsistent with what probably happens during a law-enforcement confrontation in the field.
TASER ECDs can produce cardiac capture in humans.
Cao et al31 published a case report of a 53-year-old man with

a dual-chamber pacemaker implanted subcutaneously beneath
the left clavicle who received 2 X26 shocks with darts in the
right chest. Pacemaker interrogation revealed 2 ventricular
high-rate episodes that corresponded to the exact time of the
X26 shocks. The man was asymptomatic. The ventricular electrograms during X26 cardiac capture were different from those
during pacemaker capture, consistent with cardiac capture from
the TASER shocks directly from the X26 and not over the pacemaker lead (L. Saxon, MD, personal communication, 2013 ).
The second study26 tested a new-generation TASER ECD on
normal supine human volunteers using echocardiographic monitoring. It demonstrated “an apparent brief episode of cardiac
capture” at a rate of 240 bpm during the 10-second TASER ECD
shock. The individual had no symptoms during the capture. One
dart was slightly to the right of the midline chest with a skin-toheart distance of 2.57 cm; the second was in the right groin.
Although neither individual developed VF, the fact that a
TASER ECD could induce cardiac capture at rates exceeding
200 bpm makes it plausible that, in a given situation and given
individual, perhaps in the presence of underlying heart disease
such as an old myocardial infarction or a chemical substance
such as alcohol or perhaps after longer or repeated shocks or
during heightened sympathetic tone, TASER ­ECD–induced
VF becomes possible, as previous authors have suggested.13,17,27
Establishing that TASER X26 shocks cannot provoke VF
would require replicating potential elements of field situations:
testing shocks, some with >15-second duration, with 12- to
14-mm darts over a cardiac vector in multiple upright/prone
volunteers, some with heart disease or after ingestion of potentially arrhythmogenic drugs or after receiving epinephrine.
Such a study would require anesthetized patients in whom VF
induction is necessary for ICD implantation testing.
The videos (Figure 4, Movie I in the online-only Data Supplement,
and video at http://www.youtube.com/watch?v=b6dHpt6c6zM) in
essence show the results of such clinical studies. Although there is
no ECG recording or video of the heart, these videos of an “intact
human” serve as a substitute for those experiments that cannot
be done ethically and show what can happen in real life during a
TASER X26 deployment.

Clinical Epidemiology
Several epidemiological studies have not concluded that
TASER shocks induced VF. Gardner et al32 reported that 100
shocks in subjects 13 to 17 years old caused no significant
injuries. Eastman et al33 found 1 death in 426 uses that may or
may not have been causally related to the ECD. Strote et al34
noted that, of 1101 individuals subjected to M26 and X26
shocks, none died. Bozeman et al35 reported on 1201 uses,
almost all X26s. Deaths of 2 subjects were not attributed to
electric weapon use because of “prolonged combative behavior, cocaine use, cardiac abnormalities, and possible olanzapine toxicity,” questionable reasons to exclude an ECD death.
Apparently using the same cohort,11 they noted “no immediate
deaths in any cases…to suggest a cardiac dysrhythmia….”

108  Circulation  January 7, 2014

These surveys are too small to exclude a TASER X26
risk of inducing VF. Even so, given the claim by Amnesty
International6 of 544 deaths associated with ECD use between
2001 and 2013, it is surprising that these studies did not capture at least some of these deaths, which brings their validity
into question. Swerdlow et al,36 using an Internet-based search,
found 200 cases of ECD-associated, nontraumatic sudden
deaths from 2001 to 2008. Thus, more deaths occurred after
ECD deployment than captured by the epidemiological studies.

Prior Publications of Cases Consistent
With TASER-Induced Cardiac Arrest
Kim and Franklin37 reported that a 14-year-old adolescent
shocked with a TASER X26 immediately collapsed and was
found by paramedics to be in VF 2 minutes later. Four resuscitative shocks and drug administration restored a perfusing
rhythm, and the adolescent made a nearly complete recovery.
The ECG published, showing VF terminating after a 360-J
defibrillation shock, was not the final shock, but 1 depicting
an earlier 200-J shock converting VF to an idioventricular
rhythm. Kroll et al38 contested the accuracy of this report, but
on the basis of both the paramedic’s report and her deposition
testimony,39 the allegations of Kroll et al were shown to be
incorrect. The paramedic testified that, immediately after the
young man lost consciousness, she noted a pulse and respiration but recorded VF about 2 minutes later. A review by the
National Institute of Justice40 concluded for this case, “The
proximity of collapse to CED (conducted energy device) use
and documented VF argues in favor of an electrically induced
cardiac event.”
Another observation is of a 17-year-old boy who received
TASER X26 shocks of 25 and 5 seconds in the anterior chest,
immediately dropped to the ground, and became cyanotic and
apneic.41 The initial rhythm recorded >10 minutes later was
asystole. Resuscitation included hypothermia, and he survived
with memory impairment.
Of the 200 deaths analyzed by Swerdlow et al,36 56 subjects
collapsed within 15 minutes of the ECD shock and had the presenting rhythm reported. Four had VF and 52 had bradycardia/
asystole or pulseless electric activity. Swerdlow et al concluded
that 1 death was typical of electrically induced VF and stated,
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.” They continued, “To
the best of our knowledge, this is the first reported
fatality suggestive of [ECD]- induced VF.

Role of Underlying Heart Disease
Some of the TASER X26 ECD–induced cardiac arrests
occurred in individuals alleged to have structurally abnormal hearts or in the presence of potentially arrhythmogenic
substances such as alcohol.2 Invasive electrophysiological
testing over many years has demonstrated that it is easier to

electrically induce VF when the heart is abnormal or in the
presence of arrhythmogenic substances.42 So, rather than
preclude a diagnosis of X26-induced cardiac arrest in such a
setting, the presence of these abnormalities actually helps support that diagnosis. Arguments suggesting that heart disease or
a chemical substance, not the ECD shock, caused the cardiac
arrest must require that coincidentally at the exact time of the
TASER shock, the underlying heart disease or drugs triggered
the VF, an unlikely assumption. Some individuals may have
pacemakers31 or defibrillators43 in place, and they can be at
risk for device-device interactions.

Importance of Vital Signs and
Movement During VT/VF
Most observers, including physicians, rarely witness a person
dying of VT/VF without intervening and do not know what to
expect in terms of body movement, pulse, or respiration. In the
unfortunate death of basketball player Hank Gathers resulting
from exercise-induced VT captured on video, almost a full minute elapsed from the time he fell on court, presumably from a
syncopal episode, until he finally stopped moving. He exhibited
apparently purposeful movements, including sitting up, and
breathing until finally succumbing to VF (www.youtube.com/
watch?v=vcD5XUXfr1Y). Thus, claiming that a death cannot
be due to VT/VF resulting from a TASER X26 shock because
the individual was breathing or moving seconds or even minutes
after the shock, when there can be no other cause for the sudden loss of consciousness in an individual who was alert and
functioning immediately before the X26 shock, is without merit.
Multiple explanations exist for such events. First, VT before
VF, as noted in several pig experiments15 (Figures 6 and 7),
could provide sufficient cerebral blood flow to maintain some
bodily functions. In fact, in the case noted earlier,37,39 the paramedic present during the entire TASER X26 deployment stated
in sworn deposition testimony that she counted a pulse of 100
bpm over 15 seconds and respirations of 16 breaths per minute
immediately after the TASER X26 ECD shock when the individual was totally unconscious, with VF established by ECG 2
minutes later (explained if VT with a pulse preceded the VF).
Second, normal breathing has been documented in sheep and
pigs for as long as 1 minute and in humans for at least the first
12 to 15 seconds after the onset of VF.44,45 Therefore, normal
respirations can continue despite VF. Furthermore, confusing
agonal respirations with normal respirations, especially early
after VF onset, can confound the interpretation of the events.
Finally, accurate palpation of a pulse, particularly a radial pulse,
in the midst of the turmoil of observing an unresponsive subject
after a police altercation can be inaccurate. In a test among first
responders checking a carotid pulse in patients before and while
undergoing cardiopulmonary bypass, when no pulse was present, 10% (6 of 59) did not recognize an absent carotid pulse. In
fact, only 1 in 59 emergency medical technicians and paramedics identified pulselessness correctly in 10 seconds, making the
authors conclude that “…recognition of pulselessness by rescuers with basic CPR training is ­time-consuming and inaccurate.”46

Zipes   TASER Devices and Cardiac Arrests   109

In a study using a computerized mannequin, 64 experienced
healthcare providers checked the carotid pulse for 10 or 30 seconds. When there was no pulse, 27 of 42 responders checking for
10 seconds said there was a pulse, and 32 of 50 said there was a
pulse after checking for 30 seconds. The authors stated,
If the absence of a pulse was the only factor determining the onset of CPR maneuvers, approximately 50%
of pulseless patients simulated in our study would not
have had CPR initiated.47

Excited Delirium
Excited delirium has been reported as the cause of TASER X26–
related deaths as a result of an agitated and irrational state, usually compounded by physical restraint. The diagnosis of excited
delirium is not recognized by the American Medical Association
as a medical or psychiatric condition but is recognized by the
National Association of Medical Examiners. Many of the individuals dying with this alleged diagnosis have taken stimulant
drugs such as phencyclidine, methamphetamine, and cocaine or
have suffered from severe mental illness, were restrained with
hands bound behind them and legs shackled, and held prone on
the ground, making breathing difficult. Drug toxicity or postural
hypoxia or anoxia has been appropriately suggested as contributing to death in many of these individuals. The presence of
increased body temperature is said to be an important differentiator of excited delirium from other causes of death48; however,
“the exact signs and symptoms [of excited delirium] are difficult
to define precisely,…”49 thus hampering an accurate diagnosis.
It is possible that excited delirium is a form of takotsubo syndrome,50,51 which might be a cause of some in-custody deaths.
However, as noted above, to attribute an ECD death to excited
delirium, one must postulate that the excited delirium, if the
entity exists, caused VF at the precise time of the TASER shock.

Asystole
Untreated, VF evolves to asystole, sometimes in as short as
3 minutes52 but usually longer,53 and has been noted in some
patients after ECD-related collapse2,36 (Table and Figures 3 and
5). Waalewijn et al54 analyzed 873 patients and found the probability to record VF decreased per minute and the probability of asystole increased as time from collapse elapsed. At 10
minutes, the probability of asystole without basic life support
is ≈25%, rising to ≈35% at 15 minutes. Therefore, recording
asystole after a prolonged “down time” following X26 administration does not exonerate the X26 from causing the death.

biological mechanism), (4) TASER shock(s) with 1 or both chest
barbs near the heart (required for cardiac capture), (5) no other
plausible alternative explanation (normal heart or underlying
heart disease/drugs, if present, unlikely to cause VF at that precise time), and (6) similar cases in the literature (see above).

Conclusions and Recommendations
The animal and clinical data clearly support the conclusion
that a TASER X26 shock can produce VF in humans by the
mechanisms elaborated above. Although the risk may be low,
its number cannot be known without universal record keeping and the creation of a national database. Because of this
risk, it has been suggested that law-enforcement experts reassess ECD use to maintain a balance of safety for subjects
and officers while still achieving the goal of maintaining law
and order.55 In this regard, the Cincinnati Police Department
has revised its use-of-force policy to ban TASER chest shots
except in self-defense or the defense of another.56
The use of TASERS may be increasing. A recent Guardian
article indicated that the deployment of TASER weapons has
more than doubled in England and Wales, from ≈3500 in 2009
to 14 500 in 2010 and 2011.57 In addition, a new TASER ECD,
the X2, capable of shooting 2 cartridges, has been tested in 4
pigs exposed to 5-second shocks; it produced cardiac capture
in 17 of 71 exposures (24%) at heart rates of 206 to 313 bpm
compared with X26 capture in 45 of 71 exposures (63%) at
heart rates of 180 to 313 bpm.58 No pig developed VF. The
authors concluded that the “transcardiac” pathway was less
important for capture than the proximity of the dart to the heart.
I think ECD manufacturers should undertake an educational campaign to make all ECD users aware of the VF risk.
Educational material should stress avoiding chest shots if possible and should warn against repeated or long trigger pulls.
However, it is clear that a single 5-second shock can induce
VF. A user should be judicious with ECD deployment and
treat it with the same level of respect as a firearm, suspect cardiac arrest in any individual who becomes unresponsive after
a shock, quickly call for medical support, and be prepared to
resuscitate, including using an automated external defibrillator if needed. A national database should be mandated.

Acknowledgments
I thank John Burton, Esq, and M. Joan Zipes for reviewing the
manuscript.

Source of Funding

Causality

This work was supported by the Krannert Institute of Cardiology
Charitable Trust.

A temporal association alone does not prove causality. However,
when the following exist, in my opinion, a causal relationship
between the TASER X26 ECD and cardiac arrest in humans is
established: (1) known causal mechanism (cardiac capture at
rapid rates), (2) temporal association with loss of consciousness
and subsequent cardiac arrest (TASER shock precedes both), (3)
recorded VF (or asystole if a prolonged interval until first ECG;

The Institutional Review Board of the Indiana University School of
Medicine approved the medical information used for this article.
Written informed consent was obtained from each person or an authorized representative. The cases included have been studied as part of
litigation related to administration of ECD shocks from the TASER
X26 device. I have served (and in the future may serve) as a paid

Disclosures

110  Circulation  January 7, 2014

plaintiff expert witness in ECD-related sudden cardiac arrest/death
cases. Despite this conflict of interest, I have tried to present the salient
facts about the cases and to offer scientific evidence, credible argument,
and logic to support the conclusions. Statements in this manuscript are
my opinion, made to a reasonable degree of medical certainty.

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Response to Zipes
Mark W. Kroll, PhD; Dhanunjaya R. Lakkireddy, MD; James R. Stone, MD, PhD; Richard M. Luceri, MD
In controversies like this, transparency, absence of conflict, and adherence to the scientific method are important requisites.
In Dr Zipes’ series, not a single medical examiner postulated the ECD as the primary cause of death. The presumably unbiased Council of Canadian Academies report ­­(http://www.cahs-acss.ca/the-health-effects-of-conducted-energy-weapons-2/)
concluded that Dr Zipes’ “study…is particularly questionable” and stated that “In the [>2 000 000 ECD uses in the] field
there has not been a conclusive case of fatal ventricular fibrillation caused solely by the electrical effects….A small number
of human cases have found a temporal relationship between [ECDs] and fatal cardiac arrhythmias but they do not allow for
confirmation or exclusion of a clear causal link….” Dr Zipes cites Sherbino to support his claim that the ECD charge is equivalent to that of transcutaneous pacing; however, Sherbino does not report any pacing thresholds. Zipes himself, with Klein
as first author, reports thresholds of 2440 microcoulombs (61 mA·40 ms)—significantly greater than the 100 microcoulombs
of the ECD. The temporal coincidence argument is discussed in our article and online-only Data Supplement and is refuted
by Dr Zipes’ case 4 (our case 8) in which the probes missed the subject. Dr Zipes may also be confusing the sensitivity of a
pulse finding (which is low) with its specificity (which is high). The assertion of a “precise” timing (between the ECD and
cardiac arrest) may be ill advised when the majority of cases had a documented pulse, normal breathing for 6.1±3.1 minutes,
and abnormal underlying cardiac morphology.