Skip navigation

Taser Physiological Effects of Elec Weapon on Human Subj Annals Emerg Medicine 2007

Download original document:
Brief thumbnail
This text is machine-read, and may contain errors. Check the original document to verify accuracy.
ARTICLE IN PRESS
TRAUMA/ORIGINAL RESEARCH

Physiological Effects of a Conducted Electrical Weapon on
Human Subjects
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

From the Department of Emergency Medicine, University of California, San Diego Medical Center,
San Diego, CA (Vilke, Sloane, Levine, Neuman, Castillo, Chan); and the Department of Exercise
and Nutritional Sciences, San Diego State University, San Diego, CA (Bouton, Kolkhorst).

Study objective: Sudden death after a conducted electrical weapon exposure has not been well
studied. We examine the effects of a single Taser exposure on markers of physiologic stress in
healthy humans.
Methods: This is a prospective trial investigating the effects of a single Taser exposure. As part of
their police training, 32 healthy law enforcement officers received a 5-second Taser electrical
discharge. Measures before and for 60 minutes after an exposure included minute ventilation; tidal
volume; respiratory rate (RR); end-tidal PCO2; oxygen saturation, pulse rate; blood pressure (systolic
blood pressure/diastolic blood pressure); arterialized blood for pH, PO2, PCO2, and lactate; and
venous blood for bicarbonate and electrolytes. Troponin I was measured at 6 hours. Data were
analyzed using a repeated-measures ANOVA and paired t tests.
Results: At 1 minute postexposure, minute ventilation increased from a mean of 16 to 29 L/minute,
tidal volume increased from 0.9 to 1.4 L, and RR increased from 19 to 23 breaths/min, all returning
to baseline at 10 min. Pulse rate of 102 beats/min and systolic blood pressure of 139 mm Hg were
higher before Taser exposure than at anytime afterward. Blood lactate increased from 1.4 mmol/L at
baseline to 2.8 mmol/L at 1 minute, returning to baseline at 30 minutes. pH And bicarbonate
decreased, respectively, by 0.03 and 1.2 mEq/L at 1 minute, returning to baseline at 30 minutes.
All troponin I values were normal and there were no EKG changes. Ventilation was not interrupted,
and there was no hypoxemia or hypercarbia.
Conclusion: A 5-second exposure of a Taser X-26 to healthy law enforcement personnel does not
result in clinically significant changes of physiologic stress. [Ann Emerg Med. 2007;xx:xxx.]
0196-0644/$-see front matter
Copyright © 2007 by the American College of Emergency Physicians.
doi:10.1016/j.annemergmed.2007.05.004

INTRODUCTION
Background
There has been growing public demand for effective, less
lethal law enforcement weapons, which include blunt impact
weapons such beanbag guns or rubber bullets, mace, pepper
spray, and batons. The Taser, a conducted electrical weapon, is
an electrical law enforcement and self-defense device originally
developed in the 1970s and manufactured by Taser
International (Scottsdale, AZ). Early versions were bulky and
often ineffective. Various models of the Taser device have been
Volume xx, . x : Month 

developed, and their newest version, the X26, differs from the
previous model, the M26, mainly in the size and shape of the
device.
The National Institute of Justice reports that 9,800 US law
enforcement agencies authorize the Taser device, which is being
carried by more than 225,000 officers.1 Additionally, they
report that more than 120,000 US citizens also have a Taser
device. Although the actual number of uses is unknown, they
have reported that the Taser has been used on more than
150,000 volunteers during training and in more than 100,000
Annals of Emergency Medicine 1

ARTICLE IN PRESS
Physiological Effects of Conducted Electrical Weapons on Humans
Editor’s Capsule Summary

What is already known on this topic
The Taser delivers an electrical pulse, causing
incapacitating tetanic muscular contractions. Sudden
death has been associated with its use.
What question this study addressed
What are some measurable physiologic effects of a single
5-second Taser exposure on healthy human volunteers?
What this study adds to our knowledge
In 32 healthy individuals, there were no clinically
important changes in respiratory, cardiac, acid-base, or
electrolyte status after a single 5-second Taser exposure.
How this study might change clinical practice
Although this small study suggests that the Taser is safe
in healthy volunteers, there are insufficient data to
determine its safety profile in individuals with agitated
delirium, the population on whom the device is mainly
used.

“real-life” police confrontations. The manufacturer asserts that
the device helps officers avoid the use of deadly force while
lowering the risk of injury to officers.
The Taser X26 is designed to be deployed up to 7 m from
the subject. The operator fires the device, releasing 2 9-mm
barbs attached to the gun by thin, 7-m copper wires. When the
circuit is completed, an electrical pulse of 5 seconds’ duration is
automatically delivered through the wires to incapacitate the
subject by causing involuntary tetanic muscular contractions.
The officer may deliver continued electricity by pulling the
device trigger again.
Although the effect of the Taser is poorly studied, it is
generally regarded as safe2-4 and has been approved by the US
Consumer Product Safety Commission for the current
indication for which it is being used. Most of the data
supporting the product’s approval by the US Consumer Product
and Safety Commission was based on theoretic calculations and
not animal or human studies.5
Importance
There have been a number of reports of sudden death after
Taser administration. Amnesty International6 reports “152Taser related deaths” since 2001, and the Arizona Republic7
reports “167 cases of death following stun gun use” since 1999.
The majority of deaths in humans who were exposed to a Taser
device were associated with illicit drug use, especially
phencyclidine, methamphetamine, and cocaine.4,8,9 However,
there have been several deaths reported in individuals after Taser
exposure who were not under the influence of illicit drugs.
These cases generally involved a clinical presentation of “excited
delirium” and other comorbid factors that were likely to be
2 Annals of Emergency Medicine

Vilke et al
related as the cause of the suspect’s death.10-12 Most case reports
and police reports note that such suspects who are shocked with
a Taser go into cardiac arrest 5 to 40 minutes later.13 If a lethal
dysrhythmia, particularly ventricular fibrillation, was at fault
from the electrical discharge, cardiac arrest would be expected to
occur at the Taser activation. However, if individuals were
under the influence of sympathomimetic drugs such as cocaine,
methamphetamine, or phencyclidine or were having the clinical
presentation of excited delirium, other important clinically
significant physiologic aberrations might contribute to these
sudden deaths.
Goals of This Investigation
Because the metabolic and ventilatory effects of an acute
Taser exposure are unknown in humans, the aim of this study
was to investigate the extent of physiologic stress after exposure
to the Taser X26. We monitored cardiorespiratory and blood
characteristics in police officer volunteers before, during, and
after a 5-second Taser exposure that was part of their police
training. Because of the widespread and increasing use of Taser
devices by law enforcement agencies, it is vital to assess whether
its use on humans increases the risk of physiologic stress,
ventilatory impairment, cardiac muscle damage, or sudden
death.

MATERIALS AND METHODS
Study Design and Selection of Participants
This was a prospective study evaluating healthy police
volunteers drawn from the pool of San Diego County, CA,
Sheriff’s officers who had already volunteered to have a Taser
exposure as part of their tactical training. Inclusion criteria
included subjects who were between 18 and 60 years of age.
Before the study was conducted, each subject was screened by
the physician investigators to ensure that he or she was free of
acute illness or pregnancy that would prevent completion of the
study; all women underwent a urine pregnancy testing. In
addition, subjects weighing less than 45.5 kg or having a body
mass index less than 18 kg/m2 were excluded from the study.
Because there had been no human trials on the physiologic
effects of the Taser on humans when this trial was being
evaluated by the institutional review board and most Taser
activations used in the field were on larger individuals, a lower
limit of weight and body mass index was specified by our
institutions’ institutional review board committees. Initial
cardiovascular screening of subjects was conducted with the
Physical Activity Readiness Questionnaire (available at http://
www.csep.ca/communities/c574/files/hidden/pdfs/par-q.pdf). If
the subjects answered yes to any of the questions on the Physical
Activity Readiness Questionnaire, they were excluded from the
study. Although there were no occurrences, any subject with a
reported history of recent illicit drug use within the last 6
months or a positive point-of-care urine drug screen for illicit
drugs (Biosite urine drug assay; San Diego, CA) would have
been excluded from the study. In addition, subjects with a
baseline pulse exceeding a rate of 120 beats/min or a systolic or
Volume xx, . x : Month 

ARTICLE IN PRESS
Vilke et al
diastolic blood pressure greater than 150 or 90 mm Hg,
respectively, or an abnormal 12-lead ECG result were excluded
from participation. The study was approved by the University
of California, San Diego and the San Diego State University
institutional review boards, and all subjects provided informed
consent before participating in the study.
Intervention
Each subject was exposed to a 5-second Taser electrical
discharge. Darts from a standard Taser X-26 were shot into the
subject’s back by training personnel at a range of 2 to 3 m, with
the target laser centered on the subject’s back between the
shoulder blades.
Methods of Measurement
Vital signs, including blood pressure (systolic blood pressure/
diastolic blood pressure), pulse rate, and pulse oximetry (oxygen
saturation), were recorded before intervention and repeated at 5,
10, 15, 20, 25, 30, 40, 50, and 60 minutes post–Taser
activation. Ventilatory measures, including minute ventilation,
tidal volume, respiratory rate (RR) and end-tidal PCO2
(PETCO2), were obtained using a wireless portable metabolic
measurement system (Oxycon Mobile; VIASYS Healthcare,
Yorba Linda, CA). These ventilatory parameters were measured
before and 1 minute after the Taser activation and at 10, 30,
and 60 minutes.
A 12-lead ECG was performed at baseline before the Taser
activation and repeated at 60 minutes postactivation. These
ECGs were evaluated in a blinded manner for ischemia, as well
as for interval changes.
Venous blood samples were drawn for electrolyte measures
that included calcium, sodium, potassium, and bicarbonate
concentrations. These studies were drawn before intervention
and repeated at 1, 10, 30, and 60 minutes post–Taser
activation. Subjects had an intravenous catheter placed in
standard sterile fashion for ease of repeated blood draws.
Arterialized capillary blood was drawn from a fingerstick before
and at 1, 10, 30, and 60 minutes post–Taser activation for
determination of pH, PO2, PCO2, and lactate concentration
(i-STAT Portable Analyzer; Abbott Laboratories, Abbott Park,
IL). The hand was placed in a warm water bath (Ϸ41 °C) for
approximately 3 minutes, and blood was drawn using standard
capillary sampling techniques. A final venous blood sample was
drawn 6 hours post–Taser activation for evaluation of troponin
I, using the Advia Centaur Immunoassay System (Bayer
Diagnostics, Tarrytown, NJ).
Outcome Measures
Outcome measures were as follows: hypoxemia, as expressed
by pulse oximetry less than 95%; hypoventilation, as evidenced
by end tidal CO2 greater than 40 mm Hg and PCO2 greater
than 40 mm Hg on arterialized capillary blood sampling;
changes in pH as evaluated by arterialized capillary blood
sampling; and cardiac myocardial damage by assessing troponin
Volume xx, . x : Month 

Physiological Effects of Conducted Electrical Weapons on Humans
Table 1. Subject characteristics and baseline vital measures
(nϭ32).
Characteristic
Age, y
Weight, kg
Height, m
Body mass index, kg/m2*

Mean؎SD

Range

38.4 Ϯ 7.7
89.3 Ϯ 15.0
1.79 Ϯ 0.08
27.8 Ϯ 3.3

25–57
65.8–125.2
1.65–1.96
22.4–34.6

*Normal values for body mass indexϭ18.5 to 24.9 kg/m2.

Figure 1. Effect of a 5-second Taser exposure on pulse
rate, oxygen saturation, and systolic and diastolic blood
pressure (nϭ32). Baseline levels (timeϭ0) were obtained
within 5 minutes before Taser exposure. Individual
measures missing for systolic blood pressure (nϭ2),
diastolic blood pressure (nϭ2), oxygen saturation (nϭ1),
and pulse rate (nϭ1).

I levels at 6 hours post–Taser activation, as well as by evaluating
12-lead ECG at 1 hour postactivation. Other outcome measures
consisted of vital signs, ventilatory function, and venous and
capillary blood indicators, as mentioned above. The change in
each measure was evaluated separately to assess any relevant
change in the measure.
Primary Data Analysis
Power analysis indicated that 24 subjects with complete data
would be needed to detect a pH change of 0.15 (7.40 to 7.25),
assuming 80% power, an ␣ of 0.05, and SD of 0.30. A study
population of 32 subjects would adequately account for missing
values for specific measures. All measures were reported as
means and SDs. A 1-way repeated-measures ANOVA was used
to detect differences in respiratory, ventilatory, and blood
measurements. When the repeated-measures ANOVA results
indicated significance at PϽ.05, pairwise comparisons were
made between the baseline and the 4 or 9 subsequent measures
(1, 10, 15, 20, 25, 30, 40, 50, and 60 minutes postactivation or
5, 10, 15, 20, 25, 30, 40, 50, and 60 minutes, depending on
outcome measure), including only subjects with data for all time
measures. Changes from baseline and subsequent measures are
Annals of Emergency Medicine 3

ARTICLE IN PRESS
Physiological Effects of Conducted Electrical Weapons on Humans

Vilke et al

Table 2. Effect of Taser exposure on respiratory and ventilatory function (nϭ32).
Mean (SD)
†

Measure*

Baseline

1-Minute

10-Minute

30-Minute

60-Minute

VE, L/min‡
TV, L‡
RR, breaths/min‡
‡
PETCO2, mm Hg
PO2, mm Hg
PCO2, mm Hg

16.0 (3.7)
0.9 (0.2)
19.3 (4.4)
33.5 (3.1)
73.2 (4.8)
35.8 (2.8)

28.8 (10.5)
1.4 (0.7)
23.1 (5.7)
34.5 (4.4)
75.3 (7.2)
35.9 (2.6)

17.9 (4.0)
0.9 (0.2)
20.2 (4.6)
32.9 (3.3)
72.7 (6.9)
35.0 (3.0)

15.2 (5.3)
0.9 (0.3)
18.6 (4.4)
32.4 (2.6)
75.4 (9.8)
36.1 (3.3)

14.9 (4.3)
0.8 (0.3)
19.6 (4.5)
32.7 (2.5)
74.2 (8.1)
36.0 (2.7)

VE, Minute ventilation; TV, tidal volume.
Individual measures missing for VE (nϭ4), TV (nϭ4), RR (nϭ4), PETCO2 (nϭ4), PCO2 (nϭ9), and PO2 (nϭ9).
*Normal values: VE (4 to 7.5 L/minute), TV (0.5 L), RR (8 to 15 breaths/min), PETCO2 (35 to 45 mm Hg), PO2 (80 to 100 mm Hg), PCO2 (35 to 45 mm Hg). VE and TV
vary according to sex, size, tobacco use, and physical fitness.
†
Baseline values were obtained within 5 minutes before Taser exposure.
‡
Repeated-measures ANOVA PϽ.05.

and enrollment and did not participate (6 because of increased
baseline systolic blood pressures, 1 with an abnormal baseline
ECG result, and 3 for taking medications for hypertension or
cardiac disease). Complete cardiorespiratory measurements and
blood samples were obtained from all 32 participants for each
collection period. Subject characteristics are reported in Table 1.

Figure 2. Effect of a 5-second Taser exposure on minute
ventilation (VE), RR, tidal volume (TV), and PETCO2 (nϭ32).
Baseline levels (timeϭ0) were obtained within 5 minutes
before Taser exposure. Individual measures missing for VE
(nϭ4), TV (nϭ4), RR (nϭ4), and PETCO2 (nϭ4).

reported as mean differences and associated 95% confidence
intervals (CIs), with associated P values. Because of multiple
comparisons, a Bonferroni adjustment was used to define
statistical significance (PϽ.006 for vital measure comparisons
and PϽ.013 for all other outcome measures). However, because
limited data have been presented about the physiologic effects of
a Taser activation on healthy adults and because this was an
exploratory analysis, PϽ.05 was considered to represent
differences of possible interest. Clinical significance was
determined based on current medical practice. All analyses were
performed with SPSS for Windows, version 14.0 (SPSS, Inc.,
Chicago, IL).

RESULTS
Characteristics of Study Subjects
A total of 42 sheriff’s officers volunteered to participate in
the study. Thirty-two completed the study, which included 27
men and 5 women. Ten subjects screened out before consent
4 Annals of Emergency Medicine

Main Results
Repeated-measures ANOVA results indicated statistically
significant differences in vital sign means between measures for
systolic blood pressure (PϽ.001) but no significant differences
for pulse rate or diastolic blood pressure (Figure 1). Systolic
blood pressure decreased linearly before Taser activation (139
mm Hg at baseline) to normal (123 mm Hg at 60 minutes)
(difference of 16 mm Hg; 95% CI 12.7 to 20.3 mm Hg;
PϽ.001). There were no significant differences between baseline
(97%) and any subsequent measure for oxygen saturation, and
no measure was below 97% (data not shown). The change in
systolic blood pressure was not clinically significant.
Table 2 reports the effects of Taser exposure on respiratory
and ventilatory measures (minute ventilation, tidal volume, RR,
PETCO2, PO2 and PCO2). Repeated-measures ANOVA results
identified significant differences in means between readings for
all measures (PϽ.001 for minute ventilation, tidal volume and
RR; Pϭ.009 for PETCO2) (Figure 2) but not for PO2 or PCO2
(PϾ.05). Minute ventilation, tidal volume, and RR all had an
initial significant increase from baseline to 1 minute after Taser
activation (12.8 L/minute, 95% CI 8.5 to 17.1 L/minute,
PϽ.001 for minute ventilation; 0.5 L, 95% CI 0.3 to 0.7 L,
PϽ.001 for tidal volume; 3.8 breaths/min, 95% CI 1.6 to 5.9
breaths/min, PϽ.001 for RR). All measures returned to and
remained at baseline readings at 10-, 30-, and 60-minute
comparisons. The 30-minute PETCO2 measure was different
from baseline when not adjusting for multiple comparisons
(decrease Ϫ1.1 mm Hg; 95% CI Ϫ2.1 to Ϫ0.2; Pϭ.025), but
it was no longer significant after adjustment (PϾ.013). PETCO2
readings were not different at 1, 10, or 60 minutes compared
with baseline. There was no evidence of hypoxemia or
hypoventilation.
Volume xx, . x : Month 

ARTICLE IN PRESS
Vilke et al

Physiological Effects of Conducted Electrical Weapons on Humans

Table 3. Effects of Taser exposure on blood characteristics (nϭ32).
Mean (SD)
†

Measure*
pH‡
Bicarbonate, mEq/L‡
Lactate, mmol/L‡
Calcium, mg/dL
Sodium, mEq/L
Potassium, mEq/L

Baseline

1-Minute

10-Minute

30-Minute

60-Minute

7.45 (0.04)
23.9 (2.2)
1.4 (0.5)
9.8 (0.4)
138.3 (3.8)
4.2 (0.6)

7.42 (0.03)
22.7 (2.0)
2.8 (0.7)
9.8 (0.4)
137.8 (3.9)
4.1 (0.6)

7.43 (0.03)
22.9 (1.8)
2.4 (0.6)
9.8 (0.4)
138.4 (4.2)
4.2 (0.6)

7.43 (0.03)
23.9 (1.7)
1.5 (0.5)
9.8 (0.4)
137.8 (4.0)
4.2 (0.6)

7.44 (0.03)
23.8 (1.6)
1.3 (0.5)
9.8 (0.4)
138.3 (3.9)
4.2 (0.6)

Individual measures missing for pH (nϭ8), PCO2 (nϭ9), PO2 (nϭ9), bicarbonate (nϭ9), and lactate (nϭ9).
*Normal values: pH (7.35 to 7.45), bicarbonate (20 to 29 mEq/L), lactate (0.7 to 2.1 mmol/L), calcium (8.6 to 10.3 mg/dL), sodium (135 to 147 mEq/L), potassium
(3.5 to 5.0 mEq/L).
†
Baseline values were obtained within 5 minutes before Taser exposure.
‡
Repeated-measures ANOVA PϽ.05.

None of the blood measure changes that did occur were
clinically significant. Troponin I values for all subjects at 6
hours were less than 0.2 ng/mL, with a positive assay defined as
greater than 0.2 ng/mL.
All 32 subjects had no evidence of ischemia on ECG, and
when results were blinded and compared, there was no evidence
of interval changes from baseline to after Taser exposure.

LIMITATIONS

Figure 3. Effect of a 5-second Taser exposure on blood pH
and lactate concentration (nϭ32). Baseline levels
(timeϭ0) were obtained within 5 minutes before Taser
exposure. Individual measures missing for pH (nϭ8) and
lactate (nϭ9).

The effects of Taser-exposure blood parameters are reported
in Table 3. For arterialized capillary blood measures, there were
statistically significant differences for pH (Pϭ.021), bicarbonate
(PϽ.001), and lactate concentration (PϽ.001) in the repeatedmeasures ANOVA analysis (Figure 3). There was an initial
decrease in pH at 1 minute (Ϫ0.02; 95% CI Ϫ0.04 to Ϫ0.01;
Pϭ.001), but levels returned to normal at 10, 30, and 60
minutes. Bicarbonate levels were lower at 1 and 10 minutes
compared with baseline (Ϫ1.2 mEq/L, 95% CI Ϫ1.8 to Ϫ0.7
mEq/L, PϽ.001 at 1 minute; Ϫ1.0 mEq/L, 95% CI Ϫ1.6 to
Ϫ0.4 mEq/L, Pϭ.002 at 10 minutes) but returned to baseline
levels at 30 and 60 minutes. Lactate concentration levels were
higher at 1 minute (1.4 mmol/L; 95% CI 1.1 to 1.6; PϽ.001)
and 10 minutes (1.0 mmol/L; 95% CI 0.7 to 1.2; PϽ.001)
compared with baseline but returned to baseline levels at 30 and
60 minutes. For venous blood measures, there were no
significant differences between measures for calcium, sodium or
potassium according to repeated-measures ANOVA results.
Volume xx, . x : Month 

There are several limitations to our study. Our subjects were
generally healthy and free from chronic disease, and duration of
the Taser activation in our study did not exceed a single 5second activation, whereas individuals in the field often receive
multiple shocks. Our subjects were also not under the influence
of illicit stimulant drugs or in a state of agitated delirium.

DISCUSSION
The Taser delivers energy through a sequence of dampened
sine-wave current pulses, each lasting about 11 ␮s. This energy
is reportedly neither pure alternating current nor pure direct
current but probably akin to rapid-fire, low-amplitude, directcurrent shocks.3 The power output of the device is 26 W,
average 2-mA current, and a maximum of 50,000 V, which is
reported to be below the threshold of ventricular fibrillation.2
Studies directly stimulating canine hearts with the Taser failed
to induce cardiac arrhythmia.14,15 There is also an industrysponsored swine model study lauding the cardiac safety of the
newer Taser.16
Effect of electrical injury on the cardiac conducting system
has been studied in prospective animal studies and retrospective
human studies.17-22 The pulse duration and amplitude of
electricity in these cases are different from that of the Taser, that
is, the majority of data available about electrocutions is about
people and animals subjected to very different doses of
electricity, such as from lightning or power lines.
To date, there are only 3 published studies that have
prospectively evaluated the effects of the Taser on humans.23-25
The first 2 studies were published as abstracts and used singlelead monitoring to assess cardiac changes by monitoring
Annals of Emergency Medicine 5

ARTICLE IN PRESS
Physiological Effects of Conducted Electrical Weapons on Humans
immediately before, during, and for several seconds after a Taser
activation was being deployed.23,24 Both observed an increase in
subject pulse rate immediately before the activation and slightly
higher immediately afterwards, but no ectopy or dysrhythmias
were reported in any of the subjects in either study.
The third study, funded by Taser International, evaluated 66
human volunteers with a 5-second Taser activation and 24-hour
monitoring.25 The investigators drew blood at baseline,
immediately after activation, and at 16 and 24 hours post–Taser
exposure. Their conclusions were that they were unable to
detect any induced electrical dysrhythmias or significant direct
cardiac cellular damage that may be related to sudden and
unexpected death proximal to a Taser exposure. Because deaths
associated with the Taser may not be an electrical phenomenon,
we evaluated other physiologic effects of a Taser discharge.
These immediate physiologic effects of the Taser on these
characteristics have not been published previously. Because of its
widespread use, we believe that it is important to assess whether
the Taser use has potential effects on individuals, including
changes in the above measured physiologic characteristics.
We found no changes in electrolytes in the 60 minutes of
observation. Additionally, all our 6-hour troponin I levels were
normal, and there were no changes in ECG from baseline
compared with the ECGs taken 1 hour postexposure.
We observed a modest increase in RR and tidal volume,
which resulted in increased minute ventilation immediately after
the Taser exposure, but this increase was transient and returned
to baseline by 10 minutes. In monitoring breath-by-breath
ventilation during the Taser activation, all subjects were
observed to continue breathing during the exposure. Arterialized
capillary sampling of PO2 and PCO2 demonstrated no evidence
of hypoxia or carbon dioxide retention during or after the Taser
exposure, demonstrating no ventilatory impairment as a result
of the Taser exposure. Although statistically significant changes
in pH were observed, the mean pH remained between 7.42 and
7.45. The changes that were observed in pH were clinically
insignificant and of a degree found in mild to moderate exercise.
In summary, this preliminary work in humans demonstrates
no clinically relevant changes in ventilation, acid-base status,
electrolyte concentrations (calcium, sodium, potassium),
troponin I level, or ECGs. We conclude that a 5-second
exposure of a Taser X-26 to healthy subjects does not result in
clinically significant changes in ventilatory or blood
characteristics of physiologic stress.
Supervising editor: E. John Gallagher, MD
Author contributions: GMV and TCC conceived the project,
were coprincipal investigators, and worked on protocol
formulation. CMS, FWK, SDL, and TSN assisted with protocol
refinement. KDB assisted with analysis. GMV, CMS, FWK,
SDL, TSN, EMC, and TCC assisted with article preparation.
EMC assisted with data management and statistical analysis.
GMV, CMS, KDB, FWK, SDL, TSN, and TCC worked on data
collection. GMV takes responsibility for the paper as a whole.

6 Annals of Emergency Medicine

Vilke et al
Funding and support: By Annals policy, all authors are required
to disclose any and all commercial, financial, and other
relationships in any way related to the subject of this article,
that might create any potential conflict of interest. See the
Manuscript Submission Agreement in this issue for examples
of specific conflicts covered by this statement. This study was
funded by the National Institute of Justice (2005-IJ-CX-K051).
Publication dates: Received for publication March 9, 2007.
Revisions received April 19, 2007, and April 27, 2007.
Accepted for publication May 4, 2007.
Presented at the Society for Academic Emergency Medicine
annual meeting, May 2007, Chicago, IL.
Address for reprints: Gary M. Vilke, MD, Department of
Emergency Medicine, University of California, San Diego
Medical Center, 200 West Arbor Drive, Mailcode #8676, San
Diego, CA 92103; 619-543-6463, fax 619-543-3115; E-mail
gmvilke@ucsd.edu.

REFERENCES
1. The Commission of Accreditation for Law Enforcement Agencies
(CALEA) Less Lethal Technology Working Group Meeting. Use of
force: sudden death myths and excited equilibrium delirium.
Washington, DC. 2006.
2. Taser International. Taser promotional literature. Available at:
http://www.Taser.com. Accessed September 30, 2006.
3. Bleetman A, Steyn R, Lee C. Introduction of the Taser into British
policing. Implications for UK emergency departments: an overview
of electronic weaponry. Emerg Med J. 2004;21:136-140.
4. Kornblum RN, Reddy SK. Effects of the Taser in fatalities
involving police confrontation. J Forensic Sci. 1991;36:434-448.
5. O’Brien DJ. Electronic weaponry—a question of safety. Ann Emerg
Med. 1991;20:163-167.
6. Amnesty International. Amnesty International’s continuing
concerns about laser use. Available at: http://www.web.amnesty.
org/library/index/engamr510302006. Accessed June 28, 2007.
7. Anglen R. 167 cases of death following stun-gun use. The Arizona
Republic. January 5, 2006.
8. Koscove EM. The Taser® weapon: a new emergency medicine
problem. Ann Emerg Med. 1985; 14:109-112.
9. Ordog GJ, Wasserberger J, Schlater T, et al. Electronic gun
(Taser®) injuries. Ann Emerg Med. 1987;16:103-108.
10. Allen TB. Discussion of effect of the Taser in fatalities in
fatalities involving police confrontation. J Forensic Sci. 1991;36:
434-438.
11. Kosove EM. The Taser®: research, patients and language (Tom
Swift found). J Emerg Med. 1988;6:343-344.
12. Stratton SJ, Rogers C, Brickett K, et al. Factors associated with
sudden death of individuals requiring restraint for excited
delirium. Am J Emerg Med. 2001;19:187-191.
13. Ederheimer JA. Presentation: Critical issues in policing series,
police executive research forum; San Diego, CA; December 2005.
14. Panescu D, Webster JG, Stratbucker RA. A nonlinear electricathermal model of the skin. IEEE Trans Biomed Eng. 1994;41:
672-680.
15. Panescu D, Webster JG, Stratbucker RA. A nonlinear finite
element model of the electrode-electrolyte-skin system. IEEE
Trans Biomed Eng. 1994;41:681-687.
16. Lakkireddy D, Wallick D, Ryschon K, et al. Effects of cocaine
intoxication on the threshold for stun gun induction of ventricular
fibrillation. J Am Coll Cardiol. 2006;48:805-811.

Volume xx, . x : Month 

ARTICLE IN PRESS
Vilke et al
17. Arya KR, Taori GK, Khanna SS. Electrocardiographic
manifestations following electrical injury. Int J Cardiol. 1996;57:
100-101.
18. Chandra NC, Siu CO, Munster AM. Clinical predictors of
myocardial damage after high voltage electrical injury. Crit Care
Med. 1990;18:293-297.
19. Forrest FC, Saunders PR, McSwinney M, et al. Cardiac injury and
electrocution. J R Soc Med. 1992;85:642-643.
20. Jain S, Bandi V. Electrical and lightning injuries. Crit Care Clin.
1999;15:319-331.
21. Robinson NKM, Chamberlin DA. Electrical injury to the heart may
cause long-term damage to conducting tissue: a hypothesis and
review of the literature. Int J Cardiol. 1996;53:273-277.

Physiological Effects of Conducted Electrical Weapons on Humans
22. VanDenburg S, McKormick GM, Young DB. Investigation of
deaths related to electrical injury. South Med J. 1996;89:869872.
23. Levine S, Sloane C, Chan T, et al. Cardiac monitoring of
subjects exposed to the Taser [abstract]. Prehosp Emerg Care.
2006;10:
130.
24. Barnes DG, Winslow JE III, Alson RL, et al. Cardiac effects of the
Taser conducted energy weapon [abstract]. Ann Emerg Med.
2006;48(4 suppl 1):S102.
25. Ho JD, Miner JR, Lakireddy DR, et al. Cardiovascular and
physiologic effects of conducted electrical weapon discharge in
resting adults. Acad Emerg Med. 2006;13:589-595.

Editor’s Capsule Summary: What is already known on this
topic: The Taser delivers an electrical pulse, causing
incapacitating tetanic muscular contractions. Sudden death has
been associated with its use.What question this study addressed:
What are some measurable physiologic effects of a single 5second Taser exposure on healthy human volunteers?What this
study adds to our knowledge: In 32 healthy individuals, there were
no clinically important changes in respiratory, cardiac, acidbase, or electrolyte status after a single 5-second Taser
exposure.How this study might change clinical practice: Although
this small study suggests that the Taser is safe in healthy
volunteers, there are insufficient data to determine its safety
profile in individuals with agitated delirium, the population on
whom the device is mainly used.

Volume xx, . x : Month 

Annals of Emergency Medicine 7