Forensic Science, Medicine and Pathology (2020) 16:406-414 https://doi.org/10.1007/s12024-020-00249-w ORIGINAL ARTICLE The physiologic effects of a new generation conducted electrical weapon on human volunteers at rest Check for updates Jeffrey D. Ho1 • Donald M. Dawes2 • Sebastian N. Kunz3 • Lauren R. Klein1 • Brian E. Driver1 • Paige A. DeVries1 Gregg A. Jones1 • Jamie L. Stang1 Accepted: 19 March 2020 / Published online: 9 May 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020 Abstract Axon Enterprise, Inc. (Axon) released its newest generation conducted electrical weapon (CEW), the T7, in October 2018. In order to compare the effects of this new CEW to prior generations, we used our previously described methodology to study the physiologic effects of CEWs on human volunteers at rest. This was a prospective, observational study of human subjects consisting of two parts. Part 1 was testing a single cartridge (2-probe) exposure. Subjects received a 10-s exposure from the T7 to the back with a 30 cm (12 in.) spread between the two probes. Part 2 was testing a simultaneous two-cartridge (4-probe) exposure. Subjects received a 10-s exposure from the T7 to the back with two cartridges with a 10 cm (4 in.) spread between each probe pair. The probe pairs were arranged cephalad to caudal such that the distance between the top probe of the first cartridge and the bottom probe of the second cartridge was 30 cm (12 in.). Vital signs were measured immediately before and after the exposure. Continuous spirometry was performed. ECG monitoring was performed immediately before and after the exposure. Venous pH, lactate, potassium, CK, catecholamines, and troponin were measured before and immediately after the exposure, at 1 -h post-exposure, and again at 24 h. 11 subjects completed part 1 of the study. 9 subjects completed part 2 of the study. No subjects had a dysrhythmia or morphology change in the surface ECG. There were no statistical changes in vital signs pre- and postexposure. While subjects did not have a statistical change in spirometry parameters pre-exposure to exposure except for a small drop in PETC02, there was an increase in minute ventilation after the exposure that could have several explanations. A similar pattern was seen with prior generation weapons. No subject had elevated troponin levels. Other blood parameters including venous pH, lactate, potassium, CK, and catecholamines had changes similar to prior generation weapons. Comparison of the data for the single-cartridge exposures against the simultaneous two-cartridge exposures yielded no difference in vital signs, but the minute ventilation was higher for the two-cartridge exposures. The blood data, where there was a difference, was mixed. In our study, the physiologic effects of the Axon T7 are modest, consistent with the electrically-induced motor nerve-driven muscle contraction, and were similar to prior generation weapons. Keywords Axon ■ CEW ■ Conducted electrical weapon ■ Conducted energy weapon ■ Physiology ■ TASER Introduction Conducted electrical weapons (CEW) are now ubiquitous in policing in the United States (U.S.) and many western coun- 53 Donald M. Dawes donalddawes@gmail.com 1 Hennepin Healthcare, Minneapolis, MN, USA 2 Lompoc Valley Medical Center, Lompoc, CA, USA 3 Institute of Forensic Medicine, Ulm University, Ulm, Germany tries due to their unique ability to temporarily immobilize subjects from a distance. The primary mechanism by which Axon Enterprise, Inc. (Axon), formerly TASER International (TASER), Scottsdale, AZ, CEWs are thought to operate is through the electrical stimulation of motor neuron axonal projections to skeletal muscles. Motor neurons within sufficiently strong electric fields established by the wire-tethered probes are stimulated at a sub-tetanic rate (19-22 pulses per second (PPS) depending on the CEW) leading to involuntarily fused muscle contractions and therefore incapacitation of activated muscle groups [1]. Because CEWs electrically capture excitable tissues, most of the direct safety concerns have centered on direct cardiac stimulation, respiratory impairment from Springer Forensic Sci Med Pathol (2020) 16:406-414 407 respiratory muscle contraction, and other physiologic effects related to sustained muscle contraction (e.g. acidosis, rhabdo-myolysis, and hyperkalemia). Known, but more obvious direct risks, include dart puncture wounds (especially to sensitive structures such as the eye) and minor skin burns due to electrical arcing. Indirect risks include head injuries from unprotected falls, and the possibility of severe burns from the ignition of flammable materials. Concerns have also focused on the indirect risk of increased "stress" particularly in vulnerable subjects. We have previously described a methodology for studying the physiologic effects of CEWs on human volunteers at rest [2, 3]. Axon released its newest generation CEW, the T7, in October 2018. In order to compare the physiologic effects of this new CEW to prior generations, we have used our prior method here. Because the T7 is a two-bay/cartridge weapon, we tested both single-cartridge (2-probe) and simultaneous two-cartridge (4-probe) exposures. This is the second study in the literature to study the effects of simultaneous two-cartridge exposures from a handheld CEW and the first to study the new T7. Methods This was a prospective, observational study of human volunteers consisting of two parts. Part 1 tested a one-bay exposure, and part 2 tested a simultaneous two-bay exposure with an over-all similar effective probe spread. The institutional review board at Hennepin County Medical Center (HCMC) (Minneapolis, MN) approved the study. The study was conducted at an Axon facility in Scottsdale, AZ on two different dates (one part per date). The subjects were a convenience sample of primarily law enforcement, military and security officers but also civilian volunteers. Subjects were compensated with an Axon CEW for their participation. Subjects completed a medical screening questionnaire that was reviewed by a study physician and provided informed consent (an HCMC representative was brought in specifically to do the consenting process). Pregnancy was the only specific exclusion criterion. A commercial scale (Omron Full Body Sensor HBF-5168, Omron Healthcare, Inc., Bannockburn, Illinois) was used to determine participant weight that was combined with stated height to determine body mass index (BMI). Baseline creatine kinase (CK), potassium, pH, lactate, troponin, and catecholamines (epinephrine, norepinephrine and dopamine) levels were drawn. The pH, lactate, troponin, and potassium levels were immediately analyzed after the draw using the Abbott Point-of-Care i-STAT (East Windsor, NJ) and CG4, Chem8+, and cTnl cartridges. The blood was spun on site by a contracted laboratory technician, and delivered later to Lab Corps (Phoenix, AZ) for CK and catecholamines analysis (note in part 2 of the study, the cTnl cartridges were unavailable and troponin was sent to Lab Corps). Subjects were laid supine on a padded table for testing. An "off-the-shelf Axon T7 was attached by hand-placing the probes to full dart depth (11.5 mm). Axon engineers confirmed the CEW to be operating according to manufacturer specifications prior to testing. The top probe was placed 15 cm (6 in.) below the C7 prominence and 10 cm (4 in.) laterally on the back, and, in part 1, the bottom probe was placed 30 cm (12 in.) caudally. Laterality was alternated between subjects. The 30 cm (12 in.) distance was chosen based on prior work that showed that 30 cm (12 in.) was the minimum spread between the probes that would successfully incapacitate a human subject [4]. In part 2, two cartridges simultaneously were tested, rather than a single cartridge. In part 2, the top probe of the first cartridge had the same placement as above. However, the bottom probe of the first cartridge was placed 10 cm (4 in.) caudally. The top probe from the second cartridge was placed caudally an additional 10 cm (4 in.), and the bottom probe from the second cartridge was placed caudally an additional 10 cm (4 in.) such that the distance from the top probe of cartridge 1 to the bottom probe of cartridge 2 was 30 cm (12 in). See Fig. 1. Baseline vital signs (blood pressure, heart rate, and pulse oximetry) were taken with a portable monitor (Nonin 2120, Plymouth, MN). Subjects were connected to a spirometer, and continuous respiratory data was collected with a breath-by-breath gas exchange system (Ultima Cardio 2 PFX, Med Graphics, Minneapolis, MN). The spirometer measured oxygen and carbon dioxide concentrations of breathed air, the respiratory rate, and the tidal volume on a breath-by-breath basis. Sparks Systems (Phoenix, AZ) was contracted to collect and process the spirometry data. A wireless acquisition module (Mortara, Milwaukee, WI) was used to integrate continuous ECG before and after the exposure (ECG during exposure was not possible due to electrical noise and body movement). Once baseline data were collected over about 5 min, subjects had a 10-s continuous exposure from Axon T7 CEW. Vital signs were repeated, and labs were drawn within 1-2 min after the exposure. Labs were drawn again at 1 h, and at 16-24 h. Spirometry data were collected for approximately 5 min after the exposure. Data were compiled in an Excel spreadsheet (Microsoft Corporation, Redmond, WA) and exported into Stata (Version 15, StataCorp, College Station, TX) for analysis. Median and interquartile range values were calculated for vital signs, laboratory values and respiratory values for each part. Part 1 and 2 were compared with a t-test for each value. Data were further analyzed by comparing change from baseline to point of highest clinical significance. Springer 408 Forensic Sci Med Pathol (2020) 16:406-414 Fig. 1 Set up for part two (simultaneous two-bay exposures) Bay! Bay 2 12 inches Results In part 1, the single-cartridge exposures, 11 subjects were enrolled. No subjects were excluded. All the subjects were male. Subject health histories included: depression (1), chronic pain (1), high blood pressure (1), hernia surgery (1), orthopedic surgery (3), and multiple sclerosis (1). The mean age of the subjects was 38.5, with a range from 22 to 74. The mean height was 191 cm (70.5 in), weight 96.4 kg (212 lbs), and BMIof29.6kg/m2. In part 2, the simultaneous two-cartridge exposures, 9 subjects were enrolled. No subjects were excluded. 8 subjects were male, and 1 was female. Health histories included: diabetes (1), hypertension (4), GERD (2), abdominal surgeries (1) and orthopedic surgeries (3). The mean age of the subjects was 38, with a range from 19 to 59. The mean height was 178 cm (70 in), weight 98.6 kg (217.6 lbs), an BMI of 30.8 kg/m2. There were no important adverse events observed or reported. One subject in part 1 had vasovagal syncope immediately after the exposure (his pulse was checked during the syncope and he was bradycardic) but recovered quickly and reported no persistent symptoms. Another subject hyperventilated after but responded well to reassurance. One subject with a baseline CK of 672 had a CK of 2883 at 24 h. This subject was contacted by email 1 week later and had no complaints. He denied any symptoms or signs of rhabdomy-olysis during the week after the exposure. He was on a cholesterol-lowering "supplement". He was advised to have his CK (and renal function) rechecked. No additional follow up was attempted or requested. A blinded emergency physician reviewed the ECGs from both parts. There were no changes in any subject ECGs except for small changes in heart rate (<10—12 beats per minute (BPM)). No subjects had ectopic beats or a rhythm different from sinus rhythm at any point. Data for CK, potassium, pH, lactate, troponin, and catecholamine levels for both parts is shown in Table 1. Only norepinephrine and epinephrine are given here for the catecholamines as dopamine was reported as "<30" pg/mL for 36/ 44 measurements in part 1 (the 8 exceptions ranged from 31 to 47 pg/mL) and for 34/36 measurements in part 2 (the 2 exceptions ranged from 36 to 61 pg/mL). While hemoglobin was not a primary outcome, we reported it here because one investigator had raised concerns regarding hemoglobin due to findings in swine, and because it has never been published previously. The comparative blood data is presented in Table 2. Statistical differences between the parts occurred in potassium, lactate, pH, and epinephrine. The clinical significance of these differences is uncertain, though unlikely to be important. The spirometry data for both parts is presented in Table 3. The data presented is the respiratory rate, tidal volume, end tidal 02, end tidal C02, and minute ventilation for preexposure, during exposure, the first minute post-exposure, and the second minute post-exposure. The data did not show a statistical change pre-exposure to exposure for either group (except a small change in PETC02). However, the minute ventilation increased after the exposure. Two subjects in the 2-cartridge group did not take any breaths during the exposures. The comparison spirometry data is presented in Table 4. Statistical changes occurred in PETC02 and minute ventilation. Vital sign data are presented in Table 5 and comparison data are shown in Table 6. There were no statistically significant changes. Discussion Our results are consistent with the results of prior studies. Many of the same parameters have been studied by these authors and others across several CEW models including the Springer Table 1 Blood results Laboratory Value 1 Cartridge Exposure 2 Cartridge Expo sure P Value* Pre - * 1 Cartridge/2 Cartridge Exposure Median (IQR) Median (IQR) Pre -Exposure Post Exposure 1-Hour Next Day Pre -Exposure Post Exposure 1-Hour Next Day K+ 3.9 3.7* 3.9 3.8 3.9 3.8* 3.9 3.9 0.002/0.64 (mmol/L) (3.7-4.1) (3.6-3.9) (3.8-4.2) (3.7-4.3) 3.^4.0) (3.6^.1) (3.7-4.3) (3.8^.1) Lactate 0.98 3.98* 1.12 0.88 1.10 2.10* 1.14 1.10 <0.001/0.005 (mmol/L) (0.74-1.22) (2.96-4.27) (1.05-1.69) (0.65-1.17) (0.76-1.32) (1.87-2.54) (1.10-1.14) (1.00-1.35) Hgb 15.3 15.3* 15.0 15.6 15.6 15.3* 15.3 15.6 0.34/0.01 (g/d/1) (15.0-15.6) (14.3-15.6) (14.3-15.6) (15.0-16.3) (15.0-16.3) (14.6-16.3) (14.6-15.6) (14.3-16.0) Troponin 0.00 0.00 0.00 0.00 * 0.00 0.00 0.00 0.00* -/0.35 (ng/mL) (0.00-0.00) (0.00-0.00) (0.00-0.00) (0.00-0.00) (0.00-0.00) (0.00-0.00) (0.00-0.00) (0.00-0.00) pH 7.39 7.32* 7.36 7.37 7.36 7.32* 7.34 7.37 <0.001/0.12 (7.36-7.41) (7.27-7.33) (7.35-7.38) (7.35-7.41) (7.33-7.36) (7.30-7.35) (7.33-7.35) (7.33-7.38) CK 88 88 98 156* 159 152 163 294* 0.03/0.19 (U/L) (79-143) (76-141) (79-134) (183-371) (88-198) (92-199) (122-202) (145^89) NE 485 744* 547 526 532 682* 509 559 0.01/0.01 (pg/mL) (390-715) (516-924) (453-690) (359-665) (362-580) (565-1001) (433-616) (438-595) Epi 73 460* 38 27 62 666* 61 37 0.005/<0.00 (pg/mL) (34-142) (304-592) (30-117) (16-54) (45-72) (557-1194) (45-71) (26-78) 1 p values in the rightmost column are between the pre-exposure value and the value noted by CK creatine kinase, Epi epinephrine, IQR interquartile range, NE norepinephrine 410 Forensic Sci Med Pathol (2020) 16:406-414 Table 2 Comparative blood results Comparative Blood Data Comparison Points Mean Change 1 Mean Change 2 Mean Difference p Value 95% CI Cartridge Cartridges (2 Cartridges-1 Cartridge) K+(mmol/L) Pre-Exposure-Post Exposure -0.15 +0.04 +0.19 0.05 0 to 0.38 Lactate (mmol/L) Pre-Exposure-Post Exposure +2.78 +1.39 -1.39 0.01 -2.33 to -0.44 Hgb (g/d/1) Pre-Exposure-Post Exposure -0.22 -0.21 +0.01 0.98 -0.51 to 0.53 Troponin (ng/mL) Pre-Exposure - Next Day +0.000 +0.001 +0.001 0.28 0 to 0.001 pH Pre-Exposure - Post-Exposure -0.07 -0.03 +0.04 0.02 0.01 to 0.08 CK (U/L) Pre-Exposure - Next Day +98 +341 +244 0.28 -220 to 707 NE (pg/mL) Pre-Exposure-Post Exposure +278 +253 -25 0.83 -265 to 214 Epi (pg/mL) Pre-Exposure-Post Exposure +347 +737 389 0.01 91 to 687 Means are measured as (2 cartridges - 1 cartridge) first-generation Axon X26E, and the second generation X3 and (newer) X2. Several authors have studied ECG tracings before and after CEW exposure and found no significant morphologic changes or dysrhythmias [2, 3, 5-8]. The majority of these studies involved large probe spread back exposures, although one involved chest exposures (one involved abdomen to leg exposures). Likewise, our study found no important ECG changes associated with the exposures. While not a study objective, continuous ECG recording was done during spirometry except when disconnected for the exposure and no dysrhythmias or ectopy was noted in any subject after exposure. Based on animal studies, it is very unlikely to have direct cardiac effects with exposures that do not include the chest. Several authors have studied spirometry. In a prior study by Ho et al. of 15-s trunk (front and back) X26E exposures, the study subjects had increased minute ventilation during the exposures (mean 20.9 L/min compared to 16.3 at baseline for the continuous exposures) [9]. Van Meenan et al., in a study of 5-s X26E back exposures, showed a decrease in tidal volumes (described as "cessation" of normal breathing) during exposures. However, only graphical data was presented with no statistical summary. In addition, compared to other studies, these exposures were short [10]. In a study by Dawes et al. of a 10-s X3 exposure to the chest, there was no statistical change in tidal volume, respiratory rate or minute ventilation (although minute ventilation was close to significant) during the exposure with a statistically significant increase in these parameters after the exposure [11]. In a study by Ho et al. of 10-s X2 exposures to the abdomen and leg, there were significant increases in the respiratory rate and minute ventilation but a decrease in the median tidal volume during the exposures [3]. Our data is not dissimilar to the prior X3 data. There were no statistically significant changes in spirometry parameters (except for PETC02) in both groups. In both groups, minute ventilation rose in the post-exposure period. There are several possible explanations for this. One explanation is that there was some limitation on subject breathing during the exposure to prevent full respiratory compensation for the muscle-contraction induced acidosis and this was "make up" ventilation; or simply a pain response. The significance of these findings is likely low in practice. Most field exposures are less than 15 s. In Bozeman et al. only 7% of field uses included over 3 exposures (not necessarily continuous) [12]. In a study by Ross and Hazlett of 1085 "violent" arrests over 12 months with 17 agencies, the average "trigger pulls" was 2 totaling 10 s (30% one trigger pull, 55% two, and 15% 3) [13]. It would be very unlikely even in physiologically compromised subjects for short exposures (less than 15 s), even if they caused cessation of all breathing, to cause any important effects. Of particular note, the clinically important patient-oriented outcomes of PETC02 and PET02 did not show hypercarbia or hypoxia. It is not clear why the 2-cartridge group had an increase in minute ventilation compared to the 1-cartridge group. Given the rapidity of the pulses, it would not be expected that the brief "short path" time and pulse changes would make a clinical difference in respiration but this is possible. It is also not clear why the data is different from the original X26E data (the X2 data did not involve the thorax). Exposures were more lateral in the original study that could mean less bilateral thorax involvement. The difference with the Van Meenan data may be due to the difference in duration as previously hypothesized. Several authors have also studied serum markers, including troponin. None of our subjects had a positive troponin (the LabCorp reference range is 0.00-0.04). Multiple authors have measured serum troponin after exposures and none have found a troponin elevation except one 24-h reading in Ho et al. That subject had in-hospital monitoring and testing and the result was deemed spurious [2, 3, 7, 8, [14]. Back exposures would not be expected to have direct cardiac effects but indirect effects may be possible. The data here, including the ECG data, does not suggest any indirect effects other than the possibility of vasovagal induced syncope. Springer Forensic Sci Med Pathol (2020) 16:406-414 411 > x c > c p. -si 1 c O X c p. X X 12 in. are generally are necessary for optimal incapacitation [4], While this study did not study incapacitation performance, or cardiac safety, the physiologic effects of the new T7 appear to be similar to prior generation Axon CEWs. Limitations The small number of enrolled subjects limits our conclusions. Additionally, our study only used large-spread (or large spread "equivalent") back shots. Low center of mass exposures on the front (manufacturer recommended targeting) would have mechanistically had less of a respiratory effect given that thoracic muscles would not be stimulated. Because of our small study enrollment, we decided to not study these exposures. However, this may bias our study to more respiratory effects. Lastly, we did not test a probe scenario that would yield the highest PPS rate at a probe with the adaptive cross connect algorithm. We instead chose, in order to better compare both groups, exposures that would be relatively equivalent if the adaptive cross connect technology was working (two 30 cm (12-in) equivalent exposures). Conclusions In our study, the physiologic effects of the new generation Axon T7 are similar to prior generation weapons. Springer 414 Forensic Sci Med Pathol (2020) 16:406-414 Key points 1) CEWs cause modest changes in physiology consistent with the electrically-induced motor-nerve mediated muscle contraction. 2) The T7 appears to have a similar physiologic profile to prior CEWs. References 1. Sweeney JD. Transcutaneous muscle stimulation. In: Kroll MW, Ho JD, editors. TASER conducted weapons: physiology, pathology, and law. New York: Springer; 2009. p. 51-62. 2. Ho J, Miner J, Lakireddy D, Bultman L, Heegard W. Cardiovascular and physiologic effects of conducted electrical weapon discharge in resting adults. Acad Emerg Med. 2006;13: 589-95. 3. Ho J, Dawes D, Chang R, Nelson R, Miner J. Physiologic effects of a new generation conducted electrical weapon on human volunteers. J Emerg Med. 2014;46:428-35. 4. Ho J, Dawes D, Miner J, Kunz S, Nelson R, Sweeney J. Conducted electrical weapon incapacitation during a goal-directed task as a function of probe spread. Forensic Sci Med Pathol. 2012;8:358-66. 5. 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The impact of the TASER on suspect resistance: identifying predictors of effectiveness. Crime Delinq. 2010;56:70-102. Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Springer