TASER Electronic Control Devices Can Cause Cardiac Arrest in Humans
2014; Lippincott Williams & Wilkins; Volume: 129; Issue: 1 Linguagem: Inglês
10.1161/circulationaha.113.005504
ISSN1524-4539
Autores Tópico(s)Cardiac Arrest and Resuscitation
ResumoHomeCirculationVol. 129, No. 1TASER Electronic Control Devices Can Cause Cardiac Arrest in Humans Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBTASER Electronic Control Devices Can Cause Cardiac Arrest in Humans Douglas P. Zipes, MD Douglas P. ZipesDouglas P. Zipes From the Indiana University School of Medicine, Indianapolis. Originally published7 Jan 2014https://doi.org/10.1161/CIRCULATIONAHA.113.005504Circulation. 2014;129:101–111IntroductionThe 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 111PurposeThe 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.BackgroundA 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 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.Table. Summary of the 8 Cases Reported as Having Cardiac Arrest After X26 AdministrationCaseAge, yHeight/Weight, lbLength of ECD Shock(s), sResponse to ECD ShockTime to Initial ECG AfterECD Shock, minInitial Recorded RhythmDrug ScreenCardiacFindings at AutopsyComments1486 ft 0 in/1555, 8, 5LOC toward end of last ECD cycleSeveralVT/VFBAC 0.35 g/100 mL; THC presentSurvived with memory impairment; normal echocardiogram5 AED shocks, intravenous epinephrine, and lidocaine eventually restored a perfusing rhythm2175 ft 7 in/17037, 5LOC toward end of a 37-s cycle>4.5VFNegative410 g; focal atherosclerosis; plaintiff pathologist: normal; defense pathologist: HCM3 defibrillating shocks and an additional 3 shocks from a second AED at least 9 min after the collapse failed to resuscitate3175 ft 8 in/1155ILOC>5VFBAC 0.25 g/100 mL; THC present270 g; normal heartAsystole developed after the AED shock and then PEA; subsequently, VF recurred and a second AED shock was delivered, followed by asystole/PEA; could not be resuscitated4245 ft 10 in/17611ILOC≈10AED: "shockable rhythm"; asystole after shock; no recordings availableBAC 0.319 g/100 mL400 g; plaintiff pathologist: no specific pathology; defense pathologist: lymphocytic myocarditisSaid to be breathing initially with a weak radial pulse; resuscitated in hospital; life support withdrawn after 3 d because of anoxic encephalopathy5336 ft 2 in/22013 shocks totaling 62 s in <3 minLOC toward the end of multiple shocks≈13Fine VF vs asystoleGabapentin 31 μg/mL470 g; 10%–20% narrowing of the LAD; normal histologyGabapentin taken for seizure disorder6245 ft 6 in/14449, 5LOC toward end of 49-s shock≈10VT/VFNegative366.7 g; normal gross and microscopic findingsSaid to be breathing initially; could not be resuscitated7165 ft 3 in/1305ILOC≈10VT/VFTHC380 g; medical examiner diagnosis: right ventricular cardiomyopathy, disputed by plaintiff's expert6 AED shocks for VT/VF resulted in asystole/PEA; could not be resuscitated8235 ft 9 in/17321, 7, 3LOC toward end of 21-s shock≈30AsystoleBAC 0.111 g/100 mL400 g; mild interstitial fibrosis of compact atrioventricular node; interstitial fibrosis, atrophy, and vacuolization of penetrating and branching bundleSaid to be breathing with pulse initially; could not be resuscitated; cardiac pathologist could not determine whether changes contributed to deathAED 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;125:2417–2422.2Download figureDownload PowerPointFigure 1. Picture at autopsy of case 3 with TASER X26 barbs still in place (circles). The heart at autopsy was normal.Download figureDownload PowerPointFigure 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.Download figureDownload PowerPointFigure 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;125:2417–2422.2Download figureDownload PowerPointFigure 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.Download figureDownload PowerPointFigure 5. Top, ECG during resuscitation attempt. Bottom, Picture of case 8 at autopsy showing TASER X26 barb marks (circles).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."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 7A 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 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 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 8The police video (Figure 4 and Movie I in the online-only Data Supplement.) for this case helps establish causality. A 23-year-old 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 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 CaseSince 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.IncidenceThe 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.9TASER 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.12Animal ResearchThe 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.13A 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).Download figureDownload PowerPointFigure 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.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 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:Download figureDownload PowerPointFigure 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.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.17Recent 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.20Drive-Stun CaptureTwo 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 ArrestThe 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 DistanceAs 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-to-heart 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 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 dart-to-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 ResearchMultiple 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 dar
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