Introduction

Electronic control devices (ECDs), also referred to as conducted electrical weapons, are called less lethal or nonlethal weapons because their intent is to incapacitate temporarily, not to kill. The ECD manufactured by TASER International, model X26, is the device most widely used by law enforcement, corrections, and military establishments worldwide. It is a handgun-shaped weapon that uses compressed nitrogen to shoot two 9- or 12-mm barbs from a cartridge into the clothes/skin of an individual. Wires connect the barbs through the cartridge to the gun through which is delivered an initial 50 000-V shock, followed by 100-microsecond pulses at ≈19 Hz (≈1140 times per minute), 2 to 4 amps, 100-microcoulomb charge per pulse, and ≈1200 V.¹ The standard 5-second shock cycle can be halted earlier, repeated, or sustained longer by the user. If electrical currents from both darts connect with the subject, pain and skeletal muscle contraction generally result in rapid incapacitation. The exposed electrodes of the gun can be pressed against the skin (drive stun mode) to cause pain without muscular contractions. ECDs are not considered firearms and therefore are not regulated by the Bureau of Alcohol, Tobacco, Firearms, and Explosives.

Editorial see p 2406

Clinical Perspective on p 2422

The safety of ECDs has been questioned. Amnesty International documented 334 deaths that occurred after exposure to ECDs between 2001 and 2008.² To date, no peer-reviewed publication has definitely concluded that ECD shocks can precipitate ventricular fibrillation (VF) causing sudden cardiac arrest and death in humans.

The purpose of this report is to present an analysis of sudden cardiac arrests and deaths following ECD exposure that occurred in 2006 (case 1), in 2008 (cases 2, 4, 5, and 8), and 2009 (cases 3, 6, and 7) and to weigh the existing animal and clinical data to determine whether an ECD shock can cause cardiac electrical capture and, in so doing, provoke ventricular tachycardia (VT) and/or VF in humans.

Methods

The medical information used for this article was approved by the Institutional Review Board of the Indiana University School of Medicine. Written and 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. In each instance, when available, police, medical, and emergency response records, X26 dataport interrogation, automated external defibrillator information, ECG strips, depositions, and autopsy results were analyzed.

Results

All individuals were previously clinically healthy males who received shocks from the TASER X26 ECD with 1 or both barbs in the anterior chest near or over the heart and developed loss of consciousness during or immediately after the ECD shock (Table). First recorded rhythms were VT/VF in 6 and asystole (after ≈30 minutes of nonresponsiveness) in 1 (Figure). An external defibrillator reported a shockable rhythm in 1, but no recording was made. Except for case 1, all died.

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Discussion

New Observations

This report adds detailed observations on 8 new cases of sudden cardiac arrest/death following ECD shocks to those already in the literature.

Published Reports

The first published report of sudden cardiac arrest after ECD discharge was a letter to the editor about a 14-year-old boy who immediately lost consciousness after a 17-second ECD chest shock.³ He initially had a pulse and was breathing but 2 minutes after collapse had VF documented in an ECG recorded by paramedics; he was ultimately resuscitated. The accuracy of statements made in this publication was contested,⁴ but sworn testimony by a paramedic who witnessed the entire event⁵ stated that VF was recorded 2 minutes after the ECD shock.

The second observation was of a 17-year-old man who received ECD applications of 25 and 5 seconds in the anterior chest. He immediately dropped to the ground and was observed to become cyanotic and apneic. The initial rhythm was asystole recorded >10 minutes after the ECD application. He was eventually resuscitated with hypothermia⁶ but had memory impairment.

The third publication reviewed the presenting rhythm in 56 sudden deaths temporally proximate to discharge of a TASER ECD, finding VF in 4, but concluding that only 1 could be related to ECD discharge. That individual was a 25-year-old man who received ECD shocks in the anterior chest for 16, 5, and 5 seconds. He immediately lost consciousness, and prompt application of an automated external defibrillator showed VF. After 2 shocks, he could not be resuscitated. The report stated that “…the time course and the electrode location are consistent with electrically induced VF.”⁷

Animal and Clinical Studies

The concept of cardiac capture by transthoracic electrical impulses in humans was pioneered by Zoll,⁸ replicated by many others subsequently,⁹ and is now a standard part of resuscitative equipment. The threshold for transthoracic cardiac electrical capture is 100 microcoulombs,¹⁰ which is the output of the TASER model X26.¹

Studies in pigs,^11–15 sheep,¹⁶ and humans¹⁷ established that transthoracic shocks from the TASER model X26 or a new prototype ECD¹⁸ caused cardiac electrical capture. In addition, porcine research showed that such electrical capture could provoke VF at normal^12–15 or higher-than-normal¹¹ TASER model X26 outputs. Vectors encompassing the heart and probes closer to the heart facilitated electrical capture.^11,12,15 In 1 study, standard 9-mm probes produced VF in pigs at dart-to-heart distances of 4 to 8 mm.¹⁹ In another porcine study testing barbs at 5 locations, the authors found that 5-second shocks from the TASER X26 produced cardiac electrical capture without VF at normal outputs but that VF induction at increased output was initiated when the capture ratio was ≤2:1. Bracketing the heart with darts in a sternal notch to cardiac apex position along the cardiac axis resulted in the lowest safety margin for VF induction. The authors stated that cardiac disease could reduce the VF threshold and provide a substrate for arrhythmia induction and that rapid ventricular capture was the likely mechanism of VF induction.²⁰

In addition to the importance of probe location, longer-duration shocks at normal TASER X26 outputs appear more likely to induce VF.^13,14 Although it is possible that body size might influence cardiac capture and development of VF, clearly big people can still develop VF from an ECD shock (see the Table).

Determining whether an ECD shock caused cardiac electrical capture can be difficult because the shock produces electrical interference in the ECG recording. In a clinical study of a new TASER ECD prototype, cardiac electrical capture monitored echocardiographically was shown to occur at 240 bpm in 1 volunteer.¹⁸ In addition, a case report about a man with an implanted pacemaker demonstrated cardiac electrical capture at rates exceeding 200 bpm during each of two 5-second TASER model X26 applications that was found when the pacemaker was interrogated.¹⁷

Multiple clinical studies have not shown ECD-induced VF in healthy volunteers. But, because of ethical considerations, even those few studies testing actual barbs to the anterior chest and single 15-second exposures²¹ may not be able to replicate the clinical scenario of a frightened/fleeing/fighting individual.

Several epidemiological studies have not shown a link between ECD shocks and sudden cardiac death.^22,23 However, a recent review²⁴ determined that single shocks in healthy people “…could have deleterious effects when used in the field, in particular if persons receive multiple exposures…or present with medical comorbidities.”

Proposed Mechanism of ECD-Induced Sudden Cardiac Arrest

Electrical stimulation can induce VF by causing ventricular capture during the vulnerable period of the T wave of the previous beat or ventricular capture at rates too fast for ventricular activation to remain organized. Rapid pacing also can cause a precipitous blood pressure fall, leading to ischemia. VF by rapid pacing was often the outcome of runaway pacemakers many years ago.²⁵

It is clear from the information cited above that an ECD shock to the chest can produce cardiac electrical capture at rapid rates in animals and humans.^11–18 Furthermore, it is clear that VF has been documented as early as 2 minutes after an ECD shock to humans.^3,5 What is lacking is the actual ECG recording of VF induction during an ECD shock in humans, a practical impossibility unless it fortuitously occurred in an individual with a recording device already in place. Even then, electrical interference may obscure the recording. However, ECD-induced VT and VF have been clearly and repeatedly shown in pigs.^11–15,19 In 1 example, intravenous epinephrine in an anesthetized pig, infused at a concentration that increased the spontaneous sinus rate 50% to replicate the clinical “fight or flight” situation, improved the TASER model X26 electrical capture ratio from 3:1 to 2:1 and resulted in VF induction.¹²

Thus, from the pig studies, a likely clinical scenario is that ECD induced cardiac electrical capture at rates of 200 to 240 bpm (a 6:1–4:1 ratio), as already shown in humans.^17,18 The increased rate plus sympathetic effects can shorten ventricular refractoriness to permit further ECD-induced rate acceleration that eventually causes VF from the rapid rate or R on T. Because a sharp blood pressure reduction results from the rapid rate, repeated shocks or those exceeding the recommended 5-second ECD discharge can add an ischemic component and would be more likely to provoke VF. Furthermore, on the basis of clinical electrophysiological studies performed over many years, the presence of underlying heart disease or arrhythmogenic drugs would be expected to facilitate VF induction by electrical stimulation. Finally, an individual falling forward and then lying prone may be at even greater risk for cardiac capture since the heart can move closer to the chest wall and hence, be closer to the barbs and site of stimulation. The fall might even push the barbs into the skin to a greater depth.

Certainly not every in-custody death occurring after ECD deployment is due to the effects of the ECD shock. Restraint asphyxia and the concept of “excited delirium” are among other explanations.²⁶ Excited delirium may be a form of takotsubo cardiomyopathy.²⁷ Considering the fact that extreme sympathetic stimulation likely accompanies most restraint attempts, particularly those with ECD discharge, and the relatively few reported sudden deaths, it seems more logical to conclude that the ECD rather than sympathetic stimulation was responsible for the sudden death.

Alternative explanations such as excited delirium would be more relevant when there was a significant time delay between ECD deployment and loss of consciousness/responsiveness or death.²⁸ However, when loss of consciousness/responsiveness occurs during/immediately after an ECD chest shot, as it did in each of the cases above, and the subsequent rhythm is VT/VF or asystole (if a long time has elapsed without resuscitation) with no other cause apparent, it becomes difficult to exonerate the effects of the shock. It is also possible that combinations exist. For example, prolonged QT interval in takotsubo cardiomyopathy or metabolic changes from prolonged or repeated shocks might predispose to pacing-induced VT/VF.

Several victims were alleged to have structural heart disease (cases 2, 4, 7, and 8) and/or had elevated blood alcohol concentrations (cases 1, 3, 4, and 8). Although sudden death caused by underlying heart disease or alcohol is possible, one would have to postulate that the heart disease or alcohol coincidentally induced sudden loss of consciousness precisely at the time of ECD application. Far more likely is that stimulation from the ECD in the presence of structural heart disease and/or alcohol intoxication induced VT/VF. Clinical electrophysiology studies over many years have established that the presence of structural heart disease facilitates electrical induction of VT/VF, as does alcohol.²⁹

Institutional Reviews

A contemporary review by the National Institute of Justice concluded that the case reported as a letter to the editor³ was ECD-induced VF and stated that an ECD “may induce rapid ventricular pacing or VT in an individual who appears to be in satisfactory condition…lead[ing] to VF after a short delay,” and therefore “use involving the area of the chest in front of the heart area is not totally risk free.”³⁰ The Report of the Braidwood Commission of Inquiry,³¹ after an ECD-related death recorded on video in the Vancouver, BC, airport, stated, “There is evidence that the electrical current from a conducted energy weapon is capable of triggering ventricular capture…and that the risk of ventricular fibrillation increases as the tips of the probes get closer to the wall of the heart…[I]f a person dies suddenly and from no obvious cause after being subjected to a conducted energy weapon, death is almost certainly due to an arrhythmia.”

Incidence

Sudden death occurs infrequently after ECD deployment, considering the number of ECD applications and the apparently few reported sudden deaths. However, the actual incidence of death when the darts are impaled in the chest is unknown because accurate numerators and denominators are uncertain owing to potential underreporting of total number of sudden deaths (numerator) and the actual number of chest shocks that might cause cardiac electrical capture (denominator). ECD applications without 1 or both probes in the anterior chest would not be expected to influence cardiac rhythm and likely make up a large number of the total applications (denominator) cited. Until a detailed database of ECD deployments and outcomes is created, the exact incidence will remain unknown.

Clinical Implications

It is important to stress that the purpose of this article is not to condemn ECD use by trained professionals. Law enforcement experts must make those decisions, not physicians. Intuitively, one would expect a less lethal weapon to reduce in-custody–related sudden deaths and to be preferable to firearms. Such may not always be the case, however. One study³² noted that the rate of in-custody sudden deaths increased >6-fold and the rate of firearm deaths increased >2-fold in the first full year after ECD deployment compared with the average rate in the 5 years before deployment.

The main purpose of this article is to make ECD users aware that cardiac arrest caused by VF can result from an ECD shock. Users should be judicious in how and when to use the ECD weapon, avoid chest shocks if possible, as TASER International recommended in September 2009, monitor the person after an ECD shock, and suspect this adverse response in any victim who loses consciousness. Users should be prepared to resuscitate, including deployment of an automated external defibrillator if indicated.

Limitations

The incidence of ECD-induced sudden cardiac arrest/death cannot be determined without accurate data compiled in a national registry of ECD deployments and outcomes. Such a registry should also chart precise dart locations and should be administered and reviewed by an independent oversight group.

The major limitation of this study is not having an ECG recording during ECD application, a practical impossibility in the field situation, as noted earlier. The hard facts of each encounter are 2 events separated in time: ECD deployment and the recorded ECG. The explanation of the cause of the events in between, ie, the loss of consciousness/responsiveness and sudden death, is based on the animal and clinical data detailed above. However, in cases 4, 6, and 8, reports stated that a pulse and/or respirations were recorded initially, which would seem to be incompatible with ECD-induced VF. Yet, the victims were totally unconscious/unresponsive directly after the ECD discharge without any other explanation (no head trauma, seizure activity, etc). Although it may be possible that the sudden loss of consciousness was not due to the effects of the ECD, it is my opinion that finding a pulse (often radial) could have been spurious during the tumultuous event and that agonal breathing could be mistaken for normal respirations. It is also possible that a pulse and respiration were present initially if the first rhythm was VT before VF, as has been found in the ECD animal studies.¹² In fact, in 1 porcine study,¹³ ECD discharge induced a stable monomorphic VT that remained for ≈3 minutes before degeneration to VF. An example of recording an initial pulse and respiration immediately after ECD-induced loss of consciousness was given in the published New England Journal of Medicine letter³ in which a paramedic, present during the entire ECD deployment, felt an initial pulse of 100 (counted for 15 seconds) and respirations of 16,⁵ with VF documented by ECG 2 minutes later. Normal breathing has been documented in pigs and sheep for a minute after the onset of ventricular fibrillation and in humans for at least the first 12–15 seconds.^33,34 From these observations, it is clear that continuous monitoring of vital signs and ECG, if available, in an individual unconscious following ECD deployment, should be mandatory.

Conclusions

The animal and clinical data support the conclusion that ECD shocks from a TASER model X26 delivered via probes to the chest can cause cardiac electrical capture. Furthermore, if the capture rate increases sufficiently or if R on T occurs, the development of VF, either directly or via a transition through VT, occurs in animals and, in my opinion, in humans as well. How often this happens is unknown. Although it would seem more likely to occur in individuals exposed to potentially arrhythmogenic drugs, in those who have structural heart disease, and after long or repeated ECD shocks, electrophysiological studies in humans clearly show that only 1 or 2 extra stimuli can provoke VT/VF in particularly susceptible individuals.

Sources of Funding

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

Disclosures

Dr Zipes has served (and in the future may serve) as a paid plaintiff expert witness in ECD-related sudden cardiac arrest/death cases. However, that role has provided access to critical and detailed records necessary to determine the potential for ECD-induced sudden cardiac arrest and death. Despite this conflict, the author has attempted to present the salient facts about the cases and to offer scientific evidence, credible argument, and logic to support the conclusions to a reasonable degree of medical certainty.

Footnotes