Cardiac Safety of Conducted Energy Devices: Electrophysiological mechanisms, risk assessment, and forensic interpretation

Conducted Energy Devices (CEDs) or Conducted Energy Weapons (CEWs), among which the best known are the TASER® brand of CEWs, are increasingly deployed by law-enforcement agencies. Their established cardiac safety is overshadowed by temporally-associated sudden deaths, which are often directly attributed to CED discharge. Concern remains that in rare cases, high-voltage CED pulses might directly induce fatal cardiac arrhythmias. This review considers electrophysiological evidence, computational modelling, and forensic case data to understand the mechanisms governing cardiac stimulation during CED exposure. It discusses strength–duration relationships, differential excitement of neuromuscular and myocardial tissues, and compares predicted electrical stimulation thresholds with those determined by finite element modelling. This evidence is compared with clinical evidence of CED-induced malignant arrythmias. CED pulses of 50–100 μs are both too brief and too weak to depolarise cardiac myocytes under normal anatomical conditions. Finite-element and finite-integration models show typical myocardial current densities of 0.27–0.6 mA cm -2 which are more than two orders of magnitude below the short-pulse VF threshold of ∼100–150 mA cm -2 (≈ 4 mA cm -2 RMS). Layered thoracic modelling demonstrates that muscle anisotropy and chest-wall thickness diverts almost 90% of current laterally, producing cardiac field strengths far beneath depolarisation levels. Rare trans-cardiac probe alignments or thin chest walls, however, may approach capture thresholds and therefore cannot be considered completely risk-free. Current evidence indicates that in all but extreme probe geometries or paediatric exposures, CED are at minimal risk of inducing malignant arrhythmias. Forensic assessment of CED-related deaths should consider electrophysiological principles with probe placement, the timing of the collapse, and toxicological findings in order to distinguish coincidental from causally related events. • CED pulses are too short and too weak to depolarise cardiac myocytes under normal conditions. • Finite-element models show myocardial current densities ≪ ventricular fibrillation thresholds. • Anatomical factors (muscle anisotropy, chest wall depth) divert most current away from the heart. • Rare trans-cardiac probe alignments may approach capture thresholds in thin-chest subjects. • Forensic interpretation requires correlating collapse timing, probe placement, and toxicological contribution.