Influence of physiological and pharmacological factors on conducted electrical device safety thresholds.

Abstract

Conducted electrical devices (CEDs) deliver brief, high-voltage pulses that depolarise peripheral motor nerves and produce transient neuromuscular incapacitation. Although these pulse characteristics generally remain well below myocardial stimulation thresholds, deaths temporally associated with CED exposure have raised concerns that physiological or pharmacological factors present during deployment may reduce the cardiac safety margin or precipitate fatal arrhythmias. This review examines the potential effects of sympathetic activation, metabolic acidosis, myocardial ischaemia, heart failure, hyperthermia, alcohol, antipsychotics, cocaine, methamphetamine and MDMA on myocardial stimulation thresholds and their possible contribution to arrhythmogenic collapse. These factors generally either increase myocardial rheobase or produce only modest reductions in excitation threshold, typically insufficient to permit direct myocardial capture by short-duration CED pulses. In contrast, the same factors may markedly increase baseline arrhythmia vulnerability through conduction slowing, dispersion of refractoriness, autonomic excess, abnormal calcium handling, hypoxia, acidosis and increased myocardial oxygen demand. The evidence reviewed does not support a primary role for direct CED-induced myocardial depolarisation in most reported fatalities. However, CED deployment is itself an acute painful, stressful and incapacitating event. In vulnerable individuals with stimulant intoxication, acidosis, hyperthermia, hypoxia, impaired ventilation or structural heart disease, CED exposure may contribute indirectly to a multifactorial pathway to cardiopulmonary collapse, even where direct myocardial capture is unlikely.

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