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Abstract
Controversy exists concerning the lethality of Tasers. These are conducted electrical weapons which incapacitate subjects by delivering an electrical charge that causes diffuse muscle contraction. In North America, over 440 deaths have been reported immediately following Taser use. Taser International has recently suggested that Tasers should not be aimed at the chest, although there is no conclusive proof that a discharge over the heart would cause an arrhythmia. The case history is presented of a young man who was shot in the chest by a Taser and presented to the emergency department in ventricular fibrillation.
- Resuscitation
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A 17-year-old man was intoxicated and became violent at home. His mother called the police who, on arrival, shocked the patient in the anterior chest with a Taser (figure 1). He immediately dropped to the ground and was handcuffed. He was observed to be cyanotic and apnoeic. Paramedics arrived within 4 min and found him to be in ventricular fibrillation and defibrillated three times en route to the hospital. He was intubated, given epinephrine, atropine, sodium bicarbonate and lidocaine. His initial rhythm on arrival at the emergency department was ventricular fibrillation. Amiodarone 300 mg was given intravenously as well as repeated epinephrine and vasopressin. At that point, heart motion was observed with ultrasound. Levophed was started and a pulse returned. He was cooled with a Coolgard catheter (Alsius Corporation, Irvine, California, USA) placed in the right groin to 32–34°. The patient lost his pulse again, was observed to be in ventricular fibrillation and was shocked at 360 J with a return of sinus rhythm. Initial laboratory values included: sodium 156 mEq/l, potassium 3.9 mEq/l, chloride 103 mEq/l, CO2 20 mEq/l, blood urea nitrogen 11 mg/dl, creatinine 1.5 mg/dl and glucose 132 mg/dl. The alcohol level on arrival was 235 mg/dl and the drug screen was positive for cannabinoids. The patient had no history of cardiac problems or past medical history. The patient remained on the hypothermia protocol for 24 h and then was gradually rewarmed. He had a prolonged hospital course with pneumonia and renal failure but was eventually discharged 2 months after his admission. He is currently doing well.
Penetrating wounds after removal of Taser barbs from the area overlying the precordium.
Discussion
Ventricular fibrillation can be precipitated by ischaemic heart disease, electrolyte disturbances, cardiomyopathy and myocarditis. To our knowledge, there is only one previously reported case of ventricular fibrillation triggered by Taser use.1 It is useful to discuss the possible mechanisms of Taser-induced ventricular fibrillation, although abundant research suggests that most Taser discharges do not result in arrhythmia.2
Tasers were initially thought to be completely safe because the skin formed a Faraday cage. This principle was first described by Michael Faraday who discovered that charge resides only on the exterior of a charged conductor, leaving the interior without electrical charge. However, it is known that, with sufficient current, a transthoracic charge will affect the heart, as in the case of cardiac defibrillation. Is the Taser always below the threshold for a cardiac effect?
Animal experiments show that, when the Taser is discharged across the chest in swine,3 myocardial stimulation occurred 50% of the time. When epinephrine was administered before the discharge, the myocardium was stimulated in 13 of 16 animals with one incident each of ventricular tachycardia and ventricular fibrillation. In a recent study in which echocardiography was used to determine the heart rhythm during the discharge of a Taser in swine, there was immediate ventricular capture in 52% of cases if the discharge was on the ventral surface of the animal.4 There may be mitigating factors determining whether cardiac capture occurs. It is possible that acidosis may lower the fibrillation threshold. Increased muscle activity, as would occur in a struggle or flight from law officers, could result in lactic acidosis. This acidosis is well described in marathon runners where lactic acid levels averaged 4.2–4.5 mmol/l (normal 0.5–2.2 mmol/l) in the finishers of the 2003 Boston marathon. Repeated Taser-induced muscle contraction may also cause acidosis in individuals being restrained. In addition, a condition referred to as ‘agitated delirium’ has been blamed for sudden cardiac arrest during the process of restraint. This is thought to be due to a terminal arrhythmia, most likely due to sympathetic sensitisation of the myocardium caused by the stress of the struggle or drugs such as cocaine.
Mechanical as well as electrical methods have been postulated as a cause of death after Taser use. Restraint asphyxia refers to the inability to breathe adequately in the prone position after restraint. In restraint asphyxia, hypoventilation and acidosis cause a terminal arrhythmia. In addition, Commotio cordis, a blow that has sufficient force to interrupt the electrical cycle of the heart, may be responsible for sudden death if the person drops suddenly forward onto the chest when muscle incapacitation occurs.
Although the mechanism of fibrillation will continue to be debated, rapid recognition of arrhythmia after Taser use can lead to successful resuscitation.
Footnotes
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; not externally peer reviewed.