In general, high-voltage injury is more dangerous than low-voltage injury A higher voltage is more likely to cause “locking-on” and associated deep tissue injury, although its tendency to throw victims from the source of current may mitigate this effect The possibility of head and cervical spine injuries must be considered in these cases The value of the current, or amperage, is of even greater importance than the voltage Flow as low as to 10 mA may be perceived as a tingling sensation Progressively higher flows may paralyze muscles and ventilation, precipitate ventricular fibrillation, and cause deep tissue burns Clinical Recognition Electrical injury may produce a variety of clinical sequelae, ranging from local damage to widespread multisystem disturbances Victims of the most severe accidents are commonly pulseless, apneic, and unresponsive Current that passes directly through the heart may induce necrosis and ventricular fibrillation Brainstem (medullary) paralysis or tetanic contractions of thoracic muscles may result in cardiopulmonary collapse Lightning injury is capable of inducing asystole, from which the heart may recover spontaneously, but the accompanying respiratory failure is commonly prolonged Unless ventilation is initiated promptly, hypoxia leads to secondary ventricular fibrillation and death Other cardiac disorders, including arrhythmias and conduction defects, are common among survivors Supraventricular tachycardia, atrial and ventricular extrasystoles, right bundle branch block, complete heart block, and prolongation of the QT interval are most common Complaints of crushing or stabbing precordial pain may accompany nonspecific ST–T wave changes Some patients sustain myocardial damage or even ventricular wall perforation Despite evidence of important cardiac injuries, patients without secondary hypoxic–ischemic injury usually regain good myocardial function Nervous system injury is also common and may involve the brain, spinal cord, peripheral motor and sensory nerves, and sympathetic fibers Loss of consciousness, seizures, amnesia, disorientation, deafness, visual disturbances, sensory deficits, hemiplegia, and quadriparesis occur acutely but may be transient Vascular damage may produce subdural, epidural, or intraventricular hemorrhage, and patients with brain hemorrhage or ischemic injury may become comatose Additional problems develop within hours to days after injury The syndrome of inappropriate antidiuretic hormone secretion may precipitate cerebral edema Electroencephalograms reveal diffuse slowing, epileptiform discharges, or burst suppression patterns, but these may not have prognostic significance Spinal cord dysfunction more often results in motor than sensory deficit Peripheral neuropathies with patchy distribution may reflect direct