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Mechanisms of Electrical Injury

To understand the effect of electric forces on biological systems, it is helpful to think in terms of bioelectric circuits. The major portion of cellular energy, for example, is expended in maintaining the difference in electrolyte concentrations (and secondary transmembrane potentials) across cell membranes. Ions leaking across membranes by electrodiffusion are pumped back in by ATP-driven pumps. The cell membrane properties which limit this leakage include resistance to ion transport, which in turn serves to conserve energy.


Strong electric fields can damage biological tissues by at least two mechanisms: Joule heating and electroporation (Fig. 2). When contact is through an electric arc, thermoacoustic blast force can significantly add to the injury. All these mechanisms lead to increased cell membrane permeability and energy depletion. In Joule heating, the passage of electric current through tissues causes their temperature to rise, leading to disruption of cell membranes at temperatures greater than 42°C, disruption of intramolecular bonds in proteins, with loss of conformation (denaturation) at slightly higher temperatures (<45°C), and denaturation of DNA at temperatures above 65°C. Heat damage is related to duration of exposure: The higher the temperature, the shorter the exposure time required for adverse effects. In most cases of high-voltage electrical shock (<10 kV), heat damage occurs instantaneously at contact points but requires 1-3 seconds to injure deeper tissues (6). Thermoacoustic blast can also cause a significant blunt trauma and associated fall injuries.

Because normal physiology involves so many applications of electrical forces, ranging from neuromuscular signaling to coordination of wound healing, biological systems are very vulnerable to application of supraphysiologic electric fields. Therefore, even when the injury doesn't involve any visible tissue damage, electric shock survivors may experience significant consequences.