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As shown in Chapter 14, along the track of current flow, there are measurable changes in temperature due to the effect of joule heating. That is, the tissue in the current path presents a finite resistance to the flow of current which, in turn, leads to a local dissipation of electrical energy given by I2R where I is the local current and R is the electrical resistance measured at the same point. According to the first law of thermodynamics, this energy appears as an increase in the internal energy of the tissue and manifests itself as a rise in the local temperature. Tropea and Lee (Chapter 14) show that these temperature increases can be substantial depending upon proximity to the point of entry and the type of tissue. Because of these elevated temperatures, it is highly likely that the injury experienced by tissue, and hence, the cells that make up the tissue, has two components, one electrical and the other thermal. It is also just as likely that these two modes of cellular injury can be uncoupled and addressed independently of one another. The only coupling that exists is a consequence of the fact that all the thermodynamic and electrical tissue properties depend upon the local temperature.
In order to develop therapeutic protocols for the treatment of tissue damaged by either of these modes of injury, it is essential to understand both the fundamental mechanisms and the time progression of the injury, i.e. the kinetics of the damage processes.
Rhabdomyolysis is a characteristic clinical feature of electrical trauma. The release of large quantities of myoglobin into the intravascular space and the frequent localization of technetium-99 in skeletal muscle are common manifestations. It was this attribute of electrical trauma victims that caused several experienced clinicians to liken electrical trauma to the mechanical crush injury in its clinical manifestations. More than a decade later, the pathogenic mechanisms responsible for rhabdomyolysis following electrical trauma have yet to be specifically identified by clinical studies. While heat generation by the passage of electrical current (joule heating) has commonly been believed to be the only mediator of tissue injury, over the past few decades considerable evidence has accrued suggesting that other nonthermal mechanisms may be important.
In many cases of electrical trauma, particularly when the duration of electrical contact is short, heating is predictably insignificant in some regions in the current path where skeletal muscle damage is common (see Chapter 14). This information has been the motivation to postulate that in these instances cell membrane rupture due to the induced transmembrane potential may be the important mechanism of cellular damage. This chapter describes the rationale for the hypothesis and details the results of experiments designed to test its validity.
For a given applied electric field, the magnitude of the induced transmembrane potential imposed by the field depends on the cell size and orientation in the field.
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