Irnich Werner, Kroll Mark W
Faculty of Medicine, Justus-Liebig-University, Giessen, Germany.
Pacing Clin Electrophysiol. 2015 Jul;38(7):831-45. doi: 10.1111/pace.12573. Epub 2015 Feb 14.
Electrostimulation has gained enormous importance in modern medicine, for example, in implantable pacemakers and defibrillators, pain stimulators, and cochlear implants. Most electrostimulation macromodels use the electrical current as the primary parameter to describe the conventional strength-duration relationship of the output of a generator. These models normally assume that the stimulation pulse charges up the passive cell membrane capacitance, and then the increased (less-negative) transmembrane potential activates voltage-gated sodium channels. However, this model has mechanistic and accuracy limitations.
Our model assumes that the membrane capacitance is an electromechanical transducer and that the membrane is compressed by the endogenous electric field. The pressure is quadratically correlated with the transmembrane voltage. If the pressure is reduced by an exogenous field, the compression is released and, thus, opening the pores for Na(+) influx initiates excitation.
The exogenous electric field must always be equal to or greater than the rheobase field strength (rheobase condition). This concept yields a final result that the voltage-pulse-content produced by the exogenous field between the two ends of a cell is a linear function of the pulse duration at threshold level. Thus, the model yields mathematical formulations that can describe and explain the characteristic features of electrostimulation.
Our model of electrostimulation can describe and explain electrostimulation at cellular level. The model's predictions are consistent with published experimental studies. Practical applications in cardiology are discussed in the light of this model of electrostimulation.
