Electrophysiological basis of mono-phasic action potential recordings.

Monophasic action potentials (MAPs) have been recorded for over a century, however, the exact mechanism responsible for their genesis has yet to be elucidated fully. The goal of the paper is to examine the physical basis of MAP recordings. MAP recordings are simulated by modelling a three-dimensional block of cardiac tissue. The effect of the MAP electrode is modelled by introducing a large, non-specific leakage conductance to the small region under the electrode. From the spread of the electrical activity, the equivalent extracellular current flow can be efficiently determined. These computed current sources are then input into a boundary element model of the tissue to determine the surface potentials. Finally, differences in surface potentials are used to compute waveforms that closely resemble MAP recordings. By varying model parameters, the mechanisms responsible for the MAP are determined, and a theory is put forward that can account for all observations. It is hypothesised that the leakage current causes the formation of a double-layer potential with a strength equal to the difference in transmembrane voltage between the regions under the electrode and those outside the electrode, leading to a recorded potential that mimics the transmembrane voltage outside the electrode region, although offset. Based on experimental MAP recordings, an equivalent leakage channel with a conductance of 0.1 mS cm-2 and a reversal potential of -43 mV is introduced by the electrode.