This is the first in a series of posts about the hows and whys of cardiac simulation, both electrophysiological and mechanical.
The heart is an extremely complicated organ. It’s composed of many different cell types, including cardiomyocytes, conduction system cells such as those in Purkinje fibers, fibroblasts, neurons, and adipocytes. However, the cardiomyocytes make up most of the weight of the heart, and are well-connected to each other by gap junctions. As a result, cardiac tissue can be reasonably well modeled as a syncytium (even though it is not a true syncytium as skeletal muscle is). This is usually formalized using either the monodomain formulation (which only considers current within and between cells) or the bidomain formulation (which also models the current outside of the cells).
Activity within individual cells is modeled using systems of differential equations typically referred to as ‘ionic models’ or ‘Hodgkin-Huxley-type’ models. These systems model how a cell moves ions around to effect changes in its transmembrane potential. It is fortunate that these models have been well-developed from their humble beginnings in the squid giant axon. Very sophisticated models of everything from said axon up to human ventricular myocytes have been created, based on patch-clamp experiments. Changes in transmembrane potential in one cell create a potential difference relative to neighboring cells, driving the flow of current from one cell to another. It is this effect that couples ionic models to the tissue model described above.
The next post in this series will delve into the different tissue and cell models offered by our CARP simulator.