While studies of gap junctions often cite their fundamental importance to normal electrical activation of the heart, there is little agreement on the degree of gap junction remodeling required to slow the spread of electrical activity in the heart. Our recent work suggests that cardiac myocytes may electrically communicate through very narrow extracellular clefts by a theoretical mechanism called ephaptic coupling. Ephaptic coupling is not only theoretically faster than gap junctional coupling, but may also ensure stable electrical communication under a wide variety of pathological conditions including the loss of gap junctions. Our data suggests that sodium channels necessary for depolarizing myocytes are densely localized adjacent to gap junctions across a cleft of 10-20nm; a theoretical distance that is necessary for ephaptic coupling. Disrupting ephaptic coupling either ionically or osmotically can unmask defective sodium channels or gap junctions. Additionally, we've found that changing extracellular sodium, potassium, or calcium within a physiologic range can modulate the determinants of ephaptic coupling and this suggests a more sobering issue: the foundational tool of ex vivo and in vitro biology (buffers) used to study the spread of electrical activity in the heart may yield investigator dependent results simply based on ionic buffer composition.