During cardiac disturbances such as ischemia and hyperkalemia, the extracellular potassium ion concentration is elevated. This in turn changes the resting transmembrane potential and affects the excitability of cardiac tissue. To test the hypothesis that extracellular potassium elevation also alters the stimulation mechanism, we used optical fluorescence imaging to examine the mechanism of diastolic anodal unipolar stimulation of cardiac tissue under 4mM (normal) and 8mM (elevated) extracellular potassium. We present several visualization methods that are useful for distinguishing between anodal-make and anodal-break excitation. In the 4-mM situation, stimulation occurred by the make, or stimulus-onset, mechanism that involved propagation out of the virtual cathodes. For 8-mM extracellular potassium, the break or stimulus termination mechanism occurred with propagation out of the virtual anode. We conclude that elevated potassium, as might occur in myocardial ischemia, alters not only stimulation threshold but also the excitation mechanism for anodal stimulation.