We recorded the transmembrane potential in the whole-cell recording mode from small clusters (2-4 cells) of spontaneously beating 7-day embryonic chick ventricular cells after 1-3 days in culture, and investigated the effects of adding the blockers D-600, diltiazem, almokalant, and Ba⁺⁺. Electrical activity in small clusters is very different from that in re-aggregates made up of several hundred embryonic chick ventricular cells: e.g. re-aggregates have tetrodotoxin-sensitive fast upstrokes, while small clusters have tetrodotoxin-insensitive slow upstrokes (maximum upstroke velocity ~100 V s^-1 vs. ~10 V s^-1). Based on our voltage- and current-clamp results and on data from the literature, we formulated an Hodgkin-Huxley type of ionic model for the electrical activity in these small clusters. The model contains a calcium current (I_Ca), three potassium currents (I_Ks, I_Kr, and I_K1), a background current (I_b), and a seal-leak current (I_seal). I_Ca generates the slow upstroke, while I_Ks, I_Kr, and I_K1 contribute to repolarization. All of the currents contribute to spontaneous diastolic depolarization: e.g. removal of I_seal increases the interbeat interval from 392 ms to 535 ms. The model replicates the spontaneous activity in the clusters, as well as the experimental results of applying blockers. Bifurcation analysis and simulations with the model predict that annihilation and single-pulse triggering should occur with partial I_Ca block. Embryonic chick ventricular cells have been used as an experimental model to investigate various aspects of spontaneous beating of cardiac cells, e.g. mutual synchronization, regularity of beating, and spontaneous start-up and stopping of reentrant rhythms; our model now opens the possibility of investigating these topics through numerical simulation.