Background A source-sink mechanism plays a crucial role in transmission of electrical impulse to tissue. We hypothesized that partial uncoupling of impulse source to tissue by ablation might generate ectopic beats. Methods Canine right atrial preparations (n = 5) were coronary perfused and optically mapped using ANBDQBS, a near-infrared voltage-sensitive dye, to assess the origin and spread of excitation in transmural layers. The sinus node (SN) and surrounding atrial tissue in the field of view were reconstructed after Masson-trichrome, H&E, and immunofluorescence. Masson-trichrome histology was merged with the optical mapping. Cryoablation at –70°C for >3 minutes was performed in the SN and the atrial tissue. Results At baseline, sinus impulse originated from a specific cluster of the histologically demarcated SN (n = 5, 124 ± 23 bpm). Random extensive cryoablation on the SN and atrial tissue caused de novo activation of the ectopic foci outside the field of view (n = 3/5). We also observed the ectopic focus outside the histologic SN independently producing only spontaneous electrical oscillatory waves at baseline before ablation (n = 1), which was composed of HCN4 + cells in immunohistochemistry. However, this isolated electrical activity failed to propagate to the large atrium, as evidenced by the inability of this cluster to generate P waves on the pseudo-ECG. We created partial uncoupling of the nonpropagated ectopic source to the large atrium by cryoablation. In contrast to preablation, the nonpropagated ectopic source acquired the ability to propagate to the surviving atrial myocardium and generated ectopic beats. Conclusions The current study suggests that incomplete ablation may induce ectopic beats through paradoxical improvement of impulse conduction to the cardiac tissue by reducing coupling of impulse source to atrial sink. The current study may provide a mechanistic insight and clinical implications on generation of ectopic beats.