Recent experimental studies have demonstrated that sinoatrial node cells (SANC) generate spontaneous, rhythmic, local subsarcolemmal Ca²⁺ releases (Ca²⁺clock), which occur during late diastolic depolarization (DD) and interact with the classical sarcolemmal voltage oscillator (membrane clock) by activating Na⁺/Ca²⁺ exchanger current (I_NCX). This and other interactions between clocks, however, are not captured by existing essentially membrane-delimited cardiac pacemaker cell numerical models. Using wide-scale parametric analysis of classical formulations of membrane clock and Ca²⁺ cycling, we have constructed and initially explored a prototype rabbit SANC model featuring both clocks. Our coupled oscillator system exhibits greater robustness and flexibility than membrane clock operating alone. Rhythmic spontaneous Ca²⁺ releases of sarcoplasmic reticulum (SR)-based Ca²⁺clock ignite rhythmic action potentials via late DD INCX over much broader ranges of membrane clock parameters (e.g. I_CaL and/or I_f conductances). The system Ca²⁺clock includes SR and sarcolemmal Ca²⁺ fluxes, which optimize cell Ca²⁺ balance to increase amplitudes of both SR Ca²⁺ release and late DD I_NCX as SR Ca²⁺ pumping rate increases, resulting in a broad pacemaker rate modulation (1.8-4.6Hz). In contrast, the rate modulation range via membrane clock parameters is substantially smaller when Ca²⁺clock is unchanged or lacking. When Ca²⁺clock is disabled, the system parametric space for fail-safe SANC operation considerably shrinks: without rhythmic late DD I_NCX ignition signals membrane clock substantially slows, becomes dys-rhythmic, or halts. Conclusion: The Ca²⁺clock is a new critical dimension in SANC function. A synergism of the coupled function of Ca²⁺ and membrane clocks confers fail-safe SANC operation at greatly varying rates.