In this paper, a bifurcation analysis of a recently proposed reduced order cardiac cell model is performed to obtain insights into the mechanisms of control of the sinoatrial node pacemaker activity. The objective is to improve the understanding of cardiac arrhythmias caused by abnormal automaticity. The bifurcation structure of the model is studied as a function of the maximal conductances of six sarcolemmal currents: the sodium, calcium, background calcium and potassium currents, the sodium potassium pump and the sodium calcium exchanger. All these parameters, except for the sodium current, allow when varied the annihilation of the physiological rhythmic activity through Hopf bifurcation points. The background calcium current seems to be the current responsible for cycle length sensitivity in the physiological zone and then it appears as the main control input of the pacemaker activity.