This article reviews the consequences of the need for the cardiac cell to be in calcium flux balance in the steady state. We first discuss how this steady state condition affects the control of resting [Ca(2+)]i. The next section considers how sarcoplasmic reticulum (SR) Ca content is controlled by a feedback mechanism whereby changes of SR Ca affect the amplitude of the Ca transient and this, in turn, controls sarcolemmal Ca fluxes. Subsequent sections review the effects of altering the activity of individual Ca handling proteins. Increasing the activity of the SR Ca-ATPase (SERCA) increases both the amplitude and rate constant of decay of the systolic Ca transient. The Ca flux balance condition requires that this must be achieved with no change of Ca efflux placing constraints on the magnitude of change of amplitude and decay rate. We analyze the quantitative dependence of Ca transient amplitude and SR content on SERCA activity. Increasing the open probability of the RyR during systole is predicted to have no steady state effect on the amplitude of the systolic Ca transient. We discuss the effects of changing the amplitude of the L-type Ca current in the context of both triggering Ca release from the SR and loading the cell with calcium. These manoeuvres are considered in the context of the effects of β-adrenergic stimulation. Finally, we review calcium flux balance in the presence of Ca waves.