A variety of serious complications often associated with Fontan procedure to palliate single ventricle physiology are related to elevated central venous pressure (CVP) and diminished cardiac output (CO). This “Fontan Paradox” is a fundamental challenge because some interventions benefit one of these variables at the cost of the other. Animal models employed to address the Fontan Paradox are limited, and the multiple mechanical properties affecting CVP and CO are difficult to measure, control, and scale to humans. Although complex mathematical models of the cardiovascular system have provided insights, the need to solve model equations numerically require that all parameter values are known a priori—results only apply to a subject characterized by a specific set of assumed parameter values. In contrast, it has been shown that the equations characterizing minimal closed-loop models can be solved algebraically, yielding algebraic formulas for hemodynamic variables in terms of mechanical properties of the heart and vasculature. Therefore, the purpose of the present work is to derive algebraic formulas for CVP and CO to address the Fontan Paradox. First, we utilized a modified minimal closed-loop model consisting of a single ventricle, arterial and venous vascular compartments, and systemic and pulmonary resistances. The end-diastolic pressure-volume relationship was linearized, and mean arterial pressure was assumed to be regulated by renal control of blood volume. Equations were solved algebraically for CVP, CO, and venous pressures. The resulting formulas for CVP and CO incorporate only five groups of parameters characterizing the 1) efficiency of heart-vascular interaction, 2) relative cardiac contractility, 3) relative pulmonary resistance, 4) theoretical stroke volume at zero ventricular pressure, and 5) theoretical CO at zero CVP. Of these, only mean arterial pressure (controlled by blood volume) and systemic resistance require a choice to be made of either rectifying CVP or CO. Furthermore, these general formulas indicate that altering blood volume or systemic resistance to treat low CO has a greater negative impact on CVP in subjects with diastolic dysfunction or high pulmonary resistance. The present work thus provides a novel tool for clinical investigators to explore the mechanical basis of the Fontan Paradox.