The purpose of this essay is to increase the awareness on what patients, families and those involved in the treatment and follow-up can face in the long run regarding the survivors of the Fontan operation (FO) and to provide some clues to diminish the deleterious effects of the single ventricle (SV) physiology. Although a significant number of patients survive and are initially asymptomatic, most probably due to adaptation to their limitations, an active approach without being pessimistic is needed in order to prevent problems and thereby improve the long-term prognosis of these patients. When William Harvey described the circulation he stated: "Those who believe that one ventricle can drive blood full of spirit into the body and the lungs likewise, are heretics. They forget that nature, being divine, never gave a heart to any where there was no need." When Fontan and Baudet published their procedure they advised us that "this procedure is not an anatomical correction, which would require the creation of a right ventricle, but a way of physiological pulmonary blood flow restoration, with suppression of right and left blood flow mixing".1 They also described the "Ten commandments", a list of precise recommendations regarding the indications for surgery.2 Some of the problems that we see today are the result of not following their guidelines. Although they clearly defined the main purpose of this procedure, they could not anticipate the long-term implications of this improvement. More than forty years later, we are witnessing the consequences of not having a sub-pulmonary ventricle. Although clinical experience shows that to survive we do not need a pumping chamber to drive blood into the lungs, the non-pulsatile flow of both vena cava directly connected to the pulmonary circulation results in the following unintended consequences: 1) elevated central venous pressure, and 2) suboptimal cardiac output, relative to the normal two-ventricle state due to: a) impaired chronotropic response to exercise; b) decreased capability to transport a normal blood volume across the pulmonary vascular bed, resulting in reduced ventricular filling and low stroke volume; c) inability to adequately increase stroke volume during periods of increased demand; and, d) elevated systemic vascular resistance with deprived tissue perfusion and anaerobic metabolism.