Subjects with Fontan physiology (Group I and II) have a unique physiology where both the superior vena cava (SVC) and inferior vena cava (IVC) are connected directly to the pulmonary arteries thereby bypassing the heart. This palliation scheme allows for separation of the pulmonary and systemic circulations in patients with univentricular hearts and essentially eliminates cyanosis. These patients have non-pulsitile pulmonary artery flow with elevated central venous and portal venous pressures. Therefore, it is suspected that these patients will have increased production of substance P and VIP. In addition, a fenestration (or hole), is created between the Fontan conduit and the atrium at the time of Fontan surgery in order to lower central venous pressure and increase cardiac output by creating a right to left intracardiac shunt. It is suspected that these patients will have elevated systemic venous and arterial levels of vasoactive peptides as a result of 1) increased hepatic/gut production, 2) decreased pulmonary vascular clearance, and/or 3) intracardiac right to left shunting. Studying these subjects will allow us to determine how systemic venous and systemic arterial levels of Substance P and VIP are altered by the Fontan circulation. By comparing systemic arterial and venous levels of vasoactive peptides among control, Glenn physiology and Fontan physiology groups we hope to measure differences in vasoactive peptide levels that could be responsible for the development of PLE and PB in Fontan physiology patients.