Eisenmenger Syndrome is congenital heart disease with pulmonary hypertension and shunting from right to left turning. Pulmonary vascular resistance defects cause enlargement of the pulmonary arteries, as well as enlargement of the left ventricle. Hypoxia alveoli cause reversible vasoconstriction which increases the pressure of the pulmonary wedges. Physiological effects of inhaled nitric oxide therapy result in selective pulmonary vasodilation such that the pulmonary wedge pressure can be reduced. Although it does not affect the cardiac output and systemic arterial pressure. Inhaled nitric oxide in the pulmonary vascular is selective as it is activated by hemoglobin; selective vasodilatation in the ventilated region, local hypoxia alveoli constricts the surrounding vascular tissue and redistributes better and higher intraalveolar oxygen pressure to the ventilated lungs. Inhaled nitric oxide improves this process by increasing blood flow into a well-ventilated lung; bronchodilators; pulmonary surfactant; combining high concentrations of inspired oxygen with high concentrations of inhaled nitric oxide reduces minimum surface tension.