The heart is mildly to moderately enlarged with reduced blood flow in the pulmonary circulation, a pressure difference between the enlarged right atrium and the functional right ventricle, and a right-to-left intracardiac shunt. This symptom is part of the stenosis of Ebstein’s syndrome. In Ebstein syndrome, also known as Ebstein malformation, there is often interatrial traffic. If the tricuspid valve lesion is very mild and an atrial septal defect is present, then a left-to-right shunt can occur at the atrial level; or, because the tricuspid valve lesion is mild and the foramen ovale is closed, there will be no shunt at this time. In the first two cases, there is often no clinical cyanosis; in the third case, there is cyanosis, and in a few patients, even though there is no obvious right-to-left shunt, there can be mild clinical cyanosis due to low cardiac output and increased arteriovenous oxygen difference, and in addition, in the functional right ventricle, systolic pressure can be normal, while diastolic pressure is often increased, similar to constrictive pericarditis, with elevated systolic and diastolic pressures in the atrial chambers, and there can be systolic pressure difference on both sides of the pulmonary valve. The former may be due to a tricuspid leaflet that is too long and partially obstructs the right ventricular outflow tract; the latter is due to tricuspid valve malformation and tricuspid orifice stenosis. Reasons for right-to-left intracardiac shunt: Pulmonary circulation blood flow (neuromodulation of pulmonary circulation vessels is innervated by sympathetic and vagal nerves. The direct effect of stimulation of sympathetic nerves on the pulmonary vessels is to cause constriction and increased resistance to blood flow. However, in the overall situation, vasoconstriction of the vasculature of the body circulation during sympathetic excitation squeezes some of the blood into the pulmonary circulation, which increases the blood volume within the pulmonary circulation. Catecholamines in the circulating blood have the same effect. Stimulation of the vagus nerve causes pulmonary vasodilation. Acetylcholine also causes pulmonary vasodilation, but is broken down and inactivated after flow through the lungs) is reduced, and there is a pressure difference between the enlarged right atrium and the functional right ventricle.