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These routes include moving through a patent foramen ovale (a congenital hole connecting the right and left atria of the heart), a ventricular septal defect (a congenital hole connecting the ventricles), or a pulmonary arteriovenous fistula, where arteries in the lungs connect directly to veins without capillaries in between.
Atrial septal defect (ASD) is a congenital heart defect in which blood flows between the atria (upper chambers) of the heart.Some flow is a normal condition both pre-birth and immediately post-birth via the foramen ovale; however, when this does not naturally close after birth it is referred to as a patent (open) foramen ovale (PFO).
The VSD allows deoxygenated blood to flow from the right to left side of the heart. This blood bypasses the lungs. The lack of oxygenation in the pulmonary circulation results in cyanosis. Widely split fixed S 2 and systolic ejection murmur at the left upper sternal border Classic for a patent foramen ovale (PFO) or atrial septal defect (ASD).
The foramen ovale stays open because of the flow of blood from the right atrium to the left atrium. As the lungs expand, blood flows easily through the lungs and the membranous portion of the foramen ovale (the septum primum) flops over the muscular portion (the septum secundum). If the closure is incomplete, the result is a patent foramen ...
The operation is performed under general anesthesia. The four pulmonary veins are reconnected to the left atrium, and any associated heart defects such as atrial septal defect, ventricular septal defect, patent foramen ovale, and/or patent ductus arteriosus are surgically closed. With obstruction, surgery should be undertaken urgently.
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth. [citation needed] VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, an uncorrected VSD can increase pulmonary resistance leading to the reversal of the ...
PPHN can range from mild to severe disease. In the most severe form, infants experience severe hypoxemia resulting in cardiac and pulmonary complications. [4] As a result of low oxygen levels, infants with PPHN are at an increased risk of developing complications, such as asphyxia, chronic lung disease, neurodevelopment issues, and death.
cyanotic d-TGA + VSD neonate (unpalliated and pre-operative) Due to the low oxygen saturation of the blood, cyanosis will appear in peripheral areas: around the mouth and lips, fingertips, and toes; these areas are furthest from the heart, and since the circulated blood is not fully oxygenated to begin with, very little oxygen reaches the peripheral arteries. [2]