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This can be accomplished by a ventricular septal defect (VSD) connecting the left ventricle to the pulmonary artery or by a patent ductus arteriosus (PDA) connecting the aorta to the pulmonary artery. In the latter case, prostaglandin E1 is used to maintain the PDA connection until emergency corrective surgery can be completed.
The severity of symptoms depends on the type of TGV, and the type and size of other heart defects that may be present (ventricular septal defect, atrial septal defect, or patent ductus arteriosus). Most babies with TGA have blue skin color (cyanosis) in the first hours or days of their lives, since dextro-TGA is the more common type.
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]
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Patent ductus arteriosus (PDA) is a medical condition in which the ductus arteriosus fails to close after birth: this allows a portion of oxygenated blood from the left heart to flow back to the lungs from the aorta, which has a higher blood pressure, to the pulmonary artery, which has a lower blood pressure.
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The failure of the circulatory system of the newborn to adapt to these changes by lowering PVR leads to persistent fetal circulation. [2] The newborn is therefore born with elevated PVR, which leads to pulmonary hypertension. Because of this, the condition is also widely known as persistent pulmonary hypertension of the newborn (PPHN). [3]