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A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle.
VSD: ventricular septal defect: VSR: ventricular septal rupture (see myocardial rupture) VSS: vital signs stable visual snow syndrome VT: ventricular tachycardia verotoxin VTE: venous thromboembolism: VTEC: verotoxin-producing Escherichia coli, also known as enterohaemorrhagic E. coli: VUR: vesicoureteral reflux: VWD: ventral wall defect Von ...
A ventricular septal defect is when this lower wall—the ventricular septum—has a gap in it after development. The septum is formed during development as this muscular ridge of tissue grows upward from the apex, or the tip, and then fuses with a thinner membranous region coming down from the endocardial cushions.
Taussig–Bing syndrome is a cyanotic congenital heart defect [1] in which the patient has both double outlet right ventricle (DORV) and subpulmonic ventricular septal defect (VSD).
Eisenmenger syndrome or Eisenmenger's syndrome is defined as the process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect (typically by a ventricular septal defect, atrial septal defect, or less commonly, patent ductus arteriosus) causes pulmonary hypertension [1] [2] and eventual reversal of the shunt into a cyanotic right-to-left shunt.
Heart sounds of a ventricular septal defect patient. The condition consists of atresia affecting the pulmonary valve and a hypoplastic right ventricular outflow tract. The ventricular septal defect doesn't impede the in and outflowing of blood in the ventricular septum, which helps it form during fetal life. [3] [5]
In the latter case, prostaglandin E1 is used to maintain the PDA connection until emergency corrective surgery can be completed. As oxygenated blood is mixed with deoxygenated blood in both cases, there is a reduction in the oxygen-carrying capacity. [4] It is also possible for tricuspid atresia to appear without the life-saving defects.
Reference ranges for blood tests, measured in units, including several cardiac markers. Depending on the marker, it can take between 2 and 24 hours for the level to increase in the blood. Additionally, determining the levels of cardiac markers in the laboratory - like many other lab measurements - takes substantial time.