Other structural congenital heart defects include the following: Single ventricle with or without pulmonary pulmonary atresia with an intact ventricular septum Double output in the right ventricle Ebstein’s anomaly Congenital corrected transposition spectrum of single ventricle These anomalies include any complex lesions with only one functional ventricle. Included are a hypoplastic right ventricle (RV) and left ventricle (LV) and, more rarely, a completely undifferentiated single ventricle. Surgical procedure ensures an adequate blood flow to the lungs via an anastomosis between the systemic circulation and the pulmonary artery (eg modified Blalock-Taussig shunt. [Tetralogy of Fallot: Final Operation]) in patients with a decreased pulmonary blood flow or protects the pulmonary vasculature against high pressure when pulmonary circulatory stress is by the banding of the pulmonary artery. Later, the Fontan procedure (tricuspid atresia: treatment) may be used as a final treatment, to convert the single functional ventricle to a left ventricle. Pulmonary atresia with intact septum This anomaly is most often associated with hypoplasia of the tricuspid valve and the right ventricle. Coronary artery anomalies, especially fistulous connections of the coronary arteries for hypoplastic RV and coronary stenoses are widespread and have a huge impact on the prognosis and the surgical options. Double output of the right ventricle This abnormality is associated with a very wide range in anatomy and physiology, which is dependent on both the size and the position of the VSD (VSD), as well as on the presence and extent of pulmonary stenosis. In the most common type with a subaortischen VSD complete correction is possible with a closure of the VSD by a redirection of the LV outflow is carried out in the aorta. Ebstein’s anomaly This anomaly consists of a variable apical shift and dysplasia of the septal and smaller sailing of the tricuspid valve with a dysplasia, with simultaneous normal origin of the anterior leaflet. These anomalies relocate the effective valve opening downwards, which results in a hazard of the operation of the RV in an atrial portion contiguous with the valve opening. This anomaly is associated with the use of lithium during pregnancy. Associated anomalies include atrial septal defect, pulmonary stenosis and Wolff-Parkinson-White syndrome. There is a remarkably broad spectrum of findings ranging from strongly cyanotic neonates cardiomegaly with mild cyanosis in infancy to a previously asymptomatic adults with atrial or supraventricular tachycardia reentry mechanism. The onset of symptoms depends on the degree of anatomical and functional disorder of the tricuspid valve and the presence of accessory pathways (eg. As Wolff-Parkinson-White syndrome). If the symptoms resulting from a heavy dysfunctional tricuspid valve, surgical correction should be considered. Congenital corrected transposition This anomaly is relatively rare, accounting for 0.5% of congenital cardiac malformations from. The normal embryological wrap of the fetal heart tube is reversed, resulting in atrioventricular and ventrikuloarterialen unconformity. As a result, the right atrium to connect to a right side and the left atrium LV morphological a compound having a left-side morphological RV. In almost all cases, the morphological LV connects the pulmonary artery and the morphological RV connects to the aorta. The circulation is thus “corrected” physiologically, but associated anomalies are in the majority of patients, including VSD, pulmonary stenosis, Ebstein’s anomaly, or other dysplasia of the left side tricuspid valve, congenital heart block, Mesokardie or Dextrokardie and heterotaxia syndromes. These abnormalities result in a variety of clinical manifestations. When patients reach adulthood, a common problem is the development of a dysfunction of the morphological RV, which serves as the left ventricle. This dysfunction may be subclinical or manifest as severe cardiomyopathy and heart failure, which leads to the consideration of a heart transplant. Rare structural heart defects are congenital complete atrioventricular block Congenital metabolic errors that cause long QT syndrome cardiomyopathy and torsades de pointes tachycardia to the long QT syndrome and other genetic arrhythmia syndromes with risks of serious and potentially fatal ventricular arrhythmias.

Health Life Media Team

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