Ventricular Septal Defect (Vsd)

A ventricular septal defect (VSD) is an opening in the Ventrikelseptumwand, which leads to a shunt between the ventricles. Large ventricular septal defects cause a large left-right shunt and cause breathing difficulties in feeding and slow growth in infancy. A loud, rough, holosystolic noise at the left lower sternal border is common. Frequent infections of the respiratory and heart failure may occur. The diagnosis is made by echocardiography. The defect may be spontaneous or close in childhood or must be surgically.

The ventricular septal defect (VSD; ventricular septal defect) is after the bicuspid aortic valve of the second most common heart disease and represents 20% of all heart failure. It can occur alone or in combination with other congenital disorders (eg. As Tetralogy of Fallot, complete atrioventricular canal, transposition of the great vessels).

A ventricular septal defect (VSD) is an opening in the Ventrikelseptumwand, which leads to a shunt between the ventricles. Large ventricular septal defects cause a large left-right shunt and cause breathing difficulties in feeding and slow growth in infancy. A loud, rough, holosystolic noise at the left lower sternal border is common. Frequent infections of the respiratory and heart failure may occur. The diagnosis is made by echocardiography. The defect may be spontaneous or close in childhood or must be surgically. The ventricular septal defect (VSD; ventricular septal defect) is after the bicuspid aortic valve of the second most common heart disease and represents 20% of all heart failure. It can occur alone or in combination with other congenital disorders (eg. As Tetralogy of Fallot, complete atrioventricular canal, transposition of the great vessels). Ventricular septal defect Pulmonary blood flow and volumes of LA and LV are increased. Ventricular pressures are medium pressures. RV pressure and O2 saturation are variable increases, and depending on the size of the defect. AO = aorta; IVC = inferior vena cava; LA = left atrium; LV = left ventricle, PA = pulmonary artery; PV = pulmonary veins, RA = right atrium; RV = right ventricle; SVC = superior vena cava. Classification VSD are classified according to their location: Perimembranös Subpulmonaler trabecular outflow (supra cristal or doubly bound subarterial) input perimembranous defects (70-80%) are defects in the membranous septum adjacent to the tricuspid valve and extending through a differently large amount of the surrounding muscle tissue , Most commonly, this defect occurs immediately below the aortic valve. Trabecular defects (5-20%) are completely surrounded by muscle tissue and can occur at any point of the septum. Discharge defects (5-7% in the US and 30% in Asian countries) are below the pulmonary valve. These defects are often called supra cristale, conoseptale or double undertook subarteriale defects and are often associated with an incident of the aortic leaflet, creating a regurgitation of the aorta is triggered. Input defects (5-8%) are bounded at the top by the tricuspid and are located behind the membranous septum. These defects are referred to as AV septal defects. Pathophysiology The size of the shunt depends on the size of the defect and the falling resistance, d. H. of the pulmonary outflow tract obstruction and pulmonary vascular resistance. Blood just flows over larger defects, which are therefore referred to as non-restrictive; the pressure equalizes between the right and left ventricles, and there is a large left-right shunt before. In time it causes a big shunt, if no pulmonary stenosis is likely to hypertension of the pulmonary artery to increased vascular resistance of the pulmonary artery, to increased right ventricular pressure overload and right ventricular hypertrophy. Ultimately, the increased pulmonary vascular resistance causes a shunt reversal (from the right to the left ventricle) with a Eisenmenger syndrome (Eisenmenger syndrome). Smaller defects, which are also referred to as restrictive VSDs, restrict blood flow and the transmission of high pressure into the right heart. These VSDs result in a relatively small left-right shunt; the pulmonary artery is increased or normal minimal. and Eisenmenger’s syndrome does not develop. Symptoms and signs The symptoms depend on the defect size and the size of the left-right shunt. Children with a small VSD are usually asymptomatic, grow and develop normally. In children with larger defects occur after 4-6 weeks of life, when the pulmonary vascular pressure drops, the symptoms of heart failure on such. B. dyspnoea, low weight gain, fatigue after feeding. Frequent infections of the lower respiratory tract occur. If patients are not treated, they can develop symptoms of Eisenmenger syndrome. Auscultatory findings vary with the size of the defect. Small VSD show typically with heart sounds of grade 1-2 / 6 with high, short systolic noise (due to tiny defects in fact close at the late systole) to holosystolischen heart sounds of grade 3-6 / 4 with or without palpable vibration at the lower left sternal. These heart sounds are heard shortly after birth. The heart’s apex is hyperactive and the second heart sound (S2) is normally cleaved and noisy. Moderate to large VSD produce a holosystolic sound that can be heard in an age of 2-3 weeks; S2 is closely cleaved usually with an accentuated pulmonary component. An apical diastolic rumble (due to the increased flow through the mitral valve) and the clinical signs of heart failure (tachypnea, dyspnea during feeding, failure to thrive, gallop characters, rales and hepatomegaly) may be present. At moderate high-flow VSDs the murmur is often very loud and accompanied by a buzz (grade 4 or 5 marbles). For large defects that allow a balance of left ventricular and right ventricular pressures, systolic heart murmur is often muted. Diagnostic chest X-ray and ECG echocardiography is the diagnosis, supported by a chest x-ray absorption and an EKG, made based on clinical examination and secured by echocardiography. In a large VSD, the x-ray shows cardiomegaly and increased pulmonary vascular markings. The ECG shows a right ventricular hypertrophy, or a combined ventricular hypertrophy and sometimes a left atrial enlargement. The ECG and chest X-ray are typically normal in small VSD. The two-dimensional Farbechokardiographie and Doppler studies confirm the diagnosis and can provide valuable information on the anatomy and hemodynamics as well as information on the location and size of the defect and the right ventricular pressure. A cardiac catheterization is not usually necessary. Treatment For Heart Failure: drug therapy (eg, diuretics, digoxin, ACE inhibitors.) Sometimes surgical correction Small VSD, especially muscular septal defects often close spontaneously during the first years of life. A small defect can remain open and does not require further medical or surgical treatment. Larger defects often shut themselves less spontaneous. Diuretics, digoxin and ACE inhibitors may be useful to control the symptoms of heart failure before heart surgery or in infants with medium-sized VSD, which are likely to close over time by itself, to gain time. If infants do not respond to drug treatment or bad thrive, often a surgical repair within the first months of life is recommended. Even in asymptomatic children large VSDs should be repaired, usually within the first year of life to prevent later complications. The current mortality in surgery is <2%. Surgical complications include a residual ventricular failure and / or a complete bundle branch block. Endocarditis prophylaxis is not necessary before surgery, but probably in the first 6 months after surgery or when there is a residual defect in addition to the operated site. Parche de comunicación interventricular var model = {thumbnailUrl: '/-/media/manual/professional/images/ventricular_septal_defect_patch_high_blausen_de.jpg?la=de&thn=0&mw=350' imageUrl: '/ - / media / manual / professional / images / ventricular_septal_defect_patch_high_blausen_de ? lang = en & .jpg thn = 0 ', title:' Parche en comunicación interventricular 'description:' 'credits'', hideCredits: false, hideTitle: false, hideFigure: false, hideDescription: true}; var panel = $ (MManual.utils.getCurrentScript ()) Closest ( 'image-element-panel.'). ko.applyBindings (model, panel.get (0)); Key points A ventricular septal defect (VSD) is an opening in the Ventrikelseptumwand, resulting in a left-right shunt. Over time, large left-right shunt lead to hypertension of the pulmonary artery to increased vascular resistance of the pulmonary artery, to increased right ventricular pressure overload and right ventricular hypertrophy, which results in the end, that the direction of the shunt reverses, which Eisenmenger syndrome is caused. Larger defects cause symptoms of heart failure (HF) at the age of 4 to 6 weeks. Typically, a degree is 3 to 6.4 holosystolic murmur at the left lower sternal heard shortly after birth. Children who do not respond to medical treatment of heart failure or grow poorly, should have a surgical repair during the first months of life. Even asymptomatic children should have a repair during their first year of life.

Health Life Media Team

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