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| | Annex A > Chapter 3 - Developments in the UK, in the Diagnosis and Treatment of Congenital Heart Abnormalities in Children, 1984-1995 > The specific heart abnormalities and procedures referred to in the Inquiry > Ventricular Septal Defect (VSD) << previous | next >> Ventricular Septal Defect (VSD)Figure 4: Ventricular Septal Defect The problem44 There is a hole (defect) in the wall between the two ventricles of the heart. The size of the hole determines whether or not the function of the heart will be compromised. It has been estimated that approximately 65% of all VSDs are too small to create a problem for the child and will probably become smaller with the passage of time, some even closing spontaneously. The VSDs with which the Inquiry was concerned were those which were large and therefore required surgical closure. 45 With each heartbeat, the two ventricles together pump blood out of the heart, the left ventricle to the body and the right to the lungs. In VSD, the blood flows normally from both ventricles, and also through the hole along the pathway of least resistance, i.e. from left to right ventricle and into the blood vessels to the lungs. The increased volume of blood flowing to the lungs then returns to the left atrium and to the left ventricle. The increased volume load on the left ventricle contributes to that chamber of the heart becoming `stretched' with consequent reduced function or `heart failure'. 46 There are some babies in whom a large VSD does not cause heart failure because the blood vessels to the lungs behave abnormally and provide an increased resistance to lung blood flow. In those cases, the expected increased flow of blood to the lungs with the consequent increased return of flow to the left heart chambers does not occur. Therefore, the left ventricle does not become sufficiently volume loaded for its function to become compromised. However, the problem is equally serious because the pressure in the blood vessels to the lungs increases and, in time, permanent changes take place in those vessels. This condition is known as pulmonary hypertension or pulmonary vascular disease and it progresses over the years, causing death in late adolescence or early adulthood. It is essential to recognise this problem within the first few months of life before pulmonary vascular disease becomes permanent. Diagnosis47 The baby becomes progressively more breathless to the extent that he is unable to complete feeds, fails to gain weight and becomes more hungry, requiring more frequent feeds and eventually becomes so exhausted that he has to be helped temporarily by being fed through a tube passed from the nose, down the oesophagus and into the stomach. The diagnosis is made by examining the baby and is confirmed by echocardiography. As explained above under `Echocardiography', advances in technology have considerably enhanced the accuracy of identifying the site and nature of the defect. From the mid-1980s it was common for babies to be subjected to cardiac catheterisation in addition to echocardiography. By the mid-1990s, evolving technology and experience enabled the diagnosis, in most cases, to be made sufficiently accurately using echocardiography alone. However, there continue to be some babies in whom it is necessary to obtain additional information by cardiac catheterisation. Management48 In the presence of heart failure, medical treatment is only of temporary value and a relatively early surgical operation becomes necessary. Surgical closure of a VSD is an open-heart procedure. The technical difficulty, if any, relates to the nature and position of the defect within the ventricular septum. The age and the size of the baby are also factors. During the early to mid-1980s, the mortality rate in the UK for closure of a VSD in infancy was significantly higher than in older children. During the 1990s the mortality rate reduced substantially for all age groups.
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