In the developing embryo, two endothelial tubes run in the belly and fuse in the neck region to form the single heart tube. Venous inflow and arterial outflow are at the caudal (tail) and cephalic (head) ends of the heart tube, respectively. The tube is divided into five segments: sinus venosus, atrium, ventricular inlet component, ventricular outlet component and arterial segment. During the fourth week of gestation, complex looping of the heart tube provides the basis of adult cardiac structure, with the ventricle lying beneath the atrium. The four-chambered stru

cture requires separation of the atrial and ventricular components (and also the division of the arterial segment into the aorta and pulmonary artery). These separations occur during the fifth and sixth weeks of gestation and it is this process which is most prone to erroneous development. By the end of the eighth week, cardiovascular development is complete and no further changes take place until birth.

Towards the fourth week of gestation, the common trunk of the heart tube is divided into the pulmonary artery and the aorta, accomplished by a caudad spiral growth of the truncoccal ridges. There are two theories behind the mechanism of this growth. The first suggests that the spiral motion of the blood from each potential ventricular chamber into the truncus arteriosus causes the septum to assume a corresponding spiral direction, resulting in the left ventricle emptying its blood into a vessel that becomes the aorta and the right ventricle emptying its blood into a vessel that becomes the pulmonary artery. The second theory suggests that as the bulbus cordis develops, it enlarges and rotates, carrying with it the truncoconal septum in such a way that the aorta will arise from the left ventricle and the pulmonary artery from the right ventricle. If a disruption occurs in either of these mechanisms, the septum will grow in a straight caudid fashion, disrupting the expected relationship between the great vessels and the ventricular chambers.

Patent ductus arteriosus (another defect which is more common in females than in males) occurs when an abnormal communication between the aorta (with its high pressure) and the pulmonary artery (with its low pressure) establishes, through which a volume of blood can flow (see appendix two - diagram five). During foetal life, the ductus arteriosus serves as a functioning connection between the pulmonary artery and the aorta. After birth and the commencement of respiration, the partial pressure of oxygen rises and the pulmonary arterioles dilate. This influences the ductus arteriosus to close (ultimately, it will become the ligamentum arteriosum). However, patent ductus arteriosus occurs when this vessel remains open. This places a volume burden on the lungs and on the left side of the heart. The murmur of this defect is continuous and maximal underneath the left clavicle.

Congenital heart disease represents a broad range of heart defects that are present at birth, some of which present life altering and sometimes life threatening symptoms. In the considered case study of Charles-William (appendix one) some of the more obvious symptoms such as cyanosis and clubbing are illustrated and used in the diagnosis of the cardiovascular defect. Other more subtle symptoms, such as heart murmurs, are further used by the medical profession in the initial diagnosis (as is done by Dr Wellbelove in the case study). Rapid diagnosis of CHD is essential, as some cases present a serious mortality risk (70% of untreated CHD sufferers are likely to die by the age of five) and demand medical attention. Some of the defects I have mentioned can be controlled with medication, or in more serious scenarios may demand surgical correction. Precautions may now be taken during pregnancy to minimise risks, such as Rubella vaccination and avoidance of drugs and radiation. However, CHD is still a prevalent disorder that demands our attention and understanding.

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