Valvular and Congenital Heart Diseases PDF
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Summary
This document provides an overview of valvular and congenital heart diseases, discussing their causes, effects, and different types, including mitral stenosis, mitral incompetence, aortic incompetence, aortic stenosis, and congenital heart diseases. It also details types such as atrial septal defect, and ventricular septal defect. This is suitable for medical students
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Valvular and Congenital Heart Diseases Valvular heart disease Mitral Stenosis: Aetiology: Occurs in young and middle age due to: (I) Healed rheumatic valvulitis is the commonest cause. (2) Healed mild subacute infective endocarditis. Gross picture: (1) The cusps are thickened, rigid and fused....
Valvular and Congenital Heart Diseases Valvular heart disease Mitral Stenosis: Aetiology: Occurs in young and middle age due to: (I) Healed rheumatic valvulitis is the commonest cause. (2) Healed mild subacute infective endocarditis. Gross picture: (1) The cusps are thickened, rigid and fused. (2) The mitral orifice is narrowed and slit-like “Button hole” (3) The cordae tendinae are fibrosed, thick and short. The papillary muscle show hypertrophy. Effects: (1) Hypertrophy and dilatation of the left atrium. (2) Chronic venous congestion of the lung. (3) Pulmonary hypertension. (4) Lastly the right ventricle and atrium undergo hypertrophy and dilate. The condition terminates by right-sided heart failure with chronic general venous congestion. Complications: (1) Atrial thrombosis which may give rise to cerebral embolism. (2) Haemorrhagic infarctions of the lung caused by thrombosis in pulmonary arteries or by emboli from the right atrium. (3) Subacute infective endocarditis complicates mitral stenosis. Mitral Incompetence: Causes (1)Rheumatic valvulitis is the commonest cause. (2) Subacute infective endocarditis. (3) Dilatation of the left ventricle as a result of anaemia, hypertension, healed myocardial infarct and aortic incompetence cause stretching of the mitral ring and mitral incompetence. Effects: Occur in this sequence: (1) The blood regurgitates in the left atrium during ventricular systole causing its hypertrophy and dilatation. (2) During the diastole the left ventricle receives the blood of the right side of the heart and the regurgitated blood, so it hypertrophies and dilates. Left-sided heart failure occurs. (3) Pulmonary congestion, pulmonary hypertension and right-sided heart failure may follow. Aortic Incompetence: Causes: (1) Rheumatic valvulitis. (2) Syphilitic aortitis and syphilitic valvulitis. Effects: (1) During diastole the blood regurgitates from the aorta to the left ventricle which undergoes hypertrophy and dilatation. (2) Dilatation of the left ventricle renders the mitral valve incompetent. This results in hypertrophy and dilatation of the left atrium, chronic venous congestion of the lung, then hypertrophy and dilatation of the right side of the heart. All the cardiac chambers are enlarged “Cor bovinum”. (3) The case terminates by left or right sided heart failure. Aortic Stenosis: Causes: (1) Rheumatic valvulitis. (2) Subacute infective endocarditis. (3) Atherosclerotic changes. (4) Congenital (rare). Effects: (1) Concentric hypertrophy of the left ventricle. (2) Coronary and cerebral insufficiency. (3) Left ventricular failure. CONGENITAL HEART DISEASES Incidence: 1-2% of all heart diseases and 10% of heart diseases in children. Aetiology: The real cause is unknown, but the following factors are blamed: (1) A defect of the germ cell. (2) German measles (rubella) affecting the pregnant mother especially during the first three months. (3) Drugs administered by the pregnant mother as thalidomide and cortisone. (4) Nutritional and vitamin deficiencies in pregnancy. (5) Syphilis. Types: (1) Non-cyanotic group: (a) Atrial septal defect. (d) Aortic stenosis (b) Ventricular septal defect. (e) Patent ductus arteriosus. (c) Pulmonary stenosis. (f) Coarctation of aorta. (2) Cyanotic group: (a) Fallot’s trilogy. (b) ) Fallot’s tetralogy. (c) Eisenmenger’s syndrome. Atrial Septal Defect: Cause: Large foramen ovale which fails to close. Results (1) The blood flows from the left to the right atrium. The right atrium undergoes hypertrophy and dilatation followed by hypertrophy and dilatation of the right ventricle. (2) Dilatation of the pulmonary artery. Ventricular Septal Defect: is of two types: (1) Small defect: Rare and occurs in the muscular part of the septum. Cardiac hypertrophy does not occur (Roger’s disease). (2) Big defect: More common and occurs in the membranous septum usually just below the aortic valve. The blood is shunted from the left ventricle to the right ventricle to the pulmonary artery causing slight enlargement. Patent Ductus Arteriosus: Results in: (1) Shunt of the blood from the aorta to the pulmonary artery. (2) The left ventricle increases its output to compensate for the shunted blood so it undergoes hypertrophy and dilatation. (3) The increased strain on the right ventricle causes its hypertrophy and dilatation. (4) The patient may die from right sided heart failure or the lesion gets complicated by subacute infective endocarditis. Coarctation of the Aorta: Congenital narrowing of the aorta in the region of the ductus arteriosus. Two types occur: (1) Infantile type: The narrowing is proximal to the ductus which is patent and through it the blood passes from the pulmonary artery to the aorta. The condition is fatal shortly after birth. (2) Adult type: The narrowing is distal to the ductus which is closed. The following changes occur: (a) Increased blood pressure in the arms, head and neck and decreased blood pressure in the legs. (b) Death results from left sided heart failure, aortic rupture above the narrowing, cerebral haemorrhage or subacute bacterial endocarditis. Fallot’s Trilogy: Consists of: (1) Pulmonary stenosis. (2) Right ventricular hypertrophy. (3) Atrial septal defect. Fallot’s Tetralogy: A more common lesion which consists of: (1) High ventricular septal defect. (2) Dextroposition of the aorta which over-rides the septal defect, (3) Pulmonary valve stenosis. (4) Right ventricular hypertrophy. Effects: (1) The aorta receives blood from both ventricles so it is partly non-oxygenated. (2) Severe cyanosis. (3) The anoxia causes secondary polycythaemia and clubbing of the fingers.