129. Changes in the heart, large and small circles of blood circulation with mitral defects.

Mitral valve malformation, or mitral malformation, usually develops in rheumatism and very rarely in atherosclerosis. There is mitral valve insufficiency, stenosis of the left atrioventricular (mitral) orifice and their combination (mitral disease). Pure forms of insufficiency are rare, pure forms of stenosis are somewhat more common. Their combination is often noted with the predominance of one or another type of defect, which eventually leads to stenosis of the hole. The progression of sclerosis and, consequently, the defect is caused by frequent repeated attacks of rheumatism (endocarditis) and valve hyperplasia associated with continuous traumatization of the altered valve by blood flow. As a result, vessels appear in the valves of the mitral valve, then the connective tissue of the valves thickens, they turn into scarred, sometimes calcified, fused formations. Sclerosis and petrification of the fibrous ring are noted. The chords are also sclerosed, becoming thick and shortened. With the predominance of mitral valve insufficiency due to reverse blood flow (regurgitation) into the diastole, the left heart overflows with blood, compensatory hepertrophy of the left ventricular wall develops.

The narrowing of the mitral valve opening often develops at the level of the fibrous ring, and the hole has the appearance of a narrow slit resembling a button loop, less often the valve opening has the appearance of a "fish mouth". The narrowing of the mitral orifice can reach such an extent that it barely passes the branch of the tweezers. With the predominance of stenosis, there is a difficulty in blood flow in the small circle of blood circulation, the left atrium is dilated, its wall is thickened, the endocardium is sclerosed, whitish. As a result of hypertension in the small circle of blood circulation, the walls of the right ventricle are significantly hypertrophied (up to 1-2 cm), the ventricular cavity is expanded.

(this is just in case, you don't have to dictate)

1. Atrial septal defect – DMPP (fixed opening in the atrial septum due to incomplete formation of its tissue)

Morphology: 1) Primary DMPP are located adjacent to the atrioventricular valves, 2) Venous sinus defect are located near the mouth of the superior vena cava

Etiology: pulmonary vascular resistance is significantly less than systemic and compliance (extensibility) of the right ventricle is significantly higher than that of the left ventricle.

2. An open oval window (an opening located in the oval fossa of the atrial septum, not covered with a flap of tissue).

In the fetus, venoarterial bypass surgery is provided, which allows oxygen-enriched blood from the placenta to pass through the lungs that have not yet been straightened and directly enter from the right atrium into the left.

it closes after birth as a result of increased blood pressure in the left half of the heart

pulmonary hypertension or increased pressure in the right parts of the heart can cause short-term venoarterial bypass surgery with the possibility of paradoxical embolism

3. Ventricular septal defect (Incomplete closure of the interventricular septum, leaving the possibility of communication between the right and left ventricles)

4. Open ductus arteriosus (in the fetus, blood from the pulmonary artery is discharged through the ductus arteriosus into the aorta bypassing the lungs).

Clinic: 1) The open ductus arteriosus is large – arteriovenous bypass surgery and the absence of cyanosis, in case of volume or pressure overload, obstructive changes occur in the pulmonary arteries of small diameter, leading to a change in the direction of blood bypass; 2) OAP is small – there are no symptoms

6. Defect of the atrioventricular septum (lack of adequate fusion of the upper and lower endocardial cushions of the atrioventricular canal in the embryonic period).