Daily Archive 02.10.2019

Etiology, pathogenesis of the open ductus arteriosus

The arterial ( botall ) duct (OAP) in the prenatal period connects the aorta to the pulmonary artery. This is the necessary anatomical structure of the embryonic circulation. After the birth of the baby, the duct function stops almost immediately. The process of anatomical closure of it lasts no more than 2-8 weeks . In some cases, the closure of the duct does not occur. Such a defect accounts for 10-25% of all congenital heart abnormalities. The arterial duct moves away from the aortic arch opposite the left subclavian artery, goes obliquely anteriorly and downward, falling into the bifurcation of the pulmonary trunk or into the left pulmonary artery. The duct has the shape of a cylinder or a truncated cone 10-25 mm long and up to 20 mm wide.

The primary violation of hemodynamics is associated with a difference in pressure in the aorta and the pulmonary artery, which leads to persistent systolic- diastolic aortopulmonary discharge of blood (from left to right). At the same time, there is a volume increase in pulmonary blood flow, which depends on the ratio of the diameters of the aorta and duct. With a significant diameter of the latter, most of the blood pumped into the left ventricle enters the pulmonary artery from the aorta. As a result, pulmonary blood flow may exceed that in a large circle of blood circulation. Due to chronic oxygen starvation of the body, the child lags behind in physical development. Significant volume overload of the vessels of the pulmonary circulation leads to frequent bronchitis and pneumonia. Hemodynamic compensation is initially supported by shock and minute volumes of the left ventricle due to its diastolic overload. In the future, there comes a spasm of pulmonary arterioles with their subsequent sclerosis , which leads to a significant decrease in the vascular capacity of the pulmonary circulation. This process at certain stages causes pressure balancing in the aorta and the pulmonary artery, and sometimes even leads to an inversion of blood discharge (from right to left). From this moment, blood begins to flow into the arterial bed, cyanosis appears ( cyanotization of the defect). At the same time, systolic overload of the right ventricle increases and OAA becomes its salvage drainage, the closure of which can cause acute right ventricular failure. However, in OAP, cyanotization is rare.

Clinic of the open arterial duct

The clinic depends on the magnitude of the OAA, the pressure level in the pulmonary artery and the ratio of the resistance of the vessels of the small and large circles of blood circulation. Allocate 4 stages of OAP: I – systolic pressure in the pulmonary artery is less than 40% blood pressure; II – moderate hypertension (systolic pressure in the pulmonary artery is 40-45% of blood pressure; III – severe hypertension (systolic pressure in the pulmonary artery is more than 75% of blood pressure, blood discharge is preserved from left to right); IY – state of extreme severity (systolic pressure in the pulmonary arteries is equal to or higher than blood pressure, cyanotization of the defect).

Complaints of patients with OAP are nonspecific. The most common complaints are fatigue, shortness of breath with physical exertion , sometimes sensations of interruptions in the work of the heart, palpitations, pneumonia. The lag in physical development, pallor of the skin is characteristic. When straining, cyanosis is more pronounced in the lower half of the trunk and on the lower extremities. On palpation of the chest determines the gain of the apical impulse, systolic or systolic -diastolicheskoe jitter in the projection base of the heart. The borders of the heart are expanded, but their quantitative characteristics are different. With a large arteriovenous discharge, the pulse is fast and high. Pulse pressure – with a tendency to increase. In young children, diastolic pressure can be reduced to 0. Auscultation reveals the main diagnostic sign of OAP – a rough, “machine” systolic- diastolic murmur in the second intercostal space to the left of the sternum. Noise is carried into the interscapular space and on the vessels of the neck. The diastolic component is better heard when straining ( Valsalva test ). As pulmonary hypertension there is a tendency to disappear first Diastolic – of the noise component, and subsequently – and systolic. Patients with stage IV it is virtually wrinkle ” Afonichev ” or accompanied by the appearance Protodeacon – stolicheskogo noise relative valvular insufficiency, pulmonary arterial (noise Graham Stille ). Against this background, II tone over the pulmonary artery progressively amplifies. Sometimes it can be split and the accent of the pulmonary component of II tone is heard

Diagnosis of open ductus arteriosus

In typical cases, a rhomboid-like systolo- diastolic murmur is recorded on the FCG over the pulmonary artery . As pulmonary hypertension increases, the tendency to the disappearance of the diastolic and decrease in the systolic component of the noise correlates with the amplification and splitting of II tone over the pulmonary artery. In the later stages of the defect, the protodiastolic murmur of Graham Still is recorded . There are no specific changes on the ECG. A normogram or levogram is marked . In the future, signs of hypertrophy of both ventricles with an outcome in the rightogram and isolated hypertrophy of the right ventricle are determined . When x-ray examination in the initial stages are noted: increased vascular pattern, left ventricular hypertrophy, increased aortic pulsation. In the future, a tendency to swelling and an increase in the pulse amplitude of the pulmonary artery, depletion of the pulmonary pattern, and hypertrophy of the right ventricle is determined . Dopplerographic examination in some cases captures the aorto-pulmonary shunt. When catheterization of the right heart revealed an increase in oxygen saturation of the blood in the pulmonary artery compared with the right ventricle by at least 2 vol. % Aortography makes it possible to obtain simultaneous contrasting of the pulmonary artery, into which the contrast medium enters through the OAA.