PDA (patent ductus arteriosus) - causes of its appearance, why is it dangerous and how is pathology determined? Evolution of the circulatory system What is patent ductus arteriosus in children.

Patent ductus arteriosus (PDA) occurs in 10% of all congenital heart disease cases as a separate defect. Historically, the first description of the vice was made by Galen in the 2nd century. AD Harvey then continued to study it physiological role in the fetal circulation, although the first report belongs to J. Agashsyu (1564). The name of the defect was given in honor of L. Botallo, who described the clinical symptoms a little later. In 1583, the Italian physician and anatomist L. Botallo rediscovered and described the vessel connecting the aorta and pulmonary artery, and called it the ductus arteriosus, and in 1888, the physician Munro dissected and ligated the duct on the corpse of a newborn child. In 1907, Munro, at a meeting of the Philadelphia Cardiological Society, proposed the idea of ​​prompt closure of a PDA, which met with strong opposition from colleagues, primarily pediatricians.

The discussion continued for 30 years. Finally in 1938 pediatric surgeon R. Gross at the Boston Children's Hospital was the first in the world to successfully ligate a PDA in a 7-year-old patient, opening an era in cardiac surgery medicine.

Girls suffer from this defect more often than boys (M:D ratio = 1:3). Patent ductus arteriosus can have a very different clinical picture. Although it is more often diagnosed in infants, sometimes PDA is recognized late - in school age or even in adults. The defect is registered in less than 0.02% of full-term newborns, but very often among premature and low-birth-weight children. When a child is born at a gestational age of 34-36 weeks, a patent ductus arteriosus occurs in 21%, 31-32 weeks - in 44%, 28-30 weeks - in 77%; among children with a birth weight of less than 1750 g - in 45%, with a body weight of less than 1200 g - in 80%.

Morphology
There are four clinically distinct types of PDA.

Isolated PDA in otherwise healthy children.

Isolated PDA in premature infants.

PDA in combination with other, more serious structural abnormalities hearts.

PDA as a compensatory structure that provides systemic or pulmonary blood flow in critical situations with severe blue-type congenital heart disease or with obstruction of the left heart.

Depending on membership in one of these four groups, there are differences in hemodynamic disorders, clinical symptoms, prognosis, and monitoring tactics for PDA.

In infants, the length of the PDA is 2-8 mm, the diameter is 2-12 mm. The duct usually departs from the trunk of the PA or its left branch and flows into the aorta immediately behind the origin of the left subclavian artery, defining the area of ​​the aortic isthmus. Anatomically, the ductus arteriosus is a remnant of the 6th aortic arch. It is located between the front wall of the aircraft and back wall aorta. The ductus arteriosus has a special tissue structure - its middle layer It is represented by spirally arranged smooth muscle cells, highly sensitive to prostaglandins E1, E2 and I2 (relaxation) and O2 (constriction), and its intima is thickened and has a viscous mucosal structure.

It is usually cone-shaped with a wide aortic end and narrowing towards the PA. However, variations in the shape and length of the duct are possible from short and cylindrical to long and tortuous.

The right ductus arteriosus is also found, and the ductus arteriosus may be present on both sides - left and right. Although a left-sided PDA is normal anatomical structure necessary during fetal development, the presence of a right-sided PDA is usually associated with other congenital defects of cardio-vascular system- primarily such as anomalies of the aortic arch or conotruncus. In complex heart defects, the anatomy of the PDA may be atypical. In these cases, the range of anatomical variations of the ductus arteriosus is very wide. Structures that may be mistaken for a PDA include primarily the aorta, pulmonary artery, and carotid artery.

Hemodynamic disorders
In the fetus, the ductus arteriosus is a normal structure of the heart through which blood flowing from the pancreas into the pulmonary artery enters the descending aorta. Normally, in the fetus, only 10% of the blood ejected into the pulmonary trunk of the pancreas passes through the vascular bed of the lungs.

From 6th week intrauterine development The main volume of blood ejected from the pancreas passes through the ductus arteriosus, and this volume accounts for 60% of the total cardiac output in fetal life. In the fetal period, the functioning of the duct is ensured by the local production and presence in the bloodstream of prostaglandins E2 (PGE2) and I2 (PGI2), which relax the smooth muscles of this vessel. After birth and an increase in the volume of pulmonary blood flow, locally produced prostaglandins are metabolized and at the same time their supply from the placenta stops.

But the most important role in postnatal closure of the duct is played by the vasoconstrictor effect of the increased partial pressure of O2 in the blood passing through the duct. Contraction of the smooth muscles of the duct leads to the functional closure of its lumen by thickened intima. In most full-term newborns, this occurs in the first 24 hours of life, followed by fibrous degeneration of the subintimal layer and complete obliteration of the duct over the next few weeks. In premature babies, immature ductal tissue is less sensitive to oxygen, which is why the duct closes less frequently postnatally.

After birth, a left-right discharge occurs through the duct. In other words, the ductus arteriosus allows blood to flow from the systemic circulation (systemic circulation) to the pulmonary circulation (pulmonary circulation). The volume of left-to-right shunting increases in the first 1-2 months of life due to a fall in pulmonary vascular resistance. The volume of blood in the pulmonary bed becomes excessive (hypervolemia). Overflow of the pulmonary bed with blood leads to an increase in vascular resistance in the lungs. However, the degree of response of the pulmonary bed to excess blood volume is individual and unpredictable. The magnitude of excess blood volume in the pulmonary bed depends on several factors. The wider internal diameter of the narrowest part of the ductus arteriosus contributes to the high volume of the left-to-right shunt. The presence of a long narrowed section of the duct limits the volume of shunted blood. With a long duct, the shunt is usually small.

The volume of left-right shunt is partially regulated by the ratio of vascular resistance in the pulmonary and systemic circulation. If systemic vascular resistance is high and/or pulmonary vascular resistance is low, blood shunt through the ductus arteriosus is potentially large. Starting in the ductus arteriosus, the blood flow in systole and then in diastole follows the following path: pulmonary arteries, capillaries, pulmonary veins, left atrium, left ventricle, aorta, ductus arteriosus. Therefore, large left-to-right shunt through the PDA leads to dilatation of the left atrium and ventricle.

With a large shunt volume, venous return to the left heart is significantly increased, and they experience severe volume overload. At the same time, the pressure in the pulmonary artery and right ventricle increases. The pulmonary veins and ascending aorta can also be dilated. Together, these factors can lead to pulmonary edema if the vascular resistance of the duct or pulmonary vessels is low.

Functional and anatomical closure of the PDA after birth have different timing. Functional closure of the duct by constriction occurs 12-48 hours after birth, and in 10% of full-term newborns it is delayed until 3-4 weeks of life. Perinatal asphyxia usually causes a delay in closure of the duct, but after a short period of time in these newborns it closes without additional intervention. True anatomical closure of the duct (after which the duct is no longer able to open again) occurs after several weeks or months. In the second, anatomical stage of closure, fibrous proliferation of the intima occurs, after which the duct turns into a fibrous ligament, most often this is observed 2-3 months after birth in full-term children.

In the fetus, the oxygen tension in the blood is relatively low because the lungs are not functioning. This factor, combined with increased levels of prostaglandin E in the blood, keeps the duct open. High levels of prostaglandin E are due to low pulmonary blood flow and high levels of its production by the placenta. At birth, the placenta stops functioning and the lungs expand (and prostaglandins are metabolized in them). In addition, with the onset of pulmonary respiration, O2 tension in the blood increases and pulmonary vascular resistance decreases. Normally, cessation of functioning of the ductus arteriosus occurs on average 15 hours after birth in full-term newborns. First of all, this occurs due to contraction of the muscular wall of the duct under the influence of O2, the concentration of which is high in the inhaled air.

In addition, with the opening of the pulmonary vessels, there is a shift in the discharge of blood from the right ventricle, already predominantly into the pulmonary artery. Until complete (anatomical) closure of the ductus occurs and the level of pulmonary vascular resistance falls below systemic resistance, a small residual shunt of blood through the PDA from the aorta to the pulmonary artery may persist. Although ductus arteriosus tissue in newborns is highly sensitive to increased arterial O2 levels, there are other significant factors closing it.

These include the state of vegetative nervous system, exposure to chemical mediators and the state of ductal muscles. The balance of factors influencing the relaxation/constriction of the duct determines its vascular tone. The main factors supporting ductal relaxation are: high levels of prostaglandin E, hypoxemia, and production of nitric oxide by the ductal intima. On the contrary, the main factors of duct constriction are: decreased levels of prostaglandin E, high levels of O2 in the blood, increased production of endothelin-1, norepinephrine, acetylcholine, bradykinin, decreased sensitivity of ductus arteriosus receptors to prostaglandin E.

The inability of the ductus arteriosus to close in premature infants is associated with low levels of ductus arteriosus metabolism in the immature lungs. In addition, in premature high sensitivity to PGE and low sensitivity to O2 on the part of ductal muscle cells.

The absence of duct contraction within the physiological period in full-term newborns may be a consequence of disturbances in PGE metabolism in the lungs due to hypoxemia, asphyxia or an increase in the volume of pulmonary blood flow, renal failure and respiratory disorders.

Increased production of cyclooxygenase type 2 (COX-2 - iso-forms of COX-producing PGE) can prevent duct closure. In this case, receptors for PGE-2 are activated, which leads to relaxation of smooth muscle ductal cells. In late gestation, the level of PGE decreases, which is a stage of preparation for postnatal constriction of the duct. After birth, the primary adhesion of the mucous membrane of the duct occurs after constriction of the muscular layer.

Increased sensitivity to PGE in combination with lung immaturity leads to hypoxia and, as a result, an increase in the frequency of functioning of the ductus arteriosus in premature infants.

Time of onset of symptoms
Depends on the diameter of the duct and the volume of the shunt. If they are significant, then symptoms of pulmonary edema may appear already in the first days of life. With little or medium width duct manifestations of pulmonary hypertension and heart failure are mild, and in these cases the defect is usually recognized by a systolic murmur at the base of the heart, which appears or intensifies from the 5-7th day after birth.

Symptoms
Symptoms of the defect usually appear in early age. With a small or medium duct diameter, the patient initially experiences no symptoms. However, then fatigue occurs during exercise or signs of pulmonary congestion combined with a heart murmur. At the age of 3-6 weeks, infants with PDA often experience tachypnea, sweating, and feeding difficulties. Significant loss of body weight or lack of weight gain occurs in children who have not received treatment.

For infants with a medium or large ductus arteriosus shunt, hoarse voice, cough, lower respiratory tract infections, atelectasis, recurrent pneumonia.

When examining a child, you can find following symptoms:
if the left-right shunt is large, pulsation of the heart area is visible;

The heartbeat is shifted to the left, tremors can be detected in the suprasternal region or under the left clavicle;

The first sound (S1) is usually normal, and the second sound (S2) often merges with noise or is split due to premature closure of the pulmonary valve;

PDA is characterized by systolic or systolic-diastolic murmur in the second and third intercostal spaces on the left and an increase in the second sound above the pulmonary artery;

Sometimes, upon auscultation of the PDA, multiple clicks or noises of a rumbling timbre are heard.

The most characteristic symptom of this defect is a systolic or systolic-diastolic murmur in the second and third intercostal spaces on the left and an increase in the second sound above the pulmonary artery. The noise usually appears or intensifies from the 5-7th day of life. With a large duct size, the murmur is heard from the end of the 1st day in combination with tachycardia, shortness of breath and cardiomegaly, with expansion of the borders of the heart to the left or in both directions.

If pulmonary vascular resistance begins to exceed systemic resistance, the shunt of blood through the duct becomes right-to-left and cyanosis may be visible only on the lower half of the body (differential cyanosis), since usually the site of origin of the duct from the aorta is located below its three main branches that supply blood to the upper half of the body .

With a large diameter of the ductus arteriosus, systolic blood pressure is increased and diastolic blood pressure is decreased due to retrograde outflow of blood into the pulmonary artery. At the same time, pulse blood pressure is increased, and a racing pulse appears. With significant pulmonary hypertension, the diastolic component of the murmur may not be audible. With advanced obstructive damage to the pulmonary vessels, the systolic murmur disappears. If pulmonary vascular resistance begins to exceed systemic resistance, the shunt of blood through the duct becomes right-to-left and cyanosis may be visible only on the lower half of the body (differential cyanosis), since usually the site of origin of the duct from the aorta is located below the three main branches supplying the upper half of the body. With a small PDA (0.1-0.15 cm), children usually have no clinical symptoms and often no heart murmur.

Features of the patent ductus arteriosus in newborns and premature infants

In the first 2 months of life, even in mature full-term newborns, the aortic isthmus is relatively narrow and has a diameter of about 5 mm. With a very wide PDA in diastole, a significant retrograde flow rushes from the aorta to the pulmonary artery, and this can lead to large circle steal syndrome, in which cerebral circulatory disorders are observed, including hemorrhages in the ventricles of the brain, severe anemia, intestinal ischemia with symptoms of paresis or small intestinal obstruction and the addition of necrotizing ulcerative enterocolitis, acute renal failure. Among low birth weight and premature babies, manifestations of steal syndrome occur more often and are especially dangerous.

Classic signs of PDA are usually absent in the group of premature and low birth weight infants. Auscultatory diagnosis of the defect in premature infants with low body weight can be difficult; they rarely have a systolic-diastolic murmur. The presence of a PDA should be suspected in them primarily in cases of severe respiratory distress syndrome. The classic coarse systolic murmur of a PDA can be heard in the second intercostal space at the left sternal border, but in very young children with a large PDA and significant hypervolemia of the pulmonary vascular bed, the murmur may be absent altogether. However, in this case, you should pay attention to the pulsation of the cardiac region and the racing pulse, which is caused by relatively low systemic arterial pressure due to the constant and significant outflow of blood from the aorta to the pulmonary artery.

The likelihood of persistent functioning of a PDA depends on body weight at birth. Thus, among children with a birth weight of less than 1750 g, it occurs in 45%, and with a body weight of less than 1200 g - in 60-80%. In almost half of premature infants born weighing less than 1750 g, the ductus arteriosus continues to function until 3-4 months, and then closes spontaneously in 75% of cases. However, if this does not happen, then the chance of spontaneous closure is small and is no more than 10%. The functioning of the duct during the first 3-4 months subsequently leads to BPD and COLD, which occur not only at an early age, but also in the 1st-2nd decade of life.

In premature babies, even with a small width of the ductus arteriosus, it usually functions for a long time due to low sensitivity to oxygen and a number of respiratory problems characteristic of immature lungs and maintaining increased pressure in the pulmonary circle. Among premature infants with respiratory distress syndrome, PDA occurs in at least 20%. In case of prematurity and low body weight, the criteria for hemodynamic disorders due to PDA are: ventilator dependence due to respiratory distress syndrome, hospital-acquired pneumonia, cerebrovascular accidents, symptoms of intestinal ischemia, acute renal failure.

In general, patent ductus arteriosus in premature infants is one of the main causes of hospital-acquired pneumonia and ventilator dependence, and later bronchopulmonary dysplasia. Without medical or surgical closure of the PDA, such conditions are accompanied by high mortality.

Diagnostics
On the frontal radiograph of the chest, the pulmonary pattern of the arterial type is enhanced, the cardiac shadow is expanded with signs of dilatation of the left ventricle and left atrium, and the trunk of the pulmonary artery. Cardiomegaly occurs both with and without symptoms of heart failure. Typically data plain radiography chest wall remain normal until the ratio of pulmonary to systemic blood flow begins to exceed 2:1. Bulging of a segment of the pulmonary artery trunk is a sign of increased pressure and volume of pulmonary blood flow. With significant hypervolemia, pulmonary edema may develop. Radiological signs of a hemodynamically significant ductus arteriosus in newborns include: increased vascular pattern, emphasized interlobar pleura, enlarged LA and LV.

On the electrocardiogram electric axle the heart is not abnormal; with a small PDA, the ECG is usually normal. With medium and large duct widths, sinus tachycardia, sometimes atrial fibrillation. With a large PDA diameter, signs of LA and LV hypertrophy appear. With a large PDA with pronounced pulmonary hypertension signs of pancreatic hypertrophy join or dominate.

In newborns, especially premature infants, with a large ductus arteriosus, the ECG shows T-wave inversion and ST segment depression due to ischemia against the background of systemic blood flow steal syndrome. Coronary insufficiency is also caused by an increase in the work of the LV myocardium due to a large left-to-right shunt and significant overload of the pulmonary blood flow, as well as in conditions of low systemic and coronary diastolic pressure - due to retrograde shunting of blood from the aorta to the pulmonary artery.

Laboratory data - general analysis blood and blood gas composition are normal.

With two-dimensional Doppler echocardiography, direct visualization of the duct is possible in no more than 10-15% of patients. The leading echocardiographic sign of a PDA is the detection of blood flow through the duct using Dopplerography (preferably color): diastolic turbulent flow in the pulmonary artery, turbulent flow through the PDA. Assessing the degree of diastolic flow reversal in the descending aorta helps further assess the volume of the shunt. The dimensions of LV and LA dilatation are usually increased.

If the duct is visible on two-dimensional echocardiography, then usually its aortic part is first visualized and then the area flowing into the pulmonary artery is determined by the size, shape, and location of the duct. It is most convenient to see the duct from the parasternal position along the short axis and from the suprasternal notch. In typical cases, the PDA is located between the junction of the trunk and left branch of the pulmonary artery and the aorta immediately opposite the origin of the left subclavian artery.

If there are no other heart defects, Doppler echocardiography reveals a continuous flow from the aorta to the pulmonary artery. With a large volume of shunted blood, a constant flow from the aorta into the pulmonary artery through the ductus arteriosus and retrograde blood flow from the descending aorta are clearly visible. With a large shunt volume, the LA is also enlarged due to excess blood flow to the left side through the pulmonary veins.

Cardiac catheterization and angiography are not necessary for uncomplicated PDA. Color Doppler echocardiography is more sensitive for recognizing small diameter ductus arteriosus than cardiac catheterization. However, angiocardiography may be required in cases of high pulmonary hypertension due to PDA and/or associated congenital heart disease, including to determine the response to vasodilators and assess the patient's operability. Finally, catheterization may be necessary to close the PDA with an occlusion device.

Natural evolution of vice
If surgery is not performed in a timely manner, up to 30% of patients die in infancy. The main causes of death are severe congestive heart failure or associated pneumonia. Spontaneous closure of a small-diameter PDA sometimes occurs in full-term newborns by 3-4 weeks of life, but after the 1st month of life it rarely occurs. With a large duct width in children left without surgical treatment, irreversible pulmonary hypertension develops from the 2-3rd year of life. In this case, Eisenmenger syndrome occurs and life expectancy is sharply reduced (~20 years). One of typical complications The defect in non-operated patients is bacterial endocarditis.

Observation before surgery
If there are signs of heart failure and hypervolemia in the pulmonary circulation, diuretics are prescribed, ACE inhibitors, digoxin; in premature infants and in full-term infants with symptoms of severe heart failure and pulmonary edema - respiratory support.

Timing of surgical treatment
In full-term infants with a large-diameter PDA, the likelihood of spontaneous closure after the first 3-4 weeks of life is low. These children are indicated for ligation of the duct from the moment of diagnosis. If there are symptoms of heart failure that are not relieved by conservative treatment, then surgery is performed immediately. If there are no symptoms of heart failure, then surgery should be performed within the first 3 months of life.

For premature infants, mandatory echocardiographic screening for PDA is required immediately after birth, and if it is detected, immediate medical closure is indicated. Pharmacological treatment based on suppression of the synthesis of prostaglandins - one of the main factors that maintain the duct open. For this purpose, intravenous administration of non-steroidal anti-inflammatory drugs - cyclooxygenase inhibitors - is used. For this purpose, intravenous indomethacin was previously used, and now ibuprofen. Treatment regimen: ibuprofen at a dose of 10 mg/kg intravenously and then twice more at 5 mg/kg after 24 and 48 hours.

Currently, in the Russian Federation, only one drug is registered and approved for use in the neonatal period for the treatment of PDA - a COX inhibitor - an ibuprofen solution for intravenous administration. Controlled studies of the use of ibuprofen and indomethacin conducted in 1997-2003 showed comparable effectiveness of these drugs, with a better safety profile of ibuprofen, especially for the treatment of premature infants. Early use of ibuprofen (in the first 3-4 days of life) in premature infants with a gestational age of less than 34 weeks and documented PDA is accompanied by closure of the ductus arteriosus in 75-80% of children. However prophylactic use ibuprofen in the first 3 days of life (starting 6 hours after birth) in premature newborns with a gestational age of less than 28 weeks leads to an increased incidence of side effects from the lungs and kidneys. For this reason, the drug is not recommended for prophylactic use.

Although the ductus arteriosus can be closed in more than 70% of cases in preterm infants, this occurs less frequently in full-term infants. A decrease in the effect of manipulation is also observed with a late attempt at pharmacological closure of the duct (age more than 10 days), as well as with extremely low body weight (less than 1000 g). Maximum safety and effectiveness of ibuprofen is ensured when treatment is started immediately after the diagnosis of ductus arteriosus (in the absence of contraindications) and when the course of treatment is carried out no later than the 7th day of life.

Ibuprofen preparations are not administered earlier than 6 hours after birth. In this case, the daily volume of fluid administered during treatment with ibuprofen must correspond to physiological needs, since the nephrotoxicity of the drug increases significantly under conditions of dehydration. If anuria or oliguria is observed during the administration of the first or second dose of the drug, dopamine is included in the therapy at a dose of 1-2 mcg/kg per minute, and the administration of the next dose should be postponed until diuresis normalizes. When using ibuprofen intravenously, diuresis, water balance, body weight, levels of sodium, glucose, indirect bilirubin should be monitored daily, and gastric contents should be assessed promptly to prevent the development of bleeding. Glucocorticoids should not be used simultaneously with the administration of ibuprofen intravenously due to high risk gastrointestinal bleeding, as well as other non-steroidal anti-inflammatory drugs.

If the ductus arteriosus has not closed within 48 hours after the last injection or has reopened, a second course can be administered, also consisting of three injections of the drug, as described above. If there is no effect from a repeated course, then the child should be operated on urgently - preferably in the 1st week of life until the age of 10-14 days.

Types of surgical treatment
Just as ligation of the PDA was the first cardiac surgery in the world, so later the closure of the PDA using a polyvinyl probe by W. Portsman in 1967 became the world's first transcatheter cardiac surgical procedure.

Currently, the following types of surgical interventions are used to close the PDA.

Video thoracoscopic clipping (the most preferred method for premature babies).

Transcatheter embolization with an Amplatzer Duct Occluder device or a Cook or Gianturco coil (for moderate duct width, usually over 12 months of age).

Ligation (ligation) of the duct from a left-sided thoracotomy is the method of choice for large PDA diameters, regardless of the child’s age.

The clipping method has obvious advantages for the group of premature and low birth weight babies, but it is not considered the method of choice for everyone age groups due to the fact that it has the highest frequency of recanalizations compared to other types of interventions.

Various technical devices used for interventional occlusion of the PDA are discussed in detail in the review by A. Koch et al.

Result of surgical treatment
Mortality at planned operations in full-term infants it is almost zero. In premature infants, it can reach 10-20% due to the high frequency of concomitant diseases and complications (primarily respiratory distress syndrome and hospital-acquired pneumonia, as well as cerebrovascular accidents). The result of the operation (depending on the duration of surgical treatment) with the best survival if the operation is performed in the first 2 weeks of life. In later operations, mortality is much higher, and its causes are complications of the defect (cerebral intraventricular hemorrhages, ulcerative necrotizing enterocolitis with perforation and purulent peritonitis, etc.) or hospital infections.

Recanalization occurs in less than 1% of cases; it is usually associated with late surgery or severe pulmonary hypertension.

Postoperative follow-up
In normal cases, examination by a cardiologist - once a year with electrocardiographic and echocardiographic monitoring; in case of residual pulmonary hypertension, direct chest x-ray must be performed at least once a year and the condition of the pulmonary bed is assessed over time.

Children are not immune from congenital anomalies, therefore, it is important for parents to know what signs may indicate certain developmental defects. For example, about such a pathology as patent ductus arteriosus in newborns.

The ductus arteriosus is a small vessel that connects the pulmonary artery to the fetal aorta, bypassing the pulmonary circulation. This is normal before birth because it provides fetal circulation necessary for the fetus, which does not breathe air in the womb. After the baby is born, the small duct closes in the first two days after birth and turns into a cord of connective tissue. In premature babies, this period can last up to 8 weeks.

But there are cases when the duct remains open and leads to disturbances in the functioning of the lungs and heart. More often, this pathology is observed in premature babies and is often combined with other congenital defects. If the ductus arteriosus remains open for 3 or more months, we are talking about a diagnosis such as PDA (patent ductus arteriosus).

By what signs can one suspect that the duct remains open?

The main symptoms in children under one year of age are shortness of breath, rapid heartbeat, slow weight gain, pale skin, sweating, and difficulty feeding. The reason for their appearance is heart failure, which occurs due to congestion of the vessels of the lungs, to which blood returns when the duct is open, instead of rushing to the organs.

The severity of symptoms depends on the diameter of the duct. If it has a small diameter, the disease may be asymptomatic: this is due to a slight deviation from normal pressure in the pulmonary artery. With a large diameter of the open vessel, the symptoms are more severe and are characterized by several other signs:

• hoarse voice;
• cough;
• frequent infectious diseases of the respiratory system (pneumonia, bronchitis);
• weight loss;
• poor physical and mental development.

Parents should know that if a child slowly gains weight, gets tired quickly, turns blue when screaming, breathes quickly and holds his breath when crying and eating, then it is necessary to urgently consult a pediatrician, cardiologist or cardiac surgeon.

If a patent ductus arteriosus has not been diagnosed in a newborn, then as the child grows, the symptoms usually worsen. In children over one year of age and adults, the following signs of PDA can be observed:

• rapid breathing and lack of air even with minor physical exertion;
• frequent infectious diseases of the respiratory tract, persistent cough;
• cyanosis – blue discoloration of the skin of the legs;
• weight deficiency;
• rapid fatigue even after short outdoor games.

For what reasons does the ductus arteriosus not close?

Until now, doctors cannot give an exact answer to this question. It is assumed that the risk factors abnormal development can be attributed:

• a number of other congenital heart defects (congenital heart defects);
• premature birth;
• insufficient body weight of the newborn (less than 2.5 kg);
• hereditary predisposition;
• oxygen starvation of the fetus;
• genomic pathologies, such as Down syndrome;
• diabetes mellitus in a pregnant woman;
• infection with rubella during pregnancy;
• chemical and radiation effects on a pregnant woman;
• consumption of alcoholic beverages and drugs by pregnant women;
• taking medications during pregnancy.

Moreover, statistics show that this pathology occurs twice as often in girls as in boys.

How do doctors make a diagnosis?

First of all, the doctor listens to the newborn’s heart with a stethoscope. If the noises do not stop after two days, the examination is continued using other methods.

A chest x-ray shows changes in the lung tissue, expansion of the cardiac borders and vascular bundle. High load on the left ventricle is detected using an ECG. To detect an increase in the size of the left ventricle and atrium, echocardiography or ultrasound of the heart is performed. To determine the volume of blood discharged and the direction of its flow, Doppler echocardiography is needed.

In addition, the pulmonary artery and aorta are probed, with the probe passing through the open duct from the artery into the aorta. During this examination, the pressure in the right ventricle is measured. Before performing aortography, a contrast agent is injected into the aorta with a catheter, which enters the pulmonary artery with the blood.

Early diagnosis is very important, since the risk of complications and severe consequences is very high, even with an asymptomatic course.

Spontaneous closure of the pathological ductus arteriosus can occur in children under 3 months of age. In more late period self-healing is almost impossible.

Treatment depends on the patient’s age, severity of symptoms, diameter of the pathological duct, existing complications and concomitant congenital malformations. The main methods of treatment: medication, catheterization, ligation of the duct.

Conservative treatment is prescribed in case of mild symptoms, in the absence of complications and other congenital defects. Treatment of patent ductus arteriosus with various drugs is carried out before the age of one year under constant medical supervision. For treatment, drugs can be used: non-steroidal anti-inflammatory drugs (ibuprofen, indomethacin), antibiotics, diuretics.

Catheterization is performed for adults and children over the age of one year. This method is considered effective and safe in terms of complications. The doctor carries out all actions using a long catheter, which is inserted into a large artery.

Often, a patent ductus arteriosus is treated surgically by ligating it. If a defect is detected while listening to extraneous murmurs in the heart of a newborn, the duct is closed through surgery when the child reaches the age of 1 year in order to avoid possible infectious diseases. If necessary (with a large diameter of the duct and heart failure), the operation can be performed on a newborn, but it is optimal to do it before the age of three.

Don't forget about prevention

In order to protect the unborn child from developing PDA, you should avoid taking medicines, stop smoking and drinking alcohol, and beware of infectious diseases. If there are congenital heart defects in family members and relatives, you need to contact a geneticist even before the moment of conception.

What's the prognosis?

The vice is dangerous because there is a high risk of death. Patent ductus arteriosus can be complicated by a number of diseases.

• Bacterial endocarditis is an infectious disease that affects the heart valves and can cause complications.
• Myocardial infarction, in which necrosis of an area of ​​the heart muscle occurs due to impaired blood circulation.
• Heart failure develops when the diameter of the unclosed ductus arteriosus is large if left untreated. Signs of heart failure, which is accompanied by pulmonary edema, include: shortness of breath, rapid breathing, high pulse, low blood pressure. This condition poses a threat to the child's life and requires hospitalization.
• Aortic rupture is the most severe complication of PDA, leading to death.

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Patent ductus arteriosus in children

Patent ductus arteriosus in children refers to congenital heart defects. This pathology is considered quite mild. In most cases does not cause in newborns and older children serious problems with health.

One child in every 2,000 births has this defect. And in premature babies, almost every second child is diagnosed with this condition. Manifestations of the disease and treatment tactics depend on the size of the duct.

Congenital causes

• the child was born premature, up to 37 weeks, the shorter the term and the lower the weight of the baby, the higher the risk of developing PDA;
• the child experienced oxygen starvation (hypoxia) during pregnancy and a few minutes after birth;
• during pregnancy, the mother had rubella and the child developed congenital rubella;
• a child was born with Down syndrome, Edwards syndrome or other chromosomal diseases;
• maternal use of alcohol, hormonal or sleeping pills or other toxic substances during pregnancy;
• underdevelopment of the muscle layer, which should ensure compression and closure of the ductus arteriosus;
• a high level of biologically active substances - prostaglandins, which prevent the walls of the duct from contracting.

Symptoms and external signs

Well-being

Doctors classify patent ductus arteriosus in children as “white” defects. This means that at the time of birth the baby's skin is pale and does not have a bluish tint. With such defects, venous blood with a small amount of oxygen does not enter the left half of the heart and the aorta, which means the child’s organs do not lack oxygen. Therefore, in most cases, full-term babies feel normal.

The size of the ductus arteriosus at which symptoms of the disease appear in newborns:

1. Full-term children - the size of the duct is almost equal to the diameter of the aorta, more than 9 mm;
2. Premature babies - the duct size is more than 1.5 mm.

If the duct is smaller in width, then the disease manifests itself only as a heart murmur.

Child's well-being

• rapid pulse more than 150 beats per minute;
• shortness of breath, rapid breathing;
• the child gets tired quickly and cannot breastfeed normally;
• breathing problems, the child requires artificial ventilation;
• sleeps little, often wakes up and cries;
• delay in physical development;
• poor weight gain;
• early pneumonia, which is difficult to treat;
• older children refuse active games.

Objective symptoms

In premature infants and children with medium and large defects, the following symptoms of PDA appear:

• the heart is greatly enlarged and occupies almost the entire chest, this is revealed by tapping;
• When listening, strong and frequent heart contractions are heard. In this way, the heart tries to increase the volume of blood flowing to the organs, because part of it goes back to the lungs;
• pulsation is clearly visible in large vessels, the result of increased blood pressure in the arteries after strong contraction of the ventricles;
• using a stethoscope, a heart murmur is listened to, which occurs when blood passes from the aorta to the pulmonary artery through the ductus arteriosus;
• the skin is pale due to a reflex spasm of small vessels;
• With age, an elevation appears on the chest - the “chest hump”.

Diagnostics

1. Electrocardiogram- in most cases no change. Signs of overload on the right side of the heart appear after the vessels of the lungs compress in response to blood overflow. It becomes difficult for the heart to pump blood through them and its chambers stretch.
2. Chest X-ray shows changes associated with the overflow of the pulmonary vessels with blood and the load on the right atrium and ventricle:
   • enlargement of the right half of the heart;
   • bulging of the pulmonary artery;
   • dilation of large vessels of the lungs.
3. Angiography a type of x-ray examination in which a contrast agent is injected into the vessels to study the direction of blood flow:
   • “colored” blood from the left half of the heart enters the pulmonary artery through the duct;
   • filling the pulmonary trunk with blood and a contrast agent.
4. Phonocardiography– graphic recording of heart sounds.
   • identifies specific noise, which is commonly called “machine noise”.
5. Echocardiography or ultrasound of the heart allows:
   • see the presence of a patent ductus arteriosus;
   • set the hole diameter;
   • calculate the amount and direction of blood passing through it (using Doppler ultrasound).
6. Catheterization of the heart(probing or coronogram) reveals:
   • increased pressure in the right ventricle;
   • blood oxygen saturation in the right side of the heart and in the pulmonary artery;
   • Sometimes a catheter can be inserted from the pulmonary artery into the aorta.
7. CT scan with PDA determines:
   • open duct;
   • its dimensions and location features.

More information about diagnostic methods
Electrocardiogram . The study of electrical currents that arise in the heart and cause it to contract. These discharges are detected by the device's sensitive sensors, which are attached to the chest. After electrical potentials are recorded in the form of a curve, the teeth of which reflect the spread of excitation in the heart. Changes with patent ductus arteriosus:

• overload and thickening of the walls of the left ventricle;
• overload and thickening of the right heart, develops after a significant increase in pressure in the vessels of the lungs.

Chest X-ray. Research based on the properties of X-rays. They pass through almost unhindered human body, but some tissues absorb some of the radiation. As a result, images of internal organs appear on sensitive film. Signs of PDA:

• the large vessels of the lungs are dilated. This is due to the stagnation of large amounts of blood in them;
• enlargement of the boundaries of the heart;
• an increase in the pulmonary trunk, into which an additional volume of blood flows from the aorta;
• in severe cases, signs of pulmonary edema are visible.

Phonocardiography . Registration and analysis of sounds that occur in the heart during its contraction and relaxation. Unlike conventional listening with a stethoscope, the results of phonocardiography are recorded on paper tape in the form of a curved line. Characteristic sign of the defect:

• a continuous “mechanical” noise that is heard both during contraction and relaxation of the heart.

Echocardiography (ultrasound of the heart). The diagnostic device creates an ultrasonic wave that passes into the body and is reflected from different organs or is absorbed by them. The sensor converts the “ultrasound echo” into a moving image on the monitor screen. This makes it possible to consider:

• diameter of the hole in it;
• condition and thickness of the heart muscle;
• blood flow that is thrown from the aorta into the pulmonary artery (Doppler study).

Catheterization of the heart. A small incision is made in the artery on the top of the thigh. A thin and flexible catheter (probe), hollow inside, is inserted through it. Under X-ray control, it is advanced towards the heart. The probe can measure pressure and oxygen content in the arteries and different chambers of the heart. Changes with patent ductus arteriosus:

• increased oxygen content in the right atrium, ventricle and pulmonary artery;
• increased pressure in the right heart and pulmonary trunk;
• if the hole in the duct is large enough, then a probe can be inserted from the pulmonary artery into the aorta.

The catheter can not only clarify the diagnosis, but also block the ductus arteriosus using a special device - an occluder, which is attached to its end.

Angiography . A diagnostic procedure in which a contrast agent is injected through an opening in the catheter. It spreads through the vessels with the blood flow and is clearly visible on x-rays. If a patent ductus ductus is suspected, the blood in the left ventricle is stained with “contrast” and it flows into the aorta. If the ductus arteriosus is open, then through it the colored blood enters the pulmonary artery and into the vessels of the lungs. Within a minute, an x-ray will determine the presence of this substance in the lungs.

Spiral computed tomography with 3D image reconstruction. This method combines the properties of X-ray radiation and the capabilities of a computer. After the body is scanned with X-rays from different angles, the computer creates a three-dimensional image of the area of ​​the body being examined with all the smallest details:

• its length, width;
• the presence of narrowings in its different parts;
• the structure and condition of the vessels through which the probe is planned to be inserted;
• Features of blood movement through the ductus botallus.

In most cases, this study is carried out before surgery so that the surgeon can draw up a plan of action.

Treatment

Drug treatment

Drug treatment for patent ductus arteriosus is aimed at blocking the production of prostaglandins, which prevent this vessel from closing. Diuretics and non-steroidal anti-inflammatory drugs can help with this. In the first days after birth, the chance of successful treatment is much higher.

Cycloxygenase inhibitors: Indomethacin, Nurofen.

These anti-inflammatory non-steroidal drugs block the action of substances that interfere with the natural closure of the duct. As a result, a spasm of the smooth muscle wall of the ductus arteriosus occurs, and it closes.

A regimen for administering indomethacin intravenously has been developed:

1. the first two days: initial dose of 200 mcg/kg, then 2 doses of 100 mcg/kg every 12 hours.
2. Days 2-7: initial dose of 200 mcg/kg, then 2 doses of 200 mcg/kg at daily intervals.
3. Days 7-9: initial dose of 200 mcg/kg, then 2 doses of 250 mcg/kg at daily intervals.

Diuretics, diuretics: Lasix, Furosemide, Hypothiazide

These drugs speed up the formation and elimination of urine, thereby helping to reduce the volume of blood that circulates in the body. This relieves swelling and makes it easier for the heart to work. The drugs are dosed based on a ratio of 1-4 mg/kg per day.

Cardiac glycosides: Isolanide, Celanide

They improve the functioning of the heart, helping it contract more intensely and powerfully. These drugs reduce the load on the heart muscle and give it the opportunity to rest, lengthening the periods of relaxation (diastole). At the first stage, to saturate the body, take 0.02-0.04 mg/kg per day. From the fourth day, the dose is reduced by 5-6 times.

Usually two courses of drug treatment are given. If they do not produce results and the duct does not close, then in this case an operation is prescribed.

Surgical treatment of PDA

Surgery is the most reliable method of treating patent ductus arteriosus in children and adults.

1. Drug treatment did not help close the duct.
2. There were signs of blood stagnation and increased pressure in the vessels of the lungs.
3. Long-term bronchitis and pneumonia that are difficult to treat.
4. Cardiac dysfunction - heart failure.

The optimal age for surgery is 2-5 years.

Contraindications for surgery

1. The reflux of blood from the pulmonary artery into the aorta, which indicates severe changes in the lungs that cannot be corrected with surgery.
2. Severe liver and kidney diseases.

Advantages of the operation:

1. The cause of circulatory disorders is completely eliminated,
2. Immediately after the operation, it becomes easier to breathe and lung function is gradually restored.
3. A very small percentage of mortality and complications after surgery is 0.3-3%.

Disadvantage of the operation
In approximately 0.1% of cases, the aortic duct may open again after a few years. Repeated surgery is associated with a certain risk due to the formation of adhesions.

Types of operations

1. – a low-traumatic operation that does not require opening the chest. The doctor inserts a special device into the arterial duct through a large vessel - an occluder, which blocks the flow of blood.
2. Open surgery. The doctor makes a relatively small incision in the chest and closes the defect. As a result of the operation, the blood flow stops, and the duct itself is gradually deposited connective tissue and it is overgrown.
   • suturing of the ductus arteriosus;
   • ligation of the duct with a thick silk thread;
   • clamping the duct with a special clip.

Treatment of patent ductus arteriosus
The most effective treatment for patent ductus arteriosus is surgery, during which the doctor cuts off the flow of blood from the aorta to the pulmonary artery.

At what age is it better to have surgery?

The optimal age for eliminating a medium-sized defect (4-9 mm) is 3-5 years.

If the duct is wide (more than 9 mm) or if the duct is more than 1.5 mm in a premature baby, surgery is performed a few days after birth.

In the case where the patent ductus arteriosus appears after puberty, the operation can be performed at any age.

Open surgery to close the PDA

The heart surgeon makes an incision between the ribs and closes the duct.

Indications for surgery

1. The size of the duct in full-term babies is more than 9 mm, in premature babies it is more than 1.5 mm.
2. Return of blood from the aorta to the pulmonary artery.
3. Dependence of a newborn on a ventilator when the child cannot breathe on his own.
4. Early prolonged pneumonia, difficult to treat.
5. The duct remains open after two courses of treatment with non-steroidal anti-inflammatory drugs (Indomethacin).
6. Signs of disruption of the lungs and heart due to the reflux of additional blood into the pulmonary vessels.

Contraindications

1. Severe heart failure - the heart cannot cope with pumping blood throughout the body, internal organs suffer from a lack of nutrients and oxygen. Symptoms: interruptions in the functioning of the heart, blueness of the skin and mucous membranes, pulmonary edema, impaired kidney function, enlarged liver, swelling of the extremities, accumulation of fluid in the abdomen.
2. High pulmonary hypertension is the sclerosis of small pulmonary vessels and alveoli, the vesicles in which the blood is enriched with oxygen. The pressure in the vessels of the lungs rises above 70 mm Hg. st and this leads to the fact that blood is thrown from the pulmonary artery into the aorta.
3. Heavy accompanying illnesses which can cause death during and after surgery.

Advantages of the operation

• doctors have extensive experience in performing such operations, which guarantees a good result;
• the surgeon can eliminate a defect of any diameter;
• the operation can be performed for any width of the vessels, which is especially important when the child is born ahead of schedule.

Disadvantages of the operation

• in approximately one percent of cases, the ductus arteriosus reopens;
• the operation is a physical injury and rehabilitation requires 2-6 weeks;
• During and after surgery, complications associated with bleeding or inflammation of the wound may occur.

Stages of open surgery

1. Preparation for surgery:
   • blood test for group and Rh factor, for coagulation;
   • blood test for AIDS and syphilis;
   • general blood analysis;
   • general urine analysis;
   • stool analysis for worm eggs;
   • chest x-ray;
   • Ultrasound of the heart.

   If concomitant diseases are identified, they are treated first to avoid complications after surgery.
   

2. Consultation with doctors. Before the operation, you will definitely meet with the surgeon and anesthesiologist, who will tell you about the procedure and allay your fears. You will be asked if you are allergic to medications in order to choose the right drug for anesthesia.
3. The night before surgery, it is advised to take sleeping pills to ensure you have a good rest.
4. Before the operation, the doctor administers drugs intravenously to general anesthesia. After a few minutes, deep medicated sleep occurs.
5. The heart surgeon makes a small incision between the ribs, through which he gains access to the heart and aorta. During this operation, there is no need to connect a heart-lung machine, since the heart independently pumps blood throughout the body.
6. The doctor eliminates the defect in the most appropriate way:
   • ties with thick silk thread;
   • compresses the duct with a special clamp (clip);
   • cuts the ductus arteriosus and then sutures both ends.
7. The doctor sutures the wound and leaves a rubber tube to drain the fluid. Then a bandage is applied.

The operation to close the ductus arteriosus is performed in the same way in both children and adults.

Endovascular closure of the ductus arteriosus
IN Lately Most operations are performed through the large vessels in the upper thigh.

1. If the diameter of the duct is less than 3.5 mm, then use a “Gianturco” spiral;
2. If the diameter of the duct is larger, then use the Amplatzer occluder.

Indications for surgery

1. Patent ductus arteriosus of any size.
2. Return of blood from the aorta to the pulmonary artery.
3. Ineffectiveness of drug treatment.

Contraindications

1. Return of blood from the pulmonary artery to the aorta.
2. Irreversible changes in the lungs and heart.
3. Constriction of the blood vessels through which the catheter must pass.
4. Sepsis and inflammation of the heart muscle (myocarditis).

Advantages

• does not require opening the chest;
• quick recovery after the procedure 10-14 days;
• minimal risk of complications.

Flaws

• not carried out if there is an inflammatory process or blood clots in the heart;
• not effective if the duct is not located typically;
• will not improve the condition if the pressure in the vessels of the lungs is so high that the reflux of blood from the pulmonary artery into the aorta has begun (third degree of pulmonary hypertension);
• the diameter of the femoral artery must be greater than 2 mm.

Operation stages

1. A few days before the procedure, you will need to do an ultrasound of the heart, a cardiogram and tests to make sure that there is no inflammatory process that could cause complications.
2. Consultation with a cardiac surgeon and anesthesiologist. Doctors will answer your questions, clarify your health status and response to medications.
3. Adults are operated on under local anesthesia - the site where the probe is inserted is numbed. Children are given general anesthesia.
4. The procedure is performed in an X-ray room. Using the equipment, the doctor sees how the catheter is moving and how the operation is going.
5. The surgeon disinfects the skin at the top of the thigh and makes a small incision in the artery and inserts a catheter into it. With its help, a special device is delivered to the arterial duct, which blocks the lumen and does not allow blood to enter the aorta.
6. After installing the “plug,” a contrast agent is injected through the catheter, which enters the blood vessels. The operation is considered successful if the x-ray shows that it does not pass from the aorta to the pulmonary trunk.
7. The doctor removes the catheter and sutures the artery wall and skin. After this, the person will be taken to the ward.
8. On the first day, you should not sit down or bend your legs to prevent a blood clot from forming in the artery. But then the recovery will go quickly and in 3-5 days you will be able to return home.

Rehabilitation after open surgery for PDA

From the operating room you will be transferred to the intensive care unit; you may need to be connected to special devices that will monitor your pulse, blood pressure, heart rhythm and support your body. To ensure uninterrupted breathing, a special breathing tube is inserted into your mouth; it will prevent you from speaking.

Modern anesthesia eliminates problems when waking up. To prevent chest pain from bothering you, you will be prescribed painkillers that prevent inflammation of the wound.

The first day you will have to observe strict bed rest. This means you can't get up. But within 24 hours you will be transferred to the intensive care ward and allowed to move around the ward.

Until the stitch heals, you will need to go to the dressing every day. A day later, the drainage will be removed from the wound and you will be advised to wear a special corset that will prevent the seam from coming apart.

During the first 3-4 days, the temperature may rise slightly - this is how the body reacts to the operation. It's okay, but it's best to tell your doctor.

Do breathing exercises with a jerky exit every hour and do physical therapy: stretch your hands. While lying in bed, bend your knees without lifting your feet off the bed. Move your hands to shoulder joint without getting out of bed.

You will have to stay in the hospital for 5-7 days. When the doctor is satisfied that your condition is steadily improving, you will be discharged home. At first, your capabilities will be somewhat limited, so you need to have someone nearby who will help you with the housework.

Before you leave, you will be told how to treat your stitches. They need to be lubricated with brilliant green or calendula tincture once a day. In the future, your doctor will recommend an ointment to prevent scarring: Contractubex.
You can take a shower after the wound has healed. Simply wash the seam with warm soapy water and then carefully dry it with a soft towel.

Increase physical activity gradually. Start with walks for short distances - 100-200 meters. Increase your load a little every day. In 2-3 weeks you will be almost completely recovered.

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In what cases does the botal duct not close?

This pathology is most often found in children born much prematurely. In children born at term, such a heart defect is practically undetectable. Patent ductus arteriosus is diagnosed in 50% of children born weighing less than 1.7 kg, and 80% of children born weighing less than 1 kg. Prematurely born children often have congenital defects in the structure of the genitourinary and digestive systems. Untimely closure of the embryonic canal between the aorta and the pulmonary trunk in children born prematurely is a consequence of respiratory failure, oxygen starvation during childbirth, metabolic acidosis, constant supply of highly concentrated oxygen, and improper infusion treatment.

In children born at term, this heart defect is detected more often in areas with thin air. In certain cases, insufficient closure of the canal is associated with its incorrect structure. Causes such as genetic predisposition and infectious diseases suffered by a pregnant woman, such as rubella, also lead to the appearance of the ductus botallus.

Characteristics of blood flow with a patent ductus arteriosus

The patent ductus arteriosus in children is located in the upper part of the mediastinum, it begins along with the left subclavian artery on the wall of the aorta, its reverse end is combined with the pulmonary trunk, partially affecting the left pulmonary artery. In especially severe cases, a bilateral or right-sided defect is diagnosed. The canal can have a cylindrical, cone-shaped, fenestrated structure, its length varies from 0.3 to 2.5 cm, width - from 0.3 to 1.5 cm.

The arterial canal, as well as the open foramen ovale, is a physiological component of the embryo’s circulatory system. Blood from the right side of the heart enters the pulmonary artery, from where it is directed through the arterial duct into the underlying aorta. With the onset of pulmonary respiration after birth pulmonary pressure decreases, and in the cardiac artery it increases, which leads to blood entering the pulmonary vessels. When inhaling, a spasm of the ductus arteriosus occurs due to contraction of muscle fibers. The duct soon stops working and becomes completely overgrown as unnecessary.

Heart defects in newborns are indicated by the continued functioning of the ductus 2 weeks after birth. PDA is classified as a pale type defect, since in this disease, oxygenated blood from the aorta is thrown into the pulmonary artery. This leads to the release of excess blood into the pulmonary vessels, their overflow and a local increase in pressure. High load on the left side of the heart leads to expansion of the ventricles and pathological thickening of their walls.

Impaired blood flow during a PDA depends on the size of the canal, its angle relative to the aorta, and the difference in pressure in the pulmonary circulation from the pressure in the systemic circulation. If the channel has a small lumen diameter and is located at an acute angle to the aorta, no serious disturbances in blood flow occur. Over time, such a defect may disappear on its own. The presence of a duct with a wide lumen leads to the reflux of large amounts of blood into the pulmonary vessels and severe disturbances in blood flow. Such channels do not heal on their own.

Classification of heart defects of this type

Depending on the level of pressure in the pulmonary arteries, anomalies in the structure of the heart muscle are divided into 4 types. With grade 1 PDA, the pressure in the pulmonary artery does not exceed 40% of arterial pressure, with grade 2 defects, the pressure ranges from 40 to 70% of arterial pressure, grade 3 is characterized by an increase in pressure to 75% of arterial pressure and preservation of the left shunt. A severe degree of the defect is characterized by an increase in pressure to arterial values ​​or exceeding these values.

In its natural course, the disease goes through 3 stages:

1. 1. At the first stage, the first symptoms of PDA appear; dangerous conditions often develop, which, if left untreated, lead to death.
2. 2. Stage 2 is characterized by relative compensation. Hypervolemia of the pulmonary circulation develops and persists for many years, and overload of the right side of the heart occurs.
3. 3. At stage 3, sclerotic changes occur in the pulmonary vessels. The further course of the disease is accompanied by adaptation of the pulmonary arteries with their subsequent gluing. Symptoms of a patent arterial canal at this stage are replaced by manifestations of pulmonary hypertension.

Clinical picture of the disease

The disease can occur in either asymptomatic or extremely severe forms. An arterial canal of small diameter, the presence of which does not lead to circulatory impairment, may remain undetected for a long time. With a wide ductus arteriosus, pronounced symptoms of the disease appear already at its first stage. The main signs of heart disease in newborns may be constant pallor of the skin, cyanosis of the nasolabial triangle during sucking, crying, and defecation. There is a lack of body weight and a lag in psychophysical development. Such children often suffer from pneumonia and bronchitis. During physical activity, shortness of breath, irregular heart rhythm, and excessive fatigue are noted.

The severity of the disease worsens during puberty, pregnancy, and after childbirth. Blueness of the skin is constantly present, which indicates regular veno-arterial discharge of blood and progressive heart failure. Serious complications arise when joining infective endocarditis, aneurysm and duct rupture. In the absence of timely surgical treatment, a patient with PDA lives no more than 30 years. Spontaneous fusion of the duct occurs in rare cases.

During the initial examination of a patient with a defect of this type, a curvature of the chest in the heart area and increased pulsation in the area of ​​the upper parts of the organ are detected. A characteristic symptom of a patent ductus arteriosus is a pronounced systole-diastolic murmur in the 2nd intercostal space. When diagnosing the disease, it is necessary to conduct an X-ray examination of the chest organs, electrocardiography, ultrasound of the heart and phonocardiography. The image reveals an increase in the heart muscle due to dilatation of the left ventricle, bulging of the pulmonary artery, a pronounced pulmonary pattern, and expansion of the pulmonary roots.

The cardiogram shows signs of dilation and overload of the left ventricle; with pulmonary hypertension, similar changes are observed in the right side of the heart. Echocardiography can reveal indirect symptoms heart defect, see the open arterial canal itself and determine its size. With a high degree of pulmonary hypertension, aortography, MRI of the chest, and sounding of the right ventricle are performed. These diagnostic procedures reveal accompanying pathologies. When identifying a disease, defects such as aortic septal defect, common truncus arteriosus, aortic insufficiency and venoarterial fistula should be excluded.

Methods of treating the disease

When treating low birth weight newborns, it is used conservative therapy, which involves the introduction of prostaglandin production blockers in order to stimulate the natural clogging of the duct. If the result of such treatment does not appear after 3 courses of drug administration, children older than a month are subjected to surgical intervention. In pediatric cardiac surgery, both abdominal and endoscopic operations are practiced. In open operations, the duct is ligated or secured with vascular clips. In some cases, the canal is cut and both ends are sutured.

TO endoscopic methods include: clamping of the ductus arteriosus during thoracoscopy, catheter closure of the lumen with special devices. It is better to prevent any disease than to treat it, especially for heart defects. Even a small size of the ductus arteriosus is dangerous with the risk of death. Premature death can be caused by a decrease in the compensatory capabilities of the heart muscle, rupture of the pulmonary arteries, and the occurrence of severe complications.

After surgery, blood circulation is gradually restored, good blood flow indicators are noted, life expectancy increases and its quality improves. Deaths during and after surgery are extremely rare.

To reduce the risk of having a child with abnormalities in the structure of the heart muscle, a pregnant woman must eliminate all factors leading to the occurrence of such diseases.

During pregnancy, you must stop drinking alcohol, smoking, and taking strong medications. Must be avoided stressful situations and contact with people with infectious diseases. A woman who has had a congenital heart defect should visit a geneticist at the stage of pregnancy planning.

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general information

This congenital defect, related to the pathology of the cardiovascular system, is lack of closure of the ductus arteriosus, connecting the pulmonary artery and the baby’s aorta in the prenatal period.

What happens if a child has patent ductus arteriosus? The baby begins to form a functioning “vessel” between these anatomical formations, unnecessary for an organism existing outside the womb, which leads to obvious disruptions in the functioning of not only the heart, but also the respiratory system.

Causes and risk factors

Knowledge of the etiological factors that contribute to the failure of this fetal communication is especially important not only for doctors, but also for expectant mothers, so that they can promptly sound the alarm and seek medical help in case of any suspicion. This knowledge is also no less important for preventing the occurrence of PDA.

However, some factors can affect its healing. Among the main causes of patent ductus arteriosus and congenital heart defects of the newborn generally distinguish:

Types and phases of flow

There are isolated PDA, which occurs in approximately 10% of all cases of this defect, and combined with other heart defects (atrial septal defect in children, coarctation of the aorta in newborns, forms of pulmonary artery stenosis).

It is also customary to classify open botalls by phases of its development:

• Stage 1 is called “primary adaptation” and lasts during the first 3 years of the baby’s life. This is the most intense stage in terms of severity of clinical symptoms, which can even lead to death if suitable surgical treatment is not provided.
• Stage 2 characterized by relative compensation of the clinical picture of the disease and lasts 3 to 20 years. A decrease in pressure in the vessels of the pulmonary (pulmonary) circulation and an increase in pressure in the cavity of the right ventricle develops, which leads to its functional overload during the work of the heart.
• At stage 3 Irreversible sclerosis of blood vessels in the lungs steadily progresses, which causes pulmonary hypertension.

Considering the level of pressure in the lumen of the pulmonary artery and pulmonary trunk, The following degrees of PDA are distinguished::

1. When the systolic pressure of the pulmonary artery is no more than 40% of the body's blood pressure.
2. The presence of symptoms of moderate hypertension in the pulmonary artery (40-75%).
3. When there are symptoms of severe hypertension in the pulmonary artery (over 75%) and there is blood flow from left to right.
4. When severe hypertension develops in the pulmonary vessels and the pressure equals the systemic arterial pressure, the blood flows from right to left.

Why it’s dangerous: possible complications

• Development of endocarditis bacterial nature, leading to damage to the inner layer of the wall of the heart chambers, primarily in the area of ​​the valve apparatus.
• Bacterial endarteritis.
• Myocardial infarction with risk of rhythm disturbance or death.
• Heart failure varying degrees gravity.
• Swelling of the lung tissue due to increased pressure in the pulmonary vessels, which requires extreme quick action by medical personnel.
• Rupture of the main vessel of the human body - the aorta.

Symptoms

The symptoms that appear with this type of congenital heart defect are entirely depend on the degree of hemodynamic changes in the body. In certain cases, the clinical picture will not be traced.

In others she progresses to extreme degrees of severity and manifests itself in the development of a “heart hump” (a convex deformation of the anterior chest wall in the area of ​​​​the projection of the heart), downward movement of the apical impulse of the heart along with the expansion of its zone, tremors of the heart in its lower and left parts, persistent shortness of breath with orthopnea and severe cyanosis.

The main symptoms of PDA in less severe clinical cases are:

• increased heart rate;
• increased breathing;
• enlarged liver (hepatomegaly) and spleen;
• electrocardiographic signs of left side enlargement;
• specific murmur during auscultation of the heart in the second left intercostal space near the sternum (systole-diastolic);
• rapid high pulse on the radial arteries;
• an increase in the level of systolic systemic pressure and a decrease in diastolic pressure (sometimes to zero).

When to see a doctor

Not in every case, parents can notice changes in the health of their child and suspect this congenital pathology, which, of course, worsens the prognosis for the baby.

Parents should remember that a trip to the doctor is necessary if they Have identified the following symptoms in your baby:

• sleep rhythm disturbance;
• drowsiness;
• slow weight gain;
• shortness of breath at rest or after light exertion;
• bluish discoloration of the skin after exercise;
• lethargy, refusal of games and entertainment;
• frequent acute respiratory infections and acute respiratory viral infections.

You should make your appeal to the local pediatrician, who, in the presence of pathological symptoms, can refer you for consultation to other specialists: pediatric cardiologist, pediatric cardiac surgeon.

Diagnostics

Diagnosis of patent ductus botallus includes several groups of research methods. With an objective examination of the child, the doctor can determine:

• rapid pulse;
• an increase in systolic pressure with a simultaneous decrease in diastolic pressure;
• changes from the apical impulse;
• expansion of the boundaries of cardiac dullness (borders of the heart);
• Gibson's murmur described above (systole-diastolic);
• anamnestic symptoms associated with possible exposure to risk factors for this defect.

Among the instrumental diagnostic techniques The following are in active use:

1. ECG (electrocardiography). There is a tendency towards hypertrophy of the left parts of the heart, and in more severe stages, the right parts with deviation of the cardiac axis to the right. As the disease progresses, signs of heart rhythm disturbances appear.
2. Echocardiography. It also gives information about the expansion of the left heart cavities. If you add a Doppler study, a mosaic pattern of blood flow through the pulmonary artery is determined.
3. Radiography chest organs. Characteristic is the strengthening of the contours of the lung pattern, an increase in the transverse size of the heart due to the left ventricle in the initial stages of the manifestations of PDA symptoms. If hypertension of the pulmonary vessels develops, the pattern of the lungs, on the contrary, becomes poorer, the trunk of the pulmonary artery bulges, and the heart is enlarged.

Differentiation of the diagnosis is necessarily carried out with other congenital heart defects, such as:

• combined aortic disease;
• incomplete atrioventricular canal;
• defective septum between the ventricles;
• defective septum of the aorta and pulmonary artery.

Treatment

Conservative treatment is used only in premature babies and consists of administering inhibitors of prostaglandin formation in order to medically stimulate the independent closure of the duct.

Main medicine in this group is Indomethacin. If there is no effect after repeated administration of the drug three times in children over three weeks of age, then surgical obliteration is performed.

Children are treated surgically at the age of 2-4 years, this is the most best period for this type of therapy. In extended use is the method of ligating the ductus botallus or transversely crossing it, followed by suturing the remaining ends.

Prognosis and prevention

If the duct is not operated on, death occurs in people aged about 40 years due to the development of severe hypertension in the pulmonary arteries and severe degrees of heart failure. Surgical treatment provides favorable outcomes in 98% of young patients.

Preventive actions:

1. Avoiding smoking, alcohol abuse, and drugs.
2. Avoiding stress.
3. Mandatory medical and genetic counseling both before and during pregnancy;
4. Sanitation of foci of chronic infection.

Patent ductus arteriosus is serious congenital pathology , which carries high mortality rates with untimely or inadequate treatment.

The debut of its clinical picture is the development of signs of pulmonary hypertension and cardiac failure. However, If this disease is diagnosed in time, its outcome is very favorable, which is confirmed by modern statistical data.

Patent ductus arteriosus (PDA) is a disease that occurs as a result of disruption of the normal development of the heart and great vessels in the prenatal and postnatal period. Congenital ones usually form in the first months of fetal development as a result of atypical formation of intracardiac formations. Persistent pathological changes in the structure of the heart lead to its dysfunction and development.

Arterial (Botallov) duct- a structural formation of the fetal heart, through which the blood ejected from the left ventricle into the aorta passes into the pulmonary trunk and returns again to the left ventricle. Normally, the ductus arteriosus undergoes obliteration immediately after birth and turns into a connective tissue cord. Filling the lungs with oxygen leads to the closure of the duct by the thickened intima and a change in the direction of blood flow.

In children with developmental defects, the duct does not close in time, but continues to function. This disrupts pulmonary circulation and normal heart function. PDA is usually diagnosed in newborns and infants, somewhat less frequently in schoolchildren, and sometimes even in adults. The pathology is found in full-term children living in high mountain areas.

Etiology

The etiology of PDA is currently not fully understood. Experts highlight Several risk factors for this disease:

• Premature birth
• Low birth weight
• Vitamin deficiencies,
• Hereditary predisposition
• Marriages between relatives
• Mother's age is over 35 years,
• Genomic pathologies - Down, Marfan, Edwards syndromes,
• Infectious pathology in the 1st trimester of pregnancy, congenital rubella syndrome,
• Drinking alcohol and drugs during pregnancy, smoking,
• Irradiation with X-rays and gamma rays,
• Taking medications during pregnancy,
• Impact chemical substances on the pregnant woman's body,
• Systemic and metabolic diseases of the pregnant woman,
• Intrauterine endocarditis of rheumatic origin,
• Maternal endocrinopathies – diabetes mellitus, hypothyroidism and others.

The causes of PDA are usually combined into 2 large groups– internal and external. Internal reasons associated with hereditary predisposition and hormonal changes. TO external reasons include: poor ecology, industrial hazards, diseases and addictions of the mother, toxic effects on the fetus of various substances - drugs, chemicals, alcohol, tobacco.

PDA is most often detected in premature infants. Moreover, the lower the weight of the newborn, the higher the likelihood of developing this pathology. Heart disease is usually combined with developmental anomalies of the digestive, urinary and reproductive systems. The immediate causes of non-occlusion of the ductus Botallova in in this case are respiratory distress, fetal asphyxia, long-term oxygen therapy and parenteral fluid therapy.

Video: medical animation about the anatomy of the ductus arteriosus

Symptoms

The disease can be asymptomatic or extremely severe. With a small diameter of the duct, hemodynamic disturbances do not develop, and the pathology is not diagnosed for a long time. If the diameter of the duct and the volume of the shunt are significant, the symptoms of the pathology are pronounced and appear very early.

Clinical signs:

Children with PDA often suffer from bronchopulmonary pathology. Newborns with a wide ductus arteriosus and a significant shunt volume are difficult to feed, they do not gain weight well and even lose weight.

If the pathology was not detected in the first year of life, then as the child grows and develops, the course of the disease worsens and is manifested by more pronounced clinical symptoms: asthenia of the body, tachypnea, cough, frequent inflammatory diseases of the bronchi and lungs.

Complications

Severe complications and dangerous consequences OAP:

• - infectious inflammation of the inner lining of the heart, leading to dysfunction of the valve apparatus. Patients develop fever, chills and sweating. Signs of intoxication are combined with headache and lethargy. Hepatosplenomegaly develops, hemorrhages appear in the fundus and small painful nodules on the palms. Treatment of pathology is antibacterial. Patients are prescribed antibiotics from the group of cephalosporins, macrolides, fluoroquinolones, and aminoglycosides.
• develops in the absence of timely cardiac surgery and consists of insufficient blood supply to internal organs. The heart stops pumping blood fully, which leads to chronic hypoxia and deterioration of the functioning of the entire body. Patients experience shortness of breath, tachycardia, edema lower limbs, fast fatiguability, sleep disturbance, constant dry cough. Treatment of pathology includes diet therapy, drug therapy aimed at normalizing blood pressure, stabilization of heart function and improvement of blood supply.
• - an acute disease caused by the appearance of foci of ischemic necrosis in the heart muscle. Pathology appears characteristic pain, which is not relieved by taking nitrates, agitation and anxiety of the patient, pale skin, sweating. Treatment is carried out in a hospital setting. Patients are prescribed thrombolytics, narcotic analgesics, nitrates.
• Reverse blood flow through the wide ductus arteriosus can lead to and.
• Pulmonary edema develops when fluid moves from the pulmonary capillaries into the interstitial space.

Rarer complications of PDA include: aortic rupture, incompatible with life; and rupture of the ductus arteriosus; sclerotic nature; cardiac arrest in the absence correctional therapy; frequent acute respiratory infections and acute respiratory viral infections.

Diagnostics

Diagnosis of PDA is carried out by doctors of various medical specialties:

1. Obstetricians-gynecologists also monitor the development of the fetal cardiovascular system,
2. Neonatologists examine the newborn and listen,
3. Pediatricians examine older children: they perform heart auscultation and, if pathological murmurs are detected, refer the child to a cardiologist,
4. Cardiologists make a final diagnosis and prescribe treatment.

General diagnostic measures include visual examination of the patient, and chest percussion, auscultation, instrumental methods studies: electrocardiography, radiography, ultrasound of the heart and large vessels, .

During the examination, deformation of the chest, pulsation of the heart area, and a shift of the heart impulse to the left are revealed. By palpation, systolic tremors are detected, and by percussion, an expansion of the boundaries of cardiac dullness is detected. Auscultation is the most important method in the diagnosis of PDA. Its classic sign is a rough, continuous "machine" noise caused by the unidirectional movement of blood. Gradually it disappears, and an accent of 2 tones appears above the pulmonary artery. In severe cases, multiple clicking and rumbling noises occur.

Instrumental diagnostic methods:

• Electrocardiography does not reveal pathological symptoms, but only signs.
• X-ray signs pathologies are: reticular pattern of the lungs, expansion of the shadow of the heart, bulging of a segment of the pulmonary artery trunk, flocculent infiltrate.
• Ultrasound of the heart allows you to visually evaluate the work of different parts of the heart and valve apparatus, determine the thickness of the myocardium, the size of the duct. Doppler ultrasound allows you to most accurately establish the diagnosis of a PDA, determine its width and regurgitation of blood from the aorta to the pulmonary artery. Ultrasonography heart allows you to detect anatomical defects of the heart valves, determine the location of the great vessels, and assess the contractility of the myocardium.
• Phonocardiography- a simple method that allows you to diagnose heart defects and defects between cavities by graphically recording heart sounds and noises. Using phonocardiography, you can objectively document the data obtained while listening to the patient, measure the duration of sounds and the intervals between them.
• Aortography- an informative diagnostic method that consists of supplying a contrast fluid into the heart cavity and taking a series of x-rays. Simultaneous staining of the aorta and pulmonary artery indicates patent ductus Botallus. The resulting images remain in the computer's electronic memory, allowing you to work with them repeatedly.
• Catheterization and cardiac catheterization in case of PDA, it allows an absolutely accurate diagnosis if the probe passes freely from the pulmonary artery through the duct into the descending aorta.

Probing of the cardiac cavities and angiocardiography are necessary for more accurate anatomical and hemodynamic diagnostics.

Treatment

The earlier the disease is detected, the easier it is to get rid of it. When the first signs of pathology appear, you should consult a doctor. Early diagnosis and timely therapy will increase the patient’s chances of a full recovery.

If a child loses weight, refuses active play, turns blue when crying, becomes drowsy, experiences shortness of breath, cough and cyanosis, and is often exposed to ARVI and bronchitis, he should be shown to a specialist as soon as possible.

Conservative treatment

Drug therapy is indicated for patients with mild clinical signs and the absence of complications. Drug treatment of PDA is carried out in premature infants and children under one year of age. If after 3 courses of conservative therapy the duct does not close, and the symptoms of heart failure increase, proceed to surgical intervention.

1. A sick child is prescribed a special diet that limits fluid intake.
2. Respiratory support is necessary for all premature infants with PDA.
3. Patients are prescribed prostaglandin inhibitors, which activate independent obliteration of the duct. Typically, intravenous or enteral administration of Indomethacin or Ibuprofen is used.
4. Antibiotic therapy is carried out to prevent infectious complications– bacterial endocarditis and pneumonia.
5. Diuretics - "Veroshpiron", "Lasix", cardiac glycosides - "Strofantin", "Korglikon", ACE inhibitors - "Enalapril", "Captopril" are prescribed to people with clinical heart failure

Cardiac catheterization

cardiac catheterization

Cardiac catheterization is prescribed for children for whom conservative therapy has not given the expected result. Cardiac catheterization is a highly effective method of treating PDA with a low risk of complications. The procedure is performed by specially trained pediatric cardiologists. A few hours before catheterization, the child should not be fed or watered. Immediately before the procedure, he is given a cleansing enema and a sedative injection. After the child relaxes and falls asleep, manipulation begins. The catheter is inserted into the chambers of the heart through one of the large blood vessels. There is no need to make incisions in the skin. The doctor monitors the progress of the catheter by looking at the monitor screen of a special X-ray machine. By examining blood samples and measuring blood pressure in the heart, he obtains information about the defect. The more experienced and qualified the cardiologist, the more effective and successful the cardiac catheterization will be.

Cardiac catheterization and clipping of the duct during thoracoscopy is an alternative to surgical treatment of the defect.

Surgical treatment

Surgical intervention allows you to completely eliminate PDA, reduce the patient’s suffering, increase his resistance to physical activity and significantly prolong life. Surgical treatment consists of performing open and endovascular operations. The PDA is ligated with a double ligature, vascular clips are applied to it, transected and sutured.

Classic surgery is an open operation that involves ligating the Botallo duct. The operation is performed on a “dry” heart while the patient is connected to a ventilator and under general anesthesia.

Endoscopic method surgical intervention is minimally invasive and minimally traumatic. A small incision is made in the thigh through which a probe is inserted into the femoral artery. It is used to deliver an occluder or a spiral to the PDA, which closes the lumen. The entire progress of the operation is monitored by doctors on the monitor screen.

Video: surgery for PDA, anatomy of the Botallian duct

Prevention

Preventive measures consist of eliminating the main risk factors - stress, taking alcohol and medications, and contacts with infectious patients.

After surgical correction of the pathology, the child must engage in dosed physical exercise and massage at home.

Quitting smoking and screening for genetic abnormalities will help reduce the risk of developing congenital heart disease.

Prevention of congenital heart disease comes down to careful pregnancy planning and medical and genetic counseling for people at risk.

It is necessary to carefully monitor and examine women infected with the rubella virus or with concomitant pathology.

The child should be provided with proper care: enhanced nutrition, physical activity, physiological and emotional comfort.

Ductus arteriosus I Duct arteriosus

open(ductus arteriosus; synonym) - congenital, in which after birth a constant communication between the aortic arch and the pulmonary artery remains. May be combined with other developmental defects (developmental defects) . First described in the 16th century. Botallo (L. Botallo). Among patients with congenital heart defects and great vessels, patients with open A. p. make up about 20%.

During the period of intrauterine development, the apex is open and ensures a normal fetus when the lungs are not working. Its length is about 1.5 cm, and diameter up to 2 cm. In the first days or weeks after birth, the apex spasms, and then obliterates and turns into an arterial ligament. In approximately 1% of children, the apex remains open after the child reaches 1 year of age. But in most such cases, the apex has a very small diameter and does not affect the function of the cardiovascular system.

If the artery is not closed after birth, part of the oxygenated blood from the aorta enters the pulmonary artery (from an area of ​​high pressure to an area of ​​lower pressure). The left ventricle of the heart pumps excess blood mass. Often, in response to the overflow of the blood vessels of the lungs, long-term blood occurs with the development of pulmonary hypertension (see Hypertension of the pulmonary circulation) and a decrease in the volume of discharged blood until it completely stops and even flows back from the pulmonary artery into the aorta.

Systolic pressure is usually normal, but diastolic pressure may be reduced. In cases with a large volume of blood discharged from the aorta into the pulmonary artery, it decreases to zero. may resemble that in patients with aortic valve insufficiency.

An X-ray examination reveals an increase in the size of the heart, mainly due to the left ventricle and left atrium, bulging of the pulmonary artery arch and an increase in the pulmonary pattern. There are signs of left ventricular hypertrophy, expressed in varying degrees. In some cases, especially in older children and adults, in the presence of pulmonary hypertension, there is a need for cardiac catheterization and angiocardiography.

Along with severe pulmonary hypertension and heart failure with open A., the development of subacute infectious endarteritis in the duct zone poses a danger. In this regard, establishing a diagnosis of open A. p., even without clinically pronounced symptoms, serves as an absolute indication for surgical intervention. In the USSR, the most common method is double ligation of the AP. After surgery, attention is paid to the prevention of respiratory diseases; in case of prolonged rises in body temperature, accompanied by lethargy, apathy, anemia, blood cultures are performed, active antibacterial therapy is prescribed and the patient is consulted with a cardiac surgeon. It should be limited within 1 year after surgery. Forecast with timely surgical treatment favorable.

Bibliography: Petrovsky B.V. and Keshisheva A.A. Surgical patent ductus arteriosus, M., 1963, bibliogr.

II Duct arteriosus

Blood vessel connecting the pulmonary trunk of the fetus with the aorta; formed from the left sixth (aortic) branchial arch; after birth it quickly becomes empty and is reduced to a cord; non-fusion of A. p. - congenital.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. encyclopedic Dictionary medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

See what “ductus arteriosus” is in other dictionaries:

- (lat. Ductus arteriosus; also Botal duct named after the Italian doctor Leonardo Botallo) duct, the upper part of the 6th arterial arch, connecting the e... Wikipedia

A blood vessel connecting the pulmonary artery and aorta in the fetus of vertebrate animals and humans; the same as Botall's duct... Big Soviet encyclopedia

- (ductus arteriosus, PNA; ductus arteriosus (Botalli), BNA; syn. Botalli proto) blood vessel connecting the pulmonary trunk of the fetus with the aorta; formed from the left sixth (aortic) branchial arch; after birth it quickly becomes empty and reduced... Large medical dictionary

Parts of the heart in PDA ... Wikipedia

DUCT ARTERIAL OPEN- honey Patent ductus arteriosus (PDA) is a vessel through which pathological communication between the aorta and pulmonary artery remains after birth. Subsequently, it gradually obliterates and turns into an arterial ligament. Normal obliteration... ... Directory of diseases

A fetal blood vessel that connects the pulmonary artery directly to the ascending aorta, bypassing the pulmonary circulation. Typically, the ductus arteriosus closes after the baby is born. Incomplete closure of the duct (open arterial... ... Medical terms

DUCT ARTERIAL- (ductus arteriosus) fetal blood vessel connecting the pulmonary artery directly to the ascending aorta, bypassing the pulmonary circulation. Typically, the ductus arteriosus closes after the baby is born. Incomplete closure of the duct... ... Explanatory dictionary of medicine

See Duct arteriosus.

The function of the circulatory system is to deliver oxygen and nutrients to all organs of the body, remove decay products and carbon dioxide from the body, as well as humoral function.

The circulatory system is mainly of mesodermal origin.

Evolution of the circulatory system in invertebrate animals.

In lower invertebrate animals, i.e. in sponges, coelenterates and flatworms, the delivery of nutrients and oxygen from the place of their perception to parts of the body occurs through diffuse currents in tissue fluids. But some animals develop pathways along which circulation occurs. This is how primitive vessels arise.

Further evolution of the circulatory system is associated with the development of muscle tissue in the walls of blood vessels, due to which they can contract, and even later evolution is associated with the transformation of the fluid filling the vessels into a special tissue - blood, in which various blood cells are formed.

The circulatory system can be closed or open. The circulatory system is called closed if blood circulates only through vessels, and open if the vessels open into slit-like spaces in the body cavity, called sinuses and lacunae.

The circulatory system first appeared in annelids, she is closed. There are 2 vessels - dorsal and abdominal, connected to each other by annular vessels running around the esophagus. The movement of blood occurs in a certain direction - on the dorsal side towards the head end, on the abdominal side - backwards due to the contraction of the spinal and annular vessels.

Arthropods have an open circulatory system. On the dorsal side there is a pulsating vessel, divided into separate chambers, the so-called hearts, between which there are valves. With successive contractions of the hearts, blood enters the vessels and then pours into the slit-like spaces between the organs. Having given up nutrients, the blood slowly flows into the pericardial sac, and then through paired openings into the hearts.

Mollusks also have an open circulatory system. The heart consists of several atria into which veins flow and one fairly developed ventricle from which arteries arise.

Evolution of the circulatory system in chordates.

Lower chordates, in particular the lancelet, have a closed circulatory system, but no heart. The role of the heart is performed by the abdominal aorta, from which the afferent branchial arteries depart, in the number of 100-150 pairs, carrying venous blood. Passing through the gill septa in an unbranched form, the blood in the arteries has time to oxidize and through the efferent paired gill arteries, arterial blood enters the roots of the dorsal aorta, which merge into the unpaired dorsal aorta, from which vessels carry nutrients and oxygen to all parts of the body.

Venous blood from the dorsal part is collected in the anterior and posterior cardinal veins, which merge into the left and right ducts of Cuvier, and from them into the abdominal aorta. Blood from the abdominal side collects in the intestinal vein, which carries the blood to the liver, where it is disinfected, and from there hepatic vein also flows into the Cuvier's duct and then into the abdominal vessel.

In higher chordates, in particular in lower vertebrates, i.e. in cyclostomes and fish, the complication of the circulatory system is expressed in the appearance of a heart, which has one atrium and one ventricle. The heart contains only venous blood. There is only one circulation in which arterial and venous blood do not mix. The circulation of blood throughout the body is similar to the circulatory system of the lancelet. From the heart venous blood is flowing to the gills, where it is oxidized, and from them the oxidized (already arterial) blood spreads throughout the body and returns through the veins to the heart.

With the emergence of animals on land and with the advent of pulmonary respiration, a second circle of blood circulation appears. The heart receives not only venous, but also arterial blood, and therefore the further evolution of the circulatory system follows the path of separation of two circles of blood circulation. This is achieved by dividing the heart into chambers.

Amphibians and reptiles have a three-chambered heart, which does not ensure complete separation of the two circles of blood circulation, so mixing of arterial and venous blood still occurs. True, in reptiles the ventricle is already divided by an incomplete septum, and in a crocodile there is a four-chambered heart, so the mixing of arterial and venous blood is observed to a lesser extent than in amphibians.

In birds and mammals, the heart is completely divided into four chambers - two atria and two ventricles. The two circles of blood circulation, arterial and venous blood do not mix.

Let's look at the evolution of gill arches in vertebrates.

In all embryos of vertebrate animals, an unpaired abdominal aorta is formed in front of the heart, from which the branchial arches of the arteries arise. They are homologous to the arterial arches in the circulatory system of the lancelet. But their number of arterial arches is small and equal to the number of visceral arches. So fish have six of them. The first two pairs of arches in all vertebrates experience reduction, i.e. atrophy. The remaining four arcs behave as follows.

In fish, they are divided into the gill arteries that bring them to the gills and those that carry them out from the gills.

The third arterial arch in all vertebrates, starting with tailed amphibians, turns into the carotid arteries and carries blood to the head.

The fourth arterial arch reaches significant development. From it, in all vertebrates, again starting with tailed amphibians, the aortic arches themselves are formed. In amphibians and reptiles they are paired, in birds the right arch (the left one atrophies), and in mammals the left arch of the aorta (the right one atrophies).

The fifth pair of arterial arches in all vertebrates, with the exception of caudate amphibians, atrophies.

The sixth pair of arterial arches loses connection with the dorsal aorta, and the pulmonary arteries are formed from it.

The vessel that connects the pulmonary artery with the dorsal aorta during embryonic development is called the ductus bottalus. In adulthood, it is preserved in tailed amphibians and some reptiles. As a result of disruption of normal development, this duct may persist in other vertebrates and humans. This will be a congenital heart defect and in this case surgical intervention will be necessary.

Anomalies and malformations of the circulatory system in humans.

Based on the study of the phylogenesis of the cardiovascular system, the origin of a number of anomalies and deformities in humans becomes clear.

1. Cervical ectopia of the heart- location of the heart in the neck. The human heart develops from paired mesoderm layers that merge and form a single tube in the neck. During development, the tube moves to the left side of the chest cavity. If the heart is delayed in the area of ​​the original anlage, then this defect occurs, in which the child usually dies immediately after birth.

2. Destrocardia (heterotopia) - location of the heart on the right.

3. Two-chambered heart- arrest of heart development at the stage of two chambers (heterochrony). In this case, only one vessel leaves the heart - the arterial trunk.

4. Non-closure of the primary or secondary atrial septum(heterochrony) in the area of ​​the fossa ovale, which is an opening in the embryo, as well as their complete absence leads to the formation of a three-chambered heart with one common atrium (incidence rate 1:1000 births).

5. Non-fusion of the interventricular septum(heterochrony) with an incidence of 2.5-5:1000 births. A rare defect is its complete absence.

6. Persistence(impaired differentiation) arterial, or Bottallov, duct, which is part of the root of the dorsal aorta between the 4th and 6th pairs of arteries on the left. When the lungs do not function, a person has a ductus bottallus during embryonic development. After birth, the duct closes up. Maintaining it leads to serious functional disorders, since mixed venous and arterial blood passes through. The incidence is 0.5-1.2:1000 births.

7. Right aortic arch- the most common anomaly of the branchial arches of the arteries. During development, the left arch of the 4th pair is reduced instead of the right one.

8. Persistence of both aortic arches 4th pair, the so-called " Aortic ring"- in the human embryo sometimes reduction does not occur right artery 4th branchial arch and aortic root on the right. In this case, instead of one aortic arch, two arches develop, which, going around the trachea and esophagus, connect into an unpaired dorsal aorta. The trachea and esophagus end up in the aortic annulus, which shrinks with age. The defect is manifested by impaired swallowing and suffocation.

9. Persistence of the primary embryonic trunk. At a certain stage of development, the embryo has a common arterial trunk, which is then divided by a spiral septum into the aorta and pulmonary trunk. If the septum does not develop, then the common trunk is preserved. This leads to mixing of arterial and venous blood and usually ends in the death of the child.

10. Vascular transposition- a violation of the differentiation of the primary aortic trunk, in which the septum takes on a straight rather than spiral shape. In this case, the aorta will arise from the right ventricle, and the pulmonary trunk from the left. This defect occurs with a frequency of 1:2500 newborns and is incompatible with life.

11. Open carotid duct- preservation of the commissure between the 3rd and 4th pairs of arterial arches (carotid artery and aortic arch). As a result, blood flow to the brain increases.

12. Persistence of the two superior vena cavae. In humans, a developmental anomaly is the presence of an additional superior vena cava. If both veins flow into the right atrium, the anomaly is not clinically manifested. When the left vein flows into the left atrium, venous blood is discharged into the systemic circulation. Sometimes both vena cava empty into the left atrium. Such a vice is incompatible with life. This anomaly occurs with a frequency of 1% of all congenital malformations of the cardiovascular system.

13. Underdevelopment of the inferior vena cava- a rare anomaly in which the outflow of blood from the lower part of the torso and legs occurs through collaterals of the azygos and semi-gypsy veins, which are rudiments of the posterior cardiac veins. Rarely, atresia (absence) of the inferior vena cava occurs (blood flow is through the azygos or superior vena cava).

14. Absence of the liver portal system.