Anatomical and physiological features of the cardiovascular system in children and their clinical significance. Arterial pressure in children. You may be interested

Many changes are taking place in neonatal cardiovascular system after the embryonic phase of development. They relate directly to the heart as the center of the whole mechanism, as well as blood circulation, pulse, pressure. The child after birth begins to adapt to new living conditions, which provokes these changes. Unlike the fetus, which has a placental blood supply, the newborn's blood does not mix.

The structure of the cardiovascular system of the newborn

Newborn structure of the cardiovascular system is a gradual process that completes its formation only in adolescence. The beginning of this process occurs after the activation of the systemic and pulmonary circulation. This, in turn, leads to the closure of the oval window between the atria at 6-7 months of age. The left side of the heart becomes larger than the right side due to increased workload on the left ventricle. In a newborn, the heart makes up a significant part of the body weight and, with the stages of maturation, increases it, and decreases as a percentage of the total body weight. At the same time, the structure of tissues and blood vessels changes. For example, children have much more capillaries, and the lumens of the aorta, arteries and veins increase with the growth of the child. Blood actively supplies the brain.

The position of the heart of a newborn is higher than in older children due to the growth of the body. Its shape also changes from more round to oval. Initially, the child's pulse is more frequent than that of adults, and this is associated with an intense energy metabolism due to the rapid growth of the body.

Pathology of the cardiovascular system of the newborn

At an early age, a child's heart is not yet as elastic, so it is exposed to many risks. Pathologies of the cardiovascular system can harm the health of the newborn, provoke disability, in the worst case, death. They can be congenital and acquired due to inflammatory diseases, through toxic effects, or due to illnesses suffered by the mother during pregnancy.

Congenital heart pathologies are inherent from the moment of birth and in most cases the predisposition to them is inherited. Very often they require surgical intervention and the sooner the better for the child. Therefore, during pregnancy, it is important to undergo ultrasound, which can determine this. Acquired defects can also occur when exposed to various factors or their complex, since children still have a weak protective barrier.

Hypertension and hypotension are less life-threatening for the child, but require constant monitoring to prevent complications in the future.

It is important to prevent rheumatic heart disease due to fever, which is one of the causes of acquired heart defects.

As you can see, there are a lot of diseases of the heart system, so we advise you to approximately learn their main symptoms in order to be able to recognize them if necessary and immediately seek qualified help.

CHILD FEATURES OF THE HEART

The heart of a newborn is spherical. The transverse size of the heart is equal to the longitudinal or exceeds it, which is associated with insufficient development of the ventricles and the relatively large size of the atria. The auricles are larger and cover the base of the heart. The anterior and posterior interventricular sulci are well marked due to the absence of subepicardial tissue. The top of the heart is rounded. The length of the heart is 3.0-3.5 cm, the width is 3.0-3.9 cm. The mass of the heart is 20-24 g, i.e. 0.8-0.9% of body weight (in an adult - 0.5% of body weight).

The heart grows most rapidly during the first two years of life, then at 5-9 years and during puberty. By the end of the first year of life, the mass of the heart doubles, by the age of 6, the mass increases by 5 times, and by the age of 15, it increases by 10 times compared with the neonatal period.

The interatrial septum of the heart of a newborn has a hole, which is covered by a thin endocardial fold from the side of the left atrium. By the age of two, the hole closes. There are already trabeculae on the inner surface of the atria, a uniform trabecular network is detected in the ventricles, small papillary muscles are visible.

The myocardium of the left ventricle develops faster and by the end of the second year its mass is twice that of the right one. These ratios are preserved in the future.

In newborns and infants, the heart is located high and lies almost transversely. The transition of the heart from a transverse to an oblique position begins at the end of the first year of a child's life. In 2-3 year old children, the oblique position of the heart predominates. The lower border of the heart in children under 1 year old is one intercostal space higher than in an adult (4th intercostal space), the upper border is at the level of the second intercostal space. The apex of the heart is projected in the left 4th intercostal space 1.0-1.5 cm outward from the midclavicular line. The right border is located along the right edge of the sternum or 0.5-1 cm to the right of it.

The right atrioventricular orifice and the tricuspid valve are projected onto the middle of the right border at the level of attachment to the sternum of the 15th rib. The left atrioventricular orifice and mitral valve are located at the left edge of the sternum at the level of the third costal cartilage. The openings of the aorta and pulmonary trunk and the semilunar valves lie at the level of the third rib, as in an adult.

Limits of relative cardiac dullness

(according to V.I. Molchanov)

The shape of the pericardium in a newborn is spherical. The dome of the pericardium is located high - along the line connecting the sternoclavicular joints. The lower border of the pericardium passes at the level of the middle of the fifth intercostal space. The sternocostal surface of the pericardium is covered with thymus for a considerable extent. Lower divisions the anterior wall of the pericardium is adjacent to the sternum and costal cartilages. The posterior surface of the pericardium is in contact with the esophagus, aorta, left vagus nerve, and bronchi. The phrenic nerves are closely adjacent to the lateral surfaces. The lower wall of the pericardium is fused with the tendon center and the muscular part of the diaphragm. By the age of 14, the boundary of the pericardium and its relationship with the organs of the mediastinum correspond to those in an adult.

The blood vessels of the heart at the time of birth are well developed, while the arteries are more formed than the veins. The diameter of the left coronary artery is greater than the diameter of the right coronary artery in all children age groups. The most significant difference in the diameter of these arteries is observed in newborns and children aged 10-14 years.

The microscopic structure of blood vessels changes most intensively at an early age (from 1 to 3 years). At this time, the middle shell develops intensively in the walls of the vessels. The final size and shape of the blood vessels develop by the age of 14-18.

Coronary vessels up to two years are distributed according to the loose type, from 2 to 6 years - according to the mixed type, after 6 years - as in adults - according to the main type. Abundant vascularization and loose fiber surrounding the vessels create a predisposition to inflammatory and degenerative changes in the myocardium.

The conduction system of the heart is formed in parallel with the development of the histological structures of the myocardium, and the development of the sinus-atrial and atrioventricular nodes ends by the age of 14-15.

The innervation of the heart is carried out through the superficial and deep plexuses formed by the fibers of the vagus nerves and cervical sympathetic nodes in contact with the ganglia of the atriogastric and sinus-atrial nodes. The branches of the vagus nerves complete their development by 3-4 years. Until this age, cardiac activity is regulated mainly by the sympathetic nervous system, which is partly associated with physiological tachycardia in children of the first years of life. Under the influence of the vagus nerve, the heart rate slows down and sinus arrhythmia and individual “vagal impulses” may appear - sharply elongated intervals between heartbeats.

Among the functional features of the circulatory organs in children are the following:

    A high level of endurance and working capacity of a child's heart, which is associated both with its relatively larger mass and better blood supply, and the lack of chronic infections, intoxication and harmfulness.

    Physiological tachycardia due to a small volume of the heart with high oxygen needs of the body and characteristic of children early age sympathicotonia.

    Low blood pressure due to the small volume of blood supplied with each heartbeat and low peripheral vascular resistance due to the greater width and elastic arteries.

    The possibility of developing functional disorders of activity and pathological changes due to the uneven growth of the heart, its individual parts and vessels, the peculiarities of innervation and neuroendocrine (in puberty) regulation.

Pulse rate, blood pressure and number of breaths

Pulse, beats / min

Arterial pressure, mm Hg

Number of breaths

systolic

diastolic

newborn

CHILDREN'S FEATURES OF THE circulatory system

In the vascular system of the newborn, changes are associated to a large extent with changes in the conditions of blood circulation. The placental circulation is interrupted and with the act of inhalation, the pulmonary circulation comes into force. Following this, the umbilical vessels become empty and undergo obliteration.

The umbilical vein does not completely overgrow after birth, part of the anastomoses and vessels associated with its non-obliterated segment continues to function and can be strongly expressed in a number of pathological conditions.

The umbilical arteries after the first respiratory excursions are reduced almost completely and during the first 6-8 weeks of life are obliterated in the peripheral section. The process of obliteration of the umbilical vessels consists in the growth of the connective tissue of the intima and the muscular membrane, in the degeneration of muscle fibers and their atrophy, in the hyolin degeneration and the disappearance of elastic fibers.

The process of obliteration of the umbilical arteries and veins proceeds differently: already on the 2nd day of life, the umbilical arteries are impassable at a distance of 0.2-0.5 cm from the navel, and the umbilical vein is still passable. Therefore, the umbilical vein can be the object of infection if the sterility of newborn care is violated and cause the formation of an umbilical purulent fistula and even the occurrence of sepsis.

Simultaneously with the umbilical vessels, the botallus duct is also obliterated. Its obliteration ends by 6 months (in some cases, on the 2nd week after birth). Non-closure of the ductus botulinum by 6-12 months is considered as a malformation. Infection occurs due to the contraction of muscle cells at the mouth of the duct when oxygenated blood enters it from the aorta, where the pressure after birth is higher than in the pulmonary trunk.

As the age of the child increases, due to the active function of the internal organs and the musculoskeletal system, changes occur in the entire vascular system both at the macroscopic and microscopic levels. The length of the vessels, their diameter, the thickness of the walls of arteries and veins increase, the level of branching changes, the loose type of branching of the vessels is replaced by the main one. The most significant differences in the vascular system are observed in newborns and children 10-14 years old. So, for example, in a newborn, the diameter of the pulmonary trunk is greater than the diameter of the aorta, and this proportion remains until 10-12 years old, then the diameters are compared, and after 14 years, an inverse relationship is established between this size of the aorta and the pulmonary trunk. This phenomenon is explained with an increase in the mass of blood, with the growth of the child, an increase in the whole systemic circulation, and finally, an increase in the muscular membrane of the left ventricle and the force of ejection of blood into the aorta. The aortic arch up to 12 years of age has a greater radius of curvature than in adults. In a newborn, the aortic arch is located at the level of the 1st thoracic vertebra, at the age of 15 - at the level of the 2nd thoracic vertebra, at 20-25 years - at the level of the 3rd thoracic vertebra.

Due to the unequal development of individual systems (bone, muscle, respiratory, digestive, etc.) and parts of the body, changes do not occur simultaneously in different vessels of the circulatory system. The greatest changes in the first years of life occur in the vascular system of the lungs, intestines, kidneys, and skin. For example, the arteries of the intestine in early childhood are almost all the same size. The difference between the diameter of the superior mesenteric artery and its branches is small, but as the age of the child increases, this difference increases. The capillary networks are relatively wide, and the elements of the microvasculature at the time of birth are equipped with precapillary sphincters that regulate blood flow.

Big changes in the small circle, especially in the first year of life. There is an increase in the lumen of the pulmonary arteries; thinning of the walls of arterioles; great lability of hemodynamics.

In histological relation to the birth of a child, the arteries of the elastic type are more formed than the muscular ones. In the arteries of the muscular type, there are few smooth muscle cells. The age period up to 12 years is characterized by intensive growth and differentiation of cellular elements of all membranes of the artery wall, but the middle layers grow and develop especially intensively. The increase in the muscular membrane comes from the side of the adventitia. After 12 years, the growth rate of arteries slows down and is characterized by stabilization of the structures of the wall membranes.

In the process of development, the ratio of the diameters of individual large arterial trunks also changes. So, in newborns and young children, the common carotid arteries and subclavian arteries are wider than the common iliac arteries. By puberty, the diameter of the common iliac arteries exceeds almost 1.5-2 times the common carotid arteries. Probably, such a rapid development of the carotid arteries in young children is associated with increased development of the brain (according to Lesgaft's law).

An example of a change in the course of arteries is the renal artery. In newborns and young children, it has an upward direction, and in a 15-20 year old it acquires a horizontal direction.

The topography of the arteries of the extremities changes. For example, in a newborn, the projection of the ulnar artery corresponds to the anterior-medial edge ulna, with the radius - the anterior medial edge of the radius. With age, the ulnar and radial arteries are displaced in relation to the midline of the forearm in the lateral direction. In children older than 10 years, these arteries are located and projected in the same way as in adults.

As for the age-related features of veins, it should be noted that with age their length and diameter also increase, the position and sources of formation change, and histological features of veins are also noted in different age periods. So in newborns, the division of the vein wall into membranes is not pronounced. Elastic membranes are underdeveloped even in large veins, since the return of blood to the heart occurs without the participation of the walls of the veins in this process. The number of muscle cells in the vein wall increases with increasing blood pressure on the vessel wall. Valves in the veins of the newborn are present.

Large veins such as the superior and inferior vena cava are short and relatively large in diameter. The superior vena cava is short due to the high location of the heart; by the age of 10-12, the cross-sectional area of ​​​​this vein increases, and its length increases. The inferior vena cava is formed at the level of III-IV lumbar vertebrae.

The portal vein in newborns is subject to significant anatomical variability, manifested in the variability of the sources of its formation, the number of tributaries, the place of their confluence, and the relationship with other elements of the lesser omentum. The initial section of the vein lies at the level of the lower edge of the XII thoracic vertebra or I lumbar, behind the head of the pancreas. It is formed from two trunks - the superior mesenteric and splenic.

The confluence of the inferior mesenteric is not constant, more often it flows into the splenic, less often into the superior mesenteric.

After birth, the topography of the superficial veins of the body and limbs changes. So, newborns have dense subcutaneous venous plexuses, large saphenous veins are not contoured against their background. By the age of 2, the saphenous veins of the upper and lower extremities.

In newborns and children of the first year of life, the superficial veins of the head are clearly distinguished. This phenomenon is actively used in practical pediatrics for the administration of drugs for various diseases. Moreover, the superficial veins are closely connected with the diploetic veins, which represent a delicate, finely looped network in the foci of ossification. When the bones of the skull reach a sufficiently advanced stage of development (by 5 years of age), the diploetic veins are surrounded by bony canals, and retain connections with the superficial veins of the head, as well as connections with the meningeal veins and with the superior sagittal sinus.

A rapid leap in the development of organs and systems occurs during puberty. Due to the uneven growth of various systems, there is a temporary violation of the coordination and functions of the cardiovascular system. The growth of the muscles of the heart occurs faster than the nervous tissue, therefore, there is a violation of the functions of automatism and excitability of the myocardium. The volume of the heart increases faster than the vessels - this leads to vasospasm, an increase in peripheral total resistance and can lead to a hypertrophic variant of the heart in adolescents. Vasospasm also supports the activation of the adrenal glands and pituitary gland, which leads to hypertensive conditions. There are hypoinvolutional variants (small drip heart), which is caused by a fixed lifestyle.

Any doctor will tell you that the body of a crumb is significantly different from an adult: it has its own diseases, inherent only to it, and its own principles of work - physiological features. Knowing these features is very important for parents, because many of the nuances of caring for a baby depend on them. We will talk about the special “device” of a newborn in this section.

Who does not know about the most important role played by the cardiovascular system in ensuring the vital activity of the human body? The human heart begins to contract from the first weeks prenatal development and throughout his life carries out its uninterrupted work. Speaking of the human heart, we compare it with an engine, a pump, but not only. We consider him the embodiment of sincerity, humanity because of his ability to sensitively respond to changes in our mood and the state of the whole organism.

The structure of the heart

The human heart is a hollow muscular organ consisting of four chambers: the right and left atria and the right and left ventricles. The right and left sections of the heart are separated by partitions - interatrial and interventricular. And the right and left atria are connected, respectively, to the right and left ventricles with the help of holes equipped with valves.

The division of the heart into right and left sections is not only anatomical. These two parts of the heart perform various work, taking on the provision of blood circulation in two circles - large and small.

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The systemic circulation begins in the left ventricle, continues in the aorta (the largest blood vessel that carries blood from the heart to the entire body) and then goes through all the vessels of the body, limbs, brain, internal organs (except the lungs) and ends in the right atrium.

The main tasks of the systemic circulation are:

    delivery to all organs and tissues of blood enriched with oxygen (arterial blood); the implementation of gas exchange in the capillaries of organs and tissues - oxygen enters the tissues, which is necessary for the life of cells, and carbon dioxide (an exchange product, waste products) enters the bloodstream; transport of saturated blood carbon dioxide, back to the heart.

The pulmonary circulation begins in the right ventricle, then follows the pulmonary artery, which carries blood to the lungs, and ends in the left atrium. The tasks of the pulmonary circulation are just as important: it delivers blood saturated with carbon dioxide to the vessels of the lungs, where reverse gas exchange occurs - the blood gives off carbon dioxide and is enriched with oxygen. Further, the vessels of the pulmonary circulation deliver oxygen-enriched blood to the left atrium, from where it begins its journey through the large circle.

Valves between the atria and ventricles, between the ventricles and large vessels: they prevent the reverse flow of blood from the vessels into the cavity of the heart and from the ventricles to the atria.

Important changes

Immediately after the birth of a child, at the moment of the first breath, truly revolutionary changes occur in the circulatory system. Throughout the entire period of intrauterine development, the pulmonary circulation did not function - the blood was enriched with oxygen due to the placental blood flow: the fetal blood received oxygen from the mother's blood. Blood enriched in the placenta with oxygen and other nutrients, through the umbilical vein, passing in the umbilical cord, came to the fetus. The umbilical vein carried this blood to the liver. The liver received the most oxygenated blood. Another big part

arterial blood entered the right atrium, where blood saturated with carbon dioxide was also sent from the upper half of the body. In the right atrium there was oval window, through which blood, enriched with oxygen and partially mixed with venous, oxygen-poor blood, entered the systemic circulation and further to the lower body.

In addition to the oval window in the fetus, there were two more so-called shunts (messages between the vessels) - the arterial and arrantian ducts. Their presence is characteristic exclusively for the fetus.

Thus, the most oxygen-rich blood was received by the liver and brain of the fetus. The lower part of the body received blood, the oxygen content of which is lower. These are partly due to the large size of a newborn baby compared to the size of the rest of the body, more developed upper shoulder girdle.

Immediately after crossing the umbilical cord and making the first breath by the newborn child, the uteroplacental circulation ceases to function and the small circle begins to function. Fruit communications (foramen ovale, arterial and arrantian ducts) become unnecessary and gradually, during the first day of the life of the rebbe, are closed.

But since the closure occurs at once (usually it takes from one to two or three days), during this time, murmurs can be heard in the heart of the newborn, which are not a sign of heart disease and gradually disappear.

Age features

The heart of a newborn child is much larger in relation to the size of his body than those of an adult (in a newborn, the mass of the heart is about 0.8% of body weight, and in adults - 0.4%). The right and left ventricles have approximately the same thickness, but this ratio changes with age: the load on the left ventricle increases after birth, since it drives blood through the systemic circulation and does much more work than the right one, its walls gradually become one and a half to two times thicker than the right one.

The pulse rate in newborns (120-160 beats per minute) is significantly higher than in older children (80-120 beats per minute) and even more so than in adults (60-80 beats per minute). This is due to the fact that newborns have a much higher tissue need for oxygen, and also because their pumping ability of the heart is much lower. Therefore, the cardiovascular system compensates for the high oxygen demand by increasing the number of heartbeats. With any trouble in the state of the newborn, the heart rate increases. This can happen with overheating, with dehydration, with pathology from the nervous system, respiratory system and, of course, the circulatory system.

Blood pressure in newborns is much lower than in adults. It is the lower than younger child. This pressure is due to the wider lumen of the vessels, the smaller size of the left ventricle and the lower pumping capacity of the heart than at an older age. In a newborn baby, the value of systolic pressure (the first digit in pressure indicators) is about 70 mm Hg. Art. by the year it rises to 90 mm Hg. Art.

The blood vessels of a newborn baby grow quite intensively, especially small vessels- capillaries, which, as it were, penetrate and braid all organs and tissues. Their permeability is very high, which allows more efficient gas exchange in tissues.

The lumen of large arteries and veins is large enough, which, in combination with low blood pressure, on the one hand, improves the conditions of blood circulation, and on the other hand, creates preconditions for blood stagnation. This explains the propensity of newborns to a number of inflammatory diseases, including such as pneumonia, osteomyelitis - inflammation of the bone tissue.

Thus, in general, the age-related features of the cardiovascular system of the newborn facilitate blood circulation, helping to ensure that the high oxygen needs of the growing body are fully satisfied. However, such high demands force the heart to do much more work, which, given the limited reserve capacity of the heart, makes it more vulnerable.

Prevention of cardiovascular diseases

How can possible congenital and acquired diseases of such a vital system as the cardiovascular system be prevented?

First of all, you need to remember that. that the laying of the heart occurs at the earliest stages of intrauterine development - in its 4th week. Therefore, often a woman is not yet aware of the onset of pregnancy at a time when any adverse effect can cause a violation of the formation of the heart. That is why it is important to plan pregnancy, an exceptionally healthy lifestyle for the expectant mother at the stage of preparation for pregnancy, prevention viral diseases and the complete exclusion of professional and other harmful effects when there is a possibility of a desired and planned pregnancy.

Prevention of congenital and acquired heart diseases is everything that contributes to the successful course of pregnancy - active image life, balanced diet, lack of pronounced stress factors, strengthening immune system pregnant.

Sparing delivery, a favorable course of the early neonatal period, prevention of colds and viral infections, and rational hardening also help to prevent diseases of the cardiovascular system. Based on the peculiarities of the structure of the vessels of a newborn child and the functioning of his heart, measures aimed at strengthening the walls of blood vessels and training them to the effects of temperature factors are especially important. These activities include air baths in the first month of life, to which from the second or third month you can add contrast rubbing cool and warm water.

For normal development heart muscle requires the presence in the child's diet of a number of vitamins and minerals, such as vitamins B and C, iron, copper, magnesium, zinc, potassium, phosphorus. Most of them are contained in mother's milk in the optimal ratio. Therefore, natural feeding, being the basis for the formation of the health of a growing baby, also contributes to the normal growth and development of the heart and blood vessels. The same trace elements and vitamins help to strengthen the immune defense of a small person, and the prevention of colds and viral diseases is also the prevention of heart disease.

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FUNCTIONAL HEART AND VASCULAR DISEASES IN CHILDREN

They are the most common in the structure of cardiac pathology. They occur in children of all ages, including newborns.

Etiology and pathogenesis

Currently, functional diseases are considered secondary. Various etiological factors- physical inactivity in children, toxic-infectious effects, hypoxia in childbirth, psycho-emotional overload, stressful situations cause significant damage to the central and autonomic nervous system and lead to regulatory and humoral shifts, as a result of which various organs can be affected, including the cardiovascular system.

To designate functional diseases heart and blood vessels, different terms are used: neurocirculatory dystonia (NCD), vegetovascular dystonia(VVD), myocardial dystrophy, functional cardiomyopathy (FCD). Such terminological disunity introduces great confusion into the doctrine of functional heart diseases and requires streamlining. We consider the most acceptable terms - FKP to denote changes in the heart and NCD - for vascular damage. They have advantages over the term "myocardial dystrophy", which focuses the clinician's attention only on the fact of damage - dystrophy, the presence of which remains unproven, and the term VVD, which is too general (occurs with functional diseases various organs) and therefore not orienting the doctor to the organization of specific therapeutic measures.

Classification

In pediatrics, there is no generally accepted classification of functional diseases of the heart and blood vessels. We believe that FKD should be subdivided according to the form into primary (dysregulatory and dishormonal) and secondary, arising against the background of chronic and acute infection, as well as by syndromes - cardialgic, which occurs both in primary and secondary FKD, cardiac with and without rhythm disturbances, respiratory and gynecological. NCD should be divided into hyper-, hypotensive and mixed forms.

Clinical picture

The clinical picture is characterized by a variety of symptoms and is determined by the variant of the disease. Common to FKD and NCD is an abundance of complaints of increased fatigue, weakness, headache, which often worsens in the evening, sleep disturbance, pain in the heart, often stabbing, rarely aching, quickly and most often spontaneously disappearing. Some children complain of shortness of breath, a feeling of lack of air, shortness of breath, fainting, which occur during stuffy room, bath and are often combined with hypotensive syndrome. There is a prolonged subfebrile condition, which is caused by a focal infection, but sometimes it is noted even in its absence and is associated with autonomic disorders. The manifestations of the latter are acrocyanosis, cold and wet palms, sweating, profuse juvenile acne, persistent dermographism.

BP is characterized by lability. Systolic blood pressure tends to increase or decrease (this underlies the diagnosis of hypo- and hypertensive NCD syndromes). Diastolic BP and mean BP are most often normal.

The borders of the heart (percussion, X-ray and according to echocardiography) are not changed. At the apex of the heart, at the 5th point, along the left edge of the sternum, systolic murmur decreasing in the vertical position. The pulse can be quickened, slowed down, labile. The heart rate in the upright position is much higher than in the horizontal position. The ECG reflects the existing vegetative shifts - tachycardia or bradycardia is pronounced, the P-Q interval is lengthened or shortened, the T wave is reduced, smoothed and negative in the 2nd, aVF

Ub-leads, the RST segment in these leads is displaced. Sometimes the T wave is enlarged. Since such changes also occur with myocarditis, in terms of differential diagnosis, it is necessary to carry out functional electrocardiographic tests (obsidan, atropine, orthostatic). With functional cardiopathies, they are positive.

Functional cardiopathies often occur with rhythm disturbances. There are extra- and parasystoles, atrial rhythms against the background of bradycardia, sick sinus syndrome, various blockades are possible - sinoatrial blockade different degrees, partial atrioventricular blockade of the 1st and 2nd degree (less often).

On FCG - often variable size and shape of systolic murmur at the apex of the heart and at the 5th point. On echocardiography, the dimensions of the heart are normal. Myocardial contractions of sufficient amplitude. Myocardial hyperkinesis is common interventricular septum in the absence of hypertrophy. Prolapse is sometimes diagnosed mitral valve, which can be combined with FKP. Indicators of central hemodynamics in children with FKD are close to normal. Laboratory changes in routine studies in children with primary FKD are absent. At special studies a decrease in the content of catecholamines and cholinesterase and an increase in the level of acetylcholine can be detected. In secondary FKD, biochemical and immunological changes are possible caused by the disease against which FKD occurs, the absolute content of peripheral blood lymphocytes, as well as the number of B- and T-lymphocytes, the content of the main Ig classes in FKD is the same as in healthy children . The functional ability of T-lymphocytes is often reduced.

To clarify the diagnosis of FKD, which often presents great difficulties, many clinical criteria. We consider it possible to use in pediatric practice the proposals of V. I. Makolkin, S. A. Abbakumov (1985), who give 6 signs and believe that a combination of 3 of them is sufficient to establish the diagnosis of FKD. These include: 1) pain in the region of the heart; 2) heartbeat; 3) respiratory disorders, feeling of lack of air; 4) vascular dystonia, weakness and lethargy; 5) vegetative dysfunctions - persistent dermographism, asthenoneurotic disorders; 6) headache, dizziness. No effect of anti-inflammatory therapy and good effect from the use of β-blockers also speaks in favor of FKP. The diagnosis of FKD is excluded, according to V. I. Makolkin, S. A. Abbakumov (1985), if the following signs are present: an increase in the size of the heart, at least according to X-ray and EchoCG studies, diastolic murmurs, intraventricular blockade (severe blockade of the legs bundle of His and their branches), which developed during this disease atrioventricular block II - III degree, paroxysmal ventricular tachycardia and atrial fibrillation, pronounced shifts in laboratory data, if they are not explained by concomitant diseases, chronic heart failure.

Treatment

Treatment of FKD should be etiopathogenetic whenever possible. Of the medications prescribed sedatives, tranquilizers, drugs that improve metabolic processes in the myocardium, such as riboxin. β-blockers (obzidan, trazikor) are important for tachycardia, a tendency to increase blood pressure, fainting. In FKP, proceeding with bradycardia, preparations of the Belloid type are indicated. In case of heart rhythm disturbances, antiarrhythmic therapy is carried out (see Cardiac arrhythmias), in case of hypotensive NCD syndrome, eleutherococcus, pantocrine are prescribed.

Children with FKD should be encouraged to lead a healthy lifestyle, and general physical education is required (exemption only from participation in competitions). It is important to stay outdoors for a long time, swimming (swimming pools), cycling, skiing, skating is useful. Playing football, volleyball, basketball, tennis is not contraindicated. Undesirable strength exercises, excessive physical exercise. Systematic sanitation of foci of infection is very important. shown spa treatment mainly in local sanatoriums, staying in sanatorium camps.

Surely, every person who sees a small child thinks that the baby is just a copy of an adult reduced by several times. Of course, in fact, it is so, but not quite. Like it or not, children, and especially infants, have a number of differences from the adult human body. For example, we can say that their organs do not work like adults and according to a regimen that is completely incomparable to ours.

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Photo gallery: Features of the cardiovascular system of the baby

Naturally, the most main body both an adult and a baby are the heart, or to be more precise, the cardiovascular system. Thanks to her, our body receives blood in the prescribed amount, moreover, it is responsible for the heartbeat and gives us life.

What is the heart made of?

The heart is a very complex organ that has the same complex structure. The heart has four compartments: two ventricles and two atria. All parts of the heart were invented for a reason to maintain symmetry. Each department does its job, and to be more precise, they are responsible for the transfer of blood through the small and large circles of blood circulation.

What does the systemic circulation do?

Without going into details, we can say that the systemic circulation inherently makes it possible for us to live, because it is he who sends oxygenated blood to all our tissues, from the tissues of the toes to the tissues of the brain. This circle is considered the most important. But if we have already talked about the importance, then we need to mention the pulmonary circulation. It is with its help that oxygenated blood can enter the lungs, thanks to which we can breathe.

Features of a baby heart

Few people know what changes occur in the body of a baby who has just been born into the world, but in fact they are very colossal! Only at the first breath after childbirth, the cardiovascular system of the crumbs begins to fully function. After all, when a baby lives in the womb of his mother, the small circle of his blood circulation does not work, this makes no sense. The crumbs do not need their lungs, but for everything else there is enough a large circle that interacts most directly with the mother's placenta.

Moreover, you have probably thought many times about why newborn babies have such a disproportionately large head and such a small body compared to the head. This is precisely because of the systemic circulation, which, during pregnancy, the baby’s brain and upper body were perfectly supplied with oxygen, but Bottom part was provided to them worse, because of this, the lower part of the body lagged behind in development. However, this is not at all a reason for panic and worries, because we are all normal adults and walk with normal proportions. All parts of the body will quickly catch up with each other and become absolutely proportional.

Also, initially, at the first listening, the heart doctor may hear some murmurs in the child's heart, but you should not worry about this either.

Noises in the baby's heart

Almost all parents raise a panic and begin to worry about the health of their baby when the pediatrician detects heart murmurs in the baby. Of course, this has nothing to do with the norm, but this happens very often with babies, about 20% of babies suffer from it. It happens that the heart simply does not have time to adapt with a rather rapid growth of the body, as a result of which the thymus and lymph nodes put pressure on the heart vessels and noise is obtained, while no changes in blood circulation occur. Quite often noises arise because of chords of a left ventricle which are incorrectly located, they have the name false chords. As the baby grows, it goes away on its own. There may be such a reason as prolapse (flexion) of the mitral valve.

In any case, the specialist will indicate in the baby’s card that he has detected noises and write you a referral to a cardiologist. In no case should you ignore the recommendations of a pediatrician. Go to a cardiologist without fail and go through all the examinations. He can prescribe you an ultrasound of the heart, an ECG, or something else. Basically, murmurs in the heart of the chest are not the cause of any abnormalities, but still there are situations when some pathologies are detected.

Naturally, serious illness, for example, such as heart disease, doctors detect even in the maternity hospital, but it happens that the work of the heart is disturbed a little later, and perhaps they appear after any past illnesses.

Heart murmurs can be caused by rickets, anemia, severe infectious diseases and possibly their consequences. Often, doctors begin treatment only when the baby reaches one year of age. If your child lags behind in development, growth, or his skin turns blue, then you do not need to wait for a routine examination, contact a pediatric rheumatologist immediately.

Age features

If we consider the heart of an infant in the ratio of steles, then we can see that it weighs much more than that of any adult and makes up almost one percent of the total body weight of a newborn. It is worth mentioning that at first the walls of the baby's ventricle are equal in thickness, but over time, the ventricle from which the large circle of blood circulation begins to move acquires thicker walls than the one that works with the small circle.

If suddenly you suspect that your child's heart is beating very often or the pulse is not normal, as if he had just jumped and ran, do not panic. For a baby, it is considered normal when his pulse makes more than a hundred beats in one minute. Please note that in an adult, it is considered normal when the pulse is not higher than sixty beats in the same time. Know that a baby who has just been born needs oxygen much more, because all his tissues constantly require it. Because of this, the heart with all its strength distills the blood, which is saturated with oxygen through all the capillaries, tissues and veins of the newborn.

In infants, the process of blood circulation itself is much easier than in an adult, because all capillaries and vessels have a huge lumen. Thanks to this, the blood moves better and gives oxygen to tissues, moreover, the process of gas exchange between tiny tissues in the baby's body is simplified.

Prevention of diseases of the vessels and heart of the baby

It is clear that it is necessary to do the prevention of cardiovascular diseases from the very first months of the baby. Already from the age of one month you can do the necessary procedures.

Always keep in mind how your baby has developed while in the womb, because this affects general health baby and all health problems. It is because of this that even at the beginning of pregnancy in the first trimester, you must especially carefully bear the child, because it is this period that affects his health. Often, mothers behave inappropriately at this time, perhaps due to the fact that not all women immediately find out that they are pregnant. If you notice the first signs of pregnancy, then you need to immediately find out if this is true or not, so that in the future there will be no complications.

Naturally, the birth itself can affect the baby's cardiovascular system, both positively and negatively. In some situations, it will be much better if you do a caesarean section, while maintaining the integrity of all the systems of the child's body, than in any case trying to give birth naturally.

In addition, you need to give the baby minerals and vitamins, which you can buy in pharmacies in the form vitamin complexes. If you regularly give these vitamins to the baby, then this will be the ideal prevention of diseases of the vascular tissues and the heart.

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Ministry of Health of the Republic of Belarus

Belarusian Medical Academy of Postgraduate Education

Teaching aid

Cardiovascular system in newborns

L.G. Kozharskaya

G.L. Kachan

Introduction

1. Anatomical and physiological features of the cardiovascular system in a newborn child

4. Congenital heart defects

5. Diseases of the myocardium

6. Cardiac arrhythmias in a newborn

7. Heart failure

Literature

Applications

Introduction

Authors: d.m.s. professor of the department Polyclinic Pediatrics of the Belarusian Medical Academy of Postgraduate Education Larisa G. Kozharskaya; PhD Associate Professor Polyclinic Pediatrics of the Belarusian Medical Academy of Postgraduate Education Galina Lvovna Kachan.

Reviewers: d.m.s. professor, head of department children's diseases No. 1 of the Belarusian State Medical University A.V. Sukalo; PhD assistant professor T.V. Gnedko, Laboratory of Clinical Neonatology, Rehabilitation of Newborns and Children of the First Year of Life, Republican Research and Practical Center "Mother and Child"

Data on the physiology of the blood circulation of the fetus and newborn, ECG features in newborns are given. Differential diagnostic approaches and principles of therapy for the pathology of the cardiovascular system in newborns are considered.

Intended for neonatologists, cardiologists, resuscitators, pediatricians.

1. Anatomical and physiological features of the cardiovascular system in the fetus and newborn

newborn vascular heart myocardium

The formation of the fetal heart occurs from the 2nd to the 8th week of intrauterine development. The work of the heart in the prenatal period is aimed at providing metabolic processes between the blood of the fetus and the mother, which occur in the placenta. Own blood circulation has been functioning in the fetus since the end of the second month. Oxygenated blood from the placenta is distributed through the umbilical vein into two streams: one stream enters the portal vein, the other, continuing the umbilical vein in the form of the duct of Arantia, flows into the inferior vena cava, where placental blood mixes with venous blood flowing from the pelvic organs, liver, intestines and lower extremities. The bulk of the blood flowing into the right atrium from the inferior vena cava, due to the presence of a valve-like fold in the right atrium (Eustachian valve), enters through the foramen ovale into the left atrium, left ventricle and aorta. The remainder of the blood from the inferior vena cava and blood from the superior vena cava flows from the right atrium into the right ventricle and into the pulmonary artery. From the pulmonary artery, through the open ductus arteriosus, this blood enters the descending aorta below the origin of the vessels that deliver blood to the brain.

Thus, fetal circulation is characterized by the following features:

the placenta is an active metabolic organ;

blood enters the right ventricle through the superior vena cava and coronary sinus;

pulmonary blood flow is practically absent due to the high resistance of pulmonary vessels;

blood flow through the ductus arteriosus is carried out from right to left and is approximately 60% of the total cardiac output;

the pressure in the right atrium is slightly higher than the pressure in the left atrium;

The right ventricle pumps about 2/3 of the total cardiac output.

After the birth of a child and the transition to a pulmonary type of breathing, the following occurs:

decrease in the resistance of pulmonary vessels (due to an increase in the level of PaO2), an increase in blood flow through them;

the oval window ceases to function. Its complete obliteration occurs by 5-6 days. In 50% of children, the foramen ovale may remain open but without hemodynamic function;

the arterial duct closes (its complete obliteration occurs at 2-3 months of life), a powerful stimulator of duct closure is an increase in the partial tension of oxygen in the blood (due to the transition to a pulmonary type of breathing);

empty placental communications;

each ventricle ejects 50% of the total cardiac output;

all the blood ejected by the right ventricle passes through the lungs.

Primary functional restructuring leads to an increase in left ventricular output by about 25%. Systemic arterial pressure and peripheral systemic vascular resistance become higher than pulmonary artery pressure and pulmonary vascular resistance.

The heart of a newborn is characterized by an oval shape with a predominance of transverse dimensions. The cardiovascular system of a newborn child has a number of features:

The cardiac muscle is represented by a symplast consisting of thin, poorly separated myofibrils. There is no transverse striation, there are many nuclei in the cells, few mitochondria, the activity of mitochondrial enzymes involved in the metabolism of fatty acids is reduced, which leads to L-carnitine deficiency. Myofibrils are dominated by the β-isomer of myosin with low ATPase activity and insufficient function of calcium channels. Connective tissue has few elastic fibers.

A feature of biochemical processes in cardiomyocytes is the predominance of the carbohydrate component and the use of lactate for energy needs.

Coronary circulation is characterized by a loose type of vessels and a large number of anastomoses.

A feature of the nervous regulation of the activity of the heart is the predominance of sympathetic influences.

The hemodynamics of a newborn child is characterized by instability: any deviation in homeostasis (changes in the concentration of oxygen, electrolytes, blood pH) may be accompanied by a return to the fetal type of circulation.

2. Pathology of the cardiovascular system in newborns

The pathology of the cardiovascular system in newborns is represented by:

structural anomalies in the form of congenital malformations (CHD) and minor anomalies of heart development (MAPC);

myocardial diseases;

diseases of the pericardium;

cardiac arrhythmias and conduction disturbances.

In the genesis of the formation of heart pathology, the leading role is played by genetic factors and viral infections. Transplacental transmission of the vast majority of viruses found in newborns with heart disease has been proven. A direct dependence of the severity of heart damage on the activity of the viral infection was established. There is evidence of long-term persistence of cardiotropic viruses detected in a newborn child - Coxsackie B1-5, Coxsackie A13.

The standard complex of examination of a newborn child with a lesion of the cardiovascular system should include:

Clinical examination

Blood tests general and biochemical

Resting electrocardiogram (12 leads)

Daily Holter ECG monitoring

R-gram chest

Doppler echocardiography

During clinical examination, the factors of diagnostic attention are:

intrauterine malnutrition and deviation of weight dynamics;

connective tissue dysembryogenesis stigmas, chest deformity and other phenotypic features. Their presence in a child with heart disease, intrauterine malnutrition is the basis for genetic counseling and cytogenetic examination;

lethargy, weakness or severe anxiety;

pallor skin or cyanosis, edema;

expansion of the boundaries of relative cardiac dullness;

change in the sonority of tones, arrhythmias;

7) the presence of systolic or systole-diastolic murmur. Systolic murmur in a newborn may be associated with heart defects, occurs with relative insufficiency of the mitral and 3-fold valves, in some children the murmur may be due to chordal, valvular, papillary features of the structure of the heart (the so-called small anomalies of the heart), which can cause turbulent and combination noises;

changes in the pulse (lack of it on the femoral artery, a different value on the radial arteries);

change in blood pressure - a big difference in the upper and lower extremities;

difficulty in feeding, refusal to eat, fatigue;

shortness of breath, wheezing in the lungs;

liver enlargement.

When evaluating a complete blood count, the factor of diagnostic attention is high content Hb and erythrocytes.

At biochemical research special attention is paid to an increase in the content of cardiospecific enzymes: MB-creatine phosphokinase and 1-lactate dehydrogenase (Table 1).

Table 1 Normal performance content of MB-creatine phosphokinase and 1-lactate dehydrogenase (1-LD) in healthy newborns

In an ECG study, attention is paid to the type of ECG, changes in the size and shape of the teeth, the duration of the intervals, and the nature of rhythm disturbances is specified.

3. Features of the ECG in healthy newborns

The main feature of the blood circulation of the perinatal period is the predominance of the activity of the right heart, therefore, in the fetus at a gestational age of more than 28 weeks and in newborns, a pronounced right type of ECG is recorded (angle b = + 80 + 120 °). The ECG voltage is reduced, a low-voltage ECG is especially characteristic for preterm infants. Heart rate for the first 2 days from 120 to 160 beats / min, by day 10 heart rate<146 уд/мин, на 16-30 день <140 уд/мин.

The P wave in standard leads is high, in premature babies it is pointed, serrated. PV1-V2 can only be negative in preterm infants. PV2 during the first week may be pointed, PV5-V6 - smoothed. The Q3 wave may be > 1/3 R3. The R wave may be serrated. In the right positions, the R wave is high; deep S is recorded in the left positions. The S wave is absent in lead III, present in aVR and aVL. The T wave in standard leads is reduced, smoothed and even negative (up to 7 days). TV1-V2 may be positive for the first 4 days, then becomes negative. T V3-V5 is negative. From the 7th day TV5-V6 is positive.

PQ interval 0.1-0.12 sec, QRS complex 0.04-0.05 sec, QT interval duration 0.22-0.32 sec, QTc 0.42 to 0.45 ms. QTc - corrected QT interval, calculated as the ratio of QT duration ms to the square root of the previous RR interval. Premature babies have a longer electrical systole than full-term babies.

For the diagnosis of the pathology of the cardiovascular system in newborns, electrocardiographic signs of hypertrophy and overload of various parts of the myocardium are of great importance.

Electrocardiographic signs hypertrophy right chairman R dia:

- prong P2, 3 > 3 mm;

- PaVF tooth high, pointed;

- PaVL wave is negative;

- PV1-2 tooth is high.

True hypertrophy of the right atrium in the neonatal period is rare, its temporary overload due to acute hemodynamic situations is more common. Overload is characterized by the same changes in the P wave as in hypertrophy, but with overload they quickly disappear.

Electrocardiographic signs of left atrial hypertrophy:

- tooth P1, 2 broadened> 0.08 ", split or two-humped;

- tooth PaVL, aVR broadened and double-humped;

- tooth PV3-V6 is broadened and double-humped;

- PV1-2 wave is biphasic with a predominance of the negative phase.

Electrocardiographic signs of right ventricular hypertrophy:

- right ECG type (angle b > +180°);

- high-amplitude RV1-2;

- the ventricular complex in lead Vl has the form qR;

- wave SII > RII;

- an increase in the activation time of the right ventricle in leads Vl-2> 0.03";

- positive TV1 wave after the 7th day.

Electrocardiographic signs of right ventricular overload:

A. Systolic overload:

- right type of ECG;

- tooth RV1> SV1;

- in lead Vl, the ventricular complex has the form R, qR;

- the ST segment is shifted down from the isoline in II, III, aVF, Vl-2 leads in combination with a discordant shift of the T wave in these leads.

B. Diastolic overload:

- right type of ECG;

- in leads V1-V2 signs of blockade of the right leg - the form of the complex rSr", rsR";

- Changes in the ST segment are not very pronounced.

Electrocardiographic signs of left ventricular hypertrophy:

- ECG type left (angle b< +30°);

- an increase in the amplitude of the S wave in leads Vl-2 (SV1 > 21 mm in full-term and > 26 mm in preterm);

- an increase in the activation time of the left ventricle> 0.02 in leads V5-6;

- QV6 > 3 mm.

Electrocardiographic signs of left ventricular overload:

A. Systolic:

- decrease in the deviation of the electrical axis of the heart to the right - angle b + 80 ° + 90 °;

- increase in the amplitude of the RV5-6 wave;

- shift of the ST segment down from the isoline in I, II, aVL, V5-6 leads with a discordant T wave;

B. Diastolic:

- deep Q wave in leads V5-6;

- high RV5-6;

- high, pointed TV5-6.

According to Holter monitoring data (Kravtsova L.A., 2002), newborns show significant rhythm variability during the day and at night (Table 2).

Table 2 Data on the daily heart rate in newborns

ECG indicators

Meaning

Q-T mean

Q-Tmax

Heart rate average

Heart rate maximum

Heart rate minimum

Maximum mode pauses

984 (764.2±74.3)

the difference between m / y heart rate max and heart rate min during the day

difference between m/s heart rate max and heart rate min at night

Heart rate during sleep

Circadian index (wake heart rate/sleep heart rate ratio)

A decrease in the circadian index (CI) reflects the rigidity of the rhythm and is characteristic of the organic pathology of the heart. An increase in CI is associated with an increase in the sensitivity of the myocardium to catecholamines, is observed with rhythm disturbance, and is associated with an increase in vagal influences on the heart.

Doppler echocardiography is the only available non-invasive method for studying the hemodynamics of the fetus and newborn. For examining the fetus, linear and convex sensors of 3-3.7 MHz are used; for examining the heart of a newborn, sectoral sensors of 7-5 MHz are used.

The main parameters of systolic function are end-systolic and end-diastolic diameters and volumes of the left ventricle, ejection fraction and fractional shortening of left ventricular myocardial fibers. The dimensions of the cavities and the thickness of the walls of the heart are determined by the weight of the child (Belozerov Yu. M., 1995) - Appendix 1, 2, 3, 4, 5, 6. The ejection fraction in newborns is 65-75%, the fractional shortening of myocardial fibers is 35-40 %.

The main indicators of diastolic function are: maximum speed early diastolic filling of the ventricles (E), the rate of filling in the atrial systole phase (A), the ratio of these rates (E / A), the time of isovolumetric myocardial relaxation (VIR) and the time of slowing the blood flow of early diastolic filling. In the fetus, the rate of diastolic filling through the tricuspid valve prevails over the rate of blood flow through the mitral valve. The blood flow velocity in the atrial systole phase prevails over the early filling phase, the E/A ratio< 1. У новорожденного кровоток раннего наполнения преобладает над систолой предсердий, Е/А >1. Violation of diastolic relaxation can be judged by the preservation of E / A< 1 и удлинению времени изоволюметрического наполнения левого желудочка. Задержка формирования диастолической функции миокарда в виде длительного сохранения высокой скорости кровотока в фазу систолы предсердий по сравнению с фазой раннего диастолического наполнения характерна для недоношенных детей и это является фактором риска rapid development they have cardiac decompensation.

Ultrasound of the heart is an indispensable method for diagnosing perverse communications between different parts of the heart, stenosis of the excretory tracts, which makes it possible to diagnose CHD with a greater degree of certainty.

R-logical examination provides information about the state of the pulmonary circulation, changes in the configuration of the shadow of the heart and blood vessels, the presence of cardiomegaly. The size of the heart is judged by the value of the cardiothoracic index. Normally, its value is 0.55. An increase in the index to 0.59-0.61 is considered small, up to 0.62-0.65 - moderate, with an index> 0.66, cardiomegaly is diagnosed.

4. Congenital heart defects

Among the primary heart lesions in newborns, the main share is congenital malformations. Congenital heart defects account for about 22% of all congenital malformations. To date, mortality from congenital heart defects remains high. About 50% of children with CHD die in the first year of life, including 50% in the neonatal period (A.S. Sharykin, 2000).

Table 3 Division of congenital heart defects depending on the age chronology of the first symptoms

Defects that manifest only in newborns

Defects that manifest mainly in newborns

Malformations in newborns, most often not accompanied by hemodynamic disorders

Vices that manifest in all age groups

Pulmonary valve atresia with intact ventricular septum

Subdiaphragmatic complete anomalous pulmonary venous drainage

Prenatal narrowing or fusion of the oval window

1. Complete transposition of the aorta and pulmonary artery

2. Common true truncus arteriosus

3. Two-chambered heart

1. Atrial septal defect

2. Ventricular septal defect

3. Tetralogy of Fallot (except in cases with pulmonary atresia)

1. Open ductus arteriosus

2. Coarctation of the aorta

3. Aortic stenosis

4. Stenosis of the valves of the pulmonary artery

5. Tetralogy of Fallot with pulmonary atresia

6. Atresia of the tricuspid valve

7. The only one

8. ventricle

9. Ebstein's disease

10. Complete (supradiaphragmatic) anomalous pulmonary venous drainage

11. Atrioventricular valve

Most congenital heart diseases have an age-related chronology of clinical manifestations, which can make it difficult to diagnose in the neonatal period. In the first days of life, defects are diagnosed in which hemodynamics is disturbed already in the early stages of placental circulation - valve atresia, underdevelopment of the heart, critical aortic stenosis, transposition of the main vessels with an intact interventricular septum. Another category of anomalies is observed mainly in newborns, but can also occur at an older age - complete transposition of blood vessels, a common arterial trunk, a two-chambered heart. There are malformations that may not show pathological symptoms in a newborn, such as septal defects. And, finally, there is a group of defects that can manifest themselves at any age (Table 3).

Defects that manifest only in the neonatal period are rare malformations, but they determine the lethal outcomes from CHD in the neonatal period.

Left ventricular hypoplasia syndrome

This defect includes a reduced left ventricular cavity, aortic and mitral valve defects (stenosis, atresia, hypoplasia).

In newborns, this defect is one of the most common causes of death from CHD. Children die immediately after birth in the maternity hospital or departments of newborns; congenital heart disease is most often not diagnosed in them. In this case, there may be extracardiac malformations of many organs. The defect is more common in boys. Hemodynamic disturbances are caused by hypertension of the small circle, the right ventricle provides blood circulation in the large and small circle. Arterial blood from the left atrium through the open oval window enters the right heart and pulmonary artery, through the PDA, part of the blood enters the descending aorta, a small amount - into the ascending and coronary vessels. AT big circle mixed blood circulates, resulting in moderate hypoxemia. The blood flow in a large circle is reduced (ischemic necrosis occurs in many internal organs). Right ventricular hypertrophy with cavity expansion leads to early decompensation. The first signs of CHD occur shortly after birth - adynamia, pale gray skin, pronounced shortness of breath up to 100 breaths / min with retraction of compliant places. Possible differentiated cyanosis - on the legs. The apex beat is enhanced, there is an epigastric pulsation, the pulse in the arms and legs is almost not palpable or weaker in the arms due to hypoplasia of the aortic arch. The boundaries of the heart are sharply expanded, muffled tones, tachycardia, systolic murmur may be absent. Heart failure may occur in the early days and progress. If there are concomitant defects (stenosis of the pulmonary artery, transposition of the great vessels), heart failure occurs later.

On the ECG - low voltage, EOS deviation to the right up to + 130 °, signs of hypertrophy of both atria, more than the right one, sharp hypertrophy of the right ventricle. There are no Q waves in V5-6, deep S waves are also recorded here.

An R-logical study reveals an increase in the pulmonary pattern - venous congestion. Cardiomegaly from 4-5 days of life. KTI> 65%, heart configuration is closer to spherical.

On ultrasound of the heart, atresia or hypoplasia of the orifice is detected from the parasternal access, the absence of an echo signal from the MV, or signs of its hypoplasia and stenosis, LV hypoplasia, the RV and RA are sharply dilated. There is no communication between LP and LV.

Abnormal pulmonary venous drainage (ADLV - Q.262)

A defect in which all (total) or individual (partial) pulmonary veins empty into the right atrium or into venous vessels leading to it. Partial ADLV may not manifest itself clinically for a long time. Only in the neonatal period does total drainage of the pulmonary veins into the inferior vena cava manifest itself, it is called subdiaphragmatic. This variant of the defect is characterized from the moment of birth by arterial hypoxemia, circulatory and respiratory failure. From the first days of life, pulmonary hypertension is detected. The main signs are shortness of breath, cough, difficulty in feeding, lagging behind in mass. The heart is not enlarged. In lungs rales of stagnant character.

ECG - sharp right-wing, hypertrophy and overload of the right departments.

With R-graphy of the chest in the frontal projection - a picture of a "snow woman".

Echocardiographic examination is uninformative - small sizes of the left parts of the heart are detected, an additional echo signal posterior to the left atrium.

Of the defects that occur mainly in newborns, transposition of the great vessels is most often diagnosed.

Transposition of the great vessels (TMS)

This defect is from 12 to 20% of all CHD, it is defined as the most common cause cyanosis and heart failure infants. With this defect, the aorta departs from the right, and the pulmonary artery from the left ventricle. For this defect to be compatible with at least the shortest life, there must be one or more communications between the systemic and pulmonary circulation. It can be a patent foramen ovale, VSD, ASD, or PDA. Among the concomitant defects that are not a prerequisite for life, pulmonary artery stenosis is the most common. Its presence facilitates the condition of patients and causes a more favorable prognosis.

Hemodynamics in TMS is characterized by:

dissociation of circulatory circles, while the right ventricle acts as a pump for a large circle

gas exchange is carried out due to variable discharges of blood through compensating communications, the magnitude of the discharge determines the degree of hypoxemia. But even under the most favorable circumstances, the discharge is insufficient to saturate the arterial blood with oxygen.

despite the large minute volume, heart failure develops.

In boys, the defect occurs 2 times more often than in girls. Children are born with normal weight. From the very first day there is an intense general cyanosis. Oxygen therapy does not affect the degree of its severity. Cyanosis may be the only sign of malformation during the first 2-3 weeks of life. Starting from 3-4 weeks, shortness of breath appears, difficulties in feeding, the liver enlarges, the size of the heart rapidly increases, and edema appears. In the presence of pulmonary artery stenosis, a systolic murmur is heard. From the first days of life, severe polycythemia is noted, the symptom of "drum sticks" develops early.

ECG - rightogram, hypertrophy of the right departments.

R-gram - oval, egg-shaped heart; the vascular bundle is narrow in the anteroposterior view and expanded in the lateral view.

Ultrasound: indirect signs- dilatation and hypertrophy of the right ventricle, increased excursion of the anterior cusp of the tricuspid valve; parallel orientation of the excretory tracts of both ventricles.

Patent ductus arteriosus (PDA - Q.25.0)

A PDA is considered a congenital defect if it continues to function a week after birth in full-term babies and two weeks after birth in premature babies. Clinically significant PDA occurs in 75% of newborns weighing less than 1 kg, in 10-15% - with a weight of 1.5 to 2 kg. The lower the gestational age of the newborn and the more severe his condition, the less likely the ductus arteriosus to close on its own. In practice, it never closes in children with RDS, which significantly aggravates the course of the underlying disease and forces one to resort to urgent surgical intervention. There are ductus-dependent CHD, in which a functioning duct plays the main compensatory role in maintaining adequate hemodynamics (TMS, pulmonary atresia with an intact interventricular septum, etc.). Hemodynamics in this defect depends on the direction of blood shunting through the PDA. Clinically significant malformation in the neonatal period is manifested by symptoms of heart failure and pulmonary edema. Auscultation reveals a systolic murmur in the II-Sh intercostal space to the left of the sternum. The size of the heart is enlarged, the pulmonary pattern is strengthened.

ECG shows combined hypertrophy of both ventricles. Normal position of the electrical axis of the heart. A change in pulse is characteristic - fast and high, pulse pressure above 40 mm. rt. Art.

Ultrasound - indirect signs: an increase in the cavity of the left ventricle and a change in the ratio of the size of the left atrium to the diameter of the aorta (> 1.2).

Extracardiac symptoms of a hemodynamically significant patent ductus arteriosus include:

pulmonary: negative dynamics or absence of positive carrying out IVL, Fi02 increases;

gastrointestinal - the occurrence of ulcerative necrotic enterocolitis;

renal - oliguria, decreased clearance.

Atrioventricular communications (AVK)

AVK - atrioventricular communications account for 2 to 5% of all defects. Cause severe hemodynamic disturbances. Allocate full and incomplete forms. In the full form, the development of the valvular apparatus, interventricular and interatrial septa is impaired. With an incomplete form, a defect interatrial septum associated with impaired development of the mitral valve leaflet. Hemodynamics is determined by the anatomical form of the defect. In the full form, there is an abundant discharge of blood from the right heart to the left with the development of mitral and tricuspid insufficiency. In the incomplete form, hemodynamic disturbances are associated with a large interatrial defect and mitral insufficiency. Circulatory decompensation is combined with pulmonary hypertension. With an incomplete form, the heart is sharply enlarged in size. During auscultation, two murmurs are heard - one above the pulmonary artery, the other at the apex, and a diastolic murmur may also be heard at the apex due to deformation of the mitral valve cusps and relative stenosis. In the full form, this sound symptomatology is accompanied by a very rough VSD murmur. Heart sounds are muffled.

ECG - overload of both ventricles and their hypertrophy is detected. The axis of the heart is deviated to the left - with complete AVC, the angle b > - 90 °, with incomplete angle b up to - 60 °.

R-logically - cardiomegaly.

Ultrasound data: signs of ASD, mitral valve anomalies, signs of changes in the tricuspid valve, volume overload of the right ventricle.

Common truncus arteriosus (Q.20.0)

With this defect, the trunk of the pulmonary artery is absent, its branches originate from the common trunk. The leading sign of defect is shortness of breath, cyanosis, aggravated by crying. Heart sounds are loud. A rough systolic murmur is heard in the III-IV intercostal space. Heart failure develops rapidly and steadily progresses.

The ECG shows signs of overload of the right departments.

R- logically enlargement of the heart, sometimes it is ovoid.

Echocardiography - revealed a large vessel sitting on the interventricular septum, right ventricular hypertrophy.

Tetralogy of Fallot (Q.21.3)

Tetralogy of Fallot is 10-15% of all CHD. With this defect, there is a combination of a large ventricular septal defect located at the aortic root with disturbances in the structure of the outflow tract of the right ventricle, causing equal pressure in both ventricles of the heart. Disturbances in the excretory tract can be represented by valvular or infundibular (sometimes a combination of them) stenosis or hypoplasia of the pulmonary artery. The heart is small, the right atrium and ventricle are hypertrophied. All hemodynamic disorders occur after birth. With atresia of the mouth of the pulmonary artery, its filling with blood is carried out through the PDA, after its closure - through the collaterals. In pulmonary artery stenosis, the regulators of blood shunting are the ratio of resistance of the pulmonary artery and the aorta. The higher the resistance in the pulmonary artery, the greater the level of hypoxemia. The clinic of defect is very various. With atresia of the mouth of the pulmonary artery, cyanosis in a child appears immediately from birth, it is moderately pronounced. Shortness of breath is absent. The size of the heart is enlarged, in the interscapular space one can hear a systolic-diastolic murmur of blood flow through the collaterals. With pulmonary artery stenosis, there are usually no clinical manifestations in the neonatal period, with the exception of systolic murmur, which appears by the end of 1 week of life. During the so-called. physiological anemia, the child may have hypoxemic crises - shortness of breath, crying, apnea, convulsions suddenly appear, the skin becomes gray. Crises can be 20-25 per day, they can occur during feeding, swaddling, defecation. There is usually no cyanosis during a crisis.

An ECG study revealed moderate or severe hypertrophy of the right ventricle.

R- logically, the pulmonary pattern is depleted, the cardiac shadow is enlarged in diameter, the waist is emphasized, the ascending aorta and its arch are sharply expanded.

Ultrasound can detect aortic displacement, VSD, degree of pulmonary stenosis, and right ventricular hypertrophy.

Defects with obstruction of blood flow

The most common are stenosis of the pulmonary artery, aorta and coarctation of the aorta.

Coarctation of the aorta (Q.25.1) accounts for 10–15% of all CHD and may be the leading cause of heart failure in newborns. There are infantile and adult types of aortic coarctation. In the first case, the ductus arteriosus functions, the mouth of which can flow into the aorta below the site of its narrowing (preductal variant) and above (postductal). More common preductal. In the adult type, the duct is closed, collaterals appear early. Hemodynamic disorders are determined by the degree of narrowing of the aorta, its localization and the presence of an open ductus arteriosus. With an adult type, an overload of the left departments is possible. In the upper and lower half of the body, two different circulation patterns occur. Above the site of narrowing, severe arterial hypertension develops. With an infantile type of hypertension in a large circle, there may not be, but there is a discharge of blood; in the preductal variant, the shunt is from right to left - from the pulmonary artery to the aorta; in the postductal variant, the shunt is from left to right, while the pulmonary blood flow is increased. Both variants of the infantile type are complicated by circulatory failure. Initial symptoms may occur during the first week or in the neonatal period: difficulty in feeding, shortness of breath, cough, weight loss, bouts of unreasonable crying, restlessness, vigorous movement of the legs. There may be gray-ash staining of the skin. In diagnosis, it is important to pay attention to the features of the pulse - the weakening or absence of it on the legs and the difference in blood pressure. Auscultation shows a gallop rhythm at the apex, a systolic murmur is heard very rarely.

ECG - the right type is more often recorded, overload of the right departments, less often combined hypertrophy.

R-logically, the pulmonary pattern is enhanced, the shadow of the heart is enlarged in diameter, in oblique projections, the right and left sections are enlarged.

Ultrasound - doppler echocardiography allows you to identify turbulent accelerated blood flow behind the site of stenosis and determine the pressure gradient.

Coarctation of the aorta can be combined with subaortic and mitral stenosis (complete Sean's anomaly). Sean's anomaly can be combined with genetic syndromes - congenital dysfunction of the adrenal cortex, Shereshevsky-Turner syndrome.

Pulmonary stenosis (Q.25.6)

It is from 2 to 10% of the IPU. Hemodynamics is determined by the degree of narrowing of the artery. A sharp degree of narrowing creates in the newborn such resistance to blood flow that the right ventricle is not completely emptied, it quickly dilates and circulatory failure occurs. The condition of patients is aggravated by arterial hypoxemia due to the discharge of blood through the oval window. The time of onset of the first symptoms is determined by the degree of narrowing. Serious hemodynamic disturbances occur if the area of ​​the mouth of the pulmonary artery is less than 0.7 cm2 per 1 m2 of body surface. The first symptom is moderate cyanosis, which sometimes appears during the first day after birth or occurs towards the end of the neonatal period. The heart progressively increases, there is shortness of breath, pulsation of the jugular veins, liver. During auscultation at the end of the neonatal period, half of the patients heard a systolic murmur in the II-IV intercostal space to the left of the sternum. It is usually short, but can be continuous. Due to hypoxemia, polycythemia develops.

ECG - rightogram with hypertrophy and a sharp overload of the right ventricle - RV1 tooth> 20 mm, negative TVl, 2 is combined with ST shift down from the isoline.

R-logically, the silhouette of the heart has a spherical shape, the pulmonary pattern is depleted.

Ultrasound - in the projection of the short axis at the level of the vessels, impaired opening of the valves of the pulmonary artery, doppler echo - turbulent blood flow in the region of the pulmonary valve.

Ventricular septal defect (Q.21.0)

This is one of the most common anomalies in the development of the heart, accounting for 17 to 30% of all CHD. A defect of various sizes is located under the aortic orifice or below the base of the leaflet of the 3-fold valve. Hemodynamic disorders appear after birth and consist in the discharge of blood from the left ventricle to the right. At the same time, in the neonatal period, the discharge is usually insignificant, since high vascular resistance still remains in the lungs of the child. The magnitude of the discharge can be determined by the size of the defect - with large defects, the diameter of which exceeds half the diameter of the aorta, the left ventricle acquires two equivalent outlets, one of which is the aortic orifice, the other is a septal defect. Large defects are combined with severe pulmonary hypertension due to hypervolemia. In these cases, there is a deficit of minute volume in a large circle and heart failure. Children are born with normal weight. The first symptom of defect is systolic noise. With small defects, it is heard from the first week, with large defects, at the end of the neonatal period. Noise maximum - III-IV intercostal space to the left of the sternum. A heart hump forms quickly. The heart is enlarged. There are signs of insufficiency I-II Art.

In an ECG study, there may be a normal position of the electrical axis or deviation to the left, hypertrophy of the left sections or combined ventricular overload, conduction disturbances.

R-logical increase in the left sections, bulging of the pulmonary artery, increased pulmonary pattern.

Ultrasound can determine the size and location of the defect.

Abnormal discharge of the left coronary artery from pulmonary artery (Blyde-White-Garland syndrome) (Q.24.5)

Blood in the left coronary artery with this defect comes not from the pulmonary artery, but through intercoronary anastomoses from the right CA. In this regard, the survival of these patients determines the collateral blood flow at the time of birth. The disease manifests itself in the first months of life. The first signs are lethargy, pallor of the skin, sweating, vomiting, shortness of breath, tachycardia. Sometimes the first sign is bouts of intense anxiety after or during feeding. Attacks may be accompanied by an increase in body temperature (violation of thermoregulation).

Main diagnostic value has an ECG - deviation of the electrical axis of the heart to the left, blockade of the anterior branch of the left leg, deep Q1, aVL, V 5-6, ST rise above the isoline with a decrease in the R wave, which corresponds to the picture of myocardial infarction.

Myocardial infarction is a rare, but not casuistic, pathology of the heart in newborns. The causes of myocardial infarction in the neonatal period can be different. Most often, this is a CHD - an abnormal origin of the left coronary artery (Bland-White-Garland syndrome). Other CHDs may include transposition of the great vessels, double origin of vessels from the right ventricle (Taussig-Bing's anomaly), and pulmonary stenosis. Less commonly, the cause of MI may be severe neonatal asphyxia, umbilical vein catheterization, idiopathic arterial calcification.

The diagnosis of myocardial infarction is established on the basis of characteristic electrocardiographic signs. Electrocardiographic signs of myocardial infarction in newborns (Towbin, 1992):

Wide Q wave (> 0.035");

ST segment elevation > 2 mm;

In leads V5-6, the ventricular complex has the shape of a QR, the T wave in these leads is negative;

QT interval lengthened > 0.44".

Differential Diagnosis congenital heart defects in newborns is presented in Table 4.

Table 4 Differential diagnosis of major cardiac lesions in newborns

The time of the first manifestations of the disease from birth

First symptom

Enlargement of the heart

Circulatory failure

Strengthening of the lung pattern

Note

Hypoplasia of the left side of the heart

48 hours - 7 days

sudden shortness of breath

Not palpable

Rightgram

Occurs in boys 2 times more often, 75% die in the first week of life

Pulmonary valve atresia

Since birth

Overload of the left departments

Subdiaphragmatic anomalous pulmonary venous drainage

24 hours - 7 days

Rightgram

Vascular transposition

Since birth

Rightgram

Silhouette of the heart in the form of "egg on its side". It is 2.5 times more common in boys

Coarctation of the aorta

Reinforced on the arms

Rightgram

Tricuspid valve atresia

Since birth

Levogramma

common truncus arteriosus

1-4 weeks

fast, full

Combined tipertrophy

Tetralogy of Fallot with pulmonary atresia

1-4 weeks

Rightgram

Open arterial (botallian) duct

fast, full

Combined overload

Ebstein's disease

Cyanosis (with LLC)

See note

Characterized by low-voltage, split QRSvl-v6 complexes

Principles of organization of care for newborns with congenital heart disease:

timely detection of children with suspected congenital heart disease in the maternity hospital;

topical diagnosis of defect;

adequate conservative therapy;

timely surgery.

Factors of diagnostic attention, allowing to suspect the presence of congenital heart disease:

Paleness or cyanosis of the skin;

Hypotrophy;

Poor exercise tolerance (difficulty feeding, refusal to breastfeed, shortness of breath or cyanosis when swaddling);

Enlargement of the heart;

Changing the sonority of tones;

Systolic murmur in the II, III intercostal space to the left of the sternum,

In the interscapular space, bottom corner left scapula, machine systolic-diastolic murmur at the base of the heart;

Change in pulse (different pulse on the radial arteries, no pulse on the femoral artery);

Change in blood pressure (significant difference in the apex and lower extremities);

arrhythmias;

Pathological ECG changes (signs of overload or hypertrophy);

Unusual heart shadow on R-logical examination;

- (spherical, ovoid, in the form of a "Dutch shoe");

Multiple stigmas of connective tissue dysembryogenesis.

The topical diagnosis of the defect is specified during an ultrasound examination.

When conducting conservative treatment patients with congenital heart disease are recommended a differentiated approach to infusion therapy and the use of oxygen, diuretic drugs. Infusion therapy should be aimed at improving microcirculation and correcting metabolic disorders, diuretic drugs are recommended to be used very carefully, preference is given to aldosterone antagonists.

Oxygen is considered contraindicated in ductus-dependent defects (transposition of the great vessels, arterial atresia with an intact interventricular septum). To maintain the functioning of the patent ductus arteriosus, infusions of prostaglandin E2 are used at a dose of 0.02-0.1 μg / kg / min. Duration of infusion from 30 minutes to 8 hours. Possible side effects: apnea, hypotension, hyperthermia, bronchospasm, bradycardia, convulsions, thrombocytopenia.

With a hemodynamically significant PDA with a left-right shunt, it is recommended to limit the volume of fluid from 60 ml/kg/day (in children weighing more than 1500 g) to 100 ml/kg/day (in children weighing less than 1000 g). It is possible to use diuretics (only for congestive heart failure): hydrochlorothiazide 2-4 mg / kg / day (furosemide is prescribed in exceptional cases - it prevents the ductus arteriosus from closing). Oxygenation should be maintained at a sufficient level (hypoxia stimulates the synthesis of prostaglandins, which maintains an open ductus arteriosus), if necessary, red blood cell transfusion. If there is no effect within 24-48 hours, indomethacin is prescribed (inhibits the synthesis of prostaglandins): 0.2 mg / kg intravenously slowly every 8 hours - only three injections. In the first week of life, the introduction of indomethacin is carried out after 12 hours. If there is no effect, the cycle of 3 injections is repeated after 12 hours. While maintaining the duct open after the second cycle, indomethacin is administered at a maintenance dose of 0.1 mg/kg/day for 5 days. The effectiveness of indomethacin (60%) increases with gestational age. Together with cardiac glycosides, indomethacin should be used very carefully - the risk of anuria is high. In the absence of the effect of conservative treatment or the presence of contraindications to the use of indomethacin, surgical treatment of the patent ductus arteriosus is indicated. Contraindications to the use of indomethacin: kidney failure(diuresis less than 0.7 ml/kg/hour in the last 8 hours), thrombocytopenia less than 80,000x109/l, IVH in the last 4 days, suspicion of necrotizing ulcerative enterocolitis, increased bleeding, blood in the stool, hyperbilirubinemia at a level that is an indication for exchange transfusion. Side effects of indomethacin: oliguria, inhibition of platelet aggregation, displacement of bilirubin from its association with albumin, ulcerative necrotic enterocolitis, intestinal problems.

Indications for surgical correction of congenital malformations in newborns are critical conditions not amenable to conservative therapy.

Signs of a critical course of CHD:

total cyanosis, persistent, > 3 hours (in the absence of other causes - atelectasis, diaphragmatic hernia);

symptoms of heart failure;

severe progressive malnutrition.

5. Diseases of the myocardium

Myocardial damage in newborns is most often secondary. It may be due to the effects of hypoxia, drugs, endocrine, metabolic disorders. Myocardial pathology can be genetically determined. The morphological substrate in all cases is myocardial dystrophy and sclerotic changes in it. Therefore, in relation to these variants of myocardial damage, the term cardiomyopathy can be used. If it is not possible to specify the cause, the term idiopathic cardiomyopathy is used.

In newborns, myocardial damage is also possible due to viral and bacterial infections - congenital carditis. If carditis occurs in the first 6 months of intrauterine development, the same dystrophic and sclerotic changes occur in the myocardium that are characteristic of cardiomyopathies, and fibrosclerotic processes predominate. Therefore, the so-called. early congenital carditis is identified with the concept of fibroelastosis.

Fibroelastosis is considered as a nonspecific morphological response of the endocardium to any myocardial stress. Congenital heart defects, hypoxia, infections, cardiomyopathies can act as such stress. If a damaging agent (bacteria, viruses) acts on the myocardium in the last 2-3 months of intrauterine development or at the time of the birth of a child, classic inflammation, which corresponds to the term myocarditis. It can be congenital and acquired. All of the listed variants of myocardial damage have features due to etiological factors.

Syndrome of disadaptation of the cardiovascular system

Features of the structure of cardiomyocytes in a newborn child, features of the bioenergetics of the heart cell (the leading role carbohydrate metabolism with rapid depletion of aerobic glycolysis) determine the significant role of hypoxia in the genesis of disturbances in the processes of adaptation of the cardiovascular system. Disorders of the cardiovascular system in a newborn child, arising under the influence of hypoxia, are singled out as an independent syndrome - the syndrome of maladaptation of the cardiovascular system. There are 4 clinical and pathogenetic variants of this syndrome:

Neonatal pulmonary hypertension and persistence of fetal communications (persistent fetal circulation);

Transient myocardial dysfunction with cavity dilatation, normal or increased contractility;

Transient myocardial dysfunction with dilatation of the cavities and reduced contractility;

Rhythm and conduction disturbances.

Perhaps a combination of these options in one child.

Neonatal pulmonary hypertension and persistence

fetal communications (R.29.3)

There are two variants of this pathology - with left-right shunting through the PDA and right-handed. Precapillary form pulmonary hypertension with right-to-left shunting is clinically manifested by diffuse cyanosis from birth. Cyanosis increases with crying, oxygen therapy is not effective. The boundaries of relative cardiac dullness are expanded, heart sounds are loud.

On the ECG - signs of overload of the right atrium, violation of the right leg bundle of Hiss.

An R-logical study reveals a depletion of the lung pattern, often an X-ray picture without features (“surprising norm”).

In the capillary form of pulmonary hypertension with left-right shunting, a sharp violation of the respiratory function is detected, up to pulmonary edema. On the ECG signs overload of both atria and left ventricle. Rhythm disturbances are possible in the form of supraventricular paroxysmal tachycardia, atrial flutter, extrasystole. Rhythm disturbances arise in connection with the simultaneous left-right reset through the LLC.

Transient myocardial dysfunction with normal or

increased contractility (R.29.4)

Clinically manifested by pallor of the skin, there may be oral cyanosis. Heart sounds are muffled. A systolic murmur can be heard at the apex and at the V point. On the ECG - ST depression I, II, V5-6, negative T V5-6. With echocardiography, the expansion of cavities with good contractility of the myocardium.

Transient myocardial dysfunction with dilatation of cavities and

reduced contractility (R.29.4)

As the severity of the condition worsens, a violation is detected contractility. In this case, the content of cardiospecific enzymes may be increased, which indicates the severity of subendocardial ischemia. This variant occurs under conditions of prolonged antenatal hypoxic exposure.

Rhythm and conduction disorders (R.29.1)

a) Rhythm disturbances in maladaptation syndrome are caused by changes in neurovegetative regulation, electrical instability of the myocardium and hemodynamic disturbances due to the persistence of fetal communications.

b) Most often, rhythm disturbances are represented by sinus tachycardia - this is the initial pathophysiological reaction of the cardiovascular system to hypoxia, the second most common is supraventricular tachycardia. Paroxysmal tachycardia in 50% of cases is due to the functioning of accessory pathways.

c) The occurrence of arrhythmias can be facilitated by the presence of fragments of a specialized conductive tissue of the heart that has not undergone resorptive degeneration, functional immaturity of the main regulatory centers medulla oblongata, the presence of a pronounced imbalance between the sympathetic and parasympathetic innervation of the heart due to the asynchrony of the maturation of the right and left stellate ganglia of the sympathetic nervous system.

Features of postnatal adaptation of the cardiovascular system in preterm infants

A characteristic delay in the formation of diastolic function of the myocardium is the preservation of a high blood flow velocity in the phase of atrial systole compared to the phase of early diastolic filling - a risk factor for rapid decompensation under adverse effects. With RDS, there is a violation of the systolic function of the myocardium with clinical signs of heart failure. A syndrome of persistent fetal circulation and pulmonary hypertension is common. Premature infants in the neonatal period often have electrolyte-mediated QT interval prolongation in association with ventricular forms rhythm disturbances.

Myocarditis in newborns is most often caused by Coxsackie B viruses (type 1-5) and Coxsackie A 13, may be a manifestation of an intrauterine generalized process with multiple organ damage. Clinical manifestations consist of extracardiac and cardiac symptoms. Extracardiac: sweating, restlessness, cough, cyanosis, vomiting. Cardiac: shortness of breath, deafness of tones, gallop rhythm, systolic murmur, rhythm disturbances - sinus node weakness syndrome, paroxysmal tachycardia. Most often, clinical symptoms on the part of the heart is represented by heart failure.

An ECG study reveals:

1. diffuse decrease in voltage;

2. systolic overload of the left ventricle;

3. heart rhythm disturbances in the form of extrasystole, ectopic

tachycardia, atrial flutter, blockade of the branches of the left leg;

4. smoothed T wave;

5. depression of the ST segment.

Data from ultrasound of the heart - the expansion of the cavity of the left ventricle, signs of its dysfunction, a decrease in myocardial contractility. At laboratory research- an increase in CPK, LDH, an increase in troponin T in the blood.

...

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