obstructive shock.

In the structure of infant mortality, developmental anomalies occupy the third place, and half of the cases of mortality are determined by congenital heart defects (CHDs). Among children who died from CHD and malformations large vessels, 91% of patients are infants in the first year of life, of which 35% of deaths occur in the early neonatal period (up to 6 days). About 70% of children die within the first month of life.

The scale of the problem is emphasized by the high frequency of CHD: in different countries this figure varies from 0.6% to 2.4% per year in children born alive, taking into account intrauterine fetal death and early miscarriages the overall incidence of CHD is 7.3%.

prenatal diagnosis. In order to reduce infant mortality, prenatal ultrasound screening is used, which makes it possible to detect the majority of CHD before the 24th week of gestation. If a defect is suspected, a targeted ultrasound of the fetus is performed on an expert-class apparatus. The main task is to prevent the birth of children with inoperable defects - hypoplastic left heart syndrome (HLS), hypertrophic cardiomyopathy with signs of organic myocardial damage, multiple fetal malformations. The prenatal council should offer termination of pregnancy only if accurate diagnosis incurable vice.

Classification. In the neonatal period (sometimes in the first days, hours or minutes after birth), defects called critical are manifested, since in 95-100% of cases they are accompanied by life-threatening conditions and determine early neonatal mortality. Critical malformations include great vessel transposition (TMS), HFRS, tricuspid valve atresia, or pulmonary artery with intact interventricular septum (IVS), preductal coarctation of the aorta, common truncus arteriosus, single ventricle, double outlet of the great vessels from the right ventricle, and others.

Taking into account the high lethality of newborns and infants from CHD, a classification based on the definition of the leading factor was created for this age group of patients. clinical syndrome, the effectiveness of therapeutic tactics and determining the timing surgical intervention.

Syndromic classification of CHD in newborns and children of the first year of life (Sharykin A. S., 2005)

CHD, manifested by arterial hypoxemia (chronic hypoxemia, hypoxemic status) - "ductus-dependent" defects.

CHD, predominantly manifested by heart failure (acute heart failure, congestive heart failure, cardiogenic shock).

CHD, manifested by heart rhythm disturbances (complete atrioventricular blockade, paroxysmal tachycardia).

These conditions can be combined, aggravating the severity of the condition of children, 50% of these children require surgical or therapeutic intervention in the first year of life.

Hemodynamics. Critical malformations are characterized by ductus-dependent pulmonary or systemic circulation, they are united by a sudden sharp deterioration in an outwardly safe child at birth, associated with a decrease in blood flow through the ductus arteriosus. Ductus-dependent pulmonary circulation with TMS, atresia (or critical stenosis of the pulmonary artery) with intact IVS, it provides blood flow through the duct to the pulmonary circulation, and when it is limited or terminated, severe arterial hypoxemia develops, acute hypoxia of organs and tissues.

CHD clinic with pulmonary ductus-dependent circulation

The anatomy of one of the most common critical defects - transposition of the main vessels - consists in the incorrect discharge of the aorta - from the right and pulmonary arteries - from the left ventricle, which contributes to the separation of the circulation circles: arterial blood circulates in the small circle system, venous blood circulates in the large circle system.

The supply of oxygen to life-supporting organs is possible only under the condition of functioning fetal communications - ductus arteriosus, interatrial defect. This communication between the circles of blood circulation does not provide compensation for hypoxemia. In order to compensate for the deficit peripheral circulation the minute volume of blood flow increases, there is an overload of the small circle (this happens faster in the presence of an IVS defect), pulmonary hypertension develops rapidly. That is why during the management of the patient it is necessary to constantly monitor the symptoms of arterial hypoxemia and monitor clinical signs heart failure (HF) - tab. one.

The natural course of vice is very severe. The child is born at term with normal body weight, but in the first hours after birth diffuse cyanosis of the skin appears, especially pronounced on the periphery - cyanosis of the face, hands, feet. The state of extreme severity is due to severe arterial hypoxemia. Shortness of breath, tachycardia appear 1-2 hours after clamping the umbilical cord. There is a progressive deterioration in the condition. The child is lethargic, lethargic, cools easily.

When fetal communications are closed, acute hypoxia leads to the development of multiple organ failure and death of the newborn within a few hours. If the child survives for several weeks, heart failure increases. Severe malnutrition develops rapidly. It should be noted that in the case of adequate tactics of observation and treatment, as well as timely - up to a month - surgical correction of a defect in a child (since only during this period a radical correction by arterial switching of the main vessels is possible), physiological hemodynamics, growth and development rates are completely restored, physical and subsequent social adaptation. If the defect is corrected later, the outcomes are less favorable.

Diagnostic criteria for TMS include:

Electrocardiographic signs of hypertrophy of the right atrium and right ventricle - high P wave in the "right" leads - III, V1-3, deep S waves in the "left" - I, V5-6 and high R waves in leads III, V1-3.

Radiologically, cardiomegaly and an “ovoid” shape of the heart with a narrow vascular bundle are determined as a result of combining the contours of large vessels (photo).

According to echocardiography - a parallel course of the excretory sections of the ventricles - the pulmonary artery and aorta.

The hyperoxide test is negative - when trying to supply 100% oxygen through a mask in patients with "blue" defects, after 10-15 minutes pO2 increases by no more than 10-15 mm Hg. Art. (whereas in lung diseases, the increase in pO2 is up to 100-150 mm Hg).

Scheme of examination of a newborn child with suspected congenital heart disease:

Examination of the patient (with an assessment of symptoms of hypoxemia and / or heart failure);

Evaluation of pulsation in all limbs;

Auscultation of the heart and lungs (dynamic control of heart rate, respiration);

Measurement blood pressure(BP) on all limbs (further dynamic control).

In addition, observation of a child involves monitoring blood gases (pO2, pCO2), oxygen saturation (SatO2) using pulse oximetry and metabolic indicators - pH, BE. Gas exchange in the lungs is not impaired if PaO2 is in the range of 60-80 mm Hg. Art., SaO2 - 96-98%. Arterial hypoxemia develops when PaO2 is less than 60 mm Hg. Art. and a hemoglobin saturation level of 85-75%.

Tasks of a pediatrician (neonatologist):

To ensure a decrease in the body's need for oxygen by creating thermal and physical comfort - the conditions of an incubator, with an elevated position of the upper body;

Swaddling with free chest and arms;

Limitation of energy costs for physiological load (feeding through a tube);

Support of blood flow through the ductus arteriosus (infusion of fluids, prostaglandin E);

Correction of metabolic shifts, if necessary - artificial ventilation lungs (IVL) without adding oxygen to the inhaled mixture, in a mode that excludes hyperventilation and with simultaneous infusion of prostaglandin E (the calculation of the dose of the drug is described below). When deciding on the appointment of mechanical ventilation, it must be taken into account that oxygen has a vasoconstrictor effect on the arterial duct, which makes oxygen therapy dangerous in this group of patients;

When threatened with closure ductus-dependent defects the volume of infusions and feedings is increased to 110-120% of normal requirements against the background of a constant assessment of diuresis. It has been established that a 5% increase in body weight in a newborn in 1-2 days stabilizes the function of the arterial duct.

Transportation to the cardiac surgery center is optimal during the first weeks, the first month of life. Beforehand, it is necessary to inform the cardiosurgical hospital about a patient with congenital heart disease with ductus-dependent blood circulation. The period of observation until the moment of transfer and transportation to the center is carried out against the background of infusion of the drug prostaglandin E (Alprostan, Vazaprostan).

CHD clinic with systemic ductus-dependent circulation (a group of malformations includes HFRS, severe aortic coarctation, interruption of the aortic arch). The most positive example of defects in this group is pronounced preductal coarctation, which occupies from 1% to 10% among critical CHD. With this defect, the blood flow is sharply limited or completely absent from its proximal part (below the place where the ductus arteriosus originates) to the distal one. Violation of hemodynamics, respectively, is that in the descending aorta (in big circle) a small volume of blood comes only from the pulmonary artery through the ductus arteriosus. When the ductus arteriosus closes, acute hypoperfusion of organs and tissues and multiple organ failure develop. Clinic: full-term newborn with a sharp deterioration in the first few days of life - adynamia, cold extremities, a symptom of hypoperfusion of peripheral tissues (" white spot”), pulse of small filling, high blood pressure on the arms and low or not detected on the legs, shortness of breath, tachycardia, oliguria with increasing azotemia, hepatomegaly with an increase in transaminases, necrotizing enterocolitis.

Consider the diagnosis and optimal therapeutic tactics in relation to a patient with severe coarctation of the aorta in a specific clinical example.

A full-term newborn A. was delivered to the intensive care unit in a serious condition: lethargic, does not suck at the chest, pale skin, tachypnea 120 per minute, breathing is symmetrically carried out in all fields, no wheezing. Sonorous heart sounds, 167 per minute, gentle systolic murmur in the third intercostal space to the left of the sternum, hepatomegaly (liver +5 cm from under the edge of the rib, dense). Diuresis is reduced, there is no peripheral edema. BP in the arms - 127/75 mm Hg. Art., pulsation on the femoral artery is not determined. SatO2 - 98%.

From the anamnesis: the condition suddenly worsened on the 14th day of life, when the child became lethargic, severe shortness of breath appeared, he was hospitalized by ambulance. A boy from a second, normal pregnancy, urgent delivery with a weight of 3220 g, an Apgar score of 5 (9) points. Discharged from the maternity hospital in a satisfactory condition, was breastfed. Periodically there were episodes of anxiety, flatulence.

On admission, the child was intubated and ventilated low content oxygen in the inhaled mixture. Examination in the hospital revealed cardiomegaly (cardiothoracic index - 80%), depletion of the lung pattern, according to electrocardiography - combined overload of both ventricles. Echocardiography revealed aortic hypoplasia below the origin of the left subclavian artery(and above the localization of the ductus arteriosus), in a typical place for the ductus arteriosus, there is a point blood flow (closing ductus arteriosus). After 6 hours the child's condition worsened: oliguria developed, there was an increase in creatinine to 213 mmol/l, transaminases 4-5 times higher than the laboratory norm. Humoral activity has not been established.

Rationale for the diagnosis and tactics: given the clinical presentation of severe respiratory failure and, subsequently, multiple organ failure in combination with cardiomegaly, systemic arterial hypertension, renal and hepatic insufficiency, clinical data should suggest aortic coarctation. The sudden deterioration of the child's condition in the absence of signs of infection suggests a ductus-dependent systemic circulation, taking into account the data on visualization of the heart and blood vessels, the diagnosis takes place: "CHD, preductal coarctation of the aorta, arterial hypertension 2 tbsp., secondary, multiple organ failure.

From the moment the diagnosis is confirmed according to echocardiography, it is necessary to start therapy with Vazaprostan 0.02 (with an increase in dose to 0.05 μg / kg / min) in order to restore blood flow through the ductus arteriosus. With this defect, the shunt is directed from the pulmonary artery to the descending aorta, and only this small portion of blood provides the entire systemic circulation.

Dose calculation and method of administration. The weight of the child at admission is 3220 g. 1 ampoule contains 20 µg of Vazaprostan. In this case, the administration of the drug was started with a dose of 0.02 µg/kg/min, i.e. it took 0.02 ´ 3.2 = 0.064 µg/kg/min. For an hour, the dose of the drug was 0.064 ´ 60 = 3.8 µg/hour. To administer the drug, 1 ampoule (20 µg of Vazaprostan) was diluted in 20 ml physiological solution(in 1 ml - 1 mcg). In the absence of effect within two hours, the dose was increased to 0.04-0.05 mcg / kg / min: accordingly, the rate of drug administration increased to 7.6-9.5 ml / hour. In this case, the control of therapy was very indicative - after 6 hours of infusion, an improvement in the condition was noted, an increase in the blowing systolic murmur in the second intercostal space on the left, an increase in the size of the flow through the arterial duct according to EchoCG. Transferred to a maintenance dose of Vazaprostan - 0.01 and then 0.005 mcg / kg / min, which was maintained during the entire observation period in the pediatric hospital and during transportation when transferred to a cardiac surgery hospital. In this clinical case it was impossible to completely move away from mechanical ventilation (given the severity respiratory failure), on the 5th day of hospitalization (19th day of life), the child was transferred to the clinic named after A.I. Meshalkin, where the defect was successfully corrected - the formation of an aortopulmonary bypass.

In cases of development of heart failure in newborns with defects accompanied by a massive discharge of blood into the pulmonary circulation, the same principle of monitoring the main indicators and symptomatic therapy is applied:

Restriction of fluid administration by diuresis, in severe cases - up to 1/3 of the age norm (but fluid restriction to 50% of the daily physiological need is unacceptable);

The presence of volume overload requires the use of diuretics (for edematous syndrome, preference is given to Furosemide / Lasix at a dose of 1-2 mg / kg; a combination with Veroshpiron is possible (1-3 mg / kg / day orally in 2-3 doses);

Digoxin is used to stop tachycardia (economically unfavorable for the myocardium and ineffective volume for peripheral circulation) (Table 2).

If symptoms of small circle overload appear (auscultatively - amplification, splitting of the 2nd tone on the pulmonary artery, on EchoCG - an increase in pressure in the pulmonary artery more than 30 mm Hg after six days of life), as well as signs of a violation of the diastolic function of the heart, it is recommended to use drugs from the group of angiotensin-converting enzyme inhibitors (ACE inhibitors). Capoten (captopril) is used at a dose of 0.5-1 mg / kg, subject to control of systemic blood pressure. Therapeutic action ACE inhibitors are associated with a decrease in peripheral vascular resistance and partial deposition of blood, resulting in a decrease in the volume of blood returned to the right heart. Accordingly, the volume of the shunt and the load on the left chambers and vessels of the small circle are reduced. In addition, it is known that ACE inhibitors are an inhibitor of apoptosis stimulated by hypoxia, which explains the angio- and cardioprotective effect of the drugs.

Thus, the tactics of the pediatrician, including early diagnosis critical congenital heart disease and therapy that controls intracardiac, central and peripheral hemodynamics, as well as, if possible, early coordination with the cardiac surgery center can significantly improve the prognosis of patients and reduce infant mortality.

Literature

Burakovsky V. A., Bukharin V. A., Podzolkov V. P. et al. Congenital heart defects. In book. Cardiovascular surgery. Ed. V. I. Burakovsky, L. A. Bokeria. M.: Medicine, 1989; 345-382.

Congenital heart defects. Reference book for doctors. Ed. E. V. Krivosheeva, I. A. Kovaleva. Tomsk, 2009; 285.

Sharykin A.S. Congenital heart disease. Guide for pediatricians, cardiologists, neonatologists. M.: Publishing house "Teremok", 2005; 384.

Sharykin A.S. Perinatal cardiology. Guide for pediatricians, cardiologists, neonatologists. M.: Publishing house "Teremok", 2007; 347.

Even highly qualified cardiologists with vast practical experience will not be able to give an exact answer to the question of how long they live with heart disease. The causes of the development of pathology are diverse, as are its manifestations. Sometimes the disease proceeds quietly and does not make itself felt. long years. Serious defects require lifelong therapy, and sometimes urgent surgical intervention. But it is one thing when a person finds himself in such a situation due to reasons beyond his control. And it is quite another if the threat to his life arose due to inaction, delay or some kind of prejudice.

What is heart disease

Heart disease is a pathology characterized by anatomical disorders of the structures of the heart muscle, valves, partitions or large vessels that supply it with blood. The heart cannot cope with its job of supplying the organs with oxygen. They experience oxygen starvation, being exposed to serious danger. Distinguish between acquired and congenital heart defects.

birth defect

Congenital heart disease is an anomaly in the structure of blood vessels and the heart, according to different reasons arising during prenatal development fetus. Pathology occupies one of the first places among congenital deformities of organs that can cause the death of newborns before they reach one year of age.

Often, congenital heart disease does not manifest itself in the prenatal phase. It happens that the pathology goes unnoticed during the first years of the baby's life. But over time, she will definitely remind of herself.

The responsibility for the appearance of pathology lies primarily with the parents of the child. Their diseases, heredity and lifestyle directly affect the health of the unborn baby. Provoke the development of heart disease can:

• infectious diseases;
• taking certain medications;
• addiction to alcohol;
• drug use;
• exposure to radiation;
• pathology of the endocrine system;
• severe toxicosis during childbearing;
• old age of the mother;
• bad heredity;
• chromosomal disorders.

There are several types of congenital heart defects:

• open holes in the heart muscle;
• difficulties with blood flow;
• pathology of blood vessels;
• heart valve defects;
• tetrad of Fallot;
• aortic stenosis;
• common trunk of arteries;
• Ebstein anomaly;
• simultaneous manifestation of several species.

An anomaly detected immediately after birth will allow it to be treated in a timely manner and reduce the threat of death of the baby during the first days of life. Before planning offspring, it is necessary to find out how healthy future parents are. You should ask the second "halves" if they have genetic problems and cases of congenital heart disease in their next of kin.

If, during development, a heart pathology is detected in the fetus, the mother is prescribed appropriate therapy during pregnancy. It should support the baby's heart function until he is born.

Heart disease in children

Timely treatment of pathology prevents the occurrence of complications. Children can grow and develop on a par with healthy peers. Not all heart defects require emergency operation. If so, the specialists adhere to a wait-and-see attitude, keeping the cardiac activity of the wards under control. But in any case, a child with heart disease needs special conditions growing up.

Visually, the symptoms of pathology usually appear when the baby is three years old. At this time, attentive parents may notice:

• delayed physical development baby;
• pallor skin, sometimes their cyanosis;
• the appearance of shortness of breath during habitual movements.

Children with congenital heart disease are characterized by psycho-emotional experiences - due to problems with development and learning. Usually sick children begin to walk, talk, read and write later than their healthy peers. Over time, the situation can be aggravated by the appearance of excess weight, although initially, babies with congenital heart disease are underweight. Immunity in a sick child is low, so he is threatened with infectious diseases.

But children are not only affected by congenital heart defects. Adolescents are often diagnosed with acquired defects. This type of pathology can occur with exacerbation of various ailments. Harmful bacteria can enter the bloodstream:

• by infection by injection (contaminated syringes and needles);
• in case of violations of sanitation during the medical manipulations(including dental);
• when abscesses occur.

Blue and white vices

There are blue and white heart defects. When blue, there is a cast venous blood into the arterial line. In this case, the heart muscle “pumps” oxygen-depleted blood. Pathology is characterized by early manifestation of symptoms of heart failure:

• cyanosis (cyanosis);
• dyspnea;
• nervous excitement;
• fainting.

With white defects, venous and arterial blood do not mix, oxygen enters the organs in the required amount. Pathology is characterized by the same attacks that are observed with blue defects, but they appear later - at 8-12 years.

Medical practice shows that often people with heart disease live a full life, without suffering and discomfort.

Acquired Vice

Acquired heart defects affect the heart valves. Serious pathologies become the “trigger” to their development:

• chronic vascular diseases (atherosclerosis);
• systemic lesions of connective tissues (rheumatism, dermatomyositis, scleroderma);
• inflammation of the endocardium (infective endocarditis);
• systemic diseases of the joints (Bekhterev's disease);
• systemic venereal diseases(syphilis).

The cause of acquired heart defects is often the death of cells of the heart valves. Injuries can provoke the course of pathology.

There are compensated and decompensated acquired defects. In the first case, there are no obvious symptoms of circulatory failure, in the second, these symptoms are present.

Symptoms of pathology are similar to manifestations of other diseases of the vessels and heart. Therefore, the diagnosis is made only on the basis of the results of the examination, including echo and electrocardiography. Among the acquired heart defects are:

1. Mitral - manifested by prolapse (sagging of the leaflets) of the mitral valve. Treatment is symptomatic. In parallel with it, drug therapy pathology that caused heart disease. In case of serious lesions of the valve, its surgical correction is indicated;
2. Aortic - the aortic valve is affected. The main pathology is treated with medication. Therapy of heart disease may require surgical intervention - up to valve transplantation;
3. Combined - two or more valves of the heart muscle are affected. Mitral, tricuspid and aortic valves can undergo deformities, which will cause difficulties in diagnosing and treating pathology. Most often, mitral valve insufficiency and mitral stenosis. Under such circumstances, cyanosis and severe dyspnea appear;
4. Combined - one valve undergoes several violations. Usually it is stenosis and insufficiency. Diagnosing this type of heart disease, find out the severity of the lesions and the predominance of one of them. This is necessary in order to prescribe adequate treatment and the type of possible surgical intervention;
5. Compensated - difficult to diagnose, asymptomatic pathology. Violations of the functions of some parts of the heart muscle in fully offset by an increased load on other parts of the heart. Only an experienced cardiologist, who has at his disposal high-tech special equipment, is able to diagnose this defect.

"Simple" isolated vices hearts are much less common than "complex", combined. Infectious diseases have been haunting patients for years, affecting muscle tissue. As a result, one vice is added to another.

Life expectancy with heart disease

Even a very competent cardiologist will not undertake to predict how long a patient with heart disease can live. It is necessary to make efforts for the sake of recovery and prevention of complications of pathology on your own - sometimes overcoming Bad mood and banal unwillingness.

Uncomplicated heart defects

Often people do not even know that they live with a disease under the formidable name "heart disease". The life expectancy of patients with heart defects is influenced by objective and subjective factors. A huge role is played by the characteristics of the patient's body and the conditions of his life. Reduce the likelihood of developing pathology or even reduce its manifestations to a minimum:

• strict adherence to all recommendations of the doctor;
• healthy lifestyle;
• giving up bad habits;
• regular physical education;
• dosing of physical activity;
• complete sleep.

A balanced approach to the course of the disease will save the patient from pain, discomfort and other consequences. Careful medical examination will help determine the severity of the pathology, and modern medications and physiotherapy will improve the patient's condition.

Complicated forms of pathology

For many types of heart defects, surgery is optional or impossible. Under such circumstances, the body needs medical support. If there is no treatment, the pathology progresses. The only outcome in this case is lethal. The heart muscle refuses to perform its direct functions, disrupting the body's blood supply. If a surgical intervention- the only possible chance to prolong life or improve its quality, you should not refuse it. A very small percentage surgical treatment heart failure leads to death. Over 97% of operated patients live a full life in the future.

What is this “heart threshold”, how long do they live with a diagnosed heart disease? These questions are of concern to many. Some are concerned about their own diagnosis, others care about the health of their future children. In any case, you should not tune in to the worst outcome. There are reasons for a positive outlook on the situation. The latest equipment, advanced medical technologies and high level medical qualifications can provide a long full life even people with severe forms of heart disease.

Ductus-dependent circulation. With some defects in newborns, an open arterial duct (ductus) may be the main or even the only source of blood entering the pulmonary artery or aorta. In these cases, the closure of the duct leads to a significant deterioration in the condition, often incompatible with life. In other pathologies, the presence of a patent ductus arteriosus (PDA) may exacerbate hemodynamic problems, but is not a vital factor. In this regard, the affiliation of the defect to ductus-dependent or ductus-independent anomalies is determined.

1. Ductus-dependent congenital heart defects:
- with the provision of pulmonary blood flow through the PDA (malformations with pulmonary atresia or critical pulmonary stenosis, transposition of the main arteries);
- with the provision of systemic blood flow through the PDA (break of the aortic arch, sharp coarctation of the aorta, critical aortic stenosis, left heart hypoplasia syndrome).

2. Ductus independent congenital heart disease: VSD, ASD, abnormal pulmonary vein drainage, etc.

Critical heart disease.

Critical situation characterized by severe deficiency cardiac output, rapid progression of heart failure, oxygen starvation of tissues with the development of decompensated metabolic acidosis and dysfunction of vital organs. Critical conditions in CHD occur most often during the transition from prenatal to postnatal type of circulation.

To the main reasons for the development critical condition include (in brackets - the most typical heart pathology):
1) closure of the PDA in ductus-dependent circulation;
2) severe obstruction of blood flow (aortic stenosis, coarctation of the aorta, hypoplastic left heart syndrome, critical pulmonary stenosis);

3) inadequate return of blood to the left heart (total anomalous pulmonary venous drainage, pulmonary atresia with an intact interventricular septum);
4) severe hypervolemia of the pulmonary circulation and volume overload of the heart (common arterial trunk, large VSD, insufficiency of atrioventricular valves);

5) severe arterial hypoxemia (transposition of the main arteries, pulmonary atresia);
6) myocardial ischemia or hypoxia (abnormal discharge of the left coronary artery from the pulmonary artery, transposition of the main arteries).

Some of these reasons can be combined. characteristic feature of critical congenital heart defects in newborns is the absence or weak severity of compensatory reactions (myocardial hypertrophy, collateral circulation etc.). If emergency therapy or surgery is not performed, the child dies within a few days or weeks. Some researchers consider CHD to be critical if it results in death within the first year of life.

• Place of residence. For example, if a person lives in the mountains, then he has to be in conditions of rarefied air, hence the adaptability of the body in the form of an increase in hemoglobin.
• What you do matters too. Those who are engaged in rock climbing, skiing, as well as pilots elevated level hemoglobin is considered normal. This is typical for everyone who experiences great physical exercise.
• Bad habits. Perhaps not surprisingly, smoking also has an effect, because in people addicted to this activity, the capillaries constrict, the lungs receive less air, and this all leads to a lack of oxygen.
• congenital defects. Diseases of the heart, lungs or irregular shape red blood cells, as well as many other genetic abnormalities.
• cancer diseases, diabetes, erythrocytosis, diseases internal organs, cholelithiasis are frequent companions of elevated hemoglobin.
• Excess amounts of vitamins B9 and B12.
• Problems with ecology.
• Hemoglobin can rise from an increase in the size of red blood cells or from the fact that there are more of them. It is usually associated with diseases such as true polycythemia. Or erythrocytosis - a disease in which the quantitative content of red blood cells and hemoglobin increases. Malignant and hemolytic anemia also cause an increase in this protein. With pernicious anemia, the number of red blood cells also decreases.
• The presence of artificial heart valves.

It is worth noting that there are cases when a high level of hemoglobin in men is the norm. This is due primarily to heredity, frequent pastime in the air and the territory of residence.

Symptoms

Unfortunately, without special tests, we cannot determine the exact level of hemoglobin, but its increase can be understood by outward signs. Pay attention to symptoms such as:

• Constant desire to sleep.
• Rapid loss of strength and energy.
• Visual impairment.
• Bad appetite.
• Skin blanching.
• Problems with urination and sexual function.

At the first detection of these symptoms, you should immediately consult a doctor. If you delay, there may be consequences in the form of blood clots, blood clotting, up to a stroke or heart attack.

diet

Get tested for hemoglobin levels. And if it turned out to be elevated, then in addition to medication, it is worth limiting yourself to some food.

1. First, avoid animal fats. They increase cholesterol levels, which in turn leads to blockage of blood vessels.
2. Nuts, fruits, vegetables. These foods are rich in iron, which you should reduce. Also, do not lean on greens, they are also rich in iron.

Add seafood, chicken and legumes, and fish to your diet. Sea food and fish are very rich in iodine, it helps to strengthen the walls of blood vessels, fatty fish also have a lot of polyunsaturated fatty acids that thin the blood. You can buy at the pharmacy fish fat and consume it as a source of unsaturated fats.

You need to keep a close eye on your diet. Problems with hemoglobin often haunt people with a sick stomach. Poor functioning of the gastric mucosa does not beneficial substances absorbed, and also causes difficulty in digestion.

Diseases of the stomach have a negative complex effect on the human body. Remember, we are what we eat.

Do not take vitamins without a doctor's prescription. Since they may contain vitamins of group B, copper, folic acid. These elements increase the absorption of iron, which increases hemoglobin. Excess iron in the body is one of the the most important reasons why high hemoglobin in men.

• Get rid of bad habits such as smoking.
• Try not to experience serious physical exertion. But it is worth doing walking and light jogging, they will make the blood move faster through the vessels, which will prevent the formation of blood clots. Normalized physical activity will also keep your blood vessels in good shape and make them stronger.
• Try to get enough sleep and rest well. A rested body restores all body processes faster.
• Follow your diet.
• See your doctor regularly and follow his instructions.

Some folk recipes can help:

• Mummy, helps well with elevated hemoglobin sold in a pharmacy. A piece no larger than a match head should be dissolved in water. The resulting solution is taken at night for ten days. Then take a five-day break and repeat.
• Drink lemon juice dissolved in water.
• Take buckwheat oats and pearl barley until hemoglobin levels return to normal.

It will not be superfluous to consider some extraordinary methods. For example, donating blood at donor sites. This allows you to start the process of hematopoiesis.

The procedure with leeches can also help, they will not only suck out blood, but also secrete saliva, which has properties favorable for blood.

It makes sense to take blood thinners. As such a drug, you can use aspirin or Cardionmagnyl or Trental.

But remember that before you self-medicate, consult a doctor.

In especially severe cases, it is necessary to apply the procedure - erythrophoresis for treatment. During this procedure, some red blood cells are removed from the blood.

Treatment should not be left for later. The consequences can be irreversible and even fatal. Use the above recommendations for the prevention and prevention of the disease. Take care of your health.

In newborns

General activities:

Removing mucus from respiratory tract, monitoring of heart rate, respiratory rate and SaO2 - if necessary, provide venous access.

Gentle feeding regimen: expressed breast milk or a mixture in frequent small doses or by tube.

Monitoring the level of glucose, electrolytes, urea, etc.

Thermal comfort

Special _____Events, determined by hemodynamic disorders:

1. Ductus-dependent malformations: (pulmonary artery atresia with VSD or intact VSD, CHD with severe pulmonary stenosis, TMA, interruption of the aortic arch, SHL, severe coarctation of the aorta).

2. Ductus-independent defects: (VSD, OSA, TADLV, aortic stenosis, single ventricle without pulmonary stenosis. ASD).

With ductus-dependent malformations, oxygen therapy cannot be prescribed to prevent early closure of the PDA, even in cases of mechanical ventilation.

With increased pulmonary blood flow, the most important thing is to maintain hydrobalance with limited fluid intake into the body. The main means of therapy are diuretics, then inotropic support.

Treatment regimen for cyanotic congenital heart disease:

1.Correction of body temperature.

2. Correction of acidosis (dose of 4% sodium bicarbonate = deficiency of BE * t of the body * 0.3).

3. Determination of the nature of pulmonary blood flow (reduced, enhanced, normal).

4. Determination of ductus dependence.

5. Correction of BCC (increase with reduced pulmonary blood flow; decrease with increased pulmonary blood flow) with glucose infusion or diuretics.

b. Oxygen therapy in ductus-independent patients with reduced pulmonary blood flow.

7. The use of inotropic drugs in concomitant SP.

8. Use of group E prostaglandins in ductus-dependent patients.

9. The use of mechanical ventilation for the treatment of heart failure with oxygen concentrations corresponding to the defect.

After making a preliminary (or accurate) diagnosis and conducting the necessary primary therapy, it is advisable to classify the patient in one of three groups based on the combination of heart damage and somatic status:

1. Patients with congenital heart disease, in which the operation is necessary and possible soon after birth.

2. Patients with congenital heart disease, in which early surgery is not indicated due to minor hemodynamic disorders.

3. Patients with uncorrectable CHD or inoperable due to their somatic condition.

Cyanotic dyspnoea

Shortness of breath-cyanotic attack - an attack of hypoxia in a child with congenital heart disease of the blue type, most often with Fallot's tetralogy, associated with spasm of the output section of the right ventricle.

An attack of hypoxia develops mainly in children early age from 4-6 months to 3 years.

Provoking factors of a shortness of breath-cyanotic attack can be: psycho-emotional stress, increased physical activity, intercurrent diseases accompanied by dehydration (fever, diarrhea), Iron-deficiency anemia, a syndrome of neuro-reflex excitability with perinatal lesion CNS etc.

Clinical diagnostics

A shortness of breath-cyanotic attack is characterized by a sudden onset. The child becomes restless, groans, cries, while cyanosis and shortness of breath increase. He takes a forced position - lies on his side with his legs brought to his stomach or squats down. On auscultation of the heart - tachycardia, systolic murmur of pulmonary artery stenosis is not heard. The duration of a hypoxic attack is from several minutes to several hours. In severe cases, convulsions, loss of consciousness up to coma and death are possible.

Urgent care:

1. Reassure the child, unfasten tight clothes. Lay on the stomach in the knee-elbow position (with brought to the chest and bent in knee joints feet).

2. Inhalation of humidified oxygen through the mask.

3. In case of a severe attack, provide access to a vein and prescribe:

1% solution of morphine or promedol at a dose of 0.1 ml / year of life s / c or / in (children over 2 years old in the absence of symptoms of respiratory depression);

If there is no effect, introduce carefully (!) A 0.1% solution of obzidan at a dose of 0.1-0.2 ml / kg (0.1-0.2 mg / kg) in 10 ml of a 20% glucose solution IV slowly ( at a rate of 1 ml/min or 0.005 mg/min).

4. In case of convulsions, inject a 20% solution of sodium hydroxybutyrate 0.25-0.5 ml / kg (50-100 mg / kg) intravenously slowly.

5. With an intractable attack and the development of hypoxemic coma, a transfer to mechanical ventilation is indicated.

Cardiac glycosides and diuretics are contraindicated!

Hospitalization of children with shortness of breath and cyanotic attacks is indicated if the above therapy is ineffective. With the success of first aid measures, the patient can be left at home with the recommendation of the subsequent use of obzidan at a dose of 0.25-0.5 mg / kg per day.

Pulmonary edema

Pulmonary edema -a critical condition due to increasing left ventricular failure, leading to hypertension in the pulmonary circulation and congestion in the lungs.

Causes of pulmonary edema:

1. Myocardial diseases in the stage of decompensation (myocarditis, cardiomyopathy of various origins).

2. Hemodynamic overload of the volume of the left heart in case of heart defects: defects of the interatrial and interventricular septa; open aortic duct; aortic insufficiency and mitral valves;

3. Hemodynamic pressure overload of the left parts of the heart with heart defects: aortic coarctation; stenosis of the mitral and aortic valves; hypertrophic cardiomyopathy; tumors of the heart; malignant arterial hypertension.

4. With heart rhythm disturbances (paroxysmal tachycardia, atrial fibrillation).

With the development of cardiogenic pulmonary edema, anxiety is noted at the beginning, children can thrash around in bed, and subsequently there may be a violation of consciousness. The skin is at first pale, and then cyanotic, covered with a cold clammy sweat. Breathing is noisy, gurgling. Auscultated over the lungs a large number of moist small and medium bubbling rales, appearing first paravertebral, and then over all other departments chest. Perhaps the development of oligoanuria.

General medical level of care

1. position with a raised head end; can be applied to lower limbs soft tourniquets to delay venous blood for 15-20 minutes. (the pulse on the artery distal to the tourniquet should be maintained), subsequently, the degree of tension of the tourniquet should be gradually reduced;

2. ensure the patency of the upper respiratory tract by removing mucus from the mouth with a gauze swab;

3. Oxygenation of oxygen 40% concentration, passed through a solution of 33% alcohol;

4. lasix 2-4 mg/kg intravenously;

5. prednisolone 5-10 mg/kg;

6. call for an intensive care team.

Qualified level of assistance

oxygenation elevated concentrations oxygen passed through a solution of 33% alcohol, in the absence of effect - spontaneous breathing in the mode of positive exhalation pressure. In case of inefficiency - transfer to mechanical ventilation in the mode of positive end-expiratory pressure (PEEP);

If systolic pressure is below 70 mm Hg. or 70-80 mm Hg, start an intravenous infusion of dopamine (6-20 mcg/kg x min). If more than 20 mcg/kg x min dopamine is required to maintain blood pressure, switch to norepinephrine (0.5 x 30 mcg/kg x min);

If blood pressure is above 90-100 mm Hg. in combination with high diastolic pressure, it is necessary to prescribe:

Nitroglycerin 2-4 mcg/kg x min or pentamine 1.0 mg/kg IV;

Hospitalize in the intensive care unit.

Heart rhythm disorders

One of the leading pathophysiological mechanisms for the development of arrhythmias in children is a violation of the neurogenic regulation of the heart rhythm, leading to severe electrical instability of the myocardium. The psycho-emotional factor in the occurrence of arrhythmias in children also plays a significant role, because. strength of response to stressful situation is largely determined by the personality characteristics of the child, and not by the nature of the stressor itself.

When collecting anamnesis the doctor must determine:

The state of the premorbid background ( perinatal pathology nervous system, neurocirculatory dystonia, infectious-toxic diseases);

Congenital and hereditary pathology of the heart;

Treatment with cardiac glycosides (signs of their overdose), unplanned withdrawal of the antiarrhythmic drug

cases sudden death, syncope in the family.

On clinical examination The physician must determine:

The presence or absence of sudden cardiac arrhythmias;

The duration of the attack of arrhythmias;

Unpleasant sensations and pain in the heart;

"Beating on the neck" - a symptom of "swollen neck";

Weakness, fear of death, change of consciousness;

Paleness of the skin, cold sweat;

The presence of a pulse peripheral vessels, the value of blood pressure, the boundaries of the heart, the characteristics of tones, the heart rate; disappearance, persistence of heart murmur;

Vomiting, abdominal pain, frequent urination, appetite, liver size;

The presence of shortness of breath.

Paroxysmal tachycardia

Paroxysmal tachycardia -an attack of sudden increase in heart rate> 150-160 beats per minute. in older and >200 beats per minute. in younger children, lasting from several minutes to several hours (less often - days), with a sudden restoration of heart rate, which has specific ECG manifestations.

Heart rate in an attack in children up to a year - 260-300; from 1 to 3 years 220-250; older than 3 years 170-220.

The main causes of an attack paroxysmal tachycardia:

1. Violation of the autonomic regulation of the heart rhythm.

2. Organic lesions of the heart.

3. Dielectrolytic disorders.

4. Psycho-emotional and physical stress.

There are two main forms of paroxysmal tachycardia: supraventricular and ventricular. Supraventricular paroxysmal tachycardia in children in a large percentage of cases are functional and result from changes in the autonomic regulation of cardiac activity. Ventricular paroxysmal tachycardias are rare, they are life-threatening conditions and are usually caused by organic heart diseases (congenital heart disease, carditis, cardiomyopathy, etc.)

To select an adequate volume of emergency care, it is important to determine:

Variant of paroxysmal tachycardia: supraventricular or ventricular;

The presence or absence of signs of heart failure in a child, to clarify the diagnosis, conduct an electrocardiographic study.

Clinical manifestations

For an attack of supraventricular paroxysmal tachycardia, a sudden onset is characteristic. The child feels a strong heartbeat, lack of air, dizziness, weakness, nausea, fear of death. Pallor, increased sweating, polyuria are noted. Heart sounds are loud, clapping, heart rate cannot be counted, jugular veins swell. There may be vomiting, which often stops the attack. Heart failure (shortness of breath, hypotension, hepatomegaly, decreased diuresis) develops infrequently, mainly in children during the first months of life and with prolonged attacks. R ("not sinus").

Features of the clinic of ventricular paroxysmal tachycardia: the onset of paroxysm is not subjectively detected; always a serious condition of the child (shock!); the cervical veins pulsate at a frequency much lower than that of the arterial pulse; vagus tests are ineffective. ECG signs of ventricular paroxysmal tachycardia: rhythm rate not more than 160 per minute, variability R-R intervals, altered ventricular complex, absence of P wave.

Emergency care for an attack of supraventricular tachycardia:

Reflex effects that enhance tone vagus nerve: straining with a pinched nose at maximum inspiration (Valsalva test), provocation of a gag reflex, massage of the carotid sinus on one side for 10-20 seconds.

Sedatives and psychotherapy: seduxen (1/4 - 1 tablet), tincture of valerian, motherwort, valocordin (2 drops per year of life), Pavlov's mixture and 1/2-2 panangin tablets, depending on age.

If there is no effect after 30-60 minutes, antiarrhythmic therapy is used. Since children usually react negatively to injections, you need to start with the use of drugs by mouth - Isoptin 1 mg / kg and 1-2 tablets of Panangin, if the attack has not stopped, then you can give the drug again, and another hour later at half the dose. In the case of persistent continuation of the attack, ATP is sequentially administered intravenously in a stream without dilution at a dose of: 6 months. - 0.5 ml; 6 months-1 year - 0.7 ml; 1-3 years -0.8 ml; 4-7 years - 1.0 ml;

8-10 years -1.5 ml; 11-14 years old - 2.0 ml.

With a narrow ventricular complex, IV isoptin (verapamil) 0.25% solution at a dose of 0.1-0.15 mg / kg (in an ampoule with 2 ml of 5 mg of the drug) per 20 ml of isotonic sodium chloride solution or 5% glucose solution , i.e. in dose:

up to 1 month -0.2-0.3 ml; up to 1 year -0.3-0.4 ml; 1-5 years - 0.4 - 0.5 ml; 5-10 years - 1.0-1.5 ml; more than 10 years - 1.5-2.0 ml in combination with 2-5 ml of panangin and seduxen (0.1 ml per year of life). The effect is shown "on a needle". After 20-30 minutes, the introduction can be repeated at the same dose.

In the absence of ECG data or registration of a wide ventricular complex, a 2.5% solution of gilurithmal is slowly injected intravenously in 15-20 ml of isotonic sodium chloride solution at a dose of 1 mg / kg, but not more than 50 mg (25 mg in 1 ml of solution)

Digoxin is the drug of choice for stopping an attack of paroxysmal tachycardia in children, including those suffering from heart failure (not used for PT with aberrant wide complex). The initial dose should be administered intravenously (half daily dose). Calculate the dose of saturation (0.03-0.05 mg/kg of weight) with its uniform introduction in three divided doses per day. Digoxin is combined with isoptin or obzidan. After the use of cardiac glycosides, it is undesirable to use defibrillation, since the electrical discharge can excite treatment-resistant ventricular disorders rhythm.

In the absence of ECG data and registration of a wide complex, cordaron 5% solution is used slowly intravenously in 5% glucose solution at a dose of 5 mg / kg (50 mg in 1 ml of solution).

Means for stopping an attack of PT, including in the presence of aberrant complexes - novocainamide, obzidan. Novocainamide is less desirable (severe hypotension, blockade with intravenous administration), it is not used in heart failure and is not combined with cardiac glycosides. A dose of novocainamide (0.15-0.2 ml/kg) is administered as a 10% solution (no more than 10 ml), preferably with mezaton (0.1 ml per year of life, no more than 1 ml). Obzidan intravenously should be administered very carefully at a dose of 0.01 - 0.02 mg / kg (in 1 ampoule of 1 or 5 mg) at a rate of 0.005 mg / min. Contraindicated in cardiomegaly (carditis, cardiomyopathy).

If the attack continues for a long time and signs of heart failure appear, diuretics should be added.

In case of inefficiency complex therapy defibrillation is indicated. Defibrillator electrodes are wrapped with a cloth moistened with isotonic sodium chloride solution. The active electrode is placed above the lower third of the sternum, the passive electrode is placed under the left shoulder blade. Voltage power electrical impulse: newborns - 250-500 V, children infancy- 500-1000 V, older than 1 year - 1000-4000 V.

If the first impulse is ineffective, it can be repeated 2-3 times with an increase in voltage by 1/3 - 1/2.

Medical defibrillation is indicated in cases where there is no possibility of using a defibrillator.

Methodology: 7.5% solution of potassium chloride (1 - 1.5 ml per year of life) and 1% solution of novocaine (1 ml per year of life) are intracardiacly injected - transferring fibrillation to complete cardiac arrest, followed by neutralization of excess potassium by introducing a 10% solution of calcium chloride (0.1-0.2 ml per year of life) and continued closed heart massage. Defibrillation may occur after 5-10 minutes, since this time is necessary for the distribution of drugs in the heart muscle. In case of inefficiency, a 0.1% solution of adrenaline is added (0.05 ml per year of life).

Intracardiac administration of cardiostimulating agents: chest puncture in newborns and infants is performed in the third intercostal space at the left edge of the sternum, in other ages - in the fourth-fifth intercostal space at a distance of 0.5-1 cm to the left of the sternum. The puncture is carried out with a syringe with a needle 0.8 mm in diameter and 80 mm long. The syringe plunger is constantly pulled towards itself and, as soon as blood appears in the syringe, adrenaline and calcium chloride are injected into the heart cavity with atony of the myocardium, previously diluted 10 times with 10% glucose solution.

Complications: pneumothorax during puncture lateral to the parasternal line, hemipericardium when using large-diameter needles.

Emergency correction of metabolic acidosis during cardiopulmonary resuscitation: 4% sodium bicarbonate solution or 3.6% trisamine solution 0.1 ml/kg per minute is administered intravenously.