Critical heart defects. Pediatrician's tactics for critical congenital heart defects in newborns

(manifested by arterial hypoxemia, "ductus-dependent")

Transposition of the great arteries (TMA) 0.22-0.33 per 1000 newborns, 6-7% of all CHD, 23% among critical CHD.

Anatomy of the defect: the pulmonary artery is the outflow tract of the left ventricle, the aorta is the outflow tract of the right ventricle. This disrupts hemodynamics: arterial blood circulates in the system of the small circle, and venous blood in the system of the large circle. The supply of oxygen to the life-supporting organs is possible only under the condition of functioning fetal communications - the ductus arteriosus, the oval window, or in the presence of an atrial defect. At birth, the child immediately has diffuse cyanosis, a state of extreme severity, severe arterial hypoxemia. With survival for several weeks, heart failure and severe malnutrition increase. When the communications are closed, acute hypoxia leads to the development of multiple organ failure and death of the newborn within several hours. Optimal timing of surgical correction : with intact IVS in the first 3-4 weeks of life, an arterial switch operation (radical) can be performed, which has top scores than the Rastelli procedure. With the combination of TMA + VSD, arterial switching can be performed within 1 year of life.

Atresia (critical stenosis) pulmonary artery with intact interventricular septum (ALA + VMI) 0.06-0.07 / 1000, 1-3% of all CHD, 3-5% of critical CHD.

Anatomy : there is no exit from the pancreas, LA is hypoplastic, hypoplasia of the right heart. Hemodynamics: blood does not enter the pulmonary artery, it is shunted to the left heart through the LLC (PDA), that is, the condition for survival is "ductus-dependent" blood circulation. The left ventricle pumps blood into both circles of the blood circulation. A full-term baby is born. In the first hours of life, the condition worsens. Increasing cyanosis from birth, shortness of breath, tachycardia, hepatomegaly, peripheral edema. The condition is very serious. The noise of the PDA is heard. Anxiety or lethargy of hypoxic genesis may be accompanied by a "cry of pain" in coronary disorders, loss of consciousness. A similar violation of hemodynamics, and a similar clinical picture noted with atresia of the tricuspid valve. Optimal terms of surgical correction: in the first months of life, the problem of decompression of the right ventricle with the restoration of effective blood flow through it should be solved, which will contribute to the growth and development of its cavity by creating intersystem anastomoses, pulmonary valvotomy.

Left heart hypoplasia syndrome (LHSS) 0.12-0.21 / 1000 newborns, 3.5-7.5% of all CHD, 16% - among critical CHD.

Anatomy: Various combinations of atresia, stenosis or hypoplasia of the aortic and / or mitral valve, hypoplasia or absence of the left ventricle, hypoplasia of the aorta. Hemodynamics: pronounced obstruction of blood flow through the left heart, blood from the left atrium through oval window enters the right sections, the pulmonary artery, then a small volume of blood through the PDA - into the descending aorta and the great circle, which is accompanied by a pronounced impoverishment of the small circle. Immediately after birth, the clinic resembles RDS, CNS damage and / or septic shock: gray skin, weakness, cold extremities, cyanosis (more on the legs), severe shortness of breath, oligo-, anuria. Optimal timing of surgical correction: if a decision is made on surgical correction, it is performed in the first 3-4 weeks of life in the form of: heart reconstruction, when the functions of the systemic ventricle are transferred to the right ventricle, heart transplantation, or (in case of moderate hypoplasia - as biventricular correction)

Severe preductal coarctation / break of the aortic arch (CA) 0.02 / 1000 newborns, 0.4% of all CHD, 1-10% among critical CHD.

Anatomy: the blood flow from the proximal part of the aorta to the distal one (below the place of origin of the arterial duct) is sharply limited or completely absent. Hemodynamics: in the descending aorta (into the great circle), a small volume of blood comes only from the pulmonary artery through the ductus arteriosus When the arterial duct closes, hypoperfusion of organs and tissues and multiple organ failure develop. . Clinic. Outwardly safe newborn with a sharp deterioration in the first 1-3 days of life - weakness, cold extremities, symptom " white spot», Pulse of small filling, high blood pressure on the arms and low (not determined) on the legs, shortness of breath, tachycardia, oliguria with increasing azotemia, hepatomegaly with an increase in transaminases, necrotizing enterocolitis. Optimal terms of surgical correction: after the stabilization of the child's condition is achieved, surgical correction of the defect is performed - the creation of a direct anastomosis between the segments of the aorta or the interposition of a synthetic prosthesis in the event of a break in the arc, similar correction tactics for preductal coarctation.

In newborns

General activities:

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

Gentle feeding mode: expressed breast milk or a mixture in frequent small doses or by gavage.

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

Thermal comfort

Special _____Events, determined by hemodynamic disorders:

1. Ductus-dependent defects: (atresia of the pulmonary artery with VSD or intact IVS, CHD with sharp pulmonary stenosis, TMA, break of the aortic arch, SGFS, sharp coarctation of the aorta).

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

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

With increased pulmonary blood flow, the most important is the observance of the hydrobalance with the restriction of the flow of fluid into the body. The main means of therapy are diuretics, then inotropic support.

Treatment regimen for cyanotic CHD:

1.Correction of body temperature.

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

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

4. Determination of ductus dependence.

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

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

7. Use of inotropic drugs with concomitant joint ventures.

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

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

After a preliminary (or accurate) diagnosis has been made and the necessary primary therapy has been carried out for the combination of heart damage and somatic status, it is advisable to assign the patient to one of three groups:

1. Patients with CHD, in whom surgery is necessary and possible soon after birth.

2. Patients with CHD, in whom early surgery is not indicated due to minor hemodynamic disturbances.

3. Patients with incorrect CHD or somatic inoperable.

Dyspnea-cyanotic attack

A dyspnea-cyanotic attack is an attack of hypoxia in a child with a congenital blue-type heart defect, most often with Fallot's tetrad, associated with spasm of the right ventricular outlet.

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

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

Clinical diagnostics

A dyspnea-cyanotic attack is characterized by a sudden onset. The child becomes restless, groans, cries, while cyanosis and shortness of breath intensify. Takes a forced pose - lying on its side with legs brought to the stomach or squatting down. With auscultation of the heart - tachycardia, systolic murmur of pulmonary 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. Calm down the child, unbutton the embarrassing clothing. Lay on the stomach in the knee-elbow position (with the legs brought to the chest and bent at the knee joints).

2. Carry out the inhalation of humidified oxygen through the mask.

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

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

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

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

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

Cardiac glycosides and diuretics are contraindicated!

Hospitalization of children with dyspnea-cyanotic attacks is indicated if the above therapy is ineffective. If the first aid measures are successful, the patient can be left at home with a recommendation for 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 the growing left ventricular failure, leading to hypertension in the pulmonary circulation and congestion in the lungs.

Causes of pulmonary edema:

1. Diseases of the myocardium in the stage of decompensation (myocarditis, cardiomyopathy of various origins).

2. Hemodynamic volume overload of the left heart in heart defects: atrial and ventricular septal defects; open aortic duct; insufficiency of the aortic and mitral valves;

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

4. In case of heart rhythm disturbances (paroxysmal tachycardia, atrial fibrillation).

With the development of cardiogenic pulmonary edema, anxiety is noted at the beginning, children can rush in bed, in the future there may be a violation of consciousness. The skin is pale at first and then cyanotic, covered with cold, clammy sweat. Breathing is noisy, bubbling. Above the lungs, a large number of moist fine and medium bubbly rales are heard, appearing first paravertebrally, and then over all other parts chest... Development of oligoanuria is possible.

General medical level of care

1. position with a raised head end; can be superimposed on lower limbs loose tourniquets for delaying venous blood for 15-20 minutes. (the pulse on the artery distal to the tourniquet should be maintained), then gradually reduce the degree of tension of the tourniquet;

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

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

4. lasix 2-4 mg / kg intravenously;

5. prednisolone 5-10 mg / kg;

6. Calling the intensive care team.

Qualified level of assistance

Oxygenation with increased oxygen concentrations, passed through a solution of 33% alcohol, in the absence of effect - spontaneous breathing in the mode of positive pressure on exhalation. If ineffective - transfer to mechanical ventilation in the mode of positive pressure at the end of expiration (PEEP);

If the 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 a dopamine injection rate of more than 20 μg / kg x min is required to maintain blood pressure, it is necessary to switch to norepinephrine (0.5 x 30 μg / 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 μg / kg x min or pentamine 1.0 mg / kg IV;

Hospitalized in the intensive care unit.

Heart rhythm disturbances

One of the leading pathophysiological mechanisms of 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 psychoemotional factor in the occurrence of arrhythmias in children also plays a significant role, because the strength of the response to stressful situation is largely determined by the personality traits of the child, and not by the nature of the stress factor itself.

When taking anamnesis the doctor must establish:

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

Congenital and hereditary heart disease;

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

Cases sudden death, fainting in the family.

On clinical examination the doctor must determine:

The presence or absence of sudden heart rhythm disturbances;

Duration of an attack of arrhythmias;

Unpleasant sensations and pain in the heart;

"Throbbing in the neck" - a symptom of a "swollen neck";

Weakness, fear of death, change in consciousness;

Pallor skin, cold sweat;

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

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

Shortness of breath.

Paroxysmal tachycardia

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

Heart rate in an attack in children under one year old - 260-300; from 1 to 3 years 220-250; over 3 years old 170-220.

The main causes of an attack paroxysmal tachycardia:

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

2. Organic lesions of the heart.

3. Dielectrolyte disturbances.

4. Psycho-emotional and physical stress.

There are two main forms of paroxysmal tachycardia: supraventricular and ventricular. Supraventricular paroxysmal tachycardias 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, are life-threatening conditions and are usually caused by organic heart diseases (congenital heart disease, carditis, cardiomyopathy, etc.)

To select an adequate volume emergency care it is important to define:

Variant of paroxysmal tachycardia: supraventricular or ventricular;

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

Clinical manifestations

An attack of supraventricular paroxysmal tachycardia is characterized by a sudden onset. The child feels a strong heartbeat, shortness of breath, dizziness, weakness, nausea, fear of death. Pallor, increased sweating, polyuria are noted. Heart sounds are loud, clapping, heart rate cannot be counted, neck veins swell. There may be vomiting, which often stops the attack. Heart failure (shortness of breath, hypotension, hepatomegaly, decreased urine output) develops infrequently, mainly in children of the first months of life and with prolonged attacks .. ECG signs of paroxysmal supraventricular tachycardia: rigid rhythm with a frequency of 150-200 beats, unchanged ventricular complex, the presence of an altered tooth P ("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 rate much lower than the arterial pulse rate; vagal tests are ineffective. ECG signs of ventricular paroxysmal tachycardia: rhythm rate no more than 160 per minute, variability intervals R-R, altered ventricular complex, absence of P wave.

Emergency care for an attack of supraventricular tachycardia:

Reflex effects that increase the tone of the vagus nerve: straining with a pinched nose at maximum inspiration (Valsalva test), provoking the 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, antiarrhythmic therapy is used after 30-60 minutes. 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 after another hour in a half dose. In case of persistent continuation of the attack, ATP is sequentially injected 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 old - 1.0 ml;

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

With a narrow ventricular complex, intravenous 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 a dose:

up to 1 month -0.2-0.3 ml; up to 1 year -0.3-0.4 ml; 1-5 years old - 0.4 - 0.5 ml; 5-10 years old - 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 manifested “on the needle”. After 20-30 minutes, the administration 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 giluritmal 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)

The means of choice for stopping an attack of paroxysmal tachycardia in children, including those suffering from heart failure, is digoxin (not used for PT with an aberrant wide complex). The initial dose should be given intravenously (half the daily dose). The dose of saturation (0.03-0.05 mg / kg of weight) is calculated with its uniform introduction in three doses per day. Digoxin is combined with isoptin or obzidan. Defibrillation is undesirable after cardiac glycosides have been used, as the electrical discharge can induce treatment-resistant ventricular disturbances rhythm.

In the absence of ECG data and registration of a wide complex, cordaron 5% solution is used slowly intravenously in a 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. The dose of novocainamide (0.15-0.2 ml / kg) is administered in the form of 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 with extreme caution 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, then diuretics must be added.

In case of inefficiency complex therapy defibrillation is shown. Wrap the defibrillator electrodes with a cloth dampened with isotonic solution sodium chloride. The active electrode is placed over the lower third of the sternum, and the passive electrode is placed under the left shoulder blade. Voltage power electrical impulse: newborns - 250-500 V, infants - 500-1000 V, over 1 year old - 1000-4000 V.

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

Medical defibrillation is indicated when a defibrillator cannot be used.

Methodology: a 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 injected intracardiacally - 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 the continuation of a closed heart massage. Defibrillation can appear in 5-10 minutes, as this time is necessary for the distribution of drugs in the heart muscle. If ineffective, add 0.1% adrenaline solution (0.05 ml per year of life).

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

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

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

Even highly qualified cardiologists with a huge practical experience... The reasons for the development of pathology are varied, as are its manifestations. Sometimes the disease proceeds calmly and does not make itself felt for many years. Serious defects require lifelong therapy and sometimes urgent surgical intervention... But it's one thing when a person finds himself in such a situation for reasons beyond his control. And it is completely different - 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, septa or large vessels supplying it with blood. The heart cannot cope with its job of supplying organs with oxygen. They experience oxygen starvation and are in serious danger. Distinguish between acquired and congenital heart defects.

Congenital defect

Congenital heart disease - an anomaly in the structure of blood vessels and the heart, according to different reasons arising during the intrauterine development of the fetus. Pathology is one of the first places in the number of 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 intrauterine phase. It happens that the pathology remains unnoticed during the first years of a baby's life. But over time, she will definitely remind of herself.

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

• infectious diseases;
• taking certain medications;
• addiction to alcohol;
• drug use;
• exposure to radiation;
• endocrine system pathology;
• severe toxicosis while carrying a child;
• middle age of the mother;
• poor heredity;
• chromosomal abnormalities.

There are several types of congenital heart defects:

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

An anomaly detected immediately after birth will allow it to start treatment in a timely manner and reduce the threat of death of the baby during the first days of life. Before planning offspring, you need to find out how healthy the 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 the development of the fetus, a heart pathology is found, the mothers are prescribed appropriate therapy during pregnancy. It should support the baby's heart function before birth.

Heart disease in children

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

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

• slow physical development baby;
• pallor of the 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 developmental and learning problems. 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 have a reduced body weight. A sick child's immunity is low, so he is at risk of infectious diseases.

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

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

Blue and white vices

Distinguish between blue and white heart defects. With blue, venous blood is thrown into the arterial bed. In this case, the heart muscle "pumps" oxygen-depleted blood. Pathology is inherent early manifestation symptoms of heart failure:

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

With white defects, venous and arterial blood do not mix, oxygen is supplied to 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 old.

Medical practice testifies: often people with heart disease live a full life, without suffering and unpleasant sensations.

Acquired vice

Acquired heart defects affect the heart valves. Serious pathologies become a "trigger" to their development:

• chronic vascular disease (atherosclerosis);
• systemic lesions of connective tissues (rheumatism, dermatomyositis, scleroderma);
• endocardial inflammation (infective endocarditis);
• systemic diseases of the joints (ankylosing spondylitis);
• systemic venereal diseases(syphilis).

The cause of acquired heart defects is often the death of heart valve cells. 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 the pathology are similar to the manifestations of other vascular and heart diseases. Therefore, the diagnosis is made only based on the results of the examination, which includes 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 for heart disease may require surgical intervention - up to a valve transplant;
3. Combined - two or more valves of the heart muscle are affected. Mitral, tricuspid and aortic valves can undergo deformations, which will cause difficulties in the diagnosis and treatment of pathology. Most often, mitral valve insufficiency and mitral stenosis are simultaneously manifested. Under similar circumstances, cyanosis and severe shortness of breath appear;
4. Combined - one valve is exposed to several violations. This is usually 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... Dysfunctions of some parts of the heart muscle in to the fullest are compensated by the increased load on other parts of the heart. Only an experienced cardiologist, who has high-tech special equipment at his disposal, is capable of diagnosing this defect.

"Simple", isolated heart defects are much less common than "complex", combined. Infectious ailments haunt patients for years, affecting muscle tissue. As a result, another vice is added to one vice.

Life expectancy with heart disease

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

Uncomplicated heart defects

Often people do not even know that they are living with a disease called "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. They will reduce the likelihood of developing pathology or even reduce its manifestations to a minimum:

• strict adherence to all the doctor's recommendations;
• healthy lifestyle;
• rejection of addictions;
• regular exercise;
• dosing of physical activity;
• full sleep.

A balanced approach to the course of the disease will save the patient from pain, discomfort and other consequences. Meticulous 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 unnecessary or impossible. Under such circumstances, the body needs medication support. If there is no treatment, the pathology progresses. The only outcome in this case is fatal. The heart muscle refuses to perform its direct functions, disrupting the body's supply of blood. If a surgery- the only possible chance to extend life or improve its quality, you should not give it up. Very small percentage surgical treatment heart defects leads to lethality. Over 97% of the operated patients live a full life in the future.

What is this “heart threshold”, how long do they live with a diagnosed heart defect? These questions are troubling to many. Some are worried about their own diagnosis, others are concerned 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 technology and high level medical qualifications can ensure long-term full life even people with severe heart disease.

Introduction
Obstructive shock is a condition in which a decrease in cardiac output is caused by a physical obstruction to blood flow. The reasons for the development of obstructive shock include:

• Heart tamponade
• Tension pneumothorax
• Ductus-dependent congenital heart defects
• Massive pulmonary embolism

Physical obstruction to blood flow leads to decreased cardiac output, insufficient tissue perfusion, and a compensatory increase in systemic vascular resistance... Early clinical manifestations obstructive shock can be indistinguishable from hypovolemic shock, although a careful clinical examination can reveal signs of venous stasis in the pulmonary or pulmonary circulation, which is not typical for ordinary hypovolemia. As the condition worsens, increased respiratory effort, cyanosis, and signs of venous congestion become more evident.
Physiology and clinical manifestations of obstructive shock
The physiological features and clinical manifestations of obstructive shock depend on the cause that caused it. This chapter describes the 4 main causes of obstructive shock and the main distinguishing features of each of them.
Heart tamponade
Cardiac tamponade is caused by accumulation of fluid, blood, or air in the pericardial space. An increase in pressure in the pericardial cavity and compression of the heart leads to a decrease in venous return from the large and pulmonary circulation, a decrease in the end-diastolic volume of the ventricles, and to a decrease in cardiac output. Left untreated, cardiac tamponade leads to cardiac arrest, which is characterized as electrical activity without a pulse.
In children, cardiac tamponade is most often found in penetrating wounds or in cardiac surgery, although the cause of this condition may be pericardial effusion as a complication of the inflammatory process.

Features:

• Muffled heart sounds
• Paradoxical pulse(decrease in systolic blood pressure during inspiration by more than 10 mm Hg. Art.)
• Swelling of the neck veins (may be difficult to see in children with severe hypotension)

Note that in children after cardiac surgery, signs of tamponade may be indistinguishable from signs cardiogenic shock... A successful outcome depends on prompt diagnosis and prompt treatment. The diagnosis can be made by echocardiography. The ECG shows a low amplitude of QRS complexes with a large volume of fluid in the pericardial cavity.
Tension pneumothorax
The cause of a tense pneumothorax is the accumulation of air in the pleural cavity. Air can enter the pleural space from a damaged lung, which can occur with an internal rupture or with a penetrating chest wound. With a simple pneumothorax, a limited amount of air enters the pleural cavity, followed by the closure of the defect. With the continued supply and accumulation of air, the pressure in the pleural cavity becomes positive. This can occur as a result of barotrauma during positive pressure ventilation, when air from a damaged lung enters the pleural space. With an increase in pressure in the pleural cavity, the lung collapses, and the mediastinum shifts in the opposite direction. The collapse of the lung quickly leads to the development of respiratory failure, and high pressure in the pleural cavity and compression of the structures of the mediastinum (heart and large vessels) reduce venous return. This leads to a rapid drop in cardiac output. If untreated, tension pneumothorax leads to cardiac arrest, which is characterized by pulseless electrical activity.
Suspect a tension pneumothorax in a victim with a chest trauma, as well as in any intubated child whose condition suddenly worsens during positive pressure ventilation (including overly vigorous ventilation with a mask bag).
Typical signs of tension pneumothorax:

• Tympanic percussion sound on the affected side
• Decreased breathing on the affected side
• Swelling of the neck veins (may be difficult to see in infants or if hypotension is severe)
• Tracheal deviation to the opposite side of the lesion (may be difficult to assess in children younger age)
• Tachycardia, quickly replaced by bradycardia and a rapid deterioration of blood circulation with a drop in cardiac output

A successful outcome depends on prompt diagnosis and prompt treatment.
Ductus-dependent congenital heart defects
Ductus-dependent defects are congenital heart defects in which a child's life is possible only with the functioning of the ductus arteriosus (ductus arteriosus). As a rule, the clinical manifestations of ductus-dependent defects occur in the first week of life.
Ductus-dependent defects include:

• A group of cyanotic congenital heart defects in which pulmonary blood flow depends on the functioning of the ductus arteriosus
• Congenital heart defects with obstruction of the left heart, in which systemic blood flow depends on the functioning of the ductus arteriosus (coarctation of the aorta, break of the aortic arch, critical aortic stenosis, and left heart hypoplasia syndrome)

Defects in which pulmonary blood flow depends on the functioning of the ductus arteriosus usually manifest as cyanosis without signs of shock. Defects with obstruction of the left heart of the heart are often manifested by the development of obstructive shock in the first two weeks of life, when the ductus arteriosus ceases to function. Maintaining a patent ductus arteriosus as a bypass pathway for left heart obstruction is critical to survival.

Distinctive signs of defects with obstruction of the left heart:

• Rapid deterioration of systemic perfusion
• Congestive heart failure
• Different levels of blood pressure in the vessels proximal and distal to the ductus arteriosus (coarctation of the aorta, break of the aortic arch)
• Cyanosis of the lower half of the body - areas of postductal blood flow (coarctation of the aorta, break of the aortic arch)
• Lack of pulse in the femoral arteries (coarctation of the aorta, break of the aortic arch)
• A rapid decline in the level of consciousness
• Respiratory failure with signs of pulmonary edema or insufficient respiratory effort

Massive pulmonary embolism
Pulmonary embolism is a complete or partial obstruction of the pulmonary artery or its branches by a blood clot, fat, air, amniotic fluid, a catheter fragment, or an intravenous substance. The most common cause of pulmonary embolism is a thrombus that migrates into the pulmonary circulation. Pulmonary embolism can lead to pulmonary infarction.
In childhood, pulmonary embolism is relatively rare, but there are conditions that predispose to the development of pulmonary embolism in children. Examples of such conditions and predisposing factors are indwelling central venous catheters, sickle cell anemia, malignancies, diffuse diseases connective tissue, hereditary coagulopathies (for example, deficiency of antithrombin, protein S, and protein C).
With pulmonary embolism, a vicious circle of disorders is formed, including:

• Violation of the ventilation-perfusion ratio (proportional to the size lung infarction)
• Systemic hypoxemia
• Increased pulmonary vascular resistance, resulting in right ventricular failure and a drop in cardiac output
• Displacement of the interventricular septum to the left, which leads to a decrease in left ventricular filling and a further decrease in cardiac output
• Rapid drop in end-expiratory CO2 concentration

Symptoms of this condition can be mild, which makes diagnosis difficult, especially in the absence of alertness in the researcher. The manifestations of pulmonary embolism are mostly nonspecific and include cyanosis, tachycardia, and hypotension. However, symptoms of right ventricular failure and blood stasis distinguish it from hypovolemic shock.
conclusions
The choice of treatment for obstructive shock depends on the underlying cause. Quickly identifying and treating the cause of the obstruction can be life-saving. Therefore, the most important tasks of the resuscitator are the rapid diagnosis and treatment of obstructive shock. In the absence of emergency care, the condition of patients with obstructive shock progresses rapidly to cardiopulmonary failure and cardiac arrest.
Bibliography

1. Carcillo JA. Pediatric septic shock and multiple organ failure. Crit Care Clin. 2003; 19: 413-440, viii.
2. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005; 6: 2-8.

• 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 organism in the form of an increase in hemoglobin.
• What you do also matters. For those who are engaged in rock climbing, alpine skiing, as well as for pilots, an increased level of hemoglobin is considered the norm. This is typical for everyone who experiences great physical exercise.
• Bad habits. Perhaps few people will be surprised, but smoking has an impact, because people who are addicted to this activity have narrowed capillaries, the lungs receive less air and this all leads to a lack of oxygen.
• Congenital malformations. Diseases of the heart, lungs or irregular shape red blood cells, as well as many other genetic abnormalities.
• Oncological diseases, diabetes, erythrocytosis, diseases internal organs, cholelithiasis - frequent companions of high hemoglobin.
• Excessive amounts of vitamins B9 and B12.
• Ecological problems.
• Hemoglobin can increase from an increase in the size of red blood cells or from the fact that there are more of them. This is usually associated with diseases such as polycythemia vera... Or erythrocytosis - a disease in which the quantitative content of erythrocytes and hemoglobin increases. Malignant and hemolytic anemia also cause an increase in this protein. With pernicious anemia, the number of erythrocytes also decreases.
• The presence of artificial heart valves.

It is worth noting that there are times when a high level of hemoglobin in men is the norm. This is due primarily to heredity, frequent spending time outdoors 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... It is worth paying attention to symptoms such as:

• Constant desire to sleep.
• Rapid loss of strength and energy.
• Deterioration of vision.
• Poor appetite.
• Pale skin.
• Problems with urination and sexual function.

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

The diet

Get tested for hemoglobin levels. And if it turned out to be elevated, then in addition to medication treatment, you should limit 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 should be reduced. Also, do not lean on greens, they are also rich in iron.

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

You need to closely monitor your diet. Hemoglobin problems often plague people with stomach problems. Poor work of the gastric mucosa does not give useful substances absorbed, and also causes difficulty in digestion.

Diseases of the stomach have a negative complex effect on the human body. Don't forget - we are what we eat.

You should not take vitamins without a doctor's prescription. Since the composition can contain B vitamins, 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 activity. 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. Normal physical activity will also keep your blood vessels in good shape and make them stronger.
• Try to get enough sleep and get a good rest. A rested body quickly restores all body processes.
• Follow your diet.
• See your healthcare provider regularly and follow their instructions.

Some folk recipes can also help:

• Shilajit, good for high hemoglobin, is sold in the pharmacy. A piece no larger than a match head should be dissolved in water. Take the resulting solution 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 the hemoglobin level returns to normal.

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

The leech procedure can also help, they will not only suck blood, but also secrete saliva, which has properties favorable to blood.

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

But remember that before self-medication, consult a doctor.

In especially severe cases, it is necessary to use a procedure for treatment - erythrophoresis. 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 to prevent and prevent illness. Take care of your health.