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Taking into account the nature, localization of pain sensations and ECG changes in patients with acute pericarditis, MI is most often misdiagnosed. In differential diagnosis, it should be taken into account that a significant duration, connection with

respiration, and the occurrence simultaneously with a temperature reaction are not characteristic of is genesis. Pericardial friction noise in myocardial infarction is less pronounced and occurs later

longer time after the onset of pain than with pericarditis. With MI, a discordant shift of the ST segment and the formation of a pathological Q wave are recorded, while with pericarditis, a unidirectional shift of the ST segment is observed in opposite ECG leads and a pathological Q wave is not formed. Echocardiographic examination reveals the most important sign of effusion pericarditis -

divergence of the sheets of the pericardium, while violations of local contractility of the heart muscle, characteristic of MI, are not observed in patients with acute pericarditis.

Having ruled out the diagnosis of MI, in practice it is often necessary to make a differential diagnosis of various clinical variants of effusion pericarditis. It is important to distinguish pericarditis due to connective tissue diseases (systemic red

lupus, scleroderma, periarteritis nodosa, rheumatoid arthritis, etc.), from acute idiopathic pericarditis. In acute rheumatic fever, pericarditis is usually

accompanied by inflammation of other membranes of the heart with signs of severe pancarditis. Tuberculous pericarditis can be acute (with its symptoms combined with

other signs of active tuberculosis), as well as in the form of subacute constrictiveexudative pericarditis and classic chronic constrictive pericarditis. Uremic pericarditis develops in every third patient with chronic uremia.

Pericarditis in patients with malignant neoplasms may be due to

metastasis or germination of tumors in the pericardium. Most often, pericarditis develops in patients with tumors of the lungs, breast, malignant melanoma, and lymphoma.

Within 1 to 5 years after radiation therapy for cancer,

develop radiation pericarditis. Significant, but not accompanied by severe

Clinical symptomatic fluid accumulation in the pericardial cavity is observed in some patients with myxedema.

To clarify the etiology of pericarditis, in addition to a thorough analysis of anamnestic and physical data, the results of the study of fluid obtained from the pericardial cavity are of

great importance. Transudate, the hallmark of which is a protein content of less than 30 g/l, is characteristic of congestive heart failure, Dressler'ssyndrome, radiation pericarditis. Serous exudate is usually found in viral and idiopathic

pericarditis. Purulent exudate is a sign of bacterial pericarditis. With pericarditis, caused by oncological diseases, as a rule, hemorrhagic

effusion. Subsequent examination of the pericardial fluid using various

methods, the choice of which is carried out taking into account the individual characteristics of the disease, allows you to find out the cause, and in infectious pericarditis - to identify the causative

agent of the inflammatory process, which is of great importance for determining the prognosis and tactics of treating the patient.

Flow. Acute pericarditis in most cases is characterized by a benign course. Severe course, as a rule, is noted in patients with uremic, tumor and other pericarditis of secondary origin. In 10–20% of cases, a recurrent course of pericarditis is observed. Chronic constrictive pericarditis develops in 5

- 8% of patients.

Forecast and outcomes. Most patients with acute pericarditis recover within

2 - 6 weeks The best prognosis is typical for effusion serous pericarditis. Development

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cardiac tamponade significantly worsens the prognosis. This complication is diagnosed in 10-15% patients, most often - with tuberculous, purulent and tumor pericarditis. Pressure

exudate in the pericardial cavity can increase to critical within a few days

and even weeks. The most common cause of acute tamponade is hemopericardium due to aortic dissection or rupture of the ventricular wall in patients with MI. Chronic constrictive pericarditis with the formation of a "shell heart" in most cases is

is the outcome of tuberculous, purulent or radiation pericarditis.

Treatment. The diagnosis of acute pericarditis is the basis for hospitalization of the patient and the appointment of bed rest (in the first days of illness) or semi-bed rest. If there

is an effusion in the pericardial cavity, it is necessary to monitor blood pressure and heart rate, and regular echocardiographic study. The appearance of signs of cardiac tamponade - an indication

to immediately perform pericardiocentesis as a life-saving procedure. Puncture

the pericardium is justified in cases of accumulation of a significant volume of fluid even without signs of cardiac tamponade. In aortic dissection, pericardiocentesis is

contraindicated, since the removal of blood from the pericardial cavity increases bleeding and worsens the Drug treatment is determined by the etiology of pericarditis. With tuberculosis

pericarditis, a long-term (for 6-12 months) combined anti-tuberculosis therapy is carried out. In the case of purulent pericarditis, systemic antibiotic therapy is combined with the introduction of antibiotics into the pericardial cavity. Most patients use

open surgical drainage and irrigation of the pericardial cavity with proteolytic enzymes. Formation of adhesions, encysted effusion, recurrent cardiac tamponade,

an increase in signs of constriction are considered as indications for pericardiectomy. AT treatment of patients with fungal pericarditis, antifungal drugs are used

means: ketoconazole, fluconazole, itraconazole, amphotericin B. Patients with tumor

pericarditis, systemic antitumor treatment is prescribed, pericardio

centesis and intrapericardial administration of cytostatics or sclerosing agents.

Most patients with pericarditis are prescribed drugs that have

anti-inflammatory action. The basis for the use of non-steroidal anti-inflammatory drugs is fibrinous pericarditis, accompanied by persistent pain syndrome, and effusion serous pericarditis with a small amount of exudate. First-line drugs in the treatment of acute pericarditis are acetylsalicylic acid.

(aspirin) and ibuprofen. Aspirin is given in large doses (500-1000 mg every 6 hours) within 3 - 5 days. Then during the week aspirin is used at a dose of 1500 mg / day and for

2 more weeks at a dose of 500 mg / day. Ibuprofen is prescribed according to the scheme of 300-800 mg every 6-8 hours

until the complete disappearance of manifestations of pericarditis. Ibuprofen is the drug of choice in the treatment of postinfarction pericarditis (Dressler'ssyndrome), as it can improve

coronary perfusion. Active treatment with non-steroidal anti-inflammatory drugs should be combined with medical gastroprotection.

For the treatment of patients who, during therapy with non-steroidal anti-inflammatory drugs, have a fever for 5 to 7 days or after the symptoms subside

pericarditis recurrence of the disease, it is recommended to add colchicine 1 mg / day. Colchicine can be used not only in combination, but also instead of non-steroidal antiinflammatory drugs in case of their individual intolerance.

Corticosteroids are indicated only in patients who are seriously ill

(unstable hemodynamics, severe cardiac or respiratory failure). The recommended dose of prednisolone is 1-1.5 mg per 1 kg of patient weight (60-90 mg) per day

for up to 1 month. followed by a gradual decrease in dose until the drug is completely discontinued within 3 months. Patients with purulent and tuberculous pericarditis corticosteroids for

contraindicated.

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A radical method of treating patients with constrictive pericarditis is a partial resection of the pericardium. During preparation for surgery, diuretics are used. Mortality in pericardiectomy is 10%, a pronounced improvement in the condition after surgery is observed in 50% of patients.

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1.8. HEART DEFECTS

Heart defects are divided into congenital and acquired. Congenital heart defects are anatomical changes in the heart and/or large vessels that

formed in the embryonic period. Acquired heart defects are

morphological and / or functional disorders of the valvular apparatus that occur due to illness and injury. In some cases, structural changes in the valvular apparatus and related disorders of intracardiac hemodynamics are the result of a

combination of anomalies in the development of the cardiovascular system and diseases suffered by the patient.

1.8.1. congenital heart defects

The incidence of congenital heart defects in children born alive averages 8:1000. Every third congenital heart disease is regarded as critical and requires surgical treatment during the first year to save the child'slife.

More than half of children with congenital heart defects undergo surgery or die in childhood and adolescence.

The detection of congenital heart defects in adults is in most cases the result of inadequate diagnosis of heart disease in children. Among the developmental anomalies of the cardiovascular system, most often detected in adults, include defects

atrial and interventricular septa, patent ductus arteriosus, pulmonary stenosis and coarctation of the aorta.

Atrial septal defect

Atrial septal defect is the most common congenital

heart disease in adults. The share of atrial septal defect among other congenital malformations detected in adults is 15%.

There are two main morphological variants of the defect. In 20% of patients, a primary atrial septal defect is diagnosed, which is localized in its lower part. Primary atrial septal defect is often associated with splitting

mitral and/or tricuspid valve cusps. In 70% of patients, a secondary

atrial septal defect. With this variant of the defect, communication between the atria occurs due to the presence of a tissue defect in the region of the oval fossa, i.e., the middle part of the septum, which is formed later than its upper and lower sections. About

in 10% of cases, a defect of the venous sinus is detected, which is characterized by the location tissue defect in the upper part of the interatrial septum, near the confluence of the hollow veins. With all variants of this defect, there is a hole in the interatrial septum,

as a result of which there is a constant communication between the atria. In cases of open

oval window, the septal tissue can anatomically completely separate the left and right

atrium, but due to the lack of fusion between non-simultaneously formed parts partitions in it a kind of valve is formed. The volume of blood that passes through an open oval window, is determined by the difference in pressure in the atria.

Blood flow through the opening in the interatrial septum usually occurs on the left

to the right, since in the left atrium the pressure is on average higher than in the right. Increased the volume of blood entering the right atrium moves to the right ventricle, then -

into the pulmonary artery, pulmonary veins and left atrium, from where it is again discharged into the right

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atrium. With a small hole, the disturbance of intracardiac hemodynamics is insignificant and may remain invisible throughout the patient'slife.

At large orifice sizes, the additional blood volume causes volume overload.

and expansion of the right chambers of the heart. Entry into the pulmonary trunk of excess blood pressure causes pulmonary hypertension, increased resistance to blood flow

and systolic overload of the right ventricle. With the depletion of the resources of the right ventricle, increase in diastolic pressure in its cavity. The development of right ventricular failure

causes an increase in pressure in the right atrium. As a result, the shedding of blood through the hole in the atrial septum can change direction, and venous blood

will enter the systemic circulation.

Patients with a significant atrial septal defect complain of

shortness of breath, fatigue and palpitations. Patients with a dilated right ventricle palpation reveals an elevated cardiac impulse and epigastric pulsation. Auscultatory signs of pathological blood flow are absent for a long time, since

due to the low pressure gradient, the movement of blood through the shunt occurs at a low speed. The most specific auscultatory sign of an atrial septal defect is a wide fixed splitting of the second tone. The volume of both components

II tone does not change depending on the phases of breathing. In almost all patients, a systolic murmur is heard to the left of the sternum, the cause of which is the

expulsion of an increased volume of blood into the dilated pulmonary artery. With a secondary defec noise intensity is determined in the II intercostal space, with a primary defect - in the III - IV

intercostal space. With a significant increase in blood flow through the tricuspid valve and the developmen diastolic overload of the right ventricle, a diastolic murmur appears over the lower

part of the sternum and at the xiphoid process, as well as preceding the diastolic murmur right ventricular III tone.

With insignificant dimensions of the atrial septal defect, any changes

ECG is often absent. At the same time, many patients have a blockade of the right legs of the bundle of His, atrial arrhythmias. With significant defects, signs of hypertrophy of the right atrium and right ventricle appear. X-ray examination reveals hypervolemia of the pulmonary circulation, and at later stages of the disease - signs

of pulmonary hypertension, expansion of the pulmonary trunk, enlargement of the right

chambers of the heart.

Direct visualization of an atrial septal defect is possible using two-dimensional echocardiography. Doppler echocardiography can detect the

presence of pathological shunting of blood. In addition, cardiac ultrasound can evaluate the state of the mitral and tricuspid valves, determine the size of the chambers of the heart, quantify pulmonary hypertension. In difficult-to-diagnose cases, transesophageal echocardiography is used, which has a higher resolution than transthoracic echocardiography.

An atrial septal defect with appropriate clinical symptoms is an indication for surgical treatment. In most cases, open heart surgery is performed with a patch of own tissue or an artificial heart.

material. With a secondary atrial septal defect in a number of patients, it is possible performing a catheter operation using an occluder in the form of a double umbrella, which opens on both sides of the septum and is fixed along the edges of the defect.

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Ventricular septal defect

Ventricular septal defect is detected in 10% of adults with congenital heart defects. Some children born with a ventricular septal defect

it spontaneously closes.

The opening(s) through which communication occurs between the ventricles can located in any part of the interventricular septum. In more than 80% of cases, a defect in the upper, membranous part of the septum near the aortic valve is found.

In 10% of patients, the defect is located in the muscular part of the septum. Occasionally meet defects in the outlet section of the septum, bordering the membranous part, closer to the pulmonal valve, as well as its inlet section, which is located in the posterior part of the interventricular septum, near the atrioventricular valves. Output and input defects

sections of the interventricular septum are usually an integral part of more complex congenital anomalies of the heart.

The size of the ventricular septal defect varies greatly: from a few millimeters to the complete absence of septal tissue with the formation of a single ventricular

cavities. A defect in the muscular part of the septum often consists of many small holes (Tolochinov-Roger disease).

Through the hole in the interventricular septum during systole, a discharge occurs

blood from the left ventricle to the right. With a small reset for a long time, the dimensions of the chambers hearts do not change significantly, i.e., the state of successful compensation of intracardiac hemodynamics is preserved. A large shunt causes a volume overload of the right ventricle, an

increase in the volume of blood entering the pulmonary artery, hypervolemia

pulmonary circulation, pulmonary hypertension and an increase in the amount of blood entering the left chambers of the heart with their volume overload. The development of pulmonary hypertension is promoted by reflex spasm of the pulmonary arterioles. Over time, morphological changes develop in the wall of small pulmonary arteries, leading to their narrowing.

lumen, stabilization and further increase in pulmonary hypertension, increased pressure in the right ventricle. Because of this, the obstacle to resetting from left to right increases and its

the value decreases. In cases where the pressure in the pulmonary artery becomes higher than the pressure in the systemic circulation, discharge through the hole in the interventricular septum may even acquire the opposite direction. As a result of volume overload and associated pressure overload, dilatation of the right ventricle and relative tricuspid valve insufficiency develop. In 5– 10% of cases, patients with ventricular septal defect develop aortic insufficiency, which is associated with

localization of the defect in the membranous part of the interventricular septum under the noncoronary cusp of the aortic valve and violation of its attachment to the septum. Aortic insufficiency contributes to an increase in the volumetric load on the left ventricle.

Patients with a small ventricular septal defect usually do not experience discomfort. With large defects, accompanied by the development of pulmonary

hypertension, symptoms of heart failure develop: increased fatigue,

shortness of breath, cyanosis. An objective examination of patients with a small ventricular septal defect does not reveal significant changes in the size of the heart. With a significant discharge of blood through the defect, systolic trembling ("cat'spurr") is detected

in the precordial region, expansion of the boundaries of relative cardiac dullness due to dilatation of all chambers of the heart and absolute cardiac dullness due to dilatation of the right ventricle, increased cardiac impulse. With the development of right ventricular failure, swelling and pulsation of the cervical veins appear, signs of stagnation in the systemic circulation.

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The main auscultatory sign of the defect is an intense pansystolic

noise in the III-IV intercostal space along the left edge of the sternum. Noise intensity depends on the gradient

pressure between the ventricles, so the loudest noise is with small defects. As the pressure gradient decreases, the noise decreases. The formation of pulmonary hypertension is accompanied by the appearance of additional auscultatory phenomena: accent and splitting of the II tone over the pulmonary artery, pulmonary expulsion tone and systolic

murmur of relative pulmonary stenosis. In patients with severe dilatation of the pulmonary artery and its valvular ring, a diastolic murmur of the pulmonary artery is heard.

regurgitation (Graham Still noise). During the formation of aortic insufficiency, a protodiastolic murmur of aortic regurgitation appears.

Small defects are not accompanied by changes in the ECG and chest x-ray. With severe violations of intracardiac hemodynamics and significant

pulmonary hypertension, electrocardiographic signs of hypertrophy of both ventricles, and radiography reveals cardiomegaly and dilated pulmonary artery. Echocardiography is the main method of diagnosing the defect. Two-dimensional

echocardiography allows you to visualize the defect, determine its size and localization, color

Doppler echocardiography - to identify and evaluate blood flow in the area of the defect, which is especially important for the diagnosis of small multiple defects.

Surgical treatment is used in cases of distinct clinical symptoms.

in combination with cardiomegaly and increased pressure in the pulmonary artery to values above 50 mmHg Art. Contraindications to surgery are morphological changes in the vessels of the lungs, for the detection of which functional tests and lung biopsy are used.

fabrics. Closure of a ventricular septal defect is carried out by applying

patches. If the defect is localized in the membranous part of the septum, it is possible to use catheter surgery.

Open ductus arteriosus

Patients with an open ductus arteriosus (Botallo) account for about 10% of total number of adult patients with congenital heart disease. Women have this vice occurs 2-3 times more often than in men.

The ductus arteriosus departs from the aorta at the level of the left subclavian artery and flows into the trunk of the pulmonary artery at the level of its bifurcation. Normally, the ductus

arteriosus closes shortly after birth. If this does not happen, conditions are created for the discharge of blood from the aorta to the pulmonary artery. The degree of hemodynamic disturbance is determined

by the anatomical features of the ductus arteriosus. The duct diameter varies from 2 to 30 mm, length - from 3 to 25 mm. The narrow duct does not cause significant hemodynamic disturbances. Through the wide duct, an additional volume of blood enters the pulmonary artery, which passes small circle of blood circulation and returns to the left chambers of the heart, causing their volume overload and dilation. The flow of excess blood into the pulmonary artery stimulates the development of morphological changes in the vascular wall, which together leads to the formation of pulmonary hypertension and overload of the right heart. Due to

Since the left ventricle is forced to eject an additional volume of blood into the aorta, its hypertrophy gradually develops.

With a significant discharge of blood, the main complaints of patients with open arterial the duct is shortness of breath and palpitations as manifestations of left ventricular failure. Physical examination reveals pathological current

blood trembling over the pulmonary artery, increased and shifted to the left apex beat,

expansion of the boundaries of relative cardiac dullness, first at the expense of the left, and then the right

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departments. The most characteristic sign of an open ductus arteriosus is a rough,

prolonged systole-diastolic murmur, increasing during systole and weakening towards the end

of diastole (“machine” murmur) with a maximum in the 2nd intercostal space to the left of the sternum. The intensity of the noise weakens with the development of pulmonary hypertension, as this leads to decrease in the pressure gradient between the aorta and the pulmonary artery. First, the diastolic

and then the systolic component of the murmur weakens. When pressure equalizes in the pulmonary artery and aorta, the murmur may disappear.

ECG changes in the form of signs of hypertrophy of the left ventricle, left atrium and

of the right ventricle are noted only with a significant amount of blood shunt and the formation of high pulmonary hypertension. In patients with a hemodynamically significant defect,

radiography reveals an expansion of the heart shadow due to the left chambers and pulmonary trunk, signs hypervolemia of the pulmonary circulation. In high pulmonary hypertension, there is

expansion of the right chambers of the heart. Visualization of the patent ductus arteriosus is possible using two-dimensional echocardiography. Color Doppler echocardiography detects abnormal shunting and calculates systolic pressure gradient

between the aorta and the pulmonary trunk.

Identification of an open ductus arteriosus in an adult patient is an indication to close it. Ducts of small and medium diameter are closed with a special

occluder by catheter surgery. In cases where the diameter of the duct exceeds 8 - 10 mm, a major surgical intervention is applied.

Coarctation of the aorta

Narrowing of the aorta that obstructs blood flow is usually localized at the junction of the ductus arteriosus with the descending aorta below the origin of the left subclavian

arteries. The prevalence of coarctation of the aorta among other congenital heart defects in adults is about 5%. In men, this defect is diagnosed 2-3 times more often than

among women. Often coarctation of the aorta is combined with other congenital heart defects: ductus arteriosus, bicuspid aortic valve, ventricular septal defect.

In the part of the aorta above the site of obstruction, there is an increase in pressure. It causes dilatation of the proximal part of the aorta, hypertrophy of the walls, and then the expansion of

the cavity of the left ventricle. With a significant narrowing, despite the compensatory

development of collaterals, there is a deterioration in the nutrition of organs located in the blood supply pool. abdominal aorta. The main clinical manifestation of aortic coarctation is an increase in blood

pressure in the brachial arteries with normal or reduced blood pressure and a weakening of the pulsation in the arteries of the lower extremities. A characteristic auscultatory sign of coarctation of the aorta - systolic murmur, which is localized in the left subclavian region and interscapular

space to the left of the spine. In addition, the strengthening of the II tone above the aorta is determined. Electrocardiographic examination reveals signs of hypertrophy

left ventricle. X-ray examination reveals expansion of the ascending aorta

and large arteries extending from it, as well as the usuration of the ribs, which occurs due to the development of collaterals. Two-dimensional echocardiography makes it possible to visualize the narrowing of the aorta, to determine its degree and extent. With the help of color Doppler echocardiography, the severity of the intra-aortic pressure gradient can be assessed. To identify coarctation of the aorta, computed tomography and magnetic resonance imaging are used. Angiography is usually performed immediately before surgery.

property.

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Patients with clinical symptoms of the defect are shown surgical treatment. In most cases, resection and plasty of the narrowing of the aorta are performed. In children, balloon dilatation is often used to relieve narrowing of the aorta.

1.8.2. Acquired heart defects

mitral stenosis

Definition. Mitral stenosis is a narrowing of the left atrioventricular orifice, which makes it difficult to empty the left atrium, resulting in an increase in the degree of

diastolic pressure between the left atrium and left ventricle.

Prevalence. Mitral stenosis is the most common heart defect.

Cases of isolated mitral stenosis account for about 25% of all valve defects.

hearts. Combined mitral valve disease is diagnosed in 40% of patients with heart defects. vice. In women, mitral stenosis is detected 3 times more often than in men.

Etiology. The most common cause of mitral stenosis is rheumatic endocarditis. In rare cases, narrowing of the left AV foramen occurs due to infective endocarditis and atherosclerosis. Congenital mitral stenosis occurs exclusively

very rare and usually associated with other cardiac anomalies.

Pathogenesis. The normal area of the mitral orifice is 4-6 cm2 . The movement of blood through the left AV foramen is normally provided by a pressure gradient of 5 mm rt. Art. Hemodynamically significant is the narrowing of the mitral orifice to a value

less than 2 cm2 . In these cases, higher than normal pressure in the left atrium is required to move blood into the left ventricle. Increased pressure in the left atrium

causes an increase in pressure in the pulmonary veins and capillaries, i.e., the development of the so-called passive pulmonary hypertension. At the initial stage, an

increase in the transmitral pressure gradient is recorded only during exercise, i.e., under conditions whe passing through the mitral opening increases. With further narrowing of the mitral orifice,

the increase in pressure in the left atrium becomes constant, which entails

followed by its gradual hypertrophy and dilatation, stabilization of pulmonary hypertension. The rise in pressure in the pulmonary capillaries to the level of plasma oncotic pressure creates conditions for extravasation of fluid from blood vessels into lung tissue and alveoli. The

development of pulmonary edema is hindered by increased lymph flow and reflex constriction of the lun arterioles. However, arteriolar vasoconstriction causes an increase in pressure in the

pulmonary artery, i.e., the formation of the so-called active pulmonary hypertension, the

stabilization of which is facilitated by morphological changes in the walls of the pulmonary arterioles (pr smooth muscle, media thickening, fibrosis). As a result, there is an increase

pressure in the right ventricle. An increase in the load on the right ventricle causes its hypertrophy. A significant increase in pressure in the right ventricle and a decrease in its elasticity obstruct the emptying of the right atrium. With the exhaustion of the compensatory

resources of the right ventricle, it dilates, the pressure in the pulmonary artery decreases,

but the load on the right atrium increases and stagnation develops in the systemic circulation. Morphology. There are three morphological variants of mitral stenosis: commissural,

valvular, and chordal.

The commissural variant is characterized by fusion of the mitral valve leaflets along edges with the formation in most cases of isolated mitral stenosis. At

valvular variant develops fibrosis (sometimes with calcification) of the valve leaflets and

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the combined defect of the mitral valve is usually formed. Chordal is called

a variant of mitral defect, in which changes in the valves are combined with sclerosis and shortening of the chords. Altered chords draw into the cavity of the left ventricle deformed and fused along the edges of the mitral valve cusps, as a result of which an inactive funnel-like formation is formed, which does not provide a full-fledged

opening or complete closure of the left AV foramen.

Classification. In Russia, the most widespread classification of mitral stenosis, proposed by A. N. Bakulev and E. A. Damir (1955). In this classification, the stages of development of the defect are determined on the basis of clinical symptoms,

spare the mitral orifice and the size of the left atrium.

Stage I - complete compensation of blood circulation. There are no symptoms of HF, but objective examination reveals signs of mitral stenosis. The area of the mitral orifice is 3–4 cm2 .

The size of the left atrium is no more than 4 cm.

Stage II - moderate heart failure. Symptoms of HF occur only during exercise.

The area of the mitral orifice is about 2 cm2 . The size of the left atrium is from 4 to 5 cm.

Stage III - the initial stage of severe heart failure. There are symptoms of stagnation in small and a large circles of blood circulation, an increase in the size of the heart. The area of the mitral

orifice is 1–1.5 cm2 . The size of the left atrium is 5 cm or more.

Stage IV - the stage of pronounced CH. Significant stagnation in the systemic circulation: peripheral edema, liver enlargement, ascites is possible. Heart significantly

enlarged in size. The area of the mitral orifice is less than 1 cm2 . The size of the left atrium exceeds 5 cm.

Stage V is the terminal stage of heart failure. Severe peripheral edema, hepatomegaly,

ascites, persistent dyspnea, cardiomegaly. The area of the mitral orifice is less than 1 cm2 . The size of the left atrium is more than 5 cm.

clinical picture. The earliest symptom and main complaint of patients

mitral stenosis is shortness of breath. With moderately severe stenosis, shortness of breath occurs only during physical exertion. As the degree of mitral valve narrowing increases

holes, the level of load at which shortness of breath occurs decreases, then it begins

disturb the patient at rest, becomes constant, aggravated in the supine position. Patients with severe mitral stenosis occasionally experience attacks of cardiac asthma,

pulmonary edema. The second sign of mitral stenosis is palpitations. Raise

Heart rate, as well as shortness of breath, is a mechanism for compensating for violations of the systemic hemodynamics due to a decrease in the stroke volume of the left ventricle. In most patients,

palpitations occur during physical exertion. Patients with severe heart failure or patients in whom mitral stenosis has become complicated experience persistent palpitations

permanent form of AF. A common symptom of mitral stenosis is cough due to congestive bronchitis. Sometimes, with severe stagnation in the pulmonary circulation, hemoptysis occurs due to rupture of pulmonary capillaries and arterioles in patients with mitral stenosis. Thromboembolism occurs in 15-20% of patients with mitral stenosis

into the systemic circulation. This complication is associated with an increased likelihood of thrombus formation in the cavity of the dilated left atrium. In most cases, thromboembolism occurs against the background of AF.

The classic external sign of mitral stenosis is facies mitralis - a youthful face with a peculiar blush on the cheeks. In the stage of complete compensation of blood circulation, the boundaries of relative cardiac dullness do not change significantly, however, even at

At this stage, diastolic trembling is detected in many patients with palpation of the heart. ("cat'spurr") due to difficult, turbulent blood flow through the narrowed

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