home Audience 1 Liver cirrhosis as a consequence of heart failure. Cirrhosis. Causes, symptoms, methods of diagnosis and effective treatment of the disease

Liver cirrhosis as a consequence of heart failure. Cirrhosis. Causes, symptoms, methods of diagnosis and effective treatment of the disease

In case of heart failure, not only the patient’s heart suffers, but also other organs, since they are closely interconnected in the functioning of the body. With increasing pressure in big circle blood circulation, the right parts of the heart muscle are overloaded. As a result, the liver is affected: painful sensations occur and an increase in size is observed. Congestive liver in heart failure is quite rare, but if such symptoms appear, the patient needs treatment.

Congestive liver is a pathological condition characterized by stretching of the organ due to stagnation of blood under the influence of high pressure in the veins.

One of secondary causes liver congestion is a cardiac sign. This means that the primary factor in the development of pathology was not a disease of the organ itself, but a dysfunction in the work of the heart. late stages chronic heart failure is observed in cardiac cirrhosis of the liver.

Insufficiency means the inability of the heart to disperse blood through the vessels at the required speed. This leads to its accumulation in the organs, pressure rises, liver edema occurs. Stagnant blood reduces tissue oxygen saturation, and oxygen starvation. This inevitably leads to necrosis of liver cells, causing ischemia. Dead hepatocytes are replaced by fibrous tissue cells, cirrhosis gradually develops.

Factors that provoke congestion in the liver include:

The primary manifestations of a decompensated state of the heart are shortness of breath and arrhythmia during physical exertion. Gradually, shortness of breath occurs at rest, tachycardia accompanies the patient everywhere. With insufficiency of the left ventricle, there is an accumulation of blood in the pulmonary circle.

The following manifestations are characteristic:

wheezing in the lungs;
sputum interspersed with blood;
blue tint of lips, fingers.

A cirrhotic liver is a manifestation of a disease on the right side of the heart. If a decrease in the performance of the right ventricle is not a primary phenomenon, blood stagnation secondarily accompanies the pathology of the left side of the heart muscle.

When opened, the internal organ is heavy and dense in composition. The color depends on the duration of stagnation, it varies from red to purple or bluish-brown. Sometimes yellowish spots are observed at the edges of the lobules due to fatty degeneration of the liver cells. In the center of the lobule, the vein cavity has a bluish-red color. This type of liver is called “nutmeg” liver. With a long stagnant process, drawing liver lobules erased. Fibrous tissue formed at the site of dead hepatocytes forms “false lobulation.” When stagnation suddenly occurs, many hemorrhages are recorded.

Anatomical changes and dysfunction of the liver appear when exposed to increased venous pressure and lack of oxygen at the same time.

Often, people with heart failure experience symptoms congestive liver predetermined. This disease inevitably occurs when cardiac muscle dysfunction is diagnosed in the later stages.

Signs of congestion with a weak heart are the same for all types of cirrhosis:

Increase in size (In the first stages, the organ grows in front and behind, is not palpable. With the progression of heart pathology, an enlargement of the liver is visible, it is determined at the bottom of the right rib. Pain is caused by stretching of the liver capsule).
Intense pain under the right rib with heaviness and pressure.
Swelling of the limbs.
Increase in body temperature.
Nausea, vomiting, loss of appetite.
Lethargy, weight loss, fatigue.
Aggressiveness, Bad mood, sleep problems.
Increase in abdominal size.
Symptoms of jaundice.

These manifestations are a reflection of an abnormal process occurring in the liver itself. The patient may simultaneously experience pain associated with impaired functioning of the heart.

The cardiac cause of congestion is indicated by symptoms that occur with failure of the right ventricle of the heart: swelling of the arms and legs, shortness of breath at rest or during exercise.

In cardiac cirrhosis, ascites usually occurs, which is not treatable with drugs.

A stagnant internal organ is always an unfavorable phenomenon. Cirrhosis causes activation of the pathological chain and leads to further complications.

When a patient first contacts a doctor, a general examination is carried out and the patient’s complaints are clarified. Disease for a long time may be asymptomatic due to the high compensation of liver cells.

Doctors distinguish cardiac cirrhosis from other types of liver damage by the following symptoms:

At the beginning, the enlarged liver has a soft density. Then it hardens and decreases in volume.
Treatment of the heart, which is the main cause of congestive processes, leads to an improvement in the patient’s condition.
When you press on the liver, the veins in the neck swell.

To detect blood stagnation, comprehensive examination, including the following methods:

Blood biochemistry (total protein, enzymes, bilirubin, alkaline phosphatase).
Analysis of the structure and volume of the liver using ultrasound.
Hemostasiogram (blood test for clotting).
X-ray chest(examination of the lungs, determination of the size of the heart).
Electrocardiography, echocardiography (analysis of heart function).
Laparocentesis (sampling of fluid from abdominal cavity).
Study of the coronary vessels of the heart using angiography.
Liver puncture biopsy (for heart muscle transplantation).

To make a correct diagnosis, the presence of hepatitis, inflammation, the presence of toxic elements in the blood (from alcohol, hazardous industries) and other types of pathology should be excluded.

Advanced conditions with congestion in the liver are almost always asymptomatic. They are discovered only during clinical studies in laboratory conditions.

The only method of preventing congestive cirrhosis is a timely visit to a cardiologist. Success therapeutic methods depends entirely on the correct recognition of the main disease - cardiac dysfunction. Doctors are not able to completely cure a sick person, but they can prolong life and alleviate the condition.

The life expectancy of patients suffering from cardiac cirrhosis is 3-7 years. Usually leads to death internal bleeding or the onset of hepatic coma.

A moderate rhythm of life, reduced physical activity and an individually selected course are indicated. physical activity. Limited use table salt and liquids. It is useful to follow a diet, balanced diet. Products that burden the liver are strictly prohibited: spices, smoked meats, alcohol, fried and fatty foods.

With low efficiency general events medications are prescribed:

Cardiac glycosides (digoxin) for the treatment and normal functioning of the heart muscle.
Beta blockers (metoprolol) to normalize blood pressure and heart rhythms.

Liver damage in acute left ventricular and chronic heart failure is observed in all patients. The development of passive venous stagnation, hypoxemic necrosis, liver fibrosis and, in rare cases, cardiac cirrhosis is possible.

The basis of liver damage in isolated left ventricular failure in patients with myocardial infarction complicated by cardiogenic shock is a decrease in cardiac output. The development of central hepatic necrosis is especially promoted by insufficient blood supply to the liver due to a sharp decrease in systemic blood pressure. This situation occurs with bleeding, postoperative complications, heatstroke, severe burns and septic shock. Therefore, a significant correlation is found between the frequency of detection of liver necrosis at autopsy and the presence of severe hypotension in the terminal period, renal failure, acute necrosis of the renal tubules and adrenal cortex at the border with the medulla, characteristic of shock. Acute heart rhythm disturbances (ventricular paroxysmal tachycardia, atrial fibrillation or fibrillation, etc.) can lead to acute heart failure and acute congestive liver with pain in the right hypochondrium, hyperaminotransferasemia and sometimes jaundice. Most often, congestive liver develops with weakness of the right ventricle of the heart.

Hypodiastole, caused by insufficient expansion of the heart cavities during diastole, is associated with hemodynamic disturbances and venous stasis in the systemic circulation with compressive (constrictive) pericarditis. A similar mechanism of circulatory failure, but with a predominance of changes in the left ventricle of the heart, underlies other “constrictive” cardiopathy that occurs without damage to the pericardium: myocardiosclerosis of various etiologies, primary amyloidosis, hemochromatosis with heart damage, Loeffler’s parietal endocarditis and alcoholic cardiomyopathy, which can be combined with alcoholic cirrhosis liver.

The special vulnerability of the liver in case of right heart failure is explained by the fact that the liver is the reservoir closest to the heart, capable of depositing a large amount of blood and thereby significantly facilitating the work of the right ventricle of the heart. In heart failure, the blood deposited in the liver can account for up to 70% of the organ's mass (normally about 35%). Increased pressure in the right atrium directly spreads to the inferior vena cava, subhepatic veins, sinusoids and system portal vein, leading to a relative decrease in arterial blood supply to the liver in proportion to the decrease in cardiac output, hypoxia and ischemic necrosis of hepatocytes. Portal hypertension with congestive heart failure has its own characteristics. The gradient of the wedged subhepatic and free portal pressure is not increased (the pressure in the portal vein and in both vena cava is the same), therefore the portacaval collateral circulation and varicose veins There are no esophageal veins.

With rapidly developing venous stagnation, enlargement and hardening of the liver is accompanied by stretching of the Glissonian capsule with sharp pain in the right hypochondrium and severe pain and protective muscle tension during palpation, simulating acute surgical disease. Slight jaundice often develops, initially due to hypoxemic hemolysis in the liver (unconjugated hyperbilirubinemia, urobilinuria). Later, with the development of hypoxemic central lobular atrophic changes in hepatocytes and necrosis, hepatocellular jaundice occurs with an increase in the level of direct blood bilirubin, aminotransferase activity and often blood alkaline phosphatase. Massive necrosis of the liver parenchyma with acute venous congestion can cause the development of a picture of fulminant hepatitis with intense jaundice, high ALT activity and hepatic encephalopathy.

In typical cases, the liver in chronic right-sided heart failure is enlarged, hardened and painful. Its surface is smooth. Patients are often bothered by a feeling of heaviness or prolonged dull pain in the right hypochondrium and epigastric region. In patients with chronic pulmonary heart disease and constrictive pericarditis, cyanosis and shortness of breath occur without orthopnea and significant stagnation in the pulmonary circulation.

With tricuspid valve insufficiency, characteristic systolic pulsation of an enlarged liver, orthopnea and painful swelling of the legs are observed. The spleen is enlarged in 40% of patients, and hydrothorax and ascites may develop. Biochemical changes often amount to moderate hyperbilirubinemia and hypoalbuminemia, hyperaminotransferasemia. At advanced stages, hypoproteinemia and hypoprothrombinemia are observed. The size of the liver often quickly decreases under the influence of rest, salt-free regimen, diuretic and cardiotonic therapy. With congestive hepatomegaly, there are no skin telangiectasia, palmar erythema, or signs of collateral circulation. Edema-ascitic syndrome is combined with shortness of breath and cyanosis; a high protein content in ascitic fluid is characteristic (30-40 g/l). An echographic examination reveals hepatomegaly, expansion of the inferior vena cava and the absence of fluctuations in its diameter during respiratory movements.

Adhesive pericarditis often develops without connection with known etiological factors - tuberculosis, pyogenic infection, rheumatism or heart injuries, i.e. can be idiopathic. This is characterized by a combination of early massive and resistant to diuretic therapy ascites with a large dense, painless, non-pulsatile liver (“Pick’s pseudocirrhosis” due to fibrous perihepatitis) with radiological symptoms of pericardial calcification and pleuropericardial adhesions with normal or mildly enlarged heart sizes. An X-ray examination of the chest organs is mandatory for any form of liver pathology.

In liver punctures in chronic heart failure (liver puncture is indicated for this pathology), signs of chronic venous congestion are most often found: dilation and overflow of blood in the sublobular veins, central veins and adjacent sinusoids, expansion of the spaces of Disse, which are located between the sinusoids and hepatocytes and function such as lymphatic vessels, hepatocyte atrophy and centrilobular necrosis, often in combination with fatty degeneration. During laparoscopy, the liver is enlarged, the edge is rounded, the capsule is thickened, the surface of the liver has a characteristic “nutmeg” appearance with the presence of dark red and brown-yellow areas ( nutmeg liver). With constrictive pericarditis, extensive grayish-white shiny deposits of fibrin, sclerosis and thickening of the capsules of the liver and spleen are visible on the surface of the liver.

Cardiac cirrhosis of the liver, like liver cirrhosis of other etiologies, is accompanied by dysproteinemia with a predominant decrease in the level of total protein and blood albumin and an increase in the level of γ-globulins and α2-globulins.

Sometimes clinical symptoms liver damage in patients with acute or chronic circulatory failure - heaviness or pain in the epigastric region, flatulence, nausea, bitter taste in the mouth, hepatomegaly and jaundice - come to the fore and neutralize the underlying heart disease. In such cases, doctors make diagnostic errors, assuming independent liver disease.

In the presence of heart failure in patients with hepatomegaly, it is necessary to take into account the possibility of development of chronic heart damage with hyperkinetic syndrome in liver cirrhosis, which can clinically manifest itself as cyanosis, severe shortness of breath at rest and during exercise, tachycardia, high pulse pressure, expansion of the right ventricle of the heart due to significant arteriovenous shunting of blood in the lungs.

Damage to the liver and heart with hyperdynamic or hypodynamic heart failure is also possible with idiopathic hemochromatosis, amyloidosis, sarcoidosis and chronic alcoholism. In rare cases, with cirrhosis of the liver or with long-term therapy of CAH with immunosuppressants, subacute development of infective endocarditis, which requires differential diagnosis with chronic active liver disease, as it occurs with hepatosplenomegaly, hyperproteinemia, hypergamma-globulinemia, positive protein sediment tests, moderate hyperenzymeemia (aminotransferases, alkaline phosphatase) and sometimes with hyperbilirubinemia due to concomitant reactive hepatitis. Hyper-a 2 -globulinemia, severe increase in ESR, auscultatory phenomena indicating damage to the heart valves, vasculitis, thrombosis or embolism internal organs, kidney damage and positive results repeated bacteriological blood tests.

Pathogenetic treatment of heart diseases, cardiovascular and pulmonary insufficiency, which usually leads to regression of the clinical and biochemical manifestations of cardiac cirrhosis of the liver.

Additionally, hepatoprotectors and antioxidant vitamins are prescribed: legalon, simepar, essentiale N, livolin, namacite, alvitil, gensamine, formaton, triovit, multitabs with ß-carotene in usual dosages for 1-2 months. In the presence of chronic cardiac cirrhosis of the liver, the administration of hepabene in the doses described above is indicated. Surgical treatment is performed according to indications.

A rare disease is calcium deposition in the Glissonian capsule of the liver and pericardium during pericarditis of tuberculous etiology, classified according to old terminology as “shell heart”, in which Pick’s pseudocirrhosis develops. Moreover, in some cases, the functional state of the liver improved after surgical removal parts of the calcified pericardium. As a result of the operation, the symptoms of chronic vascular insufficiency and as a consequence of the manifestation of “stagnant” nutmeg liver.

... the special vulnerability of the liver in case of right heart failure is explained by the fact that the liver is the reservoir closest to the heart, capable of depositing a large amount of blood and thereby significantly facilitating the work of the right ventricle of the heart.

Liver enlargement is a central link in the development of right heart failure. This especially applies to diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, cor pulmonale, as well as other diseases of the heart, pleura, lungs, diaphragm, leading to weakness of right ventricular systole.

CONGESTIVE LIVER

The most common picture of liver congestion is observed. As a result of various heart lesions, congestion occurs in the right atrium, pressure in the hepatic veins increases and dilatation of the central veins occurs. The slowdown in blood circulation increases the blood overflow of the central veins, the central part of the lobules, and central portal hypertension develops, which is predominantly of mechanical origin, then hypoxia occurs. Using catheterization of the liver veins in patients with circulatory failure, it was shown that they contain less oxygen than under normal conditions.

Persistently increased pressure in the hepatic veins causes centrilobular necrosis of liver cells, which occurs in all forms of heart disease, but especially in tricuspid valve insufficiency, mitral stenosis and adhesive pericarditis.

Along with the expansion of capillaries and centrilobular necrosis, the proliferation of connective tissue begins. At the periphery of the lobules, where the blood supply is worse, obesity of liver cells occurs. If venous congestion is eliminated, centrilobular cells are regenerated and the liver restores its original structure. True, a number of authors have noted that reducing venous pressure does not always eliminate venous congestion, and the same applies to the histological picture of the liver.

Congestion is clinically expressed in enlarged liver, its lower edge reaches the navel, hard, smooth and sensitive to palpation. The sensitivity of an enlarged liver is an early sign of stagnation, which precedes edema. Sometimes it moves and pulsates, so that the hepatic pulse can be observed. Ripple occurs during ventricular systole, and hepatic-jagular reflux is important. These dynamic phenomena are observed more often with tricuspid valve insufficiency.

Patients may complain for spontaneous pain in the right half of the abdomen, similar in intensity to those that occur during early stage infectious hepatitis. Obviously, they are associated with tension in the nerve endings of the liver capsule. There is often a feeling of heaviness, tension and fullness that occurs during eating and persists long after it. Appetite worsens, nausea and vomiting appear, and poor health occurs. Dyspeptic symptoms are also associated with congestion in the gastrointestinal tract.

With congestive liver, ascites may develop, the origin of which is: increased pressure in the veins of the liver, decreased serum albumin and sodium retention. Patients who develop ascites are more likely to have particularly high venous pressure, low cardiac output in combination with severe centrilobular cell damage.

Liver function tests usually change. The bilirubin content increases slightly and the level of albumin in the blood serum decreases. The most pronounced changes are observed when using functional tests, reflecting the actual functions of the liver (bromsulfalein test, radioisotope study). True, the clinical symptoms of congestive liver are masked by other signs of circulatory disorders.

Comparison morphological studies And functional state liver in patients with cardiac decompensation and congestive liver shows that changes in functional tests are combined with centrilobular necrosis and atrophy of liver cells. These changes can also be considered as indicators of liver cirrhosis, which is important to note, since often in practice the appearance of changes in functional tests is mistakenly identified with liver cirrhosis.

Congestive liver does not require special treatment. The use of leeches on the liver area during cardiac therapy promotes the effect of diuretics. A salt-free, high-calorie diet with sufficient amounts of protein and vitamins is also indicated.

CARDIAC CIRRHOSIS

Fibrous changes in the liver they occur secondarily as a result of anoxia, centrilobular necrosis and reparative processes. this central fibrosis can further lead to centrilobular cirrhosis. Sustained and frequently repeated increases in pressure in the veins lead to gradual condensation and collapse reticular tissue with proliferation of connective tissue. With continued damage to the heart, threads of connective tissue extend to the central veins of adjacent fields, connecting them to each other and causing the formation of false lobules.

!!! We can talk about cardiac cirrhosis of the liver in those cases when there are changes in the architectonics, that is, three main conditions are observed: (1) destruction of parenchymal cells; (2) regeneration processes; (3) proliferation of connective tissue.

The relative rarity of these changes, and therefore the development of true cirrhosis, depends on the fact that with cardiac decompensation, not true, but permanent liver damage occurs. Most patients die before development connective tissue proliferation and regenerative phase. It is also important that in the final stage of decompensation, stagnant and degenerative processes in the liver are constant, and that there are no periods of remission when conditions for nodular regeneration appear. True cirrhosis of the liver accounts for 0.4% of all autopsies.

Cardiac cirrhosis of the liver has the following pathological picture. The walls of the dilated central veins are sclerotic and thickened. The number of capillaries and anastomoses between the hepatic and portal veins increases. As a result of the proliferation of connective tissue, the central vein is difficult to recognize. Biliary tract proliferate and islands of regeneration appear. The most characteristic of cardiac cirrhosis is a pronounced degree of fibrosis in the central zones and compression of the portal vein by overgrown connective tissue. Obviously, this is why the term cardiac fibrosis arose, which many authors recommend calling this liver damage.

Despite some features morphological development cardiac cirrhosis, its clinical symptoms are largely identical to portal cirrhosis. When examining a patient, a slight yellowness of the skin is often noted. The combination of jaundice with existing cyanosis gives the skin a peculiar appearance.

The liver in these cases is not very large, but hard, with a sharp edge and finely nodular surface; sometimes the spleen is enlarged. Liver pulsation disappears, ascites develops. It is especially difficult to decide whether ascites is caused by cardiovascular failure or liver damage. The development of ascites after a long period of edema, the ensuing reduction and hardening of the liver, enlargement of the spleen and hypoalbuminemia give grounds for the diagnosis of cardiac cirrhosis. In these cases, ascites, like other signs of cirrhosis, persist even after successful treatment cardiovascular failure (edema disappears, etc.).

Patients with cardiac cirrhosis of the liver often have poor tolerance to medications, especially increased sensitivity to digitalis and strophanthin, apparently with a violation of the neutralizing function of the liver.

The basis for the diagnosis of cardiac cirrhosis is the presence of prolonged decompensation in diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, cor pulmonale. Functional study liver reveals severe violations of its function. Thus, along with hypoalbuminemia, the level of gammaglobulins and bilirubin may increase, sediment reactions become positive, and sometimes the Kwik-Pytel test indicators decrease. At radioisotope study liver function, its pronounced violations are observed.

The presence of cardiac cirrhosis in itself does not significantly worsen the prognosis and, if cardiac damage is treated, cirrhosis can proceed latently, without a tendency to periodic exacerbations of the process.

CARDIAC JAUNDICE

Despite the fact that overt jaundice in patients with symptoms of liver congestion and cardiac cirrhosis is rare, the concentration of bilirubin in the serum increases relatively often. Jaundice occurs with equal frequency both with congestion in the liver and with cardiac cirrhosis. Many authors have obtained a statistical correlation between the intensity of jaundice and venous pressure in the right heart. In addition, pulmonary infarction plays a role in the development of jaundice. Thus, out of 424 autopsies of those who died from heart disease, 4% had jaundice, of which 10.5% of cases had a heart attack (Kugel, Lichtmann).

The yellowness of the skin and sclera in cardiac cirrhosis is slight, pruritus absent. The uneven coloring of the skin is noteworthy. Thus, in places of massive edema, the skin is not yellow due to the fact that bilirubin circulating in the blood is bound to protein and does not enter the edematous fluid. In a small number of patients, jaundice acquires the features of mechanical jaundice: intense, with a grayish tint, coloring of the skin, pigments in the urine and light-colored feces are noted.

The mechanism of jaundice in circulatory disorders is different.

(1 ) Hepatic jaundice. There is an assumption that when the heart is damaged, liver cells inadequately excrete all pigments and, indeed, the most intense jaundice is observed in patients with severe and widespread necrosis of liver cells. However, there are exceptions to this rule, when in case of tricuspid valve insufficiency with severe liver damage, jaundice is not observed.

(2 ) Obstructive jaundice. Compression of the bile capillaries due to a sharp increase in venous pressure inside the lobules, as well as the formation of blood clots in the bile canaliculi, as a consequence of the slow flow of bile in the biliary system, create conditions for cholestasis.

(3 ) Hemolytic jaundice often combined with tissue hemorrhages, especially pulmonary infarctions. The sudden appearance of jaundice in the clinical picture of a heart attack is known: be it of the lung, spleen or kidneys, while heart attacks of the same location, but without damage to the heart, do not produce jaundice.

An additional hemoglobin depot is created at the site of the infarction, from which bilirubin is formed. This excess pigment cannot be bound by the altered liver cells. Rich and Resnik injected into the tissue of patients with heart disease an amount of blood corresponding to that found in pulmonary infarction, and noted an increase in serum bilirubin. There is also an excess of pigment in the tissues during congestion in the lungs due to heart damage, since even without a heart attack, congestion in the lungs leads to the destruction of hemoglobin.

Consequently, jaundice with heart lesions in most cases mixed type; highest value have damage to liver cells and overload them with pigment as a result of heart attacks, which is confirmed by laboratory data. The urine is dark with an increased amount of urobilin; with intense jaundice, other bile pigments are also detected; dark stool with an increased amount of stercobilin, in some cases gray with a decrease in pigment release. An increased amount of bilirubin is detected in the blood, often with a direct van den Berg reaction.

Treatment is aimed mainly at the prevention and treatment of the underlying disease. In addition, the presence of liver damage requires a diet - table No. 5, a complex of vitamins, if necessary, choleretic drugs, and corticosteroids according to strict indications.

Heart failure (HF) is in most cases associated with dysfunction of the heart muscle. With heart failure, the level of supply of the body with metabolic needs decreases.

Heart failure can be divided into:

Systolic;
Diastolic.

Systolic heart failure is characterized by impaired contractility of the heart. And diastolic is characterized by a failure of the relaxation ability of the heart muscle and an imbalance in the filling of the ventricles.

Organic disorders;
Functional disorders;
Birth defects;
Acquired diseases, etc.

Symptoms of HF

Physically, HF manifests itself in a decrease in work capacity and exercise tolerance. This is demonstrated by the appearance of shortness of breath in heart failure and rapid fatigue. All these symptoms are associated with a quantitative decrease in cardiac output or fluid retention in the body.

As a rule, right ventricular heart failure is characterized by a whole list of liver disorders. Severe congestion in the liver is almost always asymptomatic and is detected only during laboratory and clinical studies. The main pathologies of the development of liver dysfunction include:

Passive venous stasis (due to increased pressure due to filling);
Impaired blood circulation and decreased cardiac output.

Complications of heart failure

With an increase in CVP (central venous pressure), as a result, the level of liver enzymes and direct and indirect serum bilirubin may increase.

Deterioration in perfusion resulting from a sharp decrease in cardiac output can result in hepatocellular necrosis with elevated serum aminotransferase levels. “Shock liver” or cardiogenic ischemic hepatitis is the result of pronounced hypotension in patients suffering from heart failure.

Cardiac cirrhosis or fibrosis can result from long-term hemodynamic dysfunction, which is fraught functional disorder liver, accompanied by coagulation problems, as well as deterioration in the absorption of certain cardiovascular drugs and making them undesirably toxic, reducing albumin production.

Unfortunately, it is difficult to determine the exact dosage of these drugs.

If we consider this problem from the point of view of pathophysiology and histology, we will see that liver problems associated with venous stagnation are typical for patients with right-sided type of heart failure adjacent to high blood pressure in the right stomach. and it doesn’t matter what causes right-sided heart failure. Any case can be the starting point of hepatic stagnation.

Factors causing congestion in the liver

These reasons include:

Constrictive pericarditis;
Severe pulmonary hypertension;
Mitral valve stenosis;
Tricuspid valve insufficiency;
Pulmonary heart;
cardiomyopathy;
Consequences of the Fontan operation for pulmonary atresia and hypoplastic left heart syndrome;
Tricuspid regurgitation (in 100% of cases). It occurs due to right ventricular pressure on the veins and sinusoids of the liver.

With a close study of the structure of the congestive liver, its general increase is observed. The color of such a liver takes on a purple or reddish tint. At the same time, it is equipped with full-blooded hepatic veins. The section clearly shows areas of necrosis and hemorrhage in the 3rd zone and intact or occasionally steatotic areas in the 1st and 2nd zones.

Microscopic examination of hepatic venous hypertension shows us congested central veins with sinusoidal congestion and hemorrhages. Indifference and inaction in this matter leads to cardiac fibrosis and liver cirrhosis of the cardiac type.

Profound systemic hypotension in myocardial infarction, exacerbation of heart failure, and pulmonary embolism are often strong reasons for the development of acute ischemic hepatitis. Conditions such as: obstructive sleep apnea syndrome, respiratory failure, increased metabolic demand is a signal of ischemic hepatitis.

Hepatitis and HF

The use of the term "hepatitis" in this case is not entirely correct, since the inflammatory conditions that infectious hepatitis, we don't observe.

the development of chronic hypoxia in the liver is accompanied by specific protective processes. This process is characterized by an increase in the production of oxygen by liver cells from past (through the liver) flowing blood. But there are conditions under which this protective mechanism does not work. These are persistent inadequate perfusion of target organs, tissue hypoxia and acute hypoxia. In case of damage to hepatocytes, a sharp increase occurs: ALT, AST, LDH, prothrombin time in the blood serum. The onset of functional renal failure is also possible.

The temporary development of cardiogenic ischemic hepatitis varies from 1 day to 3 days. Normalization of the disease occurs from the fifth to the tenth day from the moment of the first episode of the disease.

Clinical manifestations in patients with left-sided HF are:

Shortness of breath;
Orthopnea;
Paroxysmal nocturnal dyspnea;
Cough;
Rapid onset of fatigue.

Right-sided heart failure is characterized by:

Peripheral edema;
Ascites;
Hepatomegaly;
Dull stretching pain in the upper right quadrant of the abdomen (rare).

Hepatomegaly is characteristic of right-sided chronic heart failure. But it happens that hepatomegaly also develops in acute heart failure.

Only 25% of the total number of patients is allocated for ascites. As for jaundice, it is mostly absent. There is presystolic pulsation of the liver

Ischemic hepatitis, in the majority of cases, proceeds benignly.

Diagnostics

Diagnosed inadvertently when an enzymatic increase is detected after systemic hypotension. But systemic hypotension does not only lead to elevated liver enzymes. Also, after such episodes, createnine increases, nausea, vomiting, and disturbances may appear. eating behavior, pain symptoms in the right upper abdominal quadrant, oliguria, jaundice, tremor, hepatic encephalopathy.

When heart failure develops, symptoms increase gradually, sometimes taking more than 10 years to develop the disease. For many, the disease is detected already when, due to the inability of the heart to provide adequate blood supply to organs, people develop various complications. But complications can be avoided if treatment for the disease is started in a timely manner. But how to recognize the first symptoms?

How does pathology develop?

Before answering the question: “How to recognize heart failure?”, it is worth considering the mechanism of development of the disease.

The pathogenesis of heart failure can be described as follows:

under the influence of unfavorable factors, the volume of cardiac output decreases;
to compensate for insufficient output, compensatory reactions of the body are activated (thickening of the myocardium occurs, increased heart rate);
for some time, compensation processes make it possible to ensure adequate blood supply to organs and tissues due to the work of the organ with increased load;
but the increased size of the myocardium requires a larger volume of blood to function properly, and coronary vessels can transport only the same volume of blood and cease to cope with providing the muscles with nutrients;
insufficient blood supply leads to ischemia of certain areas of the heart and myocardium due to lack of oxygen and nutrients contractile function decreases;
as the contractile function decreases, the cardiac output decreases again, the blood supply to the organs deteriorates, and signs of heart failure increase (the pathology becomes incurable, you can only slow down the progression of the disease).

Symptoms of heart failure may develop:

Slowly. Chronic heart failure (CHF) progresses over years and often occurs as a complication of heart or vascular disease. In most cases, timely identified at an early stage stages of CHF is reversible.
Fast. Acute heart failure occurs suddenly, all symptoms increase rapidly and compensatory mechanisms often do not have time to stabilize blood flow. If problems that arise are not eliminated in a timely manner acute disorders, they will end in death.

Having understood what heart failure is, we can consider how it manifests itself.

Symptoms of the disease

Manifestations of heart failure will depend on the degree of the compensatory mechanism and on which part of the heart is more impaired. There are types of heart failure:

left ventricular;
right ventricular;
mixed.

Left ventricular

It is characterized by stagnation in the pulmonary circulation and a decrease in the supply of oxygen to the blood. Chronic heart failure with damage to the left ventricle will manifest itself:

shortness of breath;
a constant feeling of fatigue, drowsiness and impaired concentration may occur;
sleep disturbance;
pale and bluish skin;
The cough is dry at first, but as the disease progresses, scanty sputum appears.

As the disease progresses, a person begins to suffocate while lying on his back; such patients prefer to sleep in a semi-sitting position, placing several pillows under their back.

If treatment for heart failure is not started in a timely manner, the person develops cardiac asthma, and in severe cases, pulmonary edema may occur.

Right ventricular

Symptoms of chronic heart failure with impaired functioning of the right ventricle will appear depending on the tissues or organs in which congestion occurs. But general symptoms will become:

feeling of chronic fatigue;
feeling of pulsation of the veins in the neck;
the appearance of swelling first in the legs, and then in the internal organs;
rapid pulse;
shortness of breath occurs first during physical activity and then at rest, but cardiac asthma or pulmonary edema rarely develops;
there are signs of general intoxication.

Compared with left ventricular, right ventricular cardiac failure progresses much faster. This is due to the fact that during its development most important organs suffer.

Mixed

It is characterized by dysfunction of both ventricles. Mixed type chronic heart failure syndrome occurs when dysfunction of one of the ventricles is accompanied by failure of the other. Almost always the mixed appearance is accompanied by atrial hypertrophy. In this case, the heart increases significantly in size and cannot fully perform its function of pumping blood.

The influence of age on the severity of symptoms

The age of the patient also influences the symptoms of the disease. By age groups there are:

newborns;
children of preschool and early school age;
teenagers;
young and middle age;
aged people.

Newborns

Heart failure in newborns occurs due to disruption of the intrauterine development of the heart or blood vessels. Newborns are always diagnosed with acute heart failure, which is characterized by a rapid increase in clinical symptoms.

In newborns, the pathology manifests itself:

severe shortness of breath;
increased heart rate;
cardiomegaly;
enlarged spleen and liver;
sluggish sucking or complete refusal to eat;
cyanosis of the skin.

Such children are immediately sent to the intensive care unit.

Children of preschool and primary school age

At this age, chronic heart failure often develops and its first signs will be decreased concentration and lethargy.

Such children try to move less, avoid active games and find it difficult to concentrate on completing a specific task. Schoolchildren's performance is falling dramatically.

Parents should remember that problems with school performance may be associated with heart disease. If treatment is not started in a timely manner, the symptoms will increase and there may be complications of heart failure, which will negatively affect child development.

Teenagers

Due to hormonal maturation, CHF in adolescents is difficult to diagnose without examination. This is due to the fact that hypersensitivity occurs in adolescents due to hormonal changes. nervous system, which means symptoms such as fatigue, palpitations or shortness of breath may be temporary and transient.

But it is dangerous to ignore the manifestation of symptoms in adolescents associated with breathing or the heart, because the consequences of heart failure can be serious, and complications will cause disruption of the functioning of vital organs.

If CHF is suspected, it is necessary to conduct a full examination of the teenager in order to promptly identify the pathology.

If a person does not have chronic diseases that give similar symptoms, for example, shortness of breath with asthma and COPD or swelling of the legs with varicose veins, then in the majority the symptoms are pronounced and suggest the presence of pathology.

Aged people

In older people, the body's defenses are weakened and the symptoms become more pronounced even with the onset of severe heart failure, which means it becomes much more difficult to treat. This is due to the fact that a person associates a gradual deterioration in well-being with the gradual efforts of the body, and not with the development of the disease.

How are manifestations of pathology classified?

Cardiologists classify chronic heart failure according to:

stages of development of the compensatory mechanism;
phases of contractile dysfunction.

Stages of compensation

On how much the body's defenses compensate pathological disorders in the work of the heart, the following degrees of cardiac pathology are distinguished:

Compensated or degree 1. It is quite difficult to diagnose the disease in this period, the first signs may not appear in any way or occur only after a significant physical activity. If changes in the myocardium are detected at the initial stage, then in most cases it is possible to cure heart failure by eliminating the provoking factor and conducting a course of maintenance therapy. But at the first degree, the disease is detected only by chance, during a routine medical examination.
Decompensated. Moderate heart failure appears first, with dyspnea on exertion and feeling increased fatigue. Gradually, the symptoms increase, shortness of breath appears at rest, the skin becomes pale bluish, swelling of various localizations appears, a rapid pulse may be long time. What is the danger of untreated chronic heart failure? The fact that with the development of stagnation of blood circulation, irreversible ischemic disorders occur in the vital systems of the body. Heart failure in the decompensation stage cannot be completely cured; the treatment process is aimed at alleviating symptoms and slowing down the progression of pathological processes.
Terminal. Medicines at this stage are ineffective, the patient has experienced dystrophic changes in all vital important organs, and water-salt metabolism was disrupted. Such patients are in the hospital and the nursing process for chronic heart failure in terminal stage aimed at relief pain patient and providing comprehensive care.

Phases of violation

Depending on the phase in which the contractile dysfunction occurred, the following are distinguished:

systolic (the stomach wall contracts too quickly or too slowly);
diastolic (the ventricles cannot fully relax and the volume of blood flowing into the ventricular chamber decreases);
mixed (contractile function is completely impaired).

But what are the causes of chronic heart failure? Why is heart function disrupted?

Causes of chronic disease

The reasons why heart failure occurs may vary, but chronic heart failure is always a complication of another pathological process in organism.

CHF can become a complication:

cardiomyopathy;
cardiosclerosis;
chronic pulmonary heart disease;
hypertension;
anemia;
endocrine diseases (more often with dysfunction of the thyroid gland);
toxic infections;
oncological processes.

The etiology of the disease affects the choice of tactics, how to treat heart failure and the reversibility of the resulting process. In some cases, for example, with infections, it is enough to eliminate the provoking factor and full heart function can be restored.

Acute form of pathology

Acute heart failure occurs suddenly when the heart malfunctions and is a life-threatening condition.

The causes of acute heart failure are varied. It could be:

The diagnosis of acute heart failure is established quickly:

the pulse increases sharply, but the pulse wave becomes weak, sometimes it can only be detected in the cervical artery;
breathing becomes shallow and frequent;
the skin turns pale and acquires a bluish tint;
consciousness is confused or disappears.

The sooner treatment for acute heart failure is started, the more favorable the prognosis for the patient. If you suspect acute heart failure syndrome, you should immediately call an ambulance. While waiting for the medical team, the patient must be laid down with his head and back elevated, and care must be taken that the person can breathe freely.

No drugs should be given to the victim, but you can wet them cold water a napkin and place it on the sick person’s head.

Applying for medical assistance cannot be neglected; treatment of acute heart failure requires the help of a cardiologist. Even if it seems that the patient has become better, this does not mean that the victim’s myocardial function is restored to full function: when acute heart failure has developed, the symptoms may subside before death. This is due to the fact that the body’s defenses are completely depleted and will fail at a certain point.

Diagnostic measures

The main methods for diagnosing heart failure are:

initial examination of the patient (the pulse is checked, the skin is examined, the heart function is heard through a phonendoscope);
taking an ECG.

An ECG is the most reliable diagnostic method for clarifying pathological changes in the heart: the pulse and the main signs of ventricular dysfunction can be seen on the electrocardiogram. During an external examination and an ECG, the attending physician

The etiology of the disease is determined through additional examinations:

CT scan. Most exact method: how to determine the degree of circulatory disorders and tissue areas with impaired trophism.
Ultrasound and Dopplerography. This hardware examination allows you to identify the uniformity of the blood flow and how fully the blood supply to the organs occurs. Doppler ultrasound can check cardiac blood flow and determine the degree of myocardial ischemia.
Biochemistry of blood. Violation of the biochemical formula will indicate which organs have already suffered from impaired blood supply.

Diagnosis and treatment chronic failure, if it is first identified, it is carried out only in a hospital setting, where the attending physician individually selects medications and their dosage regimen. When heart failure has already been established, treatment can be carried out at home, taking medications prescribed by the doctor.

Features of the treatment process

But drugs to relieve symptoms and treatment brought relief, are not the most important thing in healing process. Of course, to prevent the symptoms characteristic of heart failure from further progressing, treatment with tablets and injections is necessary. But in order to reduce the risk of complications, the lifestyle with heart failure should exclude all provoking factors:

timely treatment acute and chronic diseases;
getting rid of bad habits;
compliance with the work and rest regime;
exclusion of harmful foods from the diet (smoked meats, canned food, pickles);
ensuring adequate physical activity (walking, dosed exercise).

To prevent heart failure from worsening, prevention by changing lifestyle and diet is no less important than the medications that must be taken to maintain proper myocardial function.

It is necessary to perceive cardiac failure as a serious pathological deviation of the myocardium and, at the first suspicion of its development, do an ECG. This procedure takes only a few minutes and will identify the disease at an early stage of development. And timely detected cardiac abnormalities can be easily cured.

Cardiac cirrhosis of the liver - the end of heart failure

Cirrhosis of the liver is chronic illness, in which there is a violation of the structure of the liver: the location of cellular elements, bile ducts, as well as dysfunction of hepatocytes - liver cells.

This condition often develops due to exposure to toxic substances (alcohol, toxins) or is a consequence of inflammation, usually caused by hepatitis viruses or autoimmune reaction. But there is also a special type of this condition - cardiac cirrhosis of the liver, which develops against the background of long-term heart failure.

The fact is that with a decrease in the pumping function of the heart (heart failure), blood stasis develops in all organs, and the liver, being an organ rich in blood vessels, suffers from this stagnation more than others.

Due to the increase in venous pressure, the liquid part of the blood, as it were, sweats into the liver tissue and squeezes it. This significantly disrupts the blood supply to the organ and the outflow of bile, and therefore its function. If this situation persists for a long time, then irreversible transformations in the structure of the liver develop - cardiac cirrhosis of the liver.

It is sometimes impossible to distinguish ordinary liver cirrhosis from cardiac cirrhosis based on complaints, examination, tests or ultrasound data. Most often, such patients are bothered by heaviness and pain in the right hypochondrium, yellowness of the skin and visible mucous membranes, itching of the skin due to the accumulation of bilirubin in it. Also, due to effusion into the abdominal cavity, “edema of the abdomen”—ascites—develops.

With severe stagnation, the outflow of blood through the liver is sharply complicated and the blood begins to look for workarounds, as a result of which the blood flow is redistributed in favor of the superficial veins, veins of the esophagus and intestines.

Vein expansion gastrointestinal tract is often complicated by bleeding, and the expansion of the abdominal veins with a simultaneous increase in its size gives it a special appearance - the “head of a jellyfish”.

When diagnosing, you most often have to rely on medical history: alcohol abuse, hazardous work, it is imperative to exclude chronic viral hepatitis, by testing the blood for antibodies to the virus.

Unfortunately, cardiac cirrhosis of the liver is an extremely unfavorable condition that aggravates the course of an already severe cardiac pathology. If it is still noted high level bilirubin, then damage to the central nervous system may occur, against the background of which patients lose criticism of their condition.

There is no effective treatment for liver cirrhosis, especially cardiac cirrhosis; all measures are aimed at the root cause of the disease and elimination of symptoms: combating edema syndrome, detoxification and slowing the progression of cirrhosis.

The prognosis, unfortunately, is unfavorable.

Acquired heart defects in children and adults

Classification
Mechanism of occurrence
Most frequent vices hearts
Diagnostics
Treatment

Acquired heart defects – persistent violations structures of the heart valves that appear as a result of disease or injury.

What is damaged by heart defects? Brief anatomical information

The human heart is four-chambered (two atria and ventricles, left and right). The aorta, the largest blood artery in the body, originates from the left ventricle; the pulmonary artery emerges from the right ventricle.

Between the various chambers of the heart, as well as at the initial sections of the vessels extending from it, there are valves - derivatives of the mucous membrane. Between the left chambers of the heart is the mitral (bicuspid) valve, and between the right chambers is the tricuspid (three-leaf) valve. At the exit to the aorta there is the aortic valve, at the beginning of the pulmonary artery there is the pulmonary valve.

The valves increase the efficiency of the heart - they prevent the backflow of blood during diastole (relaxation of the heart after its contraction). When the valves are damaged by a pathological process, the normal function of the heart is disrupted to one degree or another.

Classification of valve problems

There are several criteria for classifying heart defects. Below are some of them.

According to the causes of occurrence (etiological factor), defects are distinguished:

rheumatic (in patients rheumatoid arthritis and other diseases of this group, these pathologies cause almost all acquired heart defects in children and most of them in adults);
atherosclerotic (valve deformation due to the atherosclerotic process in adults);
syphilitic;
after endocarditis (inflammation of the inner lining of the heart, the derivatives of which are the valves).

According to the degree of hemodynamic disturbance (circulatory function) inside the heart:

with minor hemodynamic impairment;
with moderate impairments;
with severe impairments.

By disturbance of general hemodynamics (on the scale of the whole organism):

compensated;
subcompensated;
decompensated.

According to the location of the valvular lesion:

monovalve – with isolated damage to the mitral, tricuspid or aortic valve;
combined - a combination of damage to several valves (two or more), possible mitral-tricuspid, aortic-mitral, mitral-aortic, aortic-tricuspid defects;
three-valve - involving three structures at once - mitral-aortic-tricuspid and aortic-mitral-tricuspid.

According to the form of functional impairment:

simple – stenosis or insufficiency;
combined – stenosis and insufficiency on several valves at once;
combined – insufficiency and stenosis on one valve.

The mechanism of heart defects

Under the influence of a pathological process (caused by rheumatism, atherosclerosis, syphilitic lesions or trauma), the structure of the valves is disrupted.

If fusion of the leaflets or their pathological stiffness (rigidity) occurs, stenosis develops.

Cicatricial deformation of the valve leaflets, wrinkling or complete destruction causes their insufficiency.

As stenosis develops, resistance to blood flow increases due to mechanical obstruction. If the valve fails, some of the pushed-out blood flows back, forcing the corresponding chamber (the ventricle or atrium) to do extra work. This leads to compensatory hypertrophy (increase in volume and thickening of the muscle wall) of the heart chamber.

Gradually, in the hypertrophied part of the heart, dystrophic processes and metabolic disorders develop, leading to a decrease in performance and, ultimately, to heart failure.

The most common heart defects

mitral stenosis

Narrowing of the communication between the left chambers of the heart (atrioventricular orifice) is usually a consequence of a rheumatic process or infective endocarditis, causing fusion and hardening of the valve leaflets.

The defect may not manifest itself for a long time (remain in the compensation stage) due to proliferation muscle mass(hypertrophy) of the left atrium. When decompensation develops, blood stagnates in the pulmonary circulation - the lungs, the blood from which is obstructed when entering the left atrium.

Symptoms

When a disease occurs in childhood the child may be delayed in physical and mental development. Characteristic of this defect is a “butterfly” blush with a bluish tint. An enlarged left atrium compresses the left subclavian artery, therefore, a pulse difference appears on the right and left hands (less filling on the left).

Mitral regurgitation

In case of mitral valve insufficiency, it is not able to completely block the communication of the left ventricle with the atrium during heart contraction (systole). Some of the blood returns back to the left atrium.

Given the large compensatory capabilities of the left ventricle, external signs of failure begin to appear only with the development of decompensation. Gradually, congestion in the vascular system begins to increase.

The patient is worried about palpitations, shortness of breath, decreased exercise tolerance, and weakness. Then swelling of the soft tissues of the extremities occurs, enlargement of the liver and spleen due to stagnation of blood, the skin begins to acquire a bluish tint, jugular veins swell.

Tricuspid insufficiency

Insufficiency of the right atrioventricular valve is very rare in isolated form and is usually part of combined heart defects.

Since the vena cavae flow into the right heart chambers, collecting blood from all parts of the body, venous stasis develops with tricuspid insufficiency. The liver and spleen are enlarged due to overflow venous blood, fluid collects in the abdominal cavity (ascites occurs), and venous pressure increases.

The function of many internal organs may be impaired. Constant venous congestion in the liver leads to the growth of connective tissue in it - venous fibrosis and a decrease in the activity of the organ.

Tricuspid stenosis

Narrowing of the opening between the right atrium and the ventricle is also almost always a component of combined heart defects, and only in very rare cases can it be an independent pathology.

For a long time there are no complaints, then atrial fibrillation and congestive heart failure quickly develop. Thrombotic complications may occur. Externally, acrocyanosis (blueness of the lips, nails) and a jaundiced tint of the skin are determined.

Aortic stenosis

Aortic stenosis (or aortic stenosis) serves as an obstruction to blood flowing from the left ventricle. There is a decrease in the release of blood into the arterial system, from which, first of all, the heart itself suffers, since the coronary arteries feeding it depart from the initial part of the aorta.

Deterioration of the blood supply to the heart muscle causes attacks of chest pain (angina). A decrease in cerebral blood supply leads to neurological symptoms - headaches, dizziness, periodic loss of consciousness.

Decreased cardiac output is manifested by low blood pressure and weak pulse.

Aortic insufficiency

When the aortic valve, which normally should block the exit from the aorta, is insufficient, some of the blood returns back to the left ventricle during its relaxation.

As with some other defects, due to compensatory hypertrophy of the left ventricle, heart function remains unchanged for a long time. sufficient level, so there are no complaints.

Gradually, due to a sharp increase in muscle mass, a relative discrepancy in blood supply arises, which remains at the “old” level and is unable to provide nutrition and oxygen to the enlarged left ventricle. Attacks of angina pain appear.

In the hypertrophied ventricle, dystrophic processes increase and cause a weakening of its contractile function. Blood stagnation occurs in the lungs, which leads to shortness of breath. Insufficient cardiac output causes headaches, dizziness, loss of consciousness when taking vertical position, pale skin with a bluish tint.

This defect is characterized by a sharp change in pressure in different phases of the heart, which leads to the appearance of the “pulsating man” phenomenon: constriction and dilation of the pupils in time with the pulsation, rhythmic shaking of the head and changes in the color of the nails when pressing on them, etc.

Combined and associated acquired defects

The most common combined defect is a combination of mitral stenosis with mitral insufficiency (usually one of the defects predominates). The condition is characterized by early shortness of breath and cyanosis (bluish discoloration of the skin).
Combined aortic disease (when narrowing and insufficiency of the aortic valve coexist) combines the signs of both conditions in an unexpressed, mild form.

Diagnostics

A comprehensive examination of the patient is carried out:

When interviewing the patient, it becomes clear past illnesses(rheumatism, sepsis), attacks of chest pain, poor tolerance to physical activity.
Examination reveals shortness of breath, pale skin with a bluish tint, swelling, and pulsation of visible veins.
An ECG reveals signs of rhythm and conduction disturbances, phonocardiography reveals a variety of murmurs during heart function.
X-ray is determined by hypertrophy of one or another part of the heart.
Laboratory methods are of auxiliary value. Rheumatoid tests may be positive, cholesterol and lipid fractions may be elevated.

Treatment methods for acquired heart defects

Elimination of pathological changes in the heart valves caused by a defect can only be achieved through surgery. Conservative treatment serves as additional means to reduce the manifestations of the disease.

Main types of operations for heart defects:

In case of mitral stenosis, the welded valve leaflets are separated with simultaneous expansion of its opening (mitral commissurotomy).
In case of mitral insufficiency, the incompetent valve is replaced with an artificial one (mitral replacement).
For aortic defects, similar operations are performed.
In case of combined and combined defects, replacement of damaged valves is usually performed.

The prognosis for timely surgery is favorable. If there is a detailed picture of heart failure, the effectiveness surgical correction in terms of improving the condition and prolonging life, it sharply decreases, so timely treatment of acquired heart defects is very important.

Prevention

Prevention of valve problems, in essence, is the prevention of the incidence of rheumatism, sepsis, and syphilis. Needs to be addressed promptly possible reasons development of heart defects - sanitize infectious foci, increase the body's resistance, eat rationally, work and rest.