Blood stagnation in the liver treatment. Cirrhosis

Congestive liver is observed in chronic heart failure, which is a common complication all organic heart diseases (valvular heart disease, hypertension and coronary disease, constrictive pericarditis, myocarditis, infective endocarditis, fibroelastosis, myxoma, etc.), a number chronic diseases internal organs(lungs, liver, kidneys) and endocrine diseases (diabetes, thyrotoxicosis, myxedema, obesity).

The appearance of the first signs of heart failure depends on a number of reasons, including a combination of several diseases, the patient’s lifestyle, and the addition of intercurrent diseases. In some patients, from the moment organic disease decades pass before the first signs of heart failure appear, and sometimes it develops quite quickly after organic damage hearts.

Clinical picture

The first signs of chronic heart failure are palpitations and shortness of breath during exercise. Over time, tachycardia becomes constant, and shortness of breath occurs at rest, and cyanosis appears. IN lower parts Moist rales are heard from the lungs. The liver enlarges, swelling appears in the legs, then fluid accumulates in subcutaneous tissue and on the body, in the serous cavities, anasarca develops.

In the first stages of heart failure, the liver enlarges in the anteroposterior direction and is not palpable. An enlarged liver can be detected using instrumental studies(rheohepatography, ultrasound). With the increase of heart failure, the liver noticeably enlarges, and it is palpated in the form of a painful edge protruding from the hypochondrium. Liver pain on palpation is associated with stretching of its capsule. The severity and pressing pain in the right hypochondrium, bloating. The liver is noticeably enlarged, sensitive or painful, its surface is smooth, its edge is sharp. Jaundice is often observed. Liver function tests were moderately altered. These changes are in most cases reversible.

At histological examination Liver biopsies reveal dilation of the central veins and sinusoids, thickening of their walls, atrophy of hepatocytes, and the development of centrilobular fibrosis (congestive liver fibrosis). Over time, fibrosis spreads to the entire lobule (septal congestive cirrhosis of the liver develops).

Diagnostics

Identify a disease that may be causing heart failure. Correct assessment of tachycardia and detection of signs plays an important role venous stagnation. Of no small importance is the favorable dynamics of symptoms during treatment with cardiac glycosides and diuretics.

Treatment

Treatment is successful if the underlying disease that led to heart failure is correctly recognized and appropriate causal therapy is carried out. Patients are limited in physical activity, fluid intake and table salt.

In case of insufficient effectiveness general events cardiac glycosides are used internally, long-term or permanently (digoxin, digitoxin, isolanide, celanide, acetyldigitoxin, adonis infusion), thiazides (furosemide, brinaldix, hypothiazide, yurinex, burinex, uregit, etc.) and potassium-sparing diuretics (triamterene, triampur, amiloride, moduretic, veroshpiron). The choice of a diuretic drug and the method of its use are determined by the degree of edema syndrome, the stage of heart failure and tolerability.

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Liver at cardiovascular failure

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 number of blood and thereby significantly facilitate 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 various lesions heart, stagnation 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 has predominantly 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.
Constantly high blood pressure in the hepatic veins causes centrilobular necrosis of liver cells, which occurs in all forms of heart damage, 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 stagnation; the same applies to histological picture liver.
Congestion is clinically expressed in an enlarged liver, its lower edge reaches the navel, is hard, smooth and sensitive to palpation. Sensitivity of an enlarged liver – early sign 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 of spontaneous pain in right half abdomen, similar in intensity to those that occur on early stage infectious hepatitis. Obviously they are related to tension nerve endings liver capsules. 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, bad feeling. 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, coupled with severe centrilobular cell damage.
Liver function tests are usually abnormal. 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). Is it true, clinical symptoms congestive liver are masked by other signs of circulatory disorders.
Comparison of 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 special treatment does not require. The use of leeches on the liver area during cardiac therapy promotes the effect of diuretics. a salt-free, high-calorie diet with sufficient quantity protein and vitamins. CARDIAC CIRRHOSIS
Fibrous changes in the liver occur secondary to 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 cases where 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 dystrophic processes in the liver are constant, so that there are no periods of remission when conditions for nodal 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, central vein 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 of the morphological development of cardiac cirrhosis, its clinical symptoms are largely identical to portal cirrhosis. When examining the patient, slight jaundice is often noted. skin. 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. Development of ascites after long period edema, ongoing shrinkage and hardening of the liver, enlarged spleen and hypoalbuminemia provide 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.).
In patients with cardiac cirrhosis of the liver, it is often observed poor tolerance 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, and cor pulmonale. Functional study liver reveals pronounced disturbances in 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 research liver function, pronounced disturbances 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 process. CARDIAL 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 received 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, itchy skin absent. The uneven coloring of the skin is noteworthy. Thus, in places of massive edema, the skin is not colored 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 bile capillaries due to sharp increase 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. Known sudden appearance jaundice with clinical picture heart attack: be it of the lung, spleen or kidney, while heart attacks of the same location, but without damage to the heart, do not cause 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 an increase in serum bilirubin was noted. There is also an excess of pigment in the tissues during congestion in the lungs due to heart damage, as well as without a heart attack, congestion in the lungs lead 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. Determined in blood increased amount bilirubin, often with a direct van den Berg reaction.
Treatment is aimed mainly at prevention and therapy 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, By strict indications corticosteroids

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Prolonged venous congestion in the liver in severe chronic right ventricular failure can lead to damage to hepatocytes and the development of cirrhosis. In contrast to acute venous congestion in the liver during acute heart failure and from ischemic hepatitis (“shock liver”), which develops with arterial hypotension as a result of decreased hepatic blood flow, cardiac cirrhosis, like any other, is characterized by pronounced fibrosis and formation regeneration nodes.

Pathological anatomy and pathogenesis. Right ventricular failure leads to increased pressure in the inferior vena cava and hepatic veins and stagnation of blood in the liver. The sinusoids are dilated and filled with blood, the liver is enlarged, and its capsule is tense. Prolonged venous stasis and ischemia associated with low cardiac output lead to centrilobular necrosis. As a result, centrilobular fibrosis develops; From the central veins towards the portal tracts, connective tissue septa diverge like rays. The alternation of red areas of venous stagnation and pale areas of fibrosis creates a characteristic “nutmeg liver” picture on the section.

Thanks to the successes of modern cardiology, and especially cardiac surgery, cardiac cirrhosis is now much less common than before.

Changes in laboratory parameters are quite varied. Bilirubin level. as a rule, it is slightly increased; both direct and indirect fractions may predominate. Possible moderate growth alkaline phosphatase activity and prolongation of PT. AST activity is usually slightly increased; pronounced arterial hypotension sometimes leads to the development of ischemic hepatitis (“shock liver”), clinically resembling viral hepatitis or toxic hepatitis. and a sharp short-term increase in AST levels. With tricuspid insufficiency, liver pulsation is sometimes observed. but with the development of cirrhosis this symptom disappears.

In chronic right ventricular failure, the liver is enlarged. dense and usually painless. Bleeding from esophageal varices is rare, but hepatic encephalopathy may develop. which is characterized by a wave-like course in accordance with fluctuations in the severity of right ventricular failure. Ascites and edema. initially associated only with heart failure, they can increase with the development of cirrhosis.

Diagnostics. One should think about cardiac cirrhosis of the liver if a patient has suffered from acquired heart disease for more than 10 years. constrictive pericarditis or pulmonary heart. an enlarged dense liver was found in combination with other signs of cirrhosis. The diagnosis can be confirmed with a liver biopsy, but with increased bleeding and ascites it is contraindicated.

In cases where liver and heart damage are simultaneously detected, hemochromatosis should be excluded. amyloidosis and other infiltrative diseases.

TREATMENT. The main thing in the treatment and prevention of cardiac cirrhosis of the liver is the treatment of the underlying disease. Reducing right ventricular failure helps improve liver function and prevents the progression of cirrhosis.

Cardiac cirrhosis (liver cirrhosis due to heart failure)

Pathogenesis of cardiac cirrhosis of the liver

The disease develops relatively rarely. With stagnation of blood in the liver, along with dilation and overflow of small veins with blood, expansion of the perisinusoidal spaces, atrophy of hepatocytes, and sometimes centrilobular necrosis are detected, which in some cases are combined with fatty degeneration. These changes may be accompanied by fibrosis and regeneration of some hepatocytes with the formation of nodules. The development of liver cirrhosis appears to be promoted by episodes of acute heart failure. It is known that acute necrosis hepatocytes occurs during shock (shock liver), but in Lately Attention is drawn to the significance of small output syndrome in chronic heart failure. Thus, hepatic O-cell failure and cardiac cirrhosis of the liver are often observed in diseases characterized by a combination of venous stagnation and decreased cardiac output(chronic cardiac aneurysm, aortic stenosis, dilated cardiomyopathy).

Clinic for cardiac cirrhosis of the liver

A congestive liver is characterized by pain in the right hypochondrium due to stretching of its capsule. With established liver cirrhosis, a moderate increase in levels is usually observed. indirect bilirubin, as a consequence of concomitant hemolysis and heart failure. The activity of aminotransferases usually increases slightly, but during periods of acute disturbance of blood flow in the liver (shock), a significant increase in the level of aminotransferases and other enzymes is possible, as in acute viral hepatitis. Over time, signs of hepatocellular failure may appear.

Portal hypertension is rare. In some cases, clinical symptoms of liver damage may come to the fore, mainly with a decrease in cardiac output.

True cardiac cirrhosis usually develops no earlier than 10 years after the first symptoms of congestive heart failure appear. At the same time, in diseases accompanied by a decrease in cardiac output, as well as repeated episodes sharp decline Blood pressure caused by one reason or another (in particular, acute disorders heart rhythm), cirrhosis of the liver can form earlier. Pronounced changes in the liver are observed with constrictive pericarditis, in which it is possible to develop as Pick's pseudocirrhosis ( portal hypertension, ascites, enlarged liver in the presence of moderate fibrosis), and true cirrhosis of the liver.

Liver enlargement in chronic heart failure

Congestive liver is observed in chronic heart failure, which is a frequent complication of all organic heart diseases (defects, hypertension and coronary disease, constrictive pericarditis, myocarditis, infective endocarditis, fibroelastosis, myxoma, etc.), a number of chronic diseases of internal organs (lungs, liver, kidneys) and endocrine diseases (diabetes mellitus, thyrotoxicosis, myxedema, obesity).

The appearance of the first signs of heart failure depends on a number of reasons, including a combination of several diseases, the patient’s lifestyle, and the addition of intercurrent diseases. In some patients, decades pass from the moment of organic heart disease to the appearance of the first signs of heart failure, and sometimes it develops quite quickly following organic heart failure.

Clinical picture

The first signs of chronic heart failure are palpitations and shortness of breath during exercise. Over time, tachycardia becomes constant, and shortness of breath occurs at rest, and cyanosis appears. Moist rales are heard in the lower parts of the lungs. The liver enlarges, swelling appears in the legs, then fluid accumulates in the subcutaneous tissue and on the body, in the serous cavities, anasarca develops.

In the first stages of heart failure, the liver enlarges in the anteroposterior direction and is not palpable. Liver enlargement can be detected using instrumental studies (rheohepatography, ultrasound). With the increase of heart failure, the liver noticeably enlarges, and it is palpated in the form of a painful edge protruding from the hypochondrium. Liver pain on palpation is associated with stretching of its capsule. Heaviness and pressing pain in the right hypochondrium and bloating are detected. The liver is noticeably enlarged, sensitive or painful, its surface is smooth, its edge is sharp. Jaundice is often observed. Liver function tests were moderately altered. These changes are in most cases reversible.

Histological examination of liver biopsies reveals dilation of the central veins and sinusoids, thickening of their walls, atrophy of hepatocytes, and the development of centrilobular fibrosis (congestive liver fibrosis). Over time, fibrosis spreads to the entire lobule (septal congestive cirrhosis of the liver develops).

Diagnostics

Identify a disease that may be causing heart failure. Correct assessment of tachycardia and detection of signs of venous stagnation play an important role. Of no small importance is the favorable dynamics of symptoms during treatment with cardiac glycosides and diuretics.

Treatment

If general measures are insufficiently effective, cardiac glycosides are used internally, long-term or permanently (digoxin, digitoxin, isolanide, celanide, acetyldigitoxin, Adonis infusion), thiazides (furosemide, brinaldix, hypothiazide, Yurinex, Burinex, Uregit, etc.) and potassium-sparing diuretics (triamterene , triampur, amiloride, moduretic, veroshpiron). The choice of a diuretic drug and the method of its use are determined by the degree of edema syndrome, the stage of heart failure and tolerability.

Drugs that improve metabolism in the myocardium are also prescribed - anabolic steroid(nerobolil, retabolil, etc.), ATP, vitamins B, C, E.

In the presence of cyanosis, oxygen therapy is indicated; severe violations rhythm - antiarrhythmic treatment. Many patients require sedative therapy.

I.I.Goncharik

“Enlarged liver in chronic heart failure” and other articles from the section Diseases of the liver and gallbladder

Additional Information:

Congestive (cardiac) cirrhosis is a chronic progressive liver disease, manifested by necrosis of hepatocytes, caused by congestion in the cardiovascular system, and in particular in the portal vein system. In the literature you can also find the term “congestive liver”. This disease occurs most often over the age of 45-55 years, in combination with long-term severe heart failure. Men and women suffer from this cirrhosis on average in the same proportion. Development speed congestive cirrhosis is 5-10 years from the onset of the process to the development of severe liver failure.

Causes

The main causes of congestive cirrhosis:

Chronic cor pulmonale;
Tricuspid (three-leaf) valve insufficiency;
Mitral valve insufficiency;
Myxoma in the right atrium;
Pericarditis, constrictive form;
Cardiosclerosis.

The process of development of cardiac cirrhosis of the liver is quite simple. As a result of insufficiency venous circulation and stagnation of blood in the right ventricle of the heart, excessive filling of the center of the liver and its central veins with blood occurs (central portal hypertension). This leads to the development of local hypoxia ( oxygen starvation hepatocytes). Dystrophy occurs in the liver lobules, then atrophy and necrosis. For replacement dead cells the body produces collagen and liver fibrosis develops, which further aggravates the situation.

Symptoms of congestive cirrhosis

The main signs of the development of congestive cirrhosis of the liver:

Pain in the right hypochondrium, discomfort and heaviness in the liver area. Quite strongly expressed, they bother the patient much more than in other forms of cirrhosis;
Bloating;
Minor jaundice ( this symptom may be absent);
Vomiting and nausea (can occur up to several times a day);
Slight enlargement of the spleen;
General weakness;
Decreased appetite;
Edema;

Diagnostics

To diagnose congestive cirrhosis, anamnesis is first of all important, during the collection of which the doctor notes the presence cardiological pathology at the patient. During examination and palpation, an increase in the size of the liver is noted (the lower edge reaches the navel), its edge is smooth, dense and painful.

Additional examination methods:

Blood test for liver tests. There is a moderate increase total bilirubin and its fractions, a decrease in albumin levels, a moderate increase alkaline phosphatase and ASaT.
Ultrasound of the liver. Characterized by a significant enlargement of the liver and signs of cirrhosis of the central lobes. If available free liquid V abdominal cavity reveals signs of ascites.
Liver biopsy. Congestion in the liver lobules, signs of sclerosis and necrosis are detected.

Treatment of congestive cirrhosis

Treatment of congestive liver cirrhosis is based on therapeutic activities to compensate for heart failure. If you stabilize the heart, the progression of cardiac cirrhosis stops.

As maintenance therapy in case of of this disease an albumin solution is administered. It allows you to support and improve protein metabolism, somewhat improves the functioning of hepatocytes, reduces swelling and ascites.

Diuretics are also prescribed to eliminate edema and ascites. The most effective in this case is Veroshpiron. He deduces excess liquid and maintains ionic balance in cells.

Diet is also necessary for liver congestion. Food should be rich in protein and slightly increase fat in the diet. These are products such as milk, kefir, cottage cheese, sour cream, any meat, fish, eggs, caviar, soybeans, and legumes. Also, any dietary supplements based on amino acids are good as a supplement to food.

Complications

The most common complications of congestive cirrhosis include:

Hepatic coma;
Varicose veins of the esophagus, rectum and portal vein;
Bleeding from varicose veins;
Hepatocellular carcinoma;
Ascitic sepsis and peritonitis;
Death.

Prevention

The only method of preventing the development of congestive cirrhosis is a timely visit to a cardiologist with heart problems, quality treatment of these diseases and maintaining the heart and blood vessels in a state of compensation.

WHAT IS A STAGNANT LIVER? The work of all organs is closely interconnected. It is difficult to find a disease that affects only one system of the body. In patients with heart failure, it's not just the heart that suffers. When its right sections are overloaded, the liver is affected, as the pressure in the big circle blood circulation If it enlarges and becomes painful, one must assume that it is a congestive liver, the treatment of which is mandatory. Definition and causes Congestive liver or cardiac cirrhosis is pathological condition, in which the liver due to high pressure the inferior vena cava and hepatic veins are filled with blood. As a result, it overstretches. Blood remaining inside for a long time stagnates, disrupting the supply of oxygen to the organ parenchyma (ischemia occurs). Ischemia inevitably leads to necrosis of liver cells (hepatocytes). Dead hepatocytes become fibrotic (replaced by connective tissue), which is the morphological essence of cirrhosis. The area where fibrosis occurred turns pale, there is no blood supply there; it drops out completely as a functional unit. Congestion in the liver is observed with mitral stenosis, pericarditis, and tricuspid valve insufficiency. Clinical picture The development of cardiac cirrhosis in patients with heart failure is often predicted. If heart disease is diagnosed at late stage, then we should expect the detection of this disease. It is characterized by the following symptoms: - hepatomegaly (liver enlargement) - the boundaries of the organ expand, the edge of the liver can be easily palpated below the right rib, which should not normally be observed; - intense pain in the right hypochondrium, caused by strong stretching of the liver capsule; - weakness, lethargy, quick loss weight; - lack of appetite, nausea, vomiting: - swelling of the lower extremities; - yellowing of the skin and mucous membranes. These signs are a reflection pathological process in the liver. But the patient may also be concerned about manifestations caused by heart failure: - severe shortness of breath during physical activity, even minimal, or at rest; - orthopnea (forced sitting position) - to facilitate breathing during an attack of shortness of breath; - the appearance of paroxysmal (maximally severe) shortness of breath at night: - cough accompanying shortness of breath; - feeling of fear, anxiety, severe anxiety. Stagnation of blood in the liver is always unfavorable. Cirrhosis can continue the pathological chain and lead to complications. Due to the increase in pressure in portal vein portal hypertension develops. Its main manifestations include ascites (fluid in the abdominal cavity), varicose veins esophageal veins, strengthening the pattern of subcutaneous vessels on the anterior wall of the abdomen. Development is possible liver failure. As cirrhosis progresses in the liver, everything large quantity functioning hepatocytes replaces connective tissue. The remaining cells are unable to withstand ischemia for a long time; they increase in size to take on the load. This allows the liver to be in the compensation stage for some time, when symptoms are absent or hardly bother the patient. As soon as compensatory capabilities are exhausted, decompensation occurs - liver failure. Diagnosis To identify congestion in the liver, you need to conduct a comprehensive examination. It includes the following methods: Biochemical blood test (level of liver transaminases (enzymes), total protein, bilirubin, alkaline phosphatase). Coagulogram (study of the blood coagulation system). Electrocardiography, echocardiography (determining the functional state of the heart). X-ray of organs chest(detecting an increase in heart size, concomitant pathology lungs). Ultrasound examination of the liver (determining its size and structure). Liver biopsy (only indicated for heart transplant candidates). Laparocentesis (taking fluid from the abdominal cavity). Coronary angiography (assessment of coronary vessels hearts). Treatment Therapy for cardiac cirrhosis consists of a sodium-restricted diet and elimination of the cardiac pathology that provoked it. Drug treatment involves the prescription of diuretics (diuretics), as well as drugs from the group of beta blockers and ACE inhibitors. Shown is an individually selected range of moderate physical activity. Surgery It is not used to eliminate liver congestion itself.