Enlarged liver with heart failure, what to do. Congestive liver with heart failure symptoms

Chronic heart failure is a chronic pathological condition, which is due to a decrease contractility myocardium.

This condition can be caused by many factors, including high blood pressure, heart defects, alcohol abuse, diabetes mellitus, inflammatory heart diseases, ischemic disease hearts, etc.

There are left and right ventricular heart failure. It is chronic failure of the right ventricle in the final stages that leads to cardiac cirrhosis of the liver.

Chronic heart failure develops under the influence of pathological factors that lead to the following:

Organic or functional disorders heart muscle, heart valves (heart defects)
Excessive heart work (alcoholism, diabetes, blood pressure, etc.)
Combination of the first two factors

For these reasons, symptoms of chronic right ventricular heart failure develop:

Shortness of breath, first during exercise, then at rest
Decreased performance
Edema of the upper and lower extremities
Liver damage

Causes of development of cardiac cirrhosis of the liver

Right ventricular failure means that the heart does not fully perform its function as a blood pump. The speed of blood flow through the systemic circulation, which includes the liver, decreases.

Blood stagnation begins, both in the liver and in other organs. Due to increased blood pressure the liquid part of the blood passes into the liver tissue, causing swelling.

Hypoxia of hepatocytes
Reduction and necrosis of hepatocytes
Development portal hypertension
Collagen formation, fibrosis
With increased blood stagnation, the proliferation of connective tissue and the destruction of the liver structure intensify

Symptoms of cardiac cirrhosis of the liver

Liver cirrhosis associated with cardiac pathology is characterized by all the symptoms of other types of disease:

Fatigue, loss of appetite, weight loss
Violations gastrointestinal tract(flatulence, vomiting, nausea)
Varicose veins
Abdominal enlargement, ascites
Edema of the lower extremities
Bleeding from the esophagus, stomach, etc.
Jaundice
Increased body temperature
Signs of hepatic encephalopathy (changes in the rhythm of sleep and wakefulness, difficulty performing usual activities, changes in behavior, etc., up to impairment of consciousness)
Pain in the right hypochondrium
Enlarged liver, spleen
Jellyfish head - dilation of veins on the skin of the abdomen

There are also signs that are typical for congestive liver:

Disappearance or reduction of symptoms of cardiac cirrhosis after treatment of heart failure, bringing positive results
On initial stages during the process, the liver is enlarged, soft to the touch, later the liver becomes of a typical dense consistency
With palpation and pressure on the liver area, the veins of the neck swell

However, with further development of the process, treatment of heart failure does not affect liver pathology. This means that cardiac cirrhosis of the liver has fully developed.

Also, cardiological cirrhosis of the liver is characterized by changes in blood tests (anemia, leukocytosis), urine (erythrocytes, protein), feces (acholia - decreased stercobilin), blood biochemistry (increased transaminases, alkaline phosphatase, gamma-GGT, fructose-1-phosphate aldolase, arginase, prothrombin time, bilirubin, globulin, decreased albumin, cholesterol, fibrinogen, prothrombin.

Ultrasound reveals an enlarged liver with uniformly increased echogenicity and an enlarged spleen. Liver biopsy gives a characteristic picture of cirrhosis if possible.

Cardiac cirrhosis of the liver: treatment

First of all, a diet is prescribed with a limit on fatty, fried, smoked foods, salt and spices are limited. Required complete failure from bad habits.

The following drugs are used to correct chronic heart failure:

Cardiac glycosides (digoxin, dobutamine) are used to strengthen and protect the myocardium
Beta-blockers (atenolol, bisoprolol, metoprolol, propronalol, bopindolol, timolol) are necessary to normalize blood pressure
Diuretics (hypothiazide, spironolactone, furosemide) reduce swelling, they also help in the treatment of ascites

For the treatment of cardiac cirrhosis of the liver, various groups of drugs are used, depending on the degree of activity and stage of compensation:

Vitamin therapy (vitamins of groups B, C are prescribed)
Hepatoprotectors – drugs that protect the liver from damage (Essentiale, Heptral)
If complications occur, they are treated

Cardiac cirrhosis of the liver: prognosis

The prognosis, as in the case of other types of cirrhosis, depends on the stage of compensation. Compensated cirrhosis allows you to live quite a long time, often more than 10 years.

Decompensated cardiac cirrhosis of the liver has a much worse prognosis: most often the life expectancy is no more than 3 years. If bleeding develops, the prognosis is poor: mortality is about 40%.

Ascites also affects life expectancy for the worse. The 3-year survival rate is only 25%.

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When there is stagnation in the systemic circulation, the liver is usually short time able to accept significant amount blood. Its role in infancy and childhood is of paramount importance. Congestive liver is always a sign of failure of the right half of the heart, even if the depletion of the right half of the heart is not primary, but secondary to the failure of the left half of the heart. Pathological changes and functional disorders occur under the influence of the combined effect of increased venous pressure and hypoxia.

Upon autopsy, the liver appears larger, heavier, and denser than normal. With fresh stagnation its color is red, with older stagnation it is bluish-brownish-red. With prolonged stagnation, the liver capsule thickens. Due to secondary fatty degeneration, the liver may have yellowish spots. With short-term stagnation, the pattern on the section is pronounced, in the center of the lobules the central veins gape red and at the edges of the hepatic beams - capillaries. The color of the hepatic ligaments is very pale compared to the red spots of the gaping vessels. After long-term stagnation, the liver cells at the edges of the lobules undergo fatty degeneration and therefore acquire yellowish color, and in the center of the lobule there is central vein, filled with bluish-red blood (“nutmeg liver”). With long-term stagnation, the pattern of the hepatic lobules is erased, and the connective tissue that takes the place of the dead hepatic substance leads to the appearance of “false lobulation.” In the center of these false lobules there is yellow liver tissue that has undergone fatty degeneration; seemingly gaping vessels are distributed along the edges. With sudden congestion in the liver substance and under the capsule, many hemorrhages are visible. The microscopic picture is characterized by dilated central veins and capillaries, compressed between them by liver cells with fat droplets and pigment grains. In the center of the lobules, liver cells often die. Microscopic hemorrhages are common.

When liver congestion occurs suddenly, the patient usually feels a sharp pain in the liver area, which may be similar to the pain caused by a gallstone. Often confused with pleurisy. The pain is caused by sudden tension of the liver capsule. Muscular protection may exist over the liver area. A congested liver also affects the function digestive tract: it is accompanied by vomiting, nausea, flatulence, diarrhea and lack of appetite.

In infancy with acute infectious diseases Sometimes it is difficult to decide whether a sudden enlargement of the liver is a consequence of heart failure or toxic damage. In such cases, you can navigate based on other symptoms (increased venous pressure, tachycardia, ECG, etc.). It should be noted here that although the basis of liver congestion is venous stasis However, severe liver congestion may still occur without an increase in venous pressure. Veins because of their great ability expand sometimes over time able to balance high blood pressure, and by the time the increase in venous pressure becomes measurable, liver congestion has long since occurred.

IN childhood Recognizing and clarifying liver congestion is now easier. The lower edge of the liver extends beyond the costal arch; percussion can also establish that the liver is enlarged upward. It raises the right side of the diaphragm and can compress the lower parts of the lungs. In such cases, the percussion sound above the diaphragm is shortened, and bronchial breathing is heard. Palpation usually reveals a uniformly compacted liver with a smooth surface and a hard, sharp or rounded edge. It rarely pulsates. In childhood, even with insufficiency of the tricuspid valves, it is very difficult to recognize the pulsation of the liver, because the liver tissue is very elastic and the greater ability to accept blood equalizes the intense action of the blood flowing back. In chronic decompensation, the proliferation of connective tissue makes the liver so hard that its pulsation can no longer be taken into account. In cardiac pseudocirrhosis, the size of the liver, despite stagnation, may be less than normal.

The functional disorder of the liver with a slight stagnation is insignificant, however, with a larger or long-term stagnation it is still significant. A functional disorder has to be taken into account even if it is not detected by functional liver tests, because based on the literature data and our own experience We believe that functional tests in some cases do not reflect changes in the liver. The content of urobilinogen in urine increases. Some authors attach a relationship between the severity of hepatic congestion and the content of urobilinogen in the urine diagnostic value. According to other authors positive result The Ehrlich reaction is caused not by urobilinogen, but by stercobilinogen. A significant increase in the concentration of lactic acid in the blood is explained by a disorder of liver function. Serum bilirubin increases significantly only after severe or prolonged stagnation. In such cases, the patient develops mild jaundice. The reason for this phenomenon is not entirely clear. It is assumed that liver damage resulting from hypoxia and hemolysis play a role in the occurrence of this jaundice. The latter is supported by the observation of Magyar and Toth: an increase in the content of bilirubin in the urine. Jaundice develops slowly and also disappears slowly. In feces, the amount of coloring substances formed from bile pigment increases.

Disorder of liver function is, with its long-term existence, one and perhaps the most important cause of hypoproteinemia accompanying failure of the right half of the heart. The decrease in the content of serum proteins in heart patients is partly explained by insufficient nutrition, poor absorption conditions, and loss of protein with edematous fluid, but undoubtedly the leading role is played by a decrease in the ability of the liver to form proteins. Due to hypoproteinemia, drug removal of edema is often unsuccessful after restoration of heart strength for a long time.

With scarring of the pericardium or with prolonged decompensation, so-called cardiac cirrhosis often occurs. With abundant growth of connective tissue, it is characterized by the death of the liver substance and, in places, islands of regenerating liver cells. The growth of connective tissue occurs not only around the lobules, but also in their central part. If the growth of connective tissue merges, then the pattern of the hepatic substance becomes unidentifiable. With prolonged stagnation, the capsule thickens due to perihepatitis. The occurrence of liver cirrhosis is characterized by the fact that the liver becomes hard, small, with sharp edges, its size is fixed. At the same time, due to portal hypertension, the spleen begins to swell. It becomes larger and harder. In this state, under the influence of treatment acting on the heart and blood circulation, neither the magnitude nor functional disorder livers do not change. Cardiac cirrhosis is usually accompanied by ascites that is not amenable to drug treatment.

Liver enlargement- hepatomegaly - noted in cases where the size of this the most important body exceeds natural, anatomically determined parameters. As doctors emphasize, this pathology cannot be considered a separate liver disease, since it is a symptom characteristic of many diseases, including those affecting other human organs and systems.

The danger of liver enlargement lies in complications liver failure and other pathological conditions, which disrupt the normal functioning of this organ and create many serious health problems.

Therefore, it is worth talking about such a common pathology as liver enlargement in more detail.

Causes of liver enlargement

Perhaps the list below, including the causes of liver enlargement, is incomplete, but it should make one realize the true scale of its pathogenesis and get an answer to the question - is liver enlargement dangerous?

So, an enlarged liver in an adult can be a consequence of:

As a rule, there is an increase in the lobe of the liver, and an increase in the right lobe of the liver (which has a higher functional load in the functioning of the organ) is diagnosed more often than an enlargement of the left lobe of the liver. However, there is nothing good in this either, since left lobe is so close to the pancreas that it may be this gland that is causing the problem.

Simultaneous enlargement of the liver and pancreas is possible due to inflammation of the pancreas (pancreatitis). Inflammation is accompanied by intoxication, and it removes toxins from the blood liver. If the course of pancreatitis takes especially severe forms, the liver may not cope with its task and increases in size.

Diffuse enlargement of the liver is a clearly non-localized change in the size of its lobules, consisting of hepatocytes (liver cells). For one of the above reasons, hepatocytes begin to die, and glandular tissue gives way to fibrous. The latter continues to grow, thereby enlarging (and deforming) individual areas of the organ, squeezing the hepatic veins and creating the preconditions for inflammation and swelling of the parenchyma.

Symptoms of liver enlargement

A person may not feel a slightly pronounced pathology - an enlargement of the liver by 1 cm or an enlargement of the liver by 2 cm. But the process of changing the natural size of the liver sooner or later begins to manifest itself with more obvious clinical symptoms.

Most typical symptoms liver enlargement: weakness and fatigue, which patients feel even in the absence intense loads; discomfort(heaviness and discomfort) in abdominal cavity; attacks of nausea; weight loss. Further heartburn, halitosis (permanent bad smell from the mouth) itchy skin and dyspepsia.

An enlarged liver due to hepatitis is accompanied not only by general malaise, but also by yellowness skin and sclera, increased temperature, aching in all joints, nagging pain in the right hypochondrium.

Liver enlargement in cirrhosis occurs against the background of the same set of symptoms, which are accompanied by such signs of this disease: abdominal pain and increase in its size, a quickly onset feeling of fullness when eating, increased drowsiness during the day and insomnia at night, nosebleeds and bleeding gums, weight loss, hair loss, decreased ability to remember information. In addition to the enlargement of the liver with cirrhosis (first of both lobes, and then more of the left), the size of the spleen in half of the patients also increases, and doctors determine that they have hepatosplenomegaly - an enlargement of the liver and spleen.

In the clinical manifestation of damage to the body by the human immunodeficiency virus, liver enlargement in HIV is diagnosed at stage 2B - in acute HIV infection without secondary diseases. In addition to the enlargement of the liver and spleen, at this stage there is a fever, skin swelling and rashes on the mucous membranes of the mouth and pharynx, enlarged lymph nodes, as well as dyspepsia.

Fatty hepatosis with liver enlargement

Fatty hepatosis (or steatosis), according to the latest WHO data, affects 25% of European adults and up to 10% of children and adolescents. In Europe, “fatty liver” develops in 90% of alcohol abusers and 94% of obese people. Regardless of the underlying cause of the pathology, fatty hepatosis with liver enlargement progresses to cirrhosis within eight years in 10-12% of patients. And with concomitant inflammation of the liver tissue - into hepatocellular carcinoma.

In addition to alcohol intoxication of the liver and obesity, this disease is associated with impaired glucose tolerance in type II diabetes mellitus and pathology of the metabolism of cholesterol and other fats (dyslipidemia). From the point of view of pathophysiology, fatty hepatosis with or without liver enlargement develops due to metabolic damage fatty acids, which can be caused by an imbalance between energy consumption and energy expenditure. As a result, an abnormal accumulation of lipids, in particular triglycerides, occurs in the liver tissue.

Under the pressure of accumulated fat and the resulting fatty infiltrates, parenchyma cells lose viability, the size of the liver grows, and normal operation the organ is disrupted.

In the early stages, fatty hepatosis may not have obvious symptoms, but over time, patient complaints of nausea and increased gas formation in the intestines, as well as heaviness or pain in the hypochondrium on the right.

Liver enlargement in heart failure

The functional interaction of all body systems is so close that liver enlargement in heart failure is an indicator of a decrease in blood output from the right ventricle of the heart and a consequence of circulatory disorders.

At the same time, blood circulation in the liver vessels slows down, venous stagnation forms (hemodynamic dysfunction), and the liver swells, increasing in size. Since heart failure is most often chronic, prolonged oxygen deficiency inevitably leads to the death of some liver cells. In their place, connective tissue cells grow, forming entire areas that disrupt the functioning of the liver. These zones enlarge and thicken, and at the same time the liver (most often its left lobe) enlarges.

In clinical hepatology, this is called hepatocellular necrosis and is diagnosed as cardiac cirrhosis or cardiac fibrosis. And cardiologists in such cases make a diagnosis of cardiogenic ischemic hepatitis, which, in essence, is an enlargement of the liver in heart failure.

Enlarged liver in a child

There are many reasons for an enlarged liver in a child. So, it could be syphilis or tuberculosis, generalized cytomegaly or toxoplasmosis, congenital hepatitis or bile duct abnormalities.

With this pathogenesis, not only a moderate enlargement of the liver, but also a strong enlargement of the liver with significant compaction of the parenchyma can be established by the end of the first year of the child’s life.

Enlarged liver and spleen in children infancy- the so-called hepatolienal syndrome or hepatosplenomegaly - is the result of congenital higher level levels of immunoglobulins in the blood (hypergammaglobulinemia). This pathology, in addition to the enlargement of these organs, manifests itself in a delay general development child, poor appetite and very pale skin. Enlargement of the liver and spleen (with icteric symptoms) occurs in newborns with congenital aplastic anemia, which occurs due to the destruction of red blood cells, as well as due to extramedullary hematopoiesis - when red blood cells are formed not in the bone marrow, but directly in the liver and spleen.

Fatty hepatosis with liver enlargement in children develops in almost half of the cases due to a significant excess of body weight for age. Although this pathology can occur with some chronic diseases Gastrointestinal tract, after long-term use non-steroidal anti-inflammatory drugs, antibacterial or hormonal therapy.

Diagnosis of liver enlargement

Diagnosis of liver enlargement begins with a physical examination of the patient and palpation of the internal organs of the abdominal cavity to the right of the midline of the abdomen - in the epigastric region.

During a medical examination, the doctor may detect severe enlargement of the liver. What does it mean? This means that the liver protrudes from under the edge of the costal arch much more than expected by the anatomical norm (in an adult of average height this is no more than 1.5 cm), and can be felt significantly below the edge of the ribs. Then it is stated that the liver is enlarged by 3 cm, the liver is enlarged by 5 cm, or the liver is enlarged by 6 cm. But the final “verdict” is made only after a comprehensive examination of the patient, primarily using ultrasound.

An enlarged liver on ultrasound confirms that there is, for example, “an enlarged liver of a homogeneous hyperechoic structure with a displacement towards the stomach, the contours are unclear” or that “diffuse hyperechogenicity of the liver and unclear vascular pattern and borders of the liver have been identified.” By the way, in an adult, a healthy liver has the following parameters (on ultrasound): the anteroposterior size of the right lobe is up to 12.5 cm, the left lobe is up to 7 cm.

In addition to ultrasound examination, the following is used in the diagnosis of liver enlargement:

laboratory tests

Enlarged liver lymph nodes during ultrasound examination are noted by hepatologists in all types of liver cirrhosis, viral hepatitis, tuberculosis of the lymph nodes, lymphogranulomatosis, sarcoidosis, Gaucher disease, drug-induced lymphadenopathy, HIV infection, pancreatic cancer.

Treatment of liver enlargement

Treatment of liver enlargement is treatment of the symptom, but, by and large, it is necessary complex therapy specific disease which led to pathological change of this body.

Drug therapy for a hypertrophied liver must be supported by proper nutrition, diet and vitamin intake. According to experts, in some diseases accompanied by liver enlargement, damaged parenchyma and normal sizes the organ can be restored.

To regenerate liver cells, their normal functioning and protection from negative effects, hepatoprotective drugs are used - special medications for liver enlargement.

The drug Gepabene is a hepatoprotector plant origin(synonyms - Karsil, Levasil, Legalon, Silegon, Silebor, Simepar, Geparsil, Hepatofalk-Planta). The active substances of the drug are obtained from extracts of fumaria officinalis (protipin) and milk thistle fruits (silymarin and silibinin). They stimulate the synthesis of proteins and phospholipids in damaged liver cells, inhibit the formation of fibrous tissue and accelerate the process of parenchyma restoration.

This medicine is prescribed for toxic hepatitis, chronic inflammatory diseases of the liver, disorders of its metabolism and functions with liver enlargement of various etiologies. It is recommended to take one capsule three times a day (with meals). The minimum course of treatment is three months. Among the contraindications of this drug are: sharp forms inflammation of the liver and bile ducts, age up to 18 years. For hemorrhoids and varicose veins, Gepabene is used with caution. During pregnancy and lactation, the drug is used only as prescribed by a doctor and under his supervision. Possible side effects include laxative and diuretic effects, as well as the appearance skin rash. Taking Gepabene is incompatible with drinking alcohol.

The therapeutic effect of the drug Essentiale (Essentiale Forte) is based on the action of phospholipids (complex fat-containing compounds), which are similar in structure to the natural phospholipids that make up human tissue cells, ensuring their division and restoration in case of damage. Phospholipids block the growth of fibrous tissue cells, due to which this drug reduces the risk of developing liver cirrhosis. Essentiale is prescribed for liver steatosis, hepatitis, liver cirrhosis and its toxic lesions. The standard dose is 1-2 capsules three times a day (with meals). Side effects (in the form of diarrhea) are rare.

The drug Essliver differs from Essentiale in the presence in its composition - along with phospholipids - of vitamins B1, B2, B5, B6 and B12. And the combined hepatoprotective medicine Phosphogliv (in capsules), in addition to phospholipids, contains glycyrrhizic acid, which has anti-inflammatory and antioxidant properties. It helps reduce damage to hepatocyte membranes during inflammation and liver enlargement, as well as normalize metabolic processes. The method of administration and dosage of the last two drugs are similar to Essentiale.

Medicines for liver enlargement include a drug based on the artichoke sativum plant - Artichol (synonyms - Hofitol, Cynarix, Artichoke extract). This medicine helps improve the condition of liver cells and normalize their functioning. Doctors recommend taking this drug 1-2 tablets three times a day (before meals). The course of treatment lasts from two weeks to a month, depending on the severity of the disease. As side effects Heartburn, diarrhea, and stomach pain may occur. And contraindications to its use are obstruction urinary tract and bile ducts, stones in gallbladder, as well as severe forms of renal and liver failure.

Besides the fact that medicinal plants are the basis of many hepatoprotective drugs; herbs for liver enlargement are widely used in the form of infusions and decoctions prepared at home. For this pathology, herbalists advise using dandelion, corn silk, calendula, sandy immortelle, yarrow, peppermint. Standard recipe water infusion: for 200-250 ml of boiling water, take a tablespoon of dry herbs or flowers, brew with boiling water, infuse until cool, strain and take 50 ml 3-4 times a day (25-30 minutes before meals).

Diet for liver enlargement

A strictly followed diet for liver enlargement is the key to successful treatment. With a hypertrophied liver, you need to completely avoid eating fatty, fried, smoked and spicy foods, since such foods overload the liver and the entire digestive system.

In addition, the diet for liver enlargement is incompatible with foods such as legumes, radishes, radishes, spinach and sorrel; sausage and spicy cheeses; margarine and spreads; white bread and pastries; vinegar, mustard and pepper; cream confectionery, chocolate and ice cream; carbonated drinks and alcohol.

Everything else (especially vegetables and fruits) can be eaten, at least five times a day, but little by little. It is not recommended to eat after 7 p.m. healthy liver, and especially if the liver is enlarged, it is strictly forbidden. Here's a glass of water with a spoon natural honey possible and necessary.

The daily diet should contain 100 g of animal proteins, approximately the same vegetable proteins and 50 g vegetable fats. The volume of carbohydrate food is 450-500 g, while sugar consumption should be reduced to 50-60 g per day, and salt to 10-12 g. The daily volume of liquid (excluding liquid food) is at least 1.5 liters.

Prevention of liver enlargement

Best prevention of liver enlargement caused by overweight or an addiction to strong drinks, you know what it is. Nothing will work out here without following the principles of a healthy lifestyle...

Unfortunately, it is impossible to predict how the liver will behave and how much it may enlarge, for example, with hepatitis, mononucleosis, Wilson's disease, hemochromatosis or cholangitis. But even in such cases, a balanced diet, consumption of vitamins, physical activity, hardening and giving up bad habits will help the liver cope with cleansing the blood of toxins, producing bile and enzymes, regulating protein, carbohydrate and fat metabolism in the body. Also, to help the liver when there is a threat of hepatomegaly, B vitamins, vitamin E, zinc (to restore liver tissue) and selenium (to increase overall immunity and reduce the risk of inflammatory liver diseases) are especially needed.

Forecast for liver enlargement

The prognosis for liver enlargement is quite alarming. Since the pronounced signs of this pathology do not appear immediately, treatment in a third of cases begins when the process reaches the “point of no return.” And the most likely consequences of liver enlargement are partial or complete loss of its functionality.

Liver in congestive heart failure

Morphological changes

In those who die from heart failure, the process of autolysis in the liver occurs especially quickly. Thus, the material obtained during autopsy does not make it possible to reliably assess intravital changes in the liver in heart failure.

Macroscopic picture. The liver, as a rule, is enlarged, with a rounded edge, its color is purple, the lobular structure is preserved. Sometimes nodular accumulations of hepatocytes (nodular regenerative hyperplasia) can be detected. The section reveals dilatation of the hepatic veins, their walls may be thickened. The liver is full of blood. Zone 3 of the hepatic lobule is clearly defined with alternating yellow (fatty changes) and red (hemorrhage) areas.

Microscopic picture. As a rule, the venules are dilated, the sinusoids flowing into them are full-blooded in areas of varying length - from the center to the periphery. In severe cases, severe hemorrhages and focal necrosis of hepatocytes are determined. They contain various degenerative changes. In the area of the portal tracts, hepatocytes are relatively preserved. The number of unchanged hepatocytes is inversely related to the degree of atrophy of zone 3. On biopsy, pronounced fatty infiltration detected in a third of cases, which does not correspond to the usual picture at autopsy. Cellular infiltration is insignificant.

The brown pigment lipofuscin is often found in the cytoplasm of degenerative zone 3 cells. When hepatocytes are destroyed, it can be located outside the cells. In patients with severe jaundice, bile thrombi are detected in zone 1. In zone 3, hyaline bodies resistant to diastase are detected using the PHIK reaction.

The reticular fibers in zone 3 are compacted. The amount of collagen is increased, sclerosis of the central vein is determined. Eccentric thickening of the venous wall or occlusion of zone 3 veins and perivenular sclerosis extend deep into the hepatic lobule. In long-term or recurrent heart failure, the formation of “bridges” between the central veins leads to the formation of a ring of fibrosis around the unchanged area of the portal tract (“reverse lobular structure”). Subsequently, as the pathological process spreads to the portal zone, it develops mixed cirrhosis. True cardiac cirrhosis of the liver is extremely rare.

Pathogenesis

Hypoxia causes degeneration of zone 3 hepatocytes, dilation of sinusoids and slower bile secretion. Endotoxins entering the system portal vein through the intestinal wall, can aggravate these changes. The absorption of oxygen from the blood of the sinusoids increases compensatoryly. A slight impairment of oxygen diffusion may result from sclerosis of the space of Disse.

A decrease in blood pressure with low cardiac output leads to necrosis of hepatocytes. The increase in pressure in the hepatic veins and the associated stagnation in zone 3 are determined by the level of central venous pressure.

Thrombosis occurring in the sinusoids can spread to hepatic veins with the development of secondary local portal vein thrombosis and ischemia, loss of parenchymal tissue and fibrosis.

Clinical manifestations

Patients are usually slightly icteric. Severe jaundice is rare and is found in patients with chronic congestive failure against the background of ischemic heart disease or mitral stenosis. In hospitalized patients, the most common cause of elevated serum bilirubin concentrations is heart and lung disease. Long-term or recurrent heart failure leads to increased jaundice. In edematous areas, jaundice is not observed, since bilirubin is bound to proteins and does not enter the edematous fluid with low content squirrel.

Jaundice is partly hepatic in origin, and the greater the extent of zone 3 necrosis, the greater the severity of the jaundice.

Hyperbilirubinemia due to pulmonary infarction or stagnation of blood in the lungs creates an increased functional load on the liver under hypoxic conditions. In a patient with heart failure, the appearance of jaundice in combination with minimal signs of liver damage is characteristic of a pulmonary infarction. An increase in the level of unconjugated bilirubin is detected in the blood.

The patient may complain of pain in the right abdomen, most likely caused by stretching of the capsule of the enlarged liver. The edge of the liver is dense, smooth, painful, and can be detected at the level of the navel.

Increased pressure in the right atrium is transmitted to the hepatic veins, especially with tricuspid valve insufficiency. When using invasive methods the curves of pressure changes in the hepatic veins in such patients resemble the pressure curves in the right atrium. Palpable expansion of the liver during systole can also be explained by pressure transmission. In patients with tricuspid stenosis, presystolic pulsation of the liver is detected. Liver swelling is detected by bimanual palpation. In this case, one hand is placed in the projection of the liver in front, and the second - on the area of the posterior segments of the right lower ribs. Increasing the size will make it possible to distinguish liver pulsation from pulsation in epigastric region, transmitted from the aorta or hypertrophied right ventricle. It is important to establish the connection between pulsation and the phase of the cardiac cycle.

In patients with heart failure, pressure on the liver area leads to increased venous return. Disturbed functionality the right ventricle is not allowed to cope with the increased preload, which causes an increase in pressure in the jugular veins. Hepatojugular reflux is used to detect the pulse in the jugular veins, as well as to determine the patency of the venous vessels connecting the hepatic and jugular veins. In patients with occlusion or block of the hepatic, jugular or main veins of the mediastinum, reflux is absent. It is used in the diagnosis of tricuspid regurgitation.

Pressure in the right atrium is transmitted to the vessels up to the portal system. Pulsed duplex Doppler can detect increased portal vein pulsation; in this case, the amplitude of the pulsation is determined by the severity of heart failure. However, phasic fluctuations in blood flow are not found in all patients with high pressure in the right atrium.

Ascites has been associated with significantly increased venous pressure, low cardiac output, and severe necrosis of zone 3 hepatocytes. This combination is found in patients with mitral stenosis, tricuspid valve insufficiency, or constrictive pericarditis. In this case, the severity of ascites may not correspond to the severity of edema and clinical manifestations of congestive heart failure. High content protein in ascitic fluid (up to 2.5 g%) corresponds to that in Budd-Chiari syndrome.

Brain hypoxia leads to drowsiness and stupor. Sometimes a detailed picture of hepatic coma is observed. Splenomegaly is common. Other signs of portal hypertension are usually absent, except in patients with severe cardiac cirrhosis in combination with constrictive pericarditis. At the same time, in 6.7% of 74 patients with congestive heart failure, autopsy revealed esophageal varices, of which only one patient had an episode of bleeding.

With CT scan immediately after intravenous administration contrast agent retrograde filling of the hepatic veins is noted, and in the vascular phase there is a diffuse uneven distribution of the contrast agent.

In patients with constrictive pericarditis or long-term decompensated mitral disease heart with the formation of tricuspid insufficiency, one should assume the development cardiac cirrhosis of the liver. With implementation surgical methods treatment of these diseases, the incidence of cardiac cirrhosis has decreased significantly.

Changes in biochemical parameters

Biochemical changes are usually moderate and are determined by the severity of heart failure.

The serum bilirubin concentration in patients with congestive heart failure usually exceeds 17.1 µmol/L (1 mg%), and in a third of cases it is more than 34.2 µmol/L (2 mg%). Jaundice may be severe, with bilirubin levels greater than 5 mg% (up to 26.9 mg%). Bilirubin concentration depends on the severity of heart failure. In patients with advanced mitral heart disease normal level serum bilirubin during its normal uptake by the liver is explained by the organ’s reduced ability to excrete conjugated bilirubin due to a decrease in hepatic blood flow. The latter is one of the factors in the development of jaundice after surgery.

Alkaline phosphatase activity may be slightly elevated or normal. There may be a slight decrease in serum albumin concentration, which is facilitated by protein loss through the intestines.

Forecast

The prognosis is determined by the underlying heart disease. Jaundice, especially severe, is always an unfavorable sign in heart disease.

Cardiac cirrhosis in itself is not a bad prognostic sign. At effective treatment heart failure can be compensated for cirrhosis.

Liver dysfunction and cardiovascular abnormalities in childhood

In children with heart failure and “blue” heart defects, liver dysfunction is detected. Hypoxemia, venous stagnation and decreased cardiac output lead to an increase in prothrombin time, an increase in bilirubin levels and serum transaminase activity. The most pronounced changes are found with reduced cardiac output. Liver function is closely related to the condition cardiovascular system.

Liver with constrictive pericarditis

In patients with constrictive pericarditis, clinical and morphological characteristics Budd-Chiari syndrome.

Due to significant compaction, the liver capsule resembles icing sugar (“ glazed liver » — « Zuckergussleber"). At microscopic examination reveal a picture of cardiac cirrhosis.

There is no jaundice. The liver is enlarged, compacted, and sometimes its pulsation is detected. There is pronounced ascites.

It is necessary to exclude liver cirrhosis and hepatic vein obstruction as a cause of ascites. Diagnosis is facilitated by the presence of paradoxical pulsus, venous pulsation, pericardial calcifications in the patient, characteristic changes with echocardiography, electrocardiography and cardiac catheterization.

Treatment is aimed at eliminating cardiac pathology. Patients who have undergone pericardiectomy have a favorable prognosis, but recovery of liver function is slow. Gradual improvement is observed within 6 months after successful surgery functional indicators and reduction in liver size. A complete reversal of cardiac cirrhosis cannot be expected, but fibrous septa in the liver become thinner and become avascular.

Cardiac cirrhosis of the liver

Cardiac, or cardiac cirrhosis of the liver develops as a consequence of chronic heart failure.

This type of cirrhosis is classified as secondary, because It is not caused by liver pathology, but by a disease of another organ.

What is chronic heart failure?

Chronic heart failure is a chronic pathological condition that is caused by a decrease in myocardial contractility.

This condition can be caused by many reasons, including high blood pressure, heart defects, alcohol abuse, diabetes, inflammatory heart disease, coronary heart disease, etc.

There are left and right ventricular heart failure. It is chronic failure of the right ventricle in the final stages that leads to cardiac cirrhosis of the liver.

Chronic heart failure develops under the influence of pathological factors that lead to the following:

Organic or functional disorders of the heart muscle, heart valves (heart defects)
Excessive heart work (alcoholism, diabetes, blood pressure, etc.)
Combination of the first two factors

For these reasons, symptoms of chronic right ventricular heart failure develop:

Shortness of breath, first during exercise, then at rest
Decreased performance
Edema of the upper and lower extremities
Liver damage

Causes of development of cardiac cirrhosis of the liver

Right ventricular failure means that the heart does not fully perform its function as a blood pump. The speed of blood flow through the systemic circulation, which includes the liver, decreases.

Blood stagnation begins, both in the liver and in other organs. Due to high blood pressure, the liquid part of the blood passes into the liver tissue, causing swelling.

Hypoxia of hepatocytes
Reduction and necrosis of hepatocytes
Development of portal hypertension
Collagen formation, fibrosis
With increased blood stagnation, the proliferation of connective tissue and the destruction of the liver structure intensify

Symptoms of cardiac cirrhosis of the liver

Liver cirrhosis associated with cardiac pathology is characterized by all the symptoms of other types of disease:

Fatigue, loss of appetite, weight loss
Gastrointestinal disorders (flatulence, vomiting, nausea)
Varicose veins
Abdominal enlargement, ascites
Edema of the lower extremities
Bleeding from the esophagus, stomach, etc.
Jaundice
Increased body temperature
Signs of hepatic encephalopathy (changes in the rhythm of sleep and wakefulness, difficulty performing usual activities, changes in behavior, etc., up to impairment of consciousness)
Pain in the right hypochondrium
Enlarged liver, spleen
Jellyfish head - dilation of veins on the skin of the abdomen

There are also signs that are typical for congestive liver:

Disappearance or reduction of symptoms of cardiac cirrhosis after treatment of heart failure, bringing positive results
At the initial stages of the process, the liver is enlarged and soft to the touch; at later stages, the liver becomes a typical dense consistency
With palpation and pressure on the liver area, the veins of the neck swell

However, with further development of the process, treatment of heart failure does not affect liver pathology. This means that cardiac cirrhosis of the liver has fully developed.

Also, cardiac cirrhosis of the liver is characterized by changes in blood tests (anemia, leukocytosis), urine (erythrocytes, protein), feces (acholia - decreased stercobilin), blood biochemistry (increased transaminases, alkaline phosphatase, gamma-GGT, fructose-1-phosphate aldolase, arginase , prothrombin time, bilirubin, globulin, decreased albumin, cholesterol, fibrinogen, prothrombin.

Ultrasound reveals an enlarged liver with uniformly increased echogenicity and an enlarged spleen. Liver biopsy gives a characteristic picture of cirrhosis if possible.

Cardiac cirrhosis of the liver: treatment

First of all, a diet is prescribed with a limit on fatty, fried, smoked foods, salt and spices are limited. A complete rejection of bad habits is necessary.

The following drugs are used to correct chronic heart failure:

Cardiac glycosides (digoxin, dobutamine) are used to strengthen and protect the myocardium
Beta-blockers (atenolol, bisoprolol, metoprolol, propronalol, bopindolol, timolol) are necessary to normalize blood pressure
Diuretics (hypothiazide, spironolactone, furosemide) reduce swelling, they also help in the treatment of ascites

For the treatment of cardiac cirrhosis of the liver, various groups of drugs are used, depending on the degree of activity and stage of compensation:

Vitamin therapy (vitamins of groups B, C are prescribed)
Hepatoprotectors – drugs that protect the liver from damage (Essentiale, Heptral)
If complications occur, they are treated

Cardiac cirrhosis of the liver: prognosis

The prognosis, as in the case of other types of cirrhosis, depends on the stage of compensation. Compensated cirrhosis allows you to live quite a long time, often more than 10 years.

Decompensated cardiac cirrhosis of the liver has a much worse prognosis: most often the life expectancy is no more than 3 years. If bleeding develops, the prognosis is poor: mortality is about 40%.

Ascites also affects life expectancy for the worse. The 3-year survival rate is only 25%.

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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 large number 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 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 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.
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 an enlarged liver, its lower edge reaching the navel, 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 at an 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, feeling unwell. 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 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 occur secondary to anoxia, centrilobular necrosis and reparative processes. this central fibrosis can further lead to centrilobular cirrhosis. Sustained and frequently repeated increases in venous pressure lead to gradual condensation and collapse of the 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 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 the 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 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.).
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 quite 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 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; the stool is dark with an increased amount of stercobilin, in some cases gray in color with a decrease in the release of pigment. An increased amount of bilirubin is detected in the blood, 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, according to strict indications, corticosteroids

The site administration does not evaluate recommendations and reviews about treatment, drugs and specialists. Remember that the discussion is being conducted not only by doctors, but also by ordinary readers, so some advice may be dangerous to your health. Before any treatment or use medicines We recommend contacting specialists!

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. As pressure increases in big circle blood circulation, the right parts of the heart muscle are overloaded. As a result, the liver is affected: painful sensations, there is an increase in size. Congestive liver in heart failure is quite rare occurrence, but when 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 primary factor The development of the pathology was not caused by a disease of the organ itself, but by dysfunction in the functioning of the heart. late stages Chronic heart failure is observed in cardiac cirrhosis of the liver.

Failure means the heart's inability to pump blood through its vessels. required speed. This leads to its accumulation in the organs, pressure increases, and swelling of the liver occurs. Stagnant blood reduces oxygen saturation of tissues, causing oxygen starvation. This inevitably leads to necrosis of liver cells, causing ischemia. Dead hepatocytes are replaced by cells of fibrous tissue, and cirrhosis gradually develops.

Factors that provoke congestion in the liver include:

Pulmonary heart.
Compressive pericarditis.
Mitral valve stenosis.
Tricuspid valve insufficiency.
Cardiomyopathy.
Consequences of the Fontan operation.
Severe pulmonary hypertension.

The primary manifestations of a decompensated heart condition are shortness of breath and arrhythmia during physical activity. Gradually, shortness of breath occurs at rest, and tachycardia accompanies the patient everywhere. With left ventricular failure, 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 the 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.

Upon opening internal organ It can be 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, the pattern of the liver lobules is 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, in people with heart failure, the symptoms of liver congestion are 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 identify blood stagnation, a comprehensive examination is carried out, 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).
Chest X-ray (examination of the lungs, determination of the size of the heart).
Electrocardiography, echocardiography (analysis of heart function).
Laparocentesis (sampling of fluid from the 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 detected only when clinical studies in laboratory conditions.

The only method of prevention congestive cirrhosis- timely contact with a cardiologist. The success of 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.

Shown moderate rhythm life, reduction of physical activity and an individually selected course of physical activity. The consumption of table salt and liquids is limited. Following a diet and a balanced diet is useful. 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.