Why does the liver enlarge in heart failure? Traditional methods of treating congestion in the liver

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 is clearly defined hepatic lobule with alternating yellow ( fatty changes) and red (bleeding) 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 is determined central vein. 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 it spreads pathological process develops into the portal zone 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 portal vein system through intestinal wall, may exacerbate 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.

Decline blood pressure at 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 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. 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. Using pulse duplex Doppler study increased portal vein pulsation can be determined; 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 congestive heart failure. The high protein content in ascitic fluid (up to 2.5 g%) corresponds to that in Budd-Chiari syndrome.

Brain hypoxia leads to drowsiness and stupor. Sometimes there is a detailed picture hepatic coma. 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 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. Maybe slight decrease Serum albumin concentrations, which are facilitated by intestinal protein loss.

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 congestion, and decreased cardiac output lead to increased prothrombin time, increased bilirubin levels, and increased serum transaminase activity. The most pronounced changes are found with reduced cardiac output. Liver function is closely related to the condition of cardio-vascular 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. Within 6 months after successful operation there is a gradual improvement functional indicators and reduction in liver size. You can't expect complete reverse development cardiac cirrhosis, but fibrous septa in the liver become thinner and become avascular.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 systemic circulation increases. 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 occurs when mitral stenosis, pericarditis, 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 to find 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 of the 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 increased pressure in the portal vein, it develops portal hypertension. Its main manifestations include ascites (fluid in 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 (definition functional state hearts). X-ray of the chest organs (detecting an increase in the size of the heart, 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.

Today, 4 out of 5 people in our country have liver disease. Most of them are men from 18 to 65 years old. Among the most common diseases is congestive liver, which is accompanied by heart failure.

Liver congestion is a common phenomenon, because every day the organ performs extensive work to secrete bile

Causes

Liver congestion is a common phenomenon, because every day the organ performs extensive work to secrete bile. The mechanism is very complex and due to the branching of the ducts, the process is not always successful, which leads to cholestasis. Common reasons the following factors become:

Liver dysfunction, if left unchecked, begins to affect the functioning of the heart. Which leads to heart failure. With this tandem, the disease can last for decades. It is necessary to conduct an examination for liver enlargement if the heart malfunctions.

Symptoms and diagnosis

Let's look at three main reasons.

First reason. Blocking of the biliary tract with a calculus (stone). This is a complication that occurs when gallstone disease. In this case, stones form in the liver, interfering with normal functioning.

The symptom is expressed suddenly acute pain under the ribs in right side, as a result of overvoltage and poor nutrition. The occurrence of discomfort is due to the closure of the duct, its subsequent enlargement and growth of the liver. Other signs of liver dysfunction may include nausea, vomiting, and chills.

The second reason. Gallbladder deformity. Bend is often a congenital problem. Only sometimes can it appear unexpectedly for a person during a period of life. The bend occurs in the neck, in the organ itself, the fundus or in the excretory duct.

The symptoms are not pronounced and may not appear at all. From possible phenomena I'm worried about slight discomfort in the right hypochondrium, bloating, lack of appetite, nausea before and after eating. However, severe pain can visit if there is a blockage of the duct or cervix.

Third reason. Cancerous tumors very insidious, because they appear only when the patient’s standard of living decreases and this is outwardly noticeable. The tumor grows into the ducts and causes cholestasis. Moreover, its initial position may not be in the liver itself, but in nearby organs.

Congestive liver in heart failure affects the entire body. People with weak veins, for example, experience increased clinical symptoms of dilated and blocked veins. Allergy sufferers experience suffocation, dryness and itching of the skin. With cancer, the tumor grows in patients due to the accumulation of poisons and toxins, which gallbladder unable to withdraw. Rheumatic patients, even after curing rheumatism, get complications. People with headaches are at risk of having more frequent attacks. Symptoms may be accompanied by blood stagnation in the liver.

Let's look at the classic signs of liver congestion:

Heart problems indicate liver congestion

1. Chronic fatigue.
2. Decreased attention.
3. Anxiety.
4. Violation of the heart.
5. Worsening of chronic diseases.
6. Inflammatory processes in the lymph nodes.
7. Weight gain.
8. Increase or decrease in blood pressure.
9. Increased sweating.
10. Problems with dryness and excessive fat content skin.
11. Cracks around the mouth, on the heels.
12. Various types of skin fungi.
13. Long-term inflammation of the nail plates on the hands and feet, etc.

Any weakness in the body can make itself felt in cardiac cirrhosis. To confirm the disease, you need to consult a specialist and undergo a series of examinations. Take a blood test to check for increased bilirubin and undergo an abdominal ultrasound.

Treatment

Helps against annoying itching antihistamines and hepatoprojectors. For example, Heptal.

If a mechanical obstruction is detected in the ducts, then endoscopic intervention surgeon

Prevention and diet

Congestive liver requires prevention. The rules are extremely simple:

Prevention of congestive liver is proper nutrition

1. Eat right.
2. Control your physical activity.
3. Support your liver with medication.
4. Do not abuse alcoholic beverages.

A diet is recommended for patients with this diagnosis. It includes a ban on neutral fats. The amount of these substances allowed for consumption is up to 40 grams per day. Meals in small portions in 6 meals. Include plant and animal protein in your diet. Onions, garlic, radishes, sorrel, spinach, mushrooms, turnips, and radishes are prohibited. It is strictly forbidden to consume alcohol, fried, fatty foods, fatty types meat.

Include in your diet fat soluble vitamins. This will help fill the gap useful substances. Take calcium.

Individual diet program A nutritionist will help you determine the extent of the disease. It will take into account the daily needs of microelements. And it will help avoid problems with weight and liver function. Balances your diet and improves your overall condition.

Video

Breathing practice for treating the liver and gallbladder.

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 in alkaline phosphatase and ACaT.
• Ultrasound of the liver. Characterized by a significant enlargement of the liver and signs of cirrhosis of the central lobes. If available free liquid in the 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 the case 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.