Stagnation of venous blood in the liver is treated with drugs. Congestive liver in heart failure

Viral cirrhosis of the liver

Viral cirrhosis of the liver has the following clinical and laboratory features that must be taken into account when diagnosing it.

1. Most often, viral cirrhosis of the liver is observed in young and middle age, and more often in men.

2. It is possible to establish a clear connection between the development of liver cirrhosis and acute viral hepatitis. E. M. Tareev identified two variants of viral cirrhosis of the liver: early, developing during the first year after acute hepatitis B, and late, developing over a long latent period. Hepatitis D and C viruses have pronounced cirrhotic properties. Chronic hepatitis caused by these viruses often transforms into liver cirrhosis. Chronic hepatitis C can have a clinically rather benign course for a long time and still naturally leads to the development of liver cirrhosis.

3. Viral cirrhosis of the liver is most often macronodular.

4. The clinical picture during periods of exacerbation of liver cirrhosis resembles the acute phase of viral hepatitis and is also manifested by severe asthenovegetative, dyspeptic syndromes, jaundice, and fever.

5. Functional impairment liver with viral form cirrhosis appears quite early (usually during periods of exacerbation of the disease).

6. At the stage of established liver cirrhosis varicose veins veins of the esophagus and stomach, hemorrhagic syndrome with viral etiology of cirrhosis is observed more often than with alcoholic cirrhosis.

7. Ascites in viral cirrhosis of the liver appears much later and is observed less frequently than in alcoholic cirrhosis.

8. Indicators thymol test with viral cirrhosis they reach the highest values compared to alcoholic cirrhosis of the liver.

9. Viral cirrhosis of the liver is characterized by the identification of serological markers viral infection(cm. " ").

Alcoholic cirrhosis of the liver

Alcoholic cirrhosis of the liver develops in 1/3 of people suffering from alcoholism within a period of 5 to 20 years (S. D. Podymova). The following clinical and laboratory features are characteristic of alcoholic cirrhosis of the liver:

1. Anamnestic indications of long-term abuse alcohol (however, most patients, as a rule, hide this).

2. The characteristic “look of an alcoholic”: a puffy face with reddened skin, small telangiectasias, a purple nose; tremor of the hands, eyelids, lips, tongue; swollen cyanotic eyelids; slightly bulging eyes with injected sclera; euphoric demeanor; swelling in the area of the parotid glands.

3. Other manifestations of chronic alcoholism (peripheral polyneuropathy, encephalopathy, myocardial dystrophy, pancreatitis, gastritis).

4. Severe dyspeptic syndrome (loss of appetite, nausea, vomiting, diarrhea) in the advanced stage of alcoholic cirrhosis of the liver, caused by concomitant alcoholic gastritis and pancreatitis.

5. Telangiectasia and Dupuytren's contracture (in the area of the tendons of the palm), as well as testicular atrophy and hair loss are more typical for alcoholic cirrhosis of the liver than for other etiological forms of cirrhosis.

6. Portal hypertension(including one of its most important manifestations - ascites) develops much earlier than with viral cirrhosis of the liver.

7. The spleen enlarges much later than in viral cirrhosis of the liver, in significant amount In patients with splenomegaly there is no splenomegaly even in the advanced stage of the disease.

8. Leukocytosis (up to 10-12x10 9 /l) with a band shift, sometimes up to the appearance of myelocytes and promyelocytes (leukemoid reaction of the myeloid type), anemia, increased ESR. The causes of anemia are blood loss due to erosive gastritis, toxic effect alcohol on Bone marrow; malabsorption and nutritional deficiency folic acid (this may cause the megaloblastoid type of hematopoiesis); disturbance of pyridoxine metabolism and insufficiency of heme synthesis (this causes the development of sideroachrestic anemia); sometimes hemolysis of red blood cells.

9. Characteristic high content in the blood IgA, as well as an increase in the activity of γ-glutamyl transpeptidase in the blood - 1.5-2 times (the normal value for men is 15-106 U/l, for women - 10-66 U/l). High levels of γ-glutamyl transpeptidase in the blood usually indicate long-term alcohol abuse, alcohol impairment liver and is considered by many authors as a biochemical marker of alcoholism. The test can be used to screen alcoholics and control during the period of abstinence (only after 3 weeks of stopping alcohol intake, enzyme activity is reduced by half). However, it should be taken into account that the activity of γ-glutamyl transpeptidase can be increased in diabetes mellitus, myocardial infarction, uremia, pancreatic tumors, pancreatitis, taking cytostatics, antiepileptic drugs, barbiturates, anticoagulants indirect action. At chronic alcoholism the blood level of acetaldehyde (a product of alcohol metabolism, more toxic than alcohol itself) is increased, and the urinary excretion of salsolin (a condensation product of acetaldehyde and dopamine) is increased. Often with alcoholic cirrhosis of the liver, the level of uric acid in the blood is increased.

10. Liver biopsy samples reveal the following signs:

Mallory bodies (accumulation of alcoholic hyaline in the center of the hepatic lobule);
accumulation of neutrophilic leukocytes around hepatocytes;
fatty degeneration of hepatocytes;
pericellular fibrosis;
relative safety of the portal tracts.

11 Stopping alcohol use leads to remission or stabilization pathological process in the liver. With continued alcohol intake, liver cirrhosis progresses steadily.

“Congestive liver” and cardiac cirrhosis of the liver

Congestive liver is liver damage caused by stagnation of blood in it due to high pressure in the right atrium. A congested liver is one of the main symptoms of congestive heart failure.

Its most common causes are mitral valves heart, tricuspid valve insufficiency, chronic cor pulmonale, constrictive pericarditis, right atrium myxoma, myocardiosclerosis of various sockets (for more details, see “Chronic circulatory failure”).

The main mechanisms for the development of “congestive liver” are:

blood overflow of the central veins, the central part of the hepatic lobules (development of central portal hypertension);
development of local central hypoxia in the liver lobules;
dystrophic, atrophic changes and necrosis of hepatocytes;
active collagen synthesis, development of fibrosis.

As congestion progresses in the liver, further development occurs connective tissue, connective tissue cords connect the central veins of neighboring lobules, the architecture of the liver is disrupted, and cardiac cirrhosis develops.

Characteristic features of “congestive liver” are:

hepatomegaly, the surface of the liver is smooth. IN initial stage circulatory failure; the consistency of the liver is soft, its edge is rounded, later the liver becomes dense, and its edge is sharp;
liver pain on palpation;
positive Plesch’s symptom or hepatojugular “reflex” - pressing on the area of the enlarged liver increases the swelling of the neck veins;
variability of liver size depending on the state of central hemodynamics and the effectiveness of treatment ( positive results treatment of congestive heart failure is accompanied by a decrease in liver size);
slight severity of jaundice and its reduction or even disappearance with successful therapy congestive heart failure.

In severe congestive heart failure, edematous-ascitic syndrome develops, in which case there is a need differential diagnosis with cirrhosis of the liver with ascites.

Differential diagnostic features are presented in the table.

Signs	Cirrhosis of the liver	"Congestive liver"
Pain and feeling of heaviness in the right hypochondrium	Available	Very significantly expressed
Flatulence	Available	Significantly expressed
Nausea, vomiting	Can be	Frequently observed
Hemorrhagic syndrome	Very characteristic	Uncharacteristic
Jaundice	Happens often	May be slightly expressed
Liver edge	Sharp, dense, low-painful	Rounded, tightly elastic, painful
Plesch's sign (hepatojugular "reflex")	Absent	Available
Splenomegaly	Significantly expressed, observed in almost all patients	It happens sometimes
"Spider veins", "liver palms"	Very characteristic	Uncharacteristic
Signs of collateral blood flow (esophageal varices, stomach, etc.)	Characteristic	Uncharacteristic
Effect of diuretic therapy	Reduction of ascites	Reducing edema and liver size
Cytolysis syndrome	Characteristic, significantly expressed in the active stage	Less pronounced and observed mainly in severe stages of circulatory failure
Hypoalbuminemia	Extremely characteristic	Less typical
Hypocholesterolemia	Very characteristic	Little characteristic
Mesenchymal inflammatory syndrome	Expressed	Uncharacteristic
Hyperbilirubinemia	Pronounced and characteristic	Less typical and small

With the development of cardiac cirrhosis, the liver becomes dense, its edge is sharp, its size remains constant and does not depend on the effectiveness of treatment of heart failure. When diagnosing cardiac cirrhosis, the underlying disease that caused heart failure, the absence of signs of chronic alcohol abuse and markers of viral infection are taken into account.

Right ventricular failure leads to increased pressure in the inferior vena cava and hepatic veins and stagnation of blood in the liver. 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. Congestion in the liver is always unfavorable. Linex is prescribed 2 capsules 3 times a day, 2-4 weeks. There are no nerve receptors in the liver itself.

Since venous blood comes from gastrointestinal tract straight to the liver, it is these organs that are loaded with poisons and toxins in the first place. First, due to stagnation in the liver, various complications may appear in the digestive tract: nausea, loss of appetite, pain or colic in the stomach and intestines, diarrhea, constipation, hemorrhoids. TO typical symptoms Also include bloating and so-called “stagnant fungi”.

In fact, all allergies are much easier to diagnose at this time. After eliminating congestion, allergies weaken to the previous level achieved before congestion occurred in the liver. In cancer patients, poisons accumulate primarily in the tumor and can provoke its growth. This also applies to everyone benign tumors: cysts, lipomas, myomas and fibromas. If you are prone to headaches or migraines, they may reappear as a result of congestion in the liver.

The liver, along with the kidneys and intestines, are the most important organs and play a central role in metabolism. Based on experience, vaccinations against hepatitis A and hepatitis B weaken the constitution of the liver if they were not normally tolerated by the body. Middle-aged men are more likely to get sick than women, in a ratio of approximately 3:1, this is associated with chronic alcohol consumption, so the alcoholic form of cirrhosis is more common.

The life expectancy of a patient with cirrhosis depends on the cause of its development and the stage at which the disease was detected. The liver is an organ digestive system, weighing approximately 1500 grams, located in upper section abdominal cavity(belly), more on the right.

The liver consists of two large lobes (left and right), and 2 small lobes (quadrate caudate). On bottom surface right lobe, there is a depression with vessels called the porta hepatis, the portal vein and hepatic artery enter them, and the inferior vena cava and the common bile duct exit.

Congestive liver: causes and consequences

Interlobular arteries, accompanied by interlobular veins, they saturate the liver with oxygen, which are a continuation hepatic arteries. Bile canaliculi pass between the liver cells, which flow into the bile ducts, with the help of which the bile formed by the liver is carried into the gallbladder for further participation in digestion. Detoxification function of the liver: destruction (neutralization) harmful substances and removing them from the body (toxins, medications, poisons and others), as a result of various chemical reactions.

Participates in the processes of coagulation and hematopoiesis: some blood clotting factors and anticoagulants, erythrocytes (red blood cells) are formed in the liver. Protective function body: forms substances (antibodies) involved in the formation of immunity (protection) of the body from harmful external and internal factors.

Chronic stagnation of bile in the ducts leads to excessive accumulation of bile in the liver, its toxic effect on liver cells, their inflammation and the development of cirrhosis. Observe for vascular and heart diseases: heart failure, pericarditis, heart defects and others. In approximately 20% of patients, cirrhosis of the liver is asymptomatic (without manifestations visible to the patient) and is detected by chance during examination for another disease.

Aching, worse after eating or physical activity, are the result of an increase in liver volume and stretching of the capsule. Heaviness in the right hypochondrium, loss of appetite, nausea, possibly vomiting, bitterness in the mouth, bloating, diarrhea. They develop as a result of a lack of bile secreted by the liver for normal digestion.

Causes of development of cardiac cirrhosis of the liver

Hepatoprotectors (Essentiale, Liv.52, vitamin B), protect liver cells from damage, improve metabolic processes in them, and increase the secretion of bile by liver cells. They are the group of choice for liver diseases.

Vitamins are prescribed to all patients, due to their deficiency in the body (the production of vitamins by the affected liver is impaired), with improvement metabolic processes in the liver. Adsorbents ( Activated carbon, Enterosorbent), are used to cleanse the intestines and increase the detoxification function of the liver, as a result of their adsorption toxic substances.

Diuretics (Veroshpiron, Furosemide) are used in patients with ascites (fluid in the abdomen) and edema. Probiotics (Linex, Bifidumbacterin), for recovery normal microflora intestines, contain intestinal bacteria that are involved in digestion.

First of all, quit alcohol and smoking. Food consumed by patients with cirrhosis of the liver should be lightly salted, without seasonings, not fried (boiled), without semi-finished products. Eat a lot of salads and fruits, as they contain vitamins. Seafood (fish various types), is useful in that it contains microelements (magnesium, phosphorus) necessary for a patient with liver cirrhosis, but not in large portions (up to 100 g per day).

With severe cirrhosis of the liver (overgrowth of connective tissue over a large area), severe general state, not amenable drug treatment, liver transplantation is prescribed. For liver transplantation, a donor is required; if there is a donor, then the operation is performed (under general anesthesia). But only approximately 80 - 90% of patients with a transplanted liver have a favorable outcome, the rest develop life-threatening complications, or the development of cirrhosis of the transplanted liver.

Consequently, effective liberation of the body from poisons is possible only if healthy function liver, kidneys and intestines. Specific pain and colic in the liver area are usually associated with the gallbladder and bile ducts. 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. In allergy sufferers, as a result of stagnation in the liver, all allergic symptoms, since accumulated poisons additionally load and weaken the immune system.

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

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

CONGESTIVE LIVER

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

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

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

Congestion is clinically expressed in enlarged liver, its lower edge reaches 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 for spontaneous pain in right half abdomen, similar in intensity to those that occur on early stage infectious hepatitis. Obviously they are related to tension nerve endings liver capsules. There is often a feeling of heaviness, tension and fullness that occurs during eating and persists long after it. Appetite worsens, nausea and vomiting appear, and poor health occurs. Dyspeptic symptoms are also associated with congestion in the gastrointestinal tract.

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

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

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

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

CARDIAC CIRRHOSIS

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

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

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

Cardiac cirrhosis of the liver has the following pathological picture. The walls of the dilated central veins are sclerotic and thickened. The number of capillaries and anastomoses between the hepatic and portal veins increases. As a result of the proliferation of connective tissue, central vein difficult to recognize. The bile ducts proliferate and islands of regeneration appear. The most characteristic of cardiac cirrhosis is a pronounced degree of fibrosis in the central zones and compression portal vein 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. Development of ascites after long period edema, ongoing shrinkage and hardening of the liver, enlarged spleen and hypoalbuminemia provide grounds for the diagnosis of cardiac cirrhosis. In these cases, ascites, like other signs of cirrhosis, persist even after successful treatment cardiovascular failure(edema disappears, etc.).

In patients with cardiac cirrhosis of the liver, it is often observed poor tolerance medications, especially increased sensitivity to digitalis and strophanthin, apparently with a violation of the neutralizing function of the liver.

The basis for the diagnosis of cardiac cirrhosis is the presence of prolonged decompensation in diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, 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. Radioisotope studies of liver function reveal pronounced disturbances.

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

CARDIAL JAUNDICE

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

The yellowness of the skin and sclera in cardiac cirrhosis is slight, there is no itching. The uneven coloring of the skin is noteworthy. Thus, in places of massive edema, the skin is not yellow due to the fact that bilirubin circulating in the blood is bound to protein and does not enter the edematous fluid. In a small number of patients, jaundice acquires the features of mechanical jaundice: intense, with a grayish tint, coloring of the skin, pigments in the urine and light-colored feces are noted.

The mechanism of jaundice in circulatory disorders is different.

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

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

(3 ) Hemolytic jaundice often combined with tissue hemorrhages, especially pulmonary infarctions. Known sudden appearance jaundice with clinical picture heart attack: be it of the lung, spleen or kidney, while heart attacks of the same location, but without damage to the heart, do not cause jaundice.

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

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

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

The special vulnerability of the liver in case of right heart failure is explained by the fact that the liver is the reservoir closest to the heart, capable of depositing a large amount of blood and thereby significantly facilitating the work of the right ventricle of the heart.
Liver enlargement is a central link in the development of right heart failure. This especially applies to diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, cor pulmonale, as well as other diseases of the heart, pleura, lungs, diaphragm, leading to weakness of right ventricular systole. CONGESTIVE LIVER
The most common picture of liver congestion is observed. As a result of various heart lesions, congestion occurs in the right atrium, pressure in the hepatic veins increases and dilatation of the central veins occurs. The slowdown in blood circulation increases the blood overflow of the central veins, the central part of the lobules, and central portal hypertension develops, which is predominantly of mechanical origin, then hypoxia occurs. Using catheterization of the liver veins in patients with circulatory failure, it was shown that they contain less oxygen than under normal conditions.
Persistently increased pressure in the hepatic veins causes centrilobular necrosis of liver cells, which occurs in all forms of heart disease, but especially in tricuspid valve insufficiency, mitral stenosis and adhesive pericarditis.
Along with the expansion of capillaries and centrilobular necrosis, the proliferation of connective tissue begins. At the periphery of the lobules, where the blood supply is worse, obesity of liver cells occurs. If venous congestion is eliminated, centrilobular cells are regenerated and the liver restores its original structure. True, a number of authors have noted that reducing venous pressure does not always eliminate venous congestion, and the same applies to the histological picture of the liver.
Congestion is clinically expressed in an enlarged liver, its lower edge reaches the navel, is hard, smooth and sensitive to palpation. The sensitivity of an enlarged liver is an early sign of stagnation, which precedes edema. Sometimes it moves and pulsates, so that the hepatic pulse can be observed. Ripple occurs during ventricular systole, and hepatic-jagular reflux is important. These dynamic phenomena are observed more often with tricuspid valve insufficiency.
Patients may complain of spontaneous pain in the right half of the abdomen, similar in intensity to those that occur at the early stage of infectious hepatitis. Obviously, they are associated with tension in the nerve endings of the liver capsule. There is often a feeling of heaviness, tension and fullness that occurs during eating and persists long after it. Appetite worsens, nausea and vomiting appear, and poor health occurs. Dyspeptic symptoms are also associated with congestion in the gastrointestinal tract.
With congestive liver, ascites may develop, the origin of which is: increased pressure in the veins of the liver, decreased serum albumin and sodium retention. Patients who develop ascites are more likely to have particularly high venous pressure, low cardiac output, 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 that reflect the actual functions of the liver (bromsulfalein test, radioisotope study). True, the clinical symptoms of congestive liver are masked by other signs of circulatory disorders.
A comparison of morphological studies and the functional state of the 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 the development of connective tissue proliferation and the 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. The bile ducts proliferate and islands of regeneration appear. The most characteristic of cardiac cirrhosis is a pronounced degree of fibrosis in the central zones and compression of the portal vein by overgrown connective tissue. Obviously, this is why the term cardiac fibrosis arose, which many authors recommend calling this liver damage.
Despite some features of the morphological development of cardiac cirrhosis, its clinical symptoms are largely identical to portal cirrhosis. When examining 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 of cardiovascular failure (edema, etc. disappear).
Patients with cardiac cirrhosis of the liver often have poor tolerance to medications, especially increased sensitivity to digitalis and strophanthin, apparently with a violation of the neutralizing function of the liver.
The basis for the diagnosis of cardiac cirrhosis is the presence of prolonged decompensation in diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, and cor pulmonale. A functional study of the 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. Radioisotope studies of liver function reveal pronounced disturbances.
The presence of cardiac cirrhosis in itself does not significantly worsen the prognosis and, if cardiac damage is treated, cirrhosis can proceed latently, without a tendency to periodic exacerbations of the process. CARDIAL JAUNDICE
Despite the fact that overt jaundice in patients with symptoms of liver congestion and cardiac cirrhosis is rare, the concentration of bilirubin in the serum increases relatively often. Jaundice occurs with equal frequency both with congestion in the liver and with cardiac cirrhosis. Many authors have obtained a statistical correlation between the intensity of jaundice and venous pressure in the right heart. In addition, pulmonary infarction plays a role in the development of jaundice. Thus, out of 424 autopsies of those who died from heart disease, 4% had jaundice, of which 10.5% of cases had a heart attack (Kugel, Lichtmann).
The yellowness of the skin and sclera in cardiac cirrhosis is slight, there is no itching. The uneven coloring of the skin is noteworthy. Thus, in places of massive edema, the skin is not yellow due to the fact that bilirubin circulating in the blood is bound to protein and does not enter the edematous fluid. In a small number of patients, jaundice acquires the features of mechanical jaundice: intense, with a grayish tint, coloring of the skin, pigments in the urine and light-colored feces are noted.
The mechanism of jaundice in circulatory disorders is different.
(1) Hepatic jaundice. There is an assumption that when the heart is damaged, liver cells inadequately excrete all pigments and, indeed, the most intense jaundice is observed in patients with severe and widespread necrosis of liver cells. However, there are exceptions to this rule, when in case of tricuspid valve insufficiency with severe liver damage, jaundice is not observed.
(2) Obstructive jaundice. Compression of the bile capillaries due to a sharp increase in venous pressure inside the lobules, as well as the formation of blood clots in the bile canaliculi, as a consequence of the slow flow of bile in the biliary system, create conditions for cholestasis.
(3) Hemolytic jaundice is often combined with tissue hemorrhages, especially pulmonary infarctions. The sudden appearance of jaundice in the clinical picture of a heart attack is known: be it of the lung, spleen or kidneys, while heart attacks of the same location, but without damage to the heart, do not produce jaundice.
An additional hemoglobin depot is created at the site of the infarction, from which bilirubin is formed. This excess pigment cannot be bound by the altered liver cells. Rich and Resnik injected into the tissue of patients with heart disease an amount of blood corresponding to that found in pulmonary infarction, and noted an increase in serum bilirubin. There is also an excess of pigment in the tissues during congestion in the lungs due to heart damage, since even without a heart attack, congestion in the lungs leads to the destruction of hemoglobin.
Consequently, jaundice with heart lesions is in most cases of mixed type; The most important are lesions of liver cells and their overload 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 feces are 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, and 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!

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

How does pathology develop?

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

The pathogenesis of heart failure can be described as follows:

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

Symptoms of heart failure may develop:

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

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

Symptoms of the disease

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

left ventricular;
right ventricular;
mixed.

Left ventricular

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

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

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

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

Right ventricular

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

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

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

Mixed

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

The influence of age on the severity of symptoms

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

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

Newborns

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

In newborns, the pathology manifests itself:

severe shortness of breath;
increased heart rate;
cardiomegaly;
enlarged spleen and liver;
sluggish sucking or complete refusal from food;
bluishness of the skin.

Such children are immediately sent to the intensive care unit.

Children of preschool and primary school age

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

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

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

Teenagers

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

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

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

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

Aged people

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

How are manifestations of pathology classified?

Cardiologists classify chronic heart failure according to:

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

Stages of compensation

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

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

Phases of violation

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

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

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

Causes of chronic disease

The reasons why heart failure occurs may be different, but chronic heart failure is always a complication of another pathological process in the body.

CHF can become a complication:

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

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

Acute form of pathology

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

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

cardiac tamponade;
valve malfunction;
heart attack;
pericardial thromboembolism;
atrial fibrillation;
blood loss;
left chest injury.

The diagnosis of acute heart failure is established quickly:

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

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

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

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

Diagnostic measures

The main methods for diagnosing heart failure are:

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

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

The etiology of the disease is determined through additional examinations:

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

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

Features of the treatment process

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

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

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

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

Cardiac cirrhosis of the liver - the end of heart failure

Liver cirrhosis is a chronic disease in which there is a violation of the structure of the liver: the arrangement of cellular elements, bile ducts, as well as dysfunction of hepatocytes - liver cells.

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

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

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

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

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

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

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

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

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

The prognosis, unfortunately, is unfavorable.

Acquired heart defects in children and adults

Classification
Mechanism of occurrence
Most frequent vices hearts
Diagnostics
Treatment

Acquired heart defects are permanent abnormalities in the structure of the heart valves that appear as a result of diseases or injuries.

What is damaged by heart defects? Brief anatomical information

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

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

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

Classification of valve problems

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

For reasons of occurrence ( etiological factor) distinguish vices:

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

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

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

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

compensated;
subcompensated;
decompensated.

According to the location of the valvular lesion:

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

According to the form of functional impairment:

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

The mechanism of heart defects

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

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

Scar deformation of the valve leaflets, wrinkling or complete destruction causes their deficiency.

As stenosis develops, resistance to blood flow increases due to mechanical obstruction. In case of valve insufficiency, part of the ejected blood returns back, causing the corresponding chamber (ventricle or atrium) to perform extra work. This leads to compensatory hypertrophy (increase in volume and thickening of the muscle wall) of the heart chamber.

Gradually in hypertrophied section heart, dystrophic processes and metabolic disorders develop, leading to decreased performance and, ultimately, to heart failure.

The most common heart defects

Mitral stenosis

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

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

Symptoms

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

Mitral regurgitation

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

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

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

Tricuspid insufficiency

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

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

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

Tricuspid stenosis

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

There are no complaints for a long time, then it develops rapidly atrial fibrillation and congestive heart failure. Thrombotic complications may occur. Externally, acrocyanosis (blueness of the lips, nails) and a jaundiced tint of the skin are determined.

Aortic stenosis

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

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

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

Aortic insufficiency

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

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

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

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

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

Combined and associated acquired defects

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

Diagnostics

Held comprehensive examination patient:

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

Treatment methods for acquired heart defects

It is possible to achieve the elimination of pathological changes in the heart valves caused by defects only operationally. Conservative treatment serves as additional means to reduce the manifestations of the disease.

Main types of operations for heart defects:

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

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

Prevention

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