Stagnation of venous blood in the liver treatment drugs. Association of liver damage with heart failure

Liver is a gland involved in the metabolism of proteins, fats, vitamins. The liver produces bile, the lack of which in the body leads to violations of the digestive process. The liver filters the blood that circulates through the body to keep out toxic substances and microorganisms that are absorbed into the blood through the gastrointestinal tract. The most common liver diseases are hepatitis A and B, fatty liver in alcoholism, gallstones formed due to stagnation of bile, infection, impaired cholesterol metabolism.

Traditional healers offer many ways liver cleansing. There is a cleaning technique according to G. Malakhov, according to E. Shchadrin, according to A. Zaraev, according to O. Eliseeva according to K. Nishi, according to N. Walker. In general, a lot and with the use of various ingredients. The procedures are responsible, and the attending physician should recommend them, as he knows what condition your liver is, and general state health. Before applying the author's methods of cleansing the liver and gallbladder, you should undergo an examination. Large stones are not removed, they can only be removed surgically. Moreover, if you proceed to the expulsion of stones from the gallbladder without examining, you can provoke emergency surgery. Be extremely responsible for your health.

But the fact that the liver will need to constantly help to cope with its functions should be known to everyone who has deviations in the health of the liver. Doctors often prescribe choleretic herbs and drugs in such cases.

Folk methods treatment of congestion in the liver offer to cleanse the liver with choleretic herbs and fees.

Liver signals about problems with bitterness in the mouth, heaviness and pain in the right hypochondrium, instability of the stool, as well as health problems of the pancreas.
Of course, in such cases, consultation with the attending physician should be.
But there are also folk remedies, herbs that have choleretic diuretic and analgesic effects.

10 gr. (1.5 tablespoons) St. John's wort herbs placed in an enamel bowl, pour a glass of boiling water (200 ml), close the lid and steam in a water bath for 30 minutes. Cool, strain, add boiled water to 200 ml. Drink 1/3 cup 3 times a day 30 minutes before meals. The decoction can be stored at a cool age for no more than 2 days.

Wash 3 fresh beets. cut into small cubes, put in a three-liter jar, add 2 tablespoons of white flour, 500 grams of sugar. Close the jar with a plastic lid and put in a dark place at room temperature for two days. Stir twice a day. Then add 700 grams of pitted and tailless raisins, 4 cups of sugar, ½ cup of water and leave to ferment for 7 days. Strain, you get 1 liter of beet kvass. The course of cleansing requires 3 liters of beet kvass. Take 1 tablespoon before meals for 30 minutes. After a 3-month break, repeat the course.

Take 1 tablespoon of a mixture of wild strawberry berries and leaves, brew, insist for 20 minutes. Then strain the infusion and take ½ - 1 cup of infusion 3 times a day for up to 3 weeks. After 2 weeks, the treatment can be repeated. Not only the liver is treated, but also the vascular system from salt deposits. ethnoscience recommends it for diseases of the gastrointestinal tract, gastritis, kidney stones, beriberi. And fresh fruits, and leaves, their water infusion, used for general loss of strength, anemia, liver disease and biliary tract, at uterine bleeding, jaundice, rickets, hemorrhoids. For children, especially weakened after an illness, fresh berries with milk and sugar are very useful - as a nutritious and tonic. The outstanding Swedish botanist Carl Linnaeus, who suffered from gout for many years, got rid of this disease using only one medicine - fresh strawberries.

With the help of smoke, you can remove the bitterness in the mouth, and with the help of chicory, increase the secretion of bile and eliminate congestion in the liver.
Infusion: 2.tsp. dry grass dymyanka insist 2 hours in 2 cups of boiling water, strain. Drink 0.5 cup 3 times a day before meals for diseases of the liver and biliary tract, cholelithiasis.

Decoction: 1 teaspoon of crushed chicory roots pour 2 tbsp. boiling water, boil for 10-15 minutes. Drink 0.5 tbsp. 3 times a day half an hour before meals.

Infusion: 1 tbsp. crushed chicory roots pour 1 cup of boiling water, leave for 2 hours, strain. Drink ¼ cup 3-4 times a day before meals.

There are many choleretic herbs, such as immortelle, St. John's wort, milk thistle, calendula, corn stigmas, strawberry leaves, rose hips, etc. It is important when choosing herbs to select anti-inflammatory properties, choleretic properties, blood-purifying properties, antispasmodic properties.

Pay attention to milk thistle, which not only has a choleretic property, but also restores liver cells during inflammation, restores intestinal motility. Milk thistle is the king herb for liver repair. You can use it for a long time up to a year or more, until the liver cells are completely restored. Solyanka hilly has the same property. Milk thistle oil has the same properties. But, I emphasize, it is best to use ground milk thistle powder,. The main component of milk thistle is a rare biologically active substance- silymarin. It is silymarin that has a hepatoprotective effect, restoring the affected areas of the liver. It stimulates the formation of new liver cells, protects the liver and kidneys from destruction by alcohol, has an anti-inflammatory and wound-healing effect in diseases of the gastrointestinal tract. Also used for cirrhosis, hepatitis, jaundice, with weakened immunity. Method of application, during meals, you can use 1 teaspoon of dry powder, or pour a little boiled water and eat with food.

You can use up to 3 times a day, depending on your health condition. Doctors often recommend us Karsil, medicine with liver disease, medicinal beginning there is also silymarin. The course of treatment with Karsil is up to 3 months. But, I think that it is easier and more reliable to cook it yourself. given that our pharmacology is now far from reliable.

Pay attention to the fact that the herbs used do not thicken your blood, as this complicates the work of the liver.

Grind 1 cup of rose hips in a porcelain or wooden mortar (vitamin C is oxidized in an iron mortar), pour 1 liter of boiling water, wrap well and leave to infuse for a day. 3 cups oats, rinsed warm water, pour into a 5-liter enameled pan and pour 4 liters of cold water, then close the lid and insist for a day, then add 2 tablespoons of birch buds, 3 tablespoons of lingonberry leaves, bring the mixture to a boil and simmer over low heat 5 minutes. Then add 2 tablespoons corn silk and 3 tablespoons of knotweed and boil over low heat for 15 minutes. Leave the mixture for 45 minutes, strain. Add the prepared rosehip infusion, pour the mixture into dark glass bottles and refrigerate. Take 150 ml 4 times a day half an hour before meals. The last appointment should be no later than 19 hours. The course of treatment is 10 days, i.e. you need to prepare 2 such portions of the medicinal composition.

Take a few heads of beets, peel, wash and boil. Then boil this mixture until it becomes like syrup. Drink ¾ cup several times a day. Experts say that gallstones dissolve pretty quickly.

And yet, to cleanse the liver of toxins, of stagnant bile, of cholesterol, of mucus, one sometimes has to do liver tube. This procedure is simple, it can be done with different ingredients. True, the pebbles during this procedure are not expelled and do not dissolve. But to alleviate and help the liver, this procedure will undoubtedly help, although you should not abuse this procedure, it is better to do it no more than once a week.

With honey: dilute 1 tablespoon of honey in 1 glass of warm mineral water, drink in sips, put warm heating pad lie on the liver area for 30 minutes. Then another 1 glass of warm mineral water and lie down for 45 minutes. Then have a light breakfast.

With cholenzym: 5-6 dragees pour 1 tbsp. warm mineral water and then on the same principle as described above.

With xylitol: dilute 2-3 teaspoons in 0.5 liters warm water divided into 2 doses. And take the same as in the first two methods.

With biliary dyskinesia, pay attention to the nervous system, eliminate stress in your life.

When heart failure develops, the symptoms increase gradually, sometimes the process of developing the disease takes more than 10 years. In many, the disease is detected already when, due to the inability of the heart to provide a full blood supply to the organs, various complications arise in people. But complications can be avoided if the treatment of 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 the development of the disease.

The pathogenesis of heart failure can be described as follows:

under the influence adverse factors volume decreases cardiac output;
to compensate for insufficient emission, compensatory reactions of the body are connected (there is a thickening of the myocardium, an increase in heart rate);
for some time, compensation processes make it possible to ensure a full blood supply to organs and tissues due to the work of the organ with an increased load;
but the enlarged myocardium requires more blood to full-fledged work, and the coronary vessels can only transport the previous volume of blood and cease to cope with providing the muscle with nutrients;
insufficient blood supply leads to ischemia individual sections heart and myocardium due to lack of oxygen and nutrients contractile function decreases;
as you go down contractile function the value of cardiac output decreases again, the blood supply to the organs worsens, 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 the years and often occurs as a complication of heart or vascular disease. In most cases, timely identified early stage CHF is reversible.
Fast. Acute heart failure occurs suddenly, all symptoms grow rapidly and compensatory mechanisms often do not have time to stabilize blood flow. If the acute violations that have arisen are not eliminated in a timely manner, they will end in death.

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

Symptoms of the disease

Manifestations of heart failure will depend on the degree compensatory mechanism and on which part of the heart is more disturbed. Types of heart failure are distinguished:

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;
constant feeling of fatigue, drowsiness and impaired concentration may occur;
sleep disturbance;
pallor and cyanosis of the skin;
the cough is initially dry, but as the disease progresses, scanty sputum appears.

With the development of the disease, a person begins to suffocate while lying on his back, such patients prefer to sleep in a semi-sitting position, putting several pillows under their backs.

If the treatment of heart failure was not started in a timely manner, then 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 manifest themselves taking into account the tissues or organs in which congestion has occurred. But the general symptoms will be:

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

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

mixed

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

Effect of age on symptom severity

The age of the patient also affects the symptoms of the disease. By age groups allocate:

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

newborns

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

In newborns, pathology manifests itself:

severe shortness of breath;
increased heart rate;
cardiomegaly;
enlargement of the spleen and liver;
sluggish sucking or complete failure from food;
cyanosis of the skin.

Such children are immediately sent to the intensive care unit.

Children of preschool and primary school age

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

Such children try to move less, avoid outdoor games, and it is difficult for them to concentrate on a specific task. Schoolchildren's performance is declining.

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

Teenagers

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

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

If CHF is suspected, it is necessary to conduct full examination adolescent, in order to timely 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 disease, then in most cases the symptoms are pronounced and suggest the presence of pathology.

Elderly people

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

How are manifestations of pathology classified?

In cardiologists, the classification of chronic heart failure is adopted according to:

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

Stages of compensation

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

Compensated or degree 1. It is quite difficult to diagnose the disease in this period, the first signs may not appear in any way or occur only after a significant physical activity. If changes in the myocardium are detected on initial stage, it is possible in most cases to cure heart failure by eliminating the provoking factor and conducting a course of maintenance therapy. But at the first degree, the disease is detected only by chance, during a routine medical examination.
Decompensated. First, moderate heart failure appears with shortness of breath on exertion and a feeling of increased fatigue. Gradually, the symptoms increase, shortness of breath appears at rest, the skin becomes pale cyanotic, swelling appears different localization, rapid heart rate may be long time. What is the danger of chronic heart failure not treated in a timely manner? The fact that with the development of congestive phenomena of blood circulation, irreversible ischemic disorders occur in the vital systems of the body. Heart failure of the decompensation stage is not completely cured, the treatment process is aimed at relieving symptoms and slowing down the progression of pathological processes.
Terminal. Medicines at this stage are ineffective, the patient has undergone dystrophic changes in all vital important organs, and violated water-salt exchange. These patients are in the hospital and nursing process in chronic heart failure in the terminal stage is aimed at alleviating pain patient and provide comprehensive care.

Phases of violation

Depending on the phase in which the violation of the contractile function occurred, there are:

systolic (gastric 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 (completely impaired contractile function).

But what are the causes of chronic heart failure? Why is the work of the heart disturbed?

Causes of chronic disease development

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 cor pulmonale;
hypertension;
anemia;
endocrine diseases (more often with impaired thyroid function);
toxic infections;
oncological processes.

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

Acute form of pathology

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

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

cardiac tamponade;
malfunction of valves;
heart attack;
pericardial thromboembolism;
ciliated ventricular arrhythmias;
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 determined on the cervical artery;
breathing becomes shallow and frequent;
the skin becomes sharply pale and acquires a bluish tint;
consciousness is confused or disappears.

The sooner treatment of acute heart failure is started, the more favorable the prognosis for the patient. If there is a suspicion of acute heart failure syndrome, then 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 can be given to the victim, but you can wet cold water a napkin and put the sick person on the head.

Seeking medical help cannot be neglected; for the treatment of acute heart failure, the help of a cardiologist is necessary. Even if it seems that the patient has become better, this does not mean that the victim is recovering full-fledged work of the myocardium: 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 exhausted and will fail at some 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 work of the heart is heard through the phonendoscope);
taking an ECG.

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

The etiology of the disease is clarified with the help of additional examinations:

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

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

Features of the treatment process

But drugs to stop the symptoms and treatment brought relief to well-being, not the most important thing in the treatment process. Of course, so that the symptoms characteristic of heart failure do not progress further, treatment with pills and injections is necessary. But, in order to reduce the risk of complications, lifestyle in heart failure should exclude all provoking factors:

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

In order not to aggravate heart failure, prevention by changing lifestyle and diet is no less important than the drugs that must be taken to maintain the full functioning of the myocardium.

It is necessary to perceive cardiac insufficiency as a serious pathological deviation of the work of the myocardium and, at the first suspicion of its development, make an ECG. This procedure takes only a few minutes and will allow you to identify the disease at an early stage of development. A timely identified cardiac abnormalities are easily treatable.

Cardiac cirrhosis of the liver - the end of heart failure

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

This condition often develops due to exposure toxic substances(alcohol, toxins) or is the result 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 with a decrease in the pumping function of the heart (heart failure), blood stasis develops in all organs, and the liver, being an organ rich in blood vessels, suffers from this stagnation more than others.

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

It is sometimes impossible to distinguish ordinary liver cirrhosis from cardiac cirrhosis based on complaints, examination, tests or ultrasound data. Most often, such patients are concerned about the severity and pain in the right hypochondrium, icterus of the skin and visible mucous membranes, itching of the skin due to the accumulation of bilirubin in it. Also, due to the effusion in the abdominal cavity, "abdominal dropsy" - ascites - develops.

With a pronounced stagnation, the outflow of blood through the liver is sharply hampered 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.

Expansion 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 "jellyfish head".

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

Unfortunately, cardiac cirrhosis of the liver is an extremely unfavorable condition that aggravates the course of already severe cardiac pathology. If it is also marked 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 the elimination of symptoms: the fight against edematous syndrome, detoxification and slowing down the progression of cirrhosis.

The prognosis, unfortunately, is unfavorable.

Acquired heart defects in children and adults

Classification
Origin mechanism
Most common heart defects
Diagnostics
Treatment

Acquired heart defects are persistent disorders of the structure of the heart valves that have appeared as a result of diseases or injuries.

What is damaged in heart defects? Brief anatomical note

The human heart is four-chambered (two atria and two ventricles, left and right). The aorta originates from the left ventricle, the largest blood duct in the body, and 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 departing from it, there are valves - derivatives of the mucous membrane. Between the left chambers of the heart is the mitral (bicuspid) valve, between the right - tricuspid (tricuspid). At the exit to the aorta is the aortic valve, at the beginning pulmonary artery- pulmonary valve.

Valves increase the efficiency of the heart - they prevent the return of blood at the time of diastole (relaxation of the heart after its contraction). When the valves are damaged by a pathological process, the normal function of the heart is impaired to one degree or another.

Classification of valve problems

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

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

rheumatic (in patients with 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 (deformation of the valves due to the atherosclerotic process in adults);
syphilitic;
after suffering endocarditis (inflammation of the inner heart membrane, the derivatives of which are valves).

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

with a slight violation of hemodynamics;
with moderate impairments;
with severe impairments.

By violation general hemodynamics(whole body scale):

compensated;
subcompensated;
decompensated.

According to the localization of the valvular lesion:

monovalvular - with isolated damage to the mitral, tricuspid or aortic valve;
combined - a combination of damage to several valves (two or more), mitral-tricuspid, aortic-mitral, mitral-aortic, aortic-tricuspid defects are possible;
three-valve - with the involvement of 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 occurrence of heart defects

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

If at the same time there is an fusion of the valves or their pathological rigidity (rigidity), stenosis develops.

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

With the development of stenosis, resistance to blood flow increases due to a mechanical obstruction. In case of valve insufficiency, some of the ejected blood returns back, forcing the corresponding chamber (ventricle or atrium) to do additional work. This leads to compensatory hypertrophy (increase in volume and thickening of the muscular wall) of the heart chamber.

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

Most common heart defects

mitral stenosis

The narrowing of the message between the left chambers of the heart (atrioventricular orifice) is usually the result of a rheumatic process or infective endocarditis, which causes fusion and hardening of the valve leaflets.

vice can for a long time not manifest itself in any way (remain in the compensation stage) due to the growth muscle mass(hypertrophy) of the left atrium. When decompensation develops, blood stagnation occurs in the pulmonary circulation - the lungs, the blood from which is obstructed when it enters the left atrium.

Symptoms

If the disease occurs in childhood, the child may lag behind in physical and mental development. Characteristic for this defect is a blush in the form of a "butterfly" with a bluish tint. The enlarged left atrium compresses the left subclavian artery, so there is a pulse difference on the right and left hand (on the left of less filling).

Mitral insufficiency

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

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

The patient is concerned about palpitations, shortness of breath, decreased exercise tolerance, weakness. Then, swelling of the soft tissues of the limbs joins, an increase in the liver and spleen due to stagnation of blood, the skin begins to acquire a bluish tint, the jugular veins swell.

Tricuspid insufficiency

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

Since the vena cava, collecting blood from all parts of the body, flows into the right heart chambers, venous congestion develops with tricuspid insufficiency. The liver and spleen increase due to overflow with venous blood, fluid collects in the abdominal cavity (ascites occurs), and venous pressure rises.

May interfere with the function of many 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

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

For a long time there are no complaints, then it develops rapidly atrial fibrillation and congestive heart failure. Thrombotic complications may occur. Outwardly, acrocyanosis is determined (cyanosis of the lips, nails) and an icteric skin tone.

aortic stenosis

Aortic stenosis (or stenosis of the aortic mouth) is an obstacle to the blood coming from the left ventricle. There is a decrease in the release of blood into arterial system, from which, first of all, the heart itself suffers, since those who feed it coronary arteries depart from the initial section of the aorta.

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

A decrease in cardiac output is manifested by low blood pressure and a weak pulse.

Aortic insufficiency

In case of insufficiency of the aortic valve, which normally should block the exit from the aorta, part 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 for a long time, the function of the heart remains at a sufficient level, so there are no complaints.

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

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

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

Combined and associated acquired malformations

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

Diagnostics

Held comprehensive examination patient:

When questioning the patient, they find out past illnesses(rheumatism, sepsis), bouts of chest pain, poor tolerance physical loads.
Examination reveals shortness of breath, pale skin with a bluish tint, swelling, pulsation of visible veins.
The ECG reveals signs of rhythm and conduction disturbances, phonocardiography reveals a variety of noises during the work of the heart.
Radiographically determined hypertrophy of one or another part of the heart.
Laboratory methods are of secondary importance. Rheumatoid tests may be positive, cholesterol and lipid fractions are elevated.

Methods of treatment of acquired heart defects

To achieve the elimination of pathological changes in the heart valves caused by a defect, it is possible only by surgery. Conservative treatment serves as an additional means to reduce the manifestations of the disease.

The main types of operations for heart defects:

At mitral stenosis the soldered valve leaflets are separated with a simultaneous expansion of its opening (mitral commissurotomy).
At mitral insufficiency the failed valve is replaced with an artificial one (mitral prosthesis).
At aortic defects similar operations are carried out.
With combined and combined defects, prosthetics of destroyed valves are usually performed.

The prognosis for a timely operation 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 valvular problems, in fact, is the prevention of the incidence of rheumatism, sepsis, syphilis. It is necessary to timely eliminate the possible causes of the development of heart defects - to sanitize infectious foci, increase the body's resistance, eat rationally, work and rest.

The liver is a severe chronic liver disease characterized by the irreversible death of liver cells as a result of chronic inflammation, followed by the destruction of the liver tissue and the growth of connective tissue in it (a tissue that does not contain cells, only collagen fibers), as a result, it increases in size, and violation of all its functions. The word "cirrhosis" comes from the Greek word "kirrhos", translated as "yellow", which characterizes the connective tissue that replaces the liver tissue.

In economically developed countries, it is one of the main causes of death in the return from 40 to 60 years. High mortality is associated with the rapid progression of the disease, severe complications, and most often incidental discovery of the disease and late referral for medical care. Middle-aged men are more likely to get sick than women, in a ratio of about 3:1, this is associated with chronic alcohol use, so the alcoholic form of cirrhosis is more common. In second place viral form, develops as a result of contact "blood with infected blood" by specific viruses, the risk group is blood transfusions, drug addicts, medical personnel.

Cirrhosis of the liver develops very slowly (many years, up to about 15 years or more), but its rapid development is also possible, when adverse factors are exposed to the body. The life expectancy of a patient with cirrhosis depends on the cause of its development, and the stage at which the disease was detected. Patients with undiagnosed cirrhosis of the liver, unaware of their disease, are admitted to the hospital with other causes (chronic gastritis, cholecystitis, peptic ulcer, etc.).

Liver anatomy

The liver is an organ of the digestive system, weighing approximately 1500 grams, located in the upper abdomen (belly), more on the right. In shape, it resembles a hat of a large mushroom, red-brown in color, soft texture. The liver consists of two large lobes (left and right), and 2 small lobes (square caudate). There is an indentation in the liver where it is located gallbladder, it accumulates bile formed by the liver, which enters the intestine under the action of which the digestion of certain products (fats) occurs. On the lower surface of the right lobe, there is a depression with vessels, called the gates of the liver, the portal vein and the hepatic artery enter them, and the inferior vena cava and the common bile duct exit.

The liver is covered with a serous membrane, supplied with blood vessels and nerves. Liver tissue formed by liver cells (hepatocytes), which are arranged radially in groups and form hepatic lobules, each 1–2 mm in size. Around each lobule are interlobular veins, which are branches of the portal vein, blood flows from the organs through them for further purification (detoxification) in the liver. Purified by liver cells, blood central veins(located in the center of the lobule), enters the hepatic veins and then into the inferior vena cava (which gives blood to the heart). Interlobular arteries, accompanied by interlobular veins, they saturate the liver with oxygen, which are a continuation of the hepatic arteries. Bile tubules pass between the liver cells, which flow into the bile ducts, with the help of which the bile formed by the liver is carried to the gallbladder for further participation in digestion.

Video about the structure of the liver

Liver functions

Detoxification function of the liver: destruction (neutralization) harmful substances and removing them from the body (toxins, medicines, poisons and others), as a result of various chemical reactions.
Excretory function: the formation of bile in the liver cells (from 500 to 2000 ml is formed per day) and its secretion into the bile ducts to participate in digestion.
Metabolism: participates in the metabolism of fats, proteins, carbohydrates, produces (synthesizes) vitamins, participates in the destruction of hormones (female sex hormones estrogen, adrenaline and norepinephrine), forms enzymes involved in digestion, produces the necessary energy for the life of the body.
Participates in the processes of coagulation and hematopoiesis: some blood coagulation 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.
It is a warehouse containing the necessary substances for the body: if necessary, it supplies the body with vitamins, minerals (iron), energy and others.
Control normal composition blood: in case of liver disease, the blood changes its composition, as a result of which the functions of organs, the most sensitive brain, are disrupted, as a result, various deviations occur.

Causes of cirrhosis

Alcohol and smoking	As a result of chronic alcohol consumption, smoking occurs toxic effect on liver cells and their chronic inflammation, later they are replaced by connective tissue and the development of liver cirrhosis.
Viral hepatitis	More often and faster, hepatitis C leads to cirrhosis of the liver (persons become infected when a large volume of infected blood enters their blood: blood transfusion), as a result of infection with hepatitis B and D, chronic inflammation of the liver occurs, and cirrhosis develops after many years, in the absence of treatment. Infection with hepatitis B and D occurs with minimal contact "blood with infected blood", risk groups are: blood transfusion, drug addicts, donors, surgical interventions, medical staff).
Diseases of the bile ducts	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. lead to stasis of bile the following diseases: narrowing of the biliary tract (congenital anomalies of the biliary tract or their absence, surgical interventions), blockage of the biliary tract (stones, tumors, congenital pathology immune system).
Long term use toxic medicines	Antibiotics, sleeping pills, antiviral, anti-inflammatory drugs with constant and dilute intake have a chronic toxic effect on liver cells, their inflammation with the further development of liver cirrhosis.
Prolonged stagnation of venous blood in the liver	It is observed in diseases of the vessels and the heart: in heart failure, pericarditis, heart defects and others. The pressure in the inferior vena cava increases, and therefore in the hepatic veins. The liver overflows with blood and increases in size, this leads to compression of the arteries that feed the liver cells, as a result they die and are replaced by connective tissue, thus developing cirrhosis of the liver.
Autoimmune liver disease	The process by which the body perceives its own cells as foreign, due to congenital disorder there is a production of substances in the body that destroy liver cells (or other cells), autoimmune hepatitis develops and further development of cirrhosis.
Metabolic disorders(hemochromatosis)	hereditary disease transmitted genetically, accompanied by the accumulation of iron in various bodies and tissues, including in the liver, a violation of the structure of cells with subsequent proliferation of connective tissue.

Read more about gallstone disease in the article: gallstones .

Symptoms of cirrhosis

	Approximately 20% of patients with cirrhosis of the liver are asymptomatic (without manifestations visible to the patient) and are detected by chance during examination for another disease. In other patients, cirrhosis of the liver is manifested by some signs, their number and degree of manifestation depends on the level of damage to the liver cells and the activity of the process:
Enlargement of the liver in volume	Due to the growth of connective tissue in it, which occupies a large area.
Pain in the right hypochondrium	Aching, aggravated after eating or exercise, are the result of an increase in the liver in volume and stretching of the capsule. The capsule contains sensitive nerve receptors that form a pain symptom.
Dyspeptic manifestations	Heaviness in the right hypochondrium, decreased 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.
General weakness	Fatigue, decreased performance due to insufficient liver production essential substances, for the organism.
Temperature rise	Occurs as a result of chronic inflammation in the liver
Increased bleeding	Frequent bleeding from the nose, gums - the result of insufficient production of blood clotting factors, or massive bleeding from the veins of the esophagus (due to increased pressure in the portal vein, it in turn connects to the veins of the esophagus)
Jaundice of the skin and sclera of the eyes	Dark urine and light feces, develops as a result of a high level of bilirubin in the blood (due to stagnation of bile and destruction of the small bile ducts) and a violation of its outflow into the digestive tract.
Skin itching	The skin itches due to the accumulation of bile acids in it (contained in bile), more often this symptom is present during the development of cirrhosis as a result of a violation of the outflow of bile.
Anemia	An increase in the concentration of toxic substances in the blood has a damaging effect on red blood cells, life cycle which is shortened.
Enlargement of the spleen	Blood flows from the spleen into hepatic vein. Due to impaired blood flow in the liver, there is an increase in pressure in the splenic vein, which leads to its overfilling with blood and an increase in size.
Vascular asterisks	Reddening of the palms "liver palms" develop as a result of expansion of the capillaries of the skin (due to advanced level estrogen)
Thickening of the mammary glands in men	It develops as a result of disruption of the breakdown and an increase in the concentration of female sex hormones (estrogens)
Abdominal fluid and enlargement (ascites)	Occurs due to a significant increase in pressure in the hepatic (portal vein). Blood, which normally should flow from the intestines to the liver, stagnates from the intestinal vessels, and its liquid part sweats into the abdominal cavity.
Edema	Elastic, appear on any part of the body, at any time of the day and persist for a long time until the effect of treatment (due to the lack of protein production by the affected liver)
Weight loss	Associated with a lack of providing the body with proteins, fats, carbohydrates
Decreased immunity	Insufficient production of proteins (antibodies) involved in the formation of immunity (colds, flu, and other infections quickly join)
Encephalopathy	Develops in late stage, or in the absence of treatment, manifests itself in the form of drowsiness, tremor, later confusion, disorientation in time and / or space, with this condition the patient must be urgently hospitalized.

Diagnosis of cirrhosis: laboratory parameters (blood biochemistry and coprology), ultrasound, CT

	General analysis blood	decrease in hemoglobin ( decrease in the level of red blood cells (12), decrease in platelets (9), an increase in the number of leukocytes (> 9 * 10 9), increased erythrocyte sedimentation rate (>15mm/h).
	Biochemical analysis blood	Decreased total protein Increase in ALAT>46U/L, and ASAT>41U/L An increase in the level of total: bilirubin> 20.5 μmol / l, more often due to bound bilirubin> 15.5 μmol / l Increase in glucose >5.5 mmol/l Decreased fibrinogen Decreased prothrombin Increase in alkaline phosphatase>270 U/l Decreased Na Decreased Ca
	Viral hepatitis markers	If cirrhosis has developed as a result of viral hepatitis, then there will be positive markers for hepatitis: HBsAg, Anti-HBs, Anti-HBc, HCV-RNA.
	Coprological analysis	steatorrhea (fat in the stool due to fat metabolism), creatorrhea (undigested proteins in the stool), discoloration of feces (due to lack of bilirubin).
	Ultrasound of the liver	The liver is enlarged, fibrosis manifests itself in the form of a decrease in echogenicity, and inflammatory areas where fibrosis has not yet formed, manifests itself in the form of an increase in echogenicity, the contour of the liver is not even, a wavy surface, the walls of the portal vein are thickened, the gallbladder is deformed and enlarged, increased diameter of the lower vena cava.
	Liver scan	Liver function assessment, absorption healthy cells radioisotope, if there are few of them, then absorption decreases and the result is a depletion of the liver pattern.
	CT scan	Study on the screen of transverse and longitudinal sections of the liver (its size, irregularities, nodes in cirrhosis).
	Liver biopsy	the most informative, invasive method allows you to determine which tissue forms the liver (with cirrhosis, it consists of connective tissue).

Read more about the diagnosis of liver diseases in the articles: liver tests, diagnosis of viral hepatitis B.

Treatment of cirrhosis

Medical treatment

The use of drugs for liver cirrhosis is determined by the attending physician individually, depending on the clinical manifestations and severity of the disease.
Groups of drugs used in liver cirrhosis:

Hepatoprotectors (Essentiale, Liv.52, vitamin B group), protect liver cells from damage, improve metabolic processes in them, increase the secretion of bile by liver cells. They are a group of choice for liver diseases. Lif.52 is used 2 tablets 3 times a day, treatment with this group of drugs is long, it can last for a month, depending on the degree of liver damage.
Vitamins are prescribed to all patients, due to their deficiency in the body (the production of vitamins by the affected liver is disrupted), metabolic processes in the liver. Appointed by courses of treatment, at least 2 times a year. Vitamin B1 20-50 mg once a day (1 ml-2.5-5%).
Glucocorticoids (Prednisolone, Dexamethasone) are used for active cirrhosis (cirrhosis that progresses very quickly) of viral origin, with active cirrhosis, which develops as a result of a violation of the outflow of bile, the presence of encephalopathy.
Pancreatic enzymes (Mezim, Pancreatin), eliminate dyspeptic symptoms (nausea, vomiting, constipation, bloating), in case enzyme deficiency liver and pancreas, medications of this group, make up for this deficiency and digestion is normalized. Mezim is used 2 tablets during meals, the duration of treatment with enzymes is set individually by the attending physician.
Prokinetics (Metoclopramide) - eliminate bloating and have an antiemetic effect, by increasing intestinal motility. Assigned to patients with severe vomiting and bloating, one tablet (10 mg) 3 times a day. The duration of treatment with this group of drugs depends on the patient's condition (complete or partial elimination of the above symptoms).
Adsorbents (Activated carbon, Enterosorbent) are used to cleanse the intestines and increase the detoxification function of the liver, as a result of their adsorption of toxic substances. Activated charcoal is taken 1 tablet (250 g) for every 10 kg of the patient (50 kg - 5 tablets, but not more than 7 tablets) at one time 20-30 minutes before meals, 3 times a day, the course of treatment is 10-14 days.
Bile acids(Ursodeoxycholic acid), are used for all patients with cirrhosis of the liver, as they stimulate the contraction of the walls of the gallbladder, the excretion of bile, preventing its stagnation. Medium daily dose up to 10 mg / kg, taken in the evening before bedtime, the duration of treatment depends on the severity of congestion, it is determined by the attending physician.
Diuretic drugs (Veroshpiron, Furosemide), used in patients with ascites (fluid in the abdomen), and with edema.
Antivirals(interferon) are prescribed to patients with liver cirrhosis of viral origin.
Probiotics (Linex, Bifidumbacterin), to restore normal intestinal microflora, contain intestinal bacteria that are involved in digestion. They are prescribed to patients suffering from diarrhea, not cured by antibiotics, and bloating. Linex is prescribed 2 capsules 3 times a day for 2-4 weeks.
Transfusion therapy is used in a hospital (blood products: erythrocyte mass, plasma, electrolytes), is used for massive bleeding, the presence of ascites (fluid in the abdomen), encephalopathy.

Diet and folk remedies

Folk methods are only an addition to other methods of treatment (medication, surgery). First of all, avoid alcohol and smoking. Secondly, all patients should have a lot of rest, walk in the fresh air, eat right. The food consumed by patients with cirrhosis of the liver should be lightly salted, without seasonings, not fried (boiled), without semi-finished products. Do not eat fatty foods, eat only dietary meat (rabbit, chicken). Eat a lot of salads and fruits, as they contain vitamins. Seafood (fish of various types) is useful because it contains trace elements (magnesium, phosphorus) necessary for a patient with cirrhosis of the liver, but not in large portions (up to 100 g per day). legume products(beans, peas), all types of cereals have a positive effect on patients with cirrhosis. Do not use canned food, smoked meats. In the presence of edema or fluid in the abdomen, limit fluid intake to 1000 ml per day.

Herbal medicine for cirrhosis of the liver is used to cleanse the liver and improve the excretion of bile. Liver cleansing should be carried out on a clean intestine, in the absence of constipation, and if they are, then they can be treated with a decoction of hay leaves. Some decoctions and preparations to improve liver function: boil willow bark in water, leave for a couple of days, drink 1/3 cup before meals 3 times a day. Drink one glass of radish and red beet juice every day. Collection of oats, birch buds, lingonberry leaves drink 1/3 cup every day, improves the excretion of bile.

Surgical treatment (liver transplantation)

With severe cirrhosis of the liver (proliferation of connective tissue over a large area), a severe general condition that cannot be drug treatment, liver transplantation (transplantation) is prescribed. For liver transplantation, a donor is needed, if there is a donor, then an operation is performed (under general anesthesia). But only about 80 - 90% of patients with a transplanted liver have a favorable outcome, the rest develop life-threatening complications, or the development of cirrhosis on the transplanted liver.

Liver damage in acute left ventricular and chronic heart failure is observed in all patients. It is possible to develop a passive venous congestion, hypoxemic necrosis, liver fibrosis and, in rare cases, cardiac cirrhosis.

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

With hypodiastole due to insufficient expansion of the cavities of the heart during diastole, hemodynamic disturbances and venous congestion in the systemic circulation are associated 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" cardiopathies that occur without damage to the pericardium: myocardiosclerosis various etiologies, primary amyloidosis, hemochromatosis with cardiac involvement, Loeffler's parietal endocarditis, and alcoholic cardiomyopathy, which may be combined with alcoholic cirrhosis of the 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 greatly facilitate the work of the right ventricle of the heart. In heart failure, the blood deposited in the liver can be up to 70% of the mass of the organ (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 a 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 the portal vein and in both vena cava is the same), so the porto-caval collateral circulation and varicose veins there are no esophageal veins.

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

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

With tricuspid valve insufficiency, a characteristic systolic pulsation of an enlarged liver, orthopnea, and painful swelling of the legs are observed. The spleen is enlarged in 40% of patients, hydrothorax and ascites may develop. Biochemical changes are often reduced to moderate hyperbilirubinemia and hypoalbuminemia, hyperaminotransferazemia. At advanced stages, hypoproteinemia and hypoprothrombinemia are observed. The size of the liver often decreases rapidly under the influence of rest, salt-free regimen, diuretic and cardiotonic therapy. With congestive hepatomegaly, there are no skin telangiectasias, palmar erythema, 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 injury, i.e. is idiopathic. This is characterized by a combination of early massive ascites resistant to diuretic therapy with a large, dense, painless, non-pulsating liver ("Peak'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 of the chest organs is mandatory for any form of liver pathology.

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

Cardiac cirrhosis of the liver, as well as cirrhosis of the liver of other etiologies, is accompanied by dysproteinemia with a predominant decrease in the level of total protein and blood albumin and an increase in the level of y-globulins and a 2 -globulins.

Sometimes clinical symptoms liver damage in patients with acute or chronic circulatory failure - heaviness or pain in the epigastric region, flatulence, nausea, bitter taste in the mouth, hepatomegaly and jaundice - come to the fore and level out 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 developing chronic heart damage with hyperkinetic syndrome in liver cirrhosis, which can be clinically manifested by cyanosis, severe dyspnea at rest and during exercise, tachycardia, high pulse pressure, expansion of the right ventricle of the heart due to significant arteriovenous shunting 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 treatment of CAH with immunosuppressants, subacute infective endocarditis may develop, 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. Hyper-a 2 -globulinemia is also said to be an infectious process, sharp rise ESR, auscultatory phenomena, indicating damage to the heart valves, vasculitis, thrombosis or embolism of the internal organs, kidney damage and positive results of repeated bacteriological blood tests.

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

Additionally, hepatoprotectors and vitamins - antioxidants are prescribed: legalon, simepar, Essentiale N, livovin, namacite, alvitil, gensamin, formaton, triovit, multitabs with ß-carotene in usual dosages for 1-2 months. In the presence of chronic cardiac cirrhosis, the appointment of hepabene in the above doses is indicated. According to indications, surgical treatment is carried out.

A rare disease is the deposition of calcium in the Glisson capsule of the liver and pericardium in tuberculous pericarditis, classified according to the old terminology as "shell heart", in which Pick's pseudocirrhosis develops. At the same time, 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 phenomena of chronic vascular insufficiency and as a consequence of the manifestation of "stagnant" nutmeg liver.

Liver in heart disease.

Professor Ambalov Yuri Mikhailovich — Doctor of Medical Sciences, Head of the Department of Infectious Diseases of the Rostov State Medical University, Member of the Russian Academy of Natural Sciences, Chairman of the Association of Infectious Diseases Rostov region, Head of the Rostov branch of the RANH, Chief Consultant of the Hepatological Center in Rostov-on-Don, Hepatologist of the highest qualification category

Khomenko Irina Yurievna — Candidate of Medical Sciences, Head infectious department No. 4 MBUZ "City Hospital No. 1 named after. ON THE. Semashko, Rostov-on-Don", Chief Freelance Specialist-Hepatologist of the Ministry of Health of the Rostov Region, Member of the Russian Society for the Study of the Liver (ROPIP), Infectious Disease Doctor, hepatologist of the highest qualification category

Book: "Liver Diseases" (S.D. Podymova; 1981)

Liver in heart disease.

In heart disease, the liver is affected due to an acute or chronic increase in central venous pressure, as well as a decrease in cardiac output. Usually there are phenomena of stagnation, necrosis, fibrosis, less often cirrhosis, which can exist separately, but are often combined depending on clinical situation. The term "cardiogenic liver" is proposed to refer to these disorders.

Speaking about the importance of hemodynamic disorders in the pathogenesis of liver damage in heart disease, it should be emphasized that the liver's need for oxygen is comparable to the need for the brain and heart, and hypoxia significantly impairs its functions.

In the clinical picture, however, one factor of liver damage often prevails: either congestion due to right ventricular failure, then arterial perfusion failure of the liver due to left ventricular failure, or signs of liver cirrhosis against the background of prolonged stagnation. This division allows a better understanding of the mechanism of formation of individual symptoms.

Congested liver. Any heart disease that causes an increase in pressure in the right atrium leads to stagnation of blood in the liver. Most often the cause is mitral defects, tricuspid valve insufficiency, cor pulmonale in chronic respiratory failure or recurrent thrombosis of small branches of the pulmonary artery, constrictive pericarditis, right ventricular myocardial infarction, right atrial myxoma.

The dependence of the blood filling of the liver on the functional state of the right heart is determined by the topographic relationship between the right atrium and the hepatic veins, the liver is called a reservoir for stagnant blood, a manometer of the right atrium.

Increased central venous pressure is transmitted to the hepatic veins and interferes with blood flow to the central part of the lobule. The slowdown in blood circulation increases the overflow of blood in the central veins, the central part of the lobules. Developing central portal hypertension is predominantly mechanical origin followed by hypoxia.

Localized central hypoxia causes atrophy and even necrosis of hepatocytes. Cell loss leads to collapse and condensation of the reticulum, active necrosis stimulates the formation of collagen, causes sclerosis of the veins. Further, the development of connective tissue leads to the movement of the central veins to the place of the portal veins. Connective tissue strands connect the central veins of neighboring lobules, the architectonics of the liver is disturbed.

Macroscopically, the liver in heart failure is enlarged, dark red, plethoric, it is rarely nodular. Expanded, distended veins protrude on the cut surface, the liver looks like a nutmeg (centrolobular red areas of stagnation and the rest of the lobules yellow).

Microscopically, there is an expansion of the central veins and sinusoids containing erythrocytes; in some cases, the centers of the hepatic lobules look like "blood lakes". The trabecular structure is erased in the central regions, atrophy of hepatocytes, balloon dystrophy develops here, and with the progression of the process, centrilobular focal necrosis is detected. Lipofuscin pigment in the form of delicate or coarse accumulations of golden yellow or brown color is contained in the center of hepatocytes.

clinical picture. The first symptom of congestive liver is its enlargement. When pressing on the liver area, a hepatojugular reflex (Plesha symptom) occurs - swelling of the cervical veins. In the initial stage of circulatory failure, the liver protrudes slightly from under the costal arch, its edge is rounded, smooth, the surface is soft.

In the future, the organ can reach a huge size, descend below the iliac crest. The edge of the liver is sharpened, the surface becomes dense. A. L. Myasnikov (1949) rightly emphasizes the variety of clinical manifestations of congestive liver: severe heart failure is possible with large edema and ascites and a slight increase in the liver, and, conversely, the liver can increase significantly with other mild symptoms of congestion. A different reaction of the liver to stagnation in it depends on its previous lesions - alcoholism, medicinal effects, as well as on the duration of stagnation.

Attention is drawn to the sensitivity, and in some cases, soreness of the congestive liver during palpation. With acute developing insufficiency circulatory system, intense spontaneous pain in the right side of the abdomen associated with stretching of the liver capsule can be observed. Characterized by a feeling of heaviness, fullness that occurs during meals, sometimes there is nausea. A distinctive feature of the congestive liver is the variability of its size, associated with the state of central hemodynamics and treatment, in particular with cardiac glycosides and diuretics.

Jaundice is usually mild. The combination of jaundice and cyanosis creates a peculiar color of the skin. An increase in bilirubin, mainly due to the bound fraction, is detected in 20-50% of patients [Bondar 3. A., 1970; Bluger A. F., 1975]. Usually it is moderately increased - up to 34.2-51.3 µmol/l (2-3 mg%), rarely up to 68.4-85.5 µmol/l (4-5 mg%). The mechanism of hyperbilirubinemia consists of a violation of excretion, regurgitation and capture of bilirubin by the liver.

Sometimes, against the background of chronic stagnation in the liver, jaundice quickly and significantly increases, which requires differential diagnosis with a number of diseases.

A. A. Krylov, O. G. Sprinson (1982) observed 25 patients in whom increasing jaundice had no additional etiological factors and arose as a result of congestive liver. Bilirubinemia crises in these patients with an increase in bilirubin from 71.1 to 167.6 µmol/l (4.16-9.8 mg%) due to the predominance of the direct fraction were accompanied by right ventricular circulatory failure.

An increase in venous pressure, a positive venous pulse, an increase and induration of the liver were noted. Most often, increasing jaundice was preceded or accompanied by pain in the right hypochondrium.

The causes of bilirubinemia crises in congestive liver are not entirely clear. The main significance in their origin, apparently, is further, sometimes paroxysmal, deterioration of intrahepatic circulation, increasing liver hypoxia, the appearance of hepatocyte necrosis, impaired bile excretion through the intrahepatic bile ducts due to increasing intravascular pressure in the sinusoids of the liver.

Hemolytic jaundice is rare. The sudden appearance of jaundice with indirect bilirubin is characteristic of infarcts of the lung, spleen, or kidneys, which do not cause jaundice without heart failure. This is due to the fact that an additional depot of hemoglobin is created in the focus of the infarction, and bilirubin is formed from it. Excess pigment cannot bind altered liver cells. Congestion in the lungs also leads to increased hemolysis and an increase in the indirect fraction of bilirubin.

In the study of the functional state of the liver, the most pronounced changes are detected with a bromsulfalein test, as well as a study of blood flow and absorptive-excretory fraction of the liver from 1311. In some cases, moderate hypoalbuminemia, a decrease in the prothrombin index, and a mild increase in the activity of aminotransferases in blood serum are noted.

Insufficient perfusion of the liver. Both functional and morphological disorders of the liver can occur with a decrease in arterial blood supply. The cause of such disorders may be acute left ventricular failure or prolonged collapse.

They are sometimes referred to as ischemic hepatitis. It should be highlighted acute infarction myocardium complicated by cardiogenic shock, arrhythmogenic collapses, post-resuscitation conditions, pulmonary embolism.

With a decrease in perfusion pressure in the liver, sufficient oxygen saturation of the blood is observed only in the periportal zones and quickly decreases when approaching the central part of the lobule, which is most sensitive to metabolic damage. Severe hypoxia of centrilobular hepatic cells leads to the development of necrosis and, in some cases, infarction.

Direct damage to the liver acute disorders blood circulation in patients with myocardial infarction is described by B. I. Vorobyov, L. I. Kotelnitskaya (1976). Ch. Stambolis et al. (1979), V. Aroidi et al. (1980), W. Beckert (1980) observed massive centrilobular necrosis of the liver in patients who died from circulatory failure.

In the clinical picture, the most important are jaundice, sometimes intense, and a high level of aminotransferases (usually 5-fold increase against the norm), which is often interpreted as acute viral hepatitis.

O.Nouel et al. (1980) described the development of acute liver failure in 6 patients with transient episodes of acute heart failure on the background of chronic stagnation in the liver. Jaundice and hepatic encephalopathy developed 1-3 days after episodes of acute circulatory failure, when hemodynamic parameters had already returned to normal. All patients had massive centrilobular necrosis without inflammatory cell infiltration.

Cardiac cirrhosis of the liver. According to various authors, the incidence of cirrhosis in patients with congestive liver ranges from 0.7 to 6.9% [Bondar 3. A., 1970; Valkovich E. I., 1973; Filippova L. A., Tikhonova G. N., 1975; Sherlock S., 1968]. Most often, it is detected against the background of prolonged stagnation in the liver with tricuspid valve insufficiency or constrictive pericarditis.

However, cirrhosis of the liver cannot be considered a common consequence of heart failure. A number of authors propose the term "cirrhosis of the liver in heart diseases occurring with circulatory failure", while emphasizing the multifactorial genesis of the disease. In addition to chronic stagnation, insufficient perfusion with the formation of necrosis in the liver, long-term drug therapy, and protein-vitamin deficiency can be noted.

Morphological examination, in addition to changes characteristic of stagnation, reveals periportal fibrosis, regenerated nodes, restructuring of lobular architectonics.

The clinical picture of cardiac cirrhosis does not have characteristic features. In the foreground, increasing heart failure, congestive liver, which is becoming increasingly dense, often with acute and jagged edge; sometimes the spleen is enlarged. Ascites develops after a long period of edema and is usually refractory to digitalis-diuretic therapy. Other signs of portal hypertension are seen late in the disease.

Cardiac cirrhosis of the liver occurs at the dystrophic stage of heart failure, when emaciation (up to cachexia), asthenia, anorexia, darkening of the skin, hair loss, brittle nails are expressed.

A functional study of the liver reveals a slight hyperbilirubinemia, hypoalbuminemia, hypoprothrombinemia, a moderate increase in gamma globulins, a decrease in cholinesterase activity, an increase in aminotransferases and gamma-glutam yltranspeptidase. Cardiac cirrhosis proceeds latently, without pronounced exacerbations.

AI Khazanov among 603 patients with cirrhosis in 22 cases found nutmeg cirrhosis with a pronounced restructuring of the liver; histological examination revealed layers of fibrous tissue and regenerated nodes. The majority of patients were found to have pronounced disorders of liver function tests, in the terminal period, 5 people developed a deep coma.