Stagnation of venous blood in the liver is treated with drugs. Relationship between liver damage and heart failure

Liver is a gland involved in the metabolism of proteins, fats, and vitamins. The liver produces bile, the lack of which in the body leads to disturbances in the digestive process. The liver filters the blood circulating throughout the body to prevent toxic substances and microorganisms from entering the body through the gastrointestinal tract. The most common liver diseases are hepatitis A and B, fatty liver due to alcoholism, gallstones formed due to stagnation of bile, infection, and impaired cholesterol metabolism.

Traditional healers offer many ways liver cleansing. There is a cleaning method 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 using various ingredients. The procedures are responsible, and the attending physician should recommend them, since he knows what the condition of your liver is, and general condition health. Before using 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 expel gallstones without examining them, you may provoke an emergency surgical intervention. Be extremely responsible in relation to your health.

But the fact that the liver will need to be constantly helped to cope with its functions is something everyone who has abnormalities in liver health needs to know. Doctors often prescribe choleretic herbs and drugs in such cases.

Traditional methods treatment of congestion in the liver They suggest cleansing the liver with choleretic herbs and herbs.

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

10 gr. Place (1.5 tbsp) St. John's wort herb in an enamel bowl, pour a glass of boiling water (200 ml), close the lid and simmer in a water bath for 30 minutes. Cool, strain, add boiled water to 200 ml. Drink 1/3 glass 3 times a day 30 minutes before meals. The decoction can be stored in a cool place 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 place in a dark place at room temperature for two days. Stir twice a day. Then add 700 grams of seedless and stemless 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 cleansing course requires 3 liters of beet kvass. Take 1 tablespoon before meals 30 minutes. After a 3-month break, repeat the course.

Take 1 tablespoon of a mixture of wild strawberry berries and leaves, brew and leave for 20 minutes. Then strain the infusion and take ½ - 1 glass of infusion 3 times a day for up to 3 weeks. After 2 weeks, treatment can be repeated. Not only the liver is treated, but also the vascular system from salt deposits. Traditional medicine recommends it for diseases of the gastrointestinal tract, gastritis, kidney stones, and vitamin deficiencies. 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 those weakened after illness, fresh berries with milk and sugar are very useful - as a nutritious and restorative remedy. 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 weed you can remove bitterness in your mouth, and with the help of chicory you can increase the secretion of bile and eliminate congestion in the liver.
Infusion: 2.tsp. Infuse dry fume grass for 2 hours in 2 cups of boiling water, strain. Drink 0.5 cup 3 times a day before meals for liver and biliary tract diseases, cholelithiasis.

Decoction: 1 teaspoon of chopped 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 glass 3-4 times a day before meals.

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

Pay attention to milk thistle, which not only has choleretic properties, but also restores liver cells during inflammation and restores intestinal motility. Milk thistle is the king herb for liver restoration. You can use it for a long time, up to a year or more, until the liver cells are completely restored. Kholmovaya Solyanka 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 biologically rare 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, and has an anti-inflammatory and wound-healing effect in diseases of the gastrointestinal tract. Also used for cirrhosis, hepatitis, jaundice, and weakened immunity. Directions for use: during meals you can take 1 teaspoon of dry powder, or pour a little boiled water and eat with food.

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

Make sure that the herbs you consume do not thicken your blood, as this complicates the functioning of the liver.

Grind 1 cup of rose hips in a porcelain or wooden mortar (vitamin C is oxidized in an iron mortar), pour in 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 enamel pan and add 4 liters of cold water, then close the lid and leave for 24 hours, 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 simmer 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 must be no later than 19:00. The course of treatment is 10 days, i.e. you need to prepare 2 such servings of the medicinal composition.

Take a few beets, peel, wash and cook. Next, cook this mixture until it becomes like syrup. Drink ¾ glass several times a day. Experts say that gallstones will dissolve fairly quickly.

And yet, to cleanse the liver of toxins, stagnant bile, cholesterol, and mucus, you sometimes have to do liver tubage. This procedure is simple and can be done with different ingredients. True, the stones are not expelled or dissolved during this procedure. But this procedure will undoubtedly help relieve and help the liver, 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 leave for 45 minutes. Then have a light breakfast.

With cholenzyme: pour 5-6 dragees into 1 tbsp. warm mineral water and then according to the same principle as described above.

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

If you have biliary dyskinesia, pay attention to your nervous system and eliminate stress in your life.

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, various complications arise. 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:

under the influence unfavorable factors volume decreases cardiac output;
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, timely identified early stage CHF 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 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 failure, 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. Chronic heart failure syndrome mixed type 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;
elderly people.

Newborns

Heart failure in newborns occurs due to disruption of the 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, 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 with hormonal changes in adolescents, hypersensitivity of the nervous system occurs, which means that 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 related to 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 carry out full examination teenager in order to detect pathology in a timely manner.

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 most the symptoms are pronounced and suggest the presence of pathology.

Elderly 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 activity. If changes in the myocardium are detected on 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. First, moderate heart failure appears with shortness of breath during exercise and a feeling of increased fatigue. Gradually, symptoms increase, shortness of breath appears at rest, the skin becomes pale bluish, and 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 in chronic heart failure in the terminal stage, aimed at providing relief pain patient 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.

Seeking medical help should not be neglected; to treat 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’s myocardial function is fully restored: 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.

ECG is the most reliable diagnostic method to clarify 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 an ECG, the attending physician

The etiology of the disease is determined through additional examinations:

Computed tomography. 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 chronic failure, if it is first identified, it 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 the treatment process. Of course, to prevent the symptoms characteristic of heart failure from further progressing, treatment with tablets 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 of acute and chronic diseases;
getting rid of bad habits;
compliance with the work and rest regime;
exclusion of harmful foods from the diet (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.

It is necessary to perceive cardiac failure as a serious pathological deviation 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

Cirrhosis of the liver is chronic disease, in which a disorder of the liver structure occurs: location cellular elements, bile ducts, as well as dysfunction of hepatocytes - liver cells.

This condition often develops due to exposure 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.

Dilation 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 - “jellyfish head”.

When diagnosing, you most often have to rely on anamnesis data: alcohol abuse, harmful production, 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
The most common heart defects
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 pulmonary artery– pulmonary valve.

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, the normal function of the heart is disrupted 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 valves 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 violation 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.

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

As stenosis develops, resistance to blood flow increases due to mechanical obstruction. If the valve fails, some of the expelled blood flows back, forcing the corresponding chamber (the ventricle or atrium) to do extra work. This leads to compensatory hypertrophy (increase in volume and thickening of the muscle wall) of the heart chamber.

Gradually, in the hypertrophied part of the heart, dystrophic processes and metabolic disorders develop, leading to a decrease in 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 orifice) is usually a consequence of a rheumatic process or infective endocarditis, causing 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 growth 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

If the disease occurs in childhood, the child may lag behind 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 cava, which collects blood from all parts of the body, flows into the right heart chambers, 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 rare cases can it 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 blood flow into arterial system, from which, first of all, the heart itself suffers, since those who feed it coronary arteries originate from the initial section of the aorta.

Deterioration of the 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

If 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 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 “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

The most common combined defect is 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

Conducted comprehensive examination patient:

When interviewing the patient, it becomes clear previous diseases(rheumatism, sepsis), attacks of chest pain, poor tolerance physical activity.
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

Elimination of pathological changes in the heart valves caused by a defect can only be achieved through surgery. Conservative treatment serves as an additional means to reduce the manifestations of the disease.

Main types of operations for heart defects:

At mitral stenosis The welded valve leaflets are separated with simultaneous expansion of its opening (mitral commissurotomy).
At 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. It is necessary to promptly eliminate possible causes of the development of heart defects - sanitize infectious foci, increase the body's resistance, eat rationally, work and rest.

Liver disease is a severe chronic liver disease characterized by irreversible death of liver cells as a result of chronic inflammation, followed by destruction of liver tissue and the growth of connective tissue in it (tissue containing no cells, only collagen fibers), resulting in an increase in its 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 mortality in people aged 40 to 60 years. High mortality is associated with rapid progression of the disease, severe complications, and most often accidental discovery of the disease and late treatment medical care. 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. In second place viral form, develops as a result of contact “blood with infected blood” with specific viruses, the risk group includes people who receive blood transfusions, drug addicts, and medical personnel.

Liver cirrhosis develops very slowly (many years, up to about 15 years or more), but rapid development is also possible when the body is exposed to unfavorable factors. 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 undetected liver cirrhosis, unaware of their disease, are admitted to the hospital for other reasons (chronic gastritis, cholecystitis, gastric ulcer, etc.).

Anatomy of the liver

The liver is an organ of the digestive system, weighing approximately 1500 grams, located in the upper abdominal cavity (stomach), more on the right. In shape it resembles the cap of a large mushroom, red-brown in color, and soft in consistency. The liver consists of two large lobes (left and right), and 2 small lobes (quadrate caudate). There is a depression in the liver where the gallbladder, bile formed by the liver accumulates in it and enters the intestines under the action of which certain foods (fats) are digested. On the lower surface of the 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.

The liver is covered with a serous membrane, supplied with blood vessels and nerves. Liver tissue is formed by liver cells (hepatocytes), which are arranged in radial groups and form hepatic lobules, each 1–2 mm in size. Around each lobule there are interlobular veins, which are branches of the portal vein; blood flows through them from the organs for further cleansing (detoxification) in the liver. Blood purified by liver cells, through central veins(located in the center of the lobule), enters the hepatic veins and subsequently into the inferior vena cava (which gives blood to the heart). Interlobular arteries are accompanied by interlobular veins; they saturate the liver with oxygen, which are a continuation of the 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.

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, medications, poisons and others), as a result of various chemical reactions.
Excretory function: the formation of bile in liver cells (from 500 to 2000 ml is formed per day) and its release 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 estrogens, adrenaline and norepinephrine), forms enzymes involved in digestion, produces the necessary energy for the functioning of the body.
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.
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: with liver disease, the blood changes its composition, as a result of which the functions of organs, the most sensitive brain, are disrupted, resulting in various abnormalities.

Causes of cirrhosis

Alcohol and smoking	As a result of chronic alcohol consumption and smoking, toxic effects 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 (individuals 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 transfusions, drug addicts, donors, surgical interventions, medical personnel).
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 stagnation 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 medications	Antibiotics, sleeping pills, antiviral, anti-inflammatory drugs, when taken continuously and over a long period of time, have a chronic toxic effect on liver cells, their inflammation with the further development of liver cirrhosis.
Long-term stagnation of venous blood in the liver	Observe for vascular and heart diseases: heart failure, pericarditis, heart defects and others. The pressure in the inferior vena cava increases, and therefore in the hepatic veins. The liver fills with blood and increases in size, this leads to compression of the arteries feeding the liver cells, as a result they die and are replaced by connective tissue, thus developing cirrhosis of the liver.
Autoimmune liver damage	The process by which the body perceives its own cells as foreign due to congenital disorder Substances are produced in the body that destroy liver cells (or other cells), autoimmune hepatitis develops and cirrhosis further develops.
Metabolic disorders(hemochromatosis)	Hereditary disease transmitted genetically, accompanied by the accumulation of iron in various organs and tissues, including the liver, disruption of cell structure with subsequent proliferation of connective tissue.

For detailed information on cholelithiasis, read the article: gallstones .

Symptoms of cirrhosis

	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. In other patients, cirrhosis of the liver manifests itself with some signs, their number and degree of manifestation depend on the level of damage to liver cells and the activity of the process:
Increased liver 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 physical activity, is the result of an increase in liver volume and stretching of the capsule. The capsule contains sensitive nerve receptors that form a pain symptom.
Dyspeptic manifestations	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.
General weakness	Fatigue, decreased performance, associated with insufficient liver production necessary substances, for the body.
Temperature rise	Occurs as a result of chronic inflammation in the liver
Increased bleeding	Frequent bleeding from the nose and gums is 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, which in turn connects to the veins of the esophagus)
Jaundice of the skin and sclera of the eyes	Dark colored urine and light stool, develops as a result of a high level of bilirubin in the blood (due to stagnation of bile and destruction of small bile ducts) and a violation of its outflow into the digestive tract.
Itchy skin	The skin itches due to the accumulation of bile acids (contained in bile); more often, this symptom is present with the development of cirrhosis as a result of a violation of the outflow of bile.
Anemia	Increased concentrations of toxic substances in the blood have a damaging effect on red blood cells, life cycle which is shortened.
Enlarged spleen	Blood from the spleen flows into hepatic vein. Due to impaired blood flow in the liver, pressure in the splenic vein increases, which leads to its overfilling with blood and an increase in size.
Spider veins	Redness of the palms "liver palms" develop as a result of dilation of the capillaries of the skin (due to higher level estrogen)
Induration of the mammary glands in men	Develops as a result of disruption of the breakdown and increase in the concentration of female sex hormones (estrogens)
Fluid in the abdomen and increase in its volume (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 in 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 remain for a long time until the effect of treatment (due to lack of protein production by the affected liver)
Weight loss	Associated with a lack of provision of 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 follow)
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 scatology), ultrasound, CT

	General analysis blood	decrease in hemoglobin ( decreased red blood cell levels (12), decrease in platelets (9), increase in the number of leukocytes (>9*10 9), increased erythrocyte sedimentation rate (>15mm/h).
	Biochemical analysis blood	Decrease in total protein Increase in ALAT>46U/l, and AST>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 Decrease in fibrinogen Decrease in prothrombin Increased alkaline phosphatase>270 U/l Decrease in Na Decrease in Ca
	Markers of viral hepatitis	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.
	Scatological analysis	steatorrhea (fat in stool as a result of fat metabolism), creatorrhea (undigested proteins in stool), discoloration of stool (due to lack of bilirubin).
	Ultrasound of the liver	The liver is enlarged in size, 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 smooth, the surface is wavy, the walls of the portal vein are thickened, the gallbladder is deformed and enlarged, the 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.
	Computed tomography	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 what tissue the liver is formed of (in 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

Drug 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 for liver cirrhosis:

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. Lif.52 is used 2 tablets 3 times a day, treatment with this group of drugs is long-term, it can last months, 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 impaired), with improvement metabolic processes in the liver. Treatment courses are prescribed 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, for active cirrhosis that develops as a result of a violation of the outflow of bile, and 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 taken 2 tablets with meals; the duration of enzyme treatment is determined individually by the attending physician.
Prokinetics (Metoclopramide) - eliminate bloating and have an antiemetic effect by enhancing intestinal motility. Prescribed 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 carbon is taken 1 tablet (250 g) for every 10 kg of the patient (50 kg - 5 tablets, but not more than 7 tablets) per dose 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. Average daily dose up to 10 mg/kg, taken in the evening before bed, the duration of treatment depends on the severity of congestion, it is determined by the attending physician.
Diuretics (Veroshpiron, Furosemide) are used in patients with ascites (fluid in the abdomen) and edema.
Antiviral drugs(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. Prescribed to patients suffering from diarrhea that cannot be cured by antibiotics, and bloating. Linex is prescribed 2 capsules 3 times a day, 2-4 weeks.
Transfusion therapy is used in a hospital (blood products: red blood cells, plasma, electrolytes), used for massive bleeding, the presence of ascites (fluid in the abdomen), encephalopathy.

Diet and traditional methods of treatment

Traditional methods are only an addition to other methods of treatment (medication, surgery). First of all, quit alcohol and smoking. Secondly, all patients should get plenty of rest, walk in the fresh air, and eat right. 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 microelements (magnesium, phosphorus) necessary for a patient with liver cirrhosis, but not in large portions (up to 100 g per day). Bean products(beans, peas), all types of cereals have a positive effect on patients with cirrhosis. Do not eat canned food or smoked meats. If there is swelling or fluid in the abdomen, limit fluid intake to 1000 ml per day.

Herbal medicine for liver cirrhosis 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 there is any, then they can be treated with a decoction of senna leaves. Some decoctions and mixtures 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. A 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 (overgrowth of connective tissue over a large area), severe general condition that cannot be treated drug treatment, liver transplantation is prescribed. For liver transplantation, a donor is needed, 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.

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

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 occurs with bleeding, postoperative complications, heatstroke, severe burns and septic shock. Therefore, a significant correlation is found between the frequency of detection of liver necrosis at autopsy and the presence in the terminal period of severe hypotension, renal failure, acute necrosis of the renal tubules and adrenal cortex at the border with the medulla, characteristic of shock. Acute heart rhythm disturbances (ventricular paroxysmal tachycardia, atrial fibrillation or fibrillation, etc.) can lead to acute heart failure and acute liver congestion with pain in the right hypochondrium, hyperaminotransferasemia and sometimes jaundice. Most often congestive liver develops with weakness of the right ventricle of the heart.

Hypodiastole, caused by insufficient expansion of the cavities of the heart during diastole, is associated with hemodynamic disturbances and venous congestion in the systemic circulation with compressive (constrictive) pericarditis. A similar mechanism of circulatory failure, but with a predominance of changes in the left ventricle of the heart, underlies other “constrictive” cardiopathy that occurs without damage to the pericardium: myocardiosclerosis of various etiologies, primary amyloidosis, hemochromatosis with cardiac involvement, Loeffler's parietal endocarditis and alcoholic cardiomyopathy, which can be combined with alcoholic cirrhosis 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 large number blood and thereby significantly facilitate the work of the right ventricle of the heart. In heart failure, the blood deposited in the liver can account for up to 70% of the organ's mass (normally about 35%). An increase in pressure in the right atrium directly spreads to the inferior vena cava, subhepatic veins, sinusoids and the portal vein system, leading to a relative decrease in arterial blood supply to the liver in proportion to the decrease in cardiac output, hypoxia and ischemic necrosis of hepatocytes. Portal hypertension in congestive heart failure has its own characteristics. The gradient of the wedged subhepatic and free portal pressure is not increased (the pressure in the portal vein and in both vena cava is the same), therefore the portacaval collateral circulation and varicose veins There are no esophageal veins.

With rapidly developing venous stagnation, enlargement and hardening of the liver is accompanied by stretching of the Glissonian capsule with sharp pain in the right hypochondrium and severe pain and protective muscle tension during palpation, simulating acute surgical disease. Slight jaundice often develops, initially due to hypoxemic hemolysis in the liver (unconjugated hyperbilirubinemia, urobilinuria). Later, with the development of hypoxemic central lobular atrophic changes in hepatocytes and necrosis, hepatocellular jaundice occurs with an increase in the level of direct bilirubin blood, aminotransferase activity and often blood alkaline phosphatase. Massive necrosis of the liver parenchyma with 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 pulmonary heart disease and constrictive pericarditis, cyanosis and shortness of breath occur without orthopnea and significant stagnation in the pulmonary circulation.

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

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

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

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

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

In the presence of heart failure in patients with hepatomegaly, it is necessary to take into account the possibility of development of chronic heart damage with hyperkinetic syndrome in liver cirrhosis, which can clinically manifest itself as cyanosis, severe shortness of breath at rest and during exercise, tachycardia, high pulse pressure, dilatation 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 liver cirrhosis or with long-term therapy 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, sharp increase ESR, auscultatory phenomena indicating damage to the heart valves, vasculitis, thrombosis or embolism of 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 the clinical and biochemical manifestations of cardiac cirrhosis of the liver.

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

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

Liver for heart disease.

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

Khomenko Irina Yurievna — Candidate of Medical Sciences, Head infectious diseases department No. 4 MBUZ "City Hospital No. 1 named after. N.A. Semashko, Rostov-on-Don", Chief freelance 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 for 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, and less often cirrhosis, which can exist separately, but are often combined depending on the clinical situation. The term “cardiogenic liver” has been 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 of the brain and heart, and hypoxia significantly impairs its functions.

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

Congestive liver. Any heart disease that causes increased pressure in the right atrium leads to stagnation of blood in the liver. More often the cause is mitral valves, 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 supply to 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 pressure gauge of the right atrium.

The increased central venous pressure is transmitted to the hepatic veins and interferes with the flow of blood to the central part of the lobule. Slowing blood circulation increases the overflow of blood into the central veins, the central part of the lobules. Developing central portal hypertension has predominantly mechanical origin, hypoxia joins it.

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, causing 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 cords connect the central veins of neighboring lobules, and the liver architecture is disrupted.

Macroscopically, the liver in heart failure is enlarged, dark red, congested, it is rarely nodular. Dilated, stretched veins protrude on the cut surface, the liver has the appearance of a nutmeg (centrilobular red areas of stagnation and the rest of the lobules are yellow).

Microscopically, expansion of the central veins and sinusoids containing red blood cells is observed; in some cases, the centers of the hepatic lobules look like “lakes of blood.” The trabecular structure is erased in the central areas, hepatocyte atrophy and balloon degeneration develop here, and as the process progresses, centrilobular focal necrosis is revealed. The pigment lipofuscin in the form of delicate or coarse clusters of golden yellow or brown color is contained in the center of hepatocytes.

Clinical picture. The first symptom of liver congestion is its enlargement. When pressing on the liver area, a hepatojugular reflex occurs (Plesch's symptom) - swelling of the neck veins. In the initial stage of circulatory failure, the liver protrudes slightly from under the costal arch, its edge is rounded, smooth, and the surface is soft.

In the future, the organ can reach enormous sizes and descend below the iliac crest. The edge of the liver becomes sharper, the surface becomes dense. A. L. Myasnikov (1949) rightly emphasizes the variety of clinical manifestations of congestive liver: severe heart failure with large edema and ascites and a slight enlargement of the liver is possible, and, on the contrary, the liver can become significantly enlarged with other mild symptoms of stagnation. The 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.

Noteworthy is the sensitivity and, in some cases, pain of the congestive liver upon palpation. In acute developing failure blood circulation, intense spontaneous pain may be observed in the right half of the abdomen, associated with stretching of the liver capsule. A characteristic feeling of heaviness and fullness that occurs during eating, sometimes nausea. A distinctive feature of a 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 elevated - 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 impaired excretion, regurgitation and uptake 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 did not have additional etiological factors and arose as a result of congestive liver. Bilirubinemic crises in these patients with a rise 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 circulatory failure of the right ventricular type.

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

The causes of bilirubinemic crises in congestive liver are not entirely clear. The main significance in their origin, apparently, is the further, sometimes paroxysmal, deterioration of intrahepatic circulation, increasing liver hypoxia, the appearance of hepatocyte necrosis, impaired excretion of bile 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 infarctions of the lung, spleen or kidneys, which do not cause jaundice without heart failure. This is due to the fact that an additional hemoglobin depot is created at the site of the infarction, and bilirubin is formed from it. Excess pigment cannot bind to altered liver cells. Pulmonary congestion also leads to increased hemolysis and an increase in the indirect bilirubin fraction.

When studying 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 the absorptive-excretory fraction of the liver with 1311. In some cases, moderate hypoalbuminemia, a decrease in the prothrombin index, and a mild increase in the activity of serum aminotransferases are noted.

Insufficient liver perfusion. Both functional and morphological liver disorders 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 heart attack myocardium, complicated by cardiogenic shock, arrhythmogenic collapses, post-resuscitation conditions, pulmonary embolism.

With a decrease in perfusion heat pressure in the liver, sufficient oxygen saturation of the blood is observed only in the periportal zones and quickly drops 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 liver damage from acute disorders blood circulation in patients with myocardial infarction was 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 high levels of aminotransferases (usually a 5-fold increase above normal), 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 against the background of chronic congestion 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 Z. 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 congestion in the liver with tricuspid valve insufficiency or constrictive pericarditis.

However, liver cirrhosis cannot be considered a common consequence of heart failure. A number of authors propose the term “liver cirrhosis in heart diseases occurring with circulatory failure,” 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 and vitamin deficiency can be noted.

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

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

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

A functional study of the liver reveals slight hyperbilirubinemia, hypoalbuminemia, hypoprothrombinemia, a moderate increase in gamma globulins, a decrease in cholinesterase activity, an increase in aminotransferases and gamma-glutamyl transpeptidase. Cardiac cirrhosis occurs latently, without significant exacerbations.

Among 603 patients with cirrhosis, A.I. Khazanov discovered muscat cirrhosis with a pronounced restructuring of the liver structure in 22 cases; Histological examination revealed layers of fibrous tissue and regenerated nodes. In the majority of patients, severe disturbances in liver function tests were found; in the terminal period, 5 people developed a deep coma.