Congestion in the liver symptoms. Liver enlargement in chronic heart failure

Long venous stasis in the liver with severe chronic right ventricular failure can lead to damage to hepatocytes and the development of cirrhosis. In contrast to acute venous congestion in the liver during acute heart failure and ischemic hepatitis (“shock liver”), which develops with arterial hypotension as a result of decreased hepatic blood flow, for cardiac cirrhosis The liver, like any other, is characterized by pronounced fibrosis and the formation of regeneration nodes.

Pathological anatomy and pathogenesis. Right ventricular failure leads to increased pressure in the inferior vena cava and hepatic veins and stagnation of blood in the liver. The sinusoids are dilated and filled with blood, the liver is enlarged, and its capsule is tense. Prolonged venous stasis and ischemia associated with low cardiac output lead to centrilobular necrosis. As a result, centrilobular fibrosis develops; From the central veins towards the portal tracts, connective tissue septa diverge like rays. The alternation of red areas of venous stagnation and pale areas of fibrosis creates a characteristic “nutmeg liver” picture on the section.

Thanks to the advances of modern cardiology, and especially cardiac surgery, cardiac cirrhosis is now much less common than before.

Changes in laboratory parameters are quite varied. Bilirubin level. as a rule, it is slightly increased; both direct and indirect fractions may predominate. Possible moderate growth alkaline phosphatase activity and prolongation of PT. AST activity is usually slightly increased; pronounced arterial hypotension sometimes leads to the development of ischemic hepatitis (“shock liver”), clinically resembling viral hepatitis or toxic hepatitis. and a sharp short-term increase in AST levels. With tricuspid insufficiency, liver pulsation is sometimes observed. but with the development of cirrhosis this symptom disappears.

In chronic right ventricular failure, the liver is enlarged. dense and usually painless. Bleeding from esophageal varices is rare, but hepatic encephalopathy may develop. which is characterized by a wave-like course in accordance with fluctuations in the severity of right ventricular failure. Ascites and edema. initially associated only with heart failure, they can increase with the development of cirrhosis.

Diagnostics. One should think about cardiac cirrhosis of the liver if a patient has suffered from acquired heart disease for more than 10 years. constrictive pericarditis or cor pulmonale. an enlarged dense liver was found in combination with other signs of cirrhosis. The diagnosis can be confirmed with a liver biopsy, but with increased bleeding and ascites it is contraindicated.

In cases where liver and heart damage are simultaneously detected, hemochromatosis should be excluded. amyloidosis and other infiltrative diseases.

TREATMENT. The main thing in the treatment and prevention of cardiac cirrhosis of the liver is the treatment of the underlying disease. Reducing right ventricular failure improves liver function and prevents the progression of cirrhosis.

Cardiac cirrhosis (liver cirrhosis due to heart failure)

Pathogenesis of cardiac cirrhosis of the liver

The disease develops relatively rarely. With stagnation of blood in the liver, along with dilation and overflow of small veins with blood, expansion of the perisinusoidal spaces, atrophy of hepatocytes, and sometimes centrilobular necrosis are detected, which in some cases are combined with fatty degeneration. These changes may be accompanied by fibrosis and regeneration of some hepatocytes with the formation of nodules. The development of liver cirrhosis appears to be promoted by episodes of acute heart failure. It is known that acute necrosis hepatocytes occurs during shock (shock liver), but in lately Attention is drawn to the significance of small output syndrome in chronic heart failure. Thus, hepatic O-cell failure and cardiac cirrhosis are often observed in diseases characterized by a combination of venous stasis and decreased cardiac output (chronic cardiac aneurysm, aortic stenosis, dilated cardiomyopathy).

Clinic for cardiac cirrhosis of the liver

A congestive liver is characterized by pain in the right hypochondrium due to stretching of its capsule. With established liver cirrhosis, a moderate increase in levels is usually observed. indirect bilirubin, as a consequence of concomitant hemolysis and heart failure. The activity of aminotransferases usually increases slightly, but during periods of acute disturbance of blood flow in the liver (shock), a significant increase in the level of aminotransferases and other enzymes is possible, as in acute viral hepatitis. Over time, signs of liver cell failure may appear.

Portal hypertension is rare. In some cases, clinical symptoms of liver damage may come to the fore, mainly with a decrease in cardiac output.

True cardiac cirrhosis usually develops no earlier than 10 years after the first symptoms of congestive heart failure appear. At the same time, in diseases accompanied by a decrease in cardiac output, as well as repeated episodes sharp decline Blood pressure caused by one reason or another (in particular, acute heart rhythm disturbances), cirrhosis of the liver can form earlier. Pronounced changes in the liver are observed with constrictive pericarditis, in which the development of both Pick's pseudocirrhosis (portal hypertension, ascites, liver enlargement in the presence of moderate fibrosis) and true cirrhosis of the liver is possible.

Liver enlargement in chronic heart failure

Congestive liver observed in chronic heart failure, which is a common complication all organic heart diseases (valvular heart disease, hypertension and coronary disease, constrictive pericarditis, myocarditis, infective endocarditis, fibroelastosis, myxoma, etc.), a number of chronic diseases of internal organs (lungs, liver, kidneys) and endocrine diseases (diabetes mellitus, thyrotoxicosis, myxedema, obesity).

The appearance of the first signs of heart failure depends on a number of reasons, including a combination of several diseases, the patient’s lifestyle, and the addition of intercurrent diseases. In some patients, from the moment organic disease In the heart, decades pass before the first signs of heart failure appear, and sometimes it develops quite quickly following organic damage to the heart.

Clinical picture

The first signs of chronic heart failure are palpitations and shortness of breath during exercise. Over time, tachycardia becomes constant, and shortness of breath occurs at rest, and cyanosis appears. IN lower parts Moist rales are heard from the lungs. The liver enlarges, swelling appears in the legs, then fluid accumulates in subcutaneous tissue and on the body, in the serous cavities, anasarca develops.

In the first stages of heart failure, the liver enlarges in the anteroposterior direction and is not palpable. Liver enlargement can be detected using instrumental studies (rheohepatography, ultrasound). With the increase of heart failure, the liver noticeably enlarges, and it is palpated in the form of a painful edge protruding from the hypochondrium. Liver pain on palpation is associated with stretching of its capsule. Heaviness and pressing pain in the right hypochondrium and bloating are detected. The liver is noticeably enlarged, sensitive or painful, its surface is smooth, its edge is sharp. Jaundice is often observed. Liver function tests are moderately altered. These changes are in most cases reversible.

Histological examination of liver biopsies reveals dilation of the central veins and sinusoids, thickening of their walls, atrophy of hepatocytes, and the development of centrilobular fibrosis (congestive liver fibrosis). Over time, fibrosis spreads to the entire lobule (septal congestive cirrhosis liver).

Diagnostics

Identify a disease that may be causing heart failure. Correct assessment of tachycardia and detection of signs of venous stagnation play an important role. Of no small importance is the favorable dynamics of symptoms during treatment with cardiac glycosides and diuretics.

Treatment

Treatment is successful if the underlying disease that led to heart failure is correctly recognized and appropriate causal therapy is carried out. Patients are limited in physical activity, fluid intake and table salt.

In case of insufficient efficiency general events cardiac glycosides are used orally, long-term or permanently (digoxin, digitoxin, isolanide, celanide, acetyldigitoxin, adonis infusion), thiazides (furosemide, brinaldix, hypothiazide, yurinex, burinex, uregit, etc.) and potassium-sparing diuretics (triamterene, triampur, amiloride, moduretic, veroshpiron). The choice of a diuretic drug and the method of its use are determined by the degree of edema syndrome, the stage of heart failure and tolerability.

Drugs that improve metabolism in the myocardium are also prescribed - anabolic steroid(nerobolil, retabolil, etc.), ATP, vitamins B, C, E.

In the presence of cyanosis, oxygen therapy is indicated; severe violations rhythm - antiarrhythmic treatment. Many patients require sedative therapy.

I.I.Goncharik

“Enlarged liver in chronic heart failure” and other articles from the section Diseases of the liver and gallbladder

Additional information:

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 of unfavorable factors, the volume of cardiac output decreases;
to compensate for insufficient output, compensatory reactions of the body are activated (thickening of the myocardium occurs, increased heart rate);
for some time, compensation processes make it possible to ensure adequate blood supply to organs and tissues due to the work of the organ with increased load;
but the increased size of the myocardium requires a larger volume of blood for full-fledged work, And coronary vessels can transport only the same volume of blood and cease to cope with providing the muscles with nutrients;
insufficient blood supply leads to ischemia individual plots heart and myocardium due to lack of oxygen and nutrients contractile function decreases;
as the contractile function decreases, 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 problems that arise are not eliminated in a timely manner acute disorders, 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 manifest themselves taking into account 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 exercise and then at rest, but cardiac asthma or pulmonary edema rarely develops;
there are signs of general intoxication.

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

Mixed

It is characterized by dysfunction of both ventricles. 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 to eat;
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 associated with breathing or the heart, because the consequences of heart failure can be serious, and complications will cause disruption of the functioning of vital organs.

If CHF is suspected, it is necessary to 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 the majority the symptoms are pronounced and suggest the presence of pathology.

Elderly people

In older people, the body's defenses are weakened and the symptoms become more pronounced even 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. Initially, moderate heart failure appears with shortness of breath on exertion and a feeling 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 vital important systems 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 are ineffective at this stage, the patient has experienced dystrophic changes vital in everyone important organs, and water-salt metabolism was disrupted. 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 vary, 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;
injuries chest left.

The diagnosis of acute heart failure is established quickly:

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

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

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

Applying for medical assistance cannot be neglected, for the treatment of heart failure in acute form Need help from a cardiologist. 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 (checking the pulse, examining skin, through a phonendoscope the work of the heart is heard);
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 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 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 healing process. Of course, to prevent the symptoms characteristic of heart failure from further progressing, treatment with pills and injections is necessary. But in order to reduce the risk of complications, the lifestyle with heart failure should exclude all provoking factors:

timely treatment acute and chronic diseases;
getting rid of bad habits;
compliance with the work and rest regime;
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

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

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

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

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

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

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

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

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

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

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

The prognosis, unfortunately, is unfavorable.

Acquired heart defects in children and adults

Classification
Mechanism of occurrence
Most frequent vices hearts
Diagnostics
Treatment

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

What is damaged by heart defects? Brief anatomical information

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

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

Classification of valve problems

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

For reasons of occurrence ( etiological factor) distinguish vices:

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

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

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

By 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. In case of valve insufficiency, part of the ejected blood returns back, causing the corresponding chamber (ventricle or atrium) to perform extra work. This leads to compensatory hypertrophy (increase in volume and thickening of the muscle wall) of the heart chamber.

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

The most common heart defects

Mitral stenosis

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

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

Symptoms

When a disease occurs in childhood the child may 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.

Considering the large compensatory capabilities of the left ventricle, external signs deficiencies 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 abdominal cavity(ascites occurs), venous pressure increases.

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

Tricuspid stenosis

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

For a long time there are no complaints, then atrial fibrillation and congestive heart failure quickly develop. 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 the coronary arteries that supply it depart from the initial part of the aorta.

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

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

Aortic insufficiency

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 an upright position, and pale skin with a bluish tint.

This defect is characterized by a sharp change in pressure in different phases 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

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

Main types of operations for heart defects:

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

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

Prevention

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

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

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

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

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

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

Pathogenesis

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

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

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

Clinical manifestations

Patients are usually slightly icteric. Severe jaundice is rare and is found in patients with chronic congestive insufficiency due to ischemic heart disease or mitral stenosis. In hospitalized patients, the most common cause An increase in the concentration of bilirubin in the serum is caused by diseases of the heart and lungs. Long-term or recurrent heart failure leads to increased jaundice. In edematous areas, jaundice is not observed, since bilirubin is bound to proteins and does not enter the edematous fluid with low content squirrel.

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

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

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

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

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

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

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

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

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

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

Changes in biochemical parameters

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

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

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

Forecast

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

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

Liver dysfunction and cardiovascular abnormalities in childhood

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

Liver with constrictive pericarditis

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

Due to significant compaction, the liver capsule resembles icing sugar (“ glazed liver» - « Zuckergussleber"). Microscopic examination reveals a picture of cardiac cirrhosis.

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

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

Treatment is aimed at eliminating cardiac pathology. Patients who have undergone pericardiectomy have a favorable prognosis, but recovery of liver function is slow. Within 6 months after successful operation there is a gradual improvement functional indicators and reduction in liver size. You can't expect complete reverse development cardiac cirrhosis, but fibrous septa in the liver become thinner and become avascular.

Liver 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 it from entering the body. toxic substances and microorganisms absorbed into the blood 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 disruption of 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 the condition of your liver and the general state of 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 of treating 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 is 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, top up boiled water up 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 to make 1 liter 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, them water infusion, used for general loss of strength, anemia, liver disease and biliary tract, with uterine bleeding, jaundice, rickets, hemorrhoids. For children, especially those weakened after illness, fresh berries with milk and sugar are very useful - both 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 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 cups 3 times a day before meals for diseases of the liver and biliary tract, 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, up to full recovery liver cells. 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 to us karsil, a 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. Rinse 3 cups of oats with warm water, pour into a 5-liter enamel pan and pour 4 liters 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 for 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 of these servings 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 the stones in gallbladder dissolve pretty soon.

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 a warm heating pad on the liver area and lie down 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.

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