Congestion in the liver treatment. Congestive liver in heart failure

Temporary hyperemia of the liver, which develops during digestion, sometimes turns into a persistent increased blood supply to the organ, which causes its enlargement, painful sensations in the right hypochondrium, indigestion, temporary slight icteric coloration of the skin, etc. The above-described painful condition often occurs in practice.

Often, in obese people accustomed to a luxurious lifestyle, a clearly palpable, enlarged liver is found. However, it is unlikely that in these cases we are dealing only with active hyperemia of the liver, or rather with hyperplasia of the liver, congestive hyperemia with the onset of circulatory disorder, light forms diffuse hepatitis of various etiologies, liver swelling due to gout, etc.

Most often, congestion in the liver is hidden behind the diagnosis when cholelithiasis or beginning .

Regarding the course and duration of active liver hyperemia, we must say that we cannot give general instructions on this matter. Depending on the reason that caused the stagnation, its intensity and duration, stagnation in the liver can appear acutely, quickly disappear, recur or be chronic.

Treatment depends solely on an accurately established diagnosis underlying the stagnation. In persons leading an inappropriate lifestyle. List of factors that will improve the patient’s condition

• careful regulation of diet (moderate lifestyle, prohibition of all alcoholic beverages)
• sufficient exercise in the fresh air (horse riding)
• prescribing laxatives
• water treatment in Carlsbad, Marienbad, Kissingen, Hamburg, etc.

Congestive heart failure (CHF) is the inability of the heart muscle to pump enough blood to support the body's metabolic processes. If the pumping function of the heart weakens, then venous blood begins to stagnate and blood circulation is impaired. To compensate for the deficiency, certain areas of the myocardium begin to enlarge to perform the function of pumping blood. This makes the patient feel better, but only temporarily.

The deformed parts wear out quickly, and the symptoms almost immediately return with a vengeance. After the onset of organ hypertrophy, surgical intervention may be required. There are right ventricular and left ventricular failure, which can be acute or chronic. The clinical picture of congestive heart failure in the initial stages may be similar to chronic bronchitis, bronchial asthma and emphysema.

Clinical picture

Depending on which part of the heart muscle is affected, the signs of the disease vary. When the right ventricle is damaged, disturbances in the systemic circulation are observed. As a result, swelling of the extremities appears, in particular, the legs become swollen, pain occurs in the right hypochondrium, and dry mouth appears. The liver enlarges and becomes painful on palpation.

Nocturia is often observed, which implies a violation of the urination process. Due to stagnation of blood in the veins during the day, metabolism becomes difficult and becomes more active at night, when the body is at rest. A person suffering from heart failure usually experiences the urge to urinate at night. Nocturia is considered one of the first signs of the disease.

Due to the accumulation of fluid in the body, the patient's weight increases.

Symptoms of left-sided heart failure are caused by impaired functioning of the pulmonary (pulmonary) circulation, which is responsible for saturating the blood with oxygen. The first indicators of the development of pathology in this case are:

• pale skin, cyanosis;
• shortness of breath, lack of air;
• high arterial pressure and tachycardia;
• rapid heartbeat, which causes insomnia;
• general weakness;
• rapid onset of fatigue with minimal physical activity;
• dry cough;
• difficulty breathing when lying down (orthopnea).

However, every body is different, and symptoms may manifest differently. Congestive heart failure in acute form may be accompanied by a strong dry cough at night with foam or blood. As a result of circulatory disorders, the organs of the abdominal region suffer, primarily the kidneys: fibrosis of the organ develops.

In the absence of proper treatment and the development of the disease, shortness of breath is observed even at rest; the patient can only sleep in a semi-sitting position. Absorption of food in the intestines deteriorates, which causes diarrhea. Thus, disruption of the heart’s function of pumping blood negatively affects most vital important organs, other diseases develop. Heart failure can also lead to death.

Causes

The development of this pathology is often provoked by increased load on the myocardium. If it is not a congenital heart defect and there is no genetic predisposition, then congestive heart failure occurs as a complication after past illness or during its course. The risk group includes people suffering from:

• thyroid dysfunction (hyperthyroidism, diabetes mellitus);
• disorders of the cardiovascular system (ischemia, hypertension, angina, myocardial infarction, pericarditis);
• acute and chronic infectious diseases (pneumonia, diphtheria, purulent tonsillitis, scarlet fever and even influenza).

Any of the above conditions significantly weakens the myocardium. A heart rate that is too fast, too slow, or simply uneven (arrhythmia) also has a negative impact. In the presence of heart and vascular diseases, NMS can also develop during pregnancy, as the load on the heart increases. The disease is also provoked by smoking, alcohol or drug addiction.

Whatever the cause, the symptoms of congestive heart failure cause the patient a feeling of discomfort, develop rapidly and affect the body as a whole. Therefore, you should immediately consult a doctor at the first signs of pathology (rapid pulse, shortness of breath, nocturia, edema, cyanosis, tingling in the heart area).

Diagnosis and treatment

Before starting treatment, the patient must undergo diagnostic examination which includes:

• examination by a cardiologist;
• load tests;
• chest x-ray;
• blood analysis;
• cardiac catheterization (according to indications);
• pulmonary function assessment;
• electrocardiogram, echocardiogram.

Treatment includes several areas: eliminating the cause of the disease, mitigating its symptoms, and preventing complications. In the presence of edema, salt is excluded from the patient's diet. The maximum amount of fluid consumed per day should not exceed 0.8–1 liter.

To normalize the function of fluid excretion, diuretics are prescribed, which increase urine formation and relieve swelling. Usually, after giving up table salt, the patient’s shortness of breath decreases and cyanosis (blueness) of the skin disappears.

Depending on the stage of development of the disease, restrictions are also imposed on physical activity, and specifically on those actions during which the patient experiences shortness of breath. Congestive heart failure causes sleep disorders. It is recommended that the patient sleep with his head elevated, since breathing is difficult in a supine position.

Medicines are also prescribed to prevent the formation of blood clots in the vessels. To enhance the pumping function of the heart and restore the correct heartbeat rhythm, glycosides and beta-blockers are used. Sometimes, to increase the effectiveness of treatment, drugs are prescribed that retain potassium in the body, which is so beneficial for the myocardium. If necessary, medications are used to stabilize blood pressure.

Signs of heart failure will help eliminate complete abstinence from fatty, fried and especially spicy food. It is better to eat only fruits and vegetables; eating dried apricots is especially beneficial. Doctors recommend eating according to diet number 10.

If there is no positive effect from therapy, the option of surgical intervention by correcting deformed areas of the heart or organ transplantation is considered.

Prevention

Congestive heart failure can be prevented preventive measures. The best prevention is healthy image life, which includes proper nutrition, active rest and moderate physical activity. A little exercise promotes recovery if it does not cause shortness of breath in the patient. It is necessary to completely give up smoking, alcoholic beverages, drugs, coffee and strong tea. General strengthening immunity also plays an important role, as it is general prevention diseases that can lead to NMS.

A person must have normal weight, corresponding to growth. With deviations up or down, the load on the heart also increases. For normal functioning of the heart muscle it is necessary healthy sleep, which is 7–8 hours a day. Stressful situations, depression, and overexertion should be avoided.

Viburnum is very good for the heart. You can grind it, add water and add honey. You need to take this remedy twice a day for a month. To prevent swelling, you should brew parsley seeds or eat it raw. It perfectly strengthens the walls of the heart.

Freshly squeezed juices are also useful for heart failure, for example, beet juice normalizes blood pressure, and pumpkin juice eliminates heart palpitations. Has a beneficial effect on the body and Spa treatment. Therapeutic baths, massages, aromatherapy, exercise therapy, just sea ​​air help strengthen the cardiovascular system. So, following everyone preventive recommendations, you will never know what congestive heart failure is.

Pulmonary hypertension: occurrence, signs, forms, diagnosis, therapy

Pulmonary hypertension (PH) is characteristic of diseases that are completely different both in the reasons for their occurrence and in their defining characteristics. LH is associated with the endothelium (inner layer) of the pulmonary vessels: as it grows, it reduces the lumen of arterioles and disrupts blood flow. The disease is rare, with only 15 cases per 1,000,000 people, but survival rate is very low, especially in the primary form of PH.

Resistance in the pulmonary circulation increases, the right ventricle of the heart is forced to increase contractions in order to push blood into the lungs. However, it is anatomically not adapted to long-term pressure load, and with PH in the system pulmonary artery it rises above 25 mm Hg. at rest and 30 mmHg during physical stress. First, during a short period of compensation, thickening of the myocardium and enlargement of the right parts of the heart are observed, and then a sharp decline contraction strength (dysfunction). The result is premature death.

Why does PH develop?

The reasons for the development of PH have not yet been fully determined. For example, in the 60s in Europe there was an increase in the number of cases associated with excessive use of contraceptives and weight loss products. Spain, 1981: complications in the form of muscle damage that began after the popularization of rapeseed oil. Almost 2.5% of the 20,000 cases were diagnosed with pulmonary arterial hypertension. The root of the evil turned out to be tryptophan (an amino acid) present in the oil; this was scientifically proven much later.

Impaired function (dysfunction) of the pulmonary vascular endothelium: the cause may be hereditary predisposition, or the influence of external damaging factors. In any case, the normal balance of nitric oxide metabolism changes, vascular tone changes towards spasm, then inflammation, the endothelium begins to grow and the lumen of the arteries decreases.

Impaired synthesis or availability of nitric oxide (NO), decreased production of prostacyclin, additional excretion of potassium ions - all deviations from the norm lead to arterial spasm, proliferation of the muscular wall of blood vessels and endothelium. In any case, the final development is a violation of blood flow in the pulmonary artery system.

Signs of the disease

Moderate pulmonary hypertension does not produce any pronounced symptoms, and this is the main danger. Signs of severe pulmonary hypertension are determined only in the later periods of its development, when pulmonary arterial pressure rises two or more times compared to the norm. Normal pressure in the pulmonary artery: systolic 30 mmHg, diastolic 15 mmHg.

Initial symptoms of pulmonary hypertension:

• Unexplained shortness of breath, even with little physical activity or at rest;
• Gradual loss of body weight even with normal, nutritious nutrition;
• Asthenia, a constant feeling of weakness and powerlessness, depressed mood - regardless of the season, weather and time of day;
• Constant dry cough, hoarse voice;
• Discomfort in the abdominal area, a feeling of heaviness and “bloating”: the beginning of stagnation of blood in the portal vein system, which carries venous blood from the intestines to the liver;
• Dizziness, fainting – manifestations of oxygen starvation (hypoxia) of the brain;
• Rapid heartbeat, over time, pulsation of the jugular vein becomes noticeable in the neck.

Later manifestations of PH:

1. Sputum streaked with blood and hemoptysis: signal increasing pulmonary edema;
2. Angina attacks (chest pain, cold sweat, fear of death) are a sign of myocardial ischemia;
3. Arrhythmias (violation heart rate) of the ciliated type.

Pain in the hypochondrium on the right: already involved in the development of venous stagnation big circle blood circulation, the liver has enlarged and its shell (capsule) has stretched - therefore pain has appeared (the liver itself does not have pain receptors, they are located only in the capsule)

Swelling of the legs, legs and feet. Accumulation of fluid in the abdomen (ascites): manifestation of heart failure, peripheral blood stagnation, decompensation phase - a direct danger to the patient’s life.

End stage PH:

• Blood clots in the arterioles of the lungs lead to death (infarction) of active tissue and increased suffocation.

Hypertensive crises and attacks acute edema lungs: most often occur at night or in the morning. Begins with a feeling of sudden lack of air, then joins coughing, bloody sputum is released. The skin takes on a bluish tint (cyanosis), and the veins in the neck pulsate. The patient is excited and frightened, loses self-control, and may move chaotically. At best, the crisis will end with copious discharge of light-colored urine and uncontrolled passage of feces; at worst, death. The cause of death may be blockage of a pulmonary artery by a blood clot (thromboembolism) and subsequent acute heart failure.

Main forms of PH

1. Primary, idiopathic pulmonary hypertension (from the Greek idios and pathos - “a peculiar disease”): is fixed by a separate diagnosis, in contrast to secondary PH associated with other diseases. Variants of primary PH: familial PH and hereditary predisposition of blood vessels to dilation and bleeding (hemorrhagic telangiectasias). Reason – genetic mutations, frequency 6 – 10% of all cases of PH.
2. Secondary PH: manifests itself as a complication of the underlying disease.

Systemic connective tissue diseases - scleroderma, rheumatoid arthritis, systemic lupus erythematosus.

Congenital heart defects (with blood shunting from left to right) in newborns, occurring in 1% of cases. After corrective blood flow surgery, the survival rate of this category of patients is higher than that of children with other forms of PH.

Late stages of liver dysfunction, pulmonary-hepatic vascular pathologies in 20% there is a complication in the form of PH.

HIV infection: PH is diagnosed in 0.5% of cases, survival within three years drops to 21% compared to the first year – 58%.

Intoxication: amphetamines, cocaine. The risk increases three dozen times if these substances were used more than three months in a row.

Blood diseases: with some types of anemia, PH is diagnosed in 20–40%, which increases mortality among patients.

Chronic obstructive pulmonary disease (COPD), the cause is prolonged inhalation of particles of coal, asbestos, shale and toxic gases. It often occurs as an occupational disease among miners and workers in hazardous industries.

Sleep apnea syndrome: partial cessation of breathing during sleep. Dangerous, detected in 15% of adults. The consequence may be PH, stroke, arrhythmias, and arterial hypertension.

Chronic thrombosis: noted in 60% after survey of patients with pulmonary hypertension.

Lesions of the heart, its left half: acquired defects, coronary disease, hypertension. About 30% is associated with pulmonary hypertension.

Diagnosis of pulmonary hypertension

Diagnosis of precapillary PH (associated with COPD, arterial pulmonary hypertension, chronic thrombosis:

• Pulmonary artery pressure: average ≥ 25 mm Hg at rest, more than 30 mm Hg during exertion;
• Increased pulmonary artery wedge pressure, blood pressure inside the left atrium, end-diastolic ≥15 mm, pulmonary vascular resistance ≥ 3 units. Wood.

Postcapillary PH (for diseases of the left half of the heart):

1. Pulmonary artery pressure: average ≥25 (mm Hg)
2. Initial: >15 mm
3. Difference ≥12 mm (passive PH) or >12 mm (reactive).

ECG: overload on the right: enlargement of the ventricle, expansion and thickening of the atrium. Extrasystole (extraordinary contractions of the heart), fibrillation (chaotic contraction of muscle fibers) of both atria.

X-ray examination: increased peripheral transparency of the lung fields, the roots of the lungs are enlarged, the borders of the heart are shifted to the right, the shadow of the arch of the dilated pulmonary artery is visible on the left along the cardiac contour.

Functional breathing tests, qualitative and quantitative analysis the composition of gases in the blood: the level of respiratory failure and the severity of the disease are revealed.

Echo-cardiography: the method is very informative - it allows you to calculate the average pressure in the pulmonary artery (MPAP) and diagnose almost all heart defects. PH is recognized already in the initial stages, with MPAP ≥ 36 – 50 mm.

Scintigraphy: for PH with blocking of the lumen of the pulmonary artery by a thrombus (thromboembolism). The sensitivity of the method is 90 - 100%, specific for thromboembolism is 94 - 100%.

Computer (CT) and magnetic resonance imaging (MRI): at high resolution, in combination with the use contrast agent(with CT), allow you to assess the condition of the lungs, large and small arteries, walls and cavities of the heart.

Inserting a catheter into the cavity of the “right” heart, testing the vascular response: determining the degree of PH, blood flow problems, assessing the effectiveness and relevance of treatment.

Treatment of PH

It is possible to treat pulmonary hypertension only in a complex manner, combining general recommendations to reduce the risks of exacerbations; adequate therapy underlying disease; symptomatic remedies impact on general manifestations LH; surgical methods; treatment with folk remedies and non-traditional methods - only as auxiliary.

Vaccination (flu, pneumococcal infections): for patients with autoimmune diseases systemic diseases– rheumatism, systemic lupus erythematosus, etc., to prevent exacerbations.

Nutrition control and dosed physical activity: for diagnosed cardiovascular failure of any origin (origin), in accordance with the functional stage of the disease.

Preventing pregnancy (or, according to indications, even terminating it): the circulatory system of the mother and child are linked together, increasing the load on the heart and blood vessels of a pregnant woman with PH can lead to death. According to the laws of medicine, priority in saving lives always belongs to the mother if it is not possible to save both at once.

Psychological support: all people with chronic diseases constantly experience stress, the balance of the nervous system is disturbed. Depression, a feeling of uselessness and burdensomeness for others, irritability over small things - typical psychological picture any “chronic” patient. This condition worsens the prognosis for any diagnosis: a person must definitely want to live, otherwise medicine will not be able to help him. Conversations with a psychotherapist, an activity you enjoy, active communication with fellow sufferers and healthy people are an excellent basis for getting a taste for life.

Maintenance therapy

• Diuretics remove accumulated fluid, reducing the load on the heart and reducing swelling. The electrolyte composition of the blood (potassium, calcium), blood pressure and kidney function must be monitored. An overdose risks too much water loss and a drop in blood pressure. When potassium levels decrease, arrhythmias begin, and muscle cramps indicate a decrease in calcium levels.
• Thrombolytics and anticoagulants dissolve already formed blood clots and prevent the formation of new ones, ensuring vascular patency. Constant monitoring of the state of the blood coagulation system (platelets) is necessary.
• Oxygen (oxygen therapy), 12 - 15 liters per day, through a humidifier: for patients with chronic obstructive pulmonary disease (COPD) and cardiac ischemia, helps restore blood oxygen saturation and stabilize the general condition. It must be remembered that too high a concentration of oxygen depresses the vasomotor center (VMC): breathing slows down, blood vessels dilate, pressure drops, and a person loses consciousness. For normal functioning, the body needs carbon dioxide, and it is after its content in the blood increases that the SDC “gives the command” to take a breath.
• Cardiac glycosides: the active components are isolated from digitalis; the most famous drug is Digoxin. Improves heart function by increasing blood flow; fights arrhythmias and vascular spasm; reduces swelling and shortness of breath. In case of overdose - increased excitability of the heart muscle, rhythm disturbances.
• Vasodilators: the muscular wall of arteries and arterioles relaxes, their lumen increases and blood flow improves, pressure in the pulmonary artery system decreases.
• Prostaglandins (PG): a group of active substances produced in the human body. In the treatment of PH, prostacyclins are used; they relieve vascular and bronchial spasms, prevent the formation of blood clots, and block the proliferation of the endothelium. Very promising drugs, effective for PH due to HIV, systemic diseases(rheumatism, scleroderma, etc.), heart defects, as well as familial and idiopathic forms of PH.
• Endothelin receptor antagonists: vasodilation, suppression of endothelial growth (proliferation). With prolonged use, shortness of breath decreases, the person becomes more active, and blood pressure normalizes. Undesirable reactions to treatment include edema, anemia, liver dysfunction, so the use of drugs is limited.
• Nitric oxide and PDE type 5 inhibitors (phosphodiesterases): used mainly for idiopathic PH, if standard therapy does not justify itself, but individual drugs effective for any form of PH (Sildenafil) Action: reducing vascular resistance and associated hypertension, facilitating blood flow, resulting in increased resistance to physical activity. Nitric oxide is inhaled daily for 5–6 hours, up to 40 ppm, course 2–3 weeks.

Surgical methods for treating PH

Balloon atrial septostomy: performed to facilitate the shunting of oxygen-rich blood inside the heart, from left to right, due to the difference systolic pressure. A catheter with a balloon and blade is inserted into the left atrium. The blade cuts the septum between the atria, and the inflated balloon widens the opening.

Lung transplantation (or lung-heart complex): performed according to vital indications, only in specialized cases medical centers. The operation was first performed in 1963, but by 2009 more than 3,000 were performed annually. successful transplants lungs. The main problem is the shortage of donor organs. Lungs are taken from only 15%, hearts from 33%, and livers and kidneys from 88% of donors. Absolute contraindications for transplantation: chronic renal and liver failure, HIV infection, malignant tumors, hepatitis C, the presence of HBs antigen, as well as smoking, drug and alcohol use within six months before surgery.

Treatment with folk remedies

They are used only in combination, as aids for general improvement of well-being. No self-medication!

Classification and prognosis

The classification is based on the principle of functional disorders in PH, the version is modified and is associated with manifestations of heart failure (WHO, 1998):

• Class I: PH with normal physis. activity. Standard loads are well tolerated, mild PH, grade 1 failure.
• Class II: LH plus decreased activity. Comfort in a quiet position, but dizziness, shortness of breath and chest pain begin even with normal exertion. Moderate pulmonary hypertension, increasing symptoms.
• Class III: PH with decreased initiative. Problems even at low loads. High degree of blood flow disturbances, worsening prognosis.
• Class IV: PH with intolerance minimal activity. Shortness of breath and fatigue are felt even at complete rest. Signs of high circulatory failure - congestive manifestations in the form of ascites, hypertensive crises, pulmonary edema.

The prognosis will be more favorable if:

1. The rate of development of PH symptoms is low;
2. The treatment improves the patient's condition;
3. The pressure in the pulmonary artery system decreases.

Poor prognosis:

1. Symptoms of PH develop dynamically;
2. Signs of decompensation of the circulatory system (pulmonary edema, ascites) are increasing;
3. Pressure level: in the pulmonary artery more than 50 mmHg;
4. With primary idiopathic PH.

The overall prognosis for pulmonary arterial hypertension is related to the form of PH and the phase of the prevailing disease. Mortality per year, with current treatment methods, is 15%. Idiopathic PH: patient survival after a year is 68%, after 3 years - 48%, after 5 years - only 35%.

Video: pulmonary hypertension in the Health program

What is heart failure: symptoms, signs and treatment of the disease

Heart failure - what is it? This is a pathological condition that appears in the event of a malfunction of the heart, when blood is not pumped in the proper volume. Acute heart failure can lead to death in a short period of time, since there is a high probability dangerous complications. Chronic heart failure develops gradually and leads to prolonged “starvation” of body tissues.

Causes of the disease

Why does heart failure occur? This condition occurs due to various etiological factors. Most often, the etiology of this disease is associated with atherosclerosis and arterial hypertension. Increased pressure in the bloodstream and atherosclerotic narrowing of the lumen of blood vessels lead to the fact that it becomes difficult for the heart to push blood. The body's resources make it possible to compensate for this pathological condition - at first there are no clinical symptoms of circulatory failure due to increased heart rate and increased strength of heart contractions. When the myocardium is depleted, decompensation of the disease occurs - this is manifested by shortness of breath, edema, and decreased tolerance to physical stress. These are all symptoms of congestive heart failure (CHF).

The pathogenesis of heart failure also includes diseases accompanied by direct damage to the heart. These are myocarditis, valve defects, infectious and autoimmune diseases, and intoxications. With lung diseases, increased pressure in the pulmonary circle can often occur. All these reasons lead to an increase in the load on the heart, due to which the efficiency of the organ is significantly reduced. This can also happen when there is fluid retention in the body, for example, with kidney disease.

In many cases, the causes of heart failure and the etiology of this condition are due to a previous heart attack. Most often this leads to acute heart failure with rapid development complications and death of the patient.

This disease is classified according to the speed of clinical development:

• acute HF – progresses in a very short period of time (several minutes – several hours). Complications of this type of disease often include pulmonary edema or cardiogenic shock. Most common reasons AHF – heart attack, valve defects (aortic and mitral), damage to the walls of the heart;
• Chronic HF – progresses over many months or years. Cause of CHF- these are compensated pathological conditions with damage to the heart and other organs (arterial hypertension, defects, chronic diseases lungs, etc.).

Classification

There are several classification options for heart failure. Depending on the severity of the clinic, the following are distinguished:

• First degree – there are no clinical symptoms.
• In the second degree of heart failure, symptoms are mild and wheezing may be present.
• The third degree is a more pronounced clinical picture, the presence of wheezing.
• The fourth degree of severity is characterized by the presence of complications, for example, cardiogenic shock, collapse (decrease in systolic blood pressure below 90 mm Hg).

According to the degree of patient resistance to physical stress, heart failure is divided into four functional classes (FC):

• 1 FC - shortness of breath and other symptoms appear during severe physical exertion, for example, while climbing to the third floor and above. Normal physical activity does not cause signs of disease.
• FC 2 – moderate heart failure, it makes itself felt only after climbing two flights of stairs or while walking quickly. The patient's daily activities may be slightly reduced.

• 3 FC – the symptoms of the disease become pronounced even with minor physical exertion and during everyday activities. At rest, shortness of breath completely disappears.
• 4 FC - in this case, shortness of breath and other manifestations bother the patient at rest. The heart is under great stress, and complications of heart failure are often observed.

Types of heart failure according to its classification by stages:

• The first stage is the beginning of the disease. It is characterized by a latent course; symptoms of circulatory failure occur only in cases where the patient experiences severe physical or emotional stress. At rest, the activity of the circulatory system is not impaired.
• The second stage is marked clinical manifestations. Signs of prolonged blood stagnation appear, this is noticeable in the absence of physical activity. Stagnation appears in the systemic and pulmonary circulation, which is primarily manifested by edema. This stage is divided into IIA and IIB. The first is characterized by dysfunction of only the left or right ventricle. In this case, shortness of breath appears during normal physical activity for a person, and his activity is noticeably reduced. Externally, the patient has bluish skin, swelling of the legs, enlarged liver and hard breathing. Stage IIB is characterized by a deeper degree of hemodynamic disturbances, the cause of which is stagnation in both circulation circles.
• The third stage of the disease is terminal. In this case, the heart ceases to cope with its function, which leads to irreversible damage in the structure internal organs, to the depletion of their resources.

Signs and symptoms of the disease

Clinical symptoms of heart failure are the same for both acute and chronic variants of this pathology. The difference lies in the speed of development of disease manifestations and the body’s ability to adapt to changes in hemodynamics. Therefore, in case of acute circulatory failure, full compensation does not occur, as a result of which the terminal stage quickly occurs and the risk increases fatal outcome. The chronic version of the disease may not manifest itself for a long time, and therefore diagnosis and treatment are often delayed.

How to recognize heart failure? The clinical picture consists of symptoms associated with stagnation of blood in the vessels due to the inability of the heart muscle to fully perform its function. As a result, swelling appears in the lower extremities and stagnation in the pulmonary circulation, which causes wheezing. The patient loses the ability to adequately cope with physical and emotional stress, so efforts of normal intensity often lead to shortness of breath.

Stagnation of blood leads to disruption of oxygen transport into tissues - hypoxia develops, metabolism changes, and cyanosis (cyanosis) of the skin of the extremities and nasolabial triangle appears.

Headache. This symptom is not typical for heart failure. Loss of consciousness, dizziness, and darkening of the eyes are more likely.

Nausea and vomiting. Such manifestations of heart failure are also not typical for this disease. However, in in rare cases they may indicate the development of metabolic disorders.

Drowsiness. Decreased performance, fatigue and drowsiness may be a consequence of circulatory failure, which leads to decreased oxygen saturation of tissues.

Heart failure in newborns and adolescents

This disease in children and newborns is quite difficult to diagnose, as it often resembles the manifestations of other pathologies. The cause of heart failure at an early age is usually associated with congenital diseases:

• heart defects;
• CNS lesions;
• glycogen disease, cardiac form;
• endocardial fibroelastosis.

It is also worth taking into account that this condition can occur with infectious diseases caused by viruses or bacteria.

There are no significant differences in how heart failure manifests itself in children. Typically, symptoms include shortness of breath, swelling, and increased heart rate. The main changes in the internal organs are the liver enlarges, the boundaries of the heart expand.

Heart failure in adolescents occurs when they have a cardiac defect. The signs of heart failure in adolescents are no different from those in children and adults, which helps establish the diagnosis.

Methods for diagnosing heart failure

Heart failure syndrome is secondary disease, which occurs against the background of other pathologies. In this regard, examination and diagnostic measures should be aimed primarily at identifying the cause of this condition. Important early diagnosis circulatory failure, when there are no pronounced clinical symptoms.

For those patients who have been diagnosed with a heart attack and other myocardial diseases, arterial hypertension, it is important to pay attention to the presence of such a symptom as shortness of breath that occurs during physical exertion. Other characteristic features, which make it possible to suspect the presence of heart failure - swelling in the lower extremities, expansion of the borders of the heart to the left side.

The pulse in patients with circulatory failure is usually low-amplitude. An increase in heart rate is also typical.

Clinical blood tests for heart failure are nonspecific or reflect changes caused by primary pathology. More specific are blood gas and electrolyte tests. It is also important to determine blood pH, creatinine, urea and indicators protein metabolism V biochemical analysis. It is possible to determine the level of cardiac-specific enzymes, which can increase both in heart failure and in myocardial ischemia.

Diagnosis of heart failure is largely determined by the indications of instrumental research methods. According to ECG data, signs of myocardial hypertrophy, which develops in response to increased load on the heart muscle. Rhythm disturbances or signs of ischemia may also be detected muscle tissue hearts.

There are special stress tests, which involve taking an ECG with physical activity. This is possible by using an exercise bike or treadmill. The load is gradually increased, thanks to which it is possible to determine the functional class of HF and the presence of signs of myocardial ischemia.

Echocardiography makes it possible to both determine heart failure and visualize the structure of the heart to determine the cause of its dysfunction. At the same time, echocardiography evaluates the functional state of the heart, for example, ejection fraction and other indicators of pumping function. MRI makes it possible to determine the presence of defects of this organ. X-ray of the lungs and chest organs shows the presence of stagnation in the pulmonary circulation.

To determine the extent of damage to other internal organs in severe circulatory failure, an abdominal ultrasound is performed. It shows changes in the spleen, liver, pancreas and other organs.

Methods of treating the disease

Treatment of heart failure involves conservative therapy. It includes the following areas:

• reduction of clinical manifestations of circulatory failure. For this purpose, cardiac glycosides are prescribed - for AHF, intravenous fast-acting drugs are used, for CHF, long-acting drugs are used;
• reducing the load on the myocardium - this is achieved by using beta-blockers, which lower blood pressure and slow down the pulse;
• prescribing diuretics to reduce the total amount of fluid in the body.

It is worth noting that it is impossible to cure heart failure, you can only reduce its symptoms and signs. The best results are obtained from treatment of first-degree heart failure. A patient who has taken all recommended medications in this case may not notice any improvement in his condition.

If the patient has a history of arrhythmia, which may have caused the development of myocardial failure, then it is possible surgery. It consists of implanting an artificial pacemaker. Surgical treatment also indicated in those cases. When there is a significant narrowing of the lumen of the arteries due to atherosclerosis, when there is pathology of the valves.

What is the danger of heart failure, consequences and complications?

Circulatory failure is progressive in nature, as a result of which, in the absence of proper treatment for this condition, the patient’s condition worsens over time, the degree of hemodynamic disorders increases, which often leads to death.

Frequent consequences of heart failure occur due to pulmonary edema, when there is stagnation in the pulmonary vessels, the liquid part of the blood penetrates into the tissues of this organ. Because of this, the ability of the lungs to saturate the blood with oxygen sharply decreases, and hypoxia develops.

With circulatory failure, signs of cerebral ischemia may appear, which is manifested by fainting, dizziness, and darkening of the eyes.

Heart failure of the 1st degree usually least often leads to serious consequences.

Disease prevention

Prevention of heart failure is based on the treatment of diseases, the development of which leads to circulatory failure - hypertension, valve defects, etc. On the other hand, it is important to adjust the patient’s lifestyle in order to reduce the number of risk factors.

If cardiac function is already impaired, then prevention of heart failure should be aimed at maintaining optimal levels of daily physical activity, constant monitoring by a cardiologist, taking prescribed medications.

What to do in case of heart failure to increase the body's chances of recovery? In addition to reception medicines In the treatment of circulatory failure, correction of the patient’s lifestyle plays an important role. For treatment to be effective, people with this disease must reduce their body weight to normal levels, since overweight– This is one of the most common causative factors of hypertension.

Patients with this pathology are advised to adhere to a diet. It consists primarily of limiting salt intake. Patients with heart failure should completely avoid this flavor enhancer, since salt reduces the excretion of fluid from the body, which leads to increased stress on the myocardium.

If the patient smokes or drinks alcohol, then these habits will have to be completely abandoned.

It is also necessary to exercise regularly. Depending on the severity of the disease, the permissible amount of stress also changes. For example, with functional class III, regular walking for about 40 minutes is sufficient, and for milder cases of circulatory failure, it is possible to add special exercises. Physical therapy is prescribed by the attending physician, so you should not increase the daily volume on your own physical exercise without knowing the whole picture of the disease. At the same time, the symptoms and treatment of severe heart failure do not allow the patient to carry out this method of rehabilitation.

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

CONGESTIVE LIVER

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

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

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

Congestion is clinically expressed in enlarged liver, its lower edge reaches the navel, hard, smooth and sensitive to palpation. The sensitivity of an enlarged liver is an early sign of stagnation, which precedes edema. Sometimes it moves and pulsates, so that the hepatic pulse can be observed. Ripple occurs during ventricular systole, and hepatic-jagular reflux is important. These dynamic phenomena are observed more often with tricuspid valve insufficiency.

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

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

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

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

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

CARDIAC CIRRHOSIS

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

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

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

Cardiac cirrhosis of the liver has the following pathological picture. The walls of the dilated central veins are sclerotic and thickened. The number of capillaries and anastomoses between the hepatic and portal veins increases. As a result of the proliferation of connective tissue, central vein difficult to recognize. Biliary tract proliferate and islands of regeneration appear. The most characteristic of cardiac cirrhosis is a pronounced degree of fibrosis in the central zones and compression of the portal vein by the overgrown connective tissue. Obviously, this is why the term cardiac fibrosis arose, which many authors recommend calling this liver damage.

Despite some features of the morphological development of cardiac cirrhosis, its clinical symptoms are largely identical to portal cirrhosis. When examining a patient, a slight yellowness of the skin is often noted. The combination of jaundice with existing cyanosis gives the skin a peculiar appearance.

The liver in these cases is not very large, but hard, with a sharp edge and finely nodular surface; sometimes the spleen is enlarged. Liver pulsation disappears, ascites develops. It is especially difficult to decide whether ascites is caused by cardiovascular failure or liver damage. Development of ascites after long period edema, ongoing shrinkage and hardening of the liver, enlarged spleen and hypoalbuminemia provide grounds for the diagnosis of cardiac cirrhosis. In these cases, ascites, like other signs of cirrhosis, persist even after successful treatment cardiovascular failure (edema disappears, etc.).

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

The basis for the diagnosis of cardiac cirrhosis is the presence of prolonged decompensation in diseases such as mitral stenosis with tricuspid valve insufficiency, adhesive pericarditis, cor pulmonale. A functional study of the liver reveals pronounced disturbances in its function. Thus, along with hypoalbuminemia, the level of gammaglobulins and bilirubin may increase, sediment reactions become positive, and sometimes the Kwik-Pytel test indicators decrease. At radioisotope research liver function, pronounced disturbances are observed.

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

CARDIAL JAUNDICE

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

The yellowness of the skin and sclera in cardiac cirrhosis is slight, itchy skin absent. The uneven coloring of the skin is noteworthy. Thus, in places of massive edema, the skin is not yellow due to the fact that bilirubin circulating in the blood is bound to protein and does not enter the edematous fluid. In a small number of patients, jaundice acquires the features of mechanical jaundice: intense, with a grayish tint, coloring of the skin, pigments in the urine and light-colored feces are noted.

The mechanism of jaundice in circulatory disorders is different.

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

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

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

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

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

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