Congestion in the liver treatment. Congested 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 an increase in it, pain in the right hypochondrium, indigestion, temporary slight icteric coloration of the skin, etc. The above-described painful condition is very often found 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 latter, congestive hyperemia with an incipient circulatory disorder, light forms diffuse hepatitis of various etiologies, swelling of the liver with gout, etc.

Most often, behind the diagnosis, stagnation in the liver is hidden during cholelithiasis or starting .

Concerning the course and duration of active hyperemia of the liver, 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 proceed chronically.

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 the diet (moderate lifestyle, the prohibition of all alcoholic beverages)
• a sufficient amount of movement in the fresh air (horse riding)
• prescribing laxatives
• water treatment in Karlsbad, Marienbad, Kissingen, Hamburg, etc.

Congestive heart failure (CHF) is the inability of the heart muscle to pump enough blood to keep the body's metabolism going. If the pumping function of the heart weakens, then the venous blood begins to stagnate, blood circulation is disturbed. To compensate for the insufficiency, certain areas of the myocardium begin to increase in order to perform the function of pumping blood. The patient thus becomes easier, but only for a while.

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. Allocate 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 also differ. At defeat of a right ventricle disturbances in a big circle of blood circulation are observed. As a result, swelling of the extremities appears, in particular, the legs swell, pain occurs in the right hypochondrium, dry mouth appears. The liver enlarges, becomes painful on palpation.

Often there is nocturia, which implies a violation of the process of urination. Due to the stagnation of blood in the veins during the day, metabolism is difficult and is activated at night, when the body is at rest. A person suffering from heart failure mostly 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 weight of the patient increases.

Symptoms of left-sided heart failure are caused by impaired functioning of the small (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, shortness of breath;
• high arterial pressure and tachycardia;
• rapid heartbeat, which causes insomnia;
• general weakness;
• rapid onset of fatigue with minimal physical exertion;
• dry cough;
• difficulty breathing when lying down (orthopnea).

However, every body is different and symptoms can vary. 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 sleep only in a half-sitting position. Absorption of food in the intestines worsens, which causes diarrhea. Thus, a violation of the function of the heart in pumping blood negatively affects most of the vital important organs develop other diseases. Heart failure can also lead to death.

Causes

The development of this pathology is often provoked by an increased load on the myocardium. If it is not a congenital heart disease 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 pectoris, 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. Too fast, slow or simply uneven heart rate (arrhythmia) also has a negative effect. In the presence of diseases of the heart and blood vessels, 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, suffocation, 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);
• assessment of lung function;
• electrocardiogram, echocardiogram.

Treatment includes several directions: elimination of the cause of the development of the disease, mitigation of the symptoms of its manifestation, prevention of complications. In the presence of edema, salt is excluded from the patient's diet. The maximum amount of liquid consumed per day should not exceed 0.8–1 liter.

To normalize the function of fluid excretion, diuretics are prescribed, which increase the formation of urine, relieve swelling. Usually, after giving up table salt, the patient's shortness of breath decreases, cyanosis (cyanosis) 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 in which the patient develops shortness of breath. Congestive heart failure provokes sleep disorders. It is recommended that the patient sleep with his head elevated, as breathing is difficult in the supine position.

Medications 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 rhythm of the heartbeat, glycosides, beta-blockers are used. Sometimes, to increase the effectiveness of treatment, drugs are prescribed that retain potassium in the body, which is so useful for the myocardium. If necessary, use funds to stabilize blood pressure.

Signs of heart failure will help remove a complete rejection of fatty, fried and especially spicy food. It is better to eat only fruits and vegetables, the use of dried apricots is especially useful. Doctors recommend eating according to Diet No. 10.

In the absence of a positive effect from therapy, the option of surgical intervention is considered by correcting deformed areas of the heart or organ transplantation.

Prevention

Congestive heart failure can be prevented preventive measures. The best prevention is healthy lifestyle life that includes proper nutrition active rest and moderate exercise. Recovery is facilitated by a small charge, if it does not cause shortness of breath in the patient. It is necessary to completely give up smoking, alcohol, drugs, coffee and strong tea. General strengthening immunity also plays an important role, as it is general prevention diseases that can lead to NMS.

The person must have normal weight corresponding to growth. With deviations up or down, the load on the heart also increases. For the normal functioning of the heart muscle, healthy sleep, which is 7-8 hours a day. Avoid stressful situations, depression, overexertion.

Viburnum is very useful for the heart. You can grind it, pour water and add honey. You need to take this remedy twice a day for a month. To prevent puffiness, parsley seeds should be brewed or eaten raw. It perfectly strengthens the walls of the heart.

Freshly squeezed juices are also useful for heart failure, for example, beetroot normalizes blood pressure, and pumpkin eliminates heart palpitations. Beneficial effect on the body and Spa treatment. Therapeutic baths, massages, aromatherapy, exercise therapy, just sea ​​air contribute to the strengthening of the cardiovascular system. Thus following all preventive advice 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 terms of their causes and defining features. LH is associated with the endothelium (inner layer) of the pulmonary vessels: growing, 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 is very low, especially in primary PH.

The 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 not anatomically adapted to long-term pressure loading, and with PH in the system pulmonary artery it rises above 25 mm Hg. at rest and 30 mmHg during exercise. First, in a short period of compensation, there is a thickening of the myocardium and an increase in the right heart, and then - a sharp decline force of contractions (dysfunction). The result is premature death.

Why does PH develop?

The causes of the development of PH have not yet been finally determined. For example, in the 60s in Europe there was an increase in the number of cases associated with the excessive use of contraceptives and weight loss agents. Spain, 1981: Complications of muscle damage following the popularization of rapeseed oil. Almost 2.5% of 20,000 patients were diagnosed with arterial pulmonary hypertension. The root of evil was the tryptophan (amino acid) present in the oil, this was scientifically proven much later.

Dysfunction (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, the vascular tone changes towards spasm, then inflammation, endothelial growth begins and arterial lumen decreases.

Violation of the synthesis or availability of nitric oxide (NO), a decrease in the level of prostacyclin production, 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 give any severe 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, compared with the norm, by two or more times. The norm of pressure in the pulmonary artery: systolic 30 mm Hg, diastolic 15 mm Hg.

Initial symptoms of pulmonary hypertension:

• Unexplained shortness of breath, even with little physical activity or at complete rest;
• Gradual weight loss even with a normal, nutritious diet;
• Asthenia, constant feeling of weakness and impotence, depressed mood - regardless of the season, weather and time of day;
• Persistent dry cough, hoarse voice;
• Discomfort in the abdomen, a feeling of heaviness and "bursting": the onset of stagnation of blood in the portal vein system, which conducts venous blood from the intestines to the liver;
• Dizziness, fainting - manifestations of oxygen starvation (hypoxia) of the brain;
• Rapid heartbeat, over time, the pulsation of the jugular vein becomes noticeable on the neck.

Later manifestations of PH:

1. Blood-streaked sputum and hemoptysis: signal increasing pulmonary edema;
2. Attacks of angina (chest pain, cold sweat, fear of death) - a sign of myocardial ischemia;
3. arrhythmias (disturbance heart rate) by the type of ciliated.

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

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

Terminal stage of HT:

• Thrombi in the arterioles of the lungs lead to the death (infarction) of the active tissue, an increase in suffocation.

Hypertensive crises and seizures acute edema lungs: more often occur at night or in the morning. Begins with a feeling of a sharp lack of air, then joins coughing, bloody sputum is produced. The skin becomes bluish (cyanotic) and the veins in the neck throb. The patient is excited and frightened, loses self-control, can move chaotically. In the best case, the crisis will end with a copious discharge of light urine and uncontrolled fecal discharge, in the worst case, with a fatal outcome. The cause of death may be the blockage of a thrombus (thromboembolism) of the pulmonary artery and subsequent acute heart failure.

The main forms of PH

1. Primary, idiopathic pulmonary hypertension (from the Greek idios and pathos - "a kind of disease"): is fixed as a separate diagnosis, in contrast to secondary PH associated with other diseases. Variants of primary PH: familial PH and a hereditary predisposition of blood vessels to dilate and bleed (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 diseases of the connective tissue - scleroderma, rheumatoid arthritis, systemic lupus erythematosus.

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

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

HIV infection: PH is diagnosed in 0.5% of cases, survival for 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: in some types of anemia, 20-40% are diagnosed with PH, which increases the mortality among patients.

Chronic obstructive pulmonary disease (COPD), caused by long-term inhalation of particles of coal, asbestos, shale and toxic gases. It often occurs as an occupational disease among miners, workers in hazardous industries.

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

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

Damage to 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: mean ≥ 25 mm Hg at rest, more than 30 mm Hg with 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: mean ≥25 (mmHg)
2. Initial: >15 mm
3. Difference ≥12 mm (passive LH) or >12 mm (reactive).

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

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

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

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

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

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

Insertion of a catheter into the cavities of the "right" heart, testing the response of blood vessels: 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 combination, combining general recommendations to reduce the risk of exacerbations; adequate therapy underlying disease; symptomatic remedies impact on common manifestations LG; surgical methods; treatment with folk remedies and non-traditional methods - only as auxiliary.

Vaccination (influenza, pneumococcal infections): for patients with autoimmune systemic diseases- rheumatism, systemic lupus erythematosus, etc., for the prevention of exacerbations.

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

Prevention of pregnancy (or, if indicated, even its termination): the circulatory system of mother and child are connected together, an increase in the load on the heart and blood vessels of a pregnant woman with PH can lead to death. According to the laws of medicine, the priority in saving a life 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, feeling of uselessness and burdensomeness for others, irritability over trifles - typical psychological picture any "chronic" patient. Such a 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, activities to your liking, active communication with fellow sufferers and healthy people are an excellent basis to feel the taste for life.

Supportive care

• Diuretic drugs remove accumulated fluid, reducing the workload on the heart and reducing swelling. Be sure to control the electrolyte composition of the blood (potassium, calcium), blood pressure and kidney function. An overdose threatens with too much water loss and pressure drop. With a decrease in potassium levels, arrhythmias begin, 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. It is necessary to constantly monitor the state of the blood coagulation system (platelets).
• Oxygen (oxygen therapy), 12 - 15 liters per day, through a humidifier: for patients with chronic obstructive pulmonary disease (COPD) and cardiac ischemia, helps to restore blood oxygen saturation and stabilize the general condition. It must be remembered that too much oxygen concentration depresses the vasomotor center (SDC): breathing slows down, blood vessels dilate, pressure drops, the person loses consciousness. For normal operation, the body needs carbon dioxide, it is after an increase in its content in the blood that the SDC "gives the command" to take a breath.
• Cardiac glycosides: active components are isolated from foxglove, Digoxin is the most famous of the drugs. Improves heart function by increasing blood flow; fights against arrhythmias and vascular spasm; reduces swelling and shortness of breath. In case of overdose - increased excitability of the heart muscle, rhythm disturbances.
• Vasodilating: 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 spasm, prevent the formation of blood clots, block the growth of the endothelium. Very promising drugs, effective in PH on the background of HIV, systemic diseases(rheumatism, scleroderma, etc.), heart defects, as well as familial and idiopathic forms of PH.
• Endothelin receptor antagonists: vasodilation, suppression of growth (proliferation) of the endothelium. With prolonged use, shortness of breath decreases, the person becomes more active, pressure normalizes. Undesirable reactions to treatment are edema, anemia, disruption of the liver, so the use of drugs is limited.
• Nitric oxide and PDE type 5 (phosphodiesterase) inhibitors: used mainly for idiopathic PH, if standard therapy does not justify itself, but individual preparations effective in any form of LH (Sildenafil) Action: reduction of vascular resistance and associated hypertension, facilitation of blood flow, resulting in increased resistance to physical activity. Nitric oxide is inhaled daily for 5-6 hours, up to 40 ppm, the course is 2-3 weeks.

Surgical treatments for PH

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

Lung transplantation (or lung-heart complex): performed according to vital indications, only in profile 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 lack of donor organs. Lungs are taken from only 15%, heart from 33%, and liver and kidneys from 88% of donors. Absolute contraindications for transplantation: chronic renal and hepatic insufficiency, 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 a general improvement in well-being. No self-treatment!

Classification and forecast

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

• Class I: PH with normal physical. activity. Standard loads are well tolerated, mild PH, grade 1 insufficiency.
• Class II: LH plus activity is reduced. Comfortable in a relaxed position, but dizziness, shortness of breath and chest pains begin with normal exertion. Moderate pulmonary hypertension, increasing symptoms.
• Class III: PH with decreased initiative. Problems even at low loads. High degree of blood flow disorders, poor prognosis.
• Class IV: LH with intolerance minimum activity. Shortness of breath, fatigue is felt and in 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 ongoing treatment improves the patient's condition;
3. The pressure in the pulmonary artery system decreases.

Unfavorable prognosis:

1. Symptoms of PH are dynamic;
2. Signs of decompensation of the circulatory system (pulmonary edema, ascites) are growing;
3. Pressure level: in the pulmonary artery more than 50 mm Hg;
4. in primary idiopathic PH.

The overall prognosis for pulmonary arterial hypertension is associated with the form of PH and the phase of the prevailing disease. Mortality per year, with current methods of treatment, is 15%. Idiopathic PH: the survival of patients 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 the blood is not pumped in the proper volume. Acute heart failure can lead to the death of a person in a short time, since there is a high probability dangerous complications. Chronic HF develops gradually and leads to prolonged "starvation" of body tissues.

Causes of the disease

Why does heart failure occur? This condition is 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 the vessels lead to the fact that it becomes difficult for the heart to push blood. The body's resources allow compensating for this pathological condition - at first there are no clinical symptoms of circulatory failure due to an increase in heart rate and an increase in the strength of heart contractions. When the myocardium is depleted, decompensation of the disease occurs - this is manifested by shortness of breath, edema, and a decrease in 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, valvular defects, infectious and autoimmune diseases, intoxications. In diseases of the lungs, an increase in pressure in the small 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 with 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 past 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 rate of development of the clinic:

• acute HF - progresses in a very short time (a few minutes - a few hours). Complications of this type of disease often become pulmonary edema or shock of a cardiogenic nature. Most common causes 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 are compensated pathological conditions with damage to the heart and other organs (arterial hypertension, defects, chronic diseases lungs, etc.).

Classification

There are several ways to classify heart failure. Depending on the severity of the clinic, the following are distinguished:

• First degree - no clinical symptoms.
• In the second degree of heart failure, the symptoms are mild, 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. Art.).

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

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

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

Types of heart failure according to its classification by stages:

• The first stage is the onset of the disease. It is characterized by a latent course, the symptoms of circulatory failure occur only in cases where the patient experiences a pronounced physical or emotional stress. At rest, the activity of the circulatory system is not disturbed.
• The second stage is marked clinical manifestations. There are signs of prolonged stagnation of blood, this is noticeable in the absence of physical activity. Stagnation appears in the large and small circles of blood circulation, which is primarily manifested by edema. This stage is subdivided into IIA and IIB. The first is characterized by impaired function of only the left or right ventricle. In this case, shortness of breath appears during normal physical exertion for a person, its activity is markedly reduced. Outwardly, the patient has blue 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 circles of blood circulation.
• 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 structure internal organs to deplete their resources.

Signs and symptoms of the disease

The clinical symptoms of heart failure are the same for both acute and chronic variant of this pathology. The difference lies in the rate of development of the manifestations of the disease and the body's ability to adapt to changes in hemodynamics. Therefore, in acute circulatory failure, full compensation does not occur, as a result of which the terminal stage quickly sets in and the risk increases. lethal outcome. The chronic variant of the disease may not manifest itself for a long time, and therefore the diagnosis and treatment are often belated.

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, edema appears on 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 the conceived efforts of normal intensity lead to shortness of breath.

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

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

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

Drowsiness. Decreased performance, fatigue and drowsiness may be the result of circulatory failure, which leads to a decrease in 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 manifestations of other pathologies. The cause of HF at an early age is usually associated with congenital diseases:

• heart defects;
• CNS lesions;
• glycogen disease, cardiac form;
• fibroelastosis of the endocardium.

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. Usually the symptomatology consists in the appearance of shortness of breath and edema, increased heart rate. The main changes in the internal organs - the liver increases, the boundaries of the heart expand.

Heart failure in adolescents occurs when they have a heart defect. Signs of heart failure in adolescents do not differ from those in children and adults, which helps to establish the diagnosis.

Methods for diagnosing heart failure

Heart failure syndrome is secondary disease that 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 insufficiency, when there are still 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 characteristics, which make it possible to suspect the presence of CH - edema 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 characteristic.

CBC in HF is nonspecific or reflects changes caused by the primary pathology. More specific are the analysis of blood gases and electrolytes. It is also important to determine the pH of the blood, the level of creatinine, urea and indicators protein metabolism V biochemical analysis. It is possible to determine the level of cardiospecific enzymes, which can increase both in HF and in myocardial ischemia.

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

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

Echocardiography makes it possible to both determine heart failure and visualize the structure of the heart in order 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 in this organ. X-ray of the lungs and chest organs shows the presence of stagnation in the pulmonary circulation.

To determine the degree 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.

Ways to treat the disease

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

• reduction of clinical manifestations of circulatory failure. For this, cardiac glycosides are prescribed - for AHF, intravenous fast-acting drugs are used, for CHF - long-acting drugs;
• reducing the load on the myocardium - this is achieved by using beta-blockers, which lower blood pressure and slow down the pulse;
• the appointment of diuretics in order 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 by the treatment of heart failure of the first degree. A patient who has taken all the recommended drugs in this case may not notice an improvement in his condition.

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

What is dangerous heart failure, consequences and complications

Circulatory insufficiency is progressive in nature, as a result of which, in the absence of proper therapy 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, hypoxia develops.

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

Heart failure of the 1st degree is usually the least likely to lead to serious consequences.

Disease prevention

Prevention of heart failure is based on the treatment of diseases, the development of which leads to the appearance of 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 heart function is already compromised, then prevention of heart failure should be aimed at maintaining an optimal level of daily physical activity, constant monitoring by a cardiologist, taking prescribed drugs.

What to do with heart failure to increase the chances of recovery of the body? In addition to receiving medicines in the treatment of circulatory failure, an important role is played by the correction of the patient's lifestyle. In order for the treatment to be effective, people with this disease must reduce body weight to normal values, since overweight is one of the most common causative factors of hypertension.

Patients with this pathology are advised to follow a diet. It consists primarily in limiting salt intake. Patients with heart failure should completely abandon this flavor enhancer, since salt reduces the excretion of fluid from the body, which leads to an increase in the load on the myocardium.

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

You also need to exercise regularly. Depending on the severity of the disease, the allowable volume of loads also changes. For example, in functional class III, regular walking for about 40 minutes is sufficient, and in milder cases of circulatory failure, the addition of special exercises. Physiotherapy exercises are prescribed by the attending physician, so you should not independently increase the daily volume 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 is especially true for 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 the systole of the right ventricle.

STAGGING LIVER

The most common picture of congestive liver. As a result various lesions of the heart, stagnation occurs in the right atrium, pressure in the hepatic veins increases and expansion of the central veins occurs. Deceleration of blood circulation increases the overflow of blood of the central veins, the central part of the lobules, and central portal hypertension develops, which is predominantly mechanical origin followed by hypoxia. With the help of catheterization of the veins of the liver in patients with circulatory failure, it was shown that they contain less oxygen than in 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. On the periphery of the lobules, where the blood supply is worse, obesity of the liver cells occurs. If the venous congestion is removed, the centrilobular cells regenerate and the liver restores its original structure. True, a number of authors noted that with a decrease in venous pressure, venous congestion is not always eliminated, the same applies to the histological picture of the liver.

Stagnation is clinically expressed in an increase in the liver, its lower edge reaches the navel, hard, even and sensitive to palpation. Tenderness of an enlarged liver is an early sign of congestion that precedes edema. Sometimes it moves, pulsates, so that a hepatic pulse can be observed. Pulsation occurs during the period of ventricular systole, hepato-jagular reflux matters. These phenomena of a dynamic nature are observed more often with tricuspid valve insufficiency.

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

With a congestive liver, ascites can develop, in the origin of which are important: increased pressure in the veins of the liver, a decrease in 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 content of bilirubin increases slightly and the level of albumin in the blood serum decreases. The most pronounced changes are observed when applying 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.

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

Congestive liver does not require special treatment. The use of leeches on the liver area against the background of cardiac therapy contributes to the action of diuretic drugs. a salt-free, high-calorie diet with enough protein and vitamins.

CARDIAC CIRRHOSIS

Fibrotic changes in the liver occur secondarily as a result of anoxia, centrilobular necrosis and reparative processes. this central fibrosis can later lead to centrilobular cirrhosis. Sustained and often 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, connective tissue filaments extend to the central veins of neighboring fields, connecting them with 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) connective tissue proliferation.

The relative rarity of these changes, and hence the development of true cirrhosis, depend on the fact that during heart 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, that there are no periods of remission, when conditions for nodal regeneration appear. True liver cirrhosis accounts for 0.4% of all autopsies.

Cardiac cirrhosis of the liver has the following pathoanatomical 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 growth of connective tissue, central vein difficult to recognize. biliary tract proliferate and there are islands of regeneration. The most characteristic for cardiac cirrhosis is a pronounced degree of fibrosis in the central zones and compression of the portal vein of the overgrown connective tissue. Obviously, therefore, the term cardiac fibrosis has arisen, which many authors recommend to call this damage to the liver.

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 with a fine nodularity of the surface, sometimes the spleen is enlarged. Liver pulsation disappears, ascites develops. It is especially difficult to decide what causes ascites - cardiovascular insufficiency or liver damage. Development of ascites after long period edema, the upcoming reduction and compaction of the liver, enlargement of the spleen and hypoalbuminemia give grounds for the diagnosis of cardiac cirrhosis. In these cases, ascites, like other signs of cirrhosis, persist even after successful treatment cardiovascular insufficiency (edema disappears, etc.).

Patients with cardiac cirrhosis often have poor tolerance medicines, especially increased sensitivity to foxglove 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 violations of its function. So, along with hypoalbuminemia, the level of gammaglobulins and bilirubin may increase, sedimentary reactions become positive, and sometimes the indicators of the Quick-Pytel test decrease. At radioisotope study liver function, its pronounced violations are observed.

The presence of cardiac cirrhosis does not in itself significantly worsen the prognosis and, if the heart disease is treated, cirrhosis may be latent, without a tendency to periodic exacerbations process.

CARDIAC JAUNDICE

Although overt jaundice is uncommon in patients with hepatic congestion and cardiac cirrhosis, serum bilirubin concentrations remain elevated frequently. Jaundice occurs with the same frequency as 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 matters in the development of jaundice. So, out of 424 autopsies of those who died from heart disease, 4% had jaundice, of which 10.5% had a heart attack (Kugel, Lichtmann).

Yellowness of the skin and sclera in cardiac cirrhosis is small, pruritus absent. Note the uneven coloration of the skin. So, in places of massive edema, the skin is not colored 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 mechanical features: intense, with a grayish tinge of skin staining, pigments in the urine and light 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, the liver cells inadequately excrete all pigments and indeed the most intense jaundice is observed in patients with severe and widespread necrosis of the liver cells. However, there are exceptions to this rule, when there is no jaundice in case of tricuspid valve insufficiency with severe liver damage.

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

(3 ) Hemolytic jaundice often combined with hemorrhages in the tissues, especially pulmonary infarctions. Known sudden appearance jaundice in the clinical picture of a heart attack: whether it be of the lung, spleen or kidneys, while heart attacks of the same localization, but without heart damage, do not give jaundice.

An additional depot of hemoglobin is created in the focus 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 which is detected by pi. lung infarction and noted an increase in serum bilirubin. There is also an excess of pigment in the tissues during stagnation in the lungs due to heart damage, since even without a heart attack, stagnation in the lungs leads to the destruction of hemoglobin.

Consequently, jaundice in lesions of the heart in most cases of a mixed type; Of greatest importance are lesions of liver cells and their overload with pigment as a result of heart attacks, which is also confirmed by laboratory data. Urine dark with an increased amount of urobilin, with intense jaundice, other bile pigments are also found; dark feces with an increased amount of stercobilin, in some cases gray color with a decrease in pigment secretion. An increased amount of bilirubin is determined in the blood, often with a direct van den Berg reaction.

Treatment It is directed mainly to the prevention and treatment of the underlying disease. In addition, the presence of liver damage requires a diet - table number 5, a complex of vitamins, if necessary, choleretic drugs, according to strict indications, corticosteroids.