Heart failure is a heart disease that is caused by poor circulation. The heart is not able to pump blood effectively, and therefore the circulation of oxygen and nutrients throughout the body is disrupted, resulting in blood stagnation. Among other things, heart failure can provoke coronary heart disease, heart disease, lung disease, myocarditis, rheumatism and arterial hypertension.

Prevention of heart failure

The main preventive actions are:

Heart failure can be caused by increased stress, so it is necessary to train the cardiovascular system. It is important that the exercises are dosed and individually selected.

In stable condition, doctors recommend walking for 20-30 minutes 3-5 times a week. An alternative is to ride a bike for 20 minutes five times a week. However, the duration of the load can be determined by the person himself; the only obligatory condition is that the state of health does not deteriorate. The first signal that you should stop exercising is the appearance of slight shortness of breath.

In medicine, there are several classifications of heart failure. Recently, the most common one is the one proposed by the New York Heart Association.

Based on subjective indicators, four functional classes are distinguished:

I functional class– has no restrictions on physical activity. Habitual physical activity does not cause fatigue, weakness, shortness of breath or palpitations.

II functional class– restrained restriction physical activity. Patients at rest do not show pathological symptoms.

III functional class– obvious limitation of physical activity. A small physical activity causes the manifestation of clinical symptoms in patients.

IV functional class– the slightest physical activity causes chest discomfort. Signs appear even in a calm state, and slight physical activity can intensify symptoms.

Causes of heart failure

The main cause of heart failure is any pathological disease that impairs the functioning of the heart. In most cases, heart failure is a natural outcome of diseases of the heart and blood vessels. Sometimes illness can serve as the first signal of a serious heart disease.

After the occurrence hypertension It may take quite a long time before the first symptoms of heart failure appear. The disease can progress quite quickly, often we're talking about not even about days and hours, but about minutes. In such cases, we can talk about acute failure. The remaining cases are classified as chronic heart failure.

The main directions of treatment of heart failure:

1. Symptomatic treatment – ​​elimination of symptoms.
2. Protecting the organs that are most affected by poor heart function. Most often these are the brain, kidneys and blood vessels.
3. Extending the patient's life and improving its quality.

Symptoms of chronic heart failure

In children, chronic insufficiency is manifested by a lag in physical development, anemia and underweight. In addition, the child may have impaired breathing, central and peripheral circulation.

In adults, chronic heart failure is accompanied by polycythemia and acrocyanosis. For patients of any age, a common symptom is pale skin.

In the early stage of chronic failure, the disease manifests itself only during physical activity. In the later stages, the symptoms are stable and can be expressed even when the patient assumes a horizontal position, resulting in shortness of breath.

First aid for heart failure

First aid for heart failure should be aimed at improving the contractility of the heart. If heart failure is associated with angina pectoris, then the patient should place one nitroglycerin tablet under the tongue. The doctor, providing first aid, must use strophanitis, corglycon and digoxin.

Eufillin is effective in reducing blood stagnation in the pulmonary vessels. The medicine can be administered intravenously in the form of a 2.4% solution and intramuscularly in the form of a 24% solution. To increase oxygen levels, the patient is given humidified oxygen to breathe. Furosemide or novorit is also administered.

How to treat heart failure?

The most important thing in treating chronic heart failure is to relieve the patient of symptoms. The treatment used must fully comply with the subjective requirements of the patient.

The following methods are used to treat the disease:

It should be remembered that the treatment of acute heart failure is a difficult process, since it often involves the treatment of accompanying diseases.

folk remedies

Since the end of the 18th century, digitalis, also called digitalis, has been considered the most effective folk remedy for the treatment of heart failure. The peculiarity of digitalis is that it affects only a diseased heart and has no effect on a healthy one. Digitalis preparations enhance the contractile function of the myocardium, the result of this effect is an increased amount of ejected blood.

Signs and treatment of heart failure

What is heart failure?

This is a disease accompanied by a certain set of symptoms, the development of which is caused by disruption of the processes of filling and emptying of the heart with the subsequent formation of hemodynamic disorders.

The following forms of deficiency are distinguished:

Acute heart failure

This pathology is a serious, life-threatening condition. It is characterized by the rapid development of the clinic as a result of a sudden drop in myocardial contractile function and a decrease in cardiac output.

The reasons leading to the development of acute failure are:

• inflammatory, dystrophic heart diseases;
• bradyarrhythmias, tachyarrhythmias;
• myocardial infarction (large focal transmural);
• pulmonary embolism;
• hypertensive crisis;
• state of decompensation of chronic heart failure.

The following clinical forms of acute failure exist:

• congestive – includes right and left ventricular failure, manifested by stagnation of circulating blood;
• hypokinetic – accompanied by the development of cardiogenic shock.

Symptoms of acute heart failure:

Left ventricular cardiovascular failure leads to a delay in circulating blood in the pulmonary circle. In this case, acute pulmonary edema develops, which is manifested by the following symptoms:

1. Increasing shortness of breath, up to suffocation.
2. Forced position of the body while sitting, since in a horizontal position the ventilation of the lungs deteriorates.
3. Cough with foamy sputum.
4. Distant moist rales in the lungs when breathing.
5. Increased heart rate.
6. Cyanosis of the skin and mucous membranes.

With significantly severe hypertension, cardiopulmonary failure develops in the pulmonary vessels. The main cause of the development of this condition is pulmonary embolism. Symptoms of the pathology are:

• sudden onset of shortness of breath at rest;
• cyanosis of the lips;
• acute chest pain;
• with a pulmonary infarction - hemoptysis.

Right ventricular failure of the heart is manifested by stagnation of circulating blood in the area of ​​the systemic circulation, which can be determined by the appearance of the following symptoms:

• swelling of the neck veins;
• pain in the right hypochondrium due to the development of portal hypertension, venous stagnation and liver enlargement, which is accompanied by stretching of the capsule;
• in case of acute necrosis of the liver parenchyma, jaundice may appear;
• development of ascites (fluid accumulation in the abdominal cavity).

The total form of the disease is characterized by combined signs of hemodynamic disturbances.

Cardiogenic shock is manifested by symptoms such as:

• decreased blood pressure, decreased pulse pressure;
• decreased urine output or complete absence urination;
• the appearance of sinus tachycardia;
• cold, sticky sweat;
• marbling of the skin.

Chronic heart failure (CHF)

It is more widespread and is the predominant form of the disease in clinical practice. The frequency of diagnosis increases with age. Thus, symptoms of CHF are most often detected in older people (in age group 60-80 years).

Reasons for the formation of CHF

Factors leading to the development of pathology include the following diseases:

• arterial hypertension;
• myocarditis, dilated cardiomyopathy;
• chronic ischemic heart disease: small focal infarction, post-infarction cardiosclerosis;
• lung diseases (chronic obstructive pulmonary disease, pneumonia);
• diabetes mellitus

In men, symptoms of the disease often develop after acute myocardial infarction. In women, the leading factor in the formation of chronic heart failure is arterial hypertension in combination with diabetes mellitus. In children, the most common cause is congenital anomalies of the heart.

Signs of CHF

At long term diseases, there are dysfunctions of all parts of the heart. In the clinical picture, the main symptoms of heart failure can be identified:

• fatigue;
• shortness of breath, cardiac asthma;
• peripheral edema;
• heartbeat.

Most patients complain of fatigue. The presence of this symptom is due to the following factors:

• low cardiac output;
• insufficient peripheral blood flow;
• state of tissue hypoxia;
• development of muscle weakness.

Shortness of breath in heart failure increases gradually - it first occurs during physical activity, then appears with minor movements and even at rest. With decompensation of cardiac activity, so-called cardiac asthma develops - episodes of suffocation that occur at night.

Signs of cardiac asthma:

• acute, sudden onset;
• feeling of lack of air, difficulty breathing;
• the appearance of suffocation;
• first a dry cough, then there may be foamy sputum.

Peripheral edema includes:

• swelling of the legs (feet, legs) – symmetrical on both limbs, from barely noticeable in the form of a mark from the elastic of socks, to pronounced;
• accumulation of fluid between the layers of the pleura and pericardium;
• the appearance of ascites, anasarca.

The skin in the area of ​​edema has a bluish color. Tachycardia is a compensation reaction due to the presence of chronic oxygen starvation of tissues. Rhythm disturbances are often present (persistent or paroxysmal atrial fibrillation, ventricular extrasystole).

Classification of heart failure

Two complementary classifications have been widely used, reflecting the severity of existing changes.

The domestic classification (Vasilenko-Strazhesko) involves division into stages:

1. Stage 1 CHF – hemodynamic disturbances occur only during physical activity.
2. Stage 2a – there are symptoms of hemodynamic disturbances in one circle of blood circulation, reduced exercise tolerance.
3. Stage 2b – severe, there are pronounced hemodynamic disturbances in both circles;
4. Stage 3 – terminal, significant hemodynamic disturbances, structural changes in organs.

The New York Heart Association distinguishes 4 functional classes depending on exercise tolerance:

1. Functional class I (FC I) – physical activity is not limited.
2. Functional class II – physical activity is moderately limited.
3. III FC – there is a pronounced limitation.
4. IV FC – inability to make any movements without discomfort.

Causes of death in heart failure

For life-threatening conditions that require urgent Care, include:

• the appearance of ventricular arrhythmias;
• acute pulmonary edema;
• exudative pericarditis, accompanied by cardiac tamponade.

Treatment of heart failure

Indications for hospitalization are:

• acute heart failure clinic;
• newly diagnosed heart failure in people of working age;
• ineffectiveness of therapy, decompensated chronic failure.

Chronic heart failure in the compensation stage is treated on an outpatient basis. At the prehospital stage, the following methods are used:

1. Compliance with nutritional principles - the diet is enriched with foods high in potassium, salt intake is significantly limited, and fluid intake is monitored.
2. Dosed physical activity - must be adequate to the patient’s capabilities; breathing exercises and walking are useful.
3. Drug therapy - using drugs with proven positive influence on prognosis and quality of life. These are drugs from the group of angiotensin-converting enzyme inhibitors, sartans, adrenergic blockers, aldosterone antagonists, cardiac glycosides. For significant edema, diuretics are prescribed, and diuretic herbs are additionally used. In addition, statins, nitrates, anticoagulants, and antiarrhythmic drugs are used.
4. Surgical methods - installation of an electrical pacemaker, implantable cardioverter-defibrillator, myocardial revascularization surgery.

Timely adequate treatment in the early stages of the disease can slow down the progression of the disease, improve the prognosis and have a significant impact on the quality and life expectancy of such patients.

Development of heart failure

In each specific case, the period during which heart failure develops may be different and depends on the type of cardiovascular disease. Heart failure is divided into left and right ventricular, depending on which of the ventricles of the heart is most affected by the effects of the disease.

At right ventricular heart failure Excessive fluid volume is retained in the vessels of the systemic circulation. The consequence of this is the development of edema, in the first stages - in the area of ​​​​the ankles and feet. In addition to the main symptoms, with right ventricular heart failure, the patient complains of rapid fatigue, which occurs due to insufficient oxygen saturation of the blood, a feeling of pulsation and fullness in the neck.

At left ventricular heart failure fluid is retained in the pulmonary circulation, resulting in a decrease in the level of oxygen entering the blood. The consequence of this is the development of shortness of breath, which increases with physical activity, and the appearance of rapid fatigue and weakness.

The severity of symptoms and the order in which they occur depends on each individual case. Symptoms of an existing disease appear more quickly in right ventricular heart failure. This is explained by the fact that the left ventricle is the most powerful section of the heart. As a rule, it takes a long time before he begins to “lose ground.” However, when this does happen, the progression of heart failure occurs rapidly.

Symptoms of heart failure

Depending on which part of the heart is most affected, the symptoms of heart failure differ. Arrhythmias may appear. shortness of breath, darkening of the eyes, dizziness, fainting, pale skin, swelling of the neck veins, leg pain and swelling, ascites (free fluid in the abdominal cavity), enlarged liver. Even minor physical activity becomes unbearable for the patient. In the later stages of the disease, symptoms appear not only during exercise, but also at rest, resulting in the patient completely loses his ability to work. All organs and systems of the body, to a greater or lesser extent, feel the negative effects of insufficient blood circulation.

Depending on which side of the heart (or both) is damaged, symptoms will vary. When the right side of the heart is not functioning well, the peripheral veins become overfilled with blood, which then leaks into the abdominal cavity (including the liver) and leg tissue. This leads to the liver increasing in size and swelling. When the left side is affected, the blood vessels of the heart and pulmonary circulation are filled with blood, some of which spreads to the lungs. This type of heart failure is characterized by a cough, rapid breathing, rapid heart rate, and pale or bluish skin. The severity of symptoms may vary, there are probability of death.

Diagnosis of heart failure

This disease is the result of various conditions and diseases, both cardiovascular and other origins. To identify existing heart failure, a routine examination by a doctor is often not enough, since it may be necessary to use certain diagnostic methods to clarify the reasons that caused it.

Help doctors identify all kinds of arrhythmias. symptoms of hypertrophy and ischemia (lack of blood supply) of the myocardium may ECG (electrocardiography). Typically, signs identified by ECG may indicate other diseases, since they are not unique to heart failure.

Based on the ECG, stress tests have been developed and are widely used, the essence of which is that the patient must overcome various levels of stress, gradually increasing. To carry out such tests, special equipment is used that helps to dose the load: treadmill - a treadmill, bicycle ergometry - a special modification of a bicycle. With the help of such tests, you can obtain data on what reserve capabilities the pumping function of the heart has.

Today, the main and accessible method for identifying diseases, the symptom of which is heart failure, is echocardiography (echocardiography) - ultrasound examination hearts. Using this procedure, you can not only find out the cause of heart failure, but also evaluate the ventricles of the heart for their contractile function. Today, using only echocardiography, it is possible to diagnose acquired or congenital heart disease, to suggest the presence of arterial hypertension, coronary heart disease and a number of other diseases. The EchoCG method can also be used to evaluate the effectiveness of prescribed treatment.

Organ examination chest Using X-rays for heart failure, it helps to detect blood stagnation in the pulmonary circulation, as well as cardiomealgia (an increase in the size of the heart cavities). A number of heart diseases (for example, valvular heart defects) have a unique X-ray picture. X-ray examination of the chest organs, like echocardiography, allows us to determine the effectiveness of treatment.

For highly accurate assessment of the contractile function of the ventricles (including the volume of blood they contain) radioisotope methods cardiac studies (eg, radioisotope ventriculography). These methods are based on the introduction and further distribution of radioisotope preparations throughout the body.

The PET (positron emission tomography) method is a nuclear diagnostic method, which is one of the most advanced achievements of modern medicine. This type of research is very expensive and is not very widespread today. The main opportunity of PET is to identify a section of viable myocardium in patients with heart failure using a certain radioactive “tag”, which will allow further adjustments to the prescribed treatment.

Treatment of heart failure

Acute heart failure requires hospitalization of the patient. It is imperative to follow a regimen with limited physical activity (the attending physician selects physical therapy); it is required to adhere to a diet that includes foods rich in proteins and vitamins and a limited salt content; if the patient has severe edema, a salt-free diet is prescribed. Diuretics, cardiac glycosides, calcium antagonists, vasodilators, and potassium supplements are also prescribed.

Modern pharmacology has made a huge step forward in prolonging and improving the quality of life of patients diagnosed with heart failure. But before proceeding directly to the treatment of heart failure, it is necessary to exclude all possible factors that can cause its occurrence (anemia, febrile states, stress, alcohol abuse, excessive consumption of table salt, as well as taking medications that contribute to fluid retention in the body, etc. .).

Treatment of heart failure involves not only getting rid of its immediate causes, but also correcting its manifestations. An important role in the treatment of heart failure is given to such a general measure as rest. Which does not at all imply that the patient should spend all the time lying down. There should be physical activity, but at the same time the patient should not get tired or experience unpleasant feelings. If the patient has difficulty withstanding stress, he should sit more, but not lie down. When there is no swelling or obvious shortness of breath, you should walk in the fresh air. It must be remembered that physical activity for patients with heart failure does not involve any elements of competition.

The bed on which a person with heart failure sleeps should have a raised head end, or he should be given a high pillow. If the patient has swelling of the legs, it is advised to sleep on a bed with the end of the leg raised or place a thin pillow under the legs (this will help reduce the manifestations of edema).

Mandatory low salt diet. You should not add salt to already prepared food. It is extremely important to reduce excess weight, as it significantly increases the load on a diseased heart. However, if heart failure has developed sufficiently, weight may decrease on its own. To control your weight and detect fluid retention in the body in time, you need to weigh yourself at the same time of day every day.

Medicines that modern medicine offers for the treatment of heart failure, aimed at:

decreased vascular tone;

increased myocardial contractility;

elimination of sinus tachycardia;

reducing fluid retention in the body;

prevention of blood clots in the heart cavities.

If modern medications do not give the desired effect, surgery may be prescribed.

– an acute or chronic condition caused by a weakening of myocardial contractility and congestion in the pulmonary or systemic circulation. It manifests itself as shortness of breath at rest or with slight exertion, fatigue, swelling, cyanosis (blueness) of the nails and nasolabial triangle. Acute heart failure is dangerous due to the development of pulmonary edema and cardiogenic shock, while chronic heart failure leads to the development of organ hypoxia. Heart failure is one of the most common causes of human death.

ICD-10

I50

General information

– an acute or chronic condition caused by a weakening of myocardial contractility and congestion in the pulmonary or systemic circulation. It manifests itself as shortness of breath at rest or with slight exertion, fatigue, swelling, cyanosis (blueness) of the nails and nasolabial triangle. Acute heart failure is dangerous due to the development of pulmonary edema and cardiogenic shock, while chronic heart failure leads to the development of organ hypoxia. Heart failure is one of the most common causes of human death.

A decrease in the contractile (pumping) function of the heart in heart failure leads to the development of an imbalance between the hemodynamic needs of the body and the ability of the heart to fulfill them. This imbalance is manifested by an excess of venous inflow to the heart and the resistance that must be overcome by the myocardium to expel blood into the vascular bed over the ability of the heart to move blood into the arterial system.

Not being an independent disease, heart failure develops as a complication of various pathologies of blood vessels and the heart: valvular heart disease, coronary artery disease, cardiomyopathy, arterial hypertension, etc.

In some diseases (for example, arterial hypertension), the increase in heart failure occurs gradually, over years, while in others (acute myocardial infarction), accompanied by the death of some functional cells, this time is reduced to days and hours. With a sharp progression of heart failure (over minutes, hours, days), they speak of its acute form. In other cases, heart failure is considered chronic.

Chronic heart failure affects 0.5 to 2% of the population, and after 75 years its prevalence is about 10%. The significance of the problem of the incidence of heart failure is determined by the steady increase in the number of patients suffering from it, the high mortality rate and disability of patients.

Reasons

Among the most common causes of heart failure, occurring in 60-70% of patients, are myocardial infarction and coronary artery disease. These are followed by rheumatic heart disease (14%) and dilated cardiomyopathy (11%). In the age group over 60 years, in addition to ischemic heart disease, heart failure is also caused by hypertension (4%). In elderly patients, a common cause of heart failure is type 2 diabetes mellitus and its combination with arterial hypertension.

Factors that provoke the development of heart failure cause its manifestation when the compensatory mechanisms of the heart decrease. Unlike causes, risk factors are potentially reversible, and their reduction or elimination can delay the worsening of heart failure and even save the patient's life. These include: overexertion of physical and psycho-emotional capabilities; arrhythmias, pulmonary embolism, hypertensive crises, progression of ischemic heart disease; pneumonia, ARVI, anemia, renal failure, hyperthyroidism; taking cardiotoxic drugs, drugs that promote fluid retention (NSAIDs, estrogens, corticosteroids), increasing blood pressure (isadrine, ephedrine, adrenaline); pronounced and rapidly progressive weight gain, alcoholism; a sharp increase in blood volume during massive infusion therapy; myocarditis, rheumatism, infective endocarditis; non-compliance with recommendations for the treatment of chronic heart failure.

Pathogenesis

The development of acute heart failure is often observed against the background of myocardial infarction, acute myocarditis, severe arrhythmias (ventricular fibrillation, paroxysmal tachycardia, etc.). In this case, there is a sharp drop in minute output and blood flow into the arterial system. Acute heart failure is clinically similar to acute vascular insufficiency and is sometimes referred to as acute cardiac collapse.

In chronic heart failure, changes developing in the heart are compensated for a long time by its intensive work and adaptive mechanisms of the vascular system: an increase in the strength of heart contractions, an increase in rhythm, a decrease in pressure in diastole due to the expansion of capillaries and arterioles, which facilitates emptying of the heart during systole, and an increase in perfusion fabrics.

Further increase in the symptoms of heart failure is characterized by a decrease in the volume of cardiac output, an increase in the residual amount of blood in the ventricles, their overflow during diastole and overdistension muscle fibers myocardium. Constant overstrain of the myocardium, trying to push blood into the vascular bed and maintain blood circulation, causes its compensatory hypertrophy. However, at a certain moment, a stage of decompensation occurs, due to the weakening of the myocardium, the development of the processes of degeneration and sclerosis in it. The myocardium itself begins to experience a lack of blood supply and energy supply.

At this stage, neurohumoral mechanisms are included in the pathological process. Activation of the mechanisms of the sympathetic-adrenal system causes vasoconstriction in the periphery, which helps maintain stable blood pressure in the systemic circulation while reducing cardiac output. The resulting renal vasoconstriction leads to renal ischemia, which contributes to interstitial fluid retention.

An increase in the secretion of antidiuretic hormone by the pituitary gland increases the processes of water reabsorption, which entails an increase in the volume of circulating blood, an increase in capillary and venous pressure, increased transudation of fluid into tissues.

Thus, severe heart failure leads to severe hemodynamic disturbances in the body:

• gas exchange disorder

When blood flow slows down, tissue absorption of oxygen from capillaries increases from 30% normally to 60-70%. The arteriovenous difference in blood oxygen saturation increases, which leads to the development of acidosis. The accumulation of under-oxidized metabolites in the blood and increased work of the respiratory muscles cause activation of the basal metabolism. A vicious circle arises: the body experiences an increased need for oxygen, and the circulatory system is unable to satisfy it. The development of the so-called oxygen debt leads to cyanosis and shortness of breath. Cyanosis in heart failure can be central (with stagnation in the pulmonary circulation and impaired blood oxygenation) and peripheral (with slow blood flow and increased utilization of oxygen in the tissues). Since circulatory failure is more pronounced in the periphery, patients with heart failure experience acrocyanosis: cyanosis of the extremities, ears, and tip of the nose.

• swelling

Edema develops as a result of a number of factors: interstitial fluid retention with increased capillary pressure and slower blood flow; water and sodium retention due to impaired water-salt metabolism; disturbances in the oncotic pressure of blood plasma due to protein metabolism disorders; reducing the inactivation of aldosterone and antidiuretic hormone with decreased liver function. Edema in heart failure is initially hidden and is expressed by a rapid increase in body weight and a decrease in the amount of urine. The appearance of visible edema begins with lower limbs, if the patient is walking, or from the sacrum if the patient is lying down. Subsequently, cavitary hydrops develops: ascites (abdominal cavity), hydrothorax (pleural cavity), hydropericardium (pericardial cavity).

• stagnant changes in organs

Congestion in the lungs is associated with impaired hemodynamics of the pulmonary circulation. They are characterized by rigidity of the lungs, decreased respiratory excursion of the chest, and limited mobility of the pulmonary edges. Manifested by congestive bronchitis, cardiogenic pneumosclerosis, hemoptysis. Congestion of the systemic circulation causes hepatomegaly, manifested by heaviness and pain in the right hypochondrium, and then cardiac fibrosis of the liver with the development of connective tissue in it.

Expansion of the cavities of the ventricles and atria in heart failure can lead to relative insufficiency of the atrioventricular valves, which is manifested by swelling of the veins of the neck, tachycardia, and expansion of the boundaries of the heart. With the development of congestive gastritis, nausea, loss of appetite, vomiting, a tendency to constipation, flatulence, and weight loss appear. With progressive heart failure, a severe degree of exhaustion develops - cardiac cachexia.

Congestive processes in the kidneys cause oliguria, increased relative density of urine, proteinuria, hematuria, and cylindruria. Dysfunction of the central nervous system in heart failure is characterized by rapid fatigue, decreased mental and physical activity, increased irritability, sleep disorders, and depressive states.

Classification

According to the rate of increase in signs of decompensation, acute and chronic heart failure are distinguished.

The development of acute heart failure can occur in two types:

• left type (acute left ventricular or left atrial failure)
• acute right ventricular failure

According to the Vasilenko-Strazhesko classification, there are three stages in the development of chronic heart failure:

I (initial) stage– hidden signs of circulatory failure, appearing only during physical activity: shortness of breath, palpitations, excessive fatigue; at rest there are no hemodynamic disturbances.

II (pronounced) stage– signs of prolonged circulatory failure and hemodynamic disorders (stagnation of the pulmonary and systemic circulation) are expressed at rest; severe limitation of working capacity:

• Period II A – moderate hemodynamic disturbances in one part of the heart (left or right ventricular failure). Shortness of breath develops during normal physical activity, and performance is sharply reduced. Objective signs are cyanosis, swelling of the legs, initial signs of hepatomegaly, hard breathing.
• Period II B – deep hemodynamic disorders involving the entire cardiovascular system (large and small circle). Objective signs – shortness of breath at rest, severe edema, cyanosis, ascites; complete disability.

III (dystrophic, final) stage– persistent circulatory and metabolic failure, morphologically irreversible disorders of the structure of organs (liver, lungs, kidneys), exhaustion.

Symptoms of heart failure

Acute heart failure

Acute heart failure is caused by weakening of the function of one of the parts of the heart: the left atrium or ventricle, the right ventricle. Acute left ventricular failure develops in diseases with a predominant load on the left ventricle (hypertension, aortic disease, myocardial infarction). When the functions of the left ventricle are weakened, the pressure in the pulmonary veins, arterioles and capillaries increases, their permeability increases, which leads to sweating of the liquid part of the blood and the development of first interstitial and then alveolar edema.

Clinical manifestations of acute left ventricular failure are cardiac asthma and alveolar pulmonary edema. An attack of cardiac asthma is usually provoked by physical or neuropsychic stress. An attack of sudden suffocation often occurs at night, forcing the patient to wake up in fear. Cardiac asthma is manifested by a feeling of lack of air, palpitations, cough with difficult to clear sputum, severe weakness, and cold sweat. The patient assumes an orthopneic position - sitting with legs down. On examination - pale skin with a grayish tint, cold sweat, acrocyanosis, severe shortness of breath. A weak, fast-filling arrhythmic pulse, expansion of the borders of the heart to the left, dull heart sounds, and a gallop rhythm are detected; blood pressure tends to decrease. There is harsh breathing in the lungs with isolated dry wheezing.

Further increase in pulmonary congestion contributes to the development of pulmonary edema. Sharp suffocation is accompanied by a cough with the release of copious amounts of foamy pink sputum (due to the presence of blood). From a distance, bubbling breathing with moist wheezing can be heard (a symptom of a “boiling samovar”). The patient's position is orthopneic, the face is cyanotic, the veins of the neck are swollen, and the skin is covered with cold sweat. The pulse is threadlike, arrhythmic, frequent, blood pressure is reduced, and there are moist rales of various sizes in the lungs. Pulmonary edema is an emergency that requires action intensive care, because it can be fatal.

Acute left atrial heart failure occurs with mitral stenosis (left atrioventricular valve). Clinically manifested by the same conditions as acute left ventricular failure. Acute right ventricular failure often occurs with thromboembolism of large branches of the pulmonary artery. Stagnation develops in the vascular system of the systemic circulation, which is manifested by swelling of the legs, pain in the right hypochondrium, a feeling of distension, swelling and pulsation of the neck veins, shortness of breath, cyanosis, pain or pressure in the heart. The peripheral pulse is weak and frequent, blood pressure is sharply reduced, central venous pressure is increased, the heart is enlarged to the right.

In diseases that cause decompensation of the right ventricle, heart failure manifests itself earlier than in left ventricular failure. This is explained by the large compensatory capabilities of the left ventricle, the most powerful part of the heart. However, with a decrease in left ventricular function, heart failure progresses at a catastrophic rate.

Chronic heart failure

The initial stages of chronic heart failure can develop according to the left and right ventricular, left and right atrial types. For aortic disease, insufficiency mitral valve, arterial hypertension, coronary insufficiency congestion develops in the vessels of the pulmonary circle and chronic left ventricular failure. It is characterized by vascular and gas changes in the lungs. There is shortness of breath, attacks of suffocation (usually at night), cyanosis, attacks of palpitations, cough (dry, sometimes with hemoptysis), increased fatigue.

Even more pronounced congestion in the pulmonary circulation develops in chronic left atrial failure in patients with mitral valve stenosis. Shortness of breath, cyanosis, cough, and hemoptysis appear. With prolonged venous stagnation in the vessels of the small circle, sclerosis of the lungs and blood vessels occurs. An additional pulmonary obstruction to blood circulation in the pulmonary circle arises. High blood pressure in the pulmonary artery system causes an increased load on the right ventricle, causing its failure.

With predominant damage to the right ventricle (right ventricular failure), congestion develops in the systemic circulation. Right ventricular failure can accompany mitral heart defects, pneumosclerosis, pulmonary emphysema, etc. There are complaints of pain and heaviness in the right hypochondrium, the appearance of edema, decreased diuresis, distension and enlargement of the abdomen, shortness of breath with movements. Cyanosis develops, sometimes with an icteric-cyanotic tinge, ascites, the neck and peripheral veins swell, and the liver increases in size.

Functional failure of one part of the heart cannot remain isolated for long, and over time, total chronic heart failure develops with venous stagnation in the pulmonary and systemic circulation. Also, the development of chronic heart failure is observed with damage to the heart muscle: myocarditis, cardiomyopathy, ischemic heart disease, intoxication.

Diagnostics

Since heart failure is a secondary syndrome that develops with known diseases, diagnostic measures should be aimed at its early detection, even in the absence of obvious signs.

When collecting a clinical history, attention should be paid to fatigue and dyspnea as the earliest signs of heart failure; the patient has coronary artery disease, hypertension, suffered a heart attack myocardium and rheumatic fever, cardiomyopathy. Detection of swelling of the legs, ascites, rapid low-amplitude pulse, listening to the third heart sound and displacement of the borders of the heart are specific signs of heart failure.

If heart failure is suspected, the electrolyte and gas composition of the blood is determined, acid-base balance, urea, creatinine, cardiospecific enzymes, indicators of protein-carbohydrate metabolism.

Based on specific changes, an ECG helps to identify hypertrophy and insufficiency of blood supply (ischemia) of the myocardium, as well as arrhythmias. Based on electrocardiography, various stress tests using an exercise bike (bicycle ergometry) and a treadmill (treadmill test) are widely used. Such tests with a gradually increasing level of load make it possible to judge the reserve capabilities of heart function.

Prognosis and prevention

The five-year survival rate for patients with heart failure is 50%. The long-term prognosis is variable, it is influenced by the severity of heart failure, concomitant background, effectiveness of therapy, lifestyle, etc. Treatment of heart failure in the early stages can completely compensate for the patient’s condition; The worst prognosis is observed in stage III heart failure.

Measures to prevent heart failure include preventing the development of diseases that cause it (coronary artery disease, hypertension, heart defects, etc.), as well as factors that contribute to its occurrence. To avoid the progression of already developed heart failure, it is necessary to adhere to an optimal regimen of physical activity, take prescribed medications, and constant monitoring by a cardiologist.

ICD-10 code

They name a set of a number of symptoms and clinical signs that arise as a result of changes in the pumping capacity of the heart. Signs of this pathology can be very diverse. In fact, they all directly depend on the form of the disease. Right now, readers will be presented with a simplified classification of this cardiac condition, as well as symptoms that are considered to be the most common. In order for the patient to maintain not only his health, but also his life, it is very important that he can recognize the presence of this disease in time. To do this, he needs to know exactly what symptoms it is accompanied by.

What are the types of heart failure?

It is a well-known fact that the heart is the main organ of the entire cardiovascular system. human body. In the event of a violation of its pumping capacity, that is, a violation of blood pumping, heart failure syndrome immediately makes itself known. As a result, a person experiences numerous signs and symptoms that point directly to the problem at hand. There are plenty of reasons that could provoke this type of violation. In this case, they do not play a special role, since the symptoms of this syndrome in most cases do not depend on the causes. They most often depend on the form of the disease.

The classification of heart failure is based primarily on the mechanisms of its development, as well as on the type of cardiac dysfunction that is observed.
Today there are several classifications of this syndrome. If we talk about the classification of this pathology depending on the speed of its development, then in this case it may be acute And chronic.
If we take into account the area of ​​the damaged area of ​​the heart, then this pathology may be right-hearted or right ventricular or left heart or left ventricular. Left ventricular heart failure is observed much more often than the right ventricular form. This is explained by the fact that the left ventricle is subjected to greater loads than the right, which, of course, “unsettles it.”

In medical practice there are also isolated heart failure. It can be either right or left ventricular, and in most cases it occurs in an acute form. But the chronic form of this disease, as a rule, is mixed.

What is acute and chronic heart failure?

Acute and chronic heart failure are the two main types of occurrence of this pathology. They differ from each other not only in the speed of their development, but also in the course of the pathology itself.

Acute heart failure develops very quickly. The development of this state takes only a few minutes, sometimes hours. The obvious symptoms of this syndrome are considered to be pulmonary edema And cardiac asthma. Both of these conditions can cause the death of the patient, which is why in this case immediate medical assistance is necessary.

Pulmonary edema and cardiac asthma are accompanied by severe attacks of shortness of breath, as well as bluish skin. In addition, the patient experiences dizziness and moist rales in the lung area. Very often in such cases, patients lose consciousness. All of these symptoms may occur along with hypertensive crisis or myocardial infarction. If this happens, it means acute decompensation of the functioning of the heart. In some cases, an acute form of heart failure occurs against the background of complications of the chronic form of this disease.

The most common causes of the development of the acute form of this pathology include:

• Acute valvular insufficiency
• Cardiac tamponade
• Myocardial infarction
• Heart rhythm disturbance
• Pulmonary embolism
• Decompensation of chronic heart failure
• Heart injuries

The chronic form of this disease is accompanied by a fairly slow development of symptoms, in which the patient’s health condition is stable. Most often, signs of this pathology appear in the patient over time, which indicates the fact of a slow disruption of the functioning of the heart. Very rarely, this condition can occur immediately after an attack of acute heart failure.

The most common causes of chronic heart failure include:

• Cardiosclerosis
• Arterial hypertension
• Chronic ischemic heart disease
• Heart valve diseases
• Chronic cor pulmonale

The most common signs of this form of chronic failure include: weakness, swelling, palpitations, chronic dry cough, shortness of breath .

Shortness of breath is considered to be one of the first signs of heart failure. At first, this condition makes itself felt only after excessive physical exertion. Then shortness of breath begins to “pursue” the patient, giving him no rest even in a supine position. In medicine, this condition is called orthopnea. In people suffering from a chronic form of this disease, this condition represents a kind of indicator of their functional potential. Since physical activity and shortness of breath are practically inseparable concepts, this was the impetus for classifying heart failure into so-called functional classes, abbreviated as FC.

I FC– the patient leads a normal life. Weakness in the muscles, shortness of breath, palpitations and some other symptoms occur only at the moment of physical stress.
II FC– the patient’s daily activity is practically unlimited. He experiences shortness of breath, as well as some other symptoms accompanying this condition, immediately during moderate physical exertion. For example, while walking. At rest, no unpleasant symptoms are felt.
III FC– the patient’s physical activity undergoes a number of pronounced restrictions. Any even minor stress immediately causes palpitations, shortness of breath, and so on.
IV FC– all the symptoms inherent in heart failure make themselves felt even at rest. They become more noticeable even during normal conversation.
Shortness of breath in this condition occurs due to impaired blood circulation in the vessels of the lungs. This is explained by the fact that the heart can no longer normally distill the blood flowing to it.

Since there is stagnation of blood in the lungs, this leads to the development of other far from pleasant symptoms, one of which is:
Dry cough– In medicine, this condition is also called cardiac cough. In most cases, this symptom is observed in patients with chronic heart failure. A dry cough is the result of swelling of the lung tissue. Most often, a cough makes itself felt during physical activity or in a lying position, since at such moments the heart must work even faster. There are also cases when attacks of dry cough transform into cardiac asthma, that is, an attack of suffocation. This fact is a signal of the onset of acute heart failure.

Since therapy for the chronic form of this condition involves taking antihypertensive drugs, including ACE inhibitors ( Captopril), the use of which may cause a side effect such as a dry cough, it is best for patients to monitor symptoms of cough and consult their doctor about this. If the patient’s cough occurs precisely because of the medications, then the medications should be replaced.

In this case, swelling usually occurs on the legs. At first they form in the ankle area. In the evenings they most often become larger, but in the mornings they practically disappear. If the disease is not treated, then it is quite possible for swelling to spread to the thighs and lower legs, as well as to some other parts of the body. In addition to edema, patients may also experience trophic changes in the skin. This could be hair loss, skin pigmentation, nail deformation, and so on.

Muscle weakness is another symptom of chronic heart failure. It occurs as a result of a decrease in blood supply to the muscles. In such cases, patients indicate excessive fatigue, as well as very severe muscle weakness, which occurs mainly during physical activity.

Pain in the right hypochondrium - this symptom of chronic heart failure is extremely rare. It occurs due to stagnation of blood in the systemic circulation, namely in the liver area. If a patient experiences this kind of pain, then he most often also experiences swelling in the legs, swelling of the jugular veins, as well as hydrothorax and ascites. All these signs of this syndrome can be combined with other unpleasant symptoms that arise due to the underlying pathology that provoked heart failure. As soon as a person notices one of these signs, he should immediately seek help from a doctor.

Conclusions

Let's remember

• In acute heart failure, there is a sharp change in the functioning of the heart;
• The obvious signs of this condition are considered to be: loss of consciousness, severe shortness of breath, which develops into an attack of suffocation, the onset of a dry cough;
• Chronic heart failure is accompanied by fairly slow disruptions in the functioning of the heart, which make themselves felt as a result of the presence of some chronic cardiovascular pathology such as angina pectoris, hypertension, and so on;
• The main signs of the chronic form of this disease include: cardiac cough, swelling of the legs, shortness of breath, muscle weakness;
• If you have this disease, you must qualified assistance medical specialists.

Heart failure: signs, forms, treatment, help with exacerbation

Today, almost every person experiences chronic fatigue syndrome, which is expressed in rapid fatigue. Many people are familiar with rapid heartbeat or dizziness that occurs without apparent reason; shortness of breath that appears when walking quickly or while climbing stairs on foot to the desired floor; swelling in the legs at the end of the working day. But few people realize that all these are symptoms of heart failure. Moreover, in one form or another they accompany almost all pathological conditions of the heart and diseases of the vascular system. Therefore, it is necessary to determine what heart failure is and how it differs from other heart diseases.

What is heart failure?

With many heart diseases caused by pathologies of its development and other reasons, circulatory disorders occur. In most cases, there is a decrease in blood flow into the aorta. This leads to the fact that in various organs occurs that impairs their functionality. Heart failure causes more blood to circulate, but the speed at which the blood moves slows. This process can occur suddenly ( acute course) or be chronic.

Video: Heart Failure – Medical Animation

Acute heart failure

All activity of the heart is carried out by the heart muscle (myocardium). Its work is affected by the condition of the atria and ventricles. When one of them stops working normally, myocardial overstrain occurs. This can be caused by damage to the heart by various diseases or abnormalities that occur outside the heart. This can happen suddenly. This process is called acute heart failure.

Etiology of acute form

This can be caused by:

1. Coronary insufficiency;
2. Valve malformations (,);
3. Chronic and acute processes in the lungs;
4. Increased blood pressure in the pulmonary and systemic circulation systems.

Symptoms

Clinically, acute heart failure manifests itself in different ways. This depends on which ventricle (right (RV) or left (LV)) the muscle overstrain occurs.

• In acute LV failure (also called) attacks mainly occur at night. A man wakes up from the fact that he cannot breathe. He is forced into a sitting position (orthopnea). Sometimes this does not help and the sick person has to get up and walk around the room. He experiences rapid (tachypnea) breathing, like a hunted animal. His face takes on a grayish, bluish color, and pronounced acrocyanosis is noted. The skin becomes moist and cool. Gradually, the patient’s breathing changes from rapid to bubbling, which can be heard even at a great distance. Occurs with pink, frothy sputum. BP - low. Cardiac asthma requires immediate medical attention.
• In acute right ventricular failure, blood stagnation occurs in the vena cava (inferior and superior), as well as in the veins of the systemic circle. The veins of the neck become swollen and blood stagnates in the liver (it becomes painful). Shortness of breath and cyanosis occur. The attack is sometimes accompanied by bubbling Cheyne-Stokes breathing.

Acute heart failure can lead to pulmonary edema (alveolar or interstitial), causing. Sudden weakness of the heart muscle leads to instant death.

Pathogenesis

Cardiac asthma (the so-called interstitial edema) occurs with infiltration of serous contents into the perivascular and peribronchial chambers. As a result, metabolic processes in the lungs are disrupted. With further development of the process, liquid penetrates into the lumen of the alveoli from the bed of the blood vessel. Interstitial swelling of the lung turns into alveolar swelling. This is a severe form of heart failure.

Alveolar edema can develop independently of cardiac asthma. It can be caused by AC (aortic valve), LV, and diffuse prolapse. Conducting clinical trials makes it possible to describe the picture of what is happening.

1. At the moment of acute failure, in the pulmonary circulation system there is a rapid increase in static pressure to significant values ​​(above 30 mm Hg), causing the flow of blood plasma into the alveoli of the lungs from the capillaries. In this case, the permeability of the capillary walls increases, and the oncotic pressure of the plasma decreases. In addition, the formation of lymph in the lung tissues increases and its movement in them is disrupted. Most often, this is facilitated by an increased concentration of prostaglandin and mediators, caused by increased activity of the sympathoadrenergic receptor system.
2. The delay in blood flow in the pulmonary circle and accumulation in the left atrial chamber is facilitated by a sharp decrease in the atrioventricular opening. It is not able to allow blood flow into the LV in full. As a result, the pumping function of the pancreas increases, creating an additional portion of blood into the pulmonary circle and increasing venous pressure in it. This is what causes pulmonary edema.

Diagnostics

Diagnosis at a doctor's appointment shows the following:

• When performing percussion (tapping to determine the configuration of the heart, its position and size) in the lungs (its lower parts), a dull, box-like sound is heard, indicating blood stagnation. Swelling of the mucous membranes of the bronchi is detected by auscultation. This is indicated by dry wheezing and noisy breathing in the lungs.
• Due to the developing emphysema of the lung, the borders of the heart are quite difficult to determine, although they are enlarged. Heart rhythm is disturbed. Develops (pulse alternation and gallop rhythm may occur). Typical for pathologies of valve mechanisms, bifurcation and intensification of the second tone can be heard above the main artery of the lung.
• Blood pressure varies over a wide range. Central pressure in the veins is also increased.

The symptoms of cardiac and bronchial asthma are similar. To accurately diagnose heart failure, a comprehensive examination is necessary, including functional diagnostic methods.

• On x-rays Horizontal shadows are noticeable in the lower parts of the lungs (Curley lines), indicating swelling of the septa between its lobules. The compression of the gap between the lobes is differentiated, the pattern of the lung is strengthened, the structure of its roots is vague. Main bronchi without visible lumen.
• During the test, LV overload is detected.

Treatment of acute heart failure requires emergency medical therapy. It is aimed at reducing myocardial overstrain and increasing its contractile function, which will relieve edema and chronic fatigue syndrome, reduce shortness of breath and other clinical manifestations. In this case, compliance with a gentle regime plays an important role. The patient must be provided with rest for several days, avoiding overexertion. He should get a good night's sleep ( night sleep at least 8 hours), rest during the day (reclining for up to two hours). A transition to a diet with limited fluid and salt is required. You can use the Carrel diet. In severe cases, the patient requires hospitalization for inpatient treatment.

Drug therapy

Video: how to treat heart failure?

Acute coronary insufficiency

With a complete cessation of blood flow in the coronary vessels, the myocardium does not receive enough nutrients and lacks oxygen. Coronary insufficiency develops. It can be acute (with sudden onset) and chronic course. Acute coronary insufficiency can be caused by severe excitement (joy, stress or negative emotions). It is often caused by increased physical activity.

The cause of this pathology is most often vasospasm, caused by the fact that in the myocardium, due to impaired hemodynamics and metabolic processes, products with partial oxidation begin to accumulate, which lead to irritation of the receptors of the heart muscle. The mechanism of development of coronary insufficiency is as follows:

• The heart is surrounded on all sides by blood vessels. They resemble a crown (crown). Hence their name - coronary (coronary). They fully meet the needs of the heart muscle for nutrients and oxygen, creating favorable conditions for its work.
• When a person engages in physical work or simply moves, cardiac activity increases. At the same time, the myocardial need for oxygen and nutrients increases.
• Normally, the coronary arteries dilate, increasing blood flow and providing the heart with everything it needs in full.
• During a spasm, the bed of the coronary vessels remains the same size. The amount of blood entering the heart also remains at the same level, and it begins to experience oxygen starvation(hypoxia). This is acute insufficiency of coronary vessels.

Signs of heart failure caused by coronary spasm are manifested by the appearance of (angina pectoris). A sharp pain squeezes the heart, preventing it from moving. It can radiate to the neck, shoulder blade or arm on the left side. An attack most often occurs suddenly during physical activity. But sometimes it can occur at rest. At the same time, a person instinctively tries to take the most comfortable position to relieve pain. The attack usually lasts no more than 20 minutes (sometimes it lasts only one or two minutes). If an attack of angina continues longer, there is a possibility that coronary insufficiency has turned into one of the forms of myocardial infarction: transitional (focal dystrophy), small focal infarction or myocardial necrosis.

In some cases, acute coronary insufficiency is considered a type of clinical manifestation, which can occur without pronounced symptoms. They can be repeated repeatedly, and the person does not even realize that he has a severe pathology. Accordingly, the necessary treatment is not carried out. And this leads to the fact that the condition of the coronary vessels gradually worsens, and at a certain moment the next attack takes on a severe form of acute coronary insufficiency. If the patient is not provided with medical assistance, a myocardial infarction may develop in a matter of hours and sudden death may occur.

– one of the main causes of coronary insufficiency

Treatment of acute coronary insufficiency involves stopping attacks of angina. For this we use:

1. Nitroglycerine. You can take it often, as it is a fast, but short acting. (For myocardial infarction Nitroglycerin does not have the required effect).
2. Intravenous administration promotes rapid relief of an attack. Eufillina (Syntophyllina, Diaphyllina).
3. A similar effect has No-shpa and hydrochloric Papaverine(subcutaneous or intravenous injections).
4. Seizures can also be stopped with intramuscular injection. Heparin.

Chronic heart failure

With the weakening of the myocardium caused by chronic heart failure (CHF), it gradually develops. This is a pathological condition in which the cardiovascular system cannot supply the organs with the volume of blood necessary for their natural functionality. The onset of the development of CHF occurs secretly. It can only be detected by testing:

• A two-stage MASTER test, during which the patient must go up and down the stairs with two steps, each height 22.6 cm, with the obligatory ECG taken before testing, immediately after it and after a 6-minute rest;
• On a treadmill (recommended annually for people over 45 years old, in order to identify cardiac disorders);

Pathogenesis

The initial stage of CHF is characterized by a violation of the correspondence between cardiac output per minute and circulating blood volume in a large circle. But they are still within normal limits. No hemodynamic disorders were observed. With the further development of the disease, all indicators characterizing the processes of central hemodynamics have already changed. They are decreasing. The distribution of blood in the kidneys is disrupted. The body begins to retain excess water.

Kidney complications are a characteristic manifestation of congestive CHF.

Both left and right ventricular cardiovascular failure may be present. But sometimes it is quite difficult to differentiate types. Blood stagnation is observed in the large and small circles. In some cases, there is stagnation of only venous blood, which overwhelms all organs. This significantly changes its microcirculation. The speed of blood flow slows down, the partial pressure sharply decreases, and the diffusion rate of oxygen in the cellular tissue decreases. A decrease in lung volume causes shortness of breath. Aldosterone accumulates in the blood due to disruptions in the excretory tract of the liver and kidneys.

With further progression of cardiovascular failure, the synthesis of hormone-containing proteins decreases. Corticosteroids accumulate in the blood, which contributes to adrenal atrophy. The disease leads to severe hemodynamic disturbances, decreased functionality of the lungs, liver and kidneys of the liver and their gradual degeneration. Water-salt metabolic processes are disrupted.

Etiology

The development of CHF is facilitated by various factors that influence myocardial tension:

• Pressure overload of the heart muscle. This is facilitated by aortic insufficiency(AN), which may be of organic origin due to chest trauma, aneurysm and atherosclerosis of the aorta, septic. In rare cases, it develops due to dilatation of the aortic mouth. In AN, blood flow moves in the opposite direction (to the LV). This helps to increase the size of its cavity. The peculiarity of this pathology is its long-term asymptomatic course. As a result, LV weakness gradually develops, causing heart failure of the left ventricular type. It is accompanied by the following symptoms:
  1. Shortness of breath during physical activity during the day and at night;
  2. Dizziness associated with sudden standing or turning of the body;
  3. and pain in the heart area with increased physical activity;
  4. The large arteries in the neck constantly pulsate (this is called “carotid dancing”);
  5. The pupils alternately narrow and dilate;
  6. The capillary pulse is clearly visible when pressing on the nail;
  7. Musset's symptom is observed (slight shaking of the head caused by pulsation of the aortic arch).
• Increased volume of residual blood in the atria. Leads to this factor. MK pathology can be caused functional disorders valve apparatus associated with the closure of the atrioventricular orifice, as well as pathologies organic origin, such as chordae sprain or valve prolapse, rheumatic lesions or atherosclerosis. Often, MV insufficiency is caused by too strong expansion of the circular muscles and the fibrous ring of the atrioventricular orifice, expansion of the LV, provoked by myocardial infarction, cardiosclerosis, etc. Hemodynamic disturbances in this pathology are caused by blood flow in the opposite direction (reflux) at the time of systole (from the ventricle back to the atrium ). This occurs because the valve leaflets sag inside the atrial chamber and do not close tightly. When more than 25 ml of blood enters the atrial chamber during reflux, its volume increases, which causes its tonogenic expansion. Subsequently, hypertrophy of the left atrial heart muscle occurs. An amount of blood will begin to flow into the LV that exceeds that required, as a result of which its walls will hypertrophy. CHF gradually develops.
• Circulatory failure can develop due to primary pathology of the heart muscle in the event of large-focal infarction, diffuse cardiosclerosis, cardiopathy and myocarditis.

It should be noted that most often the cause of the development of circulatory failure is a combination of several factors. A significant role in this is played by the biochemical factor, which is expressed in disruption of ion transport (potassium-sodium and calcium) and adrenergic regulation of the myocardial contraction function.

Congestive form of CHF

With circulatory disorders in the right atrium and ventricle, congestive heart failure of the right ventricular type develops. Its main symptoms are heaviness in the hypochondrium on the right side, decreased diuresis and constant thirst, swelling in the legs, and enlarged liver. Further progression of heart failure contributes to the involvement of almost all internal organs in the process. This causes a sharp weight loss for the patient, ascites and impaired external respiration.

CHF therapy

Treatment of chronic heart failure is long-term. It includes:

1. Drug therapy aimed at combating the symptoms of the underlying disease and eliminating the causes contributing to its development.
2. A rational regime, including restriction of work activity according to the forms and stages of the disease. This does not mean that the patient must remain in bed all the time. He can move around the room, and exercise therapy is recommended.
3. Diet therapy. It is necessary to monitor the caloric content of food. It must comply with the patient’s prescribed regimen. Fat people calorie content of food is reduced by 30%. On the contrary, patients with malnutrition are prescribed enhanced nutrition. If necessary, fasting days are carried out.
4. Cardiotonic therapy.
5. Treatment aimed at restoring water-salt and acid-base balance.

On initial stage Treatment is carried out with vasolators and alpha blockers, which improve hemodynamic parameters. But the main medications for the treatment of chronic heart failure are. They increase the ability of the myocardium to contract, reduce the heart rate and excitability of the heart muscle. The patency of impulses is normalized. Glycosides increase cardiac output, thereby reducing diastolic pressure in the ventricles. At the same time, the need of the heart muscle for oxygen does not increase. Economical but powerful work of the heart is noted. The group of glycosides includes the following drugs: Korglykon, Digitoxin, Celanide, Digoxin, Strophanthin.

They are treated according to a special scheme:

• The first three days - in a shock dosage to reduce and relieve swelling.
• Further treatment is carried out with a gradual reduction in dosage. This is necessary so as not to cause intoxication of the body (glycosides tend to accumulate in it) and not lead to increased diuresis (they have a diuretic effect). When the dosage is reduced, the heart rate is constantly monitored, and the degree of diuresis and shortness of breath is assessed.
• After it is installed optimal dosage, in which all indicators are stable, maintenance therapy is carried out, which can last quite a long time.

Diuretics remove excess fluid from the body and treat heart failure. They are divided into four groups:

1. Ethacrynic acid And Furasemide- forced action;
2. Cyclometazide, Hydrochlorothiazide, Clopamide- moderate action;
3. Daytek (Triamterene), Spiranolactone, Amiloride, Veroshpiron- potassium-sparing diuretics intended for long-term use.

They are prescribed depending on the degree of imbalance of water-salt metabolism. In the initial stage, accelerated-acting drugs are recommended for periodic use. With long-term, regular use, it is necessary to alternate moderate-acting drugs with potassium-sparing drugs. The maximum effect is achieved with the correct combination and dosage of diuretics.

For the treatment of congestive heart failure, which causes all types of metabolic disorders, drugs are used that correct metabolic processes. These include:

• Isoptin, Phytoptin, Riboxin and others - ;
• Methandrostenolol, Retabolil- anabolic steroids, promoting the formation of proteins and accumulating energy inside myocardial cells.

In treatment severe forms Plasmapheresis has a good effect. In case of congestive heart failure, all types of massage are contraindicated.

For all types of heart failure, it is recommended to take: Kaviton, Stugeron, Agapurin or Trental. Treatment should be accompanied by the mandatory prescription of multivitamin complexes: Pangexavit, Hexavit etc.

Treatment with traditional methods is allowed. It should complement the main drug therapy, but do not replace it. Useful sedative fees, normalizing sleep, eliminating cardiac anxiety.

An infusion of flowers and berries helps strengthen the heart muscle blood red hawthorn, fruits rosehip. Have diuretic properties fennel, cumin, celery, parsley. Eating them fresh will help reduce the intake of diuretics. Infusion is good for removing excess fluid from the body birch buds, bearberry (bear's ear) And lingonberry leaves.

Medicinal plants in combination with bromhexine and ambroxol effectively eliminate cough in heart failure. Soothes cough infusion hyssop. And inhalations with extracts eucalyptus help cleanse the bronchi and lungs in congestive heart failure.

During therapy and subsequent rehabilitation, it is recommended to constantly engage in physical therapy. The doctor selects the load individually. It is useful after each session to take a cold shower or douse yourself with cold water, followed by rubbing the body until slightly reddened. This helps to harden the body and strengthen the heart muscle.

Classification of CHF

Heart failure is classified according to the degree of exercise tolerance. There are two classification options. One of them was proposed by a group of cardiologists N.D. Strazhesko, V.Kh. Vasilenko and G.F. Lang, who divided the development of CHF into three main stages. Each of them includes characteristic manifestations during physical activity (group A) and at rest (group B).

1. Initial stage (CHF I) - occurs secretly, without pronounced symptoms, both at rest and during normal physical activity. Slight shortness of breath and rapid heartbeat occur only when athletes perform unusual, heavier work or increase the load during the training process before important competitions.
2. Severe stage (CHF II):
   • Group CHF II (A) - manifested by the occurrence of shortness of breath when performing even habitual work with moderate load. Accompanied by rapid heartbeat, cough with bloody sputum, swelling in the legs and feet. Blood circulation is impaired in the small circle. Partial decrease in working capacity.
   • Group CHF II (B) - characterized by shortness of breath at rest, to the main signs of CHF II (A) are added constant swelling of the legs (sometimes certain areas of the body swell), cirrhosis of the liver, cardiac, ascites. Complete loss of ability to work.
3. End stage (CHF III). It is accompanied by serious hemodynamic disturbances, the development of congestive kidneys, liver cirrhosis, and diffuse pneumosclerosis. Metabolic processes are completely disrupted. The body is exhausted. The skin takes on a light tan color. Drug therapy is ineffective. Only surgical intervention can save the patient.

The second option provides for the classification of CHF according to the Killip scale (degree of exercise intolerance) into 4 functional classes.

• I f.k. Asymptomatic CHF, mild. There are no restrictions on sports and work activities.
• II f.k. During physical activity, the heart rate increases and slight shortness of breath occurs. There is rapid fatigue. Physical activity is limited.
• III f.k. Shortness of breath and palpitations occur not only under the influence of physical activity, but also when moving around the room. Significant limitation of physical activity.
• IV f.k. Symptoms of CHF occur even at rest, intensifying with the slightest physical activity. Absolute exercise intolerance.

Video: lecture on the diagnosis and treatment of heart failure for physicians

Circulatory failure in childhood

In children, circulatory failure can manifest itself in both acute and chronic forms. In newborns, heart failure is associated with complex and combined. In infants, early and late myocarditis leads to heart failure. Sometimes the cause of its development is acquired heart defects associated with pathology of valve mechanisms.

Heart defects (congenital and acquired) can cause the development of CHF in a child of any age. In younger children school age(and older) CHF is often caused by the formation of rheumatic carditis or rheumatic pancarditis. There are also noncardiac causes of heart failure: for example, serious illnesses kidneys, hyaline membrane disease in newborns and a number of others.

Treatment is similar to drug therapy for chronic and acute heart failure in adults. But unlike adults, small patients are prescribed strict bed rest, when all the necessary movements are performed with the help of their parents. Relaxation of the regime (allowed to read in bed, draw, and do homework) for CHF II (B). You can begin to independently perform hygienic procedures and walk around the room (light regimen) when CHF moves to stage II (A). It is recommended to take magnesium supplements (Magnerot).

First aid for heart failure

Many people are in no hurry to provide themselves with the necessary medication assistance in the event of attacks of heart failure. Some people simply don’t know what to do in such cases, others simply neglect treatment. Still others are afraid that frequent use of potent drugs may cause addiction to them. Meanwhile, if symptoms of acute coronary insufficiency occur, if treatment is not started in time, death can occur very quickly.

First aid for acute attacks of heart failure consists of taking a comfortable position and taking a quick-acting drug (Nitroglycerin with Validol under the tongue).

You can take these drugs more than once. They do not accumulate in the body and are not addictive, but you should always remember that Nitroglycerin is capable significantly (and quickly) lower blood pressure, and, besides this, some patients simply cannot tolerate it.

For people diagnosed with mild heart failure (f.k. I or stage I CHF), sanatorium-resort treatment is indicated. It has preventive value and is aimed at increasing the functionality of the cardiovascular system. Thanks to a systematic, properly selected alternation of periods of physical activity and rest, the heart muscle is strengthened, which prevents the further development of heart failure. But when choosing a sanatorium, it is necessary to take into account that patients with cardiovascular diseases are contraindicated:

• A sharp change in climatic conditions,
• Moving long distances,
• Too high and low temperatures,
• High solar radiation.

Resort and sanatorium treatment is strictly prohibited for patients with severe clinical manifestations of heart failure.

Cardiac asthma(asthma cardiale; Greek asthma shortness of breath, suffocation) - attacks of suffocation from several minutes to several hours with myocardial infarction, cardiosclerosis, heart defects and other diseases associated with heart failure.

The occurrence of cardiac asthma is facilitated by an increase in blood circulation (for example, during physical exertion, fever), an increase in the mass of circulating blood (for example, during pregnancy, after introducing large amounts of fluid into the body), as well as the horizontal position of the patient; this creates conditions for increased blood flow to the lungs. Due to stagnation of blood and increased pressure in the pulmonary capillaries, interstitial pulmonary edema develops, disrupting gas exchange in the alveoli and the patency of the bronchioles, which is associated with the occurrence of shortness of breath; in some cases, breathing problems are aggravated by reflex bronchospasm.

The occurrence of cardiac asthma in the daytime is usually directly related to physical or emotional stress, increased blood pressure, and an attack of angina pectoris; sometimes an attack is triggered by eating or drinking heavily. Before an attack develops, patients often feel chest tightness and palpitations. When cardiac asthma occurs at night (observed more often), the patient wakes up from a feeling of lack of air, difficulty breathing, tightness in the chest, and the appearance of a dry cough; he experiences anxiety, a feeling of fear, his face becomes covered with sweat. During an attack, the patient, as a rule, begins to breathe through his mouth and necessarily sits up in bed or stands up, since shortness of breath decreases with an upright position of the body (orthopnea). The number of respirations reaches 30 or more per minute; the ratio of the duration of exhalation and inhalation usually changes little. In the lungs you can hear - hard breathing, sometimes (with bronchospasm) dry wheezing (usually less abundant and less “musical” than with bronchial asthma), often fine bubbling moist rales in the subscapular areas on both sides or only on the right. Subsequently, a picture of alveolar pulmonary edema may develop with a sharp increase in shortness of breath, and the release of light or pink foamy liquid when coughing. Auscultation of the heart reveals changes characteristic of a mitral or aortic defect, and in the absence of a defect, a significant weakening of the first heart sound or its replacement by systolic murmur, an accentuation of the second sound over the pulmonary trunk, often a gallop rhythm. As a rule, there is tachycardia, and with atrial fibrillation there is a significant pulse deficit.

Heart failure- a complex of disorders caused mainly by a decrease in the contractility of the heart muscle. If medical care is not provided, death is possible.

Heart failure syndrome complicates many diseases of the cardiovascular system, and heart failure develops especially often in people suffering from coronary heart disease and hypertension. The main and most noticeable manifestations of heart failure syndrome include shortness of breath, which sometimes occurs even at rest or with minimal physical activity. In addition, the possibility of heart failure is indicated increased heart rate, increased fatigue, limited physical activity and excess fluid retention in the body, causing swelling. Insufficient blood supply to the body is also the basis for such a clear sign of heart failure as blueness of the nails or nasolabial triangle (not in the cold, but at normal temperature). The inevitable result of heart failure is the appearance in the body of various abnormalities in blood circulation, which are either felt by the patient himself or determined by a cardiologist during examination.

Heart failure can occur in chronic and acute forms. Chronic heart failure usually develops as a complication of any cardiovascular disease, and can exist in a latent, asymptomatic form for quite a long time. The acute form of heart failure develops rapidly - over a few days or even hours, usually against the background of an exacerbation of the underlying disease. In some cases, they speak of the congestive phase of heart failure: its cause is a slowdown in blood flow in organs and tissues, which leads to fluid retention in the tissues of the body. It is the stagnant phase that, in its extreme manifestation, leads to the occurrence of such a life-threatening symptom as pulmonary edema.

There is also another classification of heart failure - according to the place of formation, that is, depending on which part of the heart the blood supply is impaired. On this basis, heart failure is divided into left ventricular and right ventricular. The most characteristic sign of left ventricular heart failure is shortness of breath, and the most characteristic sign of right ventricular heart failure is swelling in the feet and ankles.

Heart failure syndrome, unfortunately, is quite widespread, especially among older people. Therefore, in our time, when all statistics talk about the general aging of the population, there is an increase in the number of patients. Thus, heart failure is detected in 3-5% of people over 65 years of age and in every tenth (!) person over 70 years of age. Heart failure is more common in women because men have a high mortality rate directly from vascular disease (myocardial infarction) before it develops into heart failure.

Most patients suffering from heart failure have a chronic form. It is important to emphasize that in this case, the symptoms of heart failure develop gradually, arise softly and therefore are often mistaken by patients for natural age-related changes (“I’m getting old... So my heart is playing tricks...”). In such cases, patients often wait until the last moment to see a cardiologist, or contact them belatedly. Of course, this complicates and lengthens the treatment process, because recovery normal operation Improvement of heart and blood circulation in the initial period of heart failure is achieved more easily and with the help of smaller quantities of drugs than in the period of pronounced symptoms.

We should not forget that chronic heart failure is a progressive syndrome. Therefore, patients at the moment having “only” a latent form of chronic heart failure, within just a few years they can become the group of the most severely ill patients who are difficult to treat.

As evidence, we cite data from a study conducted several years ago in the UK. According to these data, patient survival within a year after the appearance of the first signs (symptoms) of heart failure was 57% for men and 64% for women. And after five years, these figures had dropped to 25% and 38%, respectively. In other words, 5 years after the first symptoms of heart failure appeared, only one out of four men and only every third woman remained alive! Do you need any other evidence that at the slightest suspicion of heart failure, you must IMMEDIATELY consult a cardiologist, and the case of heart failure is truly one of those cases when “delay is like death”!

Therefore, people who begin to notice “pranks” behind their hearts should always remember: early diagnosis of heart failure, and, consequently, early start treatment is the key to success in treating the syndrome. Currently, thanks to a major leap in knowledge in cardiology, heart failure can be kept “in check” for a long time. Medicines selected especially for you by a professional cardiologist will not only significantly prolong your life, but will also make it comfortable, harmonious, and free. And a patient suffering from heart failure will no longer burden the lives of those close to him.

As for acute heart failure, this is a serious but rare form of the disease. It appears unexpectedly or sudden attack Choking (cardiac asthma), often at night, and requires emergency medical attention. Acute heart failure may be complicated pulmonary edema. In such a case, the cardiologist eliminates the swelling on the spot, but, nevertheless, hospitalization of the patient is required.

Classification of heart failure:

There is a lot of debate in the cardiology community regarding the classification of chronic heart failure. In our country, the classification of V.Kh. Vasilenko and N.D. Strazhesko, proposed by them at the XII Congress of Therapists in 1935, that is, more than half a century ago, has been used for a long time, and is still used today.

According to this classification, chronic heart failure is divided into three stages: from the initial stage, with practically unexpressed symptoms, to the final dystrophic stage with severe circulatory disorders. This classification of heart failure was the first of its kind, was widely used and was long considered ideal. However, with the development of the capabilities of cardiology in the diagnosis and treatment of heart failure, the Vasilenko-Strazhesko classification, which does not provide the ability to assess the dynamics of the process of heart failure, has become somewhat outdated.

Currently, in our country, the classification of heart failure proposed by the New York Heart Association (NYHA) is increasingly used. According to this classification, patients with heart failure syndrome are divided into four functional classes (FC).

Class 1. There are no restrictions on physical activity and no impact on the patient’s quality of life.

Class 2. Weak restrictions on physical activity and complete absence of inconvenience during rest.

Class 3. A noticeable decrease in performance, symptoms disappear during rest.

Class 4. Complete or partial loss of performance, symptoms of heart failure and chest pain occur even during rest.

An easy and convenient way to determine the FC of each patient is also proposed - the so-called six-minute walk test. To carry out the test, it is enough to ask the patient to walk for six minutes at a comfortable pace along a hospital corridor of a known length and measure the time spent on this. This is sufficient to calculate the maximum oxygen consumption during exercise, and, as a result, to correctly recognize the stage of heart failure. Patients passing in 6 min. more than 551 m have no signs of heart failure; those who walk a distance from 426 to 550 m belong to FC I, those who walk a distance from 301 to 425 m belong to FC II, from 151 to 300 m belong to FC III, and patients who walk less than 150 m in 6 minutes belong to FC IV. Recently, Russian doctors are increasingly turning to this simple classification scheme.

Symptoms and signs of heart failure:

The significance of symptoms and signs of heart failure cannot be overestimated, because it is they, first of all, that allow the cardiologist to diagnose correct diagnosis and prescribe treatment. Manifestations of heart failure are a slowdown in the speed of general blood flow, a decrease in the amount of blood ejected by the heart, an increase in pressure in the heart chambers, and the accumulation of excess blood volumes that the heart cannot cope with in the so-called “depots” - the veins of the legs and abdominal cavity.

Here are the symptoms most often encountered by heart failure patients and cardiologists:

— Shortness of breath

- Weakness and fatigue

— Heartbeat

— Blueness, peripheral cyanosis and acrocyanosis

— Nocturia

The different symptoms of failure depend on which side of the heart is involved. For example, the left atrium receives oxygenated blood from the lungs and pumps it into the left ventricle, which in turn pumps blood to the rest of the organs. In case left side If the heart cannot effectively pump blood, the blood is backed up into the pulmonary vessels, and excess fluid penetrates through the capillaries into the alveoli, causing breathing difficulties. Other symptoms of left-sided heart failure include general weakness and excess mucus secretion.

Right-sided insufficiency occurs when there is difficulty in the outflow of blood from the right atrium and right ventricle, which happens, for example, when the heart valve is not functioning properly. As a result, pressure increases and fluid accumulates in the veins of the liver and legs, which end in the right chambers of the heart. The liver becomes enlarged, painful, and the legs become very swollen. With right-sided insufficiency, a phenomenon called nocturia is observed.

In congestive heart failure, the kidneys cannot handle large volumes of fluid and kidney failure develops. Salt, which is normally excreted by the kidneys along with water, is retained in the body, causing even greater swelling. Renal failure is reversible and disappears with successful treatment the main cause is heart failure.

It is important to note that almost all symptoms and clinical signs, even the “classic triad” - shortness of breath, swelling of the legs and moist rales in the lungs, not to mention fatigue and palpitations, are often found in other diseases or are leveled out by the treatment, which makes them insufficient for the diagnosis of chronic heart failure. An accurate diagnosis can only be made by a cardiologist and only using special examination methods.

Causes of heart failure:

As mentioned above, these are, first of all, various diseases of the cardiovascular system.

The most common cause of heart failure is a narrowing of the arteries that supply oxygen to the heart muscle. Vascular diseases develop at a relatively young age, sometimes they remain unattended, and then manifestations of congestive heart failure often occur in older people.

Chronic heart failure syndrome can complicate the course of almost all diseases of the cardiovascular system. But its main causes, accounting for more than half of all cases, are ischemic (coronary) heart disease and arterial hypertension, or a combination of these diseases. Often, cardiologists in their practice note the occurrence of heart failure syndrome during heart attacks and angina pectoris.

Other reasons causing the development of heart failure are changes in the structure of the heart valves, hormonal disorders (for example, hyperthyroidism - excessive function thyroid gland), infectious inflammation heart muscle (myocarditis). Myocarditis can manifest itself as a complication of almost any infectious disease: diphtheria, scarlet fever, polyarthritis, lacunar tonsillitis, pneumonia, polio, influenza, etc. It is this fact that serves as further confirmation that there are no “frivolous” viral infections, and each requires qualified treatment. Otherwise, they cause serious complications on the heart and blood vessels.

During pregnancy in women with various vascular or heart diseases, increased load on the heart can also trigger the development of heart failure. Chronic heart failure can also be caused by alcohol and drug addiction, excessive physical activity, and even a sedentary lifestyle. Thus, a recent study in the USA identified the reasons sudden deaths taxi drivers from heart failure. It turned out that heart failure is provoked by the formation of blood clots as a result of slow blood flow and blockage of blood vessels due to prolonged sitting in the car.

There is a high risk of heart failure syndrome when diabetes mellitus and diseases of the endocrine system in general. In general, we can say that heart failure is provoked by diseases in which the heart muscle is overloaded with pressure (as in hypertension) or volume (heart valve insufficiency), as well as direct myocardial diseases (myocarditis, heart attack). In addition, any factors that cause excessive stress on the heart and blood vessels can put a patient at risk.

Among the factors contributing to the exacerbation and progression of heart failure, in the first place, as you might guess, is the exacerbation or progression of the underlying disease of the cardiovascular system, as well as the addition of other diseases of the same or other systems and organs. First of all, as mentioned, this concerns diseases of the endocrine system and respiratory organs. Exacerbation of existing heart failure is caused by situations that weaken the body’s immune and nervous systems: physical overexertion, malnutrition, vitamin deficiencies, intoxication, severe stressful situations. Finally, we present this fact for those who like self-medication; the progression of heart failure can be provoked by taking certain antiarrhythmic drugs with a negative inotropic effect.

Consequences of heart failure:

Heart failure syndrome is the most difficult test for the human body, and this is not surprising. Chronic heart failure is a “time bomb” in the body. People tend to pay attention only to pronounced symptoms that clearly define the disease. The child has a rash, which means you need to show him to the doctor, it could be scarlet fever. A severe cough and pain in the side are a sure sign of pneumonia, which you also cannot ignore. But shortness of breath, fatigue, palpitations - somehow all this is not serious, and it can indicate almost any disease. So it turns out that until chronic heart failure reaches a severe stage, the patient has the opportunity to simply not pay attention to its symptoms. But we must not forget that heart failure is a PROGRESSIVE syndrome, and when the patient finally thinks about possible problems and consequences, it may already be too late. But treatment of heart failure, begun in the earliest stages, significantly improves the patient’s life prognosis; in most cases, heart failure syndrome is successfully cured in the early stages.

Cardiologists cannot predict the consequences of heart failure unambiguously and in absentia. The prognosis for each individual patient depends on the severity of the disease, concomitant diseases, age, effectiveness of therapy, lifestyle and much more. But in general, the consequences of heart failure can be extremely unfavorable. In the United States, for example, heart failure is the leading cause of hospitalization for people over 65 years of age. In patients with heart failure syndrome, the risk of death increases with myocardial infarction and stroke. In general, diseases of the cardiovascular system complicated by heart failure are more severe and less easily cured. This applies primarily to hypertension, coronary heart disease and angina.

Symptoms and clinical signs - Diagnosis of chronic heart failure

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Symptoms and clinical signs of chronic heart failure

The significance of symptoms and clinical signs is extremely high, since it is they that allow the doctor to suspect the presence of CHF in a patient and, therefore, organize the diagnostic process with maximum purposefulness and specificity in order to confirm or refute the diagnostic hypothesis. The intensive development of science and technology has contributed to the creation and implementation of numerous informative instrumental and laboratory methods for studying patients with diseases of the cardiovascular system. Nevertheless, direct clinical examination of the patient is the first stage of diagnosis. Unfortunately, we often have to deal with the fact that the clinical examination of the patient is replaced by one or another paraclinical tests. And if such a vicious approach is practiced long enough, it can lead to the atrophy of the doctor’s so-called “bedside” diagnostic skills.

Sometimes a patient comes to see a cardiologist or therapist with complaints indicating a disease of the cardiovascular system (for example, pain in the heart, “interruptions” in the heart, headache associated with increased blood pressure), in which there is a high probability of developing CHF. A nosological diagnosis (in particular, ischemic heart disease) in a case where there are no manifest manifestations of heart failure “helps” the syndromic diagnosis of the initial stage of heart failure.

In most textbooks on internal medicine, a description of the presence and severity of symptoms (complaints) and clinical signs of heart failure is given depending on the stage and form (left-, right-ventricular) CHF. As a matter of fact, it is the analysis of symptoms and clinical signs that allows one to determine the stage of the pathological process right at the bedside of a patient with chronic heart failure.

Dyspnea, as mentioned above, is the most “popular” finding in CHF. In the Great Medical Encyclopedia (2nd ed.), N. Savitsky gives the following definition of shortness of breath (dyspruxn; from Greek dyspnoia - difficulty breathing, shortness of breath) - “difficulty breathing, characterized by a violation of its frequency, depth and rhythm, accompanied by a complex of unpleasant sensations in in the form of tightness in the chest, lack of air, which can lead to a painful feeling of suffocation.”

Inspiratory dyspnea (or, according to James Mackenzie, “thirst for air”) in patients with chronic heart failure has a complex origin (the significance of each factor individually varies in different patients and in different diseases of the cardiovascular system) and there are still unresolved questions regarding it genesis. Apparently, in the formation of shortness of breath, in addition to the stagnation of blood “above” the weakened part of the heart (LV) with an increase in pressure in the pulmonary capillaries, due to which its appearance is traditionally explained, other, incompletely studied factors may also take part. In particular, the perception of difficulty breathing largely depends on the diffusion capacity of the lungs (shortness of breath is more severe, the more severe the hypoxemia), the reaction of the central nervous system to changes in blood composition (hypoxemia, hypercapnia, acidosis, etc.), the state of the peripheral and respiratory muscles and mass patient. The accumulation of fluid in the pleural and abdominal cavities, which impedes the respiratory excursion of the lungs, contributes to the appearance of shortness of breath. It is also possible that this symptom is based on a decrease in lung compliance and an increase in intrapleural pressure, which leads to an increase in the work of the respiratory muscles and auxiliary muscles. It should be added that in patients with long-term congestion of the lungs, their congestive (indurative) sclerosis develops - brown compaction (induration) of the lungs.

The sensitivity, specificity and prognostic significance of shortness of breath have already been discussed above (Table 1, 7.2). The main thing to remember is the low specificity of this symptom.

Naturally, in the initial stage of CHF, shortness of breath at rest is absent and appears only with intense muscle tension(climbing stairs or uphill, when walking quickly over long distances). Patients move freely around the apartment and can take any position convenient for themselves. As heart failure progresses, shortness of breath is observed even with minor exertion (even when talking, after eating, while walking around the room), then it becomes constant. And finally, the patient receives some relief only in a forced vertical position - a state of orthopnea. In this case, shortness of breath becomes the most serious symptom of heart disease for the patient. Severe forms of CHF are characterized by the development of painful shortness of breath at night (see below “orthopnea” and “cardiac asthma”). Very often, patients avoid the position on the left side, since this causes unpleasant sensations from the heart, which they usually cannot describe well, and increases shortness of breath (it is assumed that in this position there is a closer fit of the dilated heart to the anterior chest wall). Many patients with chronic heart failure find relief from staying in front of an open window.

With the development of hypoxia of the central nervous system in severe CHF and especially in cases complicated by atherosclerosis of the cerebral arteries, periodic Cheyne-Stokes breathing may occur.

Orthopnea (from the Greek “orthos” - straight and “rpol” - breathing) is a high degree of shortness of breath with a forced (semi-sitting or sitting) position of the patient. Orthopnea is not only a highly specific (see Table 7.2) symptom of CHF, but also its objective sign, detected during examination of the patient. Patients with severe CHF often sit in a chair, on a bed (if they still have the strength to sit down), lowering their legs and leaning forward, leaning on the back of a chair, an advanced table, or reclining on pillows (a high headboard is created with the help of several pillows or a rolled-up table). mattress). Any attempt to lie down causes them to experience a sharp increase in shortness of breath. Sometimes (in cases of untreated or “refractory” CHF) severe shortness of breath forces the patient to spend all the time - day and night (this is the only way he can short time fall asleep) - sitting. He wakes up with a feeling of lack of air if his head slips off the pillows. Sleepless nights may continue for weeks until the patient receives relief from CHF therapy. This phenomenon is especially characteristic of left heart failure. Orthopnea is explained by the fact that in the vertical position of the patient, blood moves (deposited in the veins of the lower torso and limbs) with a decrease in venous return to the right atrium, and, consequently, the pulmonary circulation becomes less full-blooded. Improving respiratory function in an upright position is facilitated by the creation better conditions for the movement of the diaphragm, as well as for the work of auxiliary respiratory muscles. Orthopnea usually disappears (or becomes significantly less severe) with increasing right ventricular heart failure secondary to left ventricular failure.

Cardiac asthma (from the Greek “asthma” - suffocation, heavy breathing) is acute asthma in a “heart” patient. An attack of severe cardiogenic shortness of breath, reaching the level of suffocation, indicates acute left ventricular heart failure (the most striking clinical manifestation of interstitial pulmonary edema), which can develop in the absence of pre-existing CHF and be the first manifestation of cardiac dysfunction. However, most cardiologists note a high positive predictive value of cardiac asthma when diagnosing chronic heart failure. Cardiac asthma can occur at any time of the day, but most often develops at night in a horizontal position. In this situation, blood leaves the depot, so-called hidden edema - extracellular fluid accumulated during the day in the tissues of predominantly the lower half of the body due to increased venous pressure - passes into the vascular bed, and a weakening of respiratory function, decreased gas exchange, and increased tone are also observed vagus nerve and bronchoconstriction. The patient awakens (if he could fall asleep before) usually after nightmares with a feeling of suffocation, tightness in the chest, fear of death, and is forced to sit up in bed. He is afraid to move, holds his hands on the bed, breathes slowly or rapidly ( breathing movements are carried out without hindrance!), often accompanied by a cough with serous sputum. If simple inspiratory dyspnea in a patient with chronic heart failure can decrease after the patient takes a vertical position on the edge of the bed, with his legs down, then in the case of acute left ventricular heart failure, severe shortness of breath and cough often persist in this position. The main cause of cardiac asthma is the discrepancy between LV dysfunction and the satisfactory “pumping” function of the right ventricle into the pulmonary circle in case of failure of the Kitaev reflex. If active therapy for heart disease is not carried out, then once it begins, attacks of cardiac asthma tend to recur more and more often. With the weakening of the contractility of the right ventricle, the addition of tricuspid valve insufficiency (this gave rise to calling it the “safety valve of the heart”) and with the development of chronic stasis as a result morphological changes in the lungs, as well as with sclerosis of the branches of the pulmonary artery, when the failure of the Kitaev reflex is lost clinical significance, relapses of cardiac asthma usually stop or their frequency is reduced. There is a common misconception among doctors that cardiac asthma is one of the criteria for stage IIB CHF, while as heart failure progresses from stage II A to stage IIB, the relevance of asthma attacks (acute heart failure!) becomes less important.

Cough (tussis). Dyspnea in patients with chronic left ventricular heart failure is often accompanied (especially at night) by a cough, dry or unproductive with mucous, difficult to separate sputum (in patients with acute left ventricular heart failure, sputum is usually not viscous and is easily excreted in the form of a thin, foamy liquid). Cough (this is a reflex act) is explained by swelling of the mucous membrane of the “congestive” bronchi (bronchitis cyanotica) or irritation of the recurrent nerve, dilated left atrium. Overflow of blood into the small vessels of the lungs may be accompanied by diapedesis of red blood cells or even minor hemorrhage and the appearance of hemoptysis (blood in the sputum). During microscopy, in addition to red blood cells, such sputum may reveal so-called “heart defect cells” (hemosiderophages).

According to the IMPROVEMENT study, fatigue is the second most sensitive symptom of heart failure after shortness of breath (Table 1), which is found in most patients even with initial symptoms of CHF. However, weakness or fatigue in patients with chronic heart failure is given unfairly little attention in many medical guidelines. Sometimes even this symptom is not classified as the main complaint of a patient with chronic heart failure, but as a “general” one (along with sweating, dizziness, irritability). There is no exact data on the specificity of the symptom under discussion, but, apparently, it is not great, since it can be observed in many other diseases. As with shortness of breath, there is no trivial explanation for the pathophysiology of fatigue. It should be noted that shortness of breath, caused by stagnation in the pulmonary circulation, is often an early sign of diastolic CHF, and increased fatigue, which is associated with impaired blood supply skeletal muscles, most often occurs with systolic CHF. Despite the fact that traditionally cardiac dysfunction is given a central place in the development of CHF, in lately Disorders of peripheral blood flow (in this case, in skeletal muscles) are becoming increasingly important in its pathophysiology.

Palpitations (palpitatio cordis - cardiac race) is the third most frequently detected symptom of CHF (Table 7.1), which is expressed in the patient feeling each contraction of his heart. More often, palpitations are felt with tachycardia (hence the synonym - cardiac race), but it can also be with a normal heart rate and even bradycardia. Apparently, for the sensation of heartbeat, not only the frequency of heart contractions matters, but also their nature and the state of the nervous system (persons with increased excitability of the nervous system complain of heartbeat more often). It is known that under normal conditions a person does not feel the activity of his heart, as well as the motor activity of other internal organs, since most reflexes from the somatic organs are closed in the reflex arcs of the areas of the central nervous system located below the cortex cerebral hemispheres, and therefore is not realized by a person in sensory perception. A change in the strength and quality of these reflexes in diseases of the cardiovascular system leads to the fact that they reach the cerebral cortex. However, sometimes with severe damage to the heart, rapid and strong contractions, which can be seen by shaking the chest wall, there are no complaints of heartbeat.

In the initial stages of CHF, the heart rate at rest does not deviate from the norm, and tachycardia occurs only during physical activity, but in contrast to the physiological increase in heart rate in patients with heart failure, it normalizes not upon cessation of exercise, but after 10 minutes or later. As CHF progresses, palpitations and tachycardia are also observed at rest. Tachycardia is a compensatory hemodynamic reaction aimed at maintaining a sufficient level of stroke (Bowditch mechanism) and minute blood volume, the effectiveness of which is rated low by most researchers (except for situations with heart valve insufficiency) - it quickly becomes untenable, leading to even greater myocardial fatigue. In patients with CHF, tachycardia is explained by humoral (activation of the sympathoadrenal system, etc.), reflex

Patients with chronic heart failure may also experience “interruptions” in the work of the heart, cardiac arrest followed by a strong beat, a sudden increase in heart rate and other subjective manifestations of rhythm and conduction disturbances.

Edema (from the Greek oidax - swell in lat. oedema - tumor, edema), detected by patients with chronic heart failure, indicates that the volume of extracellular fluid has increased by more than 5 liters and the stage of “hidden edema” has already been passed. Hidden edema can be detected by weighing or using the McClure-Aldrich test by increasing the rate (normally 40-60 minutes) of resorption of 0.2 ml saline solution(in the classic version, 0.8% NaCl solution), injected intradermally with a thin needle into the most superficial layer of the epidermis (the tip of the needle should be visible!) with the formation of a “lemon peel”, usually on the volar surface of the forearm. Also, hidden edema is indicated by a sharp increase in diuresis after the use of diuretics or cardiac glycosides.

There is a pronounced dependence of edema on the position of the body: it spreads from bottom to top. Cardiac edema is localized at first only in sloping areas - symmetrically, in areas located the lowest. In the early stages, when the patient is in a vertical position (in a lying patient, swelling begins in the lower back!), there is only swelling of the dorsum of the feet, which appears in the evening and disappears by the morning (a characteristic complaint is “shoes become tight in the evening”). As they develop, they spread to ankle joints (at the condyles), then rise to the lower leg and higher, gripping the arms and genitals. Subsequently, swelling of the legs becomes permanent and spreads to the lower abdomen and lower back up to anasarca (swelling usually does not occur on the face, neck and chest!). If a patient with already developed persistent swelling of the legs is transferred to bed rest, then they can significantly decrease and even disappear, but they appear or increase (move) in the lumbosacral region. With the long-term existence of edema, trophic changes in the skin, cracks (with massive edema, the skin often bursts and fluid leaks out of the tears), and dermatitis occur.

The pathogenesis of edema in patients with chronic heart failure can be satisfactorily explained on the basis of Starling's hydrodynamic concepts. However, the mechanical (hydrodynamic) factor is not the only one, and sometimes, apparently, the main one. The causes of edema in these patients are very diverse - it matters the whole complex neurohumoral, hemodynamic and metabolic factors.

Edema is traditionally associated with right ventricular failure, but it can also occur with decreased contractility of the left ventricle. Edema, caused predominantly by right ventricular failure and venous stagnation, usually appears later than the liver enlarges, they are extensive, dense to the touch, the skin over them is thinned, cyanotic, with trophic changes. Edema with left ventricular dysfunction occurs earlier than venous stasis, is small, soft, displaceable, located in areas of the body remote from the heart, the skin over them is pale. If the first type of edema depends on venous stagnation, then the second type of edema is the result of hypoxemic disorders, porosity of the capillary walls as a result of slow blood circulation.

Edema (both in history and according to physical examination) is an insensitive sign of CHF (see Table 2) and may be associated with disturbances of local venous or lymphatic outflow (in particular, varicose veins with venous insufficiency II-III degrees), liver and kidney diseases, etc. Therefore, the cardiac genesis of edema is established only on the basis of a comprehensive examination of the patient.

A feeling of heaviness (with slowly developing congestion) or pain (with rapidly developing congestion) in the right hypochondrium in patients with right ventricular heart failure usually precedes the appearance of edema, since the liver is the first to respond to failure right half hearts. These symptoms are caused by stretching of the liver capsule when the hepatic veins and capillaries are overflowing with blood (with rapid enlargement of the liver, stretching of the Glissonian capsule is accompanied by fairly intense pain in the right hypochondrium). With the progression of CHF, prolonged stagnation (“nutmeg liver”, cardiac cirrhosis), symptoms of liver dysfunction appear - icterus of the skin and mucous membranes. Portal hypertension occurs - at the initial stage, the patient is bothered by a feeling of bloating and fullness in the abdomen, then he notices an increase in the abdomen in volume (due to the accumulation of ascitic fluid). In this case, it is extremely rare that the complaints of a patient with chronic heart failure may be supplemented by a feeling of heaviness in the left hypochondrium (due to an enlarged spleen).

Nausea, vomiting, loss of appetite, constipation, flatulence and other symptoms of gastric and intestinal dyspepsia are almost constant companions of congestive heart failure. The functions of the gastrointestinal tract in CHF are always impaired to a greater or lesser extent, both due to hypoxia and reflex influences. Often, dyspeptic disorders are a manifestation side effect medicines, used to treat heart disease (in particular, aspirin, cardiac glycosides).

Decreased diuresis (of course not during the period of swelling) and nocturia. Impaired renal function occurs due to a significant (almost half) decrease in renal blood flow, reflex spasm of the renal arterioles and increased pressure in the renal veins (the mechanism of these phenomena was discussed above). As a result of the simultaneous (but not uniform) decrease glomerular filtration and increased tubular reabsorption of sodium and water, the daily amount of urine decreases, and the urine becomes concentrated with a high relative density. Urine is released mainly at night due to some improvement in the blood supply to the kidneys at rest and in a horizontal position, and the release of edematous fluid into the blood at this moment. In addition, central dysregulation of the diuresis rhythm appears to be important.

Changes in body weight. Sudden weight gain (sometimes 2 kg or more in 2-3 days) is a sign of increasing cardiac decompensation. Various metabolic changes in patients with chronic heart failure, barely noticeable at the beginning, in stage III lead to extremely severe nutritional disorders of all tissues and organs - a progressive decrease in body weight is observed (so-called cardiac cachexia develops, which is masked for some time by the presence of edema).

Complaints from patients with chronic heart failure about decreased mental performance and mood, irritability, insomnia at night, and then drowsiness during the day, are associated with an early change in the functional state of the central nervous system that occurs after a circulatory disorder.

Taking an anamnesis (all types) is an important part of the examination of a patient with a disease of the cardiovascular system. In this case, the following are identified: risk factors or history of coronary artery disease; the presence of arterial hypertension, diabetes, valvular pathology; family history of cardiomyopathy; the presence of recent pregnancy, a viral (“cold”) disease, risk factors for contracting AIDS and associated diseases; diseases of the thyroid gland and other systemic diseases; presence and degree of alcohol dependence. When collecting a clinical history, it is important to find out the characteristics and sequence of symptoms in a given patient. It is always important to establish the time of onset of each symptom and its relationship to the expected time of heart disease, likely provoking factors for the first manifestation and exacerbations of CHF, indications for therapeutic interventions and their effectiveness.

If possible, you should clarify the data of laboratory instrumental and other clinical studies that were carried out on the patient during the period of the present illness, obtain extracts from old medical records, copies of tests, electrocardiograms, etc. The information obtained often becomes one of the keys to recognizing CHF and largely determines the initial choice of medical actions.

It is necessary to ask the patient about physical and intellectual development, previous diseases, bad habits, living conditions, unfavorable professional factors. It is important to obtain information about the patient’s parents, relatives of the first and second degrees of kinship, find out their age, diseases, and if they died, then from what and at what age.

Clinical signs

Objective examination data can be varied. The main “findings” of the objective examination are presented in Fig. 1.

Figure 1. Main clinical signs of CHF

During a general examination of a patient with moderately severe CHF at rest, it is usually not possible to identify any signs of heart disease. When examining a patient with manifest CHF, the following signs can be detected:

1. Forced position of the patient (see above shortness of breath, orthopnea)
2. Cyanosis (Latin cyanosis - cyanosis from the Greek kyaneos - dark blue) - bluish discoloration of the skin is considered a common sign of CHF. However, qualitative studies that clearly establish the sensitivity and specificity of this clinical sign, we don't know. The appearance of cyanosis in patients with chronic heart failure is associated with a decrease in blood flow velocity and an increase in oxygen absorption in tissues, as well as insufficient arterialization of blood in the pulmonary capillaries, resulting in an increase in the content of reduced hemoglobin in the blood (has a blue color). The degree of severity of cyanosis and its nature also depend on functional and organic changes in small arteries (angiospasm, obliterating endarteritis, etc.), the diameter of small venules, the activity of arteriovenous anastomoses (the “short circuit” phenomenon). The first manifestations of cyanosis in patients with CHF are the name of acrocyanosis (from the Greek asgop - edge, limb + kyaneos - dark blue), that is, cyanosis of the areas of the body farthest from the heart (tip of the nose, earlobes, lips, fingernails and toenails). The occurrence of acrocyanosis is caused mainly by a slowdown in blood flow and therefore it is peripheral in nature (it is often called peripheral cyanosis). It is possible to distinguish peripheral cyanosis from central cyanosis caused by respiratory diseases (it is necessary to remember about functional and structural changes in the lungs in patients with chronic left ventricular failure, leading to impaired blood oxygen saturation, which significantly complicates differential diagnosis): 1) massage the earlobe until a “capillary pulse” appears - in the case of peripheral cyanosis, the cyanosis of the earlobe disappears, but in the case of central cyanosis, it remains; 2) allow the patient to breathe pure oxygen for 5-12 minutes - if after this cyanosis does not disappear, then it is of a peripheral (cardiac) nature.

With increasing cardiac weakness and oxygen deficiency, cyanosis increases (from barely noticeable cyanosis to a dark blue color) and becomes widespread (all skin and mucous membranes acquire a bluish tint) - central cyanosis, when arterial blood oxygen saturation drops to 80% or lower. In its pathophysiological essence (impaired blood arterialization) and clinical manifestations, the latter is very close to that observed in patients with respiratory diseases. Particularly severe central cyanosis is observed in patients with birth defects heart in the presence of arteriovenous communication (“black heart patients”), The so-called “blue type” defects include tetralogy of Fallot (stenosis of the pulmonary artery outlet, ventricular septal defect, dextroposition of the aorta, right ventricular hypertrophy), Eisenmenger complex (subaortic defect interventricular septum, aorta “riding” over this defect, hypertrophy and dilatation of the right ventricle, normal or dilated pulmonary artery), Ebstein’s disease (dysplasia and displacement of the tricuspid valve into the cavity of the right ventricle), pulmonary stenosis, common arterial (aortopulmonary) trunk, atresia of the tricuspid valve, variants of transposition of the great vessels, defects of the interatrial and interventricular septum. Cyanosis can also occur due to poisoning with substances that form methemoglobin, sulfagemoglobin (sulfonamides, phenacetin, aniline, nitrobenzene, berthollet salt, arsenic hydrogen, nitrates and nitrites, etc.).

Pale skin and mucous membranes in patients with chronic heart failure can be combined with cyanosis (so-called “pale cyanosis”) with aortic heart defects (aortic stenosis, aortic valve insufficiency), collapse, heavy bleeding, infective endocarditis. With mitral orifice stenosis, pallor is combined with a purple-red “blush” on the cheeks - “mitral butterfly”.

1. Jaundice (Greek icteros). Jaundice staining of the skin and mucous membranes (primarily the sclera) in patients with severe chronic right ventricular heart failure is explained by the development of congestive fibrosis (“cardiac cirrhosis”) in the liver. Jaundice in patients with chronic heart failure is usually mild (rarely up to 68-85 µmol/l). However, sometimes, against the background of chronic stagnation in the liver, jaundice quickly and significantly increases - “bilirubinemic crisis.” The latter is associated with paroxysmal deterioration of intrahepatic circulation, developing following decompensation of cardiac activity. With infective endocarditis, the yellowness of the skin is combined with its pallor, and then the color resembles the color of “coffee with milk”. In such cases, petechiae with a pale center (Lukin-Libman symptom) can be found on the skin and especially on the conjunctiva of the lower eyelid.
2. “Corvisart's face” (Jean Nicolas Corvisart) is characteristic of significant untreated or refractory CHF. It is swollen, flabby, yellowish-pale with a bluish tint, its expression is apathetic, indifferent, drowsy, its eyes are sticky, dull, its mouth is constantly half-open, its lips are cyanotic.

Fingers in the form of “drumsticks” occur with CHF, which develops in patients with infective endocarditis, some congenital heart defects.

1. Edema (see also “edema” above in the “Symptoms” section) in patients with chronic heart failure can be so pronounced that it can be detected during a general examination. However, even before pronounced swelling visible to the eye appears, one can notice by palpation the pastiness (from the Latin pastosus - pasty, flabby) of the tissues (primarily in the ankle area, on back side feet, legs) - when pressed, a disappearing dimple appears gradually (over 1-2 minutes), which is detected only by palpation. Massive, widespread swelling of the subcutaneous fat of the trunk and limbs, usually accompanied by ascites and hydrothorax, is called anasarca (from the Greek ana - on, up, up + sarx, sarcos - meat). The skin with edema, especially of the lower extremities, is pale, smooth and tense. With long-lasting edema, it becomes rigid, inelastic and acquires a brown tint due to diapedesis of red blood cells from stagnant capillaries. With pronounced edema, linear breaks may appear in the subcutaneous tissue of the abdomen, reminiscent of scars after pregnancy. A comparison of the sensitivity and specificity of edema detected by patient complaints and those detected during physical examination is presented in Table. 2.
2. Cardiac cachexia (from the Greek cachexia - exhaustion). Significant weight loss and the development of cachexia are observed in advanced stages of CHF and, in the case of treated cardiac decompensation, usually indicate the final (irreversible) stage of the disease. A patient with anasarca seems to “dry up” - “dry dystrophic type” according to V. Kh. Vasilenko:
3. activation of metabolism under the influence of additional work performed by the respiratory muscles, on the one hand, increased oxygen demand by the hypertrophied myocardium, on the other, as well as a constant feeling of discomfort associated with severe heart failure; 2) lack of appetite, nausea and vomiting caused by central disorders, intoxication with cardiac glycosides or congestive hepatomegaly and a feeling of heaviness in the abdominal cavity; 3) some malabsorption in the intestine caused by interstitial stagnation in the veins; 4) enteropathy leading to protein loss, which can be observed in individuals suffering from severe right ventricular CHF. Great importance in the development of cachexia in patients with chronic heart failure is attached to changes in cytokine status (see above). Explicit or subclinical signs of malnutrition are found in 50% of patients with severe CHF. The development of pathological weight loss should be suspected in the case. a) body weight is less than 90% of ideal; b) with documented unintentional weight loss of at least 5 kg or more than 7.5% of the initial “dry” weight (without edema) during the last 6 months; c) mass index (weight/height2)<22 кг/м2.

Swelling and pulsation of the neck veins, dilatation of the veins of the arms, which do not collapse when raising the arm. In a healthy person, the veins of the neck can only be visible if he is in a supine position. If the overflow and expansion of the neck veins is noticeable in a vertical position, it means that there is a general (right ventricular heart failure, as well as diseases that increase pressure in the chest and impede the outflow of venous blood through the vena cava) or local (compression of the vein from the outside - tumor, scars, etc. or its blockage by a blood clot) venous stagnation. Moreover, if in severe diseases of the respiratory system the neck veins swell only when exhaling, due to increased intrathoracic pressure and obstruction of blood flow to the heart, then in CHF the swelling of the neck veins is constantly observed. The Austrian pathologist G. Gflitner proposed for clinical practice a simple method for approximate determination of the level of pressure in the right atrium - the higher the hand must be raised in order for the superficial veins of the hand to collapse, the higher the pressure in the right atrium (the height to which the hand is raised from level of the right atrium, expressed in millimeters, approximately corresponds to the value of venous pressure).

In patients with chronic heart failure, pulsation of the jugular veins can be seen in the neck area - the venous pulse. The swelling and collapse of the jugular veins during one cardiac cycle is due to the dynamics of blood outflow into the right atrium in different phases of systole and diastole of the heart (slowing down of blood flow in the jugular vein and its slight swelling during atrial systole and acceleration during ventricular systole with its collapse). In healthy people, the physiological negative venous pulse is usually not visualized and can only be analyzed when it is graphically recorded. If there is difficulty in the outflow of venous blood into the right atrium, a pathological venous pulse is detected during a routine examination. Pulsation of the jugular veins, coinciding in time with ventricular systole (the carotid artery pulsates outward from the jugular veins), is called a positive venous pulse and usually indicates tricuspid valve insufficiency - the 1st symptom of Bamberger (Bamberger I). However, the cause of noticeable pulsation of the jugular veins may be hypertrophy and insufficiency of the left ventricle, even in the absence of insufficiency of the right chambers, due to the transmission of pressure through the interventricular septum.

To determine the nature of the venous pulse, the jugular vein must be pressed with a finger. If the vein pulsation remains below the point of compression, then the venous pulse is positive; if absent, it is negative.

1. Plesh's symptom is swelling of the jugular veins when pressing on the liver from bottom to top (hepatojugular reflux), which is observed with severe right ventricular heart failure (in particular, with tricuspid valve insufficiency).
2. Palpation and percussion of the heart in patients with chronic heart failure can detect signs of cardiomegaly - displacement of the apical impulse (normally located in the 5th intercostal space 1-1.5 cm medial to the left midclavicular line) outward from the left midclavicular line and below fifth intercostal space; diffuse (more than 2 cm2) nature of the apical impulse (with concentric hypertrophy of the LV - “lifting”, with eccentric hypertrophy - “dome-shaped”); the so-called cardiac impulse (pulsation of the enlarged right ventricle to the left of the sternum, spreading to the epigastric region); expansion of the boundaries of relative dullness of the heart. To determine the proper maximum size of the heart, the patient’s height is divided by 10 and 3 cm is subtracted for the length and 4 cm for the diameter. With the development of heart disease in childhood, signs of cardiomegaly can be detected already when examining the heart area - protrusion of the chest (“heart hump”).

Tachycardia, arrhythmia, weakening of the sonority of heart sounds (hydropericardium must be excluded) and protodiastolic gallop rhythm, caused by a pathological (significantly enhanced) III tone, are often heard in CHF, but are not, however, specific signs for it. Noteworthy is the data that pathological III tone often occurs in patients with reduced systolic function, while IV tone can be determined when the compliance of the ventricular wall is impaired (diastolic dysfunction). Auscultation can also reveal “direct” and additional signs of heart valve disorders. Listening to heart murmurs may be a key point in diagnosing a heart defect underlying CHF, or may indicate the presence of functional (relative) mitral and tricuspid regurgitation as a result of dilatation of the ventricles and/or atria (hence, the valve ring in the area of ​​the atrioventricular junction), or dysfunction of the papillary muscles.

1. Systemic blood pressure is elevated in patients with acute decompensation or poorly controlled hypertension, but low blood pressure with low pulse pressure is more common in advanced disease. There is an opinion that blood pressure decreases when left ventricular heart failure predominates, and when right ventricular heart failure predominates, it may increase slightly (“congestive hypertension”). However, the validity of this judgment is not always confirmed in clinical practice.

Katzenstein's symptom (M. Katzenstein) - after compression of the femoral artery, blood pressure in a healthy person increases, and in the presence of weakness of the heart muscle, it decreases.

1. Physical examination of the respiratory organs in patients with chronic heart failure may reveal signs of pulmonary congestion with wet and dry rales, as well as the presence of fluid in the pleural cavity.

The appearance of silent moist rales, mainly in the phase of inspiration and/or crepitation (crepitatio - crackling) over the basal sections (especially on the side on which the patient lies) of the lungs in patients with left ventricular heart failure is associated with high pressure in the pulmonary veins, capillaries and the accumulation of small the amount of secretion in the lumen of the small bronchi (fine rales) or alveoli (crepitus). In patients with extremely severe decompensation of the left ventricle and cardiac asthma, in addition to moist rales (up to “bubbling” rales in the late phase of development of pulmonary edema), which are heard over all pulmonary fields, high-pitched dry rales, caused by congestion of the bronchial mucosa and accumulation of viscous transudate in the lumen of the bronchi. At the same time, such wheezing can be caused not only by left ventricular failure (rule out obstructive bronchial diseases!).

An increase in pleural capillary pressure in CHF and the penetration of fluid into the pleural cavities lead to the accumulation of pleural effusion (in the right pleural cavity more often than in the left), which can be established using known physical diagnostic techniques (lag of the “sick” half of the chest in the act of breathing , a sharp weakening or absence of vocal tremor over the area of ​​fluid accumulation, a dull sound or absolute dullness is determined by percussion, during auscultation, breathing and bronchophony are sharply weakened or absent). It is a common idea that since the pleural veins drain into the veins of both the systemic and pulmonary circulation, hydrothorax develops in both left and right ventricular CHF. However, A.G. Chuchalin believes that in patients with pulmonary hypertension with signs of right ventricular heart failure, fluid accumulation in the pleural cavity does not occur, and hydrothorax is associated with left ventricular dysfunction!

1. Hepatomegaly is the first symptom of liver congestion and represents the classic manifestation of right ventricular failure.

The liver is called the "reservoir" for stagnant blood and the pressure gauge of the right atrium. Increased central venous pressure is transmitted to the hepatic veins and interferes with blood flow to the central part of the lobule - central portal hypertension develops. The latter is accompanied by hypoxia, which over time causes atrophy and even necrosis of hepatocytes with replacement fibrosis and impaired liver architecture (up to the development of cardiac cirrhosis).

In the initial period of right ventricular CHF, the liver (painful on palpation!) protrudes only slightly from under the costal arch, its edge is rounded, smooth, and the surface is soft. Characteristic variability of its size is associated with the state of hemodynamics and the effectiveness of treatment. In the future, the organ can reach enormous sizes and “sink” below the iliac crest. The Plesch symptom is determined (see above). The edge of the liver becomes sharper, the surface becomes dense. In this case, the intensity of pain during palpation may decrease. Cardiologists and hepatologists note a variety of clinical manifestations of congestive liver: a clinical situation with severe CHF, manifested by anasarca and ascites and a slight enlargement of the liver, is possible, and, on the contrary, pronounced hepatomegaly with mildly expressed other phenomena of congestion.

With prolonged right ventricular CHF, such as, for example, in patients with damage to the tricuspid valve or chronic constrictive pericarditis, splenomegaly may develop simultaneously with hepatomegaly.

Systemic venous hypertension may also manifest as liver pulsations. True venous (for example, in patients with insufficiency of the right atrioventricular valve) or arterial pulsation coinciding with the apical impulse (for example, in case of aortic valve insufficiency) pulsation of the liver itself should be distinguished from the so-called transfer pulsation in cases where heart contractions are transmitted to it.

1. Ascites (Latin ascites - abdominal dropsy from the Greek ascos - leather bag for wine or water) in a patient with right ventricular CHF develops as a result of extravasation of fluid from the veins of the liver and peritoneum, the pressure in which is increased. As a rule, massive ascites is diagnosed in patients with tricuspid valve disease or chronic constrictive pericarditis. Ascites that develops after a long period of edema in patients with cardiac cirrhosis of the liver is often refractory to digitalis-diuretic therapy.

During examination with the patient in an upright position, the abdomen with severe ascites looks saggy; in a horizontal position, the stomach is flattened, and its lateral sections bulge (“frog belly”). With so-called tense ascites, the shape of the abdomen depends little on the position of the patient (there is so much fluid in the peritoneal cavity that it does not move). The navel protruding in the patient's vertical position allows one to distinguish an enlarged abdomen with ascites from that with significant obesity.

Conn's sign (N. Conn) is a sign of severe swelling of the scrotum in patients with ascites: the patient lies on his back with his legs widely abducted.

Detecting a large amount of free fluid in the abdominal cavity (more than 1.5 liters) does not cause difficulties. A percussion examination of the abdomen of a patient in a horizontal position on his back reveals dullness over the lateral areas, and intestinal tympanitis in the middle. Moving the patient to the left side causes a dull sound to shift downwards, and it is detected above the left half of the abdominal cavity, and in the area of ​​the right flank - a tympanic sound. To detect a small amount of fluid, percussion is used with the patient standing: with ascites, a dull or dull sound appears in the lower abdomen, disappearing in a clinostatic position.

Pitfield's symptom I (R.L. Pitfield) is a sign of ascites: if a sitting patient percusses the quadratus lumborum muscle with one hand, then the second hand, palpating the anterior abdominal wall, perceives weak vibrations.

In the second issue of the journal “Heart Failure” for 2003, a scale for assessing the clinical condition in CHF, modified by V. Yu. Mareev, is presented, which consists of 10 categories and can be a good alternative to the six-minute walk test (see below) in objectifying the functional class of CHF in the case of inability for any reason to execute the latter:

1. Shortness of breath: 0 - no; 1 - under load; 2 - at rest.
2. Has your weight changed over the past week: 0 – no; 1 - increased.
3. Complaints about interruptions in heart function: 0 - none; 1 - yes.

IV What position is he in bed: 0 - horizontal; 1 - with a raised head end (+ 2 pillows); 2-1 + night suffocation; 3 - sitting.

1. Swollen neck veins: 0 - none; 1 - lying down; 2 - standing.
2. Wheezing in the lungs: 0 - no; 1 - lower sections (up to 1/3); 2 - to the shoulder blades (up to 2/3); 3 - over the entire surface of the lungs.
3. Presence of gallop rhythm: 0 - no; 1 - yes.
4. Liver: 0 - not enlarged; 1 - up to 5 cm; 2 - more than 5 cm.
5. Edema: 0 - no; 1 - pasty; 2 - swelling; 3 - anasarca.
6. Blood pressure level: 0 - >120 mm Hg; 1 - 100-120 mmHg; 2 -<120 мм рт.ст.

During the interview and examination of the patient, the doctor evaluates the clinical condition in all 10 categories of the scale. Mathematical processing of the study results consists of calculating the sum of points corresponding to the severity of clinical manifestations of CHF. In total, the maximum patient can score is 20 points (“critical” CHF). 0 points indicates a complete absence of signs of CHF. The results obtained are assessed as follows:

1. FC - up to 3.5 points
2. FC - 3.5-5.5 points
3. FC-5.5-8.5 points
4. FC - more than 8.5 points
5. Instrumental and laboratory diagnostics of chronic heart failure

The main instrumental methods for diagnosing CHF are non-invasive - ECG, echocardiography, chest radiography. According to indications, this minimum required set of studies is supplemented with more complex diagnostic techniques - stress tests, coronary angiography, cardiac catheterization, invasive hemodynamic monitoring using a Swan-Hans catheter, radioisotope methods, magnetic resonance imaging, endomyocardial biopsy, etc. However, they are rarely resorted to , since the necessary information about cardiac dysfunction can be obtained using simple non-invasive studies and primarily echocardiography.

1. ECG. Although this method does not provide direct data on the state of the systolic and diastolic functions of the heart, its sensitivity in detecting CHF is so great that a normal ECG gives reason to doubt the correct diagnosis. The probability of absence of LV systolic dysfunction (negative predictive value) with a normal ECG exceeds 90%. In other words, no more than 10% of patients with chronic heart failure fall under the exception to the rule “myocardial dysfunction, one way or another, will always be reflected on the ECG.”

The most important ECG changes for objectifying CHF are presented in Table. 6.

Table 6. ECG changes in patients with chronic heart failure

Heart failure. signs

With moderate heart failure, patients usually do not experience much discomfort at rest, except when they have to remain in a horizontal position for more than a few minutes. In more severe heart failure, pulse pressure decreases, reflecting a decrease in stroke volume. In some cases, as a result of generalized vasoconstriction, diastolic blood pressure increases. The patient becomes noticeable cyanosis of the lips and nail beds, sinus tachycardia. In heart failure, systemic venous pressure is often pathologically high, which is manifested primarily by swelling of the jugular veins to varying degrees. In the early stages of heart failure, resting venous pressure remains normal. However, it can increase significantly during or immediately after cessation of physical activity, as well as with pressure on the anterior abdominal wall (positive abdominojugular reflex).

Loud III and IV tones are often heard in heart failure, but are not, however, specific signs for it. An alternating pulse is possible, i.e. a regular rhythm, against the background of which there are strong and weak contractions of the heart, and therefore, waves of peripheral pulses of different strengths. Alternating pulse can be recorded using sphygmomanometry, and in more severe cases, with simple palpation. It often occurs after extrasystoles and is usually observed in patients with cardiomyopathies, arterial hypertension or coronary heart disease. The reason for this lies in a decrease in the number of contractile fibers during weak contraction and/or fluctuations in the end-diastolic volume of the left ventricle.

Moist rales in the lower parts of the lungs. In patients with heart failure and high pressure in the pulmonary veins and capillaries, moist crackles on inspiration and dullness on percussion of the posterior lower parts of the lungs are often detected. In patients with pulmonary edema, coarse and whistling rales, sometimes accompanied by expiratory shortness of breath, are heard over both pulmonary fields. At the same time, such wheezing can be caused not only by left ventricular failure.

Cardiac edema. The location of cardiac edema usually depends on body position. If the patient can move, then edema is more often found in symmetrical areas of the lower extremities, in particular in the pretibial region and ankles, and if he is on bed rest, then in the sacral area. Palpable swelling on the face and hands in heart failure appears rarely and only in the later stages of the disease.

Hydrothorax and ascites. An increase in pleural capillary pressure in congestive heart failure and the penetration of fluid into the pleural cavities leads to the accumulation of pleural effusion. Since the pleural veins drain into the veins of both systemic and pulmonary circulation, hydrothorax develops with a noticeable increase in pressure in both venous systems, but can be a consequence of venous hypertension in any one of them: in the right pleural cavity more often than in the left. Ascites also develops due to transudation of fluid from the veins of the liver and peritoneum, the pressure in which is increased (Chapter 39). As a rule, massive ascites is diagnosed in patients with damage to the right atrioventricular (tricuspid) valve and constrictive pericarditis.

Congestive hepatomegaly. Systemic venous hypertension is also manifested by dilatation, tension and pulsation of the liver. These changes can be observed in patients with ascites, but also in less severe forms of heart failure, regardless of the cause. With prolonged severe hepatomegaly, such as in patients with damage to the right atrioventricular (tricuspid) valve or chronic constrictive pericarditis, splenomegaly may simultaneously develop.

Jaundice. Signs of jaundice appear in the later stages of congestive heart failure. Its appearance is based on an increase in the levels of both direct and indirect bilirubin due to impaired liver function under the influence of stagnation of blood circulation in it and hepatocellular hypoxia, which leads to central lobar atrophy. At the same time, the concentrations of serum enzymes, in particular CGOT and SGPT, increase. In cases of acute liver congestion, jaundice can be severe and be accompanied by a significant increase in enzyme levels.

Cardiac cachexia. In severe chronic heart failure, significant weight loss and the development of cachexia can be observed. This occurs due to 1) activation of metabolism under the influence of additional work performed by the respiratory muscles, on the one hand, increased oxygen demand from the hypertrophied myocardium, on the other, as well as a constant feeling of discomfort associated with severe heart failure; 2) lack of appetite, nausea and vomiting caused by central disorders, intoxication with cardiac glycosides or congestive hepatomegaly and a feeling of heaviness in the abdominal cavity; 3) some malabsorption in the intestine caused by intestinal stagnation in the veins; 4) enteropathy leading to protein loss, which can be observed in individuals suffering from severe failure of predominantly the right heart.

Other manifestations. As a result of a decrease in the volume of circulating blood, the limbs become cold, become pale in color, and the skin becomes moist. Diuresis decreases; the specific gravity of urine increases, protein appears in it, and the sodium content decreases; prerenal azotemia is detected.

In patients with long-term severe heart failure, impotence and mental depression are common.

Heart failure. X-ray studies.

In addition to the enlargement of one or another chamber of the heart, the damage to which led to heart failure, signs of changes in the blood vessels of the lungs are detected, caused by increased pressure in their system (Chapter 179). In addition, chest x-ray can reveal pleural and interlobar effusions.

Heart failure. differential diagnosis.

The diagnosis of congestive heart failure can be established in the presence of its clinical manifestations in combination with characteristic symptoms of one or another etiological form of heart disease. Since chronic heart failure is often accompanied by enlargement of the heart, the preservation of normal sizes in all chambers of the heart casts doubt on this diagnosis, but in no case rejects it. Heart failure can be difficult to distinguish from lung disease. Differential diagnosis in this case is discussed in Chap. 26. Pulmonary embolism manifests itself with many symptoms characteristic of heart failure. However, hemoptysis, pleural chest pain, superior displacement of the right ventricle, and the characteristic mismatch of ventilation and perfusion of the lungs detected during lung scanning argue in favor of pulmonary embolism (Chapter 211).

Swelling of the ankles may be caused by varicose veins, a manifestation of cyclic edema, or the result of gravitational effects (Chapter 28). But in none of these cases will the edema be accompanied by hypertension of the jugular veins at rest or when pressing on the anterior abdominal wall. The renal nature of edema is usually confirmed by renal function tests and laboratory urine tests. Edema caused by kidney disease is rarely combined with increased venous pressure. Liver enlargement and ascites also occur in patients with liver cirrhosis, but in this case the jugular venous pressure remains within normal limits, and the positive abdominojugular reflex is absent.