home Audience 2 Etiology of chronic heart failure. Heart failure. Hemodynamic overload of the myocardium

Etiology of chronic heart failure. Heart failure. Hemodynamic overload of the myocardium

B.C. Gehrke
veterinarian, candidate of veterinary sciences, CJSC “Network of Veterinary Clinics”, St. Petersburg

V.S. Gerke
DVM, PhD

annotation

The article describes the main factors of chronic heart failure. The main pathogenetic aspects and stages of chronic heart failure are highlighted. Two classifications of heart failure used in humane medicine and two classifications developed and used in veterinary practice are considered. The author focuses on the classification of chronic heart failure proposed by the Veterinary Cardiological Society.

Currently, in veterinary cardiology there are three main directions with approaches to diagnosis and treatment, sometimes contradicting each other - chronic heart failure (CHF), acute heart failure (AHF) and arrhythmology. This is due to the difference in goals when treating a patient. In acute heart failure, the goal is rapid compensation without taking into account long-term prognoses in accordance with all emergency care rules. In matters of arrhythmology, the first priority is to stabilize the rhythm for the possible prevention of sudden arrhythmogenic death. Patients with arrhythmias during the stabilization period, as a rule, have a good quality of life and the main problem for them is sudden death from ventricular fibrillation or asystole. In case of CHF, the doctor has two goals - quality of life and its duration.

Of course, it is impossible to single out the more important of these areas. Moreover, both acute heart failure and arrhythmias are either combined with CHF or become the causes of CHF.

Chronic heart failure (CHF) is a pathological condition in which the work of the cardiovascular system does not meet the metabolic needs of the body, first during physical (or psycho-emotional) stress, and then at rest. It is characterized by increased fatigue, shortness of breath, cough, then accumulation of fluid in the cavities (ascites, hydrothorax), pulmonary edema, lethargy, and cachexia. If we consider CHF as a syndrome, then it is a set of symptoms and to treat the patient it is necessary to diagnose the underlying disease that causes this condition. Treatment should be aimed at the “root of evil.” However, in the development of CHF there are stages at which there may no longer be a cause (for example, myocardial dilatation after myocarditis), i.e., the underlying disease is no longer present. In this case, CHF should be considered as a disease and the patient should be treated for heart failure. That is, on the one hand, CHF is a set of symptoms of individual heart diseases, but on the other hand, CHF has its own etiological factors, stages of development, and outcomes, which means it is a disease that is a problem in itself.

So that doctors can find a common language with each other and decide on the transition of symptoms into disease, it is necessary to analyze two main points - the pathogenesis of CHF and classification. In the future, having decided on these points, we will consider the diagnostic approach, methods of basic, additional, special diagnostic tests, general and special therapeutic approaches. We will analyze individual diseases; of course, we will also pay attention to issues of arrhythmology and acute heart failure.

Cardiology in the practice of a veterinarian is closely related to diseases of the respiratory system, so in our section we will pay attention to issues of pulmonology.

Send your wishes, comments, ideas and articles on cardiology-pulmonology to This email address is being protected from spambots. You must have JavaScript enabled to view it.. We are glad to have any cooperation, it contributes to mutual professional growth.

The pathogenesis of CHF is a complex cascade of neurohumoral, hemodynamic and immunological reactions, each of which, playing a separate role, interacts with the others and contributes to the progression of the disease.

CHF is triggered by one of four main factors:

1. Volume overload (heart defects with reverse blood flow - mitral or aortic valve insufficiency, the presence of intracardiac shunts).

2. Pressure overload (stenosis of the valve orifices, ventricular outflow tract, or in the case of hypertension of the systemic or pulmonary circulation).

3. Decrease in the functional mass of the myocardium as a result of coronarogenic (chronic coronary insufficiency in endocrine diseases such as diabetes mellitus, hypothyroidism), non-coronarogenic (myocardial dystrophy, myocarditis, cardiomyopathy) and some other heart diseases (tumors, amyloidosis, etc.).

4. Impaired diastolic filling of the ventricles of the heart (pericarditis, restrictive cardiomyopathy).

It is also necessary to take into account contributing factors that accelerate the development and progression of CHF: physical and stress overload, primary and iatrogenic arrhythmias, respiratory diseases (chronic infections, brachycephalic syndrome, etc.), chronic anemia, nephrogenic hypertension.

In response to the influence of triggering factors, activation of neurohumoral mechanisms occurs, each of which ensures the strengthening of the others, and the increase in the influence of any one compared to others determines individual clinical manifestations:

Hyperactivation of the sympathetic-adrenal system;

Activation of the renin-angiotensin aldosterone system;

Hyperproduction of ADH (vasopressin);

Inhibition of the natriuretic peptide system;

Endothelial dysfunction;

Hyperactivation of pro-inflammatory cytokines (tumor necrosis factor);

Formation of hyperactive apoptosis of cardiomyocytes.

Chronic activation of neurohumoral systems, which is a key element in the pathogenesis of chronic heart failure, leads the patient from primary myocardial damage to death in a pathophysiologically similar manner, regardless of the nature of the primary damage.

As a result, structural and geometric irreversible changes in the heart occur - myocardial remodeling. The more pronounced the remodeling in a particular patient, the less important it is what was the triggering factor, and the more CHF becomes the main problem, and not just a manifestation of the underlying disease.

The progression of CHF in functional terms is characterized by an increase in clinical signs, and morphologically - by hemodynamic disorders with myocardial remodeling. As the pathogenetic aspects of CHF were studied, different authors at different times proposed many classifications in order to distinguish between separate groups of patients based on the similarity of prognosis and treatment tactics. It is worth noting that the more accurately the classification takes into account clinical and pathogenetic aspects, the more complex it is, and therefore the less applicable in clinical practice. In turn, a simple classification will not fully reflect the true picture. This means that it is necessary to look for a “golden mean”.

In modern human medicine, the two most applicable classifications are the functional classification of CHF of the New York Heart Association (NYHA, 1964) and the N.D. classification. Strazhesko and V.Kh. Vasilenko with the participation of G.F. Langa, approved by the XII All-Union Congress of Therapists (1935).

In veterinary medicine, two classifications are also proposed: the classification of the International Council on Small Animal Cardiology (ISACHC) and the classification proposed by the Veterinary Cardiological Society (A.G. Komolov, 2004).

Classification N.D. Strazhesko and V.Kh. Vasilenko distinguishes three stages:

Stage 1 (initial, latent circulatory failure): characterized by the appearance of shortness of breath, a tendency to tachycardia, and fatigue only during physical activity.

Stage 2: more significant shortness of breath with the slightest physical exertion (stage 2A, when there are signs of congestion only in the small circle, which can be eliminated and prevented with systemic maintenance therapy) or the presence of shortness of breath at rest (stage 2B, when there is insufficiency of the right parts of the heart with congestion in the systemic circle and these changes persist to varying degrees, despite the treatment).

Stage 3 (the final, dystrophic stage of chronic circulatory failure): characterized by severe circulatory disorders, the development of irreversible congestion in the pulmonary and systemic circulation, the presence of structural, morphological and irreversible changes in organs, general dystrophy, exhaustion, complete loss of ability to work.

The NYHA classification is functional. According to this classification, there are four classes, divided by load tolerance (there are recommendations for a walking test or a standard load test on a bicycle ergonometer). Let's try to extrapolate to a dog:

I - mild degree - increased fatigue compared to what was before (virtually asymptomatic stage);

II - moderate heart failure - the appearance of shortness of breath with moderate exertion;

III - severe heart failure - the appearance of shortness of breath and cough under any load, the possibility of rare manifestations at rest;

IV - severe heart failure - signs of CHF are present even at rest.

The ISACHC classification divides patients into three classes: asymptomatic (I), moderate (II) and severe (III) heart failure. And two groups: A - with the possibility of outpatient treatment, and B - patients requiring inpatient treatment.

This classification is quite easy to use, but is too ambiguous in its division into groups. The classification of the Veterinary Cardiological Society is based on determining the functional class, taking into account morphological disorders (index) identified during examination of the patient. Actually, the NYHA classification is taken as a basis, supplemented by the A, B, C index according to the degree of morphological disorders.

Thus, index A - the identified morphological disorders are reversible or do not lead to significant hemodynamic disorders; index B - signs of disturbance of intracardiac hemodynamics; index C - pronounced myocardial remodeling with hemodynamic disturbances.

The classification of CHF by the Veterinary Cardiological Society, in our opinion, is the most applicable. A general practitioner can easily determine the functional class (FC) even before referring the patient to a cardiologist, and setting the index allows one to determine the prognosis and the main treatment tactics.

Literature

1. Martin M.V.S., Corcoran B.M. Cardiorespiratory diseases of dogs and cats. M., “Aquarium-Print”, 2004, 496 p.

2. Pathological physiology. Edited by Ado A.D., Novitsky V.V., Tomsk, 1994, 468 p.

3. Kirk's modern course of veterinary medicine. Per. from English - M., “Aquarium-Print”, 2005., 1376 p.

4. X Moscow International Veterinary Congress. 2002. Komolov A. G., Classification of CHF.

5. The role of the sympathoadrenal system in the pathogenesis of chronic heart failure in dogs. Bardyukova TV., Bazhibina E.B., Komolov A.G./ Materials of the 12th Moscow All-Russian Veterinary Congress. 2002.

6. Martin M.W.S., Management of chronic heart failure in dogs: current concept. W.F., 6,1996, pp. 13 - 20.

CHRONIC HEART FAILURE

Heart failure - the inability of the cardiovascular system to adequately supply the organs and tissues of the body with blood and oxygen in quantities sufficient to maintain normal life. Heart failure is based on a violation of the pumping function of one or both ventricles.

Etiology.

Chronic heart failure develops in a wide variety of diseases that affect the heart and impair its pumping function. The causes of pumping dysfunction are varied:

1. Damage to the heart muscle, myocardial failure:

A) primary (myocarditis, dilated cardiomyopathies);

B) secondary (atherosclerotic and post-infarction cardiosclerosis, hypo- or hyperthyroidism, heart damage due to diffuse connective tissue diseases, toxic-allergic myocardial damage).

2. Hemodynamic overload of the heart muscle:

A) pressure (stenosis of the mitral, tricuspid valves, aorta and pulmonary artery, hypertension of the pulmonary or systemic circulation);

B) volume (heart valve insufficiency, presence of intracardiac shunts);

C) combined (complex heart defects, a combination of pathological processes leading to pressure and volume overload).

3. Impaired diastolic filling of the ventricles (adhesive pericarditis, restrictive cardiomyopathies, myocardial storage diseases - amyloidosis, hemochromatosis, glycogenosis).

Pathogenesis.

The main trigger of chronic heart failure (CHF) is a decrease in myocardial contractility and, as a result, a drop in cardiac output. This in turn leads to a deterioration in the blood supply to organs and tissues and the activation of a number of compensatory mechanisms, one of which is hyperactivation of the sympathetic-adrenal system (SAS). Catecholamines, mainly norepinephrine, cause constriction of arterioles and venules, which causes an increase in venous return of blood to the heart, an increase in diastolic filling of the affected left ventricle and a leveling of reduced cardiac output to normal. However, activation of the SAS, being initially compensatory, subsequently becomes one of the factors responsible for the progression of pathological changes in the organs of the cardiovascular system and the aggravation of signs of heart failure. Spasm of arterioles, in particular renal arterioles, causes activation of the renin-angiotensin system (RAS) and overproduction of a powerful vasopressor factor, angiotensin II. In addition to increasing the content of angiotensin II in the blood plasma, local tissue RAS are activated, in particular in the myocardium, which causes the progression of its hypertrophy. Angiotensin II also stimulates increased formation of aldosterone, which in turn increases sodium reabsorption, increases plasma osmolarity and, ultimately, promotes the activation of the production of antidiuretic hormone (ADH) - vasopressin. An increase in the content of ADH and aldosterone leads to a progressive retention of sodium and water in the body, an increase in the mass of circulating blood, and an increase in venous pressure (which is also caused by constriction of the venules). There is a further increase in venous return of blood to the heart, resulting in worsening left ventricular dilatation. Angiotensin II and aldosterone, acting locally in the myocardium, lead to changes in the structure of the affected part of the heart (left ventricle) - to the so-called remodeling. In the myocardium, further death of myocardiocytes occurs and fibrosis develops, which further reduces the pumping function of the heart. Reduced cardiac output (more precisely, ejection fraction) leads to an increase in residual systolic volume and an increase in end-diastolic pressure in the left ventricular cavity. Dilatation increases even more. This phenomenon initially, according to the Frank-Starling mechanism, leads to increased contractile function of the myocardium and equalization of cardiac output. However, as dilatation progresses, the Frank-Starling mechanism stops working, and therefore the pressure in the overlying parts of the bloodstream - the vessels of the pulmonary circulation - increases (hypertension of the pulmonary circulation develops according to the type of “passive” pulmonary hypertension).

Among the neurohormonal disorders in CHF, one should note an increase in the content of endothelin in the blood, a powerful vasoconstrictor factor secreted by the endothelium.

Along with vasopressor factors, the content of atrial natriuretic peptide (ANP), secreted by the heart into the bloodstream, increases, which is associated with an increase in the tension of the atrial walls, with an increase in the filling pressure of the corresponding chambers of the heart. ANP dilates the arteries and promotes the excretion of salt and water. However, in CHF, the magnitude of this vasodilatory effect is reduced by the vasoconstrictor effect of angiotensin II and catecholamines, and the potentially beneficial effect of APN on renal function is weakened. Thus, in the pathogenesis of CHF, cardiac and extracardiac (neurohormonal) mechanisms are distinguished. In this case, the triggering factor is the cardiac mechanism - a decrease in the contractile function of the heart (systolic failure) or impaired filling of the heart during diastole (diastolic failure).

Classification.

Currently, the classification of circulatory failure proposed by N.D. is used. Strazhesko. According to this classification, three stages are distinguished.

Stage I - initial: hidden circulatory failure, manifested by the appearance of shortness of breath, palpitations and fatigue only during physical activity. With rest, these phenomena disappear. Hemodynamics at rest are not disturbed.

Stage II - period A: signs of circulatory failure at rest are moderate, exercise tolerance is reduced. There are hemodynamic disturbances in the systemic or pulmonary circulation, their severity is moderate; period B: pronounced signs of heart failure at rest, severe hemodynamic disturbances in both the systemic and pulmonary circulation.

Stage III - final: dystrophic stage with severe hemodynamic disorders, metabolic disorders and irreversible changes in the structure of organs and tissues.

There is also classification of CHF proposed by the New York Heart Association (NYHA). According to this classification, there are four functional classes based on the physical performance of patients.

Class I - no restrictions on physical activity (in the presence of heart disease).

Class II - heart disease causes slight limitation of physical activity.

Class III - heart disease causes significant limitation of physical activity.

Class IV - performing minimal physical activity causes discomfort.

The advantage of this classification is that it allows for the possibility of a patient moving from a higher class to a lower one, but it does not take into account the condition of the internal organs and the severity of circulatory disorders in the systemic circulation. Circulatory disorders in the pulmonary circulation can be judged only indirectly by the degree of limitation of physical performance.

^ Clinical picture.

Manifestations of CHF are determined by the severity of disturbances in intracardiac hemodynamics and changes in the heart, the degree of circulation disturbances in the pulmonary and systemic circulation, the severity of congestion in organs and the degree of dysfunction. In addition, the clinical picture of CHF is characterized by the presence of symptoms of the disease that caused the development of circulatory failure. Thus, the clinical picture depends on whether the decrease in the contractile function of which part of the heart predominates - the left or right ventricle (hence left or right ventricular failure) or whether there is a combination of both (total heart failure).

At the first stage of the diagnostic search, shortness of breath is detected - increased and increased breathing that does not correspond to the state and conditions in which the patient is located (the appearance of shortness of breath during various physical activities or at rest). Dyspnea is a clear criterion for circulatory disorders in the pulmonary circulation; its dynamics correspond to the state of the contractile function of the heart. Patients may be bothered by a cough - dry or with the release of a small amount of mucous sputum, sometimes mixed with blood (hemoptysis), which is also a manifestation of congestion in the pulmonary circulation. Sometimes severe shortness of breath occurs in attacks; these attacks are called cardiac asthma.

Patients complain of palpitations that occur after physical activity, eating, in a horizontal position, i.e. under conditions that promote increased heart function.

With the development of heart rhythm disturbances, patients complain of interruptions in the functioning of the heart or its irregular functioning.

When stagnation occurs in the systemic circulation, complaints of decreased urine output (oliguria) or predominant urine output at night (nocturia) are noted. Heaviness in the area of the right hypochondrium is caused by congestion in the liver, its gradual increase. With rapid enlargement of the liver, quite intense pain in the right hypochondrium is possible. Stagnation in the systemic circulation causes dysfunction of the digestive tract, which manifests itself in decreased appetite, nausea, vomiting, flatulence, and a tendency to constipation.

Due to circulatory disorders, the functional state of the central nervous system changes early: rapid mental fatigue, increased irritability, sleep disturbance, and a depressive state are characteristic.

Patients are also diagnosed with complaints caused by the underlying disease that led to the development of CHF.

At stage II of the diagnostic search, first of all, signs of the underlying disease are identified, as well as symptoms, the severity of which will determine the stage of CHF.

One of the first signs of heart failure is cyanosis - a bluish coloration of the mucous membranes and skin that occurs with an increased content of reduced hemoglobin in the blood (more than 50 g/l), which, unlike oxyhemoglobin, has a dark color. Translucent through the skin, dark blood gives it a bluish tint, especially in areas where the skin is thinner (lips, cheeks, ears, fingertips). The causes of cyanosis are varied. Overfilling of the vessels of the small circle with impaired contractile function of the left ventricle and disruption of normal blood oxygenation in the lungs cause the appearance of diffuse cyanosis, the so-called central one. Slowing of blood flow and increased utilization of oxygen by tissues are the causes of peripheral cyanosis, which is observed when the phenomena of right ventricular failure predominate.

In both cases, cyanosis is promoted by an increase in circulating blood volume (which is essentially a compensatory factor) and hemoglobin content.

With the progression of CHF and increased congestion in the liver, its functions and structure are disrupted, which can lead to the addition of an icteric tint to cyanosis.

An important symptom of CHF is swelling. Fluid retention may initially be hidden and manifest only in a rapid increase in the patient’s body weight and a decrease in urine output. Visible swelling appears first on the feet and legs, and then more widespread swelling of the subcutaneous fatty tissue may develop and edema of the cavities appears: ascites, hydrothorax, hydropericardium.

When examining the respiratory organs during prolonged stagnation, the development of pulmonary emphysema and pneumosclerosis is revealed: decreased mobility of the lower pulmonary edge, small excursion of the chest. During auscultation, “congestive” wheezing (mainly in the lower parts, fine-bubbly, moist, silent) and hard breathing are determined.

From the cardiovascular system, regardless of the etiology of CHF, a number of symptoms are determined due to a decrease in the contractile function of the myocardium. These include enlargement of the heart (due to myogenic dilatation), sometimes quite significant (the so-called cor bovinum - “bull heart”); dullness of heart sounds, especially the first tone; gallop rhythm; tachycardia; Systolic murmurs appear due to relative insufficiency of the mitral and/or tricuspid valve. Systolic pressure decreases and diastolic pressure increases slightly. In some cases, “congestive” arterial hypertension develops, decreasing as the symptoms of CHF are eliminated. Symptoms of stagnation in the systemic circulation are also manifested by swelling of the jugular veins, which swell even more when the patient is in a horizontal position (due to greater blood flow to the heart).

When examining the digestive organs, an enlarged, slightly painful liver is discovered, which over time becomes denser and painless. The spleen usually does not enlarge, however, in rare cases of severe circulatory failure, a slight increase is noted (other reasons for its enlargement cannot be categorically rejected).

As CHF progresses, a progressive decrease in the patient’s body weight is observed - so-called cardiac cachexia develops, the patient seems to “dry out”. A sharp atrophy of the muscles of the limbs in combination with a significantly enlarged abdomen (ascites) is striking. Trophic changes in the skin develop in the form of thinning, dryness, and the appearance of pigmentation on the legs.

Thus, after stage II, the presence and severity of circulatory failure are established with certainty.

At stage III, the following is clarified: 1) the severity of hemodynamic disorders and the degree of decrease in the contractile function of the heart; 2) some links in the pathogenesis of CHF; 3) the degree of damage and the functional state of various organs and systems of the body. Finally, the diagnosis of the underlying disease that caused the development of circulatory failure is clarified.

The severity of hemodynamic changes is determined using non-invasive research methods, of which the most widely used method is echocardiography. This method allows you to determine the decrease in cardiac output, end-systolic and diastolic volumes of the left ventricle, the rate of circular shortening of cardiac muscle fibers, and the presence of regurgitation.

The cardiac output can also be determined using dye dilution methods or radioactive tracer(radiocardiography), as well as the direct method for probing the cavities of the heart. An increase in the volume of circulating blood is determined, as well as a slowdown in the speed of blood flow. Venous pressure clearly increases with the development of right ventricular failure.

According to x-ray examination clarify the state of the pulmonary circulation (presence and severity of signs of pulmonary hypertension) and the degree of enlargement of the chambers of the heart. With the development of heart failure (regardless of the cause that caused it), there is an expansion of the boundaries of the heart compared to the period of compensation. The degree of heart enlargement can be a measure of the state of the contractile function of the heart: the more enlarged the heart is, the more significantly the contractile function of the heart is reduced.

At electrocardiographic study no characteristic changes can be noted: the ECG shows changes typical of the underlying disease.

^ Phonocardiography (PCG) helps to clarify auscultation data, identifying a decrease in the amplitude of sounds, the appearance of an additional tone in diastole, systolic murmurs of relative insufficiency of the mitral and/or tricuspid valve.

^ Laboratory methods Determining the levels of renin in the blood plasma, some electrolytes (potassium and sodium), acid-base status, and aldosterone makes it possible to determine the severity of hormonal and metabolic disorders in each specific case. However, these studies are not mandatory in the diagnosis of CHF.

To determine the degree of damage to internal organs and systems and their functional state, appropriate instrumental and laboratory studies are used.

Complications.

With a long course of CHF, complications may develop, which are essentially a manifestation of damage to organs and systems in conditions of chronic venous stagnation, insufficient blood supply and hypoxia. Such complications include:

1) disturbances of electrolyte metabolism and acid-base status;

2) thrombosis and embolism;

3) disseminated intravascular coagulation syndrome;

4) rhythm and conduction disorders;

5) cardiac cirrhosis of the liver with the possible development of liver failure.

Diagnostics.

Recognition of circulatory failure is based on identifying its characteristic symptoms while simultaneously determining the cause that caused it. Usually, the first two stages of the diagnostic search are sufficient, and only to identify the early (preclinical) stages of CHF one has to resort to instrumental research methods (in particular, echocardiography).

^ The formulation of a detailed clinical diagnosis takes into account:

1) underlying disease; 2) chronic heart failure (indicating its stage according to Strazhesko, NYHA); 3) complications of CHF.

^ General principles of treatment

Non-drug therapy

Diet. Patients with increased body weight (especially obesity), IBO and hypercholesterolemia are advised to reduce the energy value and content of animal fats in the diet. However, with severe cachexia, easily digestible food with increased energy value is required.

It is necessary to limit the consumption of table salt (the daily diet of food products themselves contains 1.5-2 g of table salt, so its addition is not required) and liquid (up to 1.2-1.5 l).

Patients receiving diuretics should keep a record of fluid intake and output. The diet should contain a sufficient amount of animal and vegetable protein and vitamins.

It is necessary to limit or completely stop drinking alcohol due to its direct damaging effect on the myocardium and proarrhythmic effect, and also stop smoking.

^ Regular exercise moderate intensity for 4-6 months in patients with stable chronic HF helps reduce the functional class of chronic HF, increase maximum oxygen consumption and increase exercise tolerance. It has been shown that physical training, even in patients with chronic HF and LVEF equal to 16%, significantly reduces the severity of clinical manifestations and the activity of the sympathetic nervous system, while simultaneously increasing the activity of the parasympathetic nervous system. At the same time, the progression of heart failure slows down and the prognosis improves.

^ Education for patients and their loved ones is an important component of non-drug effects. The effect of therapy largely depends on the patient’s awareness of his disease, mastery of self-control methods, willingness to cooperate with the doctor and consciously participate in treatment.

Patient education must begin in the hospital and continue for several months with outpatient monitoring.

Pharmacotherapy

All drugs used in the treatment of chronic HF can be divided into 3 groups depending on the degree of evidence of their effectiveness:

Group 1. Basic Drugs whose effect has been proven in long-term, multicenter, double-blind, placebo-controlled trials and which are recommended specifically for the treatment of chronic HF. These include:

ACE inhibitors. Indicated for all patients with chronic HF, regardless of its etiology and FC;

B-blockers. These are neurohumoral modulators used in combination with ACE inhibitors;

diuretics. Indicated for all patients with clinical signs of chronic heart failure caused by excessive sodium and water retention in the body;

cardiac glycosides. In case of sinus rhythm, they are used in small doses and with caution; in case of atrial fibrillation (AF), the drugs of choice remain;

aldosterone antagonists. Used in combination with ACE inhibitors in patients with severe chronic heart failure.

Group 2. Additional Medicines, the effectiveness and safety of which have been shown in separate large studies, but require clarification. These include:

angiotensin II receptor blockers. Can be used if you are intolerant to ACE inhibitors;

vasopeptidase inhibitors. Omapatrilat is a new neurohumoral modulator that is more effective than ACE inhibitors. Its effectiveness and safety require clarification.

Group 3. Auxiliary Medicines whose effectiveness and impact on the prognosis of chronic HF are unknown or unproven. Their use is due to certain concomitant diseases. These include:

nitrates. Used for concomitant ischemic heart disease;

calcium antagonists. Used for ischemic heart disease and persistent hypertension;

antiarrhythmic drugs(III class). They are used mainly for life-threatening ventricular arrhythmias;

non-glycoside inotropic stimulants. Used for chronic hypotension with low stroke output and persistent arterial hypotension;

antiplatelet agents. Used for secondary prevention after MI;

indirect anticoagulants. They are used when there is a risk of developing thromboembolic complications, especially in patients with AF, dilatation of the heart cavities, intracardiac thrombi, after heart valve replacement;

statins. Used for hyper- and dyslipoproteinemia;

glucocorticoid agents. They are used for persistent arterial hypotension and sluggish inflammatory processes in the myocardium;

cytoprotectors(trimetazidine). They are used to improve the functioning of cardiomyocytes in chronic heart failure due to coronary artery disease.

Forecast.

The ability to cure the underlying disease (for example, effective surgical treatment of a heart defect) significantly improves the prognosis. Patients with stage I CHF are able to work, but heavy physical labor is contraindicated for them. In stage IIA, the ability to work is limited or lost; in stage IIB, the ability to work is lost. Patients with stage III CHF require constant care.

Prevention.

Prevention of the development of heart failure is achieved by systematic treatment of heart diseases (including surgery), as well as by creating an adequate work and lifestyle regimen for the patient, proper nutrition, and a categorical refusal to drink alcohol and smoke.

New articles

Effective: topical corticosteroids. Effectiveness is assumed to be: control of house dust mites. Effectiveness not proven: dietary interventions; long-term breastfeeding in children prone to atopy. go

WHO recommendations for tertiary prevention of allergies and allergic diseases: - products containing milk are excluded from the diet of children with a proven allergy to cow's milk proteins. When supplementary feeding, hypoallergenic mixtures are used (if so. go

Allergic sensitization in a child suffering from atopic dermatitis is confirmed by an allergological examination, which will identify causally significant allergens and take measures to reduce contact with them. In children. go

In infants with a family history of atopy, exposure to allergens plays a critical role in the phenotypic manifestation of atopic dermatitis, and therefore elimination of allergens at this age may lead to a reduction in the risk of developing allergens. go

The modern classification of prevention of atopic dermatitis is similar to the levels of prevention of bronchial asthma and includes: primary, secondary and tertiary prevention. Since the causes of atopic dermatitis are not up to date. go

Video

Pathogenesis and classification of CHF

Organization(s): CJSC "Network of Veterinary Clinics", St. Petersburg / "Network veterinary clinics", St. Petersburg

annotation

CHF is triggered by one of four main factors:

1. Volume overload (heart defects with reverse blood flow - mitral or aortic valve insufficiency, the presence of intracardiac shunts).

2. Pressure overload (stenosis of the valve orifices, ventricular outflow tract, or in the case of hypertension of the systemic or pulmonary circulation).

4. Impaired diastolic filling of the ventricles of the heart (pericarditis, restrictive cardiomyopathy).

· Hyperactivation of the sympathetic-adrenal system;

· Activation of the renin-angiotensin-aldosterone system;

· Hyperproduction of ADH (vasopressin);

· Inhibition of the natriuretic peptide system;

· Endothelial dysfunction;

· Hyperactivation of pro-inflammatory cytokines (tumor necrosis factor-α);

· Formation of hyperactive apoptosis of cardiomyocytes

As a result, structural and geometric irreversible changes in the heart occur—myocardial remodeling. The more pronounced the remodeling in a particular patient, the less important it is what was the triggering factor, and the more CHF becomes the main problem, and not just a manifestation of the underlying disease.

In modern human medicine, the two most applicable classifications are the Functional classification of CHF of the New York Heart Association (NYHA, 1964) and the classification of N.D. Strazhesko and V.H. Vasilenko with the participation of G.F. Lang, approved at the XII All-Union Congress of Therapists (1935). In veterinary medicine, two classifications are also proposed - the classification of the International Council on Small Animal Cardiology (ISACHC) and the classification proposed by the Veterinary Cardiological Society (A.G. Komolov 2004).

Classification by N.D.Strazhesko and V.Kh.Vasilenko distinguishes three stages:

1st stage(initial, latent circulatory failure): characterized by the appearance of shortness of breath, a tendency to tachycardia, and fatigue only during physical activity.

2nd stage: more significant shortness of breath with the slightest physical exertion (stage 2A, when there are signs of congestion only in the small circle, which can be eliminated and prevented with systemic maintenance therapy) or the presence of shortness of breath at rest (stage 2B, when there is failure of the right heart with congestion in large circle and these changes persist to one degree or another, despite the treatment).

3rd stage(final, dystrophic stage of chronic circulatory failure): characterized by severe circulatory disorders, the development of irreversible stagnation in the pulmonary and systemic circulation, the presence of structural, morphological and irreversible changes in organs, general dystrophy, exhaustion, complete loss of ability to work.

NYHA classification functional. According to this classification, there are four classes, divided by load tolerance (there are recommendations for a walking test or a standard load test on a bicycle ergonometer). Let's try to extrapolate to a dog:

I – mild degree - increased fatigue compared to what was before (virtually asymptomatic stage);

II – moderate heart failure - the appearance of shortness of breath with moderate exertion;

III – severe heart failure - the appearance of shortness of breath and cough under any load, the possibility of rare manifestations at rest;

IV – severe heart failure - signs of CHF are present even at rest.

ISACHC classification divides patients into three classes: asymptomatic (I), moderate (II) and severe (III) heart failure. And two groups: A – with the possibility of outpatient treatment, and B – patients requiring inpatient treatment. This classification is quite easy to use, but is too ambiguous in its division into groups.

The classification of the Veterinary Cardiological Society is based on determining the functional class, taking into account morphological disorders (index) identified during examination of the patient. Actually, the NYHA classification is taken as a basis, supplemented by the A, B, C index according to the degree of morphological disorders. Thus, index A – the identified morphological disorders are reversible or do not lead to significant hemodynamic disorders; index B – signs of disturbance of intracardiac hemodynamics; index C – pronounced myocardial remodeling with hemodynamic disturbances.

Literature

1. Martin M.V.S. Corcoran B.M. Cardiorespiratory diseases of dogs and cats. M. "Aquarium-Print", 2004, 496 p.

2. Pathological physiology. Edited by Ado A.D. Novitsky V.V. Tomsk, 1994, 468 p.

3. Kirk's modern course of veterinary medicine./Trans. from English – M. “Aquarium-Print”, 2005. 1376 p.

4. X Moscow International Veterinary Congress. 2002. Komolov A. G. Classification of CHF. (published http://www.vet.ru/node/149)

5. The role of the sympathoadrenal system in the pathogenesis of chronic heart failure in dogs. Bardyukova T.V. Bazhibina E.B. Komolov A.G./ Materials of the 12th Moscow All-Russian Veterinary Congress. 2002.

6. Martin M.W.S. Management of chronic heart failure in dogs: current concept. W.F. 6, 1996, R. 13 – 20.

Chronic heart failure

Pathogenesis. Basic concepts:

Preload. This is the degree of diastolic filling of the left ventricle, determined by the venous return of blood to the heart and the pressure in the pulmonary circulation. The level of preload most adequately reflects the end-diastolic pressure in the pulmonary artery (EPDP).

Afterload is the systolic tension of the myocardium necessary to expel blood. In practice, afterload is judged by the level of intra-aortic pressure and total peripheral resistance.

Frank-Starling's law: an increase in diastolic stretch of myocardial fibers (equivalent to end-diastolic pressure in the cavity of the left ventricle - LVEDP) up to a certain point is accompanied by an increase in its contractility and an increase in cardiac output (ascending leg of the curve). With further stretching of the heart in diastole, the output remains the same (does not increase) - a plateau of the curve; if the stretch in diastole increases further, exceeding 150% of the initial length of the muscle fibers, then cardiac output decreases (descending leg of the curve). In heart failure, the heart operates in the “plateau” or “descending leg” mode of the Frank-Starling curve.

The main “trigger” of heart failure is a decrease in systolic volume (equivalent to left ventricular ejection fraction), an increase in left ventricular end-diastolic pressure (LVEDP). Further events are illustrated in diagrams 6 and 7.

It can be seen that the “launch” of the neurohumoral module begins with an increase in pressure in the left atrium and in the pulmonary veins. Stimulation of baroreceptors leads to irritation of the vasomotor center and the release of catecholamines. A decrease in renal blood flow is the cause of an increase in renin secretion. Angiotensin-2 causes vasoconstriction, increased aldosterone secretion, and hypersympathicotonia. Hyperaldosteronism is the cause of Na° retention and an increase in circulating blood volume. Compensatory factors (see Diagram 6) are powerless against renin-angiotensin-aldosterone (RAA) activity. Increasing post- and preload helps reduce systolic ejection. This starts a vicious circle of heart failure.

Based on the leading pathogenetic mechanism, N.M. Mukharlyamov distinguished:

Heart failure due to volume overload (diastolic overload of the left ventricle) with aortic and mitral insufficiency, septal defects, patent ductus arteriosus;

due to resistance overload (hypertension of the systemic or pulmonary circulation, stenosis of the aorta, pulmonary artery);

Primary myocardial form with dilated cardiomyopathy, myocarditis, myocardial infarction, post-infarction cardiosclerosis;

Heart failure due to impaired ventricular filling in hypertrophic cardiomyopathy, “hypertensive heart” with severe hypertrophy without dilatation, pericardial mitral stenosis;

Conditions with high cardiac output, when tissues require more oxygen than is actually delivered.

This situation is possible with thyrotoxicosis, severe anemia, and obesity.

Clinic, classification. The leading symptoms of left ventricular heart failure: shortness of breath, tachycardia, weakness; right ventricular failure - swelling of the neck veins, enlarged liver, edema of the lower extremities.

Possibilities of additional methods:

A resting ECG clarifies the presence or absence of post-infarction scars, “diffuse” changes, tachycardia, arrhythmias and heart blocks;

X-ray examination informs about the size of the chambers of the heart, helps to clarify the nature of the valve or congenital defect, the presence and severity of stagnation in the pulmonary circulation;

The echo cardiographic method provides information about the thickness of the myocardium of the atria and ventricles, the main parameters of impaired myocardial contractile function. The most important parameter is the left ventricular ejection fraction, which is normally 65-80%.

The classification of chronic heart failure is based on the patient's tolerance to physical activity.

N.D. Strazhesko, V.Kh. Vasilenko (1935) identified three stages:

Stage 1 (initial). At rest there are no signs of heart failure. During physical activity, shortness of breath, tachycardia, and increased fatigue appear.

2A stage. Shortness of breath, tachycardia at rest (with left ventricular failure) or enlarged liver, swelling of the legs (with right ventricular failure) - monoventricular heart failure.

Stage 2 B. Dyspnea, tachycardia at rest; enlarged liver, swelling of the legs, sometimes ascites, hydrothorax. Biventricular heart failure.

Stage 3 (terminal, dystrophic). Severe biventricular heart failure, irreversible changes in organs (cardiogenic cirrhosis of the liver, cardiogenic pneumosclerosis, encephalopathy, pluriglandular endocrine insufficiency).

In Europe and America, the New York Heart Association (NYHA) classification, adopted in 1964, is used.

1st functional class (f. class). Patient with heart disease, without significant limitation of physical activity. Ordinary physical activity does not cause premature fatigue, shortness of breath, or tachycardia. The diagnosis is made using instrumental research methods using stress tests.

2nd f. class Patient with moderate limitation of physical activity. At rest there are no complaints; ordinary physical activity leads to shortness of breath and tachycardia.

3rd f. class A patient with severe limitation of physical activity feels satisfactory at rest. Fatigue, shortness of breath and tachycardia with minimal exertion.

4th f. class Symptoms of biventricular heart failure at rest.

A general practitioner and a local therapist can use any of the above classifications. It is important that the diagnosis is dynamic and reflects what the doctor managed to achieve during treatment. Chronic heart failure reduces the patient’s quality of life (W.O. Spitzer; P.A. Libis, Ya.I. Kots). A decrease in the quality of life index is due to the need for treatment, limitation of physical activity, changes in relationships with loved ones, friends and colleagues, limitation of work activity, decrease in income, demotion, restrictions in leisure activities, decrease in activity in everyday life, restrictions in diet and sex life.

Hence the psychological problems that result, depending on the basic structure of the personality, into asthenic, astheno-neurotic, hypochondriacal and other syndromes. A typology of the patient’s attitude towards the disease is formed, which is reflected in the heading “psychological status”. Knowledge of the patient’s social status is necessary to develop a treatment strategy that is adequate to the capabilities of the individual patient and his family.

Diagnostic formulations.

IHD: post-infarction cardiosclerosis.

Chronic heart failure 2 A st. (3rd class) with transformation into 1st class. (2 f.kl.). Astheno-neurotic syndrome, moderately expressed.

Rheumatism, inactive phase. Combined mitral disease with predominant stenosis of the left atrioventricular orifice. Atrial fibrillation, tachysystolic form. Chronic heart failure, stage 2 B. (4th class) with transformation into 2nd A Art. (3rd grade). Astheno-depressive syndrome, moderately expressed.

Dilated cardiomyopathy. Complex rhythm and conduction disorders: atrial fibrillation, tachysystolic form, polytopic ventricular extrasystole, right bundle branch block. Chronic heart failure, stage 2 B. (4th grade), refractory. Astheno-hypochondriacal syndrome.

Heart failure is a pathological condition consisting in the inability of the heart to provide organs and tissues with the amount of blood that corresponds to their metabolic needs of the body and is necessary for the normal functioning of the body. Heart failure can be acute or chronic. It is one of the most common causes of temporary disability, disability and death in patients suffering from diseases of the cardiovascular system. The prevalence of HF depends on age: up to 50 years it is 1-3%, after 70 years it is 9-10%. The mortality rate for HF is comparable to that for malignant diseases; after its appearance, 37% of men and 38% of women die within 2 years.

According to the Framingham study, the average five-year survival rate in the entire population of patients with chronic heart failure (CHF) was 38% for men and 58% for women. The average survival time after the onset of symptoms of HF is 1.7 years for men and 3.2 years for women.

Etiology

Heart failure (HF) can be caused by any disease of the cardiovascular system. The most common causes are ischemic heart disease (up to 40% of cases), hypertension (17%), valvular heart defects, damage to the heart muscle (cardiomyopathies, myocarditis), and less commonly, pericardial diseases. HF can also be caused by heart rhythm disturbances, bronchopulmonary diseases (“cor pulmonale”), metabolic and endocrine diseases, anemia, amyloidosis, glycogenosis, neuromuscular diseases, connective tissue diseases, drug and toxic lesions, deficiency of electrolytes: potassium, magnesium, selenium, hypovitaminosis and other reasons. In 80-90% of patients, HF is caused by dysfunction of the left ventricle of the heart, both systolic and diastolic.

Pathogenesis

In chronic heart failure (CHF), hemodynamic, neurohumoral and cellular mechanisms are included in the pathological process, performing compensatory and adaptive functions in the early stages, and as HF progresses, acting as independent pathogenetic factors. In response to volume, pressure overload, or primary myocardial damage, compensatory mechanisms are activated to maintain the pumping function of the heart. The main one is the activation of local (myocardial) neurohumoral (sympathoadrenal and reninangiotensin) systems, which contribute to the development of compensatory tachycardia, myocardial hypertrophy and moderate dilatation of the heart. As the process progresses, compensatory reactions turn into their opposite. Myocardial hypertrophy leads to increased diastolic rigidity of the left ventricle, cardiac dilatation becomes excessive, and cardiac remodeling occurs, which causes systolic dysfunction. Persistent tachycardia sharply increases the energy expenditure of the heart and limits exercise tolerance. The result is a progressive decrease in cardiac output. A new circle of systemic changes is launched in the body of a patient with CHF. Activation of the sympathoadrenal system, both local and circulating, leads to peripheral vasoconstriction. Initially aimed at maintaining a normal level of blood pressure and perfusion of vital organs, vasoconstriction, as HF progresses, causes ischemia of organs, including the kidneys, and accordingly leads to a decrease in glomerular filtration. Vasoconstriction in the arterial bed increases peripheral resistance and afterload, in the venous bed - venous return of blood and pre-load. A decrease in renal perfusion, their ischemia and increased activity of the sympathoadrenergic system stimulate the juxtaglomerular apparatus of the kidneys, which produces renin. Under the influence of renin, the formation of angiotensin I from angiotensinogen is activated, which, under the influence of ACE, is converted into angiotensin II. The latter, on the one hand, increases vascular tone , increasing vasoconstriction and worsening the perfusion of organs and tissues, on the other hand, stimulates the secretion of aldosterone by the adrenal cortex. Hyperproduction of aldosterone increases the reabsorption of sodium and water in the renal tubules, which leads to an increase in the volume of circulating blood and, as a result, to an increase in the load on heart, sodium and water retention in the body and the appearance of edema. An increase in plasma osmolarity due to an increase in sodium reabsorption in the renal tubules stimulates the production of antidiuretic hormone in the nuclei of the hypothalamus, which enhances the reabsorption of water at the level of the distal tubules and collecting ducts, which also leads to an increase in blood volume and increased edema. The vasoregulatory function of the endothelium is disrupted, the role of vasodilators (bradykinin, prostacyclin, nitric oxide) is reduced and the importance of vasoconstrictor factors (endothelin 1) increases. The secretion of atrial natriuretic hormone decreases and increases; concentration of endogenous digitalis-like factor in the blood. The latter promotes the accumulation of sodium and calcium ions in vascular smooth muscle cells and cardiomyocytes. In the early stages of heart failure, calcium accumulation in cardiomyocytes plays a compensatory role, increasing myocardial contractility. In the later stages of CHF, calcium overload of cardiomyocytes disrupts the mechanism of diastolic relaxation of the ventricular myocardium and becomes a factor in the progression of CHF. Thus, with the progression of heart failure, neurohormones determine the development of organ ischemia, fluid retention in the body, and overload of the pulmonary circulation. Neurohumoral factors not only increase the hemodynamic load on the heart due to sodium retention and peripheral vasoconstriction, but also have a direct toxic effect on the heart. This effect is mediated through changes in genetic mechanisms that regulate the growth of cardiomyocytes and their death (apoptosis). Patients with HF also show increased levels of circulating and tissue cytokines, such as tumor necrotic factor, interleukin-1, which weaken the viability and activity of cardiomyocytes. Neurohumoral factors and cytokines stimulate myocardial fibrosis, which further changes the structure and worsens the functioning of the heart. Consequently, the imbalance of neurohumoral systems plays a major role in the formation and progression of CHF at all stages of decompensation from the onset of the disease to its final stage. Moderate dysfunction of the heart caused by its congenital or acquired disease can persist for several years without clinical manifestations. Factors that provoke disruption of compensatory mechanisms in patients with cardiovascular pathology include infectious diseases, anemia, pregnancy, heart rhythm disturbances, increased blood pressure, physical overexertion, overeating, stress, excessive consumption of table salt, withdrawal of medications, overheating. Iatrogenic causes of failure of compensation in CHF include intravenous administration of large amounts of fluid, invasive cardiac examinations, use of non-steroidal and steroidal anti-inflammatory drugs, antiarrhythmic drugs of classes 1a and 1c, calcium antagonists, inhaled b2-agonists.

Clinic

Classifications of chronic heart failure The amount of blood delivered per unit time to organs and tissues decreases as a result of dysfunction and structure of the heart or blood vessels or the entire cardiovascular system. In this regard, a distinction is made between cardiac, vascular and general cardiovascular failure. Depending on the severity, there are asymptomatic, severe (symptomatic) and refractory HF.

According to the type of dysfunction, they distinguish between systolic, diastolic and mixed, and according to the predominant lesion - left ventricular, right ventricular and total HF. Classification of circulatory failure (N.

D. Strazhesko, V.

Kh. Vasilenko, 1935) I.

Acute circulatory failure: - acute heart failure: - acute left ventricular failure, - acute right ventricular failure, - acute left atrial failure; - acute cardiovascular failure; - acute vascular insufficiency (fainting, collapse, shock). II.

Chronic circulatory failure: Stage I (initial, latent): shortness of breath and/or palpitations, fatigue appear only with significant physical exertion. Stage II A (severe, reversible): there are hemodynamic disturbances in the systemic or pulmonary circulation.

Signs of circulatory failure appear after moderate physical activity at the end of the day, disappear after a night's rest, and exercise tolerance is reduced. Stage II B (severe, hardly reversible): there are severe hemodynamic disturbances in the systemic and pulmonary circulation (total, biventricular failure).

Severe signs of circulatory failure occur with minor physical activity and can be observed at rest; they do not disappear, although they may decrease, after an overnight rest. Stage III (irreversible, final, terminal, dystrophic): characterized by failure of the entire heart.

Severe phenomena of blood stagnation: congestion in the lungs: severe shortness of breath at rest, nocturnal attacks of cardiac asthma, interstitial and alveolar pulmonary edema; hepatomegapia, anasarca, fluid accumulation in the pleural, abdominal and pericardial cavities, cardiac cachexia, oliguria. Options Systolic, diastolic, undefined - with left ventricular systolic dysfunction: LV ejection fraction 40% or less; - with preserved left ventricular systolic function: LV ejection fraction more than 40%.

Functional classes of cardiac patients according to the criteria of the New York Heart Association Functional class I - patients with heart disease in whom normal physical activity does not cause shortness of breath, fatigue, or palpitations. Functional class II - patients with heart disease and moderate limitation of physical activity.

Shortness of breath, fatigue, and palpitations are observed when performing normal physical activity. Functional class III - patients with heart disease and severe limitation of physical activity.

At rest there are no complaints, but even with minor physical activity shortness of breath, fatigue, and palpitations occur. Functional class IV - patients with heart disease in whom any level of physical activity causes the above-mentioned subjective symptoms.

The latter also occur in a state of rest. Notes: 1.

The stage of HF reflects the stage of clinical evolution of this syndrome, while the functional class (FC) of the patient is a dynamic characteristic that can change under the influence of treatment; 2. Determination of the variant of CHF (with LV systolic dysfunction or with preserved LV systolic function) is possible only if appropriate data from an echocardiographic study are available; 3.

The functional class of the patient is established according to clinical criteria and can, if necessary, be objectified by instrumental research data. The clinical picture is determined by the type of heart failure - left or right ventricular failure and its stage.

Left ventricular failure is characterized by symptoms associated with stagnation in the pulmonary circulation: inspiratory shortness of breath during physical exertion, cough that worsens in a horizontal position, paroxysms of suffocation at night, orthopnea, moist rales during auscultation of the lower parts of the lungs, as well as a decrease in cardiac output: increased fatigue, decreased performance. Along with this, cardiomegaly is noted due to the left ventricle; a weakening of the 1st tone, a gallop rhythm, and an accent of the 2nd tone over the pulmonary trunk can be heard.

The skin is usually pale and cold to the touch due to peripheral vasoconstriction, and acrocyanosis is characteristic, associated with an increase in reduced hemoglobin in the venous part of the capillaries due to increased extraction of oxygen from venous blood. In severe heart failure there may be an alternating pulse.

On X-ray examination, in addition to enlargement of the left chambers of the heart, signs of pulmonary venous hypertension are observed: dilation of the upper lobe veins, perivascular and interstitial edema, and in severe cases, the presence of fluid in the alveoli. There may be pleural effusion, most often right-sided.

Echocardiography, Doppler echocardiography can reveal an increase in the size and volume of the left ventricle and left atrium, left ventricular hypertrophy, signs of segmental or diffuse impairment of its contractility, systolic and diastolic dysfunction, a decrease in ejection fraction and cardiac index. Radionuclide examination of the heart (ventriculography and myocardial scintigraphy) reveals a decrease in the ejection fraction of the left ventricle and regional disturbances in the movement of its walls.

Catheterization of the left ventricle and pulmonary artery characterizes changes in cardiac output, end-diastolic pressure and myocardial contractility. The use of ECG for diagnosing CHF is not very informative. With left ventricular failure, there may be signs of left ventricular and left atrium hypertrophy (P mitrale), decreased voltage, and impaired intraventricular conduction.

Right ventricular failure is characterized by hepatomegaly, edema, effusion in the pleural, abdominal and pericardial cavities, swelling and pulsation of the jugular veins, and high venous pressure. Pain in the right hypochondrium may occur due to stagnation of blood in the liver and an increase in its volume, loss of appetite, nausea, vomiting. Abnormal pulsation in the epigastric region can be detected, which can be caused by hypertrophy and dilatation of the right ventricle or pulsation of the liver with absolute or, more often, relative insufficiency tricuspid valve.

When pressure is applied to the liver area, the pressure in the jugular veins increases (jugular reflux, Plesch's symptom). Peripheral edema first appears in the evening and is localized on the feet, legs, and later covers the thighs and abdominal wall, lumbar region, up to anasarca.

With percussion, a displacement of the borders of the heart to the right is determined. X-ray and echocardiographic examination reveals an enlargement of the right ventricle and right atrium. The electrocardiogram may show signs of hypertrophy of the right ventricle and right atrium (Ppulmonale), blockade of the right bundle branch.

Biventricular heart failure is a combination of symptoms of left and right ventricular failure. Characteristics of stages.

Stage I (initial, latent circulatory failure) manifests itself only during physical activity; at rest, hemodynamics are not impaired. It is characterized by rapid fatigue when performing normal physical work, slight shortness of breath, tachycardia, the appearance of pasty feet and legs in the evenings, disappearing by the morning.

Exercise testing reveals a decrease in tolerance; there may be an increase in end-diastolic pressure in the left ventricle and pressure in the pulmonary artery, a decrease in ejection fraction and a slight decrease in the rate of shortening of myocardial fibers. llA Art.

Hemodynamic disturbances are moderately expressed; there is a predominant dysfunction of any part of the heart (right or left ventricular failure). Therefore, in the AN stage, clinical symptoms are associated with the nature of the hemodynamic disturbance.

Characterized by rapid fatigue, shortness of breath with moderate physical exertion, there may be a cough, hemoptysis (especially with mitral stenosis), a feeling of heaviness in the right hypochondrium, decreased diuresis, thirst, the appearance of swelling in the legs, decreasing but not disappearing by the morning. The liver is moderately enlarged, its edge is rounded and painful.

The speed of blood flow slows down, venous pressure increases, acrocyanosis is expressed, and nocturia may occur. ll B st.

Profound hemodynamic disturbances, pronounced stagnation in the small and large circles. The NB stage is characterized by shortness of breath and palpitations at the slightest physical stress, heaviness in the right hypochondrium, reduced diuresis, massive edema, weakness.

On examination, orthopnea, anasarca, and severe acrocyanosis are noted. The liver is sharply enlarged and painful.

Auscultation of the lungs reveals hard breathing and moist fine-bubbly (“congestive”) rales. Ascites and hydrothorax are often observed.

Stage Ill - final, dystrophic. Severe circulatory failure, persistent changes in metabolism and organ functions, irreversible changes in the structure of organs and tissues, complete loss of ability to work.

Stage Ill is characterized by dystrophic changes in internal organs and impaired water-salt metabolism. There is an edematous-dystrophic type, characterized by irresistible thirst, oliguria, huge edema with accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium), significant enlargement of the liver with the development of cirrhotic changes, and a dry dystrophic or cachectic type.

The latter is characterized by “cardiac” cachexia, adynamia, and brown skin pigmentation. Swelling is small, there may be ascites, hydrothorax.

Treatment

The main goals in the treatment of CHF are: improving prognosis, increasing life expectancy; improving the quality of life - eliminating the symptoms of the disease: shortness of breath, palpitations, increased fatigue, fluid retention in the body; protection of target organs (heart, brain, kidneys, blood vessels, muscle tissue) from damage; reduction in the number of hospitalizations. Treatment of the underlying disease that led to the development of CHF is essential. This applies primarily to the treatment of the inflammatory process if it is present, normalization of blood pressure in patients with arterial hypertension, the use of anti-ischemic and antianginal drugs, cessation of alcohol consumption in alcoholic cardiomyopathy, treatment of anemia, diabetes mellitus, surgical correction of heart defects, etc.

All patients need to be provided with normal sleep duration (at least 8-9 hours per day) and psycho-emotional comfort. Persons engaged in physical labor are recommended to limit physical activity, the degree of which is determined by the stage of circulatory failure.

At llB and lll st. physical work is contraindicated.

Therapeutic exercises are necessary to reduce detraining syndrome. Obese patients need to reduce body weight.

Smoking and drinking alcohol are prohibited. The diet of patients with heart failure involves reducing the energy value of food (about 2000 kcal), limiting table salt (less than 3 g/day) and liquid (table 10 and 10a according to M.

I. Pevzner), 5-6 meals a day with the consumption of a small amount of easily digestible food at one time.

Food should be rich in vitamins and potassium salts. Products rich in potassium salts include dried apricots, raisins, nuts, potatoes (baked), pumpkin, cabbage, citrus fruits, bananas, oatmeal, barley, millet, buckwheat, prunes, black currants, milk, cottage cheese, veal.

To create an optimal oxygen regime and eliminate hypxia in the early stages of CHF, it is recommended to spend maximum time in the fresh air, at stage ll B and stage 3. - oxygen therapy in the form of hyperbaric oxygenation or inhalation of humidified oxygen! through a nasal catheter.

Drug treatment is aimed at improving the function of the affected myocardium, reducing pre- and afterload, restoring vascular tone, improving circulation and metabolic processes in organs. Drugs used in the treatment of CHF can be divided into several groups: - drugs whose effect in CHF has been proven and which are recommended for use worldwide; - drugs that have not received general approval, but are recommended for certain groups of patients; - auxiliary drugs, the effect and influence on the prognosis of patients with CHF have not been proven, but their use is dictated by certain clinical situations. Group 1 drugs include diuretics, ACE inhibitors, β-blockers, cardiac glycosides (digoxin).

Diuretics are indicated for patients with CHF who have clinical signs of excessive fluid retention in the body. In the early stages of CHF, the use of diuretics is inappropriate.

Diuretics reduce sodium reabsorption in the renal tubules, increase urine volume and sodium excretion, cause volumetric unloading of the heart. The negative properties of diuretics are the electrolyte disturbances they cause (hypokalemia, hypomagnesemia), activation of neurohormones that contribute to the progression of heart failure, in particular activation of the RAS, hypotension and azotemia. Diuretics should not be used as monotherapy for CHF; they are usually combined with ACE inhibitors and b-blockers.

Preference should be given to loop diuretics (furosemide, torsemide, bumetanide). Treatment begins with low doses until the volume of urine per day increases by 800-1000 ml, and body weight decreases by 0.5-1 kg per day.

If it is necessary to correct electrolyte imbalance, low doses of potassium-sparing diuretics should be added, which are more effective in this regard than potassium or magnesium supplements. Nonsteroidal anti-inflammatory drugs may inhibit the natriuretic effect of diuretics, especially loop diuretics, and enhance the ability of diuretics to cause azotemia.

The most commonly used diuretics for the treatment of CHF include: Hydrochlorothiazide is the drug of choice for the treatment of moderate CHF. At doses up to 25 mg, side effects are minimal; at doses above 75 mg, the number of side effects increases sharply.

The maximum effect occurs 1 hour after administration, the duration of action is up to 12 hours. The absorption of hydrochlorothiazide (hypothiazide) decreases after eating, so it is recommended to take the drug in the morning, on an empty stomach.

The optimal combination is hydrochlorothiazide with ACE inhibitors (capozide, Enap-N, etc.) and with potassium-sparing diuretics (triampur-compositum in a combination of hydrochlorothiazide and triamterene).

Metolazone is a thiazide-like diuretic used in a daily dose of 2.5-5 mg. Chlorthalidone is a thiazide-like diuretic, daily dose is 25-50 mg.

Thiazides are ineffective when glomerular filtration rate decreases to less than 30 ml/min, which is often observed in patients with severe heart failure. Furosemide (Lasix) is one of the most effective loop diuretics with the onset of effect 15-30 minutes after administration, the maximum effect after 1-2 hours and the duration of the pronounced diuretic effect up to 6 hours.

Apply once, in the morning, on an empty stomach. The dose of the drug is determined by the individual sensitivity of patients and can range from 20 mg to 500 mg per day.

The diuretic effect of loop diuretics is maintained even with reduced renal function, if the glomerular filtration rate is at least 5 m.p.m.

Ethacrynic acid (uregit) is a loop diuretic; which is used in doses of 50-100 mg, if necessary, the dose can be increased to 200 mg. Bumetanide is a loop diuretic used in a dose of 0.5-2 mg per day.

In acute situations, as well as when there is a possibility of impaired absorption to the digestive canal, loop diuretics can be administered intravenously. The main side effects of loop diuretics, in addition to hypokalemia, include a decrease in circulating blood volume, which can lead to prerenal azotemia, hypotension; gastrointestinal lesions; ototoxicity, most characteristic of ethacrynic acid.

Potassium-sparing diuretics - spironolactone (veroshpiroi), triamterene, amiloride have a weak diuretic effect, but reduce the risk of hypokalemia induced by more active diuretics. They are usually used in combination with thiazide or loop diuretics.

After elimination of fluid retention, diuretic therapy is usually continued in maintenance doses under the control of diuresis and body weight. ACE inhibitors are prescribed to all patients with CHF, regardless of the etiology, stage of CHF and type of decompensation.

Ignoring ACE inhibitors in patients with CHF cannot be considered justified, and according to numerous multicenter studies, it significantly increases the risk of death. Drugs in this class block angiotensin-converting enzyme (kininase II), resulting in decreased formation of angiotensin II and increased accumulation of bradykinin.

Angiotensin II is a powerful vasoconstrictor, stimulates cell proliferation, increasing hypertrophy of the myocardium and smooth muscle cells of the vascular wall, and activates the production of catecholamines and aldosterone. Therefore, ACE inhibitors have vasodilating, natriuretic, and antiproliferative effects.

An increase in bradykinin content under the influence of ACE inhibitors both in plasma and in organs and tissues blocks remodeling processes in heart failure, enhances the vasodilating and diuretic effects of these drugs by increasing the synthesis of vasodilating prostanoids, reduces changes in the myocardium, kidneys, and vascular smooth muscles . When prescribing ACE inhibitors, one should take into account the presence of an immediate effect associated with the blockade of circulating neurohormones, and a delayed effect associated with the gradual inactivation of local (tissue) neurohormones, which determines the protection of target organs and regression of changes that have developed in them.

The incidence of side effects when using ACE inhibitors I is less than 10%. These include cough, azotemia (not caused by fosinopril), hyperkalemia, hypotension, angioedema.

To reduce the risk of hypotension, which is a consequence of rapid effects on circulating neurohormones, ACE inhibitors should not be prescribed to patients with a baseline SBP less than 85 mmHg.

The use of ACE inhibitors should be started with small doses - 1/4 and even 1/8 tablets, gradually increasing the dose, usually doubling every 1-2 weeks, under blood pressure monitoring. When starting to use ACE inhibitors, concomitant administration of drugs that help lower blood pressure - vasodilators, including nitrates - should be avoided.

After stabilization of blood pressure levels (usually after 1-2 weeks), if necessary, you can return to taking vasodilating agents. Active therapy with diuretics leads to hypovolemia and compensatory hyperreactivity of the reninangiotensin system, which significantly increases the risk of a decrease in blood pressure in response to the use of ACE inhibitors. Therefore, before prescribing them, it is necessary to avoid the use of doses of diuretics that cause large diuresis in the patient and dehydration of the patient.

In accordance with recommendations based on the results of multicenter placebo-controlled studies (“evidence-based medicine”), the following doses of ACE inhibitors are used. Captopril is prescribed at an initial dose of 6.25 mg 2-3 times a day with a gradual increase to the optimal dose of 25 mg 3 times a day.

For severe CHF, the dose of captopril can be 125-150 mg. The starting dose for enalapril is 2.5 mg.

with a gradual increase to the optimal - 10 mg 2 times a day. - Maximum dose - 40 mg / day.

Fosinopril is a safer drug - it causes cough less often, and due to the dual route of elimination from the body (by the kidneys and liver), it does not cause or increase azotemia. The starting dose is 2.5 mg, the optimal dose is 20 mg, the maximum (rarely) is 40 mg per day.

The starting dose of ramipril is 1.25 mg/day, the optimal dose is 5 mg 2 times a day, the maximum is 20 mg/day. For perindopril, the initial dose, which rarely causes hypotension, is 2 mg/day, the optimal dose is 4 mg once a day, the maximum is 8 mg/day.

With the correct dose selection, up to 90% of patients with CHF can take ACE inhibitors for a long time. Like ACE inhibitors, B-blockers interact with endogenous neurohumoral systems, mainly with the sympathoadrenal system.

Activation of the sympathoadrenal system causes peripheral vasoconstriction, decreased natriuresis, the occurrence of myocardial hypertrophy, cardiac arrhythmia, and activation of apoptosis (programmed cell death). All these effects are mediated through a1, b1 and b2 adrenergic receptors.

B-blockers reduce heart rate, myocardial ischemia and its electrical instability, have an antiarrhythmic antifibrillatory effect, block cardiac remodeling processes, prevent the death of cardiomyocytes due to necrosis and apoptosis, restore the viability of cardiomyocytes and the sensitivity of their B-receptors, improve systolic and diastolic function of the left ventricle , reduce renin activity. Multicenter clinical studies have proven the ability of three drugs - carvedilol, bisoprolol and metoprolol (a slow-release form of the drug) to prolong the life of patients with heart failure, regardless of its etiology, when added to ACE inhibitors and diuretics.

The most typical side effects when prescribing B-blockers are hypotension, exacerbation of heart failure in the first days of treatment, bradycardia and the development of atrioventricular block. The first two complications are observed at the beginning of treatment; bradycardia and atrioventricular block can also occur in the long-term period, with an increase in the dose of B-blockers.

B-blockers should not be prescribed to patients with bronchospastic syndrome or acute heart failure. Treatment with β-blockers should begin with very low doses with a gradual increase in dose if the patient tolerated the previous one (“dose titration”).

The starting dose for carvedilol is 3.125 mg 2 times a day, the target dose is 50 mg per day. The drug has a number of advantages over other beta-blockers: due to its ability to block a-adrenergic receptors, it causes vasodilation, which leads to a decrease in afterload and easier emptying of the left ventricle.

Due to antiproliferative and antioxidant effects, it reduces the processes of pathological remodeling of the heart and restores its contractility. The starting dose of bisoprolol is 1.25 mg, the target dose is 10 mg/day. It selectively blocks b1 receptors, is highly lipophilic, and penetrates well into organs and tissues, ensuring regression of cardiac remodeling.

Metoprolol (long-acting form) is prescribed at an initial dose of 12.5 mg/day, the target dose is up to 200 mg/day. Even low doses of β-blockers have been shown in clinical studies to increase ejection fraction and significantly reduce the risk of death or hospitalization due to HF.

Therefore, although it is desirable to achieve target doses of beta-blockers during treatment, lower doses can be used in case of intolerance.

In the first days of using b-blockers in complex therapy of CHF, it is advisable to prescribe them not simultaneously with diuretics or ACE inhibitors, but with an interval of 2-3 hours to reduce the risk of developing hypotension. Since dehydration can increase the risk of developing hypotension, and fluid retention increases the likelihood of worsening the course of CHF, it is necessary to select the optimal dose of the diuretic before starting the use of beta-blockers.

Cardiac glycosides have a beneficial effect in patients with heart failure by inhibiting sodium-potassium (Na+/K+) adenosine triphosphatase (ATPase). Inhibition of ATPase not only increases cardiac contractility, but also reduces sympathetic impulses.

By inhibiting this enzyme in the kidneys, cardiac glycosides reduce tubular reabsorption of sodium and indirectly inhibit the secretion of renin by the kidneys. Currently, digoxin is mainly used from the group of cardiac glycosides.

The main indications for the use of cardiac glycosides are low-output heart failure in combination with atrial fibrillation; HF functional class II-IV with an ejection fraction of less than 30-35%, if it is not possible to achieve improvement with diuretics and ACE inhibitors; for supraventricular arrhythmias (atrial fibrillation and flutter, paroxysmal supraventricular tachycardia). The greatest effectiveness of digoxin was observed in patients with CHF in the presence of atrial fibrillation.

In these cases, due to the slowdown of atrioventricular impulse conduction, the decrease in heart rate is most pronounced and is accompanied by a decrease in myocardial oxygen demand. In patients with sinus rhythm, digoxin, although it does not affect the life expectancy of patients with HF, leads to clinical improvement, increased exercise tolerance and reduces the risk of exacerbation of HF.

Glycosides reduce the automaticity of the sinus node and increase myocardial excitability, which underlies the arrhythmias associated with digitalis intoxication. The effectiveness of digoxin, as well as its toxicity, increases with a decrease in intracellular potassium and an increase in calcium.

Considering the possibility of developing glycoside intoxication, it is recommended to use low doses of digoxin in patients with sinus rhythm - up to 0.25 mg/day. (blood concentration up to 1.2 ng/ml).

A dose of 0.125 mg per day or every other day may also be effective, especially in patients over 70 years of age. Small doses of digoxin have a mainly neuromodulatory effect; as the dose increases, the positive inotropic effect begins to prevail, with which the arrhythmogenic effect and the risk of increasing the risk of sudden death begin to prevail.

When prescribing any dose of digoxin, its concentration reaches a maximum by the 8th day of treatment. This requires careful monitoring of patients after a week of treatment - monitoring heart rate and conductivity (especially at night).

The main side effects of cardiac glycosides are cardiac arrhythmias (ectopic and caused by the re-entry mechanism), and also atrioventricular heart block, and there may be failure of the sinus node; dyspeptic disorders (anorexia, nausea, vomiting); neurological disorders (impaired color perception - vision in yellow-green color, disorientation, confusion). Side effects most often occur at high concentrations of digoxin in the blood (more than 2 ng/ml), but can also occur at lower levels of digoxin, especially in cases of concomitant hypokalemia, hypomagnesemia, and hypothyroidism.

Concurrent use of quinidine, flecainide, propafenone, amiodarone, vera-pamil, spironolactone can increase the level of digoxin in the blood serum and increase the possibility of developing digitalis intoxication. There are absolute and relative contraindications to the use of cardiac glycosides.

Absolute contraindications include intoxication with cardiac glycosides or suspicion of it; atrioventricular block of the second degree; sinus bradycardia less than 50 min"1; allergic reactions to cardiac glycosides. Relative contraindications are sick sinus syndrome; sinus bradycardia less than 55 min"1, atrial fibrillation; atrioventricular block I stage.

(especially if the P-Q interval is more than 0.26 s); Wolff-Parkinson-White syndrome, acute myocardial infarction; hypocapemia; hypercalcemia; renal failure; hypertensive heart with sufficient cardiac output; pulmonary insufficiency II-III stage. In addition, there are a number of conditions in which the use of cardiac glycosides is inappropriate: impaired diastolic filling of the left ventricle: mitral stenosis (without atrial fibrillation), restrictive and hypertrophic cardiomyopathy, diastolic overload with aortic insufficiency; heart failure with high cardiac output (if with this leg atrial fibrillation): thyrotoxicosis, anemia, beriberi.

Treatment of glycoside intoxication includes drug withdrawal and correction of complications that arise. Potassium preparations (potassium chloride, panangin) are prescribed; lidocaine or diphenylhydantoin is used to eliminate ventricular arrhythmia; in case of severe bradycardia, atropine is prescribed.

If necessary, temporary cardiac stimulation is performed. Quinidine is not indicated, because

It can cause an increase in the concentration of digoxin in the blood. Cardioversion is used in exceptional cases in the absence of antiarrhythmic effect from other treatment methods.

In order to reduce the concentration of digoxin in the crop, unithiol 5% - 5 ml is administered intravenously or intramuscularly 1-2 times a day, bemegride intravenously, calcium thetacine, cholestyramine and sorbents are prescribed orally. In cases of severe intoxication, detoxification therapy is carried out: infusions of hemodez, hemosorption.

The most effective way to eliminate life-threatening digoxin toxicity is to administer IV Fab-fractions of digoxin antibodies. Each vial containing 40 mg of Fab antibody fragments neutralizes approximately 0.6 mi of digoxin.

The drugs of the second group include aldosterone antagonists, I angiotensin II receptor blockers, and the calcium antagonist amlodipine. Spironolactone (veroshpiron) is a competitive antagonist of aldosterone, blocking receptors and preventing the effects of this hormone.

Blockade of the effect of aldosterone on the receptors of the distal tubules of the kidneys suppresses the exchange of potassium for sodium, which is accompanied by moderate diuresis and natriuresis with simultaneous retention of potassium in the body. Elimination of the effect on cardiac muscle receptors helps slow fibrosis and cardiac remodeling. Blockade of the effect of aldosterone on vascular endothelial receptors is manifested by its hypotensive and vasoprotective effect.

As a diuretic, it is used in combination with other diuretics in fairly large doses (150-200 mg per day). During long-term treatment together with ACE inhibitors, spironolactone is used in small doses (25-50 mg/day) as a neurohumoral modulator that improves the prognosis and reduces mortality in patients with chronic heart failure.

Spirolactone is prescribed 1-2 times a day, in the first half of the day. The main side effects include hyperkalemia and gynecomastia (in 8-9% of patients).

An alternative approach to reducing the effect of angiotensin II in patients with heart failure is the use of drugs that block its receptors (sartans). They can be “first-line” agents in the treatment of CHF when ACE inhibitors are poorly tolerated.

In heart failure, a positive effect has been proven, which, however, does not exceed the effect of ACE inhibitors, for losartac, which is prescribed once at a dose of 50 mg/day. Other sartans (valsartan, irbesartan, candesartan, eprosartan, etc.

) recommended for use in the treatment of arterial hypertension; Their effectiveness in heart failure has not been proven. Although calcium antagonists are vasodilators that dilate resistive vessels in the systemic and coronary circulation and reduce left ventricular strain, clinical studies have not confirmed their effectiveness in the treatment of CHF.

Some exception is amlodipine, which can be used in the treatment of CHF only in combination with ACE inhibitors. An additional indication for the use of amlodipine for CHF is the presence of severe valvular (mitral or aortic) regurgitation.

The drug is prescribed in a dose of 5-10 mg/day. Adverse reactions include hypotension and edema.

The third group of drugs that play an auxiliary role in the treatment of CHF includes hydralazine and isosorbide dinitrate, antiarrhythmic drugs, and anticoagulants. Reducing the load on the heart can be achieved by reducing blood flow by dilating small peripheral veins and venules or by reducing resistance to the ejection of blood from the left ventricle, which is ensured by dilatation of arterioles.

In clinical practice, three types of vasodilating drugs are used: predominantly venous, reducing blood flow and preload; predominantly arteriolar, reducing afterload, and balanced venous and arteriolar. Venous vasodilators are prescribed mainly for overload of the pulmonary circulation: with IBO, mitral stenosis, pulmonary hypertension.

In the treatment of chronic SI, isosorbide dinitrate is often used orally at a dose of 20-40 mg 2-3 times a day. With exacerbation of chronic heart failure, intravenous infusion of a solution of nitroglycerin (nitro-5, perlinganite) under blood pressure control is possible.

The use of nitrates is often accompanied by side effects, among which headache, nausea, vomiting, and decreased blood pressure are especially poorly tolerated by patients. To prevent the development of tolerance to nitrates, it is necessary to take them intermittently, at intervals of at least 10-12 hours.

Of the arteriolar vasodilators, hydralazine is predominantly used at a dose of 25-50 mg 3-4 times a day. The drug can be used in combination with venous vasodilators (long-acting nitrates).

Hydralazine can cause tachycardia, and with prolonged use of the drug, drug-induced lupus syndrome occurs. Long-term use of peripheral vasodilators in patients with chronic HF, according to multicenter studies, did not have a significant effect on the prognosis, which may be explained by the lack of effect of vasodilators on the processes of cardiac remodeling.

Simultaneous reduction of pre- and afterload can be achieved by using sodium nitroprusside at a dose of 25-50 mg intravenously in 500 ml of 5% glucose solution. The drug is prescribed for acute left ventricular failure or for a short-term period when there is a sharp deterioration in the condition of a patient with CHF. Antiarrhythmic drugs are used only when severe heart failure is combined with life-threatening ventricular arrhythmias or with periodic or persistent atrial arrhythmias, which are accompanied by hemodynamic instability or a high frequency of ventricular contractions.

The drug of choice for the treatment of arrhythmias in patients with severe CHF is amiodarone; less commonly used is sotalol, which is prescribed, like all β-blockers for CHF, by titration, starting with small doses. Patients with chronic HF have an increased risk of thromboembolic complications due to stagnation of blood in the dilated chambers of the heart and in the vessels of the extremities, as well as due to the increased activity of procoagulant blood factors.

Since multicenter clinical studies on the effect of long-term use of anticoagulants on the risk of thromboembolism in CHF have not been conducted, the question of the need for their use remains open. The most justified is the use of the indirect anticoagulant warfarin in patients with CHF with cardiac fibrillation or in people who have already had thromboembolic complications.

In patients with critical decompensation and hypotension, when the prescription of the main means of treating CHF is ineffective or impossible, non-glycoside inotropic agents, primarily dopamine, are used. The minimum infusion rate is used (up to 5 mcg/kg/min), at which the effect on p receptors is pronounced, which is manifested by an increase in cardiac output, a gradual smooth increase in blood pressure and a decrease in filling pressure of the left ventricle.

At the same time, dopamine receptors are stimulated, which promotes dilatation of renal vessels and increased diuresis. At a higher rate of infusion, the a-stimulating effect of dopamine increases, which is realized by a significant increase in pressure and tachycardia, undesirable for patients with heart failure. The use of phosphodiesterase inhibitors (amrinone, milrenon) for the treatment of CHF, as has been shown in multicenter studies, increases the risk of mortality, and therefore these drugs are not currently used.

In severe heart failure and treatment failure, hemodialysis with ultrafiltration is used. Other methods of removing fluid (therapeutic thoracentesis, paracentesis, phlebotomy) may also temporarily relieve shortness of breath, ascites, edema, and pulmonary congestion.

Sanatorium-resort treatment is indicated only for patients with stage I circulatory failure.

Attention! The described treatment does not guarantee a positive result. For more reliable information, ALWAYS consult a specialist.

a pathophysiological condition in which the heart cannot pump the amount of blood it needs for tissue metabolism.

Etiology.

1) Volume overload (heart valve insufficiency)

2) Pressure overload (aortic stenosis, mitral stenosis, arterial hypertension)

3) Myocardial damage (ischemic heart disease, myocarditis, myocardiopathy, myocardial dystrophy, etc.).

In the general population, 87% of cases of CHF are caused by ischemic heart disease and/or arterial hypertension.

Pathogenesis of CHF.

At the moment, the dominant importance of activation has been proven neurohumoral systems(in response to a decrease in cardiac output) in the pathogenesis of heart failure. Leading importance belongs to the activation of the renin-angiotensin-aldosterone and sympathetic-adrenal systems. According to these ideas, ACE inhibitors, beta-blockers and aldosterone inhibitors currently play a dominant role in the pathogenetic treatment of heart failure.

Classification of CHF:

Stage I - initial hidden circulatory failure, manifested only during exertion (shortness of breath, palpitations, excessive fatigue). At rest, hemodynamics and organ functions are not changed. Asymptomatic LV dysfunction.

Stage II A - decompensation predominantly in one circle of blood circulation, signs of circulatory failure at rest are moderately expressed. Adaptive remodeling of the heart and blood vessels.

Stage II B - decompensation in both circles of blood circulation, severe hemodynamic disturbances.

Stage III - the final dystrophic stage - irreversible degenerative changes in the internal organs with severe hemodynamic disturbances.

Functional classes of CHF

I FC: There are no restrictions on physical activity. The patient can tolerate increased stress, but it may be accompanied by shortness of breath and/or delayed recovery.

FC II: Slight limitation of physical activity: there are no symptoms at rest, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations.

III FC: Noticeable limitation of physical activity: there are no symptoms at rest, physical activity of less intensity compared to usual exercise is accompanied by the appearance of symptoms.

IV FC: Inability to perform any physical activity without discomfort; Symptoms of heart failure are present at rest and worsen with minimal physical activity.

To determine the functional class of CHF, a simple and physiological test with a 6-minute walk is widely used. The distance in meters that the patient can walk without any discomfort is determined:

FC 0 - more than 551 meters;

FC 1 - 425-550 meters;

FC 2 - 301-425 meters;

FC 3 - 151-300 meters;

FC 4 - less than 150 meters.

Hemodynamic classification of CHF.

Diastolic heart failure. Reduced compliance and impaired filling of the left ventricle lead to an increase in diastolic pressure in the left ventricle that does not correspond to a change in its volume. A passive increase in pressure in the left atrium and pulmonary artery leads to the appearance of signs of circulatory failure in the pulmonary circulation. Pulmonary hypertension increases right ventricular afterload and leads to right ventricular failure.
Systolic heart failure. Develops when the LV ejection fraction decreases to less than 40%.

Clinic.

Left ventricular failure syndrome: shortness of breath, asthma attacks, cough, hemoptysis, orthopnea, palpitations.
Right ventricular failure syndrome: hepatomegaly, edema, ascites, hepatic reflux (swelling of the neck veins when pressing on the right hypochondrium), oliguria.
Syndrome of dystrophic changes in internal organs and tissues: cardiogenic cirrhosis of the liver, cardiogenic gastritis, cardiogenic bronchitis, trophic changes in the skin (mainly feet, legs) up to the development of trophic ulcers, cardiac cachexia.

Diagnosis of CHF.

Instrumental diagnosis of CHF.

ECG.

A pathological Q wave indicates a previous myocardial infarction, changes in the ST segment and wave

T for myocardial ischemia. Signs of left ventricular hypertrophy suggest a hypertensive heart, aortic heart disease, or hypertrophic myocardiopathy. Low R wave voltage is often seen in pericarditis, amyloidosis and hypothyroidism.

Deviation of the electrical axis of the heart to the right, blockade of the right bundle branch and signs of right ventricular hypertrophy are characteristic of CHF caused by cor pulmonale and mitral stenosis.

Chest X-ray allows you to diagnose dilatation of the heart and its individual chambers, as well as signs of venous stagnation. HF is also characterized by an unclear hilar pulmonary pattern, redistribution of blood flow, enlargement of the left atrium, and bilateral pleural effusion. The absence of radiological signs does not exclude pulmonary congestion.
EchoCG. Allows you to distinguish between systolic and diastolic dysfunction of the left ventricle and identify

congenital and acquired heart defects, left ventricular aneurysm, cardiomyopathies, exudative pericarditis, left ventricular thrombosis, etc. Typical signs of heart failure include a decrease in the ejection fraction of the left ventricle, expansion of the left ventricular cavity, an increase in its end-systolic and end-diastolic dimensions and a decrease in anteroposterior shortening.

Treatment:

1) ACE inhibitors-angiotensin converting enzyme inhibitors- is a tissue hormonal system that participates in the formation of fibrous tissue. ACE inhibitors consequently reduce fibroblast proliferation and the development of fibrosis. Since a prolonged increase in angiotensin levels II and aldosterone in the blood plasma is accompanied by necrosis of cardiomyocytes, then ACE inhibitors and aldosterone antagonists can provide an additional cardioprotective effect. Preventing the development of fibrosis in the myocardium is especially important, since the accumulation of fibrous tissue is a determining factor in the development of diastolic stiffness of the ventricles of the heart.

Captopril - 6.25 mg 3 times a day

Enalapril - 2.5 mg 2 times a day

Lisinopril — 2.5 mg 1 time per day

2)Angiotensin receptor antagonists II (ARA).

More reliably blocks the action of angiotensin II at the receptor level, and have advantages over ACE inhibitors in their action on the RAAS.

Based on currently available data, ARAs are recommended when it is impossible to use ACEIs (for example, cough when using ACEIs).

3) B-blockers.

Initial doses of drugs should be minimal. For metoprolol this dose is 5 mg 2 times a day, for bisoprolol 1.25 mg 2 times a day, carvedilol 3.125 mg 2 times a day. These doses should be doubled at 2-week intervals based on clinical response until the optimal dose is determined.

4) Aldosterone receptor antagonist.

Spironolactone (veroshpiron) - 25 mg initial dose, maximum 200 mg.

5) Diuretics.

Removing excess sodium and water from the body leads to a decrease in congestion, a decrease in pressure in the cavities of the heart and a decrease in volume overload.