Pathogenesis of CHF and the possibility of its drug correction. Chronic heart failure. Pathogenesis. Diastolic heart failure

CHF is a pathophysiological syndrome that develops as a result of various diseases of the cardiovascular system, leading to a decrease in the pumping function of the heart and insufficient blood supply to organs and tissues

Ethology:

1. Myocardial damage:
2. Hemodynamic overload of the myocardium:
3. Impaired diastolic filling of the ventricles: stenosis of the left or right atrioventricular orifice, exudative and constrictive pericarditis, restrictive cardiomyopathies)
4. Increased metabolic needs of tissues (HF with high minute volume): anemia, thyrotoxicosis.

Pathogenesis : 1. The main trigger of CHF is a decrease in myocardial contractility and a drop in cardiac output, which causes a decrease in the perfusion of a number of organs and activation of compensatory mechanisms (sympathetic-adrenal system, renin-angiotensin-aldosterone system, etc.).
2. Catecholamines (norepinephrine) cause peripheral vasoconstriction of arterioles and venules, increase venous return to the heart and level the reduced cardiac output to normal (compensatory reaction). However, further activation of the sympatheticoadrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens heart filling in diastole and other decompensation reactions).
3. Spasm of renal arterioles + renal hypoperfusion due to CHF Þ activation of the RAAS Þ hyperproduction of angiotensin II (a powerful vasopressor; potentiates myocardial hypertrophy and remodeling) and aldosterone (increases sodium reabsorption and plasma osmolality, activates the production of ADH, which retains water). An increase in blood volume, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilatation and damage to the heart (decompensation).
4. In the development of CHF, an important role also belongs to vascular endothelial dysfunction (decreased production of endothelial vasorelaxing factor), hyperproduction of a number of cytokines: IL, TNF-a (impairs the transport of calcium ions into cells, inhibits PVK dehydrogenase, leading to ATP deficiency, triggers apoptosis of cardiomyocytes ).

Classification

1.By origin: due to volume overload, due to pressure overload, primary myocardial
2. According to the cardiac cycle: systolic form, diastolic form, mixed form
3. According to clinical variant: left ventricular, right ventricular, biventricular (total)
4. According to cardiac output: with low cardiac output, with high cardiac output
Degree of severity of CHF.
1. According to Vasilenko-Strazhesko:
Stage I (initial) – latent HF, manifested only during physical activity (shortness of breath, tachycardia, fatigue).
Stage II (severe) – severe disturbances of hemodynamics, organ function and metabolism
IIA – moderately severe signs of heart failure with hemodynamic impairment in only one circle
IIB – severe signs of heart failure with hemodynamic disturbances in the large and small circles
Stage III (final, dystrophic) – severe hemodynamic disorders, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs, complete loss of ability to work.
I FC. The patient does not experience restrictions in physical activity. Normal exercise does not cause weakness (lightheadedness), palpitations, shortness of breath or anginal pain.

II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but performing normal physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

Chronic heart failure (CHF) is a pathogenic condition caused by the inability of the circulatory system to meet the metabolic needs of the body.

Acute HF (low cardiac output syndrome) is spoken of when its symptoms appear within several hours or days from the moment of exposure to the etiological factor.

Pathogenesis

Chronic heart failure (CHF) is the most common cause of disability and mortality in people with vascular anomalies. According to materials from national registries of European countries, the prevalence of CHF among adults is within four percent and increases in proportion to age, including more than ten percent among people over sixty-six years of age. In addition to its significant prevalence, CHF is also characterized by a high level of hospitalization and an unfavorable prognosis: more than 50% of patients die within 5 years after the onset of the first signs of chronic heart failure. In most countries of the world, including Russia, the proportion of the population in older age groups is growing, and the issue of studying chronic heart failure is becoming increasingly relevant. The most popular etiological factors of CHF are arterial hypertension, coronary heart disease and their combination.

It is known that lipid peroxidation (LPO) products change the processes of cell division and growth, form swelling and even decay of mitochondria, deactivate thiol enzymes that are involved in respiration and glycolysis, oxidizing SH groups of proteins, tocopherols, and phospholipids. In recent years, the role of the systemic inflammatory response in the progression of CHF has been proven. According to the results of one of the studies, changes in the functional state of the liver were found in 61% of patients with stage II A and in all patients with stage II B of chronic heart failure. In patients with stage II B CHF, cholestatic, cytolytic and mesenchymal-inflammatory syndromes were pronounced, as well as the development of hepatocellular failure. In patients with PA stage of CHF, cholestatic syndrome predominated in 42.6% of cases. Patients with chronic heart failure were characterized by disturbances in the lipid peroxidation system - antioxidant protection, the formation of a systemic inflammatory response, which was accompanied by the development of metabolic intoxication and was more pronounced in patients with stage II B CHF. A connection between pathogenetic links in the progression of CHF and impaired functional state of the liver has been identified. Thus, the acquired results indicate the need for differentiated use of hepatoprotective therapy already in the first stages of the pathological process in order to prevent disease progression, increase the effectiveness of treatment and reduce refractoriness to therapy in patients with CHF.

Diagnostics chronic heart failure

Cardiac MRI is a versatile and highly accurate non-invasive study that makes it possible to visualize ventricular volumes, assess global function, wall contractility, myocardial viability, myocardial thickness, thickening, myocardial mass and tumors, heart valves, detect congenital defects and pericardial changes.

• CT scan.
• CT angiography is used in patients with coronary artery disease with exercise or stress testing.
• Radionuclide ventriculography.Radionuclide ventriculography is recognized as a relatively accurate method for establishing LVEF and is more often performed to determine the blood supply to the myocardium, which, in turn, provides information about myocardial viability and the presence of ischemia.
• Determination of pulmonary function.It is used to identify or exclude pulmonary causes of shortness of breath and to assess the role of respiratory diseases in the patient’s shortness of breath.
• Cardiac catheterization.Cardiac catheterization is not needed for routine diagnosis and treatment of patients with heart failure (HF), but can indicate etiology and prognosis after revascularization.
• Angiography of the heart.The use of coronary angiography is considered in patients with heart failure and exertional angina or with suspected ischemic LV dysfunction. Coronary angiography is also indicated in patients with refractory heart failure of unknown etiology and in patients with confirmed severe mitral regurgitation or aortic valve disease, which can be corrected surgically.
• Right heart catheterization (RHC).CPOS provides valuable hemodynamic information about filling pressure, vascular resistance, and cardiac output. Monitoring hemodynamic changes makes it possible to evaluate the effectiveness of treatment in patients with severe HF who are refractory to treatment.
• Outpatient ECG monitoring (Holter).Ambulatory ECG monitoring is valuable in the presence of symptoms of arrhythmia (eg, palpitations or syncope) and for monitoring the ventricular rate in patients with atrial fibrillation.

Treatment chronic heart failure

Pharmacotherapy.

Treatment with ACE inhibitors for HF has been shown to improve ventricular function and patient well-being, reduce hospital visits for worsening HF, and increase survival. ACEIs are prescribed to patients if LVEF is less than 40%, regardless of symptoms.

Initiation of beta blockers.

1) Beta blockers may be initiated with caution for in-hospital relief in recent decompensation.
2) Visits every four weeks to increase the dose of beta blockers (titration may be slower in some patients). Do not increase the dose if there are signs of worsening heart failure, symptomatic hypotension (including dizziness), or excessive bradycardia (pulse less than 50 per minute).

In the presence of atrial fibrillation, digoxin is the mainstay of ventricular rate control due to its ability to suppress AV conduction. If sinus rhythm is preserved, the prescription of digoxin is also justified in case of severe systolic dysfunction - frequent paroxysms of suffocation and left ventricular failure. Digoxin is especially indicated for patients with enlarged heart sizes and ischemic heart failure.

Aldosterone antagonists (spironolactone) control only part of the sodium and are excreted by the kidneys, but this is enough for spironolactone (veroshpiron) to provide an increase in diuresis within 20-25%.

Neuroendocrine model and neuroendocrine antagonists in the treatment of CHF. Views on how to properly treat CHF have changed over the decades and it seemed that this is not such a big problem, it’s just that pharmacologists have not yet found the “ideal” means of auxiliary inotropic support for damaged myocardium, but this is a matter of time. Unfortunately, it turned out that everything is much more complicated. Strategic approaches to the treatment of myocardial dysfunction were improved in accordance with the pharmacotherapy capabilities of that time.

The heart is a “pump” that does not work well, so this pump must be constantly stimulated with digoxin. With the advent of diuretics, new treatment options have opened up. Not only the heart, but also the kidneys are to blame for severe symptoms.
Unfortunately, modern medications (valsartan, losartan) in the treatment of CHF have not demonstrated effectiveness exceeding ACE inhibitors. Therefore, their use is advisable only in cases of intolerance to ACE inhibitors.

If there is a pharmacological group with cardioprotective action, then beta-blockers (BABs) should be the first representative. Obviously, the key to the cardioprotection of beta blockade is to counteract the cardiotoxic effects of depleted doses of norepinephrine. Under its influence, cardiomyocytes become overloaded with calcium and quickly die. One of the four beta blockers - metoprolol succinate, bisoprolol, carvedilol and nebivalol, in the absence of contraindications, should be used by all patients with chronic heart failure, and what is important - only after the patient has achieved a stable condition.

In the presence of decompensation, the use of calcium channel blockers (CCBs) only aggravates the clinical course of CHF due to their pronounced cardiodepressive effect. The use of CCBs may be justified in cases of predominantly diastolic CHF. The administration of short-acting dihydropyridines (nifedipine) is accompanied by significant sympathetic activation, so they are contraindicated in patients with chronic heart failure, with rare exceptions (bradycardia).

Although chronic heart failure is a rather severe clinical syndrome, and the symptoms significantly impair the quality of life, modern pharmacotherapy makes it possible to maintain a relatively satisfactory functional state of the patient for a long time. Therefore, the constant regular use of basic treatment includes certain responsibilities.

Heart transplant

Heart transplantation is a common treatment for end-stage heart failure. Transplantation, when used with the correct selection criteria, significantly improves survival rate, exercise capacity, accelerates return to work, and improves quality of life compared to conventional treatment.

Significant breakthroughs have been made in left ventricular assist device (LVAD) and artificial heart technology. Current indications for the use of LVAD and artificial heart include transplantation and management of patients with acute severe myocarditis. Although experience is still limited, the devices may be considered for long-term use while the final procedure is being planned.

Ultrafiltration

Ultrafiltration is considered to reduce fluid overload of the lungs (pulmonary and/or peripheral edema) in selected patients and to correct hyponatremia in symptomatic patients refractory to diuretics.

Remote monitoring

Remote monitoring can be defined as the long-term collection of information about a patient and the ability to review this information without his presence.

Continuous analysis of this data and effective use of the device can activate notification mechanisms when clinically significant changes are detected, and therefore facilitate patient care. Remote monitoring may reduce healthcare resource utilization by reducing chronic HF hospitalization and readmission rates.

Thromboembolism warnings

• Antithrombotic therapy to prevent thromboembolism is recommended for all patients with AF, unless there are contraindications.

• In patients with AF at high risk of stroke/thromboembolism, long-term oral anticoagulant therapy with vitamin K antagonists is recommended unless contraindicated.

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 dilation 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

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.

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-α);

· 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 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.

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./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.

Chronic heart failure (CHF)– a syndrome of various cardiovascular diseases leading to a decrease in the pumping function of the heart (impaired contraction and, to a lesser extent, relaxation), chronic hyperactivation of neurohormonal systems and manifested by shortness of breath, palpitations, increased fatigue, excessive fluid retention in the body and limitation of physical activity.

Epidemiology: CHF is the most common cause of hospitalization in the elderly; five-year survival rate of patients with CHF: less than 50%; in case of severe CHF, half of the patients die within the first year; CHF reduces quality of life by 80%.

Etiology of CHF:

1. Myocardial damage:

a) primary myocardial failure (myocarditis, idiopathic dilated cardiomyopathy)

b) secondary myocardial failure (post-infarction cardiosclerosis, specific cardiomyopathies: metabolic, with systemic connective tissue diseases, alcoholic, toxic-allergic, etc.)

2. Hemodynamic overload of the myocardium:

a) overload due to increased ejection resistance (pressure overload): hypertension, pulmonary hypertension, aortic stenosis, pulmonary stenosis

b) overload with increased filling of the heart chambers (volume overload): heart valve insufficiency, congenital heart disease with left-to-right shunting of blood (VSD, etc.)

c) combined overload (volume and pressure): combined heart defects

3. Impaired diastolic filling of the ventricles: stenosis of the left or right atrioventricular orifice, exudative and constrictive pericarditis, restrictive cardiomyopathies)

4. Increased metabolic needs of tissues(HF with high cardiac output): anemia, thyrotoxicosis.

Pathogenesis of CHF.

1. The main trigger mechanism for CHF is decreased myocardial contractility and decreased cardiac output, which causes a decrease in the perfusion of a number of organs and activation of compensatory mechanisms (sympathetic-adrenal system, renin-angiotensin-aldosterone system, etc.).

2. Catecholamines (norepinephrine) cause peripheral vasoconstriction of arterioles and venules, increase venous return to the heart and level the reduced cardiac output to normal (compensatory reaction). However, further activation of the sympatheticoadrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens heart filling in diastole and other decompensation reactions).

3. Spasm of renal arterioles + renal hypoperfusion due to CHF Þ activation of the RAAS Þ hyperproduction of angiotensin II (a powerful vasopressor; potentiates myocardial hypertrophy and remodeling) and aldosterone (increases sodium reabsorption and plasma osmolality, activates the production of ADH, which retains water). An increase in blood volume, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilatation and damage to the heart (decompensation).

4. In the development of CHF, an important role also belongs to vascular endothelial dysfunction (decreased production of endothelial vasorelaxing factor), hyperproduction of a number of cytokines: IL, TNF-a (impairs the transport of calcium ions into cells, inhibits PVK dehydrogenase, leading to ATP deficiency, triggers apoptosis of cardiomyocytes ).

Classification of CHF.

1. By origin: due to volume overload, due to pressure overload, primary myocardial

2. According to the cardiac cycle: systolic form, diastolic form, mixed form

3. According to clinical variant: left ventricular, right ventricular, biventricular (total)

4. By cardiac output: low cardiac output, high cardiac output

Degree of severity of CHF.

1. According to Vasilenko-Strazhesko:

Stage I (initial)– latent HF, manifested only during physical activity (shortness of breath, tachycardia, fatigue).

Stage II (pronounced)– pronounced disturbances of hemodynamics, organ function and metabolism

­ IIA– moderately severe signs of heart failure with hemodynamic disturbances in only one circle

IIB– severe signs of heart failure with hemodynamic disturbances in the large and small circles

Stage III (final, dystrophic)– severe hemodynamic disorders, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs, complete loss of ability to work.

2. According to NYHA:

I class(no restrictions on physical activity) - ordinary (habitual) physical activity does not cause severe fatigue, shortness of breath or palpitations (but there is heart disease!); 6-minute walking distance is 426-550 m.

II class(mild, minor limitation of physical activity) - satisfactory health at rest, but habitual physical activity causes fatigue, palpitations, shortness of breath or pain; 6-minute walk distance 301-425 m.

III class(pronounced, noticeable limitation of physical activity) - satisfactory health at rest, but the load is less than usual leads to the appearance of symptoms; 6-minute walking distance is 151-300 m.

IV class(complete restriction of physical activity) - the inability to perform any physical activity without deteriorating well-being; symptoms of heart failure are present even at rest and intensify with any physical activity; the distance of a 6-minute walk is less than 150 m.

The main clinical manifestations of biventricular CHF:

1. Subjective manifestations:

Dyspnea is the most common and early symptom of CHF; it initially appears only during physical activity, as the disease progresses, and at rest; shortness of breath often occurs when lying down and disappears when sitting

Rapid fatigue, severe general and muscle weakness (due to decreased muscle perfusion and oxygen starvation); loss of body weight (due to activation of TNF-a and the development of malabsorption syndrome)

Palpitations (usually due to sinus tachycardia) - initially bother patients during exercise or with a rapid rise in blood pressure, as CHF progresses - and at rest

Attacks of suffocation at night (cardiac asthma) - attacks of severe shortness of breath that occur at night, accompanied by a feeling of lack of air, a feeling of fear of death

Cough - usually dry, appears after or during physical activity (due to venous stagnation in the lungs, swelling of the bronchial mucosa and irritation of cough receptors); in severe cases there may be a wet cough with the release of a large amount of foamy, pink sputum (with the development of pulmonary edema)

Peripheral edema - at first there is a slight pastiness and local swelling in the area of ​​​​the feet and legs, mainly in the evening, by the morning the swelling disappears; as CHF progresses, edema becomes widespread, localized not only in the area of ​​the feet, ankles, legs, but also in the area of ​​the thighs, scrotum, anterior abdominal wall, and lumbar region; extreme degree of edematous syndrome - anasarca - massive, widespread edema with ascites and hydrothorax

Impaired urine output (oliguria, nocturia - predominance of nighttime diuresis over daytime)

Pain, a feeling of heaviness and fullness in the right hypochondrium - appear with enlarged liver, caused by stretching of the Glissonian capsule

2. Objectively:

a) inspection:

Forced sitting or semi-sitting position of patients with legs down or horizontal position with head raised high

Acrocyanosis of the skin and visible mucous membranes, most pronounced in the distal parts of the extremities, on the lips, tip of the nose, ears, subungual spaces, is accompanied by cold skin of the extremities, trophic disorders of the skin (dryness, peeling) and nails (fragility, dullness) (due to decreased perfusion of peripheral tissues, increased tissue extraction of oxygen and increased reduced hemoglobin)

Peripheral edema (up to ascites and hydrothorax): located symmetrically, leaving a deep hole after finger pressure, which then gradually smoothes out; the skin in the area of ​​edema is smooth, shiny, soft at first, and with prolonged swelling it becomes dense; at the site of edema, blisters may form, which open and fluid flows out of them, foci of necrosis, skin tears

Swelling and pulsation of the neck veins (with the development of right ventricular failure)

Positive Plesha symptom (hepatic-jugular test) - when the patient is breathing calmly, pressure is applied with the palm of the hand to the enlarged liver, which causes increased swelling of the neck veins

Atrophy of skeletal muscles (biceps, thenar and hypothenar muscles, temporal and masticatory muscles), loss of body weight, a pronounced decrease in subcutaneous fat (“cardiac cachexia”).

b) physical examination:

1) respiratory organs: inspiratory tachypnea; percussion: dullness at the back in the lower parts of the lungs; Auscultation: crepitus and moist fine bubbling rales against the background of hard or weakened vesicular breathing in the lower parts

2) cardiovascular system: pulse is rapid, low filling and tension, often arrhythmic; Blood pressure is reduced (SBP is greater than DBP); palpation of the apical impulse is diffuse, shifted to the left and down; percussion, the borders of the heart are expanded to the left; auscultation tachycardia and various arrhythmias, often protodiastolic gallop rhythm

3) abdominal organs: bloating (flatulence), palpation - pain in the right hypochondrium; the liver is enlarged, painful on palpation, its surface is smooth, the edge is rounded, with large stagnation - systolic pulsation (bulging in systole and decreasing in diastole); ascites.

Diagnosis of CHF.

1. ECG: signs of left ventricular hypertrophy: increase in R wave V5,V6, I, aVL, signs of left bundle branch block, increase in the interval of internal deviation (from the beginning of the Q wave to the apex of the R wave) J > 0.05 sec in V5, V6, levogram , displacement of the transition zone in V1/V2, right ventricular hypertrophy: increase in R III, aVF, V 1, V 2; spelling; displacement of the transition zone in V 4 /V 5; complete/incomplete blockade of the right bundle branch; increase in the interval of internal deviation J>0.03 sec in V 1, V 2; shift of the ST interval below the isoline, inversion or biphasicity of the T wave in III, aVF, V 1, V 2, various rhythm disturbances, etc.

2. Chest X-ray: redistribution of blood flow in favor of the upper lobes of the lungs and an increase in the diameter of blood vessels (a sign of increased pressure in the pulmonary veins); Kerley lines (caused by the presence of fluid in the interlobar fissures and dilation of the lymphatic vessels of the lungs); signs of alveolar pulmonary edema (a shadow spreading from the roots of the lungs), effusion in the pleural cavity, cardiomegaly, etc.

3. Echocardiography(including stress tests: bicycle ergometry, 6-minute walk, bicycle ergometry, etc.): allows you to determine the size of the heart cavities, myocardial thickness, blood flow in various phases of the cardiac cycle, ejection fraction, etc.

4. Additional research methods: radionuclide (assessment of local myocardial contractility, EF, end-systolic and diastolic volumes, myocardial viability); invasive (catheterization of the cardiac cavities, ventriculography - more often to resolve the issue of surgical treatment).

5. Laboratory data nonspecific: OAC – there may be signs of anemia (due to decreased appetite of patients, impaired iron absorption); OAM – proteinuria, cylindruria (as a manifestation of “congestive kidney”); BAC – decrease in total protein, albumin, prothrombin, increase in bilirubin, ALT and AST, GGTP, LDH (liver dysfunction); fluctuations in electrolytes (the result of pathogenetic processes in heart failure and diuretic therapy); increased levels of creatinine and urea (“stagnant kidney”), etc.