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

Authors): V.S. Gerke, Ph.D., veterinarian / V. Gerke, PhD, DVM
Organization(s): CJSC "Network of Veterinary Clinics", St. Petersburg / "Network veterinary clinics", St. Petersburg
Magazine: №3 - 2013

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 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.

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 (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.

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.

digestive organs

kidneys

CHRONIC HEART FAILURE

( Insufficientiacordischronica)

Chronic heart failure (CHF) - This is a pathological condition in which the work of the cardiovascular system does not meet the body's oxygen needs, first during physical activity and then at rest.

Etiology. The main mechanisms leading to the development of CHF include:

1. Volume overload. It is caused by heart defects with reverse blood flow: mitral or aortic valve insufficiency, the presence of intracardiac shunts.

2. Pressure overload. It occurs in the presence of stenosis of the valve orifices, the outflow tract of the ventricles (stenosis of the left and right atrioventricular openings, the mouth of the aorta and the pulmonary artery) 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 (acute myocardial infarction, post-infarction cardiosclerosis, chronic coronary insufficiency), non-coronarogenic (myocardial dystrophy, myocarditis, cardiomyopathy) and some other heart diseases (tumors, amyloidosis, sarcoidosis).

4. Impaired diastolic filling of the ventricles of the heart, which may be caused by adhesive and exudative pericarditis, restrictive cardiomyopathy.

Pathogenesis. Any of these reasons leads to profound metabolic disorders in the myocardium. The leading role in these changes belongs to biochemical, enzymatic disorders, and shifts in acid-base balance. The biochemical basis for the development of heart failure lies in disturbances in ion transport, primarily calcium, as well as potassium-sodium, and disturbances in the energy supply of myocardial contractile function. The contractile activity of the heart muscle is associated with the rate of oxygen absorption by the myocardium. In the absence of mechanical activity (at rest), the myocardium absorbs 0 2 in an amount of about 30 μl/min/g, and under conditions of maximum load its consumption increases to 300 μl/min/g. This indicates that the main part of the energy in cardiomyocytes is produced in the process of biological oxidation.

As a result of these changes, the production of high-energy substances that provide the energy requirement of the myocardium during its contraction is disrupted.

From a modern point of view, the main stages of the pathogenesis of CHF are presented as follows. Myocardial overload leads to a decrease in cardiac output and an increase in residual systolic volume. This contributes to an increase in end-diastolic pressure in the left ventricle. Tonogenic dilatation develops and the end-diastolic volume of the left ventricle increases. As a result, according to the Frank-Starling mechanism, myocardial contractions are enhanced and the reduced cardiac output is leveled out. When the myocardium exhausts its reserves, the pathological features of this mechanism come to the fore: dilatation of the ventricle from compensatory becomes pathological (myogenic). This is accompanied by an increase in residual blood volume, end-diastolic pressure and an increase in CHF. In response, the pressure in the overlying sections of the bloodstream - the vessels of the pulmonary circulation - increases and passive pulmonary hypertension develops. As the pumping function of the right ventricle weakens, stagnation appears in the systemic circulation. As a result of a decrease in cardiac output, blood supply to organs and tissues, including the kidneys, worsens, which is accompanied by the inclusion of the renal link in the pathogenesis of CHF. To maintain blood pressure at a normal level with reduced cardiac output, the activity of the sympathetic-adrenal system increases. Increased release of catecholamines, mainly norepinephrine, leads to narrowing of arterioles and venules. Insufficient blood supply to the kidneys leads to activation of the renin-angiotensin-aldosterone system. Excess angiotensin II, a powerful vasoconstrictor, further increases peripheral vasospasm. At the same time, angiotensin II stimulates the formation of aldosterone, which increases sodium reabsorption, increases plasma osmolarity and promotes the activation of the production of antidiuretic hormone (ADH) by the posterior pituitary gland. An increase in ADH levels leads to fluid retention in the body, an increase in circulating blood volume (CBV), the formation of edema, and an increase in venous return (this is also determined by a narrowing of the venules). Vasopressin (ADH), like norepinephrine and angiotensin II, increases vasoconstriction of peripheral vessels. As the venous return of blood to the heart increases, the vessels of the pulmonary circulation become overfilled and the diastolic filling of the affected left ventricle with blood increases. There is further expansion of the ventricle and an increasing decrease in cardiac output.

With predominant damage to the left ventricle in patients with coronary artery disease, hypertension, acute and chronic glomerulonephritis, aortic defects, the clinical picture of the disease is dominated by signs of stagnation in the pulmonary circulation: shortness of breath, attacks of cardiac asthma and pulmonary edema, and sometimes hemoptysis. With predominant damage to the right ventricle in patients with mitral stenosis, chronic cor pulmonale, tricuspid valve defects, congenital heart defects, and some types of cardiomyopathies, signs of stagnation in the systemic circulation come to the fore: liver enlargement, subcutaneous and cavitary edema, increased venous pressure.

Classification of chronic circulatory failure proposed by N. D. Strazhesko, V. X. Vasilenko and G. F. Lang and approved at the XII All-Union Congress of Therapists in 1935. There are three stages of CHF.

Stage I - initial: latent NK, manifested only during physical activity in the form of shortness of breath, tachycardia, and increased fatigue. At rest, hemodynamics and organ function are not changed, work capacity is reduced.

Stage II - period A: mild hemodynamic disturbances in the systemic and pulmonary circulation; period B: profound hemodynamic disturbances in both the systemic and pulmonary circulation, pronounced signs of CHF at rest.

Stage III - final (dystrophic) with severe hemodynamic disorders, persistent metabolic disorders and the function of all organs, the development of irreversible changes in the structure of organs and tissues, and loss of ability to work.

The New York Heart Association has proposed a classification that distinguishes four classes (stages) of CHF. Functional class I of this classification corresponds to stage I of CHF, FC II - stage II A, FC III - stage N B, FC IV - stage III. In the modern domestic classification of CHF (Table 6), developed at the All-Russian Scientific Center of the Academy of Medical Sciences of the USSR (Mukharlyamov N.M., 1978), the origin, cardiac cycle, clinical variant of the course and stage of the pathological process are taken into account, and stages I and III of CHF are divided into substages A and V.

Table 6

By origin

According to the cardiac cycle

Clinical options

By stages

Overload

pressure

Systolic

failure

Mostly

left ventricular

period A

period B

Overload

volume

Diastolic

failure

Mostly

right ventricular

period A

period B

Primary

myocardial

(metabolic)

failure

Mixed

failure

Total

Hyperkinetic

Collaptoid

With saved

sinus rhythm

Bradycardic

period A

period B

Clinic. The main clinical manifestations of CHF are tachycardia, shortness of breath, cyanosis, edema, and liver enlargement.

Tachycardia - one of the fairly constant symptoms of CHF. It occurs reflexively and compensates for the lack of stroke volume by increasing the number of heart contractions. In the initial stages of CHF, an increase in heart rate is observed only during physical activity; later it is expressed at rest. Tachycardia occurs as a result of the Bainbridge reflex from the stretching mouths of the vena cava and helps maintain cardiac output at a sufficient level.

Dyspnea is the most common and early sign of CHF. Subjectively, shortness of breath is characterized by a feeling of lack of air, a sharp increase in it is like suffocation. On examination, a change in the frequency and depth of breathing is noted. A frequent accompaniment of shortness of breath is a cough, caused reflexively from congestive bronchi, or associated with expansion of the left atrium. The pathogenesis of shortness of breath is complex. As a result of stagnation in the vessels of the pulmonary circulation, the function of external respiration is disrupted, leading to the accumulation of lactic acid and carbon dioxide in the blood. This leads to the development of acidosis. The respiratory center responds to hypercapnia and acidosis by increasing and deepening breathing, and to hypoxia by only increasing it. In severe CHF, attacks of suffocation occur at night - cardiac asthma. An increase in circulating blood volume, a decrease in gas exchange, an increase in the tone of the vagus nerve and moderate bronchospasm play a role in its occurrence. Prolonged attacks of cardiac asthma can develop into pulmonary edema, which is manifested by severe suffocation, bubbling breathing, and the separation of pink, serous, foamy sputum (due to sweating of blood cells into the alveoli). On auscultation, fine and large bubble rales are heard over the entire surface of the lungs. With pulmonary edema, cyanosis increases, the pulse quickens, and its filling decreases.

Edema with CHF appear on the legs, arms, lumbar region and increase in the evening, in contrast to renal edema, which is more pronounced in the morning. In the early stages, so-called hidden edema may be observed, since retention of up to 5 liters of fluid in the body occurs outwardly unnoticed. Edematous fluid (transudate) can accumulate in serous cavities - pleural (hydrothorax), pericardial cavity (hydropericardium), in the abdominal cavity (ascites), as well as in the genital area. Edema, caused primarily by right ventricular failure and venous stagnation, appears later than the liver enlarges.

Enlarged liver with CHF helps slow blood flow in the peripheral parts of the bloodstream. The liver also enlarges due to increased production of red blood cells in conditions of bone marrow hypoxia and an increase in the mass of circulating blood. With the progression of CHF and after prolonged stagnation of blood in the liver, irreversible morphological changes develop - degeneration of liver cells, swelling of mesenchymal tissue with its induration, diffuse development of connective tissue with scarring ("nutmeg" liver). With the development of cardiac cirrhosis, icterus of the skin and mucous membranes appears, and portal hypertension occurs.

Cyanosis is one of the early symptoms of CHF. It is more pronounced on the fingers and toes, the tip of the nose, and lips. Its occurrence depends on an increase in the content of reduced hemoglobin in the blood as a result of insufficient arterialization of blood in the pulmonary capillaries. Cyanosis is also caused by excessive absorption of oxygen by tissues, caused by slowing blood flow and depletion of venous blood in oxyhemoglobin.

An increase in venous pressure in CHF is manifested by swelling and pulsation of the neck veins, and congestion of the rectal veins. These phenomena intensify in the horizontal position of the patient due to greater blood flow to the heart.

With CHF, the function of the digestive organs is impaired, which manifests itself in the form of congestive gastritis with atrophy of the gastric glands, dyspeptic disorders (nausea, flatulence, constipation, malabsorption).

Diagnostics. Along with clinical manifestations, the diagnosis of CHF is helped by instrumental research methods, which are of particular importance in the early stages of the development of circulatory failure.

There are invasive and non-invasive methods for diagnosing CHF. Invasive methods include catheterization of the cavities of the heart and great vessels with measurement of pressure in them, and ventriculography. Of the non-invasive methods, echocardiography is the most widely used. An echocardiographic study helps identify changes in the volumes of the heart chambers, the thickness of their walls, myocardial mass, and allows us to determine a decrease in EF, EDV and Vcf. Using computer echocardiography and simultaneous registration of polycardiograms (ECG, PCG, rheography of the pulmonary artery and aorta), early disturbances in diastole phases are determined. The magnitude of cardiac output and circulating blood volume are determined using dye or radioactive isotope dilution methods. To diagnose CHF, especially its latent form, a study of hemodynamics during physical activity (bicycle ergometry, treadmill load, electrical stimulation of the atria) is used.

Treatment. Therapeutic measures for CHF should be aimed at eliminating the cause that caused it and correcting disorders characteristic of a certain stage of failure. Therapy for CHF includes non-drug methods (limitation of the patient’s physical and mental activity, diet) and the prescription of medications with different mechanisms of action.

Mode: The patient's activity should not exceed the capabilities of the cardiovascular system. At stage I of CHF, semi-bed rest is prescribed for 5-7 days, then increased physical activity is limited: at stage II (period A), semi-bed rest is indicated, and at stages 11B and III, bed rest is indicated. The duration of bed rest depends on the course of CHF. With very strict and prolonged bed rest, the risk of developing phlebothrombosis and pulmonary embolism increases. These patients are prescribed breathing exercises and frequent changes in body position. Mental peace is achieved by observing a therapeutic regimen and using sedatives (bromides, valerian, motherwort, minor tranquilizers).

The diet should be rich in vitamins, which are administered in double doses, and restriction of salt and liquid is indicated. It is necessary to monitor bowel function. In stage I CHF, the amount of table salt is reduced to 5-6 g per day (10 tables). At stages II and III - up to 3 g/day (10a table). In case of severe edematous syndrome, a sharply hypochloride diet is indicated - no more than 1 g of salt per day. Along with salt restriction, fluid restriction is necessary (up to 1 l/day). Against the background of this diet, fasting days (milk, curd, fruit, etc.) are prescribed, which are especially indicated for patients with excess body weight.

Drug therapy is aimed at normalizing cardiac output, removing sodium and water, reducing peripheral vascular tone, suppressing the influence of the sympathetic-adrenal system on the myocardium.

Strengthening myocardial contractility is achieved with the help of cardiac glycosides And non-glycoside inotropic drugs. The basis for the use of cardiac glycosides (CG) is the cardiotonic effect they provide. It lies in the fact that SG increases the strength and speed of contraction of the heart muscle (positive inotropic effect). The effect of SG is to inhibit the activity of the enzyme Na + -K + -ATPase, as a result of which the active transport of sodium ions from the cell and potassium ions into the cell is suppressed during diastole. At the same time, the intracellular content of calcium ions increases. In this case, chemical energy is converted into mechanical energy and the strength and speed of myocardial contraction increases. Since Ca 2+ and SG have a complementary inotropic and toxic effect, the administration of calcium supplements is contraindicated in case of digitalis intoxication and, conversely, the administration of SG is dangerous in case of hypercalcemia. SGs also slow down the heart rate, lengthen diastole, and improve blood circulation. Venous pressure and symptoms of stagnation decrease, blood supply and kidney function improve, and diuresis increases. We must not forget that in large doses, SG can cause angina attacks.

The toxic effect of SG is characterized by the appearance of bradycardia, nausea, vomiting, and extrasystole, often of the type of ventricular bigeminy. As these disorders progress, ventricular flutter and eventually cardiac arrest may develop.

SGs are found in foxglove, adonis, lily of the valley, jaundice, strophanthus, sea onion, and lily of the valley. Despite their different origins, SGs have a similar basic structure and pharmacological properties, differing in strength and duration of action, rate of absorption and time of excretion from the body. Depending on the number of hydroxyl groups, SGs are divided into polar, relatively polar and non-polar. Polar (strophanthin, korglykon) contain 5 hydroxyl groups. They are poorly absorbed in the gastrointestinal tract, dissolve well in water, are easily excreted by the kidneys, and have the shortest duration of action. Relatively polar (digoxin, isolanide) contain 2 hydroxyl groups, are well absorbed when taken orally, and are excreted to a large extent by the kidneys. Duration of their action -5-7 days. Nonpolar (digitoxin, acedoxin) contain 1 hydroxyl group. They are highly absorbable in the intestine. The maximum duration of their action is 10 - 14 days.

Strophanthin found in strophanthus seeds. It consists of a mixture of SG. A 0.05% solution of 0.3 - 0.5 ml in a 5% glucose solution is used intravenously. The effect occurs after 5-10 minutes, maximum effect after 1.5-2 hours. Duration of action is 10-12 hours. The cumulative effect is insignificant. Strophanthin has little effect on heart rate and conduction function. Do not use immediately after taking digitalis. To prevent intoxication, a break of 3-4 days is indicated, and after taking digitoxin - 10-14 days. Strophanthin for CHF is used to obtain a quick effect or when digitalis preparations are low in effectiveness.

Korglykon is a preparation of May lily of the valley. Its action is similar to strophanthin, but it is inactivated in the body somewhat more slowly. 0.5 - 1 ml of a 0.06% solution of 5% glucose solution is administered intravenously. In terms of therapeutic activity it is inferior to strophanthin.

Preparations from foxglove purpurea, woolly, rusty and ciliated are used. When taken orally, digitalis glycosides are almost not destroyed, they are absorbed slowly and have the property of cumulation. Digitoxin is the most active glycoside of digitalis purpurea. Available in tablets of 0.1 mg and suppositories of 0.15 mg. It has a pronounced cumulative effect, which is why it is used less often than other glycosides.

Digoxin - glycoside of foxglove woolly. It has a less cumulative effect and is eliminated from the body relatively quickly. Available in tablets of 0.25 mg and in ampoules of 2 ml of 0.025% solution.

Another preparation from foxglove woolly is celanide (isolanide), having a rapid and pronounced therapeutic effect. The cumulative effect is weakly expressed. Release form: tablets of 0.25 mg, ampoules of 1 ml of 0.02% solution and drops of 0.05% solution.

There are three methods of digitalization:

1) at a fast pace, when the optimal therapeutic dose of the glycoside in the patient’s body is achieved within 24 hours;

2) at a moderately fast pace, when the optimal dose is achieved in three days;

3) at a slow pace, when saturation with glycosides is carried out over 7-10 days. Digitalization has become most widespread at a moderately fast pace.

The use of SG does not achieve a therapeutic effect in all cases. They are contraindicated in case of bradycardia, conduction disorders, especially atrioventricular. Incorrect dosing of SG leads to the development of glycoside intoxication. It manifests itself as cardiac (rhythm disturbances: extrasystoles, atrial fibrillation and flutter, atrioventricular blockades of the first and second degrees, etc., “trough-shaped” decrease in the ST segment, shortening of electrical systole, etc.), gastrointestinal (nausea, vomiting, lack of appetite, excessive salivation), neurological (insomnia, fatigue, dizziness, lethargy, confusion, delirium) and eye symptoms (coloring of all surrounding objects yellow or greenish).

In recent years, non-glycoside drugs have begun to be used that can increase myocardial contractility (positive inotropic effect) and do not cause adverse reactions characteristic of glycosides. This group of medications includes prenalterol, dopamine, levodopa, and dobutamine.

In order to correct water and electrolyte disturbances, the complex of treatment for patients with CHF includes diuretics (diuretics). Diuretics reduce circulating blood volume, increase diuresis, and natriuresis. Basic diuretics reduce the reabsorption of sodium and water in the renal tubules and, according to the primary localization of action, are divided into groups of drugs:

1) acting on the proximal tubules (osmotic diuretics, carbonic anhydrase inhibitors);

2) acting on the ascending part of the loop of Henle (thiazide diuretics, non-thiazide sulfonamides, furosemide and uregit);

3) acting on the distal tubules (potassium-sparing competitive and non-competitive aldosterone antagonists - aldactone, triamterene, pterofen, etc.).

For patients with stage II A CHF, it is advisable to start therapy with hypothiazide at a dose of 50 - 150 mg / day or brinaldix at a dose of 20 - 60 mg / day in combination with potassium-sparing diuretics such as veroshpiron at 150 - 250 mg / day (in the presence of secondary aldosteronism) or triamterene at a dose of 100 - 200 mg/day. In clinical practice, the drug triampur has proven itself well (triamterene - 25 mg, hypothiazide - 12.5 mg). It is prescribed 2-3 times a day due to its low diuretic effect. Therapy with potassium-sparing diuretics is carried out continuously: the main diuretics in the active therapy phase are prescribed daily or every other day, and when switching to maintenance therapy - 1-2 times a week under the control of diuresis and body weight. If these diuretics are ineffective, with the development of BE and stage III CHF, they switch to the use of more powerful diuretics. Furosemide at a dose of 40-200 mg/day and uregit at a dose of 50-200 mg/day are prescribed once in the morning on an empty stomach, causing pronounced diuresis within 6 hours after administration. To avoid significantly pronounced diuresis, treatment should begin with small doses, gradually moving, if necessary, to higher ones. These drugs are also combined with potassium-sparing diuretics according to the principle described above. With long-term use of diuretics, their effectiveness may decrease or even cease over time. This applies to diuretic and natriuretic effects. With long-term use of diuretics, the following unfavorable disorders of electrolyte and water metabolism develop: hyponatremia, hypochloremia and hypokalemia. Clinically, this is manifested by severe muscle weakness, convulsions, and arrhythmia. You should take a break from treatment with diuretics and administer sodium, chlorine, and potassium salts.

The treatment complex for CHF includes substances that do not act directly on the heart muscle and improve hemodynamics indirectly by influencing peripheral arterial and venous tone - peripheral vasodilators.

All peripheral vasodilators Based on the localization of the predominant action, they can be divided into 3 groups:

1) acting on venous tone (nitroglycerin, long-acting nitrates);

2) acting on the tone of arterioles (apressin, phentolamine);

3) acting simultaneously on the tone of peripheral veins and arterioles (sodium nitroprusside, prazosin).

When using vasodilators, there may be complications in the form of a sharp decrease in blood pressure. This is usually caused by an overdose of the drug. The dose of vasodilators should be selected individually and their administration should be carried out under blood pressure control. Nitrosorbide is prescribed in tablets 30 - 40 mg per dose every 5 hours (180 - 200 mg / day). To get rid of the development of tolerance, the drug must be used in courses of two weeks with breaks for two weeks. If nitrates are poorly tolerated, molsidomine (Corvaton) is used in a daily dose of 24 - 32 mg. Since intravenous administration of sodium nitroprusside requires monitoring, it should not be used on an outpatient basis. It is better to prescribe apressin in combination with nitrosorbide.

In recent years, captopril and other angiotensin-converting enzyme inhibitors have been included in the complex of therapeutic measures. This group of drugs affects the renin-angiotensin-aldosterone system, inhibiting the conversion of angiotensin I to angiotensin II. This achieves a vasodilating and hypotensive effect. Under the influence of captopril, cardiac output increases and affects the kinin and prostaglandin systems. For the treatment of CHF, small doses of the drug are recommended (no more than 100 - 150 mg/day), at which side effects are less pronounced (lowering blood pressure, leukopenia, loss of taste, hyperkalemia, skin rashes).

Calcium antagonists are also used as vasodilators: verapamil (isoptin), nifedipine (Corinfar). To reduce the tone of the sympathoadrenal system, it is prescribed b- adrenergic blockers (anaprilin, obzidan, etc.).

In complex therapy of CHF, metabolically active drugs (riboxin, inosine, etc.) are used, although their effect is controversial.

Spa treatment indicated for stages I and IIA of CHF in cardiological sanatoriums or local sanatoriums.

Work ability examination. In stage 1 CHF, patients’ ability to work is preserved, but heavy physical labor is contraindicated. At stage IIA, patients have limited ability to work. With CB stage CHF, the ability to work is completely lost (disability group II). At stage III, patients need constant care, being disabled people of group I.

Prevention of CHF includes three aspects:

1) primary prevention of diseases leading to the development of heart failure (meaning primary prevention of rheumatism, hypertronic disease, coronary disease, etc.);

2) prevention of the development of CHF in case of existing heart diseases (heart disease, hypertension, coronary disease);

3) prevention of repeated decompensations in case of already developing heart failure.

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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

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.

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.

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 to 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.