Chronic heart failure. Pathogenesis. Chronic heart failure Myocardial form of heart failure

Chronic heart failure (CHF)- a syndrome of various CVS 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 of the elderly; five-year survival rate of patients with CHF: less than 50%; in the case of severe CHF, half of the patients die within the first year; CHF reduces the quality of life by 80%.

Etiology of CHF:

1. Myocardial damage:

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

b) secondary myocardial insufficiency (postinfarction cardiosclerosis, specific cardiomyopathies: metabolic, with systemic connective tissue diseases, alcohol, toxic-allergic, etc.)

2. Hemodynamic myocardial overload:

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

b) overload with increased filling of the chambers of the heart (volume overload): heart valve insufficiency, CHD with blood shunt from left to right (VSD, etc.)

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

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

4. Increasing the metabolic needs of tissues(HF with high minute volume): anemia, thyrotoxicosis.

CHF pathogenesis.

1. The main trigger mechanism for CHF is decrease in myocardial contractility and a drop in cardiac output, which causes a decrease in 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 equalize reduced cardiac output to normal (compensatory response). However, further activation of the sympathetic-adrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens the filling of the heart in diastole, and other decompensation reactions).

3. Spasm of renal arterioles + hypoperfusion of the kidneys against the background of 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 BCC, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilation and damage to the heart (decompensation).

4. An important role in the development of CHF also belongs to endothelial vascular dysfunction (decrease in the production of endothelial vasorelaxant 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 ).

CHF 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 the clinical variant: left ventricular, right ventricular, biventricular (total)

4. According to the value of cardiac output: low cardiac output, high cardiac output

The severity of CHF.

1. According to Vasilenko-Strazhesko:

I stage (initial)- latent heart failure, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).

Stage II (expressed)– severe disorders of hemodynamics, organ function and metabolism

­ IIA- moderately pronounced signs of heart failure with hemodynamic disturbances in only one circle

IIB- strongly pronounced signs of heart failure with hemodynamic disturbances in a large and small circle

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 disability.

2. According to NYHA:

I class(lack of restrictions on physical activity) - ordinary (habitual) physical activity does not cause severe fatigue, shortness of breath or palpitations (but there is heart disease!); distance of a 6-minute walk 426-550 m.

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

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

IV class(complete limitation of physical activity) - the inability to perform any physical activity without deterioration of health; HF symptoms are present even at rest and are aggravated by 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 frequent and early symptom of CHF, at first it appears only during physical exertion, 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 a decrease in muscle perfusion and their oxygen starvation); weight loss (due to TNF-a activation and development of malabsorption syndrome)

Palpitations (more often due to sinus tachycardia) - initially disturb 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 pronounced 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 exercise (due to venous congestion in the lungs, swelling of the bronchial mucosa and irritation of cough receptors); in severe cases, there may be a wet cough with a large amount of frothy, 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 edema disappears; as CHF progresses, edema becomes widespread, localized not only in the feet, ankles, legs, but also in the thighs, scrotum, anterior abdominal wall, in the lumbar region; extreme degree of edematous syndrome - anasarca - massive, widespread edema with ascites and hydrothorax

Violation of the separation of urine (oliguria, nocturia - the predominance of nighttime diuresis over daytime)

Pain, a feeling of heaviness and fullness in the right hypochondrium - appear with an increase in the liver, due to stretching of the Glisson capsule

2. Objectively:

a) inspection:

Forced sitting or semi-sitting position of patients with legs down or horizontal position with a high headboard

Acrocyanosis of the skin and visible mucous membranes, most pronounced in the distal parts of the extremities, on the lips, tip of the nose, auricles, subungual spaces, is accompanied by cooling of the skin of the extremities, trophic disorders of the skin (dryness, peeling) and nails (brittleness, dullness) (due to a decrease in perfusion of peripheral tissues, increased oxygen extraction by tissues and an increase in reduced hemoglobin)

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

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

A positive symptom of Plesh (hepato-jugular test) - with calm breathing of the patient, pressure is made with the palm of the hand on the enlarged liver, which causes increased swelling of the jugular veins

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

b) physical examination:

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

2) cardiovascular system: the pulse is quickened, small filling and tension, often arrhythmic; BP is reduced (SBP is greater than DBP); palpation apical impulse spilled, shifted to the left and down; percussion borders of the heart expanded to the left; auscultatory 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 a large stagnation - systolic pulsation (bulging in systole and decreasing in diastole); ascites

Diagnosis of CHF.

1. ECG: signs of left ventricular hypertrophy: an increase in the R wave V5,V6, I, aVL, signs of blockade of the left leg of the His bundle, an increase in the interval of internal deviation (from the beginning of the Q wave to the top 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 ; rightgram; shift of the transition zone in V 4 /V 5 ; complete / incomplete blockade of the right leg of the bundle of His; 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 biphasic 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 the vessels (a sign of increased pressure in the pulmonary veins); Kerley lines (due to the presence of fluid in the interlobar fissures and the expansion of the lymphatic vessels of the lungs); signs of alveolar pulmonary edema (shadow spreading from the roots of the lungs), effusion in the pleural cavity, cardiomegaly, etc.

3. Echocardiography(including with 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 heart cavities, ventriculography - more often to resolve the issue of surgical treatment).

5. Laboratory data non-specific: KLA - there may be signs of anemia (due to reduced appetite of patients, impaired absorption of iron); OAM - proteinuria, cylindruria (as a manifestation of "stagnant kidney"); BAK - a decrease in total protein, albumin, prothrombin, an increase in bilirubin, ALT and AST, GGTP, LDH (impaired liver function); fluctuations in electrolytes (the result of pathogenetic processes in HF and ongoing diuretic therapy); increased levels of creatinine and urea ("congestive kidney"), etc.

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Chronic heart failure (CHF) is a syndrome of various CVD 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 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 the case of severe CHF, half of the patients die within the first year; CHF reduces the quality of life by 80%.
Etiology of CHF:
1. Myocardial damage:
a) primary myocardial insufficiency (myocarditis, idiopathic dilated cardiomyopathy)
b) secondary myocardial insufficiency (postinfarction cardiosclerosis, specific cardiomyopathies: metabolic, with systemic connective tissue diseases, alcohol, toxic-allergic, etc.)
2. Hemodynamic myocardial overload:
a) overload due to increased resistance to ejection (pressure overload): hypertension, pulmonary hypertension, aortic stenosis, pulmonary artery stenosis
b) overload with increased filling of the chambers of the heart (volume overload): heart valve insufficiency, CHD with blood shunt from left to right (VSD, etc.)
c) combined overload (by volume and pressure): combined heart defects
3. Violation of diastolic filling of the ventricles: stenosis of the left or right atrioventricular orifice, exudative and constrictive pericarditis, restrictive cardiomyopathy)
4. Increased metabolic needs of tissues (HF with high minute volume): anemia, thyrotoxicosis.
CHF pathogenesis.
1. The main trigger of CHF is a decrease in myocardial contractility and a drop in cardiac output, which causes a decrease in 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 equalize reduced cardiac output to normal (compensatory response). However, further activation of the sympathetic-adrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens the filling of the heart in diastole, and other decompensation reactions).
3. Spasm of renal arterioles + hypoperfusion of the kidneys against the background of CHF  RAAS activation  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 BCC, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilation and damage to the heart (decompensation).
4. An important role in the development of CHF also belongs to endothelial vascular dysfunction (decrease in the production of endothelial vasorelaxant factor), hyperproduction of a number of cytokines: IL, TNF- (impairs the transport of calcium ions into cells, inhibits PVK dehydrogenase, leading to ATP deficiency, triggers apoptosis of cardiomyocytes ).
CHF 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 the clinical variant: left ventricular, right ventricular, biventricular (total)
4. According to the value of cardiac output: with low cardiac output, with high cardiac output
The severity of CHF.
1. According to Vasilenko-Strazhesko:
Stage I (initial) - latent HF, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).
II stage (expressed) - expressed violations of hemodynamics, organ function and metabolism
¬IIA - moderately pronounced signs of heart failure with hemodynamic disturbances in only one circle
IIB - strongly pronounced signs of heart failure with hemodynamic disturbances in a large and small circle
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 disability.
2. According to NYHA:
Class I (no restrictions on physical activity) - normal (habitual) physical activity does not cause severe fatigue, shortness of breath or palpitations (but there is heart disease!); distance of a 6-minute walk 426-550 m.
Class II (mild, slight limitation of physical activity) - satisfactory state of health at rest, but habitual physical activity causes fatigue, palpitations, shortness of breath or pain; distance of a 6-minute walk 301-425 m.
Class III (pronounced, noticeable limitation of physical activity) - satisfactory state of health at rest, but the load is less than usual leads to the appearance of symptoms; 6-minute walk distance 151-300 m.
Class IV (complete limitation of physical activity) - the inability to perform any physical activity without deterioration of health; HF symptoms are present even at rest and are aggravated by 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:
- shortness of breath - the most frequent and early symptom of CHF, initially appears only during physical exertion, 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 a decrease in muscle perfusion and their oxygen starvation); weight loss (due to the activation of TNF-α and the development of malabsorption syndrome)
- palpitations (more often due to sinus tachycardia) - at first they disturb 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 pronounced 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 exercise (due to venous congestion in the lungs, swelling of the bronchial mucosa and irritation of cough receptors); in severe cases, there may be a wet cough with a large amount of frothy, 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 edema disappears; as CHF progresses, edema becomes widespread, localized not only in the feet, ankles, legs, but also in the thighs, scrotum, anterior abdominal wall, in the lumbar region; extreme degree of edematous syndrome - anasarca - massive, widespread edema with ascites and hydrothorax
- violation of urine separation (oliguria, nocturia - the predominance of nighttime diuresis over daytime)
- pain, feeling of heaviness and fullness in the right hypochondrium - appear with an increase in the liver, due to stretching of the Glisson capsule
2. Objectively:
a) inspection:
- forced sitting or semi-sitting position of patients with their legs down or a horizontal position with a high headboard
- acrocyanosis of the skin and visible mucous membranes, most pronounced in the distal parts of the extremities, on the lips, tip of the nose, auricles, subungual spaces, accompanied by cooling of the skin of the extremities, trophic disorders of the skin (dryness, peeling) and nails (brittleness, dullness) (due to decrease in perfusion of peripheral tissues, enhanced extraction of oxygen by tissues and an increase in reduced hemoglobin)
- peripheral edema (up to ascites and hydrothorax): located symmetrically, leaving a deep hole after pressing with a finger, which then gradually smoothes out; the skin in the area of ​​edema is smooth, shiny, initially soft, and with prolonged edema it becomes dense; blisters may form at the site of edema, which open and fluid flows out of them, foci of necrosis, skin tears
- swelling and pulsation of the cervical veins (with the development of right ventricular failure)
- a positive symptom of Plesha (hepato-jugular test) - with calm breathing of the patient, pressure is made with the palm of the hand on the enlarged liver, which causes increased swelling of the jugular veins
- atrophy of skeletal muscles (biceps, thenar and hypothenar muscles, temporal and masticatory muscles), weight loss, a pronounced decrease in subcutaneous fat ("cardiac cachexia").
b) physical examination:
1) respiratory organs: inspiratory tachypnea; percussion: dullness behind in the lower parts of the lungs; auscultatory: crepitus and moist small bubbling rales against the background of hard or weakened vesicular breathing in the lower parts
2) cardiovascular system: the pulse is quickened, low filling and tension, often arrhythmic; BP is reduced (SBP is greater than DBP); palpation apical impulse spilled, shifted to the left and down; percussion borders of the heart expanded to the left; auscultatory 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 a large stagnation - systolic pulsation (bulging in systole and decreasing in diastole); ascites
Diagnosis of CHF.
1. ECG: signs of left ventricular hypertrophy: an increase in the RV5, V6, I, aVL wave, signs of blockade of the left leg of the His bundle, an increase in the interval of internal deviation (from the beginning of the Q wave to the top of the R wave) J> 0.05 sec in V5, V6 , levogram, shift of the transition zone in V1/V2, right ventricular hypertrophy: increase in RIII, aVF, V1, V2; rightgram; shift of the transition zone in V4/V5; complete / incomplete blockade of the right leg of the bundle of His; increase in the interval of internal deviation J>0.03 sec in V1, V2; shift of the ST interval below the isoline, inversion or biphasic T wave in III, aVF, V1, V2, various arrhythmias, etc.
2. X-ray of the chest organs: redistribution of blood flow in favor of the upper lobes of the lungs and an increase in the diameter of the vessels (a sign of increased pressure in the pulmonary veins); Kerley lines (due to the presence of fluid in the interlobar fissures and the expansion of the lymphatic vessels of the lungs); signs of alveolar pulmonary edema (shadow spreading from the roots of the lungs), effusion in the pleural cavity, cardiomegaly, etc.
3. Echocardiography (including with 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 heart cavities, ventriculography - more often to resolve the issue of surgical treatment).
5. Laboratory data are non-specific: KLA - there may be signs of anemia (due to reduced appetite of patients, impaired absorption of iron); OAM - proteinuria, cylindruria (as a manifestation of "stagnant kidney"); BAK - a decrease in total protein, albumin, prothrombin, an increase in bilirubin, ALT and AST, GGTP, LDH (impaired liver function); fluctuations in electrolytes (the result of pathogenetic processes in HF and ongoing diuretic therapy); increased levels of creatinine and urea ("congestive kidney"), etc.
The goals of treatment of patients with CHF: 1) elimination of symptoms of the disease (shortness of breath, palpitations, increased fatigue, fluid retention in the body); 2) slowing down the progression of the disease by protecting target organs (heart, kidneys, brain, blood vessels, muscles); 3) improving the quality of life 4) reducing the number of hospitalizations; 5) prolongation of the patient's life.
1. General activities:
- exclusion of alcohol consumption (because ethanol retains water and is a powerful inducer of apoptosis)
- weight loss in obese patients
- correction of hypertension, hyperlipidemia and diabetes
- restriction of salt and liquid intake (up to 1-1.5 l / day)
- daily weighing to detect hidden edema
- regular moderate exercise (walking is best)
- avoid taking PAS (cardiodepressive effect), most calcium antagonists (verapamil - cardiodepressive effect, dihydropyridines - activation of the SNS), NSAIDs (retain fluid, increase blood pressure, reduce the activity of ACE inhibitors and β-AB).
2. Drug therapy for CHF:
a) the main drugs - 5 groups, the effectiveness has been reliably proven:
1) ACE inhibitors - drugs No. 1 in the treatment of CHF; improve the clinical course of the disease, reduce the risk of death, slow down the progression of the disease and the onset of decompensation.
Principles for the appointment of ACE inhibitors:
- Do not prescribe if the initial blood pressure is less than 90 mm Hg. Art. (with initial hypotension, stabilization of blood pressure is necessary before prescribing an ACE inhibitor: semi-bed rest, small doses of corticosteroids, digoxin 0.25 mg orally or intravenously and / or dopamine 2-5 mcg / kg / min, albumin / in)
- avoid concomitant use of β-blockers and vasodilators
- before using ACE inhibitors, avoid large diuresis and excessive dehydration of the patient
- ACE inhibitor dosing should be started with very low doses and very slow titers, the first dose at night
More commonly used: enalapril (starting dose 2.5 mg X 1 time / day, optimal 10 mg X 2 times / day, maximum 40 mg / day).
2) β-adrenergic blockers (BABs) - with long-term administration, they reduce the risk of decompensation and significantly prolong the life of patients (more than ACE inhibitors!), lead to an increase in EF and pumping function of the heart, inhibit and cause regression of pathological myocardial remodeling, reduce electrical instability, indirectly reduce the activity of the RAAS.
NB! The biphasic effect of β-blockers on the myocardium in patients with CHF is characteristic: in the first 2 weeks of treatment, CO may decrease and the course of CHF even worsens somewhat, then, as a result of a decrease in tachycardia and oxygen consumption by the myocardium, hibernated (sleeping) cardiomyocytes restore their activity and CO begins to grow.
Requirements for β-AB therapy:
- you can not start if the patient has an unstable condition (if the introduction of diuretics, drugs with inotropic action is required)
- the starting period of therapy should take from 2 to 6 weeks, it should start with small doses (1/8 of the treatment), titrating daily doses
- appointed for life and better in addition to ACE inhibitors
Use: metoprolol-SR (initial dose 5-12.5 mg / day, optimal - up to 100 mg / day); bisoprolol (initial dose 1.25 mg/day, optimal - up to 10 mg/day); carvedilol (initial dose - 3.125 mg / day, optimal - up to 50 mg / day - the most optimal, is a non-cardioselective -1-blocker, antioxidant)
3) diuretics - are indicated only for clinical signs and symptoms of fluid retention in the body (i.e. with congestive heart failure) mainly together with ACE inhibitors; the criterion for a sufficient dose is a decrease in body weight by 0.5-1 kg / day; loop diuretics increase sodium excretion by 20-25% and free water excretion, thiazide diuretics increase sodium excretion by 5-10%, do not increase free water clearance.
Use: thiazide diuretics (hydrochlorothiazide orally in the morning 25-75 mg), with insufficient effectiveness - loop diuretics (furosemide orally in the morning 20-500 mg)
4) cardiac glycosides (only digoxin 0.125 mg 1-2 times / day) - indicated in the presence of atrial fibrillation, in sinus rhythm - the fourth drug (after ACE inhibitors, BAB, diuretics); the use in patients with sinus rhythms in low doses does not improve the prognosis and does not slow down the progression of CHF, but improves the quality of life; it is inappropriate to prescribe in patients with heart failure in violation of diastolic filling of the left ventricle, heart failure with high ejection, cor pulmonale.
5) oral spironolactone 25-50 mg once in the morning or in 2 doses in the morning - reduces the risk of overall mortality by 30%, is used
b) additional drugs - drugs, the effectiveness and safety of which require clarification:
1) ATII antagonists - used for intolerance to ACE inhibitors (valsartan orally at an initial dose of 40 mg 2 times / day, gradually increasing to a maximum of 160 mg 2 times / day, losartan, irbesartan)
2) cardioprotectors - used in short courses to enhance the contractility of the heart (mildronate - limits the transport of long-chain fatty acids through the mitochondrial membranes, while short-chain fatty acids can freely penetrate and oxidize; trimetazidine / preductal inside 20 mg 3 times / day - inhibits beta in mitochondria -oxidation of all fatty acids, which contributes to the accumulation of activated fatty acids in mitochondria).
c) auxiliary drugs:
1) peripheral vasodilators (nitrates) - only with concomitant angina pectoris and pulmonary edema
2) calcium channel blockers (only amlodipine) - "on top" on ACE inhibitors with severe valvular regurgitation, high arterial and / or pulmonary hypertension
3) antiarrhythmics (only group III) - only for life-threatening arrhythmias
4) GCS (prednisolone, methylprednisolone) - with persistent hypotension and as a "treatment of despair" with the ineffectiveness of other drugs
5) non-glycoside inotropic stimulants (dopamine, dobutamine) - short courses during exacerbation and CHF with persistent hypotension
6) acetylsalicylic acid - used by patients after myocardial infarction
7) indirect anticoagulants (only warfarin) - with dilatation of the heart, intracardiac thrombus, atrial fibrillation, after operations on the heart valves.

a pathophysiological condition in which the heart cannot pump as much blood as it needs to metabolize tissues.

Etiology.

1) Volume overload (valvular insufficiency)

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

3) Myocardial damage (IHD, myocarditis, myocardiopathy, myocardial dystrophy, etc.).

In the general population, 87% of CHF cases are due to coronary artery disease and/or arterial hypertension.

CHF pathogenesis.

At the moment, the dominant value of activation has been proven neurohumoral systems(in response to a decrease in cardiac output) in the pathogenesis of heart failure. The leading role 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 HF.

CHF classification:

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

II A stage - decompensation mainly 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 dystrophic changes in the internal organs with severe hemodynamic disturbances.

Functional classes of CHF

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

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

Class III: Marked limitation of physical activity: at rest, there are no symptoms, physical activity of less intensity compared to habitual loads is accompanied by the appearance of symptoms.

IV FC: Inability to perform any physical activity without the appearance of 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.

1. 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. Passive increase in pressure in the left atrium and pulmonary artery leads to signs of circulatory failure in the pulmonary circulation. Pulmonary hypertension increases right ventricular afterload and leads to right ventricular failure.
2. Systolic heart failure. It develops with a decrease in the LV ejection fraction of less than 40%.

Clinic.

1. Syndrome of left ventricular failure: shortness of breath, asthma attacks, cough, hemoptysis, orthopnea, palpitations.
2. Right ventricular failure syndrome: hepatomegaly, edema, ascites, hepato-gular reflux (swelling of the neck veins with pressure on the right hypochondrium), oliguria.
3. 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, lower legs) up to the development of trophic ulcers, cardiac cachexia.

Diagnosis of CHF.

Instrumental diagnosis of CHF.

1. ECG.

Pathological tooth Q indicates a previous myocardial infarction, changes in the ST segment and tooth

T for myocardial ischemia. Signs of left ventricular hypertrophy suggest 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 leg of the His bundle and signs of right ventricular hypertrophy are characteristic of CHF caused by cor pulmonale, mitral stenosis.

1. Chest x-ray allows diagnosing dilatation of the heart and its individual chambers, as well as signs of venous congestion. HF is also characterized by an indistinct basal pulmonary pattern, redistribution of blood flow, left atrial enlargement, and bilateral pleural effusion. The absence of radiological signs does not rule out pulmonary congestion.
2. EchoCG. Allows to distinguish between systolic and diastolic dysfunction of the left ventricle, to identify

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

Treatment:

1) ACE inhibitors - angiotensin converting enzyme inhibitors- is a tissue hormonal system that is involved in the formation of fibrous tissue. ACE inhibitors consequently reduce the proliferation of fibroblasts and the development of fibrosis. Because prolonged elevations in angiotensin levels II and aldosterone in the blood plasma is accompanied by necrosis of cardiomyocytes, then ACE inhibitors and aldosterone antagonists can give an additional cardioprotective effect. Prevention of 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 ventricular stiffness.

Captopril - 6.25 mg 3 times a day

Enalapril - 2.5 mg 2 times a day

Lisinopril — 2.5 mg once a 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 the data available to date, ARAs are recommended when it is not possible to use an ACE inhibitor (for example, cough when using an ACE inhibitor).

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, depending on the clinical response, until the optimal dose is selected.

4) Aldosterone receptor antagonist.

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

5) Diuretics.

Removal of 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.

The monograph presents a new scientific concept of the study of the heart and blood vessels as a system built on the principle of the golden ratio. The structure of the heart is based on affine symmetry, and the basis of its functional activity is the symmetry of transformations. In healthy people, there is a harmony in the functioning of the heart and blood vessels, in patients with chronic heart failure, it is disturbed. Methods for diagnosing acute and chronic heart failure and its severity based on the relationship between temporal and volumetric indicators of the work of the heart are proposed. They allow you to monitor the dynamics of the course of the syndrome and the effectiveness of the treatment. An important place in the monograph is given to the principles and methods of treatment of patients with chronic heart failure and drugs used in this pathology. The publication is intended for cardiologists, internists and general practitioners.

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by the LitRes company.

PATHOGENESIS OF CHRONIC HEART FAILURE

As already discussed in the previous chapter, diseases of the cardiovascular system are considered to be the cause of the development of CHF. It sounds at least strange. According to this formulation, the disease is the cause of the development of its sign (syndrome), and not he - its manifestation. The cause of the development of CHF is a violation of the contractile function of the heart, and it is associated with systolic and diastolic dysfunction (Meyerson F. Z., 1978; Sonnenblick E. H., Downing S. E., 1963). This condition develops in patients with pathology of various structures of the heart. Therefore, the mechanism of violation of the pumping function of the heart in various diseases may be different. In some cases, primary damage to cardiomyocytes (myocardial insufficiency) occurs (A. G. Obrezan, 2007; A. G. Obrezan, I. V. Vologdina, 2002). This is observed in the following diseases:

- acute myocardial infarction;

- cardiac ischemia;

- postinfarction cardiosclerosis;

- myocarditis;

– primary cardiomyopathy;

- secondary cardiomyopathies (myocardial dystrophy).

In other cases, a violation of the contractile function of the myocardium is due to a change in intracardiac hemodynamics or an increase in the total peripheral vascular resistance, which entails an increased load on the myocardium. This picture occurs when:

- congenital and acquired heart defects;

- arterial hypertension;

– primary and secondary pulmonary hypertension;

- an increase in the volume of circulating blood.

Much less often, a violation of the propulsive activity of the heart is associated with mechanical factors, as in the following diseases:

- constrictive pericarditis and cardiac tamponade;

- amyloidosis and myocardial fibroelastosis.

Regardless of what underlies this or that disease - direct damage to the myocardium, pressure and / or volume overload, mechanical factors - this leads to a decrease in the contractile function of the heart, to a violation of CO, resulting in a decrease in blood supply to organs and tissues. The pathogenesis of CHF includes morphological disorders of the heart and blood vessels caused by the underlying disease, prolonged increased load (with arterial hypertension, the total peripheral vascular resistance increases) and a cascade of sequentially activated compensatory mechanisms, i.e. changes in the regulation of the state of the cardiovascular system.

The determining moment in the occurrence of CHF will be those morphological changes in the heart that are characteristic of cardiovascular diseases. No heart damage - no heart failure. This is an axiom.

It is well known that any disease is based on structural damage to the organ. This leads to a violation of its functions, which manifests itself in the signs of the disease. One of the signs of heart damage is heart failure.

However, the onset of symptoms does not always coincide with structural failure; it is usually delayed. This is because genetically determined and adaptive compensation mechanisms are triggered. They provide restoration of partially damaged or modification of the remaining intact structures of the affected organ and are aimed at restoring impaired functions. Regardless of the causes of diseases of the cardiovascular system, activation of a number of compensatory mechanisms aimed at maintaining cardiac activity, blood pressure and the necessary perfusion of organs and tissues is observed.

Apparently, one of the first manifestations of compensation is the regeneration of tissues with high mitotic activity or organ hypertrophy due to hyperplasia of the organelles of those cells that do not have mitotic activity (Meyerson F.Z., 1978; Sarkisov D.S., 1987). Cardiomyocytes, according to most researchers, are not able to divide, and therefore can only hypertrophy due to an increase in the number of mitochondria and other organelles. However, some authors admit the possibility of division of these cells and even the presence of stem cells in the myocardium. Myocardial hypertrophy is the main mechanism for compensating the activity of the heart. It helps to maintain the force of contraction of the heart and general hemodynamics.

The launch of such compensatory reactions is due to the activation of the gene apparatus of intact cells of the affected organ. If the tissue has a low mitotic activity, then this is manifested by an increase in the synthesis of RNA (ribonucleic acid) at some loci of DNA (deoxyribonucleic acid) and hypertrophy of cells and the organ as a whole. This fully applies to the muscle tissue of the heart. In organs with high mitotic activity, tissue regeneration is enhanced by cell DNA replication followed by division.

The material basis of the compensatory reactions of the affected heart is hyperplasia (an increase in the number of structures) or an increase in the mass of intracellular components in each cell. The compensatory process involves not only the damaged organ, but also other organs and systems that perform functions similar to it (Sarkisov D.S., 1987).

Regardless of what reasons caused the change in structures, the response (compensatory) reaction to this damage will be of the same type. The exact same reaction will follow with prolonged increased physical exertion, as well as loads associated with an increase in resistance to blood flow in the vessels, which is accompanied by an increase in blood pressure.

In medicine, unfortunately, there is no clear distinction between such concepts as "adaptation" and "compensation". Often one concept is replaced by another, and even more often the term "adaptive-compensatory reactions" or "mechanisms" is used. This can be explained by the fact that the modification of structures that occurs after damage to an organ (in particular, the heart) or is associated with a change in individual environmental factors is carried out in the same way, namely, by activating certain genes, increasing the production of RNA and protein (Khlebovich V V., 1991). However, there is still a difference between adaptation and compensation.

The meaning of the term "adaptation" used in medicine does not quite correspond to the biological understanding of this process. When individual elements of the environment change in the body, certain organs and their functions are modified to meet the conditions of the changed environment. This process is called adaptive, or phenotypic, modification and is a morphofunctional response of the body to changes in external factors, including prolonged increased physical activity (Grant V., 1991; Shmalgauzen I.I., 1982). In the medical literature, this process is called adaptation in the broad sense of the word. Adaptation (adaptation) is considered as the process of adapting a person to changing environmental conditions. It turns out to be a tautology. Compensation is an adaptive response to damage to body structures, which consists in compensating the functions of a damaged organ by modifying its undamaged tissues or other organs. Compensation is the result of genotypic (phylogenetic) adaptation. Therefore, it is stylistically incorrect to call these reactions compensatory-adaptive. If they had not been developed in the process of genotypic adaptation, then the life expectancy of living organisms would have sharply decreased. Any damage, disease of the body would lead to their rapid death.

When heart structures are damaged, it is precisely compensatory reactions and mechanisms that develop to maintain the pumping function of the heart. Myocardial hypertrophy, which occurs in patients with damage to the structures of the heart and is caused by increased load, is caused by a violation of intracardiac and / or vascular hemodynamics. The term "adaptation", proposed by F. Z. Meyerson (1978) to explain changes in the structures of the heart during its load and diseases, is not entirely successful. It does not accurately reflect the essence of the ongoing processes.

There can be no adaptation of the body to the disease, since the disease is a process of maladaptation. In this case, we can only talk about compensation for impaired functions of the body, and not adaptation to the pathological process that has developed in the human body.

After this remark, we return to the pathogenesis of CHF. The study of CHF should be based not so much on “risk factors”, largely conjectural, but on an accurate understanding of the mechanisms of the formation and development of pathological processes (Sarkisov D.S., 2000). To understand the mechanism of the occurrence of CHF, it is necessary to clearly understand the stages of the processes that lead the body to this state.

When the heart structures are damaged or overloaded with resistance to the expulsion of blood from the heart, a cascade of compensatory reactions occurs. The so-called compensatory modification of the heart develops. One of the early manifestations of compensatory reactions in the main diseases of the circulatory system is cardiac hypertrophy. This process occurs immediately after damage to the structures of the heart or exposure to increased stress. In experiments on animals, it was found that already 5-6 days after damage to the structures of the heart or increased physical activity, hyperplasia of cell organelles and hypertrophy of myocardial muscle fibers are clearly detected (Meyerson F.Z., 1978). The mass of the organ increases not due to an increase in the number of cells, but due to their hypertrophy. The experiment shows that if this process is artificially slowed down, then the life expectancy of sick animals will decrease significantly.

This is supported by biochemical data. It has been shown that suppression of RNA synthesis on structural genes by actinomycin D completely prevents the synthesis of nucleic acids and the development of myocardial hypertrophy, which leads to rapid death of animals from HF. Due to hypertrophy, the heart muscle is capable, within certain limits, of performing a greater amount of work for a long time and without signs of obvious insufficiency than a non-hypertrophied damaged muscle.

The meaning of such compensation is to maintain the force of contraction of the ventricles. The main consequence of cardiac hypertrophy is that the increase in organ function is distributed in its increased mass.

With myocardial hypertrophy, the force per unit area of ​​the cross-sectional area of ​​the heart wall remains practically unchanged. Thus, by increasing the mass of the myocardium, the contractile function of the affected heart is maintained. Thanks to this mechanism, the heart can provide the level of functioning necessary for the body for a long time. Unfortunately, myocardial hypertrophy cannot continue indefinitely. This process continues until all structures capable of hypertrophy are involved.

The increase in heart mass even in patients with initially intact myocardium under pressure load (hypertension) has its limits. The thickness of the wall of the ventricle can increase by 1.5 - 2 times, i.e., the process of hypertrophy is not unlimited. As soon as the maximum of hypertrophy is reached, there is an elongation of muscle fibers and a sharp dilatation of the heart cavities, the death of cardiomyocytes is accelerated, and connective tissue develops in their place.

To maintain vascular tone and blood pressure with reduced CO, activation of the SAS occurs - the second mechanism for compensating cardiac activity. It is manifested by tachycardia, aimed at replenishing the value of the minute volume of blood circulation. According to G. F. Lang (1958), increased heart rate is an appropriate compensation mechanism. Catecholamines enhance the function of the cardiovascular system by accelerating metabolic processes, maintain vascular tone and blood pressure at the proper level, and carry out venous vasoconstriction, which increases venous return of blood to the heart (Anthony G., 1986).

The inotropic effect of catecholamines is manifested by an increase in the force of contraction and the rate of relaxation of the ventricles. At this time, the heart works like a healthy person during exercise. There is a decrease in ESV and EDV, due to the influence of the sympathetic nervous system. As a result, myocardial contractility increases regardless of the initial stretching of the heart muscle. Such a restructuring allows, with the same BWW, to eject blood against a higher pressure, to maintain or increase the stroke volume due to the CSR. We noted similar changes in patients with CHF I FC.

In this category of patients, a clear decrease in ESV and, to a lesser extent, EDV were revealed with normal indicators of VR, i.e., their heart works, as it were, in a mode of increased load. Activation of the CAS has not only a positive inotropic, but also a positive chronotropic effect on the heart and thus supports CO and peripheral hemodynamics. With an increase in heart rate and a decrease in the duration of the cardiac cycle, diastole is shortened first of all. However, the filling of the ventricles suffers little, since the bulk of the blood enters at the beginning of diastole. Under the influence of the sympathetic nervous system, the rate of their relaxation clearly increases due to the positive chronotropic effect.

In the middle of the twentieth century. it was found that an increase in contraction force can be caused by the influence of the amplifying nerve of the heart, discovered by I. P. Pavlov, by influencing myocardial metabolism (Raiskina M. E., 1955). With the help of radioactive research methods, an increase in the intensity of the exchange of high-energy phosphorus compounds in the heart was revealed.

End of introductory segment.

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The following excerpt from the book Chronic heart failure (pathogenesis, clinic, diagnosis, treatment) (Yu. S. Malov, 2013) provided by our book partner -

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 myocardial overload:
3. Violation of diastolic filling of the ventricles: stenosis of the left or right atrioventricular orifice, exudative and constrictive pericarditis, restrictive cardiomyopathy)
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 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 equalize reduced cardiac output to normal (compensatory response). However, further activation of the sympathetic-adrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens the filling of the heart in diastole, and other decompensation reactions).
3. Spasm of renal arterioles + hypoperfusion of the kidneys against the background of 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 BCC, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilation and damage to the heart (decompensation).
4. An important role in the development of CHF also belongs to endothelial vascular dysfunction (decrease in the production of endothelial vasorelaxant 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 the clinical variant: left ventricular, right ventricular, biventricular (total)
4. According to the value of cardiac output: with low cardiac output, with high cardiac output
The severity of CHF.
1. According to Vasilenko-Strazhesko:
Stage I (initial) - latent HF, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).
II stage (expressed) - expressed violations of hemodynamics, organ function and metabolism
IIA - moderately pronounced signs of heart failure with hemodynamic disturbances in only one circle
IIB - strongly pronounced signs of heart failure with hemodynamic disturbances in a large and small circle
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 disability.
I FC. The patient does not experience restrictions in physical activity. Ordinary 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 the performance of ordinary physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.