Heart failure: signs, symptoms, diagnosis, treatment in Lyubertsy

Chronic heart failure (CHF) is a disease characterized by the inability of the heart to pump a certain volume of blood sufficient to provide the body with oxygen. CHF can be caused by many diseases of the cardiovascular system, the most common of which include coronary heart disease, hypertension, endocarditis and rheumatoid heart defects. Weakening of the heart muscle leads to the impossibility of normal pumping of blood, as a result of which the amount of blood released into the vessels gradually decreases.

The development of heart failure occurs gradually; in the early stages, the disease can manifest itself only during physical exertion, then it begins to be felt at rest.

The appearance of characteristic symptoms at rest indicates that the disease has entered a severe stage. The progression of chronic heart failure threatens a significant deterioration of the patient’s condition, a decrease in his working capacity and even disability. The development of chronic liver and kidney failure, blood clots, and strokes may occur.

Conducting timely comprehensive diagnostics and competent treatment ensures a slowdown in the development of CHF and the prevention of dangerous complications of this serious disease.

In order to stabilize the condition, a patient diagnosed with “acute and chronic heart failure” must adhere to the correct lifestyle: normalize his weight, follow a low-salt diet, limit physical and emotional stress.

Heart failure

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

Classification of the disease

In ICD 10, chronic heart failure is coded 150, divided into systolic and diastolic forms. This is not the only division of pathology; there are other bases for classification. One of the most common divisions is by stages :

Stage I - primary changes, decreased functionality of the left ventricle of the heart. At this moment, there are still no serious disturbances in blood flow, so symptoms of chronic heart failure do not appear.
Stage II A - blood moves along the bed more slowly and can form areas of stagnation in the pulmonary fields or lower segment of the body.
II B - hemodynamics suffer, affecting both circles of blood circulation at once. This stage is already characterized by noticeable changes in blood vessels and the heart muscle itself. The doctor can identify signs of the disease by recording extraneous whistling in the lungs and swelling of the lower extremities.
Stage III - swelling spreads throughout the body. Now they appear not only in the legs, but also become noticeable in the hips and lumbar area. Fluid can accumulate in the peritoneum and spread throughout the body. At this stage, irreversible changes affect vital organs: the brain, heart, bronchopulmonary system, kidneys and liver.

There is a well-known classification by functional units or classes, which is determined by the general well-being of a sick person in response to physical activity. There are 4 stages of chronic heart failure. At the first stage, activity does not cause major changes. Shortness of breath may occur during intense activities, although in many situations there is no shortness of breath.

The second functional class can be determined by normal well-being during the period of rest and increased heartbeat under light loads. When moving to stage 3, the patient experiences significant limitations in physical activity. And at the 4th stage, loads are practically inaccessible, as they cause acute discomfort. Another popular gradation is the division by zones of heart damage. Thus, experts distinguish between left-, right- and two-ventricular heart failure.

Classification of heart failure

According to the nature of the course, the classification of heart failure involves division into:

spicy;
chronic.

Acute heart failure

According to ICD-10, the code corresponds to I50.9 Heart failure, unspecified. Acute circulatory failure often leads to death (death) in the absence of timely, competent therapy.

Acute heart failure occurs suddenly, minutes or hours after a heart attack, when the body can no longer compensate. Some symptoms include:

severe difficulty breathing and/or coughing;
Gurgling sound when breathing;
Heart rhythm disturbances;
Pallor;
Cold sweat.

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

left type (acute left ventricular or left atrial failure);
acute right ventricular failure.

Chronic heart failure

Chronic heart failure is a consequence of cardiovascular diseases. It develops gradually and progresses slowly. The wall of the heart thickens due to the growth of the muscle layer. The formation of capillaries that supply nutrition to the heart lags behind the growth of muscle mass. The nutrition of the heart muscle is disrupted, and it becomes stiff and less elastic. The heart cannot cope with pumping blood.

CHF according to Vasilenko-Strazhesko (stages 1, 2, 3)

The classification was adopted in 1935 and is still used today with some clarifications and additions. Based on the clinical manifestations of the disease during CHF, three stages are distinguished:

I. Latent circulatory failure without concomitant hemodynamic disorders. Symptoms of hypoxia appear with unusual or prolonged physical activity. Possible shortness of breath, severe fatigue, tachycardia. There are two periods, A and B. Stage Ia is a preclinical variant of the course, in which cardiac dysfunction has almost no effect on the patient’s well-being. Instrumental examination reveals an increase in ejection fraction during physical activity. At stage 1b (latent CHF), circulatory failure manifests itself during physical activity and goes away at rest.
II. In one or both circles of blood circulation, stagnation is expressed that does not go away at rest. Period A (stage 2a, clinically pronounced CHF) is characterized by symptoms of blood stagnation in one of the blood circulation.
III. The final stage of the disease with signs of failure of both ventricles. Against the background of venous stagnation, severe hypoxia of organs and tissues appears in both circulation circles. Multiple organ failure and severe swelling develop, including ascites and hydrothorax. Stage 3a is treatable; with adequate complex therapy for CHF, partial restoration of the functions of the affected organs, stabilization of blood circulation and partial elimination of congestion are possible. Stage IIIb is characterized by irreversible changes in metabolism in the affected tissues, accompanied by structural and functional disorders.

The use of modern drugs and aggressive treatment methods quite often eliminates the symptoms of CHF corresponding to stage 2b to a preclinical state.

How is chronic heart failure classified?

In all cases when heart failure (symptoms and organ disorders) develops slowly, it is said to be chronic. As symptoms increase, this option is divided into stages. So, according to Vasilenko-Strazhesko there are three of them.

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

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

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

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

Depending on the symptoms that appear at different stages of the disease, the severity of the patient, functional classes (types) of heart failure are distinguished:

I – the disease does not have any effect on the patient’s quality of life. Heart failure is stage 1 and does not limit the patient’s physical activity in any way. Stage 1 deficiency responds well to therapy.

II – the patient is not bothered by anything at rest; mild restrictions are recorded during physical activity.

III – there are no symptoms at rest, but there is a noticeable decrease in performance.

IV – chest pain and signs of heart failure are recorded at rest, the patient is partially or completely incapacitated.

Publications in the media

Chronic systolic heart failure is a clinical syndrome that complicates the course of a number of diseases and is characterized by the presence of shortness of breath during exercise (and then at rest), fatigue, peripheral edema and objective signs of impaired cardiac function at rest (for example, auscultatory signs, echocardiographic data) . Statistical data. Chronic systolic heart failure occurs in 0.4–2% of the population. Its prevalence increases with age: in people over 75 years of age it develops in 10% of cases.

Etiology • Heart failure with low cardiac output •• Myocardial damage: ••• IHD (post-infarction cardiosclerosis, chronic myocardial ischemia) ••• Cardiomyopathies ••• Myocarditis ••• Toxic effects (for example, alcohol, doxorubicin) ••• Infiltrative diseases (sarcoidosis, amyloidosis) ••• Endocrine diseases ••• Nutritional disorders (vitamin B1 deficiency) •• Myocardial overload ••• Arterial hypertension ••• Rheumatic heart defects ••• Congenital heart defects (for example, aortic stenosis) •• Arrhythmias ••• Supraventricular and ventricular tachycardias ••• Atrial fibrillation • Heart failure with high cardiac output •• Anemia •• Sepsis •• Arteriovenous fistula.

Risk factors • Refusal of the patient from pharmacotherapy • Prescription of drugs with a negative inotropic effect, and their uncontrolled use • Thyrotoxicosis, pregnancy and other conditions associated with increased metabolic needs • Excess body weight • Presence of chronic pathology of the heart and blood vessels (arterial hypertension, coronary artery disease, defects hearts, etc.).

Pathogenesis • The pumping function of the heart is impaired, which leads to a decrease in cardiac output • As a result of a decrease in cardiac output, hypoperfusion of many organs and tissues occurs •• A decrease in cardiac perfusion leads to activation of the sympathetic nervous system and an increase in heart rate •• A decrease in renal perfusion causes stimulation of the renin-angiotensin systems. The production of renin increases, while excessive production of angiotensin II occurs, leading to vasoconstriction, water retention (edema, thirst, increased blood volume) and a subsequent increase in preload on the heart •• A decrease in the perfusion of peripheral muscles causes the accumulation of under-oxidized metabolic products in them, as well as hypoxia leads to severe fatigue.

CLASSIFICATIONS Classification of the XII All-Union Congress of Therapists in 1935 ( N.D. Strazhesko, V.Kh. Vasilenko). • Stage I (initial) - latent heart failure, manifested only during physical activity (shortness of breath, tachycardia, fatigue). • Stage II (severe) - prolonged circulatory failure, hemodynamic disturbances (stagnation in the systemic and pulmonary circulation), dysfunction of organs and metabolism are also expressed at rest •• Period A - the beginning of a long stage, characterized by mild hemodynamic disturbances, dysfunction hearts or only parts of them •• Period B - the end of a long stage, characterized by profound hemodynamic disturbances, the entire cardiovascular system is involved in the process. • 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.

New York Heart Association classification (1964) • Class I - ordinary physical activity does not cause significant fatigue, shortness of breath or palpitations • Class II - mild limitation of physical activity: satisfactory health at rest, but ordinary physical activity causes fatigue, palpitations, shortness of breath or pain • Class III - severe limitation of physical activity: satisfactory health at rest, but less than usual load leads to the appearance of symptoms • Class IV - 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 classification of the Society of Heart Failure Specialists (OSSN, 2002) was adopted at the All-Russian Congress of Cardiologists in October 2002. The convenience of this classification is that it not only reflects the state of the process, but also its dynamics. The diagnosis must reflect both the stage of chronic heart failure and its functional class. It is necessary to take into account that the correspondence between the stage and the functional class is not entirely clear - the functional class is set in the presence of slightly less pronounced manifestations than is necessary to assign the corresponding stage of heart failure.

• Stages of chronic heart failure (may worsen despite treatment) •• Stage I - the initial stage of heart disease (damage). Hemodynamics are not impaired. Latent heart failure Asymptomatic left ventricular dysfunction •• Stage IIA - clinically pronounced stage of heart disease (damage). Hemodynamic disturbances in one of the blood circulation circles, expressed moderately. Adaptive remodeling of the heart and blood vessels •• Stage IIB - severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels •• Stage III - the final stage of cardiac damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys). The final stage of organ remodeling.

• Functional classes of chronic heart failure (can change during treatment in either direction) •• FC I - there are no restrictions on physical activity: habitual physical activity is not accompanied by rapid fatigue, shortness of breath or palpitations. The patient can tolerate increased workload, 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 •• FC III - noticeable limitation of physical activity: at rest there are no symptoms, physical activity of lesser intensity compared to usual exercise is accompanied by the appearance of symptoms •• FC IV - inability to perform any physical activity without discomfort; Symptoms of heart failure are present at rest and worsen with minimal physical activity.

Clinical manifestations • Complaints - shortness of breath, attacks of suffocation, weakness, fatigue • • Shortness of breath in the initial stage of heart failure occurs during physical activity, and in case of severe heart failure - at rest. It appears as a result of increased pressure in the pulmonary capillaries and veins. This reduces the extensibility of the lungs and increases the work of the respiratory muscles. •• Severe heart failure is characterized by orthopnea - a forced sitting position taken by the patient to facilitate breathing with severe shortness of breath. The deterioration of health in the supine position is due to the deposition of fluid in the pulmonary capillaries, leading to an increase in hydrostatic pressure. In addition, in the lying position, the diaphragm rises, which makes breathing somewhat difficult. • Chronic heart failure is characterized by paroxysmal nocturnal shortness of breath (cardiac asthma), caused by the occurrence of interstitial pulmonary edema. At night, during sleep, an attack of severe shortness of breath develops, accompanied by coughing and the appearance of wheezing in the lungs. As heart failure progresses, alveolar pulmonary edema may occur •• Rapid fatigue in patients with heart failure appears due to insufficient oxygen supply to skeletal muscles •• Patients with chronic heart failure may experience nausea, loss of appetite, abdominal pain, abdominal enlargement (ascites) due to blood stagnation in the liver and portal vein system •• From the side of the heart, pathological III and IV heart sounds can be heard. Moist rales are detected in the lungs. Hydrothorax is characteristic, often right-sided, resulting from an increase in pleural capillary pressure and extravasation of fluid into the pleural cavity.

• Clinical manifestations of heart failure significantly depend on its stage •• Stage I - signs (fatigue, shortness of breath and palpitations) appear during normal physical activity, there are no manifestations of heart failure at rest •• Stage IIA - there are unexpressed hemodynamic disturbances. Clinical manifestations depend on which parts of the heart are predominantly affected (right or left) ••• Left ventricular failure is characterized by stagnation in the pulmonary circulation, manifested by typical inspiratory shortness of breath with moderate physical exertion, attacks of paroxysmal nocturnal shortness of breath, and rapid fatigue. Swelling and enlargement of the liver are uncharacteristic. ••• Right ventricular failure is characterized by the formation of congestion in the systemic circulation. Patients are concerned about pain and heaviness in the right hypochondrium, decreased diuresis. The liver is characterized by enlargement (the surface is smooth, the edge is rounded, palpation is painful). A distinctive feature of stage IIA heart failure is considered to be complete compensation of the condition during treatment, i.e. reversibility of manifestations of heart failure as a result of adequate treatment •• Stage IIB - there are profound hemodynamic disturbances, the entire circulatory system is involved in the process. Shortness of breath occurs with the slightest physical exertion. Patients are concerned about a feeling of heaviness in the right hypochondrium, general weakness, and sleep disturbances. Orthopnea, edema, ascites are characteristic (a consequence of increased pressure in the hepatic veins and peritoneal veins - transudation occurs, and fluid accumulates in the abdominal cavity), hydrothorax, hydropericardium •• Stage III - the final dystrophic stage with profound irreversible metabolic disorders. As a rule, the condition of patients at this stage is severe. Shortness of breath is pronounced even at rest. Characterized by massive edema, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium, edema of the genital organs). At this stage, cachexia occurs.

Instrumental data • ECG : you can identify signs of blockade of the left or right branch of the His bundle, ventricular or atrial hypertrophy, pathological Q waves (as a sign of a previous MI), arrhythmias. A normal ECG casts doubt on the diagnosis of chronic heart failure. • EchoCG allows you to clarify the etiology of chronic heart failure and assess the functions of the heart, the degree of their impairment (in particular, determine the ejection fraction of the left ventricle). Typical manifestations of heart failure are expansion of the cavity of the left ventricle (as it progresses, expansion of other chambers of the heart), an increase in the end-systolic and end-diastolic dimensions of the left ventricle, and a decrease in its ejection fraction. • X-ray examination •• It is possible to detect venous hypertension in the form of redistribution of blood flow in favor of the upper parts of the lungs and an increase in the diameter of blood vessels •• With congestion in the lungs, signs of interstitial edema are detected (Kerley lines in the costophrenic sinuses) or signs of pulmonary edema •• Hydrothorax is detected ( most often right-sided) •• Cardiomegaly is diagnosed when the transverse size of the heart increases by more than 15.5 cm in men and more than 14.5 cm in women (or when the cardiothoracic index is more than 50%). • Catheterization of the cardiac cavities reveals an increase in pulmonary capillary wedge pressure of more than 18 mm Hg. Diagnostic criteria - Framingham criteria for the diagnosis of chronic heart failure, divided into major and minor • Major criteria: paroxysmal nocturnal dyspnea (cardiac asthma) or orthopnea, distention of the jugular veins, wheezing in the lungs, cardiomegaly, pulmonary edema, pathological III heart sound, increased central venous pressure ( more than 160 mm water column), blood flow time more than 25 s, positive “hepatojugular reflux” • Minor criteria: swelling in the legs, night cough, shortness of breath on exertion, liver enlargement, hydrothorax, tachycardia more than 120 per minute, decrease in vital capacity by 1 /3 of the maximum • To confirm the diagnosis of chronic heart failure, either 1 major or 2 minor criteria are required. The symptoms detected must be related to heart disease.

Differential diagnosis • Nephrotic syndrome - a history of edema, proteinuria, renal pathology • Liver cirrhosis • Occlusive lesions of the veins with subsequent development of peripheral edema. Treatment • It is necessary to first evaluate the possibility of influencing the cause of the deficiency. In some cases, effective etiological intervention (for example, surgical correction of heart disease, myocardial revascularization in ischemic heart disease) can significantly reduce the severity of manifestations of chronic heart failure • In the treatment of chronic heart failure, non-drug and drug therapy methods are distinguished. It should be noted that both types of treatment should complement each other.

Non-drug treatment • Limiting the consumption of table salt to 5–6 g/day, liquid (up to 1–1.5 l/day) • Optimizing physical activity •• Moderate physical activity is possible and even necessary (walking for at least 20–30 minutes 3 –5 r/week) •• Complete physical rest should be observed if the condition worsens (at rest the heart rate decreases and the work of the heart decreases).

Drug therapy . The ultimate goal of treatment of chronic heart failure is to improve the quality of life and increase its duration.

• Diuretics. When prescribing them, it is necessary to take into account that the occurrence of edema in heart failure is associated with several reasons (constriction of the renal vessels, increased secretion of aldosterone, increased venous pressure. Treatment with diuretics alone is considered insufficient. In chronic heart failure, loop (furosemide) or thiazide (for example, hydrochlorothiazide) diuretics. If the diuretic response is insufficient, loop diuretics and thiazides are combined •• Thiazide diuretics. Hydrochlorothiazide is usually used in a dose of 25 to 100 mg/day. It should be remembered that if the renal GFR is less than 30 ml/min, it is not advisable to use thiazides •• Loop diuretics begin to act faster, their diuretic effect is more pronounced, but less durable than that of thiazide diuretics. Furosemide is used at a dose of 20–200 mg/day IV, depending on the manifestations of edema and diuresis. It can be prescribed orally at a dose of 40– 100 mg/day.

• ACE inhibitors cause hemodynamic unloading of the myocardium due to vasodilation, increased diuresis, and decreased filling pressure of the left and right ventricles. Indications for prescribing ACE inhibitors are clinical signs of heart failure, a decrease in left ventricular ejection fraction of less than 40%. When prescribing ACE inhibitors, certain conditions must be observed according to the recommendations of the European Society of Cardiology (2001) •• It is necessary to stop taking diuretics 24 hours before taking ACE inhibitors •• Blood pressure should be monitored before and after taking ACE inhibitors •• Treatment begins with small doses with gradual their increase •• It is necessary to monitor renal function (diuresis, relative density of urine) and the concentration of blood electrolytes (potassium, sodium ions) while increasing the dose every 3–5 days, then every 3 and 6 months •• Avoid co-administration of potassium-sparing diuretics (their can be prescribed only for hypokalemia) •• Concomitant use of NSAIDs should be avoided.

• The first positive data have been obtained on the beneficial effect of angiotensin II receptor blockers (in particular, losartan) on the course of chronic heart failure as an alternative to ACE inhibitors in cases of intolerance or contraindications to their use.

• Cardiac glycosides have a positive inotropic (increase and shorten systole), negative chronotropic (decreasing heart rate), negative dromotropic (slowing AV conduction) effect. The optimal maintenance dose of digoxin is considered to be 0.25–0.375 mg/day (in elderly patients 0.125–0.25 mg/day); The therapeutic concentration of digoxin in blood serum is 0.5–1.5 mg/l. Indications for the use of cardiac glycosides are tachysystolic atrial fibrillation and sinus tachycardia.

• b-blockers •• The mechanism of beneficial action of β-blockers in chronic heart failure is due to the following factors ••• Direct protection of the myocardium from the adverse effects of catecholamines ••• Protection against catecholamine-induced hypokalemia ••• Improvement of blood flow in the coronary arteries due to a decrease in heart rate and improvement diastolic relaxation of the myocardium ••• Reducing the effect of vasoconstrictor systems (for example, due to decreased renin secretion) ••• Potentiation of the vasodilating kallikrein-kinin system ••• Increasing the contribution of the left atrium to the filling of the left ventricle due to improved relaxation of the latter •• Currently from b -adrenergic blockers for the treatment of chronic heart failure, carvedilol is recommended for use - a b1- and a1-blocker with vasodilating properties. The initial dose of carvedilol is 3.125 mg 2 times / day, followed by an increase in the dose to 6.25 mg, 12.5 mg or 25 mg 2 times / day in the absence of side effects in the form of arterial hypotension, bradycardia, decreased left ventricular ejection fraction (according to EchoCG) and other negative manifestations of the action of b-blockers. Metoprolol is also recommended, starting with a dose of 12.5 mg 2 times / day, bisoprolol 1.25 mg 1 time / day under the control of ventricular ejection fractions with a gradual increase in dose after 1-2 weeks.

• Spironolactone. It has been established that the administration of the aldosterone antagonist spironolactone at a dose of 25 mg 1–2 times a day (in the absence of contraindications) helps to increase the life expectancy of patients with heart failure. • Peripheral vasodilators are prescribed for chronic heart failure if there are contraindications or if ACE inhibitors are poorly tolerated. Of the peripheral vasodilators, hydralazine is used at a dose of up to 300 mg/day, isosorbide dinitrate at a dose of up to 160 mg/day.

• Other cardiotonic drugs . β-Adrenergic agonists (dobutamine), phosphodiesterase inhibitors are usually prescribed for 1–2 weeks in the final stage of heart failure or in case of a sharp deterioration in the patient’s condition.

• Anticoagulants. Patients with chronic heart failure are at high risk of thromboembolic complications. Both pulmonary embolism due to venous thrombosis and thromboembolism of vessels in the systemic circulation caused by intracardiac thrombi or atrial fibrillation are possible. The administration of indirect anticoagulants to patients with chronic heart failure is recommended in the presence of atrial fibrillation and a history of thrombosis.

• Antiarrhythmic drugs. If there are indications for the prescription of antiarrhythmic drugs (atrial fibrillation, ventricular tachycardia), it is recommended to use amiodarone at a dose of 100–200 mg/day. This drug has minimal negative inotropic effects, whereas most other drugs in this class reduce left ventricular ejection fraction. In addition, antiarrhythmic drugs themselves can provoke arrhythmias (proarrhythmic effect). Surgery

• The choice of the optimal method of surgical treatment depends on the cause leading to heart failure. Thus, in case of ischemic heart disease, in many cases, myocardial revascularization is feasible; in case of idiopathic subaortic hypertrophic stenosis, septal myectomy; in case of valvular defects, prosthetics or reconstructive interventions on the valves; in case of bradyarrhythmias, pacemaker implantation, etc.

• In case of heart failure refractory to adequate therapy, the main surgical treatment is heart transplantation. • Methods of mechanical circulatory support (implantation of assisters, artificial ventricles and biomechanical pumps), previously proposed as temporary options before transplantation, have now acquired the status of independent interventions, the results of which are comparable to the results of transplantation. • To prevent the progression of cardiac dilatation, devices are implanted in the form of a mesh that prevents excessive expansion of the heart. • In case of cor pulmonale that is tolerant to treatment, transplantation of the heart-lung complex seems to be a more appropriate intervention.

Forecast. Overall, the 3-year survival rate of patients with chronic systolic heart failure is 50%. The mortality rate from chronic systolic heart failure is 19% per year.

• Factors, the presence of which correlates with a poor prognosis in patients with heart failure •• Decrease in left ventricular ejection fraction of less than 25% •• Inability to climb one floor and move at a normal pace for more than 3 minutes •• Decrease in the content of sodium ions in blood plasma less than 133 mEq /l •• Decrease in the concentration of potassium ions in the blood plasma less than 3 meq/l •• Increase in the content of norepinephrine in the blood •• Frequent ventricular extrasystole during daily ECG monitoring.

• The risk of sudden cardiac death in patients with heart failure is 5 times higher than in the general population. Most patients with chronic heart failure die suddenly, mainly from ventricular fibrillation. Prophylactic administration of antiarrhythmic drugs does not prevent this complication.

ICD-10 • I50 Heart failure

Symptoms of heart failure

In the initial stages, symptoms of heart failure occur only during physical activity. Shortness of breath appears - breathing becomes too frequent and deep, and does not correspond to the severity of work or physical exercise. If the pressure in the vessels of the lungs increases, the patient is bothered by a cough, sometimes with blood.

After physical exertion, heavy meals and in a lying position, increased heart rate occurs. The patient complains of increased fatigue and weakness.

Over time, these symptoms intensify and begin to bother you not only during physical work, but also at rest.

Many patients with heart failure have decreased urine output and go to the toilet mostly at night. In the evenings, swelling appears on the legs, at first only on the feet, and over time it “rises” higher. The skin of the feet, hands, earlobes and tip of the nose takes on a bluish tint. If heart failure is accompanied by stagnation of blood in the liver vessels, a feeling of heaviness and pain occurs under the right rib.

Over time, heart failure leads to poor circulation in the brain. The patient becomes irritable, quickly gets tired during mental stress, and often becomes depressed. He sleeps poorly at night and is constantly sleepy during the day.

Symptoms of right ventricular acute heart failure are caused by stagnation of blood in the veins of the systemic circulation:

Increased heartbeat is the result of deterioration of blood circulation in the coronary vessels of the heart. Patients experience increasing tachycardia, which is accompanied by dizziness, shortness of breath and heaviness in the chest.
Swelling of the neck veins, which increases with inspiration, is explained by an increase in intrathoracic pressure and difficulty in blood flow to the heart.
Edema. A number of factors contribute to their appearance: slower blood circulation, increased permeability of capillary walls, interstitial fluid retention, and impaired water-salt metabolism. As a result, fluid accumulates in cavities and limbs.
A decrease in blood pressure is associated with a decrease in cardiac output. Manifestations: weakness, pallor, increased sweating.
There is no congestion in the lungs.

Chronic heart failure develops in the right and left atrial, right and left ventricular types. Chronic heart failure, according to various authors, is observed in 0.5–2% of the population. The incidence increases with age; after 75 years, the pathology occurs in 10% of people. Chronic left ventricular failure develops as a complication of coronary heart disease, arterial hypertension, mitral valve insufficiency, aortic disease and is associated with stagnation of blood in the pulmonary circulation. It is characterized by gas and vascular changes in the lungs.

Clinically manifested:

increased fatigue;
dry cough (rarely with hemoptysis);
attacks of palpitations;
cyanosis;
attacks of suffocation, which often occur at night;
shortness of breath.

In chronic left atrial insufficiency in patients with mitral valve stenosis, congestion in the pulmonary circulation system is even more pronounced. The initial signs of heart failure in this case are cough with hemoptysis, severe shortness of breath and cyanosis. Gradually, sclerotic processes begin in the vessels of the small circle and in the lungs. This leads to the creation of an additional obstacle to blood flow in the pulmonary circle and further increases the pressure in the pulmonary artery basin. As a result, the load on the right ventricle increases, causing the gradual formation of its failure.

Chronic right ventricular failure usually accompanies emphysema, pneumosclerosis, mitral heart defects and is characterized by the appearance of signs of blood stagnation in the systemic circulatory system. Patients complain of shortness of breath during exercise, enlargement and distension of the abdomen, a decrease in the amount of urine discharge, the appearance of edema of the lower extremities, heaviness and pain in the right hypochondrium.

Chronic heart failure: shifting focus to the initial stages of the disease

Chronic heart failure (CHF) is one of the most severe and prognostically unfavorable complications of cardiovascular diseases [1–4]. Today, the prevalence of functional class III–IV CHF in the European part of Russia is 2.3%, and FC I–II CHF reaches 9.4%, which significantly exceeds similar foreign indicators [5]. The number of patients with left ventricular (LV) dysfunction in the country as a whole is approaching, according to some estimates, 12% (16 million people) [6]. From 55 to 295 billion rubles per year are spent on the treatment of CHF in Russia, and the cost of hospitalization for exacerbations of CHF reaches 184.7 billion rubles [7].

CHF is a progressive syndrome, and patients with asymptomatic CHF within 1–5 years can become the most severely ill patients who are difficult to treat. Therefore, early diagnosis of CHF and left ventricular (LV) dysfunction, and therefore early initiation of treatment for such patients, is the key to success in preventing mortality from heart failure. Unfortunately, in Russia, CHF is extremely rarely diagnosed at the initial stage, which indicates the absence of clear criteria for diagnosing CHF in the earliest period of its development [8].

The need to optimize the management of patients with CHF on an outpatient basis, the complexity of this work and the true state of affairs largely became obvious after the completion of the EPOCHA-O-CHF study [5]. This study was based on an analysis of visits from 4586 patients with symptoms of CHF to hospitals and clinics. The study was conducted in 22 regions of the Russian Federation for 3 months. About 2/3 (63%) of all patients with symptoms of CHF sought help in a hospital and only 1/3 (37%) - in a clinic. This can be explained by the fact that patients with CHF seek help only when decompensation becomes clinically significant and requires hospitalization and inpatient treatment. Another reason is the underestimation of the manifestations of the initial stages of CHF, especially in patients with arterial hypertension (AH) and coronary heart disease (CHD). The results of the EPOCHA study clearly demonstrate that in our country the main efforts are aimed at inpatient treatment of decompensated CHF, and not at its early diagnosis and prevention of progression in an outpatient setting. This is precisely what explains the sad fact that Russia has the worst rates in Europe of re-hospitalization of patients with CHF (31% within a month after discharge) and the length of a hospital day for the treatment of decompensation - 27 days. For comparison, similar figures in Europe are 16% and 10–12 bed days, respectively [8].

Another important point was the discovery of the fact that deterioration of systolic function was no longer a mandatory criterion for CHF. Moreover, low contractility in outpatients with CHF is rather an exception to the rule: LV ejection fraction (EF) less than 40% is detected in only 8.4% of patients. The most common finding is normal or almost normal EF in the range of 40–60% (in 52.4% of patients). And finally, 38.8% of outpatients with CHF have a hyperkinetic type of blood circulation with LVEF > 60%, which is associated with the presence of hypertension, LV enlargement (mainly due to myocardial hypertrophy), and normal cavities.

It is not surprising that in 2005, the ACC (American College of Cardiology) and the AHA (American Heart Association) proposed to classify CHF not only by exercise tolerance, but also by the degree of evolution of organ changes, as if combining the internationally accepted NYHA classification with the long-used one in our country using the Obraztsov–Strazhesko–Vasilenko classification (table).

The problem of heart failure in patients with preserved systolic function has recently received much attention. According to the Rochester Epidemiological Study, more than 43% of patients with CHF have an LVEF >50% [9]. A similar picture was observed in the Framingham study: 51% of patients with CHF had an LVEF of more than 50% [10]. Heart failure in patients with preserved systolic function is more common in older people. In this regard, according to experts, the projected number of such patients in developed countries will increase due to an increase in the proportion of elderly patients in the overall structure of CHF. Data from the EPOCHA-O-CHF study show that the situation expected in the future for Europe and America has already arrived in Russia: the proportion of patients with CHF with preserved LVEF (systolic function > 40%) exceeded 80% for outpatients [11].

For a long time, there was no clear concept for the diagnosis and treatment of patients with CHF with preserved systolic function, but with impaired diastolic function. Back in the middle of the century, in the experimental works of E. Sonnenblick, E. Braunwald, F. Z. Meerson, the postulate of the unity of systolic and diastolic disorders underlying the development of heart failure was substantiated. By the beginning of the 80s, a lot of clinical evidence had accumulated, boiling down to the fact that poor contractility and low LVEF do not always clearly determine the severity of decompensation, exercise tolerance, and even the prognosis of patients with CHF.

What are the main difficulties associated with resolving the issue of diastolic CHF today? Firstly, the “Achilles heel” of diagnosis continues to be the lack of an accurate and safe method for assessing diastolic cardiac function. Another problem is the lack of developed approaches to the treatment of diastolic CHF: despite a wide range of drugs that are potentially effective for the treatment of such patients, none of them can be considered ideal. Finally, the last and probably the most important problem is the lack of attention of researchers and doctors to this issue. Simple logic dictates that, based on the prevalence of the phenomenon, at least 1/3 of all large multicenter studies assessing the survival of patients with heart failure should be devoted to patients with diastolic CHF. In fact, such studies are very few (PEP-CHF, CHARM) [29].

According to the recommendations for the diagnosis of CHF with normal LVEF, proposed by the Association of Heart Failure and Echocardiography of the European Society of Cardiology in 2007, diastolic heart failure is also classified as heart failure with normal LVEF.

Normal or moderately reduced LVEF implies both LVEF > 50% and LV end-diastolic volume < 97 ml/m2. For diagnostic confirmation of LV diastolic dysfunction, both invasive (LV end-diastolic pressure > 16 mm Hg or pulmonary capillary wedge pressure > 12 mm Hg) and non-invasive methods can be used: tissue Doppler sonography (E/E` > 15). If the E/E` indicator is > 8 but < 15, then additional non-invasive studies are required to confirm LV diastolic dysfunction. These include determination of transmitral or pulmonary venous flow, LV myocardial mass index or left atrial mass index by echocardiography, atrial fibrillation by ECG, or plasma levels of brain natriuretic peptide [30].

In accordance with the modern model of the pathogenesis of CHF, this condition is considered, first of all, as a pathology of neurohumoral mechanisms of blood circulation regulation, one of which is an increase in the activity of the sympathoadrenal system (SAS) [12]. The initial activation of the SAS is compensatory in nature, but is subsequently characterized by a whole complex of maladaptive adverse consequences [13]. In the appearance and progression of symptoms of CHF, an important place is played by the activation of the sympathetic nervous system, which, along with an increase in the activity of the renin-angiotensin-aldosterone system, leads to the retention of sodium and water ions, to vasoconstriction and a decrease in the contractile function of the LV of the heart [17].

In this regard, to study the role of dysfunctions of the autonomic nervous system involved in regulatory mechanisms, the assessment of heart rate variability (HRV) seems to be a promising direction [14, 18]. In recent years, the method of studying HRV has begun to be used to assess the sympathetic and parasympathetic components of the regulation of cardiac activity in patients with CHF [15]. Thus, in the UK-HEART study it was shown that the standard deviation index (SDNN) is an independent predictor of overall mortality and the most significant predictor of mortality from progression of CHF [14, 16].

In patients with CHF with preserved LVEF, dyspnea is often the earliest sign due to pulmonary congestion, while skeletal muscle fatigue is characteristic of CHF with reduced LVEF due to decreased cardiac output, impaired vasodilation capacity, and decreased skeletal muscle perfusion. Dyspnea is especially difficult to interpret in the elderly and in obese patients, and these patients represent a large percentage of patients with CHF who have preserved LVEF.

Objective confirmation of a decrease in exercise tolerance can be provided by the use of a stress test in such patients - spiroergometry - with determination of maximum oxygen consumption (VO2max) (reduced VO2max < 25 ml/kg/min; low VO2max < 14 ml/kg/min) and a test with 6- minute walk (distance <300 m has an unfavorable prognosis) [30].

The functional classification of CHF (NYHA), based on a subjective assessment of symptoms by the patient and the doctor, allows only an approximate assessment of physical performance (PF), and objective and widely used indicators of the pumping function of the heart at rest, in particular, LVEF, correlate with it very weakly . The most accurate and reproducible quantitative parameter is exercise oxygen consumption, directly measured by gas analysis.

The maximum individual FR is characterized by maximum oxygen consumption (VO2max) - the highest value of oxygen consumption, which cannot be exceeded with a further increase. In patients with CHF, although it is theoretically possible to achieve it, in practice it is extremely rare, since shortness of breath or weakness stops them much earlier than this level. You can focus on peak oxygen consumption (VO2), but it should be taken into account that the duration and power of the load depend on the motivation of the patient and the doctor. The patient’s effort is considered sufficient and the test is informative if the anaerobic threshold (AT) is reached, usually 60–70% of VO2max. The anaerobic threshold (AT) is the level of O2 consumption above which energy production is supplemented by anaerobic mechanisms. With spiroergometry, it is determined at the moment when the rate of CO2 release begins to exceed the rate of O2 consumption. In stable patients with CHF, peak VO2 and AP are highly reproducible indicators.

Features of the hemodynamic effects of drugs (for example, β-blockers) can lead to differences in the assessment of their effect on RF based on the results of maximal and submaximal tests, therefore, comparison of oxygen consumption and exercise performed is of particular importance. It should be noted that multicenter studies (SOLVD, V-HeFT) did not reveal a clear connection between the effectiveness of drugs according to the results of FN tests and their effect on survival or LV contractility parameters [27]. Carrying out stress tests in patients with CHF is justified not to clarify the diagnosis, but to assess the patient’s functional status and the effectiveness of treatment, as well as to determine the degree of risk. However, a normal exercise test result in a patient not receiving specific treatment may make the diagnosis of CHF unlikely [28].

A number of studies have examined HRV and oxygen supply to the load in patients with CHF. P. Ponikovski et al. examined 102 patients with CHF (mean age 58 years, NYHA I-IV, LVEF 26%, maximum oxygen consumption (VO2max) 16.9 ml/kg/min). Within one year, 19% of the patients included in the study died. The main predictors of mortality were: NYHA functional class (p = 0.003), VO2max (p = 0.01), LVEF (p = 0.02), ventricular arrhythmias (p = 0.05), as well as such parameters of temporary and spectral analysis of HRV as SDNN (p = 0.004), SDANN (p = 0.003) and LF (p = 0.003). The study authors found that the one-year survival rate of patients with SDNN less than 100 ms was lower compared to those with SDNN greater than 100 ms (78 and 95%, respectively, p = 0.008). The combination of SDNN less than 100 ms and VO2max less than 14 ml/min/kg made it possible to identify 18 patients with the highest risk of death. The authors conclude that reduced HRV is an independent prognostic factor for the risk of mortality and complications in patients with CHF [19].

The study of the prognostic significance of HRV in comparison with LVEF and VO2max during a cardiopulmonary training test was devoted to the work of C. Kruger et al. The study included 222 patients with sinus rhythm (mean age - 54 ± 1 year, LVEF less than 40%), of which 151 were with dilated and 71 with ischemic cardiomyopathy. Over 15 ± 1 month, 17% of patients died and 20% were hospitalized due to progression of CHF. In these patients, the SDNN value was significantly lower than in patients without complications (118 ± 6 and 142 ± 5 ms, respectively). In addition, they significantly differed in LVEF (18 ± 1 and 23 ± 1%) and VO2max (12.8 ± 0.5 and 15.6 ± 0.5 ml/min/kg), respectively. Univariate analysis showed that each of these parameters is independent of the other two and significantly predictively significant for both groups. According to multivariate analysis, SDNN had greater predictive value than LVEF and VO2max. The authors believe that measuring HRV improves risk stratification in patients with CHF [20].

HRV analysis is an accessible and highly informative method for determining the state of the autonomic nervous system in patients with CHF. Along with determining parameters such as maximum VO2 and LVEF, HRV research allows us to better characterize the severity of CHF and predict the survival of this category of patients. In patients with the initial stages of CHF, as a rule, normal values of HRV indicators are detected with signs of autonomic imbalance and a predominance of the sympathetic nervous system - an increased ratio of the power of low- and high-frequency oscillations (LF/HF). As the disease progresses, both temporal and spectral indicators of heart rate variability decrease [22].

The most interesting is the correction of increased SAS activity with the help of highly selective b-blockers, which is accompanied by an improvement in both the clinical condition of patients with CHF and their prognosis.

Thus, in the work of Yu. N. Belenkov and V. Yu. Mareev, a significant increase in SDNN was noted in patients with FC II–III CHF who took carvedilol for 6 months. An increase in SDNN by 40% of the initial level indicates a positive effect of the drug on overall HRV [23].

In a study by EC Keeley et al. involved patients with post-infarction cardiosclerosis who took metoprolol for a year, against the background of which an increase in the activity of the parasympathetic nervous system was noted [24].

The SADKO-CHF study included 63 patients with CHF (class II–III) with EF <40%, randomized into groups that differed in the combination of bisoprolol, quinapril and valsartan, and bisoprolol was present in all study groups. The study revealed that the combination of drugs bisoprolol + quinapril has the effect of improving HRV parameters and sympathoadrenal activity [25].

I. V. Nesterova et al. examined 38 men (mean age 61 ± 2 years) who had suffered an MI, with class II–III CHF (NYHA) and EF < 45%. Patients were randomized into 2 groups, receiving in Group I, in addition to standard therapy, metoprolol tartrate at an average daily dose of 54.4 mg, and in Group II, nebivolol 2.3 mg. The results of the study showed that therapy with metoprolol tartrate and nebivolol leads to a decrease in the FC of CHF and normalization of the ratio of HRV indicators [26]. The studies involved patients with reduced ejection fraction, which does not answer the question related to the effect of β-blockers on the course of CHF with preserved systolic function. Potentially, β-blockers can improve the course of CHF with preserved systolic function through several mechanisms: slowing the heart rate (HR) and, as a result, improving LV diastolic filling, reducing LV hypertrophy and inhibiting renin release. However, on the other hand, activation of beta-adrenergic receptors is compensatory in nature, helping to reduce diastolic dysfunction, therefore the effectiveness of long-term use of beta-blockers in patients with EF above 45% requires further study.

Treatment of patients with CHF in the initial stages (stages A and B according to the ACC/AHA classification, 2005; functional class I according to NYHA and a risk group for the development of heart failure) with b-blockers requires further research, and it is likely that patients can receive a number of advantages, including in relation to reducing the risk of mortality and major cardiovascular complications, due to the normalization of HRV indicators. Thus, further study of heart rate variability and oxygen supply to the load in patients with the initial stages of CHF and the effect of b-blockers on these indicators is necessary to clarify adequate therapy for this strategically important group of patients.

For questions regarding literature, please contact the editor.

D. A. Napalkov , Candidate of Medical Sciences N. M. Seidova V. A. Sulimov , Professor, Doctor of Medical Sciences MMA named after. I. M. Sechenova , Moscow

Causes of heart failure

The main causes of heart failure are:

coronary heart disease and myocardial infarction;
dilated cardiomyopathy;
rheumatic heart defects.

In elderly patients, the causes of heart failure are often type II diabetes mellitus and arterial hypertension. Type 2 diabetes mellitus can lead to the development of heart failure.

There are a number of factors that can reduce the compensatory mechanisms of the myocardium and provoke the development of heart failure. These include:

pulmonary embolism (PE);
severe arrhythmia;
psycho-emotional or physical stress;
progressive coronary heart disease;
hypertensive crises; acute and chronic renal failure;
severe anemia;
pneumonia; severe ARVI;
hyperthyroidism;
long-term use of certain medications (adrenaline, ephedrine, corticosteroids, estrogens, non-steroidal anti-inflammatory drugs);
infective endocarditis;
rheumatism; myocarditis;
a sharp increase in the volume of circulating blood due to incorrect calculation of the volume of intravenously administered fluid;
alcoholism;
rapid and significant weight gain.

Eliminating risk factors can prevent the development of heart failure or slow its progression.

Acute left ventricular failure

Acute left ventricular failure is a serious condition caused by decompensation of heart pathology and requiring emergency medical care. In the structure of mortality of cardiac patients, this disease is the first cause of death. What are the main causes, symptoms, diagnostic methods, how is left ventricular failure treated - information about this is further in the article.

Risk factors

Acute cardiac left ventricular failure occurs as a result of complex pathogenetic mechanisms causing primary hypertension (increased pressure) in the pulmonary circulation. Risk factors for decompensation of severe cardiac pathology are physical or emotional stress, fluid overload of the vascular bed, infections, etc.

The development of heart failure is associated with impaired systolic or diastolic function, which is caused by various reasons. In order to understand the pathogenetic mechanism, one should recall some aspects of the anatomical and functional features of the heart.

The heart is a muscular “pump” that continuously pumps blood through 2 circles of blood circulation – large and small. Acute left ventricular failure occurs when there is difficulty in the functioning of the left sections (atrium and ventricle) of the heart and is caused by overload of the pulmonary circulation (PB).

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In a simplified manner, the ICC diagram can be described by the following sequential stages of blood circulation through the cardiovascular system:

Right ventricle.
Pulmonary trunk.
Right and left pulmonary arteries.
Arteries, arterioles, capillaries of the bronchopulmonary system.
Venules and veins.
Left atrium.

Oxygen-enriched blood through the mitral valve, during diastole, enters the left ventricle, and from there in systole, it is pushed into the aorta.

Acute left ventricular failure develops under the influence of such unfavorable factors as:

cardiac ischemia;
long-term surgical intervention;
infections;
hypertonic disease;
excess fluid in the body;
bronchial asthma;
severe kidney disease;
taking certain medications;
congenital and acquired pathology of the valve system;
diseases of the endocrine system.

Under the adverse influence, backflow occurs, overflow and volume overload of the left atrium and pulmonary vascular bed. This causes swelling of the intercellular spaces, reactive narrowing of the bronchial lumen, and foaming of the protein contents of the alveoli. All this leads to the development of a clinical picture of cardiac asthma and pulmonary edema.

Causes

The causes of acute left ventricular failure are cardiac (heart) and non-cardiac in nature. The reasons causing the development of this pathology include:

chronic heart failure in the decompensation phase;
myocardial infarction;
aortic dissection;
cardiac tamponade;
infection of arteries and valves;
severe acute myocarditis;
arrhythmia attack;
hypertensive crisis.

Factors that do not affect the anatomical structures of the heart, but significantly affect its work with the development of failure, include:

violation of treatment tactics (overdose of drugs, non-compliance with the rhythm and frequency of taking medications);
fluid overload (especially with intravenous infusions);
alcohol abuse;
tumor of the adrenal cortex (pheochromocytoma);
renal failure;
severe lung pathology (bronchial asthma, COPD, pneumonia, tuberculosis);
stroke;
sepsis.

In addition, conditions such as severe anemia and thyrotoxic crisis cause increased cardiac output syndrome, which also negatively affects the condition of the left ventricle.

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What happens

Acute left ventricular failure, according to the etiological factor or origin, can be primary and an exacerbation of chronic failure. Primary heart failure is caused by:

acute nephritis (inflammation of kidney tissue);
acute myocardial infarction;
hypertensive crisis.

And among the acute manifestations of chronic left ventricular failure are:

mitral heart defects;
defects of aortic origin;
blood stagnation in the ICC in chronic heart failure;
left ventricular aneurysm.

According to the clinical course, according to the new recommendations of the Society of Cardiology, heart failure (HF) can be:

acute decompensated (newly occurring, exacerbation of chronic HF);
hypertensive – symptoms of heart failure are combined with arterial hypertension;
pulmonary edema;
cardiogenic shock;
HF combined with high cardiac output (more often with infections).

When taking into account the clinical course together with radiographic data, acute HF is divided into 4 degrees of severity:

There are no clinical signs of heart failure.
The appearance of symptoms and radiological signs consistent with cardiac asthma.
Detailed picture of pulmonary edema.
Cardiogenic shock with a drop in blood pressure.

Based on systematic observation of the clinical course, depending on the volume of blood ejected by the left ventricle, left ventricular HF with high or low cardiac output is distinguished.

Symptoms

At the moment when acute left ventricular failure develops, assistance should be provided according to the clinical variant, each of which has its own characteristics.

Precursors and acute forms of left ventricular failure manifest themselves in the form of:

increased or onset of shortness of breath;
forced body position (orthopnea), which alleviates the condition;
rawness behind the sternum during physical activity;
cough when changing body position;
the appearance of wheezing in the lower parts of the lungs.

With stagnation in the pulmonary vessels and their increased tension, fluid leaks from the bloodstream into the intercellular tissue (interstitium). It is interstitial pulmonary edema that underlies the development of cardiac asthma, which has the following clinical manifestations:

nocturnal asthma attack;
shortness of breath accompanied by chest pain;
orthopnea;
participation of auxiliary muscles in breathing;
sticky, cold sweat on the face and chest;
cyanosis (blue discoloration) of the nasolabial triangle, lips, neck, fingertips;
dry and moist wheezing in the lungs;
pulse is rapid and arrhythmic.

If help is not provided or treatment is ineffective, the following type of manifestation of left ventricular failure develops - pulmonary edema, which is characterized by symptoms such as:

suddenness of occurrence;
bubbling breathing;
feeling of fear of death;
moist rales heard at a distance;
discharge of white-pink frothy sputum;
Moist rales are heard over all the lungs.

If acute left ventricular failure develops, pulmonary edema must be stopped immediately, since severe respiratory failure leads to acute oxygen starvation of the entire body. This is a critical condition that leads to death in a short time.

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Diagnostics

The basis of diagnostic measures aimed at confirming the diagnosis is the collection of objective data, especially auscultatory data (when listening to the lungs with a stethoscope).

The following additional laboratory and instrumental methods are used:

electrocardiography;
chest x-ray;
ECHO-cardioscopy with Dopplerography;
blood chemistry;
study of blood gas composition;
general blood and urine tests;
study of the coagulation system and D-dimer.

When recording an ECG, a number of characteristic changes are revealed that confirm decompensation of the pathological condition. On the cardiogram, changes in the isoline are recorded in the leads corresponding to the damage.

X-ray allows you to assess the presence and extent of damage to the lung tissue, displacement of the cardiac border, enlargement or displacement of the borders of the heart and mediastinum.

ECHO cardioscopy is performed using an ultrasound sensor with the function of measuring the speed and volume of blood flow through the vessels (Doppler). This study helps to visualize the site of damage, the valve apparatus, measure the volumes of the heart chambers, the thickness of the heart walls, the speed and magnitude of blood flow, and ejection fractions.

A biochemical blood test involves the identification and quantitative assessment of substances that are markers of acute cardiac pathology. Among the biochemical indicators, total protein, ALT and AST, creatine phosphokinase, haptoglobin, creatinine, potassium, sodium, urea, and sugar are taken into account.

Blood gases allow you to determine the degree of decrease in oxygen in the blood and increase in carbon dioxide. The criteria for these indicators reflect the severity of hypoxia – oxygen starvation and help monitor the patient’s condition and the effectiveness of therapeutic measures.

Treatment at different stages

If acute left ventricular failure develops, emergency care should be provided even before the ambulance arrives. The algorithm of actions is as follows:

Call an ambulance.
Position the patient in a semi-sitting position.
Provide access to fresh air.
Unbutton your shirt collar and loosen your belt.
If possible, calm down, give Valoserdin, Valocardin, Corvalol to drink.
Measure and record blood pressure and pulse, do this every 10 minutes.
When systolic (upper) pressure is above 100 mm Hg. suggest dissolving a Nitroglycerin tablet under the tongue.
Apply tourniquets to the thighs (15-20 cm below the inguinal fold), loosen them every 15 minutes.
If you lose consciousness, place yourself in a safe position on your side.
Clear your mouth of foam.
If there is no breathing or heartbeat, begin chest compressions and artificial respiration.

Acute left ventricular failure, the treatment of which must be carried out in an intensive care unit or resuscitation room, is an absolute indication for hospitalization in a cardiological or therapeutic hospital.

Therapeutic measures aimed at relieving this pathological condition include methods such as:

oxygen therapy - inhalation of heated, humidified oxygen through a mask or nasal cannulas, for pulmonary edema, passed through an antifoam agent - ethyl alcohol;
administration of narcotic analgesics (Morphine), which provide a sedative (calming) and analgesic effect;
intravenous administration of Nitroglycerin;
use of diuretics (Lasix, Furosemide, Ethacrynic acid);
prescription of cardiac glycosides (Strophanthin, Korglykon, Digoxin);
cardioversion – used for atrial flutter or fibrillation.

For successful treatment of acute HF caused by non-cardiac pathology, it is important to establish and eliminate the cause that causes it. With continued exposure to a negative factor, therapeutic measures turn out to be ineffective, which leads to rapid death.

Forecast

The prognosis for this disease is rarely favorable, and despite the achievements of modern resuscitation, pulmonary edema is very often the cause of death. The forecast largely depends on the following factors:

etiology of the development of heart failure (acutely occurring or decompensation of chronic heart failure);
the extent of damage to the cardiac structure due to cardiogenic causes;
possibilities for rapid relief of non-cardiac causes of heart failure (pneumonia, sepsis, thyrotoxic crisis);
age;
the presence of concomitant pathology.

Left ventricular failure, which occurs as a transient condition, has a more favorable prognosis, which depends on the volume and timeliness of medical intervention. Often acute heart failure is accompanied by massive damage to the heart and becomes chronic.

Disease prevention

The basis for preventing the development of acute left ventricular failure is a commitment to strict adherence to doctor’s prescriptions. It is important to exclude all provoking factors that contribute to damage to the cardiovascular system.

Measures to prevent heart disease include the following:

to give up smoking;
avoiding the consumption of alcoholic beverages;
compliance with diet therapy (limiting cholesterol-rich foods, fatty, fried, canned foods, coffee, confectionery, animal fats);
performing feasible physical exercises daily (jogging, yoga, Nordic walking, swimming);
exclusion of stressful situations and neuro-emotional experiences;
limiting physical overexertion.

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Acute left ventricular failure is based on cardiac and non-cardiac causes, which cause hypertension in the pulmonary circulation. The main manifestations of the pathology are cardiac asthma and its complication – pulmonary edema. Timely provision of emergency and specialized care for acute heart failure affects the prognosis of the disease.

How is heart failure diagnosed?

Diagnosis begins with a comprehensive assessment of a person's medical history, paying particular attention to symptoms (onset, duration, manifestation). This helps classify the severity of the symptom. The heart and lungs are examined. If a heart attack or rhythm disorder is suspected, a 12-lead resting ECG is performed. In addition, echocardiography and complete blood count. The need for catheterization is determined individually.

In diagnosis, you need to start with analyzing complaints and identifying symptoms. Patients complain of shortness of breath, fatigue, and palpitations.

The doctor asks the patient:

How does he sleep?
Has the number of pillows changed over the past week?
Did the person begin to sleep sitting instead of lying down?

The second stage of diagnosis is a physical examination, including:

Skin examination;
Assessment of the severity of fat and muscle mass;
Checking for edema;
Pulse palpation;
Palpation of the liver;
Auscultation of the lungs;
Auscultation of the heart (1st sound, systolic murmur at the 1st point of auscultation, analysis of the 2nd tone, “gallop rhythm”);
Weighing (a 1% decrease in body weight over 30 days indicates the onset of cachexia).

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

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

Using ultrasound echocardiography, it is possible to determine the cause of heart failure, as well as evaluate the pumping function of the myocardium. Using cardiac MRI, coronary heart disease, congenital or acquired heart defects, arterial hypertension and other diseases are successfully diagnosed. X-ray of the lungs and chest organs in heart failure determines congestive processes in the pulmonary circulation, cardiomegaly.

Strazhesko-Vasilenko classification (with the participation of G. F. Lang)

Was

adopted at the XII Congress of Therapists of the USSR. Classification of CHF is carried out in 3 stages:

Stage I - initial. It is characterized by the fact that hemodynamic disorders are compensated and are detected only with significant physical activity (domestic) or stress tests - treadmill, Master's test, bicycle ergometry (during diagnosis).

Clinical manifestations: shortness of breath, palpitations, fatigue at rest disappear;

Stage II - severe heart failure. When it occurs, hemodynamics are disrupted (stagnation of blood in the circulatory system), the ability to work is sharply impaired, tissues and organs do not receive the required amount of oxygen. Symptoms occur at rest. It is divided into 2 periods - IIA and IIB. The difference between them: at stage A there is failure of either the left or right parts of the heart, when at stage B there is total heart failure - biventricular;

Stage IIA - characterized by stagnation in the pulmonary or systemic circulation.
At this stage of heart failure, in the first case, left ventricular failure occurs. It has the following clinical manifestations: complaints of shortness of breath, cough with the release of “rusty” sputum, suffocation (usually at night) as a manifestation of the so-called cardiac asthma.

When examining, pay attention to pallor, cyanosis of the extremities, tip of the nose, lips (acrocyanosis). There is no swelling. The liver is not enlarged. On auscultation, you can hear dry rales; with severe congestion, signs of pulmonary edema (fine-bubble rales).

When cardiac function is impaired with the development of stagnation of the systemic circulation, patients complain of heaviness in the right hypochondrium, thirst, swelling, abdominal distension, and indigestion.

There is cyanosis of the face, swelling of the veins of the neck, external edema (later - cavitary edema: ascites, hydrothorax), enlarged liver, heart rhythm disturbances. Treatment at this stage may be especially effective.

How long can you live with stage 1 chronic heart failure?

Stage IIB - represents total heart failure with severe manifestations of circulatory failure. Combines symptoms of blood stasis BCC and MCC. This stage is very rarely reversible.

Stage III - final stage, heart failure in the decompensation stage. Deep myocardial degeneration occurs, irreversibly damaging both the heart itself and the organs experiencing ischemia and oxygen starvation due to its dysfunction. It is terminal and never undergoes regression.

How is heart failure treated?

For chronic heart failure, medications (such as ACE inhibitors, beta blockers and diuretics) are used. Medicines are used to prevent complications and improve quality of life. ACE inhibitors and beta blockers can prolong life, but they must be taken regularly to achieve a beneficial effect.

In addition, rhythm therapy (to treat cardiac arrhythmias) and implantation of a three-chamber pacemaker are used. The latter ensures timely activation of the atria and both ventricles. A defibrillator is also often implanted as part of a pacemaker to counteract dangerous heart rhythm disturbances in the setting of severe heart failure. This treatment is also known as resynchronization therapy. An important part of successful treatment is physical therapy.

In the treatment of heart failure, a properly organized diet plays an important role. Dishes should be easily digestible. The diet should include fresh fruits and vegetables as a source of vitamins and microelements. The amount of table salt is limited to 1-2 g per day, and liquid intake to 500-600 ml.

Pharmacotherapy, which includes the following groups of drugs, can improve the quality of life and prolong it:

cardiac glycosides – enhance the contractile and pumping function of the myocardium, stimulate diuresis, and increase the level of exercise tolerance;
ACE inhibitors (angiotensin-converting enzyme) and vasodilators - reduce vascular tone, expand the lumen of blood vessels, thereby reducing vascular resistance and increasing cardiac output;
nitrates - dilate the coronary arteries, increase cardiac output and improve blood filling of the ventricles;
diuretics – remove excess fluid from the body, thereby reducing swelling;
β-blockers - increase cardiac output, improve the filling of the heart chambers with blood, reduce the heart rate;
anticoagulants - reduce the risk of blood clots in blood vessels and, accordingly, thromboembolic complications;
agents that improve metabolic processes in the heart muscle (potassium supplements, vitamins).

If cardiac asthma or pulmonary edema (acute left ventricular failure) develops, the patient requires emergency hospitalization.

Prescribed drugs that increase cardiac output, diuretics, nitrates. Oxygen therapy is mandatory. Removal of fluid from body cavities (abdominal, pleural, pericardial) is carried out by puncture.

Prevention and prognosis

To prevent heart failure, you need proper nutrition, sufficient physical activity, and giving up bad habits. All diseases of the cardiovascular system must be promptly identified and treated.

The prognosis in the absence of treatment for CHF is unfavorable, since most heart diseases lead to its wear and tear and the development of severe complications. When carrying out drug and/or cardiac surgery, the prognosis is favorable, because the progression of the insufficiency slows down or a radical cure for the underlying disease occurs.