What is cardiopulmonary insufficiency. Cardiopulmonary failure: symptoms and treatment

Many of us have heard such a diagnosis as cardiopulmonary insufficiency (SLN), however, not everyone is familiar with its etiology, causes and consequences. This pathological process provokes failures of the respiratory rhythm and disorders in the cardiovascular system.

The main cause is hypertension, which develops in the pulmonary circulation. The disease is characterized by the release of blood into the pulmonary artery, which is a rather serious problem.

About what cardiopulmonary insufficiency has symptoms and treatment of pathology, we will tell in our dedicated edition.

Cardiopulmonary insufficiency is a pathological process caused by a combination of cardiac and pulmonary insufficiency. Pulmonary insufficiency develops, as a rule, with heart defects and myocarditis, characterized by circulatory failures in the pulmonary vessels.

With a pathological mechanism, the risk of blood stagnation increases, pressure increases, anastomoses are included. All these factors lead to oxygen starvation of the blood.

The disease is inherent in the elderly age category, occurs in two forms:

• acute;
• chronic.

According to ICD-10, pathology code 127.9 "Cardiopulmonary failure of an unspecified type" was assigned.

The disease is a consequence of such concomitant diseases:

• atherosclerosis;
• rheumatism;
• pulmonary pathologies;
• chronic heart disease.

As practice shows, patients who are diagnosed with a chronic form of the disease often turn to the clinic. The very first symptom indicating the development of the disease is shortness of breath, which at the initial stages appears with various physical exertion. Subsequently, shortness of breath becomes a constant accompanying symptom of such patients.

Classification

In medical practice, taking into account the mechanism of occurrence, 3 types of pulmonary insufficiency are distinguished:

1. Hypoxemic.
2. Hypercapnic.
3. Mixed.

Table number 1. Types of lung failure:

According to the rate of development of symptoms, acute and chronic forms are distinguished.

Table number 2. Forms of cardiopulmonary insufficiency:

Such a pathology as cardiopulmonary insufficiency has 3 degrees of flow.

Table number 3. Degrees of the course of cardiopulmonary insufficiency:

In medicine, the classification of the pathological process is also used depending on:

• degree of pulmonary insufficiency;
• an increase in the size of the right ventricle;
• blood oxygen saturation;
• circulatory failure.

In this context, the disease is divided into 4 stages.

Table number 4. Stages of the course of pulmonary insufficiency:

In order for the doctor to prescribe adequate and effective treatment, it is necessary to find out the cause of cardiopulmonary insufficiency. Therapy of pathology is aimed at eliminating the cause and restoring the lost functions of the body.

Attention. The acute form of SLN progresses in one of two types: left and right ventricular failure. With a left-sided lesion, the patient has a high risk of pulmonary edema, and the development of cardiac asthma is not excluded.

Etiology

The development of cardiopulmonary insufficiency occurs against the background of persistent pulmonary hypertension, which at certain stages of the course causes a violation of compensatory mechanisms. As a result, there is a malfunction in the work of the right or left ventricle, dysfunction of pumping venous blood is noted.

The main reasons for the development of a pathological condition are:

1. Cardiac pathologies. Cardiomyopathy, myocarditis, heart defects.
2. Bronchopulmonary diseases. Tuberculosis, bronchitis and chronic bronchiolitis, asthma.

In the first case, such diseases from the side of cardiac pathologies lead to dysfunction of the left ventricle, left ventricular failure develops. With this process, an increase or expansion of the cavity of the left ventricle occurs, intravenous pulmonary pressure increases, the walls of the ventricle cease to eject blood into the bloodstream. In view of these changes, the work of the right ventricle is enhanced, however, and this does not restore full blood supply.

Right ventricular failure develops against the background of pulmonary diseases, accompanied by changes in lung tissue. Even during remission, emphysema is formed in the lungs, the development of which is facilitated by the expansion of healthy tissues.

In such situations, the right ventricle begins to function for wear and tear, the blood is pushed out in an enhanced mode, which causes the development of cardiopulmonary insufficiency.

Causes of acute form of cardiopulmonary insufficiency

The acute form of cardiopulmonary insufficiency is a complication that develops against the background of:

• thrombosis;
• spasm of the pulmonary artery;
• hydro or pneumothorax;
• thromboembolism;
• bronchial asthma (with a prolonged attack);
• inflammatory process in the lung tissue;
• mitral valve insufficiency;
• mediastinal emphysema;
• various heart diseases: myocarditis, heart defects, cardiomyopathy, acute heart attack;
• mechanical injuries of the chest.

The acute form of pathology is a serious condition requiring emergency medical care. Without a qualified provision of it, the patient is in danger of death.

As a result of the above diseases, the cavity of the left ventricle expands, the contractility of the walls weakens, which makes it impossible to pump blood normally. Part of the blood stagnates and thus increases the pressure in the pulmonary artery.

At the same time, the right ventricle continues to function in the same mode, pumping blood normally, the pressure continues to grow. As a result, such severe consequences as cardiac asthma and pulmonary edema develop.

Causes of chronic cardiopulmonary insufficiency

The chronic form, in contrast to the acute form, develops slowly, gradually increasing and more and more manifesting itself clinically. The increase in pathology occurs over several months or years.

The causes of pulmonary hypertension are:

• idiopathic hypertension of a hereditary nature;
• pulmonary artery insufficiency provoked by endarteritis or secondary embolism of small branches;
• atherosclerosis;
• chronic pathological processes in the lungs: pleurisy, emphysema, obstructive bronchitis, pneumosclerosis;
• slowly developing congenital heart defects;
• acquired valvular dysfunction.

The chronic form is usually diagnosed in elderly patients. Against the background of concomitant disorders present in the body, cardiopulmonary insufficiency gradually but surely begins to develop, which is clinically activated after a few years.

Variants of the course of cardiopulmonary insufficiency and clinical manifestations

There are several options for the course of the disease process, they are determined depending on the clinical manifestations.

Table number 5. Options for the course of cardiopulmonary insufficiency:

Clinical manifestations of acute SLN

The acute form of SLN is characterized by a sudden and dramatic onset of symptoms. The patient's condition during this period is significantly deteriorating, there is a mortal threat.

With the development of an acute attack of SLN, the patient should be immediately taken to the intensive care unit, where he will be provided with emergency qualified medical care.

Attention. A mortal threat appears against the background of thromboembolism, with the active development of pain shock, as well as with extensive pulmonary edema, which occurs as a complication of the acute form of SLN.

In this case, the clinical picture has sufficiently pronounced signs, which makes it easy to make a diagnosis.

The following symptoms are noted:

• a sharp drop in blood pressure to critical levels (collapse is often diagnosed);
• difficulty breathing with frequent shallow breaths;
• expansion of the veins in the neck;
• blueness of the skin, especially discoloration, is noted on the limbs and around the lips;
• coldness of the upper and lower extremities;
• sticky sweat;
• chest pain;
• shortness of breath, often accompanied by suffocation.

Attention. Without timely assistance, a person can die in a few minutes from the development of extensive pulmonary edema or from suffocation.

First aid in such situations is to provide oxygen to the lungs. If necessary, the patient is given artificial respiration.

In some situations, the cause of an attack may be a blockage by a thrombus in the pulmonary trunk, the presence of which a person may not even be aware of.

Clinical manifestations of the chronic form of SLN

The chronic form of pathology has a mild and slow course. For many years, a person may not be aware that he has a similar problem, and only after a while certain signs begin to appear.

Important. The clinical picture depends on the underlying cause of the pathological condition. Often patients, feeling the symptoms of cardiopulmonary insufficiency, write them off as a manifestation of their diagnosis, without even thinking about the development of such a complex process, which makes further diagnosis and treatment difficult.

Chronic cardiopulmonary insufficiency can be recognized by the following signs:

• the skin of the limbs and around the lips becomes blue;
• dizziness and nausea;
• frequent heart rate;
• shortness of breath that occurs during physical exertion;
• weakness and fatigue.

The severity of symptoms depends on the stage of the disease. For example, severe shortness of breath with asthma attacks are characteristic of the later stages of the pathology. In this case, all of the above symptoms can be supplemented by signs of concomitant diseases.

Due to the further development of the chronic form of SLN, irreversible processes occur in tissues and organs, leading to a deterioration in the patient's condition. As a result, a severe form of SLN is diagnosed.

Its manifestations will be as follows:

• severe shortness of breath even in the absence of any physical exertion;
• intense pain in the region of the heart;
• a strong expansion of the veins in the neck, is noted when inhaling;
• regularly low blood pressure;
• tachycardia;
• swelling that is not amenable to therapy;
• pain in the right hypochondrium, feeling of heaviness.

When the condition has become severe, patients have a high risk of developing dangerous complications.

It:

• disorders of the brain;
• kidney failure.

Effects

The neglect of the process, as well as the lack of qualified medical care, inevitably leads to the development of serious consequences.

Sequelae of acute SLN

The acute form of cardiopulmonary insufficiency leads to such dangerous consequences as:

• pulmonary edema;
• cardiogenic shock.

Table number 6. Consequences of the acute form of SLN:

With the development of such severe consequences, the patient requires immediate anti-shock therapy. The patient should be taken to the intensive care unit as soon as possible, where he will be provided with qualified emergency medical care.

Consequences of the chronic form of SLN

The chronic process leads to a severe form of oxygen starvation, to a nutrient crisis, which is accompanied by severe shortness of breath and increased signs of cyanosis (cyanosis of the skin).

Due to a disorder of water-salt and protein metabolism, as well as high pressure in the capillaries and liver dysfunction, an accumulation of fluid appears in the soft tissues and in the body cavity, for example, the pericardium, abdominal and pleural. As a result, ascites is diagnosed, which further aggravates the patient's condition.

Ascites, in turn, leads to:

• liver dysfunction;
• digestive disorders;
• internal bleeding.

Hydrothorax (exit of fluid into the pleural cavity) provokes:

• respiratory failure;
• severe shortness of breath with attacks of suffocation.

Hydropericardium (fluid accumulation in the pericardial sac) leads to:

• pain syndrome in the sternal region;
• difficulty passing food;
• swelling of the upper half of the body;
• vein expansion.

Stagnation of fluid in the body inexorably provokes the failure of all functions and systems of the body.

The most common and dangerous consequences can be:

• pneumosclerosis;
• cardiac cirrhosis;
• liver fibrosis;
• congestive gastritis;
• pancreatitis;
• enteritis;
• sudden weight loss;
• dilated cardiomyopathy;
• mitral and aortic insufficiency;
• arrhythmia;
• tachycardia;
• extrasystole;
• lack of urine output;
• kidney failure;
• asthenia;
• sleep disorder;
• encephalopathy;
• stroke;
• thrombosis of deep vessels of the lower extremities;
• thromboembolism of the pulmonary artery.

Prevention of complications of SLN

Prevention of complications of cardiopulmonary insufficiency is based on early diagnosis and timely treatment of the problem. A complete therapy of concomitant diseases that provoke SLN excludes the likelihood of developing consequences in the form of cardiopulmonary insufficiency.

To strengthen the heart muscle, the following rules should be followed:

• stop smoking and drinking alcohol;
• eliminate stressful situations;
• timely treat infectious and bacterial diseases;
• try to take drugs that negatively affect the heart as little as possible (these are non-steroidal anti-inflammatory drugs, hormones, adrenaline);
• exclude junk food from the diet, try not to overeat;
• exercise regularly.

If a history already has such a diagnosis as cardiopulmonary insufficiency, then preventive methods are aimed at slowing down the process of its development.

In such situations, patients should do the following:

• control blood pressure and, if necessary, adjust its indicators in a timely manner;
• timely conduct therapy for heart diseases and other concomitant pathologies;
• restore lipid and carbohydrate balance;
• if indicated, agree to surgery for heart defects and coronary disease.

Diagnostics

Early diagnosis of pathological changes in the body will help to avoid an acute attack of cardiopulmonary insufficiency.

When a patient goes to the hospital, the doctor first of all listens to the patient's complaints, collects an anamnesis, and asks about addictions to bad habits. An important method of examination is listening to the heart, measuring blood pressure. After the examination, the doctor gives a referral for the examination.

Diagnostics includes:

1. X-ray examination of the chest. It makes it possible to determine the presence of changes in the lung tissue and the expansion of the mediastinum.
2. EchoCG. Allows you to determine the dysfunction of the valvular apparatus, to assess the contractility of the myocardium and disturbances in cardiac output.
3. CT. Gives an in-depth assessment of areas of the heart and lungs.
4. ECG. Shows the excitability and conduction of the heart. Based on the results of the ECG, it is possible to identify hypertrophied areas of the myocardium, determine the location of ischemic damage, and establish a heart rhythm disorder. If a doubtful situation arises, observation with the help of a Holter can be additionally assigned. This device allows for 2 hours a day to take readings at regular intervals.
5. Angiography of the pulmonary vessels. It makes it possible to visually determine the shape and lumen of blood vessels, to identify the presence of blood clots, as well as atherosclerotic changes.
6. Spirometry. This method of instrumental diagnostics shows the severity of respiratory failure.
7. Catheterization with manometer. Measures pressure in the cavity of the heart and large pulmonary vessels. It is used in the treatment of thrombosis: a special drug is injected into the catheter that dissolves the blood clots that have appeared.

If there is a diagnosis of heart failure and pulmonary hypertension, these diagnostic methods are carried out at the preclinical stage, the goal is to exclude and prevent the development of cardiopulmonary insufficiency.

Treatment

Tactics of drug therapy in acute and chronic form is distinctive. The use of drugs depends on the rate and course of SLE.

Treatment of acute SLN

The acute form of SLN requires emergency medical attention. Treatment is carried out only in the intensive care unit, as this condition poses a serious threat to the life of the patient.

Treatment includes:

1. nasal catheterization. Allows the patient to receive the necessary amount of oxygen. In severe situations, a decision is made to artificially ventilate the lungs.
2. Intra-arterial catheterization. It is carried out in order to dissolve the blood clots in the pulmonary arteries.
3. Atropine treatment. Atropine allows you to relieve spasms of the bronchial walls and normalize the respiratory rhythm.
4. Treatment with papaverine. Allows you to remove hypertension in the pulmonary circulation, normalize the tone of blood vessels.
5. Treatment with anticoagulants. This group of drugs is aimed at preventing the formation of blood clots in the heart cavity and blood vessels.
6. Eufillin treatment. This drug normalizes the contractility of the heart muscle, and also minimizes the risks of developing respiratory failure.

Attention. If signs of acute cardiopulmonary failure appear, act quickly. It is immediately necessary to call an ambulance team and provide the patient with first aid, which consists in maximizing the access of oxygen to the body. If necessary, artificial respiration is done.

Treatment of chronic SLN

In this situation, treatment is aimed at eliminating the underlying cause of the pathological condition.

Treatment includes:

1. Bronchodilators. They are prescribed in the presence of bronchopulmonary diseases.
2. Hormonal preparations. Glucocorticosteroids are prescribed as anti-inflammatory therapy.
3. cardiac glycosides. They are used to restore the lost contractility of the heart muscle.
4. Potassium-sparing diuretic drugs. Allow to eliminate the risk of congestion, remove excess fluid from the body.
5. Beta blockers. They are used to normalize blood pressure.
6. camphor and caffeine. Used for respiratory failure, drugs are able to stimulate the vasomotor center.
7. Bloodletting with replacement of blood with special solutions. This method is used for severe erythrocytosis.

Advice. As a preventive measure for the development of severe consequences and further suppression of cardiopulmonary insufficiency, patients should categorically exclude bad habits and alcohol consumption.

Emergency care for an acute attack of cardiopulmonary insufficiency

Since the acute form of SLN is dangerous with the sudden onset of severe attacks, accompanied by respiratory arrest, a significant failure of the heart rhythm, up to cardiac arrest, relatives and close friends of such patients must know the rules for providing emergency care in such situations.

Before the arrival of the ambulance, you must perform the following actions:

1. Ensure the patient is in a sitting position.
2. If possible, take the patient outside, or open all windows and doors, try to provide him with oxygen access as much as possible.
3. To reduce high blood pressure, you need to give a Nitroglycerin tablet, which is placed under the tongue and dissolves.
4. In the presence of excessively high pressure, attempts should be made to remove excess fluid from the lungs. For this purpose, heated water is poured into the basin and the patient must lower his legs into it.
5. To reduce acute symptomatic manifestations, moisten a cotton swab in alcohol and give the victim a sniff.

An inexperienced person, ignorant of the rules for providing emergency care, may not help the victim, but, on the contrary, harm him. Therefore, if there is uncertainty in your actions, it is better to call the ambulance phone and ask in detail about the actions that can be performed before the doctors arrive.

Treatment of SLN with folk methods

It should immediately be noted that treatment with alternative methods gives a positive result only in combination with drug therapy. At the same time, it must be remembered that acute SLN is not amenable to treatment with traditional medicine, in such cases, such treatment can have an effect as a restorative therapy.

There are many recipes that allow you to restore, strengthen and stimulate the heart muscle and prevent the development of consequences in the form of pulmonary insufficiency and pulmonary edema.

Table number 7. Recipes of traditional medicine in the fight against heart failure.

All of the above traditional medicine recipes are aimed at strengthening and stimulating the heart. By restoring the normal functioning of the heart muscle, you can reduce the risks of developing further pathologies and their consequences.

In addition, proper fortified nutrition is important in the fight against such a problem. It is recommended to use only natural products, fresh fruits and vegetables, juices, milk and dairy products.

Foods that have a very beneficial effect on the heart are:

• walnuts;
• raisin;
• dried apricots;
• millet;
• watermelon.

• strong tea;
• coffee;
• chocolate;
• spices;
• fried, smoked, salty and spicy dishes.

Such a breakfast is considered an excellent means of preventing heart failure: a large clove of garlic is crushed and spread on black bread, you can add a little salt. Very tasty and healthy!

To eliminate the risk of developing acute attacks of SLN, you should regularly undergo preventive examinations, and if any violations are detected, they should be treated in a timely manner. The prognosis for acute SLN depends on the quality and timeliness of the first aid provided. With a positive outcome, the patient needs a long and labor-intensive rehabilitation and compliance with the important recommendations of the attending physician.

The video in this article will introduce the risks of consequences in cardiopulmonary failure.

In recent years, the English terms or abbreviations ALI and ARDS (acute respiratory distress syndrome = acute respiratory distress syndrome = ARDS) have been used.

Pulmonary insufficiency is defined as an acute impairment of oxygenation with the presence of bilateral pulmonary infiltrates on chest x-ray in the absence of left ventricular failure.

According to the severity of acute pulmonary insufficiency, mild, moderate and severe acute respiratory distress syndrome (ARDS) are distinguished, while the difference consists mainly in the severity of oxygenation disorders.

ARDS is expressed in an acute generalized and diffuse pulmonary (multifactorial) inflammatory reaction, which leads to damage to the endothelium, followed by a violation of vascular permeability, while non-cardiogenic pulmonary edema develops and the content of extravascular pulmonary water increases significantly. Atelectasis and inflammatory infiltrates contribute to a decrease in the gas exchange surface. In the future, an increase in the pulmonary right-left shunt (as a result of hypoxic pulmonary vasoconstriction = Euler-Liljestrand effect) leads to a further disruption of gas exchange and the development of hypoxia. As a result of pulmonary vasoconstriction, pulmonary hypertension develops, followed by right ventricular loading. Changes in the lungs (high weight, loss of surfactant, inflammatory infiltrates, atelectasis) contribute to a decrease in the compliance of the lung tissue, which, in turn, often necessitates more "aggressive" ventilation strategies.

However, ventilation increases the risk of ventilator-associated lung injury (VALI = ventilator-associated lung injury due to “barotrauma and volume trauma”) due to the difference in pressure and volume loads on expiratory-collapsed and re-opened alveoli. Since the inflammatory response develops unhindered, fibrotic reorganization of the lung parenchyma occurs. Regional pathophysiological changes can vary significantly in severity.

Causes of acute lung failure

The causes or provoking factors of acute pulmonary insufficiency can be:

• Pneumonia
• (Poly-)trauma (eg, chest contusion/lung contusion)
• Sepsis/systemic inflammatory response syndrome
• Aspiration (including, for example, with incomplete drowning)
• pulmonary embolism
• Chemical substances
• Inhalation injury
• Peritonitis
• pancreatitis
• burn disease
• Heart-lung apparatus
• Transfusion
• Disseminated intravascular coagulation
• Liver/renal failure
• Intoxication/Drugs
• Preeclampsia/eclampsia.

Symptoms and signs of acute lung failure

• Severe dyspnea and tachypnea
• Possible hypotension and tachycardia
• Fever with concomitant or provoking infection
• Auscultation: bilateral rales, sometimes weakened breath sounds.

Diagnosis of acute pulmonary insufficiency

The following diagnostic measures are required:

• Laboratory data: blood, C-reactive protein, electrolytes, parameters of kidney function, parameters of blood coagulation, if pancreatitis is suspected, amylase and lipase values, if indicated, blood and urine cultures
• Blood gas analysis to assess oxygenation status:
• X-ray or CT scan of the chest with the detection of bilateral infiltrates (diffuse or solid opacities depending on the degree, effusion is usually absent)
• Echocardiography to evaluate pumping function and heart valves
• If indicated, other imaging modalities to locate a lesion in cases of unclear infection/sepsis or postoperative complications.

Treatment of acute pulmonary insufficiency

There is no specific therapy for ARDS! The basis of ARDS therapy is the elimination of the cause, in particular, adequate antibiotic therapy for pneumonia, sanitation of the focus for sepsis.

It is necessary to provide sufficient oxygenation: with clinical signs of muscle wasting (tachypnea with hypoventilation, rapid shallow breathing), early intubation and controlled mechanical ventilation are indicated. The goal of this therapy is to ensure sufficient gas exchange and reduce the increased work of breathing without causing damage to the lungs and the body as a whole due to mechanical ventilation.

Oxygen delivery in ARDS is affected by the following factors: atelectasis/dystelectasis, bronchoconstriction, edema, intrapulmonary shunts, shift in the hemoglobin oxygen saturation curve due to acidosis or alkalosis, anemia, cardiac output, and peripheral vascular tone. The goal is 90% arterial oxygen saturation, where in addition to arterial oxygen tension, hemoglobin concentration and cardiac output are also important components of oxygen delivery.

The parameter F i O 2 should be set sufficient, but as low as possible.

In the case of oxygenation disorders that are not controlled by other methods, extracorporeal lung function support (ECLA = extracorporeal lung support; iLA = interventional lung support; ECMO = extracorporeal membrane oxygenation) should be considered.

With adequate analgesic sedation, pain, fear and anxiety are controlled, and spontaneous breathing is best promoted whenever possible.
The goal of volume therapy is, on the one hand, to maintain sufficient perfusion of the organs, and, on the other hand, to prevent hypervolemia, which can become noticeable with a (further) increase in cardiac preload and increased pulmonary edema.

Restrictive volume therapy under the motto "Keep the lungs dry, but without hypovolemia" has advantages in terms of oxygenation and duration of intensive care, but this does not imply a significant advantage in terms of survival.

Gravity in patients with ARDS in the supine position causes significant fluid accumulation in dependent areas of the lungs and atelectasis, so positional therapy with repositioning can help reopen unventilated areas, recruit them for gas exchange and thereby improve oxygenation. 180° and 135° prone positions are used and discussed. The differences are in the duration and frequency of positional maneuvers (with sufficient hemodynamic stability and pulmonary tolerance 8-12 hours a day → continuous hemodynamic monitoring and periodic blood gas monitoring to confirm the effect or detect possible complications). No clear advantage in terms of survival in the supine position or in the 135° position has yet been shown, so the decision on the prone position of the patient should be made individually with an assessment of potential risks and problems.

The risks and challenges of positional therapy include:

• Displacement of the sheath, catheters and drains
• Injury due to change of position (compression, swelling of the face)
• Hemodynamic changes (hypotension, tachycardia)
• Need to adjust ventilation settings due to changes, such as pulmonary pressure ratios or lung tissue compliance
• Adequate sedation of the patient to reduce stress
• Sometimes there are clear limitations of the possibilities of positional therapy in patients with overweight, trauma or after surgery.

Currently, there is no drug therapy that would lead to a significant improvement in survival. Among other possibilities, the effects of prostaglandins, corticosteroids, surfactant, prostacyclin, N-acetylcysteine ​​and NO are being studied.

Forecast

The risk of death depends on the severity (mild ARDS 27%, moderate ARDS 32%, severe ARDS 45%). The determining moment for the prognosis is not so much the severity of hypoxemia as secondary organ damage, the cause of the syndrome, and concomitant diseases.

In addition to long-term organic consequences (eg, impaired lung function), psychiatric disorders (eg, post-traumatic stress disorder) often develop, leading to limitations in daily activities and a deterioration in quality of life.

Cardiopulmonary failure (ICD-10 code I27) is a disease characterized by a decrease in contractions of the heart muscle and the inability of the respiratory system to send the required amount of oxygen to the vessels.

The disease can take an acute or chronic form. In both cases, the quality of life of the patient is significantly reduced.

The causes of the pathology may be associated with individual or systemic disorders in the functioning of the lungs and heart. The mechanism of the development of the disease is due to increased pressure in the pulmonary circulation, which is responsible for the supply of oxygen to the blood.

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When blood is ejected into the pulmonary artery, the load on the right ventricle increases, resulting in hypertrophy (thickening of the myocardium).

The reasons

Pulmonary hypertension leads to a violation of the enrichment of blood in the alveoli with oxygen. As a result, the myocardium of the right ventricle increases cardiac output in order to reduce tissue hypoxia (lack of oxygen). Over time, due to excessive stress, the muscles of the right side of the heart grow.

Such a period is called compensated, with it complications do not develop. If the pathology progresses, compensatory mechanisms break down, which leads to irreversible changes in the heart: the stage of decompensation.

There are several groups of factors that are the causes of the disease:

Under the influence of vascular factors, the arteries narrow. This is due to blockage by a thrombus or thickening of the vascular walls due to the inflammatory process.

In the presence of deforming and bronchopulmonary factors, the vessels are compressed, the tone of their walls is disturbed, the gaps are fused with connective tissue. As a result of such processes, the tissues of the body experience a lack of oxygen.

In medical practice, the disease most often develops against the background of:

• pneumosclerosis;
• pulmonary vasculitis;
• emphysema;
• thromboembolism;
• pulmonary edema;
• stenosis of the pulmonary artery.

Severity

The chronic form of the disease is characterized by a slow and subtle increase in symptoms. Based on this, four degrees of severity of the disease are distinguished:

Diagnostics

To diagnose cardiopulmonary insufficiency and prescribe effective therapy, it is necessary to conduct a comprehensive examination.

The disease can be determined by instrumental diagnostic methods:

Treatment

The main directions of treatment of cardiopulmonary insufficiency include:

Pulmonary heart disease occurs in two types: acute and chronic.

The development of an acute form occurs as a result of a sudden blockage of a large branch or main trunk of the pulmonary artery by a thrombus or embolus, or acute pulmonary emphysema, generalized pneumothorax, and various compressions of the mediastinum. During an attack, unexpected asphyxia occurs, the right ventricle of the heart expands sharply. As a rule, disorders of the coronary circulation caused by the pulmonary-coronary reflex also join the disorders.

The main signs that characterize pulmonary heart failure are painful or constrained rapid breathing, stabbing pain in the region of a pulmonary infarction, squeezing pain behind the sternum, muffled heart tones, increased venous pressure, lowering blood pressure, sudden tachycardia, infarct changes, as well as expansion right cavities of the heart.

A similar picture can also be observed in myocardial infarction. But in this case, a sharp pain portends a drop in blood pressure, as well as a significant increase in body temperature. In the case of acute pulmonary heart failure, respiratory distress, pressure drop, tachycardia and a significant increase in body temperature occur simultaneously.

The occurrence of acute pulmonary heart syndrome is a formidable phenomenon that requires immediate intervention. When failure occurs due to tuberculosis, interstitial emphysema, or another disease that is not accompanied by a thromboembolic process, therapy must also be urgent and urgent.

Pulmonary heart failure The chronic form is much more common than the acute form. It appears as a result of a variety of chronic lung diseases, for example, bronchiectasis, pneumosclerosis, emphysema, and others. The pathogenesis of this disease is still not clear enough.

Bozhenko Alexey, cardiologist www.medicina-msk.ru

FAINTING

Fainting is a sudden short-term loss of consciousness resulting from a violation of the blood circulation of the brain.

In short, fainting is a warning to the brain that it lacks oxygen and a request for help. Often fainting is preceded by a feeling of lightheadedness, nausea, dizziness. The main symptoms of fainting are chest tightness, weakness, "flickering in the eyes", numbness of the limbs, nausea, vomiting, pallor of the skin, and a drop in blood pressure. The patient suddenly "rolls" his eyes, becomes covered with cold sweat, his pulse weakens, his limbs become cold, constriction occurs, and then the pupils expand. Most often, this state lasts for several seconds, then gradually the patient begins to come to his senses and react to his surroundings.

There is a faint with a strong fright, excitement, with pain, at the sight of blood or a weak heart. Sometimes its occurrence is facilitated by a stuffy room, overheating in the sun or in a bath, as well as a quick transition from a horizontal to a vertical position. Most often, fainting is observed in hysterical women and in debilitated patients.

First aid

First aid for fainting is to give the patient a horizontal position. Then it is necessary to provide him with an influx of fresh air: unfasten the collar or dress, loosen the belt, open the window or window. Sprinkle cold water on the face and chest of the patient, pat him on the cheeks with a wet towel or palm, give him a sniff of ammonia or burnt bird feathers, rub his limbs and warm him with heating pads. When the patient regains consciousness, he should be given hot strong tea or coffee.

COLLAPSE

Collapse differs from syncope in the longer duration and severity of the phenomena. With it, the tone of the entire arterial system sharply decreases, which leads to a drop in blood pressure and a violation of cardiac activity.

The most common cause of collapse is extensive blood loss, a blow to the stomach, a sharp change in body position. Collapse is often a complication of some disease (scarlet fever, typhoid or typhus, diseases of the cardiovascular system, food poisoning, acute pancreatitis, pneumonia, etc.).

In a state of collapse, the patient is pale, motionless, covered with cold sweat. There is cyanosis of the extremities and nail phalanges. The patient's breathing is superficial, the pulse is thready, sometimes not palpable. Body temperature is reduced by 1-2 degrees, blood pressure is very low or not detected. Consciousness is darkened, in severe cases it is absent.

If at this time the patient is not provided with emergency assistance, then convulsions, cardiac weakness, involuntary discharge of urine and feces are added to the above phenomena, and the patient dies.

First aid

First aid for collapse is aimed at eliminating the cause that caused the collapse (cessation of the traumatic agent, combating blood loss, etc.), and at combating cardiovascular insufficiency. The patient is placed in a position with legs slightly raised (to ensure a rush of blood to the brain), tight bandages are applied to the limbs (self-transfusion of blood) and an ambulance is urgently called.

Be sure to provide the patient with an influx of fresh air (see fainting).

If a patient in a state of collapse has developed a terminal state, it is necessary to start artificial respiration and chest compressions.

A serious condition that develops when exposed to extreme pain stimuli (strong stroke, myocardial infarction, perforated stomach ulcer, pancreatitis attack, etc.), after transfusion of heterogeneous blood, administration of sera and large blood loss.

Shock is a much more severe condition than collapse. In shock, the patient is lethargic, apathetic, indifferent to the environment, almost does not complain of pain. His skin is pale, his face is covered with cold sweat, there is a rare, shallow breathing, a small frequent pulse, low blood pressure. In the initial stages of shock, consciousness is preserved. These symptoms can be expressed to varying degrees depending on the stage of shock.

First aid

First aid is to eliminate or at least weaken the cause that caused the state of shock. The patient is allowed to smell ammonia, warmed with heating pads, allowed to drink tea, coffee, alcohol, vodka, analgin, amidopyrine, and be sure to call an ambulance. If immobilization has not been carried out before (for fractures), they do it.

For bleeding from superficial vessels, a pressure bandage is applied, for bleeding from deeper vessels, a tourniquet is applied (the central site of damage over clothing). If the tourniquet was applied earlier, but the bleeding continues, you need to apply another tourniquet, slightly higher than the first, and then remove the first tourniquet.

Thus, in case of shock, the following measures should be taken urgently.

1. Eliminate traumatic factors.

2. Stop bleeding.

3. Apply immobilization for fractures.

4. Control breathing and heart function. If necessary - artificial respiration and chest compressions.

5. Urgently call an ambulance.

6. Provide the victim with peace and warmth.

CHRONIC CARDIO-PULMONARY FAILURE

Circulatory failure mainly depends on two factors:

1) from a decrease in the contractility of the muscles of the heart;

2) from a decrease in the contractile strength of the muscular membrane of peripheral vessels.

If the first factor predominates, we are talking about predominantly chronic heart failure. If the second factor prevails, then we are talking about predominantly vascular insufficiency of blood circulation.

The state of blood circulation in the large and small circle is determined by the left and right sections of the heart. With a predominant lesion of one of these departments, isolated or predominant lesions of the left or right half of the heart occur. Therefore, among the forms of heart failure, left ventricular and right ventricular failure are distinguished.

The heart and lungs are very closely related in functional and anatomical terms, therefore, when one of these organs becomes ill, the other is also affected. Depending on which organ, the heart or lungs, is affected to a greater extent, cardiopulmonary or pulmonary heart failure is distinguished.

In cardiovascular insufficiency, two phases are clearly defined - compensation and decompensation.

In the compensation stage, the heart, using the reserve forces of the body, copes with its work. But there comes a period when all internal reserves are exhausted; the phase of decompensation begins - the heart cannot cope with the loads placed on it.

HEART FAILURE

Chronic heart failure is divided into three types according to the nature of the course: isolated insufficiency of only the left ventricle, isolated insufficiency of only the right ventricle and complete heart failure.

The insufficiency of each department is characterized by congestion, localized above the location of the weakened ventricle (with left ventricular failure, congestion is observed in the pulmonary circulation, with right ventricular failure - in the large one). The main symptom of heart failure is a poor supply of arterial blood to the organs, which leads to oxygen starvation.

LEFT VENTRICULAR FAILURE

It is observed with cardiosclerosis, hypertension, with insufficiency of the mitral or aortic valves, as well as with a heart attack in the region of the left ventricle. Left ventricular failure can also occur with symptomatic hypertension.

With this type of insufficiency, patients complain of shortness of breath during physical exertion (and then at rest), asthma attacks that occur most often at night (cardiac asthma), and hemoptysis. As the disease progresses, these symptoms are joined by: tachycardia, a drop in systolic pressure and a deterioration in the blood supply to the brain (which leads to dizziness, convulsions, respiratory rhythm disturbance and loss of consciousness).

RIGHT VENTRICULAR INSUFFICIENCY

Right ventricular failure occurs in diseases such as pneumosclerosis, emphysema, tuberculosis, kyphoscoliosis, i.e., in all those cases when the right ventricle has to overcome increased resistance when pushing blood into the pulmonary circulation.

With right ventricular failure, the right ventricle usually enlarges, blood stasis appears in the vessels of the systemic circulation, and tricuspid valve insufficiency occurs.

The main symptoms of right ventricular failure are: pulsation of the jugular veins, liver enlargement, dropsy (ascites) and cirrhosis of the liver. The patient develops peripheral edema, first on the feet, legs, and then throughout the subcutaneous tissue. The patient's face is edematous, with a bluish tint, blood pressure is most often elevated. Congestion in the brain can cause such manifestations from the nervous system as psychosis, delusional states, etc.

COMPLETE HEART FAILURE

With this type of insufficiency (myocarditis, cardiosclerosis, myocardial dystrophy), all the symptoms of right and left ventricular failure are present, expressed to a greater or lesser extent. Stagnation is observed both in the large and in the small circle of blood circulation, which gives the corresponding symptoms.

Acute heart failure

Acute heart failure- a clinical condition that either acutely debuts or is a worsening of the course of heart failure, which requires urgent treatment.

OSN can be with:

• rhythm disturbances
• myocardial ischemia
• neuroendocrine imbalance
• valvular lesions

The reasons

Often, AHF is caused by coronary artery disease, including:

• right ventricular infarction
• post-infarction LV defect
• acute coronary syndrome

Among the common causes are hypertension and arrhythmias, including a crisis increase in blood pressure. Valve damage can provoke AHF, namely:

• endocarditis of any valve
• significantly increased degree of regurgitation
• development of critical stenosis
• aortic dissection

AHF in some cases is caused by disorders of the peripheral and central circulation, including:

• cardiac tamponade
• anemia
• thyrotoxicosis
• septicemia
• thromboembolism of the branches of the pulmonary artery

The cause may be myocardial damage (cardiomyopathy, acute myocarditis), decompensation of chronic HF, including acute cerebrovascular accident, pneumonia, pneumonia, low compliance, exacerbation of chronic obstructive pulmonary disease, etc. Researchers divide all of the above causes into 3 arrays :

• leading to a sharp increase in preload
• leading to a sharp increase in afterload
• leading to an increase in cardiac output

Recently, the role of nonsteroidal drugs and thiazolidinediones in the development of acute heart failure has been investigated.

Symptoms are manifested by any of the following conditions (or even several of them at once):

• Pulmonary edema (orthopnea position, shortness of breath, decrease in arterial blood saturation less than 90%)
• The increase in edema (mainly occurs in patients with CHF, shortness of breath increases, free fluid appears in the cavities)
• Increased blood pressure (tachycardia, a sharp increase in peripheral vascular resistance; in some cases, pulmonary edema begins to predominate in the clinic)
• Insufficiency of blood supply to peripheral tissues and organs
• Acute coronary syndrome (a small proportion of patients with ACS have symptoms similar to AHF)
• Isolated right ventricular failure (in patients, a decrease in stroke volume develops in the absence of pulmonary edema and stagnation in the pulmonary circulation)

Diagnostics

Diagnosis of acute heart failure should begin with anamnesis. The doctor clarifies the presence of arterial hypertension, chronic heart failure and current treatment, including medications. Next, the doctor palpation evaluates the temperature of the skin and detects or does not detect swelling. Next, the central venous pressure is assessed if catheterization can be performed.

Auscultation of the heart allows you to evaluate the first tone, systolic murmur at the 1st point and its conduction, diastolic murmur at the 1st auscultation point, III tone, systolic and diastolic murmurs at the second and fifth points. Lung auscultation evaluates the number of moist rales in the lungs in relation to the angle of the scapula. The doctor should then examine the neck for swollen veins. Next, it is necessary to assess the presence of free fluid in the lungs using the percussion method.

An important diagnostic method is the ECG, an X-ray examination of the chest. In arterial and venous blood, p0 2 should be determined. pCO 2 . pH. In the blood serum, the level of glucose, urea and creatinine, ALT, etc. is determined.

Further diagnosis includes the determination of natriuretic peptides. Their normal value is possible with isolated right ventricular failure, and a preserved elevated level at discharge indicates a poor outcome. Echocardiography is the first line of procedure in patients with AHF.

All people with AHF should be admitted to the intensive care unit or intensive care unit. Invasive or non-invasive monitoring is important. These two forms are often combined. The latter includes an assessment of the number of respiratory movements, body temperature, blood pressure, heart rate, urine output, and electrocardiography.

Invasive monitoring involves placing a catheter into a peripheral artery. This is necessary for patients with unstable blood dynamics, only if intra-arterial pressure can be measured in the ward. A catheter into the central vein allows you to control the central venous pressure, administer drugs, and monitor the saturation of venous blood. Placement of a catheter in the pulmonary artery is usually not required for patients with acute heart failure. Among the limitations of the use of the catheter should include situations caused by mitral stenosis, aortic regurgitation, etc.

Coronary angiography can be used for diagnosis. In cases of ACS complicated by the development of AHF, coronary angiography is indicated for all patients who do not have absolute contraindications.

Treatment

Treatment goals are divided into three levels. The first includes minimizing the manifestation of decompensation, improving blood dynamics, improving blood supply to peripheral organs and tissues, restoring adequate oxygenation, restoring the functioning of the myocardium and kidneys, and minimizing the length of time a person stays in the intensive care unit.

The second level goals apply when a person is transferred from the intensive care unit. Titration of drugs is started, which reduces the level of deaths among patients with CHF. The need for surgical ancillary procedures, such as resynchronization, should be determined. They begin the rehabilitation of the patient and try to minimize the time spent in the hospital.

Level 3 goals are connected when a person is discharged from the hospital. The involvement of the patient in educational programs matters. Need physical rehabilitation, control of doses of life-saving drugs for the treatment of CHF. The patient's condition is monitored throughout his life.

Use of oxygen therapy

This is a mandatory procedure for all patients with AHF and arterial blood saturation.<95%. Чаще всего выбирают неинвазивную оксигенотерапию (то есть она не включает интубацию трахеи). Для этого актуальны лицевые маски. Применение неинвазивной оксигенации — первооче-редная процедура для пациентов с отеком легких и больных с ОСН, раз-вившейся на фоне повышения артериального давления, поскольку неинвазивная оксигенация снижает потребность в интубации и смертность в первые сутки после госпитализации.

Non-invasive oxygenation is carried out for half an hour every 60 minutes, starting with a positive pressure level of 5-7.5 cm of water by the end of exhalation. followed by titration of this indicator to 10 cm of water. The following side effects are possible:

• aspiration
• dry mucous membranes
• increased right ventricular failure
• hypercapnia

Morphine

This remedy is prescribed if patients with acute heart failure have agitation, a state of anxiety, severe shortness of breath. The usual dose is 2.5-5.0 mg intravenously slowly. Monitoring is necessary because nausea and/or vomiting may occur after injection.

Loop diuretics

Treatment with diuretics is described in the materials on heart failure. Their intravenous administration is the basis for the treatment of AHF in all cases of volume overload and in the presence of signs of stagnation. Do not use these medicines to treat people with blood pressure up to 90 mm Hg. as well as hyponatremia and acidosis. High doses of loop diuretics lead to hyponatremia and increase the likelihood of hypotension at the start of treatment with ACE inhibitors and ARBs.

If intravenous vasodilators are administered, this reduces the dose of diuretics. Diuretic therapy is recommended to start with 20-40 mg of furosemide or 10-20 mg of torasemide administered intravenously. After the introduction of a diuretic, the patient's urine volume must be monitored. The total dose of furosemide for the first 6 hours of treatment should be less than 100 mg, and for 24 hours less than 240 mg. Diuretic therapy in all cases entails the development of hyponatremia and hypokalemia.

With a moderate degree of AHF, loop diuretics such as furosemide and torasemide are taken. The daily dose of the first is from 20 to 40 mg, and the second from 10 to 20 mg. In severe AHF, the dose of furosemide is increased to 40-100 mg, and torasemide - up to 20-100 mg orally. With developed refractoriness, hydrochlorothiazide is added to loop diuretics at a dose of 50 to 100 mg, or spironolactones (25-50 mg) are added. The latter are preferable with an initially low level of K + and the absence of severe renal failure.

Vasodilators

These drugs are recommended for all patients with acute heart failure and systolic blood pressure above 90 mm Hg. A systolic blood pressure level of more than 110 mm Hg is considered safe. Caution in prescribing vasodilators is required at systolic blood pressure levels of 90-110 mm Hg. Vasodilators reduce systolic blood pressure and filling pressure of the left and right ventricles, reduce dyspnea and general vascular resistance.

This group of drugs is not prescribed if systolic blood pressure is less than 90 mm Hg. because there is a threat of reducing the blood supply to internal organs. During therapy with vasodilators, blood pressure levels must be monitored. The start of nitroglycerin infusion is carried out at a rate of 10-20 mcg / min, it needs to be increased to 200 mcg / min. Side effects: headache, lowering blood pressure.

Effective isosorbide dinitrate. The indication for use is:

• ICC congestion or pulmonary edema
• systolic blood pressure above 90 mm Hg

Infusion is started at a rate of 1 mg per hour, increased to 10 mg per hour. Side effects are similar to those with the introduction of nitroglycerin. The indication for the use of sodium nitroprusside is AHF against the background of arterial hypertension, systolic blood pressure >90 mm Hg. Nesiritide is also effective.

Drugs with a positive inotropic mechanism of action

Drugs with a positive inotropic effect should be used in all patients with low cardiac output, low blood pressure, signs of organ hypoperfusion. These drugs can be used together with diuretics and vasodilators. It is important to start treatment with these drugs early, stop taking them immediately after the patient's condition stabilizes. Otherwise, myocardial damage and death are likely.

Dobutamine is effective, the infusion rate is 2-20 mcgDkghmin; Dopamine, whose nephrodosis<3 мкгДкгхмин; Левосимендан. вводится болюсом в дозе 12 мкг/кг вну-тривенно за 10 минут.

Vasopressors

These drugs are not recommended as first-line drugs in the treatment of AHF. Their use is justified in cardiogenic shock, when therapy with drugs with a positive inotropic effect and fluid administration do not lead to an increase in blood pressure above 90 mm Hg. and may continue as long as signs of organ hypoperfusion persist.

Features of correction of the condition of patients with acute heart failure

With decompensation of CHF, treatment starts with vasodilators and loop diuretics. Diuretics are best given as a bolus. With persistent hypotension, drugs with a positive inotropic effect are recommended. With pulmonary edema, treatment begins with the introduction of morphine. With high blood pressure or normal blood pressure, vasodilators are used, and in the presence of stagnation and edema, diuretics are relevant.

With cardiogenic shock and systolic blood pressure less than 90 mm Hg. solutions that improve blood rheology are administered intravenously at a dose of 250 ml per 10 minutes, and drugs with a positive inotropic effect.

Cardiopulmonary insufficiency is a pathology of the respiratory and cardiovascular systems, progressing due to an increase in pressure in the pulmonary circulation. As a result, the right ventricle of the heart begins to function more intensively. If the disease progresses over a long period of time and it is not treated, then the muscle structures of the right heart will gradually increase their mass (due to increased work).

Clinicians call this period compensated - complications, as a rule, do not occur. With further progression of pulmonary heart failure, the compensatory mechanisms of the body break down, and a decompensated period sets in (changes in the heart muscle are irreversible).

Etiology

Bronchogenic, vascular and thoracophrenic factors can provoke cardiopulmonary insufficiency.

Vascular etiological factors:

• pulmonary;
• benign or malignant mediastinal tumor;
• aneurysm.

Thoracodiaphragmatic:

Bronchogenic factors:

• with a chronic course;
• bronchiectasis;
• extensive;
• emphysematous changes in lung tissues;

Symptoms

Symptoms of the disease depend on the form in which it proceeds - in acute or in chronic. It is worth noting that the acute form is a more serious condition requiring immediate ambulance.

acute form

In the case of an acute form of the disease, the symptoms appear and develop very quickly. This type of failure occurs in the following cases:

• or spasm of the trunk of the pulmonary artery;
• sternum injury of varying severity;
• damage to most of the lungs by an inflammatory process.

Acute symptoms:

• acute pain in the sternum;
• breathing becomes frequent and superficial;
• legs and arms get cold;
• decrease in blood pressure. Even possible;
• a characteristic symptom is shortness of breath (difficulty inhaling);
• veins in the neck swell;
• increased sweating;
• cyanosis;
• the patient is out of breath. Perhaps even suffocation.

Chronic form

Symptoms of the chronic form directly depend on the stage of development of the pathological process. If there is a compensated stage, then the patient has symptoms of an ailment that provoked the progression of insufficiency. Chronic insufficiency develops over a long period of time.

Symptoms of pathology:

• increased heartbeat;
• at physical shortness of breath appears on the load;
• in the epigastrium, a person can feel a pulsation;
• dizziness;
• increased fatigue;
• acrocyanosis.

In the case of progression of the decompensated stage, the symptoms also appear gradually, but they lead to destructive changes in tissues and vital organs. Symptoms of the stage of decompensation of the chronic form of the disease:

• edema. It is noteworthy that they are very resistant to treatment;
• acrocyanosis;
• in the area of ​​the projection of the heart, ischemic pain is noted;
• BP goes down;
• veins in the neck swell;
• shortness of breath manifests itself even in a state of complete rest. It tends to increase with a change in position (especially increases in the supine position);

Diagnostics

If one or more of the above symptoms appear at once, you should contact a medical institution as soon as possible for a full diagnosis. The standard plan of diagnostic measures is as follows:

• collection of a detailed anamnesis of life and disease;
• auscultation of the heart;
• measurement of blood pressure;
• angiography of the vessels of the lungs;
• spirometry;
• echocardiography;
• x-ray;

Therapeutic measures

In the case of progression of the acute form, treatment is carried out only in intensive care. Be sure to resort to oxygen therapy. In severe clinical situations, they resort to mechanical ventilation. The following pharmaceuticals are injected into a vein:

• eufillin;
• atropine;
• papaverine;
• anticoagulants;
• thrombolysis drugs.

In the chronic form of pathology, treatment is primarily aimed at eliminating the underlying pathology. The treatment plan includes hormones, anti-inflammatory drugs, and bronchodilators. If there is a pathology of the cardiovascular system, then the following pharmaceuticals are used for treatment:

• cardiac glycosides;
• magnesium and potassium preparations. They are prescribed to improve metabolism in the cells of damaged tissues;
• potassium-sparing diuretics. They are necessarily included in the treatment plan, since they remove excess fluid from the patient's body;
• selective beta-blockers;
• cardioprotectors.

Is everything correct in the article from a medical point of view?

Answer only if you have proven medical knowledge

Diseases with similar symptoms:

Heart defects are anomalies and deformations of individual functional parts of the heart: valves, septa, openings between vessels and chambers. Due to their improper functioning, blood circulation is disturbed, and the heart ceases to fully fulfill its main function - supplying oxygen to all organs and tissues.

Heart failure defines such a clinical syndrome, within the framework of the manifestation of which there is a violation of the pumping function inherent in the heart. Heart failure, the symptoms of which can manifest themselves in a variety of ways, is also characterized by the fact that it is characterized by constant progression, against which patients gradually lose adequate ability to work, and also face a significant deterioration in their quality of life.