New in the treatment of COPD with heart failure. Optimization of treatment of patients with CHF with cardiopulmonary pathology

Chronic obstructive pulmonary disease or COPD refers to chronic lung diseases associated with respiratory failure. Bronchial damage develops with emphysema complications against the background of inflammatory and external stimuli and has a chronic progressive character.

The alternation of latent periods with exacerbations requires a special approach to treatment. Development risk serious complications quite high, which is confirmed by statistical data. Respiratory dysfunction causes disability and even death. Therefore, patients with this diagnosis need to know COPD, what it is and how the disease is treated.

general characteristics

When exposed to respiratory system various irritating substances in people with a predisposition to pneumonia, negative processes begin to develop in the bronchi. First of all, the distal sections are affected - located in close proximity to the alveoli and lung parenchyma.

Against the background of inflammatory reactions, the process of natural discharge of mucus is disrupted, and small bronchi become clogged. When an infection is attached, inflammation spreads to the muscle and submucosal layers. As a result, bronchial remodeling occurs with replacement by connective tissues. In addition, lung tissue and bridges are destroyed, which leads to the development of emphysema. With a decrease in the elasticity of the lung tissues, hyperairiness is observed - the air literally inflates the lungs.

Problems arise precisely with the exhalation of air, since the bronchi cannot fully expand. This leads to a violation of gas exchange and a decrease in the volume of inhalation. Change natural process breathing manifests itself in patients as shortness of breath in COPD, which increases significantly with exercise.

Persistent respiratory failure causes hypoxia - oxygen deficiency. From oxygen starvation all organs are affected. With prolonged hypoxia, the pulmonary vessels narrow even more, which leads to hypertension. As a result, irreversible changes in the heart occur - the right section increases, which causes heart failure.

Why is COPD classified as a separate group of diseases?

Unfortunately, not only patients, but also medical workers little is known about the term chronic obstructive pulmonary disease. Doctors habitually diagnose emphysema or chronic bronchitis. Therefore, the patient does not even realize that his condition is associated with irreversible processes.

Indeed, in COPD, the nature of symptoms and treatment in remission are not much different from the signs and methods of therapy for pulmonary pathologies associated with respiratory failure. What then made physicians single out COPD as a separate group.

Medicine has determined the basis of such a disease - chronic obstruction. But the narrowing of the gaps in respiratory tract occur in the course of other pulmonary diseases.

COPD, unlike other diseases such as asthma and bronchitis, cannot be permanently cured. Negative processes in the lungs are irreversible.

So, in asthma, spirometry shows improvement after bronchodilators are used. Moreover, the indicators of PSV, FEV may increase by more than 15%. While COPD does not provide significant improvements.

Bronchitis and COPD are two different diseases. But chronic obstructive pulmonary disease can develop against the background of bronchitis or proceed as an independent pathology, just like bronchitis can not always provoke COPD.

Bronchitis is characterized by a prolonged cough with sputum hypersecretion and the lesion extends exclusively to the bronchi, while obstructive disorders are not always observed. Whereas sputum separation in COPD is not increased in all cases, and the lesion extends to structural elements, although bronchial rales are auscultated in both cases.

Why does COPD develop?

Not so few adults and children suffer from bronchitis, pneumonia. Why, then, chronic obstructive pulmonary disease develops only in a few. In addition to provoking factors, predisposing factors also affect the etiology of the disease. That is, the impetus for the development of COPD can be certain conditions in which people who are prone to pulmonary pathologies find themselves.

Predisposing factors include:

1. hereditary predisposition. It is not uncommon to have a family history of certain enzyme deficiencies. This condition has a genetic origin, which explains why the lungs do not mutate in a heavy smoker, and COPD in children develops for no particular reason.
2. Age and gender. For a long time it was believed that pathology affects men over 40. And the rationale is more related not to age, but to smoking experience. But today the number of women who smoke with experience is no less than that of men. Therefore, the prevalence of COPD among the fair sex is no less. In addition, women who are forced to breathe cigarette smoke also suffer. Passive smoking negatively affects not only the female, but also the children's body.
3. Problems with the development of the respiratory system. Moreover, we are talking about both the negative impact on the lungs during intrauterine development, and the birth of premature babies whose lungs did not have time to develop for full disclosure. In addition, and in early childhood lagging behind in physical development negatively affects the state of the respiratory system.
4. Infectious diseases. With frequent respiratory diseases infectious origin, both in childhood and at an older age, increases the risk of developing COL at times.
5. Hyperreactivity of the lungs. Initially, this condition is the cause bronchial asthma. But in the future, the addition of COPD is not ruled out.

But this does not mean that all patients at risk will inevitably develop COPD.

Obstruction develops under certain conditions, which can be:

1. Smoking. Smokers are the main patients diagnosed with COPD. According to statistics, this category of patients is 90%. Therefore, it is smoking that is called the main cause of COPD. And the prevention of COPD is based primarily on smoking cessation.
2. Harmful working conditions. People forced by their kind labor activity, inhale regularly dust of various origins, air saturated with chemicals, smoke suffer from COPD quite often. Work in mines, construction sites, in the collection and processing of cotton, in metallurgical, pulp, chemical production, in granaries, as well as in enterprises producing cement, other building mixtures leads to the development of respiratory problems to the same extent in smokers and non-smokers .
3. Inhalation of combustion products. We are talking about biofuels: coal, wood, manure, straw. Residents who heat their homes with such fuel, as well as people who are forced to be present during natural fires, inhale combustion products that are carcinogens and irritate the respiratory tract.

In fact, any external effect on the lungs of an irritating nature can provoke obstructive processes.

Main complaints and symptoms

Primary signs of COPD associated with cough. Moreover, cough, to a greater extent, worries patients in the daytime. At the same time, sputum separation is insignificant, wheezing may be absent. The pain practically does not bother, sputum leaves in the form of mucus.

Sputum with the presence of pus or a cough that provokes hemoptysis and pain, wheezing - the appearance of a later stage.

The main symptoms of COPD are associated with the presence of shortness of breath, the intensity of which depends on the stage of the disease:

• With mild shortness of breath, breathing is forced against the background of fast walking, as well as when climbing a hill;
• About shortness of breath moderate says the need to slow down the pace of walking on a flat surface due to breathing problems;
• Severe shortness of breath occurs after several minutes of walking at a free pace or walking a distance of 100 m;
• For shortness of breath of the 4th degree, the appearance of breathing problems during dressing, performing simple actions, immediately after going outside is characteristic.

The occurrence of such syndromes in COPD may accompany not only the stage of exacerbation. Moreover, with the progress of the disease COPD symptoms in the form of shortness of breath, coughing becomes stronger. On auscultation, wheezing is heard.

Breathing problems inevitably provoke systemic changes in the human body:

• The muscles involved in the breathing process, including the intercostal ones, atrophy, which causes muscle pain and neuralgia.
• In the vessels, changes in the lining, atherosclerotic lesions are observed. Increased tendency to form blood clots.
• Man facing heart problems in the form arterial hypertension, coronary disease and even a heart attack. For COPD, the pattern of cardiac changes is associated with left ventricular hypertrophy and dysfunction.
• Osteoporosis develops, manifested by spontaneous fractures tubular bones as well as the spine. Constant joint pain, bone pain cause a sedentary lifestyle.

The immune defense is also reduced, so any infections are not rebuffed. Frequent colds, at which it is observed heat, headache, and other signs of infection are not uncommon in COPD.

There are also mental and emotional disorders. Significantly reduced performance depression, unexplained anxiety.

It is problematic to correct emotional disorders that have arisen against the background of COPD. Patients complain of apnea, stable insomnia.

In the later stages, cognitive disorders also appear, manifested by problems with memory, thinking, and the ability to analyze information.

Clinical forms of COPD

In addition to the stages of development of COPD, which are most often used in medical classification,

There are also forms of the disease according to the clinical manifestation:

1. bronchial type. Patients are more likely to cough, wheezing with sputum discharge. In this case, shortness of breath is less common, but heart failure develops more rapidly. Therefore, there are symptoms in the form of swelling and cyanosis of the skin, which gave the name to the patients "blue edema".
2. emphysematous type. AT clinical picture dyspnea predominates. The presence of cough and sputum is rare. The development of hypoxemia and pulmonary hypertension is observed only in the later stages. Patients experience significant weight loss and skin acquire a pink-gray hue, which gave the name - "pink puffers".

However, it is impossible to speak of a clear division, since in practice COPD of a mixed type is more common.

Exacerbation of COPD

The disease can be aggravated unpredictably under the influence of various factors, including external, irritating, physiological and even emotional. Even after eating in a hurry, choking may occur. At the same time, the condition of a person is deteriorating rapidly. Increasing cough, shortness of breath. The use of the usual basic COPD therapy in such periods does not give results. During the period of exacerbation, it is necessary to adjust not only the methods of COPD treatment, but also the doses of the drugs used.

Usually treatment is carried out in a hospital, where it is possible to provide emergency assistance sick and spend necessary examinations. If exacerbations of COPD occur frequently, the risk of complications increases.

Urgent care

Exacerbations with sudden attacks suffocation and severe shortness of breath must be stopped immediately. Therefore, emergency assistance comes to the fore.

It is best to use a nebulizer or spacer and provide fresh air. Therefore, a person predisposed to such attacks should always have inhalers with them.

If first aid does not work and suffocation does not stop, it is urgent to call an ambulance.

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Chronic obstructive pulmonary disease

Principles of treatment for exacerbations

• Short bronchodilators are used with an increase in the usual dosages and frequency of administration.
• If bronchodilators do not have the desired effect, Eufilin is administered intravenously.
• It can also be prescribed for exacerbation of COPD treatment with beta-stimulants in combination with anticholinergic drugs.
• If pus is present in the sputum, antibiotics are used. Moreover, it is advisable to use antibiotics with a wide spectrum of action. It makes no sense to use narrowly targeted antibiotics without bakposev.
• The attending physician may decide to prescribe glucocorticoids. Moreover, Prednisolone and other drugs can be prescribed in tablets, injections or used as inhaled glucocorticosteroids (IGCS).
• If oxygen saturation is significantly reduced, oxygen therapy is prescribed. Oxygen therapy is carried out using a mask or nasal catheters to ensure proper oxygen saturation.

In addition, drugs can be used to treat diseases that frolic against the background of COPD.

Basic treatment

To prevent seizures and improve general condition patient, a set of measures is carried out, among which behavioral and drug treatment, dispensary observation.

The main drugs used at this stage are bronchodilators and corticosteroid hormones. Moreover, it is possible to use long-acting bronchodilator drugs.

Together with taking medications, it is necessary to pay attention to the development of pulmonary endurance, for which breathing exercises are used.

As for nutrition, the emphasis is on getting rid of excess weight and saturation with the necessary vitamins.

Treatment of COPD in the elderly and in severe patients associated with a number of difficulties due to the presence of concomitant diseases, complications and reduced immune protection. Often such patients require constant care. Oxygen therapy in such cases is used at home and, at times, is the main way to prevent hypoxia and related complications.

When the damage to the lung tissue is significant, cardinal measures are necessary with resection of a part of the lung.

To modern methods cardinal treatment includes radiofrequency ablation (ablation). It makes sense to do RFA when detecting tumors, when for some reason the operation is not possible.

Prevention

Basic Methods primary prevention directly depend on the habits and lifestyle of a person. Smoking cessation, the use of personal protective equipment significantly reduces the risk of developing lung obstruction.

Secondary prevention is aimed at preventing exacerbations. Therefore, the patient must strictly follow the recommendations of doctors for treatment, as well as exclude provoking factors from their lives.

But even cured, operated patients are not fully protected from exacerbations. Therefore, tertiary prevention is also relevant. Regular medical examination allows you to prevent the disease and detect changes in the lungs in the early stages.

Periodic treatment in specialized sanatoriums is recommended for both patients, regardless of the stage of COPD, and cured patients. With such a diagnosis in the anamnesis, vouchers to the sanatorium are provided on a preferential basis.

Read:

The pathogenesis of chronic cor pulmonale in chronic obstructive pulmonary disease is complex and is inextricably linked with respiratory disorders. At the same time, among the factors damaging the heart, there are:

- alveolar hypoxia and arterial hypoxemia;

- pulmonary hypertension;

- hemorheological disorders;

- neurohumoral disorders;

- infectious and toxic effects;

- immune and autoimmune damage;

- electrolyte changes;

— impact medicines used in the treatment of these patients;

- comorbidities, and especially coronary artery disease.

A decrease in the drainage function of the bronchi with a sharp increase in resistance to air flow leads to the development of uneven alveolar ventilation, alveolar hypoxia, followed by arterial hypoxemia, leading to a generalized increase in the tone of the pulmonary arterial vessels (Euler-Liljestrand reflex - spasm of the pulmonary arterioles with a decrease in RO 2 alveoli), to pulmonary hypertension and myocardial malnutrition. An increase in tone in the arterial system of the pulmonary circulation may be due exclusively to neurogenic genesis, i.e. as a result of increased function of sympathetic innervation. It should be emphasized that in most patients with chronic obstructive pulmonary diseases, pulmonary hypertension does not reach high numbers.

Hypoxemia has a direct damaging effect on the smooth muscles of the small arteries of the lungs and on the myocardium in general. With oxygen deficiency in muscle tissues, the rate of glucose utilization and the absorption of free fatty acids. Under hypoxic conditions, anaerobic glycolysis is the main source of ATP here. The release of lactate from the cell and the accumulation of H + ions. as well as products of lipid peroxidation leads to acidosis and disruption of the permeability of cell membranes. This entails a disruption in the functioning of various enzymatic systems, in particular the system of Na + /K + -ATPase, Ca 2+ -ATP-ases of cell membranes. There is an accumulation of Na and Ca in the cytoplasm and a loss of intracellular K +. These processes in chronic obstructive pulmonary diseases can increase pulmonary hypertension, cause electrical instability of the myocardium with the formation of various cardiac arrhythmias.

An important link in the chain of pathogenetic processes of the pulmonary heart in chronic obstructive pulmonary diseases are the emerging violations of the rheological properties of the blood with the development of microcirculatory disorders that exacerbate the energy hunger of the myocardium. A compensatory increase in the volume of circulating erythrocytes and a decrease in their plasticity, swelling and degranulation of platelets with the release of vasoactive substances lead to an increase in blood viscosity, a change in its aggregate state, the formation of DIC, which also contributes to an increase in pressure in the pulmonary circulation.

AT last years The attention of researchers is attracted by the role of the endothelium of the pulmonary vessels, the renin-angiotensin-aldosterone system, cytokines in the formation of pulmonary hypertension and heart failure in chronic obstructive pulmonary diseases. It has been proven that in response to hypoxia, there is an increased production of vasoconstrictor substances by the endothelium, along with a decrease in the formation of vasodilating substances, in particular, the endothelium-relaxing factor. It was also established that the level of angiotensin-converting enzyme and components of the renin-angiotensin-aldosterone system in patients with chronic obstructive pulmonary diseases increases with an increase in the degree of hypoxia. Such changes contribute to the formation of pulmonary hypertension, stimulate the processes of fibrosis in the myocardium, disrupt the systolic and diastolic function of both ventricles, leading to the development of circulatory failure.

There are more and more reports in the literature about the active participation in the formation of chronic heart failure in various heart diseases of pro-inflammatory cytokines (interleukin-1b, interleukin-6 and factor tumor necrosis-a). It is believed that the effect of cytokines on the formation and progression of chronic heart failure is realized through a direct damaging effect on cardiomyocytes and modulation of the activity of the neurohumoral system, endothelial functions, and a number of other biologically active factors.

Infectious-toxic factors also have a negative effect on the myocardium of patients with chronic obstructive pulmonary diseases. Activity inflammatory process in the bronchi and the severity endogenous intoxication at the same time, they play an important role in the development of both cardiac arrhythmias and decompensation of cardiac activity. It is known that substances of average molecular weight have a direct toxic effect on tissues, including the myocardium, worsening microcirculation.

The presence of secondary immunological deficiency in patients suffering from chronic obstructive pulmonary disease is well known. Violation of the differentiation of highly organized tissues, including immune system, due to tissue hypoxia in patients with broncho-obstructive syndrome, can lead to both a lack of anti-infective immunity and a breakthrough in immunological tolerance. There is evidence of a clear relationship between a decrease in myocardial contractility and the severity of autosensitization. With an exacerbation of the inflammatory process in the lungs in patients, sensitization to the cardiac antigen is determined. In patients with reduced myocardial contractility, sensitization to cardiac antigen persists even during the period of remission of chronic obstructive pulmonary diseases, which indicates the inclusion of autoimmune mechanisms in the development of myocardial lesions in them. Autoimmune damage to the myocardium inevitably changes its bioelectrical properties, contributing to the formation of arrhythmias in the work of the heart.

Observations made by various investigators indicate a possible involvement medicines used in the treatment of patients with chronic obstructive pulmonary diseases (eufillin, theophylline, sympathomimetics, atropine, corticosteroids), in the development of myocardial lesions and in the formation of various cardiac arrhythmias.

Particular attention in chronic obstructive pulmonary diseases deserves the pathogenesis of lesions of the left heart.

The main factors that worsen the functioning of the left ventricle in patients with chronic obstructive pulmonary disease include:

- an increase in the dilatation of the right ventricle with an increase in its final diastolic pressure and volume, leading to compression of the left ventricle;

- paradoxical movement of the interventricular septum, which protrudes into the cavity of the left ventricle and makes it difficult to fill;

- hypoxia, infectious-toxic and medicinal effects, activation of the sympathoadrenal and renin-angiotensin-aldosterone systems in relation to which the right and left parts of the heart are in the same conditions.

Myocardial damage in patients with chronic obstructive pulmonary disease may also be due to concomitant cardiac pathology (CHD, hypertension). It has been shown that the development of IHD contributes to the progression of chronic obstructive pulmonary diseases, which is associated with the commonality of some links in their pathogenesis. Thus, the formation of secondary pulmonary arterial hypertension in chronic obstructive pulmonary diseases increases the load on the right heart and left atrium. This worsens the state of the coronary reserve. Increasing ischemia of the myocardium of both ventricles leads to the progression of coronary and pulmonary heart failure.

At the next stage of the lesson, the teacher, together with the students, conducts questioning and examination of a patient with chronic pulmonary heart or a pathology that requires differential diagnosis with chronic cor pulmonale. Students, under the supervision of a teacher, participate in questioning the patient, collecting complaints, data on the anamnesis of the disease and the life of the patient.

Cor pulmonale in COPD. Diagnostics

This pathological term is right ventricular hypertrophy. caused by disorders in the pulmonary circulation. COPD is the most common cause cor pulmonale, but there is an opinion that it is less common, at least in developed countries. Cor pulmonale is diagnosed in vivo using MRI of the heart.

Diagnosis usually based on clinical assessment - ankle edema and increased jugular venous pressure in patients with persistent hypoxemia along with ECG evidence of right heart dilatation and pulmonary P wave (p-pulmonale) with or without echocardiographic dysfunction.

At COPD hypoxemia is the main factor in the development of cor pulmonale, and its correction is the most effective treatment. Although this does not lead to regression of severe pulmonary hypertension, it prevents its progression.

Two randomized controlled trials. conducted more than 25 years ago show that patients with PaO2<7,3 кПа живут дольше, если получают в домашних условиях кислород. Эти изменения необязательно соотносятся с физиологическими улучшениями в малом круге кровообращения.

Oxygen better delivered by an oxygen concentrator using a face mask or nasal prongs (these are more convenient to use). Patients should be examined in a clinically stable condition to confirm the presence of persistent hypoxemia, and that the prescribed oxygen concentration is achieved Pa02 above 8 kPa without developing hypercapnia. A detailed explanation of the goals of oxygen therapy is of great importance. It is unlikely that shortness of breath will decrease with physical exertion, and the patient should be aware of this.

Ambulatory oxygen therapy intended for patients who are able to leave the house or endure significant physical activity.

Medical therapy plays a limited role here. Diuretics are still used to reduce peripheral edema, while ACE inhibitors are widely prescribed and appear to be effective, although there are no large clinical studies to support this.

Application other cardiac drugs, such as digoxin, are not recommended unless the patient has atrial fibrillation. Vasodilators of any type, including inhaled NO, significantly impair gas exchange in cor pulmonale due to COPD. There are no studies yet showing that the use of these drugs has a beneficial effect on the natural course.

Inclusion patient into treatment Patients who adhere to treatment, even if it is a placebo, feel significantly better than those who do not. Persuading people to adhere to a treatment regimen is probably one of the best treatments we use. Identification of people with severe depression and anxiety is of great importance, and the severity of symptoms should be treated on their merits.

Selection time explaining the nature of the disease to the patient, what it means and what the treatment achieves, is always helpful, providing a realistic assessment of what can be done for them, and when it is going to be done, helps to reassure that everything is not so hopeless. Careful checks are needed to ensure that the patient is on inhalation therapy and repeat treatments are required. Special recommendations for the use of the device are mandatory.

Control of adherence to prescribed treatment is a useful criterion for determining who should be expected to have major problems in the future, especially when taking less than 80% of prescribed dosages.

Chronic obstructive pulmonary disease

Main points:

signs

The earliest symptom of COPD is a cough. In the early stages of the disease, it is episodic, but later it worries constantly, even in a dream. Cough accompanied by phlegm. Usually it is not much, but in the acute stage, the amount of discharge increases. Possible purulent sputum.

Another symptom of COPD is shortness of breath. It appears late, in some cases even 10 years after the onset of the disease.

COPD sufferers are divided into two groups - "pink puffers" and "bluish puffers". "Pink puffers" (emphysematous type) are often thin, their main symptom is shortness of breath. Even after a little physical exertion, they puff, puffing out their cheeks.

"Bluish edema" (bronchitis type) are overweight. COPD is manifested in them mainly by a strong cough with sputum. Their skin is cyanotic, their legs swell. This is due to cor pulmonale and stagnation of blood in the systemic circulation.

Description

According to the World Health Organization (WHO), COPD affects 9 men out of 1000 and about 7 women out of 1000. In Russia, about 1 million people suffer from this disease. Although there is reason to believe that there are many more.

In 90% of cases, COPD is caused by smoking. both active and passive. The remaining 10% of COPD cases develop due to:

• transferred infectious diseases of the respiratory tract (bronchitis);
• bronchial asthma;
• low birth weight;
• hereditary predisposition;
• exposure to occupational hazards (dust, vapors of acids, alkalis, SO2);
• atmospheric air pollution, kitchen fumes.

COPD may also develop due to a combination of these factors.

There are 4 stages of COPD. On the I stage (light course) the sufferer may not even notice that something is wrong with him. Often the disease is manifested only by a chronic cough, and organic disorders are minor, so the correct diagnosis at this stage is very rare.

COPD sufferers stage II (moderate course) often see a doctor for shortness of breath during exercise or due to an exacerbation of the disease and intense cough.

On the Stage III (severe course) airflows in the respiratory tract are already significantly limited, shortness of breath occurs not only during physical exertion, but also at rest, the disease often worsens.

On the IV stage (extremely severe) exacerbations of COPD become life-threatening. The bronchi become severely blocked (bronchial obstruction), and cor pulmonale develops. At this stage, COPD sufferers are assigned a disability.

The bronchi are an important part of the respiratory system. It is through them that air enters the lungs. They are tubes up to 18 mm in diameter, consisting of cartilaginous rings or plates. The main bronchi, right and left, depart from the trachea. The right bronchus is slightly wider than the left, since the volume of the right lung is larger than the left. The main bronchi are divided into lobar (bronchi of the 1st order), zonal (bronchi of the 2nd order), subsegmental (bronchi of the 3rd order), segmental (bronchi of the 4th and 5th orders), and small bronchi from 6- th to 15th orders. Gradually branching, the bronchi pass into the bronchioles.

The lumen of the bronchi is lined with a mucous membrane. On bronchoscopy, it has a grayish color. Epithelial cells of the mucous membrane have cilia to remove foreign inclusions. In addition, these cells produce mucus, which protects the bronchi from the effects of foreign bodies and microorganisms.

The disease begins with the fact that tobacco smoke or other toxic substances interact with vagus nerve receptors, resulting in bronchospasm. In addition, under the influence of various damaging factors (intoxication with tobacco smoke, gases, infections, etc.), the movement of the cilia of the bronchial epithelium stops. As a result, the mucus secreted by the bronchial mucosa is not excreted naturally. In addition, due to the impact of risk factors on the bronchial mucosa, its cells begin to produce more mucus in order to protect themselves. At this stage, a chronic cough occurs, it mainly worries a person in the morning. Many smokers at this stage are sure that nothing serious is happening, and they are coughing simply because of smoking.

However, after some time, chronic inflammation develops in the walls of the bronchi, exacerbating the blockage of the bronchi. Then, as a result of blockage of the bronchi, overstretching of the alveoli occurs. Stretched alveoli compress small bronchioles, which further contributes to the violation of airway patency.

At the onset of the disease, the blockage is reversible, as it develops as a result of bronchospasm and mucus hypersecretion. But later, when the expiratory collapse of the small bronchi and bronchioles develops, fibrosis and emphysema. blockage is irreversible.

COPD affects mainly the bronchi of the 2nd-17th order.

In the process of development of COPD, there is a reduction in the capillary bed of the pulmonary circulation. However, the body still needs a certain amount of oxygenated blood. To do this, he is forced to drive more blood through the pulmonary circulation. To make this possible, you need to increase the pressure in the pulmonary circulation. This increases the load on the right ventricle, the muscles of which are weaker than in other parts of the heart. The right ventricle enlarges, stretches - this is how the cor pulmonale is formed.

COPD can be fatal. According to WHO, now this disease is in 11th place in terms of the number of deaths, however, experts suggest that in 10 years the death rate from this disease will increase by 30%, and it will enter the top five. COPD is not only dangerous in itself, its complications are also dangerous - cor pulmonale, acute and chronic respiratory failure. heart failure. secondary polycythemia (an increase in the number of red blood cells), spontaneous pneumothorax, pneumomediastinum.

Diagnostics

The diagnosis of chronic obstructive pulmonary disease is made by a pulmonologist. The diagnosis is based on the anamnesis data, the clinical picture and the results of the study.

The gold standard for diagnosing COPD is the study of lung ventilation function. Assess the volume of forced exhaled air in the first second (FEV1). In COPD sufferers, it is reduced and decreases as the disease progresses. A pharmacological test is also made, during which FEV1 is measured 35-40 minutes after inhalation of drugs that expand the lumen of the bronchi and reduce the separation of mucus. With COPD, the increase in air volume is minimal. This test differentiates COPD with bronchial asthma, in which FEV increases significantly after inhalation of the drug.

They also do electrocardiography. which shows changes in the heart, echocardiography, which determines the presence of pulmonary hypertension and chronic cor pulmonale. In addition, they do a clinical blood test.

In severe COPD, the gas composition of the blood is determined.

If therapy is ineffective, sputum is taken for bacteriological analysis.

Treatment

Chronic obstructive pulmonary disease is an incurable disease. However, adequate therapy can reduce the frequency of exacerbations and significantly prolong the life of the patient. For the treatment of COPD, drugs are used that expand the lumen of the bronchi and mucolytics, which thin the sputum and help it to be removed from the body.

To relieve inflammation, glucocorticoids are prescribed. However, their long-term use is not recommended due to serious side effects.

During the period of exacerbation of the disease, if its infectious nature is proven, antibiotics or antibacterial agents are prescribed, depending on the sensitivity of the microorganism.

Patients with respiratory failure are given oxygen therapy.

Those suffering from pulmonary hypertension and COPD in the presence of edema are prescribed diuretics, with arrhythmias - cardiac glycosides.

A person suffering from COPD is referred to a hospital if he has:

• a significant increase in the severity of symptoms;
• lack of effect from the prescribed treatment;
• the appearance of new symptoms;
• first-time cardiac arrhythmias;
• severe concomitant diseases (diabetes mellitus, pneumonia, renal failure, liver failure);
• the impossibility of providing qualified medical care on an outpatient basis;
• diagnostic difficulties.

A patient is admitted to the intensive care unit if he has:

• severe shortness of breath, not relieved by drugs;
• disturbances of consciousness, coma.

Prevention

The main prevention of COPD is smoking cessation. Doctors recommend leading a healthy lifestyle, eating right and boosting immunity.

It is also important to treat infectious diseases of the respiratory tract in a timely manner.

Those working in hazardous industries must strictly observe safety precautions and wear respirators.

Unfortunately, in large cities it is not possible to exclude one of the risk factors - polluted atmosphere.

COPD is best treated early. For timely diagnosis of this disease, it is necessary to undergo medical examination in time.

The features of chronic heart failure (CHF) in patients with and without chronic obstructive pulmonary disease (COPD) were studied. For this purpose, 75 people were examined. The patients were divided into 2 groups based on the presence of COPD. The 1st group included 38 patients with COPD, the 2nd group included 37 patients without COPD. In patients with comorbidities, there is a decrease in exercise tolerance, aggravation of hypoxemia, an increase in heart rate, and higher systolic pressure in the pulmonary artery. An insufficient dosage of beta-blockers has been noted in patients with COPD, which can aggravate the course and progression of CHF. Thus, patients with COPD require special attention, a more detailed history taking and a thorough analysis of the data obtained for the timely diagnosis of cardiac pathology and the appointment of specific therapy, including highly selective beta-blockers.

chronic heart failure

chronic obstructive pulmonary disease

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Chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) are the leading pathologies due to hospitalizations among elderly patients. Their combination potentiates systemic inflammation and hypoxia, which in turn lead to endothelial dysfunction, increased arterial stiffness, increased platelet reactivity, accelerated atherogenesis, apoptosis of myocardial and skeletal muscle cells. The presence of both pathologies in a patient is accompanied by an increased risk of adverse events in the form of recurrent myocardial infarction, more frequent decompensation of CHF and exacerbations of COPD. Death usually occurs from a cardiovascular cause.

The prevalence of CHF in Russia is 7% (7.9 million people). Clinically pronounced CHF occurs in 4.5% (5.1 million people). One-year mortality of patients is 12%, and three-year - 36%. . Terminal CHF reaches 2.1% of cases (2.4 million people). The prevalence of CHF in patients with COPD ranges from 7.2 to 20.9%, in the Russian Federation about 13%.

Timely diagnosis of CHF in patients with COPD allows the appointment of neurohumoral modulators, thereby improving the quality and life expectancy of patients.

Target

To study the features of CHF in patients with and without COPD.

Materials and methods

In accordance with the goal, 75 people with CHF were examined, hospitalized in the State Health Institution "Regional Clinical Hospital of Saratov" in the period from 2013 to 2014, who signed an informed consent to participate in the study. The study was approved by the Ethics Committee of the Saratov State Medical University. IN AND. Razumovsky" of the Ministry of Health of Russia. Inclusion criteria were male gender, age over 40 years and under 80 years, the presence of diagnosed CHF according to the recommendations of the Russian Society of Cardiology in 2013. The exclusion criterion was the presence of unstable coronary heart disease (CHD) (myocardial infarction, acute coronary syndrome) in less than 3 months before inclusion, heart defects, myocarditis, cardiomyopathies, acute and chronic diseases in the acute phase (with the exception of COPD). The patients were divided into 2 groups, depending on the presence of COPD. All patients underwent spirography using a MicroLab device (Micro Medical Ltd. (Great Britain), echocardiography using an Apogee`CX device using a 2.75 MHz probe with simultaneous recording of a two-dimensional echocardiogram and Doppler echocardiogram in a pulsed mode, N-terminal a fragment of the brain natriuretic peptide (BNP) using a kit of reagents manufactured by BIOMEDICA, Slovakia Clinical manifestations of CHF were assessed, the clinical status assessment scale for CHF (CHCS), the modified dyspnea scale (mMRC), the Charlson comorbidity index were used.

Statistical processing was carried out using the Statistica 8 package. To count features with a normal type of distribution, a t-test was used for independent groupings. For non-normal distribution, the Mann-Whitney test, the χ2 test with Yates correction were used. Correlation analysis was carried out. The difference in the indices of the groups at p<0,05.

results

Among the examined patients, 62 (83%) patients were in the cardiology department, of which 25 (40%) had COPD. COPD was diagnosed for the first time in 13 (21%) patients hospitalized in the cardiology department. Among those who had COPD previously diagnosed, the diagnosis was confirmed in all patients. Thus, there is an underdiagnosis of respiratory pathology at the prehospital stage, and the detection of COPD among patients with CHF corresponds to the literature data.

In 38 (50.7%) patients, COPD was diagnosed during spirography (group 2), and group 1 consisted of 37 patients without signs of COPD. As shown in Table 1, patients in both groups were comparable in age, frequency and duration of arterial hypertension, history of angina pectoris, body mass index.

Table 1

General characteristics of patients with and without COPD (M±s), (Me).

There were significantly more smokers among patients of group 2 than among patients of group 1 (p<0,001). Пациенты с ХОБЛ курили дольше (p>0.05) and more intense (p<0,001), чем больные с ХСН без ХОБЛ.

The duration of dyspnea as one of the main symptoms of COPD and CHF was comparable in patients with and without COPD. At the same time, the duration of cough as one of the main respiratory symptoms of COPD was longer in patients with respiratory pathology (p<0,001).

Patients with COPD and CHF had severe respiratory dysfunction. Most of the patients (60%) suffered from severe and extremely severe COPD.

Features of CHF in the studied groups of patients are presented in Table 2. In patients with comorbidity, such manifestations of CHF as edema in the lower extremities, hydrothorax are more often observed.

table 2

Features of manifestations of CHF in examined patients with and without COPD (M±s), (Me).

The problem of differential diagnosis of shortness of breath often has a difficult solution. The cause of shortness of breath can be a wide range of pathologies: heart and respiratory failure, anemia, obesity, etc. Of particular difficulty is the identification of heart failure in patients with COPD. This is mainly due to the presence of emphysema, which is able to hide such manifestations of CHF as moist, finely bubbling rales in the lungs, displacement of the percussion borders of the heart, and in some cases, a gallop rhythm. And bronchial obstruction, as a rather specific manifestation of COPD, can also be secondary, due to interstitial pulmonary edema. In this regard, spirography data in patients with severe cardiac decompensation are often not entirely objective, but the ratio of FEV 1 to FVC is more than 0.7 in the absence of COPD. Among the patients examined by us, this sign helped to exclude COPD in 7 (19%) patients of the 1st group.

To clarify the solution of the diagnostic problem, it is possible to identify clinical signs of decompensation in a patient with COPD in the form of manifestations of cardiac asthma - the inability to take a horizontal position, as well as swelling and pulsation of the jugular veins. When collecting an anamnesis, it is important to find out whether the patient is able to lie with the usual headboard during the interictal period. Among the patients of the 2nd group, manifestations of cardiac asthma were noted in 9 (24%) patients, and pulsation and swelling of the cervical veins were detected in 4 (11%) patients.

A decrease in physical performance was established (test with a six-minute walk) (p<0,001) и более выраженная гипоксемия (p<0,001) у пациентов с ХОБЛ и ХСН по сравнению с больными без респираторной патологии.

Currently, the result of a six-minute walk test is used to establish the functional class (FC) of CHF. According to our data, in the 1st group, the majority of patients (81.1%) had the 3rd FC of CHF, in 3 (8.1%) patients - the 2nd FC and in 4 (10.8%) patients - 4th FC. In the 2nd group, the 3rd FC also prevailed (76.3%), the rest were diagnosed with the 4th FC (23.7%).

At the same time, it should be taken into account that in patients with concomitant respiratory pathology, especially in severe and extremely severe COPD, the test result may be reduced due to broncho-obstructive disorders and the formation of respiratory failure. This may lead to overdiagnosis of CHF severity in patients with concomitant cardiorespiratory pathology. In this case, the necessary study is to determine the level of the N-terminal fragment of the BNP. Among patients with COPD, its level was 309 pg/ml.

In patients with COPD and CHF, an increase in heart rate (HR) was noted compared with patients without COPD. Currently, an increase in resting heart rate is associated with an increase in overall mortality, mortality from cardiovascular causes, the frequency of re-hospitalization due to cardiovascular causes, and exacerbation of CHF. A decrease in heart rate is associated with a reduced risk of death from cardiovascular causes, sudden death, and the likelihood of reinfarction. According to our data, in the majority of patients with COPD (61%), the heart rate was more than 80 beats per minute (p<0,001 с больными без ХОБЛ). Повышение ЧСС у больных с ХОБЛ и ХСН может быть связано с активным применением бронходилататоров этой категорией пациентов, а также с недостаточным назначением бета-адреноблокаторов либо использованием их в недостаточных дозах. Так, лишь 8 (21%) пациентов с сочетанием ХОБЛ, ХСН и перенесенного инфаркта миокарда (ИМ) постоянно получали бета-блокаторы, в то время как в группе без ХОБЛ таких пациентов было 20 (54%). Бета-блокаторы ранее рекомендовались 31 (83,8 %) больному 1-й группы и 22 (57,9 %) больным 2-й группы.

Among beta-blockers, all patients with COPD and CHF were prescribed bisoprolol at an average dose of 4.84±2.54 mg/day, with an average duration of administration of 4.57±4.96 years. In the group of patients without COPD, most patients also used bisoprolol (17-85%) at a dose of 4.79±2.25 mg/day. for 2.5±1.83 years), 1 patient received carvediolol at a dose of 12.5 mg/day. during the year, 1 patient - metoprolol succinate at a dose of 100 mg / day. for 3 years, 1 patient - nebivolol at a dose of 1.25 mg / day. during a year. There was no statistically significant difference in the dose and duration of taking bisoprolol in patients of both groups.

Among patients with CHF taking beta-blockers constantly, the average heart rate was 65.85±9.16 beats per minute, and in the group of patients with COPD and CHF - 75.77±10.2 beats per minute (p<0,01). Таким образом, у больных 2-й группы отмечена недостаточная дозировка бета-блокаторов, что, вероятно, связано с чрезмерной осторожностью врачей при назначении более высоких доз.

There were 17 (45%) patients with CHF and COPD who constantly took bronchodilators. Most often, patients in this group were prescribed berodual, which patients took for 1.82±1.07 years. Three patients constantly received formoterol at a dose of 24 mg/day. within 3.00±1.73 years. The average heart rate in patients constantly taking bronchodilators was 81.24±12.17 beats per minute.

When analyzing the features of myocardial infarction in patients with COPD and CHF, it turned out that the majority (34 patients, 90%) had an anginal variant, and 4 patients had a painless variant. In 25 (66%) patients, transmural changes in the myocardium were noted. Only one patient had a history of two MI, the rest - one at a time. The anterior wall was affected in 27 (71%) patients, the interventricular septum - in 22 (58%), the apex - in 21 (55%), the posterior wall was involved in the pathological process in 14 (37%) patients.

In the group of patients without COPD, 35 (95%) patients had an anginal variant, and 2 (5%) had an asthmatic variant. Transmural myocardial damage was found in 30 (81%) patients. 23 (62%) patients had one MI, 13 (35%) had two, and one patient had a history of three MIs. The anterior wall, interventricular septum, apex were affected in 26 (70%) patients, the posterior wall - in 19 (51%) patients.

Thus, transmural changes were stated equally often in the studied groups of patients. At the same time, in the COPD group, the presence of a painless form of MI was noted, which requires more careful attention of doctors to the management of this category of patients.

Detection of exertional angina in patients with COPD is rather difficult due to the fact that often the severity of shortness of breath does not allow patients to achieve the intensity of physical activity that can cause pain. As a rule, angina pectoris of a high functional class is diagnosed, which is also confirmed by our study, where out of 28 (74%) patients with an established diagnosis, 26 (93%) of them corresponded to the 3rd functional class, in one - to the 4th functional class, and only one - the 2nd FC. In the group of patients with CHF in the absence of COPD, angina pectoris was diagnosed in 31 (84%) patients, of which 26 (70%) - 3rd FC, 2 patients - 2nd FC and 3 patients - 4th FC .

According to modern concepts, the management of a patient with COPD, evaluation of the effectiveness of therapy and survival are largely determined by the frequency of exacerbation and its severity. Severe exacerbation is the main cause of death in patients. Each such episode is associated with an accelerated progression of the disease, a decrease in the quality of life, an increase in treatment costs, and decompensation of concomitant diseases, including CHF. Among the patients with COPD we examined, 12 (32%) had one exacerbation during the previous year, 11 (29%) patients had 2 exacerbations, three had 3 exacerbations, and one patient had a history of 4 exacerbations. At the same time, the exacerbation itself was the reason for hospitalization in 9 (24%) patients. The relationship between the frequency of exacerbations and FC CHF was noted (r=0.47, p<0,01), стадией ХСН (r=0,39, p<0,05), физической работоспособностью (r=-0,47, p<0,05), SaO 2 (r=-0,49, p<0,01), индексом BODE (r=0,52, p<0,01). Найденные взаимосвязи вероятнее всего обусловлены влиянием выраженности и тяжести патологического процесса в легких, усугубляющего течение и ускоряющего прогрессирование ХСН.

The ejection fraction (EF) of the left ventricle is one of the key indicators of hemodynamics in HF and has a great prognostic value: the lower the EF, the worse the prognosis. According to our data, in patients with COPD and CHF, the LV ejection fraction is significantly higher than in patients without COPD (p<0,05). Систолическая дисфункция левого желудочка (фракция выброса менее 35%) отмечалась у 6 (16%) пациентов с ХОБЛ и ХСН, у 7 (19%) больных без ХОБЛ. Фракция выброса менее 45% (используется в ряде исследований как показатель сниженной ФВ) имелась у 30 (81%) больных без ХОБЛ и у 20 (54%) пациентов с ХОБЛ и ХСН.

Patients with intermediate EF values ​​(from 35 to 50%) belong to the so-called gray zone, and they are recommended to be considered as having minor systolic dysfunction. There were 47 (62%) such patients in the group we examined: 26 (34%) patients had no signs of COPD, and 21 (28%) patients were diagnosed with COPD.

Normal ejection fraction (more than 50%) was detected in 4 (11%) patients without COPD and in 11 (29%) patients with COPD (p<0,001).

Systolic pressure in the pulmonary artery (SPPA) in patients with COPD and CHF significantly exceeds the level of the same indicator in patients without COPD (p<0,05). У пациентов с ХОБЛ и ХСН более высокий уровень легочной гипертензии может быть связан с сочетанными механизмами ее развития. При этом, учитывая сохранную фракцию выброса ЛЖ у большинства пациентов с ХОБЛ, значимый вклад вносит формирование легочной гипертензии в рамках хронического легочного сердца.

The causes of pulmonary hypertension are factors such as hypoxia, hypercapnia and acidosis, endothelial dysfunction. The latter may be associated with chronic hypoxemia leading to a decrease in the production of vasoconstrictors such as prostacyclin, prostaglandin E2, nitric oxide, as well as chronic inflammation.

Other factors that can lead to pulmonary hypertension include capillary area reduction and pulmonary vascular compression associated with destruction of the lung parenchyma in emphysema, as well as polycythemia, which can suppress endothelium-dependent vascular relaxation in response to acetylcholine.

When conducting a correlation analysis in patients with COPD, an inverse relationship was found between SPPA and exercise tolerance (test with a six-minute walk) (r=-0.40, p<0,05), сатурацией (r=-0,55, p<0,01) и прямая - с длительностью одышки (r=0,39, p<0,05) и количеством баллов по ШОКС (r=0,33, p<0,05). При оценке взаимосвязей СДЛА с параметрами Эхо-КГ была выявлена ожидаемая сильная прямая связь с размером правого предсердия (ПП) (r=0,80, p<0,001), конечным диастолическим размером правого желудочка (КДР ПЖ) (r=0,80, p<0,001), толщиной передней стенки правого желудочка (ТПСПЖ) (r=0,62, p<0,001).

Patients without COPD showed similar inverse relationships between SPPA and SaO 2 (r=-0.62, p<0,001), переносимостью физической нагрузки (тест с шестиминутной ходьбой) (r=-0,39, p<0,05) и прямые - с ШОКС (r=0,40, p<0,05), шкалой выраженности одышки mMRC (r=0,34, p<0,05), возрастом (r=0,40, p<0,05) и функциональным классом ХСН (r=0,39, p<0,05). Выявлены сильные прямые взаимосвязи с параметрами правых отделов сердца: с ПП (r=0,81, p<0,001), с КДР ПЖ (r=0,48, p<0,01), с ТПСПЖ (r=0,67, p<0,001).

conclusions

Diagnosis of CHF in patients with COPD is quite difficult, due to the similarity of the clinical picture of both pathologies, especially in the early stages of their development. In many ways, therefore, CHF is usually diagnosed in patients with severe and extremely severe COPD. Identification of low FC of angina pectoris in patients with COPD is also difficult due to the inability of patients to achieve the level of load that can lead to the appearance of pain. In patients with comorbidities, there is a decrease in exercise tolerance, aggravation of hypoxemia, an increase in heart rate, and a higher level of SPPA. More pronounced disturbances of some clinical and instrumental parameters are associated with an increase in pressure in the pulmonary artery. In patients of both groups, systolic dysfunction of the left ventricle (EF< 35%). При анализе проводимой терапии отмечена недостаточная дозировка бета-блокаторов у больных с ХОБЛ, что может усугублять течение и прогрессирование ХСН. Таким образом, больные с наличием ХОБЛ требуют особого внимания, более детального сбора анамнеза и тщательного анализа полученных данных для своевременной диагностики кардиальной патологии и назначения специфической терапии, в том числе и высокоселективных бета-блокаторов.

Reviewers:

Kosheleva N.A., Doctor of Medical Sciences, Associate Professor of the Department of Hospital Therapy, Faculty of Medicine, SSMU. IN AND. Razumovsky, Saratov;

Nikitina N.M., Doctor of Medical Sciences, Associate Professor of the Department of Hospital Therapy, Faculty of Medicine, SSMU. IN AND. Razumovsky, Saratov.

Bibliographic link

We bring to your attention the journals published by the publishing house "Academy of Natural History"

For citation: Akhmetzyanova E.Kh., Gainitdinova V.V., Sharafutdinova L.A. Management of patients with chronic heart failure with preserved systolic function against the background of severe COPD in the acute phase // BC. 2014. No. 2. S. 138

Currently, the goals of the treatment of heart failure (HF), according to the recommendations of the European Society of Cardiology (ESC, 2012) for the diagnosis and treatment of acute and chronic heart failure (CHF), are to reduce symptoms and manifestations, prevent hospitalization and improve survival. The treatment strategy includes: drugs indicated in potentially all patients with symptomatic (FC II-IV NYNA) HF (ACE inhibitors, β-blockers, APM), and drugs with less efficacy in patients with symptomatic (FC II-IV NYNA) HF ( ARB, ivabradine, digoxin, isosorbide dinitrate, omega-3-PUFA). The results of the SHIFT study conducted in 2010 showed that elevated heart rate is a marker of an adverse outcome of CHF and proved that the concept of neurohormonal blockade in CHF can be supplemented by effective heart rate reduction with the β-channel blocker ivabradine.

Of interest is a new therapeutic approach in the treatment of CHF, which is based on the effective control of heart rate through the use of an inhibitor of if-channels ivabradine, recently included in the treatment of CHF in patients with sinus rhythm, ejection fraction (EF) ≤35%, heart rate ≥70 beats. ./min., persistent symptoms (FC II-III NYNA) with intolerance to β-blockers.

The SHIFT study also demonstrated a relative risk reduction in the primary combined outcome of CV death or hospitalization for heart failure, improved LV function and quality of life with ivabradine treatment.

In Russia, chronic obstructive pulmonary disease (COPD) as the cause of CHF, according to the Society of Heart Failure Specialists (OSSN, 2010), is noted in 13% of cases. Diagnosis of heart failure in COPD presents certain difficulties, since it is largely masked by manifestations of acute and chronic respiratory failure. Treatment of COPD, according to the global initiative GOLD 2011, 2013, includes the appointment of bronchodilators (short- and long-acting β2-agonists, short- and long-acting M-anticholinergics, methylxanthines), inhaled glucocorticosteroids (IGCS), combined long-acting β2-agonists + ICS , systemic corticosteroids (not recommended for long-term use), phosphodiesterase IV inhibitors (for GOLD III, GOLD IV). With exacerbation, antibiotics, mucolytics, oxygen therapy are prescribed.

According to an observational study, patients with HF receiving inhaled β2-agonists have an increased risk of death and hospitalization, which probably indicates the need for more careful monitoring of patients with severe HF receiving inhaled β2-agonists for COPD.

Calcium channel blockers in this category of patients can exacerbate congestive heart failure and lead to the appearance of peripheral edema.

Therapy with selective β1-blockers has a significant impact on the survival of patients with HF, and the presence of COPD is the most important reason why this category of patients does not receive full treatment.

Treatment of patients with combined pathology always presents certain difficulties; Thus, attempts at active drug treatment of one disease are associated with a real threat of iatrogenic exacerbation of concomitant pathology.

A study was made of the effect of the If-channel inhibitor ivabradine on the clinical symptoms of CHF in patients with severe COPD in the exacerbation phase.

Materials and methods

The study included 120 patients with CHF syndrome in severe COPD in the acute phase. COPD was diagnosed according to the 2010 GOLD guidelines, CHF syndrome was established according to the ESC Guidelines for CHF (2012) based on 4 criteria: typical symptoms, typical signs, normal LV EF and structural and functional changes in the heart (LA expansion, LV diastolic dysfunction ).

Criteria for inclusion in the study:

1. COPD (GOLD III, GOLD IV, 2010), exacerbation phase.

2. Sinus rhythm (heart rate above 70 bpm).

3. Pulmonary hypertension (above 20 mm Hg at rest).

4. Chronic cor pulmonale.

6. Informed consent of the patient to participate in the study.

Criteria for exclusion from the study:

1. Acute forms of cardiovascular disease (acute coronary syndrome, acute myocardial infarction, acute cerebrovascular accident).

1. Chronic form of atrial fibrillation.

2. Paroxysmal arrhythmias.

3. Diabetes.

All patients initially, after 1 and 3 weeks. ECG was performed at rest, heart rate was determined. Echocardiography was performed (at the same time intervals) using the Fillips NNVVISERCHD apparatus - standard hemodynamic parameters were studied, the size of the left ventricle in diastole (VDRd LV), the size of the left ventricle in systole (VDRs LV), the end diastolic volume of the left ventricle (EDV LV), the final left ventricular systolic volume (LV systolic volume), stroke volume (SV), left ventricular ejection fraction (LV EF), left atrium (LA), right atrium (RA), right ventricular wall thickness (RV TS), right ventricular end-diastolic size in diastole (KDRd RV), systolic pressure in the pulmonary artery (Ppa), the ratio of the E / A velocities of the LV and RV. To study the function of external respiration (RF), computer spirometry was performed using the Master Screen Body (Jaeger), the indicators of forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), and the ratio of FEV1/FVC were studied. Daily self-monitoring of blood pressure (SBP) was carried out using the Digital Automatic Blood Pressure Monitor M4 (Omron) with registration of heart rate. Exercise tolerance was assessed using a 6-minute step test followed by an assessment of the severity of dyspnea according to Borg, the assessment of the clinical condition in CHF was carried out on the SHOKS scale initially, after 1 and 3 weeks, blood oxygen saturation (SaO2) was determined before and after exercise using an MD300C finger pulse oximeter at the same time intervals.

Statistical data processing was performed using the STATISTICA V.6.0 software package (StatsoftInc, USA). The average statistics are obtained: the arithmetic mean with the error of the arithmetic mean. Friedman ANOVA, non-parametric Wilcoxon matchedpairs test, Spearman's non-parametric correlation analysis (r), and two-factor analysis of variance were used. The null hypothesis about the absence of group differences was rejected at p<0,05.

Results and discussion

The study included patients who were treated in the intensive care and pulmonology departments of the Republican Clinical Hospital. G.G. Kuvatov (Ufa) regarding the treatment of COPD exacerbation. All patients had a history of COPD with an average duration of the disease of 12.84±0.53 years, and in the last 1-2 years there was a progression of deterioration in the general condition, dyspnea increased, according to medical records, repeated (≥2) hospitalizations were recorded over the past year . 12.5% ​​of patients were treated in the intensive care unit (4.5±1.21 days on average). Among comorbidities, 24.1% of patients had ischemic heart disease, stable exertional angina of functional class II (FC), myocardial infarction (MI), 17.5% had arterial hypertension (AH) of I-II degree. Diagnostic and sanitation fibrobronchoscopy was performed in 109 (72.67%) patients.

The test with physical activity (6-minute walking test) was carried out on the 1st-2nd day. upon admission to the pulmonology department or after transfer from the intensive care unit. The clinical characteristics of the patients included in the study are presented in Table 1.

In patients, complaints of cough with the release of difficult-to-separate mucous and mucopurulent sputum, and shortness of breath at rest prevailed. Shortness of breath of varying severity was observed in all patients: in 75% of cases it manifested itself as a feeling of lack of air, in 12.5% ​​- in the form of suffocation, in 95.8% - in the form of shortness of breath with little physical exertion, in 26.6% - in the form of shortness of breath at rest. About half of the patients (46.6%) complained of pain and discomfort in the region of the heart. Palpitations, interruptions in the work of the heart were noted by the vast majority of patients - in 84.2% of cases. The patients also complained of general weakness, increased fatigue, and edema of the lower extremities (Table 2).

During an objective examination, acrocyanosis was observed in 56.6% of the examined patients, in 25% of patients there were phenomena of diffuse cyanosis. Dry wheezing rales were heard in all patients. The average frequency of respiratory movements was 23.50±1.26 per minute; a decrease in blood oxygen saturation (SaO2) to 90.74±0.69% was recorded.

The severity of dyspnea, assessed using the mMRC questionnaire, averaged 3.09±0.03 points. Increased heart rate was observed in all patients, averaging 101.02±0.81 bpm. Emphasis of tone II on the pulmonary artery was detected during auscultation in patients in 75.8% of cases. The average systolic blood pressure (SBP) was 119.31 ± 1.41 mm Hg. Art., diastolic blood pressure (DBP) - 68.34±0.77 mm Hg. Art. When assessing the clinical condition on the SHOKS scale and the distance of the 6-minute walking test, CHF syndrome corresponded to functional class III (Table 3).

An increase in the size of the liver and the presence of peripheral edema were noted in 25 (25.8%) patients.

Echocardiographic parameters of the heart in the studied patients were characterized by an increase in RV TPS, a decrease in the E/A ratio of the right ventricle, and an increase in the systolic pressure in the pulmonary artery. Along with changes in the right parts of the heart, pathological structural and functional changes in the left parts of the heart were noted. There was a slight increase in the average size of the left atrium up to 35.12±0.30 mm, which indirectly indicates an increase in filling pressure and a decrease in the function of the left ventricle (LV). Violations of LV systolic function (decrease in EF less than 50%) were not detected in any of the observed cases, the average values ​​of LV EF approached the upper limit of normal and reached 64.28±0.43%. LV diastolic dysfunction was recorded in 87.33% of patients, manifested by a decrease in the E/A ratio. The predominant type of LV diastolic dysfunction was relaxation. In 5 (3.3%) patients with an extremely severe course, a pseudonormal type of LV filling was observed.

All patients with COPD received standard therapy (GOLD 2011, 2013): bronchodilators (tiotropium bromide or its combination with long-acting β2-agonists), inhaled (IGCS) and systemic (SGCS) glucocorticoids, antibiotics, mucolytics. CHF was treated with mineralocorticoid receptor (ARM) antagonists - spironolactone 50-75 mg/day, angiotensin-converting enzyme (ACE) inhibitors - enalapril at a dose of 5-10 mg/day, or angiotensin receptor blockers (ARBs) valsartan at a dose of 40 mg/day. β-blockers were not prescribed due to the pronounced broncho-obstructive component in the observed patients, associated with the severity of the disease and the exacerbation phase.

The patients were divided into two groups: a comparison group of 60 people and a study group of 60 people. The groups were formed by random sampling, did not differ statistically significantly (p>0.05) in age, gender, clinical characteristics, baseline heart rate, standard therapy, and therefore were regarded as identical. Each group had the same number of patients with concomitant pathology of the cardiovascular system. Groups were randomized to receive ivabradine (titrated to a maximum dose of 7.5 mg 2 times a day) or standard treatment for COPD in the acute phase (GOLD 2011, 2013). Dynamic observation was carried out for 18 days.

When comparing the initial clinical and instrumental parameters in the studied groups, no statistically significant differences were observed in any case (p>0.05). Most of the patients had a reduced level of blood oxygenation. The respiratory rate in patients of both groups was 22.40±1.08 and 23.62±1.14 bpm. respectively. Sinus tachycardia was recorded in both groups, heart rate was 99.46±7.99 in the comparison group and 102.53±13.59 bpm. - in the study group. In most patients, according to the results of the test with a 6-minute walk, CHF FC III (according to NYHA) was established.

In the study of hemodynamic parameters in the comparison and study groups, an increase in the wall thickness of the right ventricle 6.0 ± 0.35 mm and 6.03 ± 0.35 mm, respectively, an increase in the level of mean pressure over the pulmonary artery to 38.0 ± 2.8 mm was observed rt. Art. and 39.15±2.46 mm Hg. Art., decrease in peak velocities E/A of the left ventricle. The LV systolic function in all groups was intact, the mean values ​​of LV EF approached the upper limit of normal and amounted to 63.64±1.02% and 62.35±1.61%, respectively. The data of our work are consistent with the results of N.A. Karoli, R. Yilmaz, M. Gencer, E. Ceylan, R.U. Demirbag. Left ventricular diastolic dysfunction manifested itself as a decrease in the ratio of LV E/A peaks and was detected in 73.0% of all patients studied. The predominant type of LV diastolic dysfunction was relaxation.

The diagram of the distribution of heart rate in the studied patients (Fig. 1) clearly shows that the most frequent heart rate was recorded in the range from 90 to 100 bpm. There were no differences in heart rate in severe and extremely severe COPD (p>0.25).

In patients treated with ivabradine, the drug was well tolerated. During the entire observation period, no side effects were registered in any case, none of the patients noted an increase in cough, shortness of breath, or the appearance of respiratory discomfort.

The assessment of the clinical condition in CHF in patients with COPD in both groups improved during treatment. Statistically significant differences between the groups were obtained according to the results of the SHOKS scale; against the background of standard treatment, there was a decrease in SHOKS to 5.25±0.18 points, against the background of ivabradine - to 4.09±0.18 points. The additional appointment of ivabradine led to an improvement in the clinical condition in patients with CHF during exacerbation of severe and extremely severe COPD (p<0,05) (рис. 2).

According to diary entries, the majority of patients in the study group noted a subjective improvement in their condition and exercise tolerance. After 3 weeks treatment, patients showed an increase in exercise tolerance, which manifested itself in a statistically significant increase in the distance traveled and a decrease in dyspnea on the Borg scale (p<0,05), по сравнению с данными группы сравнения (рис. 3).

Against the background of standard treatment, the distance traveled in 6 min. increased by 14.49% (from 237.05 to 277.23 m), against the background of the appointment of ivabradine - by 22.58% (from 236.25 to 305.48 m) (p<0,05) (рис. 4).

In all patients of the comparison groups and study groups during treatment (Fig. 5), a statistically significant decrease in heart rate was recorded (p< 0,05). Но снижение ЧСС до целевых величин (ЧСС < 70 уд./мин., ВНОК 2010 г.) было достигнуто только при назначении ивабрадина в дозе 15 мг/сут независимо от исходной ЧСС. При назначении ивабрадина в дозе 10 мг/сут снижение ЧСС наблюдалось на 4-5-й день приема препарата, целевого уровня ЧСС достичь не удалось. На фоне приема ивабрадина в дозе 15 мг/сут снижение ЧСС уже со 2-го дня приема препарата отмечалось у 92% больных, но статистически значимое снижение ЧСС наблюдалось через 2 нед. от начала лечения (p <0,001).

In order to study the dependence of the effectiveness of ivabradine in patients with severe and extremely severe COPD with CHF syndrome on the initial heart rate, a multivariate analysis of variance was performed. The analysis included two factors: heart rate (two categories - less than 100 bpm, more than 100 bpm) and treatment with ivabradine (two categories - before and after treatment). For this, the study group, taking into account the distribution of initial heart rate values ​​(Fig. 1), was divided into 2 subgroups: with heart rate<100 уд./мин. и ЧСС >100 bpm (Fig. 6, 7). The results of the analysis showed no dependence of the effectiveness of treatment with ivabradine on the initial heart rate in the studied patients.

When analyzing the influence of factors on exercise tolerance, an improvement in the indicator was noted during treatment with ivabradine, regardless of the initial heart rate (Fig. 6).

Thus, two-way analysis indicates the significance of the effect of ivabradine on the results of a 6-minute step test.

Analysis of the influence of two factors (heart rate and treatment with ivabradine) on the assessment of the clinical state in CHF SHOKS in the studied patients also showed that the positive effect of ivabradine in sinus tachycardia does not depend on the initial heart rate (Fig. 7).

Analysis of the influence of two factors (heart rate and treatment with ivabradine) on the severity of dyspnea according to the Borg questionnaire in the studied patients showed that the positive effect of ivabradine depends on the initial heart rate. In patients with baseline heart rate >100 beats/min. there was a greater degree of reduction in dyspnea, assessed by this questionnaire (p<0,05).

Thus, the improvement in the assessment of the clinical condition in CHF according to the SHOKS scale and the increase in exercise tolerance in CHF patients with severe COPD in the exacerbation phase during treatment with ivabradine do not depend on the initial heart rate. The effectiveness of treatment with ivabradine is the same both with a heart rate of 70 to 100 bpm and with severe tachycardia. The decrease in dyspnea according to the Borg questionnaire during treatment with ivabradine is more pronounced in patients with a heart rate >100 bpm.

conclusions

1. In patients with severe and extremely severe COPD, the duration of the disease for more than 10 years, CHF is recorded with preserved systolic function of the left ventricle.

2. The inclusion of ivabradine in the complex treatment of patients with CHF during exacerbation of severe COPD leads to an improvement in the clinical condition: a decrease in CHF symptoms, a statistically significant increase in exercise tolerance, an increase in functional ability, and a decrease in the severity of dyspnea. A decrease in dyspnea according to the Borg questionnaire during treatment with ivabradine is more pronounced in patients with an initial heart rate of >100 bpm.

3. Ivabradine at a dose of 15 mg/day can be recommended for the management of CHF patients with preserved systolic function in severe COPD in the acute phase.