1

The features of chronic heart failure (CHF) were studied in patients with and without chronic obstructive pulmonary disease (COPD). For this purpose, 75 people were examined. The patients were divided into 2 groups based on the presence of COPD. Group 1 included 38 patients with COPD, group 2 included 37 patients without COPD. In patients with concomitant pathology, a decrease in exercise tolerance, worsening hypoxemia, an increase in heart rate, and higher systolic pressure in the pulmonary artery are observed. 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 careful analysis of the data obtained for timely diagnosis of cardiac pathology and the prescription 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 significant CHF occurs in 4.5% (5.1 million people). The one-year mortality rate for patients is 12%, and the three-year mortality rate is 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 makes it possible to prescribe 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 stated goal, 75 people with CHF hospitalized at the Saratov Regional Clinical Hospital in the period from 2013 to 2014 were examined and signed informed consent to participate in the study. The study was approved by the ethics committee of the State Budgetary Educational Institution of Higher Professional Education "Saratov State Medical University named after. IN AND. Razumovsky" of the Russian Ministry of Health. Inclusion criteria were male gender, age more than 40 years and less than 80 years, presence of diagnosed CHF according to the recommendations of the Russian Society of Cardiology in 2013. 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 on a MicroLab device (Micro Medical Ltd. (UK), Echo-CG on an Apogee`CX device using a 2.75 MHz sensor with simultaneous recording of a two-dimensional echocardiogram and a pulsed Doppler echocardiogram, study of the N-terminal fragment of brain natriuretic peptide (BNP) using a set of reagents produced by BIOMEDICA, Slovakia.The clinical manifestations of CHF were assessed using the Clinical Status Rating Scale for CHF (CHS), the modified dyspnea scale (mMRC), and the Charlson comorbidity index.

Statistical processing was carried out using the Statistica 8 package. To count features with a normal type of distribution, a t-test for independent groupings was used. In case of non-normal distribution, Mann-Whitney tests and χ2 test with Yates correction were used. Correlation analysis was carried out. The difference in group performance was considered statistically significant at p<0,05.

results

Among the examined patients, 62 (83%) patients were in the cardiology department, of which 25 (40%) were diagnosed with COPD. COPD was first diagnosed in 13 (21%) patients hospitalized in the cardiology department. Among those who had previously been diagnosed with COPD, 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 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 presented in Table 1, patients in both groups were comparable in age, frequency and duration of arterial hypertension, history of angina pectoris, and body mass index.

Table 1

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

Index	Patients with CHF and COPD (n=38)	Patients with CHF without COPD (n=37)	Significance of differences
Age, years
Body mass index, kg/m2
Duration of shortness of breath, years
Number of smokers
Active smokers
Pack/years, conventional units
Duration of smoking, years
Duration of cough, years
Presence of arterial hypertension (%)
Duration of arterial hypertension, years
Presence of previous myocardial infarction (%)
Angina (%)
Systolic blood pressure, mm Hg. Art.
Diastolic blood pressure, mm Hg. Art.
COPD stage II
COPD stage III
COPD stage IV
Heart rate, beats In min.
6-minute walk test result, m
Left ventricular ejection fraction, %
MPAP, mm Hg. Art.
SHOKS, points
mMRC degree
Charlson Comorbidity Index, points

There were significantly more smokers among patients in group 2 than among patients in 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 shortness of breath 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. The majority of 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 concomitant pathology, such manifestations of CHF as edema in the lower extremities and hydrothorax are more often observed.

table 2

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

Index		CHF without COPD	Significance of differences
Peripheral edema
Moist rales in the lungs (+ venous congestion in the lungs according to chest x-ray)
Hydrothorax
Hydropericardium
Pulsation of the neck veins
Liver enlargement (palpation)

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: cardiac and respiratory failure, anemia, obesity, etc. Detection of heart failure in patients with COPD is particularly difficult. This is mainly due to the presence of emphysema, which can hide such manifestations of CHF as moist fine rales in the lungs, displacement of the percussion boundaries of the heart, and in some cases, a gallop rhythm. And bronchial obstruction, as a fairly specific manifestation of COPD, can also be secondary, caused by 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 remains greater than 0.7 in the absence of COPD. Among the patients we examined, this sign helped exclude COPD in 7 (19%) patients of group 1.

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

A decrease in physical performance was found (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 group 1, the majority of patients (81.1%) had FC 3 of CHF, 3 (8.1%) patients had FC 2, and 4 (10.8%) patients had FC 2. 4th FC. In group 2, FC 3 also predominated (76.3%), while the rest were diagnosed with FC 4 (23.7%).

At the same time, it is necessary to take 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 can lead to overdiagnosis of the severity of CHF in patients with combined cardiorespiratory pathology. In this case, a necessary study is to determine the level of the N-terminal fragment of BNP. Among patients with COPD, its level was 309 pg/ml.

Patients with COPD and CHF showed an increase in heart rate (HR) compared to patients without COPD. Currently, an increase in heart rate at rest is associated with an increase in overall mortality, mortality from cardiovascular causes, the frequency of re-hospitalization due to cardiovascular causes and worsening 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, the majority of patients with COPD (61%) had a heart rate of 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 use of 4.57±4.96 years. In the group of patients without COPD, the majority of 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. for a 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 were no statistically significant differences 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 were constantly taking 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. for 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 characteristics of MI 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. Transmural changes in the myocardium were noted in 25 (66%) patients. Only one patient had a history of two MIs, the rest had one each. 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 the anginal variant, and 2 (5%) had the asthmatic variant. Transmural myocardial damage was detected in 30 (81%) patients. 23 (62%) patients had one MI, 13 (35%) had two, and one patient had three MIs in their history. The anterior wall, interventricular septum, and apex were affected in 26 (70%) patients, the posterior wall - in 19 (51%) patients.

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

Detection of angina pectoris in patients with COPD is quite 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 confirmed by our study, where out of 28 (74%) patients with an established diagnosis, in 26 (93%) it corresponded to the 3rd functional class, in one - to the 4th FC, and only one - 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%) had FC 3, 2 patients had FC 2, and 3 patients had FC 4. .

According to modern concepts, the management of a patient with COPD, assessment of the effectiveness of therapy and survival are largely determined by the frequency of exacerbations and its severity. Severe exacerbation is the main cause of death in patients. Each such episode is associated with accelerated disease progression, decreased quality of life, increased treatment costs, and decompensation of concomitant diseases, including CHF. Among the COPD patients 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. Moreover, the exacerbation itself was the reason for hospitalization in 9 (24%) patients. There was a correlation between the frequency of exacerbations and the functional class of CHF (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.

Left ventricular ejection fraction (EF) is one of the key indicators of hemodynamics in HF and has great prognostic significance: 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 this indicator 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 ​​(35 to 50%) belong to the so-called gray zone and 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 (SPAP) 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 reduction in capillary bed area and pulmonary vascular compression associated with the destruction of 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 suffering from COPD, an inverse relationship between MPAP and exercise tolerance (six-minute walk test) was revealed (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).

In patients without COPD, similar inverse relationships between MPAP and SaO 2 were found (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 complex, which is due to the similarity of the clinical picture of both pathologies, especially in the early stages of their development. This is largely why CHF is usually diagnosed in patients with severe and extremely severe COPD. Detection of low FC of exertional angina in patients with COPD is also difficult due to the inability of patients to achieve a level of exercise that can lead to pain. In patients with concomitant pathology, a decrease in tolerance to physical activity, worsening hypoxemia, an increase in heart rate, and a higher level of MPAP are observed. Increased pressure in the pulmonary artery is associated with more pronounced disturbances in some clinical and instrumental parameters. In patients of both groups, left ventricular systolic dysfunction (LVEF) was equally often detected.< 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, Saratov State Medical University named after. IN AND. Razumovsky, Saratov;

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

Bibliographic link

Borodkin A.V., Karoli N.A., Rebrov A.P. FEATURES OF CHRONIC HEART FAILURE IN PATIENTS WITH AND IN THE ABSENCE OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE // Modern problems of science and education. – 2015. – No. 4.;
URL: http://site/ru/article/view?id=21327 (access date: 01/31/2020).

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Seminar "Chronic obstructive pulmonary disease in combination with chronic heart failure: complex issues of diagnosis and treatment"

Conducts: Republican Medical University

The date of the: from 09/25/2014 to 09/25/2015

Chronic obstructive disease (COPD) and chronic heart failure (CHF) are characterized by high prevalence, morbidity (morbidity is any deviation, objective or subjective, from a state of physiological or psychological well-being) and mortality, and therefore represent a serious medical and social problem. In the last two to three decades, significant progress has been made in studying their prevalence, etiology, pathogenesis and determining treatment approaches.

A very limited number of studies have been devoted to studying the prevalence, characteristics of the course and prognosis, as well as the effectiveness of various treatment regimens in patients with a combination of COPD and CHF. In this regard, a number of important issues remain insufficiently studied, including the diagnosis of COPD in patients with CHF and vice versa; the true frequency of comorbidity of COPD and CHF, the impact of such comorbidity on the prognosis and the choice of adequate treatment programs [1-6]. It should be noted that in the European Association of Cardiology Guidelines for the diagnosis and treatment of acute and chronic heart failure (2012) and the GOLD (Global Initiative for the Diagnosis and Treatment of COPD) guideline 2013, undeservedly little attention is paid to the features of diagnosis, treatment and prognosis, respectively, in patients with CHF and concomitant COPD, and in patients with COPD in the presence of CHF [,].

Terminology, epidemiology, prognosis.

It may be considered appropriate to provide the definitions of COPD and CHF presented in modern consensus documents. “COPD is a common disease characterized by persistent airway restriction (bronchial ostruction), usually progressive and associated with inflammation in the airways in response to harmful exposure to particles or gases (mainly due to smoking). Exacerbations and concomitant diseases make a significant contribution to the severity of the disease.” CHF is defined as a condition accompanied by a violation of the structure and function of the heart, in which it is not able to release into the circulation such an amount of oxygenated blood that would satisfy the needs of the tissues. From a clinical point of view, CHF is a syndrome whose typical features are decreased exercise tolerance, fluid retention in the body, a progressive nature and limited life expectancy.

The true prevalence of the combination of CHF and COPD in clinical practice is quite difficult to assess, which is explained by a number of reasons. Firstly, cardiologists, who are responsible for the diagnosis and treatment of CHF, pay insufficient attention to assessing pulmonary function, which is why the detection rate of concomitant COPD remains low. Conversely, pulmonologists, who diagnose and treat patients with COPD, underestimate the likelihood of concomitant CHF and do not perform appropriate diagnostic measures. Secondly, both CHF and COPD share significant commonality in risk factors, symptoms and physical findings. Thirdly, instrumental confirmation of the diagnosis can also be difficult; in particular, emphysema and pulmonary hyperinflation often complicate echocardiographic (EchoCG) studies, and significant congestion in the pulmonary circulation is often accompanied by the development of obstructive changes during spirometry. There have been no large-scale epidemiological studies that have assessed the true prevalence of the combination of COPD and CHF in the general population. Traditionally, the prevalence of these comorbidities was assessed separately: only in patients with CHF or only in people with COPD.

According to a large meta-analysis that included dozens of observational studies with a combined population of more than 3 million people, the worldwide prevalence of COPD is about 7%. The annual mortality rate for COPD in the general population is relatively low (about 3%), but very high after hospitalization due to exacerbations (25%) [10-12]. Experts from the World Health Organization (WHO) and the World Bank, in a study of the Global Burden of Disease, predict that in 2030 COPD will rank 3-4 in the overall mortality structure around the world.

CHF is less common than COPD, and is observed in 1-3% of people in the general population [14-17]. However, CHF is associated with distinctly negative prognostic indicators. The annual mortality rate in the general population is approximately 5-7%, and the average life expectancy after hospitalization for decompensated disease is less than 2 years [18-20].

The frequency of detection of COPD in patients hospitalized for CHF ranges from 9 to 51% in different studies [,]. Along with this, in outpatients with stable CHF it is detected with a frequency of 7-13%. This difference can be explained by the fact that with decompensated CHF, “pseudo-obstructive” spirometric changes develop, which resolve after adequate treatment of CHF.

On the contrary, characterizing the prevalence of CHF among patients with COPD, it can be noted that for quite a long time CHF was given a place primarily as a complication of severe COPD in the form of the development of right ventricular CHF, i.e. corpulmonale. Such ideas were based mainly on the results of several small studies performed in the 70s of the twentieth century in relatively young patients with severe COPD without concomitant coronary heart disease and, accordingly, left ventricular dysfunction. Only recently has sufficient data accumulated convincingly demonstrating the high prevalence of CHF in COPD (about 25%) [22-24]. In this case, the dominant place in its origin is given to left ventricular (LV) dysfunction, while the role of pulmonary hypertension and cor pulmonale in the development of CHF in COPD is important, but not of primary importance [25-27].

In general, summarizing information about the epidemiology of the combination of CHF and COPD, we can formulate a kind of “rule”: every fifth patient with CHF has concomitant COPD, and every fourth patient with COPD has CHF.

Pathogenetic mechanisms of interaction between COPD and CHF.

The mutual relationship between COPD and the cardiovascular system is far from fully understood. It is believed that a key role in the general pathophysiology of COPD and CHF is played by the common risk factors (smoking, older age), as well as the presence of systemic inflammation in both diseases. In particular, most patients with severe COPD experience a 2- to 3-fold increase in circulating levels of C-reactive protein, which is one of the most important markers of systemic inflammation [28-30]. One hypothesis to explain the higher prevalence of LV systolic dysfunction in patients with COPD is that systemic inflammation accelerates the progression of coronary atherosclerosis and coronary artery disease. In addition, circulating proinflammatory mediators may have a direct cytotoxic effect on myocardiocytes, and thus stimulate the progression of myocardial dysfunction [31-33].

In addition to the systemic effects of smoking and inflammation, COPD and CHF have other common mechanisms that cause mutual disease progression. Both diseases are accompanied by hyperactivation of the renin-angiotensin system (RAS). Angiotensin II is a potent bronchoconstrictor that can activate pulmonary fibroblasts and stimulate apoptosis of pulmonary epithelial cells, as well as increase pulmonary hypertension and impair gas exchange across the alveolar-capillary membrane [,]. COPD is also accompanied by excessive activity of the sympathetic system, which plays an extremely important role in the progression of CHF [,]. Both diseases similarly affect cellular metabolism, stimulating the replacement of glucose-dependent energy processes with lipid-dependent ones, resulting in the progression of muscle dysfunction and loss of muscle mass with the development of cachexia in the final cascade of both diseases [,].

Probably the most important pulmonary effects of CHF are increased pulmonary capillary herniation pressure, pulmonary congestion, and the presence of interstitial and peribronchiolar edema. These phenomena can lead to a decrease in the diffusion capacity of the lungs and stimulate remodeling of the pulmonary vascular bed with the development of hypertrophy of the walls of the pulmonary arterioles [,]. In addition, a secondary increase in pulmonary artery pressure may develop due to LV dysfunction. On the other hand, the alveolar hypoxia inherent in COPD and, as a consequence, pulmonary vasoconstriction further enhances the remodeling of the pulmonary vascular bed due to: 1) redistribution of blood flow from insufficiently ventilated areas to better ventilated areas of the lungs; 2) additional hypertrophy of the walls of the pulmonary arteries; 3) proliferation of vascular smooth muscle cells in those vessels of the pulmonary circulation that should normally be non-muscular [,]. With corresponding damage to a large part of the lungs, increased pulmonary vascular resistance and pulmonary arterial hypertension develop, which thus leads to an increase in the load on the right ventricle and can lead to dilatation and hypertrophy of the right ventricle and, finally, failure of the right heart (cor pulmonale) [ , 38-42].

Are common questions diagnostics combinations COPD And CHF.

Often, making a correct diagnosis and differential diagnosis of COPD and CHF is associated with certain difficulties and requires various laboratory and instrumental studies. Below we summarize the main diagnostic and differential diagnostic signs that are used in the diagnosis of COPD in the presence of concomitant CHF.

The clinical manifestations of COPD and CHF are very similar [, , ,]. Dyspnea on exertion is the main complaint in both conditions. In most cases, in both diseases there is mixed dyspnea, in patients with CHF it is often with a predominance of the inspiratory component, and in COPD - the expiratory component. Patients with CHF may experience orthopnea, which is not typical for COPD. An important symptom characteristic of CHF is paroxysmal nocturnal shortness of breath, which usually clearly decreases in an upright position, which can serve as a differential sign with attacks of breathlessness, sometimes observed in COPD. Increased fatigue is also very common in both diseases. Cough, both with sputum production and dry, is predominantly found in COPD, however, it is not uncommon in severe CHF. Episodes of acute cardiac decompensation can lead to the development of pulmonary obstruction with wheezing and prolongation of expiration, which can sometimes be difficult to distinguish from bronchospasm attacks. Depressive and anxiety symptoms are very common in both patients with COPD and patients with CHF.

Objective examination of the heart and chest is usually difficult due to the presence of pulmonary hyperinflation, and therefore has neither sufficient sensitivity nor specificity. In patients with severe COPD, the chest acquires a characteristic emphysematous (“barrel-shaped”) shape, and upon percussion a box sound is observed, which is not typical for patients with CHF. In CHF with a reduced ejection fraction of the left ventricle, the first sound is usually significantly weakened, a proto- or presystolic gallop rhythm and a blowing pansystolic murmur are often heard, carried outward, which is not typical for most patients with COPD.

Plain radiography of the chest is not a sensitive method for diagnosing the combination of COPD and CHF. On the one hand, emphysema and or hyperinflation of the lungs can mask and reduce the shadow of the heart, reducing the value of the cardiothoracic index. In addition, pulmonary vascular remodeling and areas of change in lung tissue density characteristic of COPD can both mask and imitate the phenomena of congestion and interstitial pulmonary edema. However, plain radiography is an important and useful method for identifying other important pathologies localized in the chest cavity. In particular, it remains an important screening method, playing an auxiliary but very significant role in the diagnosis of CHF.

X-ray symptoms in favor of the presence of CHF are considered to be an increase in the cardiothoracic index > 0.50, signs of redistribution of blood flow in the lungs (increased vascular pattern and enlargement of the caliber of veins in the upper lobes of the lungs, possibly a slight expansion of the root and an increase in the caliber of orthogonal shadows of vessels in the central parts of the lungs), signs of interstitial edema (increased pattern, polymorphic pattern, honeycomb deformation of the pattern, blurred vessels and bronchi, presence of Kerley lines, pleural lines) and alveolar edema (multiple confluent focal shadows due to the accumulation of transudate in the alveoli). It has been proven that a careful analysis of plain chest radiographs in patients with exacerbation of COPD can not only significantly improve the diagnosis of concomitant CHF, but also identify a group of patients with a negative prognosis for survival.

DiagnosticianA COPD in the presence of comorbid CHF.

Approaches to diagnosing COPD in the presence of concomitant CHF are generally the same as in patients without comorbidity. The above definition of COPD identifies two fundamental aspects inherent in COPD: firstly, persistent (i.e. permanent and not completely reversible) bronchial obstruction, and secondly, the relationship with pathogenic inhalation exposure. Thus, their presence is necessary and mandatory for a correct diagnosis. According to the guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD 2014), the diagnosis of COPD should be considered in all patients over 40 years of age with characteristic clinical manifestations and exposed to risk factors. It can be separately noted that when assessing inhalation risk factors, the dominant place is occupied by smoking (more than 10 pack-years, more often 20-30 pack-years), which is the direct etiological factor in the development of COPD in at least 75-80% of patients. In the remaining 20-25% of patients with COPD, the main causative exposure is household and industrial pollution (usually combustion products of fossil fuels) or occupational inhalation pollution. In patients over 40 years of age who present with characteristic complaints and have been exposed to inhalational risk factors, the likelihood of having irreversible bronchial obstruction is about 30-40%. Such patients must undergo a spirometric study to verify the diagnosis.

Spirometric study external respiratory function is the most important and mandatory stage in the diagnosis of COPD. A mandatory diagnostic criterion, without which a diagnosis of COPD is impossible, is confirmation of the presence of incompletely reversible bronchial obstruction. Incompletely reversible bronchial obstruction is understood as obstruction that, after using a high dose of bronchodilators (usually 400 mcg of salbutamol), does not resolve completely, regardless of the degree of increase in ventilation function indicators. Typically, to determine whether obstruction is reversible, spirometry is used, which calculates the ratio of forced expiratory volume in the first second (FEV 1) to forced vital capacity (FVC).

The criterion for incompletely reversible obstruction is that the FEV1/FVC ratio remains below a certain threshold value (diagnostic criterion) after a test with a bronchodilator [,]. However, despite significant efforts by international and national expert groups and professional associations, there is still no consensus on a single spirometric criterion for bronchial obstruction, and, accordingly, a functional diagnosis of COPD.

The most commonly used spirometric criterion for bronchial obstruction, proposed in the GOLD Guidelines, is the FEV1/FVC ratio<0,7 (так называемый фиксированный критерий) . Его основным преимуществом является простота вычисления, однако ему присущи существенные ограничения, потому что он не принимает во внимание физиологический феномен возрастного снижения легочной функции, следствием чего является высокая частота гипердиагностики ХОБЛ у пожилых лиц и недостаточная диагностика обструктивных изменений у молодых. Зато в общих рекомендациях Американского торакального общества и Европейского респираторного общества (American Thoracic Society / European Respiratory Society (ATS/ERS 2005)) предлагается использование критерия, основанного на популяционных статистических расчетах (нижняя граница нормы, lower limit of normal – LLN) . Он сложнее вычисляется, однако его основное преимущество в том, что он является абсолютно традиционным для расчета любых норм в медицине вообще. Как и в случае нормы почти любого лабораторного или инструментального показателя, 95% относительно здорового населения имеет ОФВ 1 /ФЖЕЛ больше, чем LLN. Поэтому данный показатель лишен риска ложно-положительной диагностики ХОБЛ в старшей возрастной группе и ложно-отрицательной диагностики у молодых лиц. LLN не представлен тем или другим цифровым значением, так как сильно зависит от пола, этнической принадлежности, роста, и, главное, возраста. Чтобы наглядно проиллюстрировать взаимоотношения фиксированного критерия ОФВ 1 /ФЖЕЛ<0,7 и статистически обоснованного ОФВ 1 /ФЖЕЛ

Rice. 1. Comparison of the fixed criterion FEV 1 /FVC<0,7 и LLN, в зависимости от возраста и роста у мужчин европейской этнической принадлежности.

As you can see, FEV 1 /FVC<0,7 (обозначен красной пунктирной линией), не зависит от демографических показателей больного, в то время как соответствующие значения ОФВ 1 /ФЖЕЛ и LLN (изогнутая плоскость серого цвета) существенно и нелинейно меняются с изменением возраста и роста. В данном случае график построен с учетом одинакового пола и этнической принадлежности (у мужчин белой расы). Если же учитывать гетерогенность этих параметров, то указанная на рисунке плоскость имеет еще более нелинейный характер, что делает несоответствие LLN фиксированному критерию 0,7 особенно подчеркнутой.

It has been established that, in contrast to the fixed criterion FEV 1/FVC arbitrarily chosen by experts<0,7, использование ОФВ 1 /ФЖЕЛ

The choice of the optimal diagnostic criterion is especially relevant in the context of COPD in combination with CHF, since both of these diseases are more common in older people. In addition, pulmonary congestion, cardiomegaly, pleural effusion and other phenomena inherent in CHF can further alter spirometric parameters, complicating the diagnosis and assessment of the severity of COPD. In particular, during decompensation of CHF, approximately 20% of patients experience the development of “pseudo-obstructive” spirometric changes with a significant decrease in FEV 1 /FVC. After diuretic therapy is prescribed, these phenomena resolve spontaneously without the use of bronchodilators. Preliminary data have now been published on the benefits of using the FEV1/FVC parameter

In contrast to the actual diagnosis of bronchial obstruction, the criteria for assessing its severity in patients with COPD are agreed upon and are almost not discussed. In previous editions of the GOLD recommendations (until 2011), a gradation based on the assessment of post-bronchodilation FEV 1 was proposed and widely used: with FEV 1 ≥ 80% – mild obstruction; at 50% ≤ FEV 1<80% – среднетяжелая обструкция; при 30% ≤ ОФВ 1 <50% – тяжелая обструкция и при ОФВ 1 <30% – очень тяжелая обструкция. Однако эти градации с 2011 года фактически имеют описательный или научный, но не практический интерес, так как в новой редакции GOLD (с 2011 года) эксперты фактически оставили 2 категории – тяжелая и нетяжелая (ОФВ 1 менее и более 50%, соответственно). Классификация заболевания и выбор тактики лечения базируются только на таком распределении.

Although widely used, an approach to assessing the severity of obstruction based on calculating percentages of predicted FEV 1 values ​​potentially has the same disadvantages as using a fixed criterion of obstruction compared with LLN. First, it is based on the false premise that a given percentage of the target is equivalent for all individuals, regardless of age, height, gender and ethnicity. The inconsistency of this premise with the truth can be demonstrated by an example: LLN for FEV 1 in a man of average height at the age of 30 years can be 74% of the predicted value, and at the age of 70 years 63% of the predicted value. Secondly, all of the above cut-off values ​​for the distribution of severity categories are arbitrarily selected based on expert opinion. The result of these shortcomings of the traditional approach to assessing the severity of obstruction may be an underestimation of the severity of violations of the ventilation function of the lungs in young people and, which is especially important for patients with COPD and CHF, overestimation in older people.

Bronchodilation test. According to established tradition, for more than half a century, one of the key signs to distinguish between COPD and bronchial asthma (BA) was the reversibility of bronchial obstruction under the influence of bronchodilators. Currently, the study of the reversibility of obstruction using a bronchodilator test (BD) has become firmly established in clinical practice, and is regulated by modern consensus documents for the diagnosis of both BA and COPD [,]. However, back in the 80s of the last century, the differential diagnostic value of RDT was subject to justified criticism. Test results are highly dependent on many factors that cannot be controlled (drug, dose, natural response variability, different standards, etc.). This leads to frequent cases of misdiagnosis, which leads to inadequate therapy and poor patient outcomes.

It is very difficult to provide an unambiguous definition of the term “reversibility of bronchial obstruction”. Firstly, this is due to the use of different criteria in various clinical guidelines, and secondly, due to the difficulties of adapting generally accepted English terms. In particular, the analogue of the concept that is most widely used – “bronchodilator reversibility” – is the Russian-language term “reversibility of bronchial obstruction”. This term carries with it a certain ambivalence. On the one hand, reversible obstruction is spoken of when obstructive phenomena are completely resolved (if, after using a bronchodilator, FEV 1/FVC becomes greater than 0.7 or LLN). On the other hand, the concept of reversibility of obstruction is also used to describe a significant increase in spirometric parameters after bronchodilation. In the GOLD 2014 recommendations, an increase in FEV 1 after bronchodilation of ≥ 12% and ≥ 200 ml is considered significant. In the ATS/ERS 2005 recommendations, in addition to FEV 1, reversibility can also be assessed using the FVC indicator (the same numbers).

To illustrate the conflicting manifestations of the same term, we can give an example of mild obstruction, which after RDT was completely resolved, but the increase in FEV 1 was only 4% and 110 ml. In this case, the criteria for both “reversible” and “irreversible” obstruction apply. To avoid such terminological conflicts, in foreign literature the concept of “bronchodilator responsiveness” is often used to describe the increase in lung volumes and flows, which can be designated as “response to a bronchodilator” [,]. Thus, the results of RDT allow us to describe two parameters: the reversibility of bronchial obstruction (reversible / not reversible) and the response to a bronchodilator (pronounced / not expressed).

All modern international recommendations regarding spirometry state that the presence of a pronounced response to a bronchodilator is not a sufficient diagnostic criterion for diagnosing asthma, as was previously believed. This is due to a number of factors.

Firstly, a pronounced response to a bronchodilator is often observed in patients with “pure” COPD, without concomitant asthma. The results of the large-scale UPLIFT study are indicative, in which about 40% of COPD patients responded significantly to a bronchodilator.

Secondly, the “reversibility” of bronchial obstruction is an unstable characteristic, variable over time. In a study by P.M. Calverley et al. (2003) the status of “reversibility” of obstruction changed repeatedly in half of patients with COPD during 3 months of observation. A similar multiple change in “reversibility” was also demonstrated in patients who are traditionally considered least prone to the effects of bronchodilators - in 13% of patients with pulmonary emphysema.

Thus, when assessing a patient with suspected COPD, the main diagnostic value of using RDT is to improve the quality of diagnosis of COPD by excluding cases of completely reversible obstruction (usually due to the presence of asthma).

Diagnosis of CHF in the presence of comorbid COPD.

According to the recommendations of the European Society of Cardiology (2102), the diagnosis of CHF is based on assessing the presence of subjective symptoms and objective signs of CHF and objective evidence of the presence of structural and functional lesions of the heart (systolic and/or diastolic dysfunction, dilatation or hypertrophy of the heart chambers), obtained using instrumental examination (primarily EchoCG). An auxiliary criterion is also a positive clinical response to treatment of CHF.

There are two main types of CHF: with reduced LV systolic function (LV ejection fraction (EF)<40%) и с сохраненной систолической функцией ЛЖ (фракция изгнания (ФВ) ЛЖ>40%). To establish the first option, it is necessary to have: (1) characteristic complaints (2) objective data inherent in CHF; (3) confirmed decrease in LVEF. Installing the second option requires (1) complaints; (2) objective data inherent in CHF; (3) confirmed preserved LV systolic function in the absence of LV dilatation; (4) the presence of LV hypertrophy / left atrial dilatation and/or EchoCG data on the presence of diastolic dysfunction (preferably based on tissue Doppler sonography).

It should be noted that the diagnostic criteria presented in the above recommendations are not discrete, but probabilistic in nature (in the categories “reduces the likelihood” or “increases the likelihood” of the diagnosis) and in many cases does not provide a basis for an unambiguous interpretation of the totality of clinical data. In the situation of concomitant COPD, accurate diagnosis of CHF (especially the variant with preserved LV systolic function) becomes especially difficult.

Performing echocardiography in patients with COPD can be difficult due to the presence of a poor acoustic window due to the presence of hyperinflation of the lungs. The incidence of inadequate imaging depends on the severity of COPD, and according to several studies, it is 10%, 35% and more than 50% in people with non-severe, severe and extremely severe COPD, respectively [, , 57-59]. A normal echocardiogram allows one to completely exclude the presence of CHF. Detection of left ventricular ejection fraction (LVEF)< 40% позволяет говорить о ХСН со сниженной ФВ ЛЖ. Постановка диагноза ХСН с сохраненной ФВ ЛЖ (при ФВ ЛЖ >40% and the presence of dilatation of the heart chambers or an increase in LV myocardial mass or signs of LV diastolic dysfunction) is a difficult question even in the absence of concomitant COPD. And the presence of this comorbidity can further complicate the assessment of both symptoms and data from all laboratory and instrumental research methods.

Studying the levels of BNP and NT-proBNP is useful to exclude CHF in individuals with acutely developed or worsened shortness of breath. The criterion that allows us to exclude the presence of CHF with 98% reliability is low levels of these peptides (NT-proBNP< 300 пг/мл или BNP < 100 пг/мл). У больных ХОБЛ уровни BNP от 100 до 500 пкг/мл могут свидетельствовать о наличии правожелудочковой недостаточности, левожелудочковой недостаточности или о сочетании обоих вариантов. Уровни BNP >500 pg/ml in a patient with characteristic symptoms can be considered a sign of acute heart failure, which should lead to the initiation of appropriate treatment. However, it should be remembered that natriuretic peptides are often false-positive, i.e. have low specificity and positive predictive value, and thus play only an auxiliary role in confirming the diagnosis of CHF. This remark is especially relevant in the presence of concomitant COPD, since the diagnostic properties of natriuretic peptides have been studied very limitedly in such patients.

Impaired structure and function of the LV in patients with COPD. By the beginning of the 2000s, symptoms of CHF in a patient with COPD were traditionally considered a sign of failure of the right heart (cor pulmonale). This stereotype was based on data from a number of small studies of the comorbidity of COPD and CHF published in the 70-80s of the last century, which included relatively young patients (average age 53-68 years) with severe COPD and, importantly, without concomitant coronary heart disease. Clinically significant LV dysfunction was observed in 0-16%. Based on this, the idea prevailed for a long time that in patients with COPD with signs of CHF, left ventricular dysfunction does not play a significant role, but in 2003 P.A. McCullough et al. and later in 2005 F.H. Rutten et al. found that every fifth patient with COPD has undiagnosed left-sided CHF [,]. Subsequently, much evidence accumulated that in real clinical practice, patients with COPD very often experience undiagnosed LV hypertrophy (in 43.2% of women and 21.4% of men, respectively), as well as systolic and diastolic dysfunction of the LV (in 22% and 71% of cases, respectively) [, , 63-71]. Gradually, the academic community came to the conclusion (and now it dominates) that disturbances in the structure and function of the LV are key factors in the development of symptoms of CHF in the vast majority of patients with COPD, including because concomitant cardiovascular diseases are the most common comorbidity of COPD (up to 70% of patients).

The above, of course, does not exclude the role of structural and functional changes in the pancreas both in the development of symptoms of overload of the systemic circulation and in the deterioration of LV function through the inherent mechanisms of interventricular interaction [, , ,]. In addition, there are a number of factors that simultaneously negatively affect the functioning of both the left and right hearts. For example, pulmonary hyperinflation, especially during exercise, has the effect of compressing both ventricles, resulting in decreased diastolic filling, decreased stroke volume, and decreased cardiac output [ , , , ]. On the other hand, during exacerbations of COPD, decompensation of right ventricular dysfunction is often observed, which leads to the development or intensification of systemic congestion and peripheral edema. It should be noted that such episodes are not always accompanied by an increase in mean pressure in the pulmonary artery system, which proves the role of other factors in the genesis of decreased RV contractility. Moreover, exacerbations of COPD are often accompanied by the appearance of peripheral edema, even without signs of pancreatic decompensation due to hypercapnia and respiratory acidosis, which are accompanied by sodium retention and fluid retention.

The role of chronic pulmonary heart disease and pulmonary hypertension in the assessment of a COPD patient with symptoms of CHF. In 1963, WHO experts gave the following definition of chronic pulmonary heart disease (CPC): “Cor pulmonale is hypertrophy of the right ventricle, developing as a result of diseases that impair the function and/or structure of the lungs, except in cases where pulmonary changes are the result of primary lesions of the left heart or congenital heart defects". Despite the fact that the concept of “pulmonary heart” is very popular in clinical practice, the given definition is more pathomorphological than clinical, and is not best suited for clinical use, which results in a very broad and heterogeneous interpretation of this concept. Considering that the key phenomenon in the development of cor pulmonale is pulmonary hypertension (PH) and it is the diagnosis and treatment of various types of PH (not only associated with lung diseases) that is emphasized in most modern international consensus documents, many experts consider the optimal definition of CHL given by E Weitzenblum (2003): “CHS is the consequences of PH caused by diseases affecting the structure and/or function of the lungs, in the form of hypertrophy and/or dilatation of the right ventricle (RV) of the heart with symptoms of right-sided heart failure.”

PH is a common complication of COPD, although the increase in pulmonary artery pressure is usually small to moderate. In patients with mild obstruction, increased pulmonary artery pressure is atypical, and in COPD with an FEV of 1<50% частота клинически значимой ЛГ с развитием симптомов может достигать 5-10%. Распространенность клинически значимых проявлений ХЛС составляет 2-6 случаев на 1000 человек, а количество ежегодно регистрируемых новых случаев ХЛС – 1-3 на 10 000 человек.

It should be noted that if earlier in the development of CHL the main role was assigned to chronic hypoxemia with the development of PH, subsequent overload of the RV and the formation of right ventricular failure and stagnation in the systemic circulation, then in recent years this concept has been the subject of increasing debate. In particular, it has been shown that in a significant number of COPD patients with clinically significant congestion, only minor PH occurs with relatively preserved structure and function of the pancreas. In this regard, the development of symptoms of CLS (especially edematous syndrome) is mainly explained by hypercapnia, associated systemic vasodilation, activation of neurohumoral systems and renal retention of sodium and water. Therefore, for the diagnosis of CLS, the assessment of clinical symptoms has low sensitivity and specificity, and the basis for verification of the diagnosis is the study of the structure and function of the pancreas and the state of the pulmonary circulation.

The most commonly used method in routine practice for assessing PH and structural and functional changes in the pancreas is echocardiography. In particular, it has been proven that in the general population, LH levels assessed by Doppler ultrasound are highly correlated with pulmonary artery pressure levels assessed by invasive methods. But, unfortunately, COPD patients are an exception to this rule. First, the hyperinflation of the lungs inherent in COPD makes it impossible to adequately visualize the heart in half of patients with severe disease, that is, in those in whom CHL is more common. Second, the average error in pulmonary artery pressure estimation using Doppler compared with the invasive gold standard is about 10 mmHg. . In a large study (n = 374) of candidates for lung transplantation (primarily due to COPD), systolic pressure in the pulmonary artery using Doppler ultrasound could be assessed in only 44% of patients, and in 52% of cases the estimates were significantly incorrect compared with invasive estimate (difference > 10 mmHg) . In addition, it should be added that any international clinical guidelines for diagnosing PH use exclusively indicators obtained during cardiac catheterization (mean pulmonary artery pressure > 25 mm Hg).

Due to the lack of accuracy in assessing pulmonary artery pressure based on echocardiography, experts from the Working Group of the European Society of Cardiology and the European Respiratory Society on the Diagnosis and Treatment of PH in their general recommendations indicate that the diagnosis of PH can only be determined at a systolic pressure level of pulmonary artery > 50 mm Hg, i.e. at least twice the usual diagnostic threshold. It is traditionally believed that the main benefit of echocardiography in diagnosing PH lies in its high negative predictive value, that is, it allows one to exclude with high confidence the presence of PH at low pulmonary artery pressures, but requires additional verification by cardiac catheterization at high pulmonary artery pressures. pulmonary artery. It is also noteworthy that high levels of mean pulmonary artery pressure (more than 40 mm Hg on invasive examination) are quite atypical for COPD and always require a search for additional causative factors (obstructive sleep apnea, left ventricular dysfunction, pulmonary embolism and others ). Very rarely (in 1-3%) significant PH occurs in patients with non-severe COPD, in such cases it is called “disproportional” PH. Patients with this variant of PH have mild obstruction, significantly reduced diffusion capacity of the lungs, severe hypoxemia and hypocapnia, and are characterized by an extremely negative prognosis.

General approaches to the treatment of the combination of CHF and COPD.

Treatment of CHF in patients with COPD should be carried out in accordance with standard approaches. Most patients with CHF with reduced LVEF are treated with β-blockers. The use of selective β 1 -blockers (nebivolol, bisoprolol) is considered quite safe even with significant bronchial obstruction. It has been established that the use of β-blockers in patients with COPD may lead to some decrease in FEV 1 (especially when using non-cardioselective agents), but this phenomenon is not accompanied by an increase in dyspnea or deterioration in quality of life, and is probably not of significant clinical significance [ , , ]. Moreover, observational studies and their meta-analyses have repeatedly demonstrated that patients chronically taking β-blockers have a lower incidence of exacerbations of COPD, regardless of the degree of cardioselectivity of the agents [81–84]. There is only one caution when using β-blockers in people with COPD. In a recently published large epidemiological study in persons with extremely severe oxygen-dependent COPD, the use of β-blockers was associated with an adverse effect on prognosis. In general, for all other patients the rule is true: the benefits of using selective β 1 -blockers for CHF significantly outweigh any potential risk.

A number of small studies requiring further validation have found that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor antagonists (ARAs), which are a mandatory component of the treatment of CHF with reduced LVEF, have a number of “pulmonary” effects useful in COPD. They are able to influence bronchial obstruction by reducing angiotensin II levels, improve alveolar gas exchange, reduce pulmonary inflammation and vasoconstriction of pulmonary vessels. Two recently published observational studies in patients with COPD showed beneficial effects of ACEIs and ARB II not only on cardiac endpoints, but also on a number of important pulmonary endpoints, such as exacerbations of COPD, hospitalizations and respiratory mortality [ , ].

The use of statins is an integral component of the treatment of coronary heart disease, which is the most common cause of CHF. The presence of concomitant COPD does not affect the choice of lipid-lowering drug or its regimen. At the same time, based on the results of a number of studies, it has been established that the use of statins can have a beneficial effect on the course of COPD, reducing the frequency of exacerbations, hospitalizations, slowing the progression of pulmonary function and reducing mortality [88-90]. However, these results were not confirmed in the only randomized study to date, STATCOPE, in which treatment with 40 mg simvastatin was not associated with a reduction in the frequency of exacerbations compared with placebo.

Treatment of COPD in patients with CHF should be standard in accordance with international recommendations, since there is no convincing evidence that COPD in the presence of concomitant CHF should be treated differently. There have been no special randomized studies of the effectiveness and safety of inhaled therapy for COPD in patients with CHF. Therefore, this expert recommendation is based primarily on the results of extensive studies in which long-term use of long-acting bronchodilators in patients both without and with CHF not only did not increase the incidence of cardiovascular complications, but was also accompanied by a decrease in the risk of myocardial infarction and a number of cardiovascular events. events (fluticasone salmeterol in the TORCH trial, tiotropium in the UPLIFT trial) [,].

Along with this, the cardiovascular safety profile of some anticholinergic agents is currently being actively discussed, especially in the context of the development or decompensation of CHF. According to the results of several meta-analyses, the use of the short-acting anticholinergic drug ipratropium may increase the incidence or severity of CHF.

According to one study, patients with CHF taking β2-agonists had an increased risk of mortality and hospitalization. It should be noted that the observational nature of this study does not allow us to draw confident conclusions about the presence of relevant cause-and-effect relationships. Therefore, there is no need to refrain from using this class of bronchodilators for CHF. However, it may be prudent to more closely monitor patients with severe CHF who are receiving inhaled β2-agonists for COPD.

1. Rutten, F.H., Diagnosis and management of heart failure in COPD, in COPD and Comorbidity. 2013, European Respiratory Society Journals Ltd. p. 50-63.

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Chronic obstructive pulmonary disease or COPD refers to chronic lung diseases associated with breathing failure. Damage to the bronchi develops with emphysema complications against the background of inflammatory and external irritants and has a chronic progressive nature.

Alternating periods of latent course with exacerbations requires a special approach to treatment. The risk of developing serious complications is quite high, which is confirmed by statistical data. Impaired respiratory function 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 the respiratory system is exposed to various irritants, people with a predisposition to pneumonia begin to develop negative processes in the bronchi. First of all, the distal sections are affected - located in close proximity to the alveoli and pulmonary parenchyma.

Against the background of inflammatory reactions, the process of natural mucus discharge is disrupted, and small bronchi become clogged. When an infection occurs, inflammation spreads to the muscle and submucosal layers. As a result, remodeling of the bronchi occurs with replacement by connective tissue. In addition, lung tissue and bridges are destroyed, which leads to the development of emphysema. When the elasticity of the lung tissue decreases, 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 disruption of gas exchange and a decrease in inspiratory volume. A change in the natural breathing process manifests itself in patients as shortness of breath in COPD, which significantly increases with exercise.

Constant respiratory failure causes hypoxia - oxygen deficiency. All organs suffer from oxygen starvation. With prolonged hypoxia, the pulmonary vessels narrow even more, which leads to hypertension. As a result, irreversible changes in the heart occur - the right side enlarges, which becomes the cause of heart failure.

Why is COPD classified as a separate group of diseases?

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

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

Medicine has determined the basis of this disease – chronic obstruction. But narrowing of the lumens in the respiratory tract also occurs during other pulmonary diseases.

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

Thus, in asthma, spirometry shows improvements after bronchodilators are used. Moreover, the indicators of PEF and 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 occur as an independent pathology, just as bronchitis cannot always provoke COPD.

Bronchitis is characterized by a prolonged cough with hypersecretion of sputum and the lesion extends exclusively to the bronchi; obstructive disorders are not always observed. While sputum production in COPD is not increased in all cases, and the damage extends to the structural elements, although bronchial wheezing is heard on auscultation in both cases.

Why does COPD develop?

Quite a few adults and children suffer from bronchitis and pneumonia. Why then does chronic obstructive pulmonary disease develop only in a few people? In addition to provoking factors, predisposing factors also influence the etiology of the disease. That is, the impetus for the development of COPD can be certain conditions in which people 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 is of genetic origin, which explains why the lungs of a heavy smoker do not undergo mutations, and COPD develops in children for no particular reason.
2. Age and gender. For a long time, it was believed that the pathology affects men over 40. And the rationale is largely related not to age, but to smoking history. But today the number of experienced women smokers 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 women, but also children’s bodies.
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 to full expansion. In addition, in early childhood, retardation in physical development negatively affects the condition of the respiratory system.
4. Infectious diseases. With frequent respiratory diseases of infectious origin, both in childhood and at an older age, the risk of developing CHOL increases significantly.
5. Hyperresponsiveness of the lungs. Initially, this condition is the cause of bronchial asthma. But in the future, the addition of COPD is not excluded.

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

Obstruction develops under certain conditions, which may include:

1. Smoking. Smokers are the main patients diagnosed with COPD. According to statistics, this category of patients makes up 90%. Therefore, smoking is called the main cause of COPD. And prevention of COPD is based, first of all, on smoking cessation.
2. Harmful working conditions. People who, due to the nature of their work, are forced to regularly inhale dust of various origins, air saturated with chemicals, and 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 and other building mixtures leads to the development of respiratory problems to the same extent in smokers and non-smoking workers .
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 forced to be present during wildfires, inhale combustion products, which are carcinogenic and irritate the respiratory tract.

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

Main complaints and symptoms

The primary symptoms of COPD are associated with cough. Moreover, cough bothers patients to a greater extent during the daytime. In this case, sputum production is insignificant, wheezing may be absent. The pain hardly bothers me, the sputum comes out in the form of mucus.

Sputum with the presence of pus or a hacking cough, provoking 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 during fast walking, as well as when climbing to a hill;
• Moderate shortness of breath is indicated by the need to slow down the pace of walking on a level 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;
• Stage 4 shortness of breath is characterized by the appearance of breathing problems while getting dressed, performing simple actions, or immediately after going outside.

The occurrence of such syndromes in COPD may accompany not only the exacerbation stage. Moreover, as the disease progresses, the symptoms of COPD in the form of shortness of breath and cough become 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 muscles, atrophy, which causes muscle pain and neuralgia.
• Changes in the lining and atherosclerotic lesions are observed in the vessels. The tendency to form blood clots increases.
• A person faces heart problems in the form of arterial hypertension, coronary artery disease and even heart attack. For COPD, the pattern of cardiac changes is associated with left ventricular hypertrophy and dysfunction.
• Osteoporosis develops, manifested by spontaneous fractures of tubular bones, as well as the spine. Constant joint pain and bone pain cause a sedentary lifestyle.

Immune defense is also reduced, so any infections are not resisted. Frequent colds, in which there is a high temperature, headache and other signs of infection, are not a rare picture in COPD.

Mental and emotional disorders are also noted. Performance decreases significantly, depression and unexplained anxiety develop.

It is problematic to correct emotional disorders that arise against the background of COPD. Patients complain of apnea and stable insomnia.

In later stages, cognitive disorders also occur, 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 based on clinical manifestation:

1. Bronchial type. Patients often experience coughing, 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 gives the patients the name “blue swelling”.
2. Emphysematous type. The clinical picture is dominated by shortness of breath. The presence of cough and sputum is rare. The development of hypoxemia and pulmonary hypertension is observed only in the later stages. Patients experience a sharp decrease in weight, and the skin acquires a pink-gray tint, which gives it the name “pink puffers.”

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

Exacerbation of COPD

The disease can worsen unpredictably under the influence of various factors, including external, irritating, physiological and even emotional. Even after eating food in a hurry, choking may occur. At the same time, the person’s condition is rapidly deteriorating. Cough and shortness of breath intensify. The use of conventional basic therapy for COPD during such periods does not produce results. During the period of exacerbation, it is necessary to adjust not only the methods of treating COPD, but also the doses of the drugs used.

Typically, treatment is carried out in a hospital, where it is possible to provide emergency care to the patient and conduct the necessary examinations. If exacerbations of COPD occur frequently, the risk of complications increases.

Urgent Care

Exacerbations with sudden attacks of 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, you must urgently call an ambulance.

Video

Chronic obstructive pulmonary disease

Principles of treatment for exacerbations

Treatment of chronic obstructive pulmonary disease during an exacerbation in a hospital is carried out according to the following scheme:

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

In addition, drugs can be used to treat diseases caused by COPD.

Basic treatment

To prevent attacks and improve the general condition of the patient, a set of measures is carried out, not least of which is behavioral and drug treatment, and clinical observation.

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

Along 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 losing excess weight and saturating yourself with essential vitamins.

Treatment of COPD in elderly people, as well as in severely ill patients, is associated with a number of difficulties due to the presence of concomitant diseases, complications and reduced immune defense. Often these patients require constant care. Oxygen therapy in such cases is used at home and, sometimes, is the main method aimed at preventing hypoxia and associated complications.

When the damage to the lung tissue is significant, drastic measures are necessary, including resection of part of the lung.

Modern methods of radical treatment include radiofrequency ablation (ablation). It makes sense to do RFA when identifying tumors when, for some reason, surgery is not possible.

Prevention

The main methods of primary prevention directly depend on a person’s habits and lifestyle. Quitting smoking and using personal protective equipment significantly reduces the risk of developing pulmonary obstruction.

Secondary prevention is aimed at preventing exacerbations. Therefore, the patient must strictly follow medical recommendations for treatment, and also eliminate provoking factors from his life.

But even cured and operated patients are not completely 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 at a preferential rate.

Chuchalin A.G.

In modern society (COPD), along with arterial hypertension, coronary heart disease and diabetes mellitus, constitute the leading group of chronic diseases: they account for more than 30% of all other forms of human pathology. The World Health Organization (WHO) classifies COPD as a disease with a high social burden, as it is widespread in both developed and developing countries. The forecast compiled by WHO experts until 2020 indicates that COPD will not only become one of the most common forms of human pathology, but will be among the leading causes of death, while a decrease in deaths from myocardial infarction, cancer, etc. is expected. .d.

The modern concept of COPD, developed by WHO (GOLD, 2006), is based on the fact that this disease is one of those whose development can be prevented and treated quite successfully; Often the severity and prognosis are determined by extrapulmonary manifestations. I would like to emphasize that the course of the disease, treatment and preventive programs largely depend on the concomitant diseases against which COPD occurs. In clinical practice, it is necessary to distinguish between those diseases that manifest themselves during the natural course of COPD. Such diseases include a group of cardiovascular diseases, osteoporosis and others. A different clinical scenario may develop in patients who have been suffering from cardiovascular diseases for a long time, which is accompanied by a violation of the pulmonary ventilation function of the obstructive type. Often the appearance of shortness of breath in this category of patients is associated not so much with manifestations of heart failure, but with respiratory failure or with a combined manifestation of reduced function of both the lungs and the heart. Among the very diverse clinical picture of COPD and concomitant diseases, it is necessary to highlight those stages of the underlying disease at which signs of systemic effects of COPD appear. Abnormal in nature, the inflammatory process is initially localized in the respiratory tract and pulmonary parenchyma, but at certain stages of the disease its systemic effects appear. Tobacco smoking is a risk factor for the development and progression of COPD, but it is also associated with the development of a large group of concomitant diseases. Smoking is associated with the appearance of pathological processes in the lungs and the development of systemic inflammatory reactions; systemic oxidative stress; vascular endothelial dysfunction; increased activity of procoagulant factors; oncogene amplification and other systemic effects.

The most common concomitant diseases in COPD are: cachexia, wasting and atrophy of skeletal muscles, arterial hypertension, coronary heart disease, heart failure, vasculopathies of the pulmonary circulation, infectious diseases of the respiratory tract and cancer. The prognosis is most unfavorable when COPD is combined with a group of cardiovascular diseases.

Patients suffering from severe forms of COPD are at high risk of sudden death. One of the reasons that may underlie the development of sudden death is a violation of the heart rhythm. This clinical problem is one of those that requires more detailed study than is currently presented.

Supraventricular and ventricular forms of cardiac arrhythmias are a fairly common clinical problem in patients with COPD. However, it should be emphasized that there is considerable variation in the data presented in the literature. Significant fluctuations in data on arrhythmias in patients with COPD are explained by the different population of patients participating in the study; The phases of the disease and the severity of clinical manifestations of COPD, as well as the methodological conditions for recording and monitoring ECG, are different. Undoubtedly, concomitant coronary heart disease and the presence of ventricular failure play a major role. In cases of COPD, another important cause of episodes of arrhythmia is associated with the use of certain medications: theophylline, digoxin, β-receptor agonists. The entire range of listed conditions for the occurrence of arrhythmias in patients with COPD makes it difficult to obtain a complete picture of this clinical problem. However, in recent years there has been some progress in its study.

The epidemiology of arrhythmias in patients with COPD and their relationship with deaths was studied in a study by Danish scientists, the Copenhagen City Heart Study. This unique epidemiological study showed that COPD is associated with a high incidence of cardiac arrhythmias. The frequency of atrial fibrillation depends on indicators of impaired ventilation function of the lungs. Thus, in patients with COPD who had no history of myocardial infarction, atrial fibrillation occurred twice as often with FEV1<60%. Контрольной группой служили больные ХОБЛ с показателями FEV1>60% .

Sudden death in patients with COPD during exacerbation of the disease is relatively common. Fuso L., RA Incalzi., R Pistelli., R Muzzolon., S Valente., G Pigliari., F Gliozzi., Ciappi (Predicting mortality of patients for acutely exacerbated chronic obstructive pulmonary disease. Am J Med 1995 Mar; 98( 3):272-7) studied a group of 590 patients during an exacerbation of COPD and admitted to a university clinic. The outcome of the disease was assessed retrospectively. The mortality rate was over 14%; Logistic regression analysis established four independent factors: age, alveolus - arterial gradient exceeded 41 mm Hg, ventricular tachycardia, atrial fibrillation. The authors concluded that varying degrees of myocardial dysfunction are the leading cause in the possible mechanism of sudden death in patients with COPD during an exacerbation.

In recent years, increasing attention has been drawn to the problem of arrhythmias in patients with COPD at various stages of the disease and during periods of exacerbation. Thus, Kleiger, RE, RM, Senior (Long-term electrocardiographic monitoring of ambulatory patients with COPD. Chest 1974; 65:483) found that arrhythmia occurs in 84% of the observed patients, among whom ventricular forms of disorders prevailed (74%) , supraventricular tachycardia occurred in 52%. The authors also concluded that a decrease in FEV1 values ​​is a factor influencing the frequency of recorded arrhythmic episodes.

Another study conducted by Shih HT., CR Webb, WA Conway, E Peterson, B Tilley (Frequency and significance of cardiac arrhythmias in COPD. Chest 1988 Jul; 94(1):44-8) showed that when severe hypoxemia in patients with COPD, supraventricular tachycardia was recorded in more than 69%; ventricular forms of heart rhythm disturbances could be detected more often - 83%. In patients who had peripheral leg edema, hypercapnia and other signs of cor pulmonale, ventricular forms of arrhythmia were more common. These observations allowed the authors to conclude that with the development of cor pulmonale in patients with COPD, it is possible to predict the development of ventricular forms of cardiac arrhythmia, which may be the cause of sudden death in this category of patients.

However, it should be emphasized that epidemiological studies on the issue of arrhythmias in patients with COPD are clearly insufficient; There are many unresolved questions, in particular, the role of secondary pulmonary hypertension is practically not studied. The same little-studied issues include the role of medications prescribed to cardiac patients to control blood pressure, heart rate, and b-blockers.

The pathogenesis of the development of arrhythmias in patients with COPD is multifactorial in nature. Among the factors that provoke the development of arrhythmia are medications prescribed to patients with COPD, dysfunction of the autonomic conduction system of the heart, coronary heart disease, arterial hypertension, dysfunction of the left and right ventricles, increased levels of catecholamines in the blood with the development of hypoxemia. Among other arrhythmogenic factors, hypokalemia, hypomagnesemia, and respiratory acidosis are also indicated.

Among the significant variety of drugs that have historically been used by patients with COPD, the arrhythmogenic effects of theophylline and its derivatives have been the most studied. Arrhythmias such as sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, unifocal and multifocal atrial tachycardia, and ventricular arrhythmias are associated with the administration of xanthine derivatives. The occurrence of both atrial and ventricular arrhythmias is directly dependent on the concentration of theophylline in the blood serum. The therapeutic window for theophylline ranges from 10-15 mq/L. Tobacco smoking, taking macrolides, and antihistamines can contribute to the toxic effects of theophylline. Age and concomitant diseases such as coronary heart disease, liver disease and some others play a certain role in the development of the arrhythmogenic effects of theophylline. In a study conducted by Bittar G., HS Friedman (The arrhythmogenicity of theophylline. A multivariate analysis of clinical determinants. Chest 1991 Jun; 99(6): 1415 - 20), the authors on a cohort of COPD patients who were admitted to the clinic in period of exacerbation of the disease, the relationship between the concentration of theophylline in the blood serum and the development of episodes of arrhythmias was studied. The study was carried out on a group of 100 patients. Many factors were taken into account in the occurrence of arrhythmias, such as the concentration of digoxin, β-agonists, potassium concentration and a number of other parameters. The authors concluded that the arrhythmogenic effects were primarily due to theophylline intake. Cardiac arrhythmias, some of which were classified as life-threatening (for example, ventricular tachycardia, polytopic ventricular extrasystole and other forms), developed even against the background of therapeutic concentrations of theophylline. Particular attention should be paid to the period of exacerbation of COPD, when respiratory failure develops in severe patients, manifestations of hypoxemia increase, and doctors include intravenous administration of aminophylline in treatment programs. During this period, conditions are created for the manifestation of the arrhythmogenic effect of aminophylline. The fight against hypoxemia is an important part of the treatment program for patients with COPD, which allows the patient not only to overcome an exacerbation, but also to prevent unwanted side reactions from a significant group of drugs (including theophylline).

The next group of drugs that is widely used in treatment programs for patients with COPD are β-receptor agonists. In everyday clinical practice, salbutamol is most widely used. It is prescribed in the form of dosed inhalations, a solution of salbutamol in a dose of 5 mg is inhaled through a nebulizer, it can be administered intravenously as a solution. Little is taken into account the fact that salbutamol administered through a nebulizer is prescribed in a fairly high dose (from 2.5 to 5 mg), and in especially severe cases its dose may be higher. At these doses, its effect on the activity of the sinus node is manifested: the ratio between the duration of the node’s activity changes (the time is shortened) and the time for restoration of its activity. Salbutamol increases the impulse conduction time through the atrioventricular node, reducing the refractory time of excitability of the node, as well as the myocardium. All of the above allows us to classify salbutamol as a drug with a proarrhythmogenic effect. However, in widespread clinical practice, the development of serious heart rhythm disturbances is not associated with the prescription of salbutamol. A meta-analysis of 33 randomized placebo-controlled trials of β-agonists in chronic obstructive pulmonary disease found that a single dose of the drug increased heart rate by an average of 9 beats per minute. Other effects include a decrease in potassium concentration by an average of 0.36 mmol/L and chlorine concentration by 0.18-0.54 mmol/L. Beta-adrenergic agonists are associated with adverse cardiac effects, primarily related to the development of sinus tachycardia. Potentially, this group of drugs should be considered as drugs that have the following undesirable effects: increase sinus tachycardia, myocardial ischemia, heart failure, cardiac arrhythmias and may cause sudden death. It should be especially emphasized that the above side effects of agonists manifest themselves especially in those patients in whom COPD occurs against the background of concomitant cardiovascular disease.

In recent years, attention has been focused on the side effects of long-acting β-agonists. The debate arose after a discussion of cases of sudden death in the African American population after taking salmeterol. The modern interpretation of the data obtained is based on the assessment of QT syndrome. When the QT interval is prolonged above 0.45 ms, the arrhythmogenic effect of agonists may occur. These changes can be congenital or acquired by a person while taking the drug. This clinical experience formed the basis of modern clinical recommendations. When prescribing agonists, it is recommended to take an ECG and measure the duration of the QT interval; in cases where the QT duration exceeds 0.45 ms, it is not recommended to prescribe agonists for a long time. In cases where patients began to regularly use this group of drugs, it is recommended to examine the duration of the QT interval using an ECG after a month. If it begins to exceed the physiological parameters indicated above, then further use of β-agonists should be abandoned.

Autonomic cardiac dysfunction manifests itself in prolongation of the QT interval. Long QT syndrome is both congenital and acquired.

Many factors can influence QT prolongation. Among them there are patients with congenital disorders in the conduction system of autonomic cardiac activity: Jervell, Lange-Nielsen, Romano-Ward syndromes; There are also idiopathic cases of conduction disorders. In cases of acquired prolonged QT interval, great importance is attached to metabolic disorders (hypokalemia, hypomagnesemia, hypocalcemia, hypothyroidism, anorexia). Taking certain medications may affect the duration of the QT interval - quinidine, amiodarone, sotalol, disopyramide, as well as antimicrobial drugs - macrolides, pentamidine, fluoroquinolones, antihistamines, drugs with psychotropic effects.

Relatively little studied is the connection between respiratory failure developing in patients with COPD, on the one hand, and, on the other, left ventricular dysfunction and the occurrence of ventricular arrhythmias. In a study by Incalzi RA, R Pistelli, A. Cocchi, MG Bonetti, A Giordano (Cardiac arrhythmias and left ventricular function in respiratory failure from chronic COPD. Chest 1990 May;97 (5);1092-7) in patients with COPD, the relationship between left ventricular function and cardiac arrhythmias. Ventricular arrhythmia was monitored for 24 hours, and the study was repeated as the clinical manifestations of respiratory failure improved. Left ventricular diastolic dysfunction is one of the factors contributing to the development of ventricular arrhythmias. The authors found a direct relationship between the severity of manifestations of respiratory failure and left ventricular diastolic dysfunction, while blood gas parameters and the clinical picture do not correlate with arrhythmic episodes. In clinical practice, it is recommended to carry out a more detailed diagnostic assessment of episodes of ventricular arrhythmias that occur against the background of diastolic dysfunction of the left ventricle, since these manifestations may be hidden myocardial ischemia, painless forms of angina and overload of the right ventricle during the formation of cor pulmonale. It must be emphasized that with the development of arrhythmia, there is always a deterioration in the clinical manifestations of respiratory failure. Cheong TH, S Magder, S Shapiro, JG Martin, RD Levy (Cardiac arrhythmias during exercise in severe chronic obstructive pulmonary disease. Chest 1990 Apr; 97(4):793-7) found that when maximum exercise was achieved in patients with COPD, new arrhythmic episodes occur. Unfortunately, in subsequent years this topic was not addressed by researchers of heart rhythm disturbances that occur in patients with COPD.

Multifocal atrial tachycardia occupies a special place in the study of cardiac arrhythmias in patients with COPD. The main morphological signs of this form of cardiac arrhythmia are the discreteness of the “P” wave, at least in three forms, which is better recorded in leads I, II, III; the number of heart contractions is more than 100 beats per minute, the intervals P-P and P-R, R-R are different.

Multifocal atrial tachycardia is associated to a large extent with the development of respiratory failure, and functional changes in the functioning of the heart muscle are associated with its occurrence. The prognosis for the course of COPD with the appearance of this type of cardiac arrhythmia is considered to be unfavorable.

Treatment programs for cardiac arrhythmias in patients with COPD have a number of features. An important place in treatment programs is given to the correction of acid-base balance, as well as hypokalemia, hypomagnesemia, and oxygen therapy. An important place is occupied by therapeutic measures aimed at preventing or treating myocardial ischemia. It is necessary to exclude the prescription of those medications that may affect the prolongation of the QT interval. Such drugs include: macrolides, antifungal drugs, antihistamines. It is usually recommended to discontinue theophylline if QT interval prolongation is observed on the ECG.

Specific antiarrhythmic therapy varies significantly depending on the severity of the clinical manifestations of COPD, concomitant diseases and a number of individual reactions of each patient.

Patients in whom asymptomatic ventricular arrhythmia is recorded when taking an ECG, as a rule, do not need to be prescribed special medications (at least, it is necessary to adhere to restraining tactics when prescribing treatment). With the development of clinical symptoms of hemodynamic collapse, myocardial ischemia, acute left ventricular failure, cardioversion is indicated. The most common drugs of choice are class IA antiarrhythmic drugs: quinidine, procainamide and disopyramide. In 2006, the American and European Heart Associations developed joint recommendations for the treatment of atrial fibrillation in patients with obstructive pulmonary disease. These recommendations emphasize the great importance of combating hypoxemia and acidemia; preference is given to prescribing non-dihydropyridine calcium channel blockers (diltiazem, verapamil). The recommendations indicate avoiding theophylline, b-agonists, b-blockers, and adenosine.

For supraventricular tachycardia, it is recommended to prescribe calcium channel blockers, amiodarone, digitalis, flecainide. The greatest antiarrhythmic effect was achieved with intravenous administration of verapamil. For multifocal atrial tachycardia, verapamil is preferable, and metoprolol is also recommended. Of all the existing b-blockers, metoprolol has the least effect on the tone of bronchial smooth muscles. When discussing antiarrhythmic therapy in patients with COPD, it is necessary to emphasize the role of verapamil, which is most often prescribed in this category of patients. An important point of the program is compliance with the conditions of the protocol for its appointment. Verapamil is initially administered intravenously at a dose of 1 mg. The effectiveness of the antiarrhythmic action is assessed after 1-2 minutes; if ineffective, the dose can be increased to 4 mg, which is administered slowly over five minutes. If the antiarrhythmic effect has not occurred and there are no conduction disturbances in the atrioventricular node, then an additional dose of 5 mg can be administered. The interval between administration of verapamil should be 10 minutes, and ECG monitoring is necessary. When the antiarrhythmic effect is achieved, therapy must be continued by prescribing verapamil 80 mg per os. every 6 hours. A contraindication to the use of verapamil is AV blockade, previous use of b-blockers and other drugs that block calcium channels. Verapamil, especially when administered intravenously, may cause hypotension. To avoid this undesirable effect, it is recommended to combine it with intravenous administration of calcium gluconate, which should be administered before the administration of verapamil.

Of all the existing b-blockers, as already discussed above, preference should be given to metoprolol, which is prescribed in a dose of 50-100 mg twice a day. Data are accumulating on the safety of esmolol use in patients with obstructive respiratory dysfunction.

The combination of arterial hypertension and chronic obstructive pulmonary disease is quite common in clinical practice. Often patients with these forms of combined diseases represent the same age group. Difficulties in managing this category of patients are primarily due to the fact that some antihypertensive drugs can have a bronchoconstriction effect, thereby aggravating the course of bronchial asthma and COPD. General recommendations are based on extremely careful prescribing of b-blockers; to a lesser extent, these recommendations apply to the group of angiotensin-converting enzyme inhibitors (ACEIs). It is necessary to emphasize the pathogenetic role of hypoxemia in the development of arterial hypertension. In the domestic literature, N.M. has dealt quite a lot with the problem of pulmonary arterial hypertension. Mukharlyamov. When managing patients with COPD and signs of respiratory failure, treatment of arterial hypertension should begin with oxygen inhalation and try to improve the ventilation parameters of external respiration function. Oxygen inhalation or more active respiratory support, such as non-invasive ventilation, as well as combined inhaled therapy with β-agonists and corticosteroids often bring positive results in controlling the course of arterial hypertension.

Currently, extensive literature has been accumulated on the effectiveness and safety of b-blockers in the treatment of patients with bronchial asthma and COPD. If patients have signs of reversible airway obstruction, then it is highly likely that beta-blockers will exhibit bronchoconstriction effects and, moreover, contribute to the development of resistance to the action of beta-receptor agonists. β-blockers, which are prescribed in the form of eye drops in the treatment of glaucoma, have these properties. The clinical effectiveness of selective b1 blockers has been studied. Salpeter S., T Ormiston, E Salpeter (Cardioselective beta - blocker use in patients with revesible airway disease. Cochrane Databese Syst Rev 2001; (2):CD002992) conducted a meta-analysis that included data from randomized, placebo-controlled, blinded trials . Data on single use of cardioselective b-blockers, their effect on forced vital capacity in one second and assessment of the effectiveness of short-acting b-receptor agonists were analyzed. Thus, 19 studies with a single dose of blockers and 10 studies when this group of drugs were used for a long time were analyzed. A decrease in FEV1 was noted by 7.9%, but there was a good response to bronchodilators - more than 13%. This meta-analysis concludes that cardioselective b-blockers do not lead to a significant deterioration in ventilation function in broncho-obstructive syndrome. However, it should be emphasized that we were talking about patients with mild to moderate obstruction. It is advisable to preserve this group of drugs when treating patients with coronary heart disease and arterial hypertension. Long-term use of b-blockers was not accompanied by a deterioration in respiratory function in patients with COPD. The exact mechanism of development of bronchoconstriction after the administration of b-blockers remains poorly understood. The development of bronchospasm is assumed to involve the parasympathetic nervous system, therefore, the use of oxytropium bromide is indicated for prophylactic purposes.

Angiotensin-converting enzyme inhibitors (ACEIs) cause a dry, nonproductive cough in more than 20% of cases, and a small group of patients may even develop typical asthma attacks. This group of drugs cannot be considered as first-line therapy in the treatment of arterial hypertension in patients with COPD.

Alternative medications are angiotensin receptor blockers. The development of cough is not associated with this group of drugs, and cases of iatrogenic bronchial asthma have not been described. In terms of their effectiveness and safety, they can be comparable to calcium channel blockers.

Diuretics are another group of drugs that are widely used in the treatment of arterial hypertension. However, long-term use can lead to such undesirable effects as hypokalemia, hypomagnesemia, which can be aggravated by constant use of b-receptor agonists and glucocorticosteroids. Another problem that may be exacerbated when diuretics are prescribed to patients with COPD is their negative effect on metabolic alkalosis. Decompensated forms of metabolic alkalosis may be accompanied by suppression of ventilation draveir, which leads to an increase in the degree of hypoxemia. Of the various existing groups of drugs with a diuretic effect, it is recommended to prescribe moderate doses of hydrochlorothiazide (up to 25 mg). Low doses may be more effective than the rapid, but more dangerous, undesirable side effects of other groups of drugs with a diuretic effect.

Calcium channel blockers play a leading role in the treatment of arterial hypertension in patients with COPD. Dihydropyridine derivatives, such as nifedipine and nicardine, have found widespread use. With the prescription of this group of drugs, as a rule, it is possible to quickly establish control over arterial hypertension. It should also be emphasized their positive effects on the regulation of bronchial smooth muscle tone, the effect of inhibiting mast cell degranulation and the potentiation of the dilatation effect of b-agonists. Clinical recommendations for the treatment of arterial hypertension include the prescription of calcium channel blockers as monotherapy or in combination with low doses of thiazide derivatives.

The last group of drugs that should be discussed relates to blockers with sympathetic activity: a2-receptor agonists clonidine and methyldopa should be prescribed with caution when treating arterial hypertension in this category of patients.

Coronary heart disease (CHD) and chronic obstructive pulmonary disease (COPD) are quite often concomitant diseases. In clinical practice, it is sometimes difficult to determine which disease is leading in a given patient in a given clinical situation. This is confirmed by the study Behar S., A. Panosh, H. Reicher - Reiss, M. Zion, Z. Schliezinger, U. Goldbourt (Prevalence and prognosis of COPD among 5839 consecutive patients with acute myocardial infarction. Sprint Study Group. Am J Med 1992 Dec;93(6):637-41). The main goal of this study was to diagnose COPD in patients undergoing myocardial infarction. The authors found that COPD was detected in more than 7% of cases and was more often observed in those patients who were tobacco smokers. In the same group of patients with concomitant pathology, a higher mortality rate and a higher percentage of patients with the development of pulmonary heart failure were observed. In Russia L.I. Kozlova conducted a study on a group of patients with coronary artery disease who received b-blockers for a long time. More than 300 patients were observed for 10 years, and some were observed for up to 15 years. During this entire period, in addition to the cardiological program, a dynamic study of the parameters of external respiration function was carried out. The author came to the conclusion that over time, most patients with coronary artery disease also became patients with obstructive disorders of external respiration function. Often the provoking factor for respiratory dysfunction was a transmitted acute viral disease of the respiratory tract. The main conclusion made in the doctoral dissertation of L.I. Kozlova, is that long-term use of b-blockers may be a risk factor for the development of obstructive respiratory dysfunction. Undoubtedly, the question remains open whether these changes in the ventilation function of the lungs occur due to already existing changes in the respiratory system, when b-blockers act as one of the risk factors, or whether many reasons underlie such frequent development of obstruction of the respiratory system in patients initially patients with coronary artery disease. Nevertheless, it is necessary to state the fact that most often COPD is combined with ischemic heart disease. N. Amposino indicates that IHD of varying severity occurs in almost every second COPD patient. These data must also be taken into account in situations when patients with emphysema are being prepared for surgery to reduce lung tissue. If the coronary reserve has not been assessed, it is unlikely that it will be possible to achieve the desired positive results from surgery. Sin D.D., S.F. Man (COPD as a risk factor for cardiovascular morbidity and mortality. Proc Am Thorax Soc 2005;2(1):8-11) concluded that COPD increases the risk factor for death in patients with coronary artery disease by 50%. With the addition of ventricular arrhythmia, the risk of sudden death increases even more. The general conclusion is made that a decrease in FEV1 by 10% increases the likelihood of death in a patient with concomitant pathology by 14%. In a study conducted by Jousilahti P., E. Vartianen, P. Puska (Symptoms of chronic ponchitis and the risk of coronary disease. Lancet 1996 Aug 31; 348 (9027):567-72), 20 thousand patients were analyzed, observed for 13 years. The main conclusion of this study is that chronic bronchitis is a risk for developing coronary disease.

A major role is assigned to the development of hypoxemia, which significantly worsens the course of IHD. A decrease in oxygen saturation to 80% and a duration of hypoxia of more than 5 minutes have a particularly detrimental effect. The most dangerous group of patients are those in whom hypoxia is combined with hypercapnia. The treatment programs for this category of patients necessarily include the administration of oxygen. It has been repeatedly shown that long-term oxygen therapy (inhalation time exceeding 15 hours per day) significantly increases the survival of patients. Current indications for long-term oxygen therapy sessions:

arterial oxygen tension (PaO2) less than 55 mm Hg. or oxygen saturation (SaO2) less than 89%. Clinical signs: cor pulmonale, right ventricular decompensation, erythrocytosis (hematocrit>56%);

PaO2>60 mmHg, saturation>90% (but these indicators are in patients with clinical manifestations of coronary artery disease). It is necessary to emphasize the need to prescribe oxygen inhalation, especially at night, when respiratory function deteriorates and coronary reserve decreases.

Drug therapy for the combined course of coronary artery disease and COPD is one of the most pressing problems of internal medicine. Currently, there are no rigorous studies on the adequate choice of medications in this category of patients. For COPD, salbutamol, salmeterol, formoterol and their combinations with glucocorticosteroids are most often prescribed. The group of sympathomimetics has a significant effect on myocardial metabolism: hypokalemia, hypomagnesemia, oxygen debt. The use of these drugs is associated with the development of arrhythmias, which can also occur when theophylline is prescribed, as discussed above. Preference is given to combination drugs that include small doses of b-agonists and glucocorticosteroids, and due to the sparring effect, their maximum effect on the tone of the smooth muscles of the respiratory tract is achieved. Of the existing bronchodilator drugs, the cardiotoxic properties are least pronounced in tiotropium bromide.

Beta blockers, which are considered basic drugs in the treatment of coronary artery disease, in this particular case are prescribed either with great caution, or they are completely abandoned. Metoprolol is considered the drug of choice if there is an urgent need for the prescription of b-blockers. Clinical recommendations give priority to the prescription of combined b-blockers (labetalol, carvedilol).

Chronic heart failure is a clinical problem indicating a poor prognosis for patients with COPD. According to N. Amposino, heart failure occurs in more than 20% of cases and, as a rule, develops against the background of coronary heart disease, arterial hypertension, type 2 diabetes, and osteoporosis. Diagnosis of heart failure presents certain difficulties, since it is largely masked by manifestations of acute or chronic respiratory failure. The problem of changes in central hemodynamics that arises during an exacerbation of COPD has already been discussed above; This condition is characterized by the development of left ventricular diastolic dysfunction. Apparently, manifestations of heart failure caused by left ventricular dysfunction are more common than it is detected in patients with COPD. Diagnosis is complicated by the fact that with respiratory and heart failure, the clinical manifestations can be very similar. Thus, the leading place is occupied by shortness of breath, the intensity of which increases with physical activity. The experience of a physician skilled in the art of taking anamnesis may enable him, using the instrument of the language of dyspnea, to note certain features in its clinical manifestation. Such signs include an orthoptic position, a reaction to physical activity, a feeling of lack of air and some other nuances. However, patients need this clinical problem to receive clear diagnostic resolution. The diagnostic algorithm includes studying the oxygen pulse, conducting an X-ray examination of the chest organs, taking an ECG and echocardiography. Biochemical markers of heart failure include determination of the level of brain sodium hormone, which is highly specific for patients with heart failure. The implementation of this diagnostic program is not academic in nature. Determination of heart failure and reduction of ejection fraction can be considered as an important prognostic sign that can predict 5-year survival. Triboulloy C., D. Rosinaru., H. Mahjoub., V. Souliere., F., Levy., M. Peltier., M., Slama., Z. Massy (Prognosis of heart failure with preserved ejection fraction: a A 5-year prospective population-based study. Eur Heart J, 2007 Dec) examined the long-term outcomes of patients who were admitted to the hospital with the first established signs of heart failure. Observing 799 patients for five years, the authors found that mortality in this category of patients exceeded 55%. Mortality rates were especially high among those patients who had low ejection fractions. When respiratory and heart failure are combined, the life expectancy prognosis for patients is unfavorable. One of the methods that has been developed in recent years in the treatment of this category of patients is the use of non-invasive ventilation and long-term therapy with oxygen inhalation. Against this background, conventional therapy, which is prescribed for heart failure, has a noticeably better effect, at least the short-term prognosis for the patient’s recovery from an exacerbation is more favorable if non-invasive ventilation is not performed.