Chronic Obstructive Bronchitis - Symptoms

The clinical picture of COPD consists of various combinations of several interrelated pathological syndromes.

COPD is characterized by a slow, gradual progression of the disease, which is why most patients seek medical attention late, at the age of 40-50 years, when there are already quite pronounced clinical signs of chronic inflammation of the chest and broncho-obstructive syndrome in the form of cough, difficulty breathing and reduced tolerance to daily physical activity.

Interrogation

When questioning, it is usually possible to find out that the appearance of these symptoms is preceded by cigarette smoking for at least 15-20 years and/or more or less prolonged exposure to the corresponding occupational hazards. Often the patient notes frequent bronchopulmonary infections ("colds", viral infections, "acute bronchitis", etc.), as well as chronic diseases of the ENT organs or aggravating heredity.

In most cases, it is important to conduct a semi-quantitative assessment of one of the most important risk factors for COPD - smoking. For this purpose, it is recommended to calculate the so-called smoking index. To do this, the average number of cigarettes smoked per day is multiplied by the number of months in a year, i.e. by 12. If the index exceeds 160, then smoking in this patient is considered a serious risk factor for the development of COPD. If the index exceeds 200, such a patient should be classified as a "heavy" smoker.

Other methods of quantitative assessment of smoking have also been proposed. For example, to determine the total number of so-called "pack-years" of smoking, the average number of cigarettes smoked per day is multiplied by the number of years during which the patient continues to smoke, and the result is divided by 20 (the number of cigarettes in a standard pack). If the number of "pack-years" reaches 10, the patient is considered an "absolute" smoker. If this figure exceeds 25 "pack-years", the patient is classified as a "hardcore" smoker.

It is very important to find out in detail the possible impact on the patient of various unfavorable environmental factors and industrial hazards, in particular, long-term residence in an ecologically unfavorable area, work in a hazardous industry, contact with volatile pollutants, etc.

Finally, no less important is information about frequent “cold” diseases, primarily respiratory viral infections, which have a powerful damaging effect on the mucous membrane of the respiratory tract and the parenchyma of the lungs.

Complaints

The earliest symptom that appears in patients with COPD at a young age, long before seeking medical help, is a cough with a small amount of mucous or mucopurulent sputum, which for a long time occurs only in the morning ("smoker's morning cough"). Just as in patients with chronic non-obstructive bronchitis, cough is an important mechanism for clearing the bronchi of excess bronchial secretions, which are formed due to insufficiency of mucociliary transport, which initially manifests itself only at night. The immediate cause of cough is irritation of cough reflexogenic zones located at the division points of large bronchi and in the area of the tracheal bifurcation.

Over time, the cough becomes "habitual" and bothers the patient during the day and especially at night, when patients are lying down in bed. The cough usually intensifies in cold and damp seasons, when COPD exacerbations most often occur. As a rule, such exacerbations are characterized by relatively scanty symptoms and occur with normal or slightly elevated subfebrile body temperature. However, already during this period, patients note difficulty breathing, shortness of breath, as well as malaise, general weakness, rapid muscle fatigue, and decreased performance. The cough intensifies and becomes more constant. Sputum becomes purulent, its quantity increases. The duration of such exacerbations becomes longer and reaches 3-4 weeks, especially if they develop against the background of respiratory viral infections.

Exacerbations of chronic purulent bronchitis are particularly severe, characterized by febrile body temperature, severe intoxication and inflammation laboratories (leukocytosis, left shift in the blood count, increased ESR, increased levels of acute phase inflammation proteins in the blood, etc.).

The immediate causes of exacerbation of chronic bronchitis are hypothermia, viral infections, massive exposure to volatile irritants (for example, excessive smoking or exposure to industrial or household pollutants), as well as severe intercurrent diseases, physical fatigue, etc.

The second obligatory symptom, characteristic of almost all patients with COPD, is shortness of breath, indicating the formation of broncho-obstructive syndrome and damage to the respiratory parts of the lungs.

In most cases, COPD patients develop shortness of breath several years after the onset of the disease, i.e. significantly later than the onset of cough with sputum. Often, the initial manifestations of obstructive syndrome and respiratory failure are perceived by patients only as a slight difficulty in breathing, respiratory comfort that occurs during physical exertion. Moreover, patients during this period may not independently complain of shortness of breath or difficulty breathing, and only a careful analysis of all subjective sensations of the patient allows the doctor to identify the initial manifestations of respiratory failure.

In these cases, patients with COPD may notice a progressive decrease in exercise tolerance, which is manifested by an intuitive decrease in walking pace, the need to stop for rest, for example, when climbing stairs, etc. Often, a feeling of severe muscle fatigue occurs when performing physical activity that was previously habitual for the patient.

Over time, difficulty breathing becomes more and more obvious and patients themselves pay attention to this important symptom of the disease. Moreover, shortness of breath becomes the main complaint of a patient with COPD. In the advanced stage, shortness of breath becomes expiratory in nature, increasing with physical exertion and exacerbations of chronic bronchitis. Inhalation of cold air, a decrease in atmospheric pressure (high altitude, flights on airplanes) also cause increased shortness of breath.

Finally, in severe cases, broncho-obstructive syndrome manifests itself in attacks of a hacking, unproductive cough, the diagnostic and prognostic significance of which is fundamentally different from a cough caused by insufficiency of mucociliary transport and hypersecretion of mucus. Attacks are often accompanied by a short-term increase in the signs of obstructive respiratory failure - dyspnea, cyanosis, tachycardia, as well as swelling of the jugular veins, which may be associated with the manifestation of early expiratory collapse of small bronchi. As is known, this mechanism of bronchial obstruction is based on two main reasons:

1. When air movement through small bronchi is obstructed by the presence of sputum, mucosal edema or bronchospasm during exhalation, intrapulmonary pressure increases sharply, which leads to additional compression of small bronchi and an even greater increase in their resistance to air flow. The role of this mechanism increases during attacks of painful, unproductive cough and pulmonary emphysema, accompanied by a marked decrease in the elasticity of lung tissue.
2. The Bernoulli phenomenon is the second most important mechanism of early expiratory collapse of the bronchi during their narrowing. The sum of the air pressure along the longitudinal axis and the lateral pressure on the bronchial walls is a constant value. With a normal lumen of the bronchi and a relatively small linear air flow rate during exhalation, the lateral air pressure on the bronchial walls is large enough to prevent their early collapse.

When the bronchi narrow and during coughing, the linear velocity of air flow increases and the lateral pressure decreases sharply, which contributes to the early collapse of the small airways at the very beginning of exhalation.

Thus, the most characteristic sign of COPD is the early appearance of cough with sputum, and only after several years - the addition of expiratory dyspnea. Only in rare cases can dyspnea be a manifesting symptom of the disease, occurring simultaneously with productive cough. This feature of the development of clinical manifestations of COPD is typical for patients exposed to the simultaneous intensive action of several risk factors, for example, malicious smoking in combination with work in a hazardous industry in an atmosphere of volatile pollutants.

Physical examination

During a general examination of patients with COPD in the initial stages of the disease, significant differences from the norm are usually not found. With further progression of the disease, the formation of broncho-obstructive syndrome and severe respiratory failure, cyanosis appears in patients with COPD. Being a consequence of arterial hypoxemia, a decrease in oxyhemoglobin and an increase in the concentration of reduced hemoglobin in the blood flowing from the lungs, cyanosis usually becomes diffuse and has a peculiar grayish tint (diffuse gray cyanosis). It is more noticeable on the face and upper half of the body. The skin is warm to the touch, if there are no signs of cardiac decompensation in patients with chronic pulmonary heart disease. It should be remembered that there is no direct correlation between the degree of respiratory failure and the severity of cyanosis.

In the presence of concomitant bronchiectasis or chronic purulent bronchitis, in some cases, upon examination, it is possible to detect a peculiar thickening of the terminal phalanges of the fingers in the form of drumsticks and a change in the nails in the form of watch glasses (symptom of "drumsticks" and "watch glasses").

Finally, the development of decompensated chronic pulmonary heart disease and right ventricular failure may be accompanied by the appearance of peripheral edema, as well as a change in the nature of cyanosis - it becomes mixed: against the background of diffuse coloration of the skin, a more intense blueness of the lips, fingertips, etc. is revealed (acrocyanosis).

Almost all patients with COPD have an emphysematous chest mark when examined. In typical cases, the following is observed:

• an increase in the transverse and especially the anteroposterior size of the chest (in some cases it becomes “barrel-shaped”);
• “short neck” due to the fact that the chest seems to freeze at the height of inhalation;
• expanded (more than 90°) epigastric angle;
• smoothing or bulging of the supraclavicular fossae;
• more horizontal direction of the ribs and increase in intercostal spaces;
• tight fit of the shoulder blades to the chest, etc.

Vocal fremitus due to the development of pulmonary emphysema is weakened, but is the same in symmetrical areas of the chest.

Percussion reveals a box percussion sound over the entire surface of the lungs. The lower borders of the lungs are shifted downwards, and the upper borders are shifted upwards. The respiratory excursion of the lower edge of the lungs, normally 6-8 cm, is reduced.

During auscultation, weakened vesicular breathing is most often heard, acquiring a particularly low tone (cotton breathing), which is also associated with the presence of pulmonary emphysema. Weakening of breathing, as a rule, is expressed equally over symmetrical areas of the lungs. An extension of the expiratory phase is also noted, due to the presence of broncho-obstructive syndrome (normally, the ratio of inhalation and exhalation is 1: 1.1 or 1: 1.2). At the initial stages of COPD development, when inflammatory changes in the bronchi predominate, and pulmonary emphysema is not yet so pronounced, harsh breathing can be heard over the lung fields.

The most characteristic auscultatory sign of chronic obstructive bronchitis is diffuse dry wheezing. Their tone depends on the caliber of the bronchi in which they are formed. High (treble) dry wheezing indicates a significant narrowing of the distal (small) bronchi due to the presence of a large amount of viscous sputum, mucosal edema, or spasm of the small bronchi. Wheezing is best heard during exhalation and changes with coughing (usually disappears or decreases). Forced exhalation, on the contrary, leads to an increase or appearance of high-pitched dry wheezing.

Low (bass) buzzing and “humming” dry wheezing indicates the presence of viscous sputum in the proximal (large and medium) bronchi.

In some relatively rare cases, patients with COPD may also have moist, fine- and medium-sized bubbling rales, indicating the presence of liquid sputum in the bronchi or in cystic formations associated with the bronchi. In these cases, bronchiectasis is most often the case.

An important auscultatory phenomenon in patients with chronic obstructive bronchitis and COPD is distantly auscultatory wheezing. They usually have the character of long, drawn-out, multi-tonal dry wheezing, usually more pronounced on exhalation.

In severe bronchial obstruction syndrome, distant wheezing is often heard much better than dry wheezing detected during auscultation of the chest.

In patients with COPD, it is always important to correctly assess the physical data obtained during the examination of the cardiovascular system, which may indicate the presence of pulmonary arterial hypertension and pulmonary heart disease. Such signs include an increased and diffuse cardiac impulse and epigastric pulsation, indicating the presence of pronounced hypertrophy and dilation of the right ventricle. In these cases, percussion can reveal a shift to the right of the right border of relative cardiac dullness (dilation of the right ventricle and right atrium), and auscultation can reveal a weakening of the first heart sound and a soft systolic murmur of tricuspid regurgitation, which usually develops with pronounced dilation of the right ventricle in patients with decompensated pulmonary heart disease. The murmur often increases during deep inspiration (Rivero-Corvallo symptom), since during this period of the respiratory cycle, the blood flow to the right heart increases and, accordingly, the volume of blood regurgitating into the right atrium.

In severe cases of the disease, accompanied by the development of pulmonary arterial hypertension and pulmonary heart disease, patients with COPD may exhibit a paradoxical pulse - a decrease in systolic blood pressure during a calm deep breath by more than 10 mm Hg. The mechanism of this phenomenon and its diagnostic significance are described in detail in Chapter 13 of the first volume of this guide.

It should be noted that most of the listed symptoms appear with the development of pronounced signs of pulmonary heart disease and chronic heart failure. The sensitivity of the most characteristic clinical sign of right ventricular hypertrophy - increased cardiac impulse and epigastric pulsation - even in severe cases of the disease does not exceed 50-60%.

The most characteristic signs of broncho-obstructive syndrome in patients with COPD are:

• Shortness of breath, mainly of an expiratory nature, appearing or intensifying with physical exertion and coughing.
• Attacks of a hacking, unproductive cough, in which a large number of coughing efforts are required to cough up a small amount of sputum, the strength of each of which is noticeably reduced.
• Lengthening the exhalation phase during calm and especially forced breathing.
• Presence of secondary pulmonary emphysema.
• Scattered high-pitched dry wheezing in the lungs, heard during calm or forced breathing, as well as distant wheezing.

Thus, chronic obstructive bronchitis is a slowly progressing disease with a gradual increase in the severity of clinical symptoms and the obligatory occurrence at different stages of disease progression:

• syndrome of impaired mucociliary transport (cough, sputum);
• broncho-obstructive syndrome;
• respiratory failure of the obstructive type, accompanied by arterial hypoxemia and then hypercapnia;
• pulmonary arterial hypertension;
• compensated and decompensated chronic pulmonary heart disease.

The possibility of various combinations of clinical manifestations of the listed syndromes explains the diversity of the individual clinical course of the disease.

Of practical importance are various combinations of signs of chronic bronchitis and pulmonary emphysema, depending on which two main clinical types of COPD are distinguished:

The emphysematous type (type A, "dyspnea", "pink puffer") is characterized by a significant predominance of morphological and functional signs of pulmonary emphysema, while the symptoms of chronic bronchitis proper are expressed to a much lesser degree. The emphysematous type of COPD often develops in individuals with an asthenic build and reduced body weight. The increase in airiness of the lungs is ensured by the valve mechanism ("air trap"): during inhalation, the air flow enters the alveoli, and at the beginning or in the middle of exhalation, the small airways close due to the expiratory collapse of the small bronchi. During exhalation, therefore, the resistance of the airways to the air flow increases significantly.

The presence of pronounced, usually panacinar, pulmonary emphysema and increased elasticity of the lung tissue, which does not provide noticeable resistance to inhalation, causes a significant increase in alveolar ventilation and minute respiratory volume. Therefore, breathing at rest is usually rare and deep (hypoventilation is absent).

Thus, in patients with the emphysematous type of COPD, a normal vertical gradient of ventilation and blood flow in the lungs is maintained, therefore, at rest, there are no significant disturbances in ventilation-perfusion relationships and, accordingly, gas exchange disturbances, and the normal gas composition of the blood is maintained.

However, the diffusion capacity of the lungs and the reserve volume of ventilation are sharply reduced due to a decrease in the total surface area of the alveolar-capillary membrane and a reduction in capillaries and alveoli. Under these conditions, the slightest physical activity leads to an acceleration of pulmonary blood flow, while there is no corresponding increase in the diffusion capacity of the lungs and the volume of ventilation. As a result, PaO2 decreases, arterial hypoxemia develops, and dyspnea appears. Therefore, in patients with the emphysematous type of COPD, dyspnea appears for a long time only during physical activity.

The progression of the disease and further reduction of the diffusion capacity of the lungs is accompanied by the appearance of dyspnea at rest. But even at this stage of the disease, a clear dependence of the severity of dyspnea on the amount of physical activity remains.

In accordance with such dynamics of respiratory disorders in patients with emphysematous type of COPD, a detailed picture of respiratory failure, pulmonary arterial hypertension and chronic pulmonary heart disease is formed comparatively late. Cough with a small separation of sputum in these patients, as a rule, appears after the onset of dyspnea. According to Mitchell RS, all symptoms of COPD develop 5-10 years later than in the bronchitis type of COPD.

The presence of shortness of breath during physical exertion, after which patients "puff" for a long time, puffing out their cheeks, intuitively achieving an increase in intrapulmonary pressure, which somewhat reduces the phenomenon of early expiratory collapse of the bronchi, as well as the prolonged absence of cyanosis and signs of pulmonary heart disease served as the basis for the fact that patients with the emphysematous type of COPD are called "pink puffers".

The bronchitis type (type B, "blue bloater") generally corresponds to the above-described manifestations of chronic obstructive bronchitis in combination with centroacinar pulmonary emphysema. In this variant of the course of COPD, as a result of mucus hypersecretion, mucosal edema and bronchospasm, there is a significant increase in resistance to both exhalation and inhalation, which determines the occurrence of general and alveolar hypoventilation mainly in the lower parts of the lungs, a change in the vertical ventilation gradient and early-onset disturbances in ventilation-perfusion relationships, leading to the appearance of arterial hypoxemia and dyspnea. At later stages of the disease, due to fatigue of the respiratory muscles and an increase in the functional dead space, PaCO2 increases and hypercapia occurs.

In patients with the bronchitis type of COPD, pulmonary arterial hypertension develops earlier than in the emphysematous type, and signs of decompensated chronic pulmonary heart disease appear.

Auscultatory signs of broncho-obstructive syndrome (dry wheezing, prolonged exhalation) are detected in the lungs; cyanosis, peripheral edema and other signs of respiratory failure and chronic pulmonary heart disease are more often observed, which is why such patients are sometimes figuratively called “blue-eyed edematous” (bloater).

The two described clinical variants of the disease course in pure form are quite rare, especially the emphysematous type of COPD. A practicing physician more often encounters a mixed variant of the disease course.

Complications of chronic obstructive bronchitis

The most significant complications of chronic obstructive bronchitis include:

• pulmonary emphysema;
• respiratory failure (chronic, acute, acute on the background of chronic);
• bronchiectasis;
• secondary pulmonary arterial hypertension;
• pulmonary heart disease (compensated and decompensated).

It is worth paying attention to the high frequency of acute pneumonia in patients with chronic obstructive bronchitis. This is explained by the blockage of the bronchi with viscous sputum, the disruption of their drainage function and a sharp decrease in the function of the local bronchopulmonary protection system. In turn, acute pneumonia, which can be severe, aggravates the disorders of bronchial patency.

An extremely severe complication of chronic obstructive bronchitis is acute respiratory failure with the development of acute respiratory acidosis. The development of acute respiratory failure is often caused by the influence of an acute viral, mycoplasmal or bacterial infection, less often by pulmonary embolism, spontaneous pneumothorax, iatrogenic factors (treatment with beta-blockers; sleeping pills, sedatives, narcotics that depress the respiratory center).

One of the common and prognostically unfavorable complications of long-term chronic obstructive bronchitis is chronic pulmonary heart disease.

Course and prognosis

The course of COPD is characterized by a steady progression of bronchial obstruction and respiratory failure. If in healthy non-smoking individuals over 35-40 years of age FEV1 decreases annually by 25-30 ml, then the rate of decrease of this integral indicator of pulmonary ventilation in patients with COPD and smoking patients is significantly higher. It is believed that the annual decrease in FEV1 in patients with COPD is at least 50 ml.

The main factors that determine an unfavorable prognosis in patients with COPD are;

• age over 60 years;
• a long history of smoking and a large number of cigarettes currently smoked;
• frequent exacerbations of the disease;
• low initial values and rates of decline in FEV1;
• development of pulmonary arterial hypertension and chronic pulmonary heart disease;
• the presence of severe concomitant diseases;
• male gender;
• low social status and general cultural level of COPD patients.

The most common causes of death in patients with COPD are acute respiratory failure and chronic heart failure. Less commonly, patients with COPD die from severe pneumonia, pneumothorax, cardiac arrhythmias, and pulmonary embolism.

It is known that approximately 2/3 of patients with severe COPD die within the first 5 years after the onset of signs of circulatory decompensation against the background of formed chronic pulmonary heart disease. According to research data, 7.3% of patients with compensated COPD and 29% of patients with decompensated pulmonary heart disease die within 2 years of observation.

Prescribing adequate therapy and performing preventive measures can reduce the rate of increase of bronchial obstruction and improve the prognosis of the disease. Thus, just stopping smoking after a few months can lead to a noticeable decrease in the rate of increase of bronchial obstruction, especially if it is largely due to the reversible component of obstruction, this leads to an improvement in the prognosis of the disease.

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