Pulmonary syndromes

Based on the data obtained using the main and additional methods of examining the patient, i.e. specific symptoms and signs, it is possible to identify a number of syndromes in which these signs are interconnected by a single mechanism of development, common pathogenesis, and are united by the features of the changes that arise. Such a syndromic stage of disease diagnostics, although it is intermediate, is very important, since, on the one hand, it allows eliminating the disunity of assessing each of the identified signs and giving a more complete picture of the disease, on the other hand, it makes the next stage of diagnostics necessary - determining the nosological essence of the syndrome, since the clinical picture of a specific syndrome can often be characteristic of several different diseases, and one of the final goals of the diagnostic path is to determine a specific nosological form.

There are several pulmonary syndromes: pulmonary consolidation syndrome, pleural syndrome, cavity syndrome, broncho-obstructive syndrome, hyper-inflated lung syndrome, Pickwickian syndrome, sleep apnea syndrome (sleep apnea syndrome), respiratory failure syndrome. It should be borne in mind that within the same large syndrome there are a number of variants, the diagnosis of which is certainly important, since the treatment methods will be different.

Major pulmonary syndromes

Pulmonary consolidation syndrome:

1. Infiltrate (pneumonic, tuberculous, eosinophilic).
2. Pulmonary infarction (thromboembolism, thrombosis).
3. Atelectasis (obstructive, compression, middle lobe syndrome).
4. Congestive heart failure (fluid buildup in the lower parts of the lungs).
5. Tumor.

Pleural syndrome:

1. Fluid in the pleural cavity (transudate, exudative pleurisy).
2. Air in the pleural cavity (pneumothorax).

Cavity syndrome (disintegrating abscess and tumor, cavern).

Broncho-obstructive syndrome:

1. Obstruction or narrowing of the bronchus.
2. Bronchial spasm.

Hyperinflation syndrome (various types of emphysema).

Pickwickian syndrome and sleep apnea syndrome (sleep apnea syndrome).

Respiratory distress syndrome:

1. Acute respiratory failure (including adult distress syndrome).
2. Chronic respiratory failure.

The identification of the indicated syndromes occurs primarily through the use of basic methods of examining the patient - inspection, palpation, percussion, auscultation.

Cavity in the lung syndrome

The cavity syndrome includes symptoms, the appearance of which is associated with the presence of a cavern, abscesses, cysts, i.e. formations with a dense, more or less smooth wall, often surrounded by an infiltrative or fibrous shaft. The cavity can be filled entirely with air only (empty cavity) or contain, in addition to air, a certain amount of liquid, remain closed or communicate with the draining bronchus. All this, of course, is reflected in the features of the symptoms, which also depend on the size of the cavity and the depth of its location.

In large, superficial and isolated cavities, regardless of their contents, vocal fremitus is weakened. If the cavity communicates with a bronchus and at least partially contains air, the percussion sound will have a tympanic tint; over a cavity filled with fluid, dullness or absolute dullness is noted. During auscultation over an isolated air cavity, breathing is not heard; if the air cavity communicates with a draining bronchus, bronchial breathing will be heard, which is easily conducted from the place of formation (glottis) along the air column and can acquire a metallic tint (amphoric breathing) as a result of resonance in a smooth-walled cavity. A cavity partially containing fluid is a source of formation of moist rales, which, as a rule, have a ringing character, since their conduction is enhanced by the surrounding compacted (infiltrated) tissue. In addition, auscultation can detect an independent stenotic noise that increases bronchial breathing and occurs at the site of communication between the cavity (cavern) and the draining bronchus.

It should be noted that all the above symptoms characterizing the cavity syndrome are often quite dynamic, since there is a staged development of the cavity formation, especially a lung abscess: partial or complete emptying is replaced by accumulation of fluid, which is reflected in the features of the above-mentioned symptoms of the presence of a cavity containing air or fluid.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ]

Broncho-obstructive syndrome

Broncho-obstructive syndrome ( bronchial obstruction syndrome ) is manifested by severe productive, less often unproductive cough, as well as symptoms of the naturally developing consequences of its long-term existence - signs of pulmonary emphysema. The clinical manifestations of broncho-obstructive syndrome are based on impaired bronchial patency, associated with it difficult and uneven ventilation (mainly due to limitation of the exhalation rate) and an increase in the residual volume of the lungs. In the case of true bronchial obstruction syndrome, we are talking about a change in the patency of the small bronchi (they are called in this regard the "Achilles heel" of the bronchi). Obstruction of the small bronchi occurs most often due to inflammation and swelling of the bronchial mucosa ( chronic bronchitis, allergic component), bronchospasm, usually with swelling of the mucous membrane (bronchial asthma), less often - with diffuse peribronchial fibrosis, compressing the bronchi from the outside.

Chronic bronchitis most often leads to the development of irreversible inflammatory-cicatricial changes in the small bronchi and is the basis of chronic obstructive pulmonary disease, the main clinical signs of which are the following:

1. cough with thick and viscous sputum;
2. clinical and functional signs of airway obstruction;
3. increasing shortness of breath;
4. development of " pulmonary heart disease " (cor pulmonale), terminal respiratory and cardiac failure.

Cigarette smoking is the most common etiologic and disease progression supporting factor. Due to the frequency of cyanosis and heart failure, patients with chronic obstructive bronchitis are described as "blue edema patients". In this variant of obstructive syndrome, following inflammatory edema of the mucous membrane of the terminal bronchioles, leading to hypoventilation of the alveoli, decreased partial pressure of oxygen and increased partial pressure of carbon dioxide - hypoxemia and hypercapnia, spasm of the alveolar capillaries and hypertension of the pulmonary circulation occur. Pulmonary heart disease is formed, decompensation of which is manifested by peripheral edema.

Another common cause of chronic obstructive pulmonary disease is obstructive emphysema, in which cyanosis is usually not expressed, patients are called "pink puffers". In this case, bronchial obstruction is also noted, but it is especially evident on exhalation, when there is a collapse of the bronchioles with a loss of elastic properties of the alveoli, which is associated with an increase in the volume of the alveoli, a decrease in the number of alveolar capillaries, the absence of blood shunting (in contrast to the first option, maintaining ventilation-perfusion relations) and normal gas composition. Smoking in pulmonary emphysema is the main etiologic factor, although in some patients the cause of the disease may be inhalation of air pollutants and a deficiency of a1-antitrypsin.

Most often, chronic obstructive pulmonary disease is a combination of the above conditions, which makes broncho-obstructive syndrome very common, and, given the seriousness of the consequences, timely detection of the syndrome and the diseases that cause it, their treatment, and most importantly, prevention are of utmost importance.

Since there are significantly fewer objective symptoms in broncho-obstructive syndrome than in other major pulmonary syndromes, it should be noted that cough is extremely important clinically not only as a patient's complaint and a sign of bronchial damage, but also as a factor that aggravates changes in the pulmonary parenchyma in bronchial obstruction syndrome. The main signs of this syndrome are the symptoms of its complication, the symptoms of pulmonary emphysema, which are described below. However, there are still signs of impaired bronchial patency as such. These primarily include those detected by auscultation - harsh vesicular breathing with prolonged exhalation, wheezing, and the characteristics of the wheezing can be used to judge not only the degree of bronchial narrowing, but also the level of obstruction. An important auscultatory indicator of bronchial obstruction is a violation of the ratio of inhalation and exhalation, the appearance of an extended rough exhalation. Finally, the indicators of external respiration function, especially the speed indicators, in particular using a formed exhalation (the aforementioned Tiffeneau test and others), are of great clinical importance for detecting impaired bronchial patency.

[ 6 ], [ 7 ], [ 8 ]

Hyperinflation syndrome

The hyper-inflated lung syndrome is most often a consequence of long-standing difficult exhalation (bronchial obstruction), which leads to an increase in the residual volume of the lungs, chronic mechanical impact on the elastic apparatus of the alveoli, their stretching, irreversible loss of the ability to collapse, increasing the value of the residual volume. A typical variant of this syndrome is pulmonary emphysema, which usually develops gradually. Acute pulmonary inflation is rare.

Thus, there is a close connection between broncho-obstructive syndrome and pulmonary emphysema, which is therefore most often of an obstructive nature. Much less common is compensatory (including vicarious) emphysema, which develops in response to a slow increase in diffuse pulmonary fibrosis. Due to the fact that broncho-obstructive syndrome is often generalized, pulmonary emphysema is a bilateral process. Its clinical signs are a barrel-shaped chest with reduced respiratory mobility, weak conduction of vocal fremitus, the presence of a widespread box percussion sound that can replace the zone of absolute cardiac dullness, downward displacement of the lower edge of the lungs, uniform weakening of vesicular breathing, auscultatory signs of broncho-obstructive syndrome (wheezing, prolonged expiration).

It should be emphasized that the above-mentioned signs are revealed in advanced emphysematous processes; of course, the detection of earlier symptoms is important, which essentially include one - a decrease in the respiratory excursion of the lower pulmonary edge, which gradually increases over time, which is detected long before the appearance of signs of pronounced pulmonary distension.

Pickwickian syndrome and sleep apnea syndrome

Of interest are Pickwickian syndrome and sleep apnea syndrome (a symptom of nocturnal apnea), which are usually mentioned in the section on diseases of the respiratory system (although they have no direct relation to lung diseases), since their main manifestation - respiratory failure with hypoxia and hypoxemia - develops in the absence of primary lung disease.

Pickwickian syndrome is a symptom complex that includes severe alveolar hypoventilation and the resulting hypoxia and hypercapnia (PCO2 _above 50 mm Hg), respiratory acidosis, as well as irresistible daytime sleepiness, polycythemia, high hemoglobin levels, and episodes of apnea. The cause of such hypoventilation is considered to be significant obesity with predominant fat deposition in the abdominal area with a small height; apparently, genetic sensitivity to such hypoventilation is important. These patients are characterized by a prolonged period of severe (morbid) obesity with an additional sharp increase in body weight, the development of pulmonary heart disease, dyspnea during exertion, cyanosis, leg edema, morning headaches, but the most typical symptom is pathological sleepiness, including during conversation, eating, reading and in other situations. It is interesting that weight loss leads to a reversal of the main signs of the symptom complex in some patients.

Although the connection between sudden sleepiness and periodic apnea and massive obesity was first pointed out in the early 19th century, the term "Pickwick syndrome" came into use after W. Osler discovered these symptoms in the hero of Charles Dickens's "The Posthumous Papers of the Pickwick Club" - an obese boy, Joe: "... On the box sat a fat, red-faced fellow, deep in slumber... - An intolerable boy, - said the elderly gentleman, - he has fallen asleep again! - A wonderful boy, - said Mr. Pickwick. - Does he always sleep like that? - He does! - confirmed the old gentleman. - He always sleeps. In his sleep he carries out orders and snores, waiting at table."

Pickwickian syndrome, like being overweight in general, is often accompanied by recurrent sleep apnea.

Currently, more and more attention is paid to sleep breathing disorders, in particular obstructive sleep apnea syndrome. It is believed that about 1% of the population suffers from such disorders. The most important anamnestic sign of this syndrome is chaotic and loud snoring ("heroic" snoring), interrupted by long pauses, sometimes reaching 2 minutes. Such respiratory arrests lead to hypoxia, which causes cerebral and cardiac disorders. In addition to this sign, such people have, at first glance, significantly limited work capacity during the day, for no apparent reason.

Sleep apnea is a syndrome characterized by episodes of respiratory arrest lasting 10 seconds or more, periodically recurring during sleep, hypoxemia, and heart-rending snoring. Pathogenetically, there are 2 types of sleep apnea: central, caused by disorders of the central regulation of breathing, and obstructive, caused by seizure of the soft palate, root of the tongue, hyperplasia of the tonsils, adenoids, developmental defects of the lower jaw, tongue, causing temporary obstruction of the upper respiratory tract. From a practical standpoint, it is important to distinguish the obstructive mechanism of breathing arrest during sleep, since it significantly increases the risk of sudden death, especially in overweight individuals, as well as in those who abuse alcohol. This risk can be reduced by persistent weight loss treatment.

The clinical picture of sleep apnea syndrome consists of the described episodes of cessation of breathing, loud snoring, daytime sleepiness, decreased memory and ability to concentrate, increased daytime fatigue, and arterial hypertension in the morning hours that is not controlled by conventional treatment. It is more common in middle-aged men, as already noted, with excess body weight, but can also occur in children. It should be noted that hypothyroidism and obstructive sleep apnea can be combined.

To diagnose the syndrome, they use sleep monitoring with recording of the electroencephalogram, breathing patterns, ECG (to register possible arrhythmias), and oxygenometry to determine the level of hypoxemia.

Sleep apnea syndrome is considered severe and potentially dangerous if it occurs more than 5 times per hour and lasts more than 10 seconds each. Some authors believe that a prolonged attack can lead to sudden death during sleep.

Weight loss, avoidance of alcohol and sedatives, but especially constant breathing during sleep using a special mask that provides air flow through the nose under pressure, are now considered the most effective treatment methods for obstructive sleep apnea syndrome. The optimal pressure level for inhalation, selected with the help of monitoring, allows the flow of inhaled air to overcome resistance, apnea does not occur, daytime sleepiness is reduced, and blood pressure is normalized.

Respiratory distress syndrome

Respiratory failure syndrome is one of the largest and most important pulmonary syndromes, since its occurrence indicates the appearance of changes in the main function of the respiratory system - the gas exchange function, including, as already mentioned, pulmonary ventilation (air flow into the alveoli), diffusion (gas exchange in the alveoli) and perfusion (oxygen transport), as a result of which the maintenance of normal gas composition of the blood is disrupted, which at the first stages is compensated by more intensive work of the external respiratory system and heart. Respiratory failure usually develops in patients suffering from chronic lung diseases, leading to the appearance of pulmonary emphysema and pneumosclerosis, but it can also occur in patients with acute diseases accompanied by the exclusion of a large mass of the lungs from breathing (pneumonia, pleurisy). Recently, acute adult distress syndrome has been specifically identified.

Respiratory failure is primarily a consequence of impaired ventilation of the lungs (alveoli), therefore there are two main types of this syndrome - obstructive and restrictive.

Obstructive respiratory failure is based on the obstruction of the bronchi, therefore the most common diseases leading to the development of the obstructive type of respiratory failure are chronic bronchitis and bronchial asthma. The most important clinical sign of obstructive respiratory failure is dry wheezing against the background of prolonged exhalation. The Tiffno test and pneumotachometry are important methods for confirming and assessing the dynamics of bronchial obstruction, as well as for clarifying the degree of bronchospasm as the cause of obstruction, since the introduction of bronchodilators in these cases improves the Tiffno test and pneumotachometry indicators.

The second type of respiratory failure - restrictive - occurs due to the impossibility of full expansion of the alveoli when air enters them, freely passing through the respiratory tract. The main causes of restrictive respiratory failure are diffuse damage to the pulmonary parenchyma (alveoli and interstitium), for example, fibrosing alveolitis, multiple pulmonary infiltrates, difficult to expand massive compression atelectasis of the lung in pleurisy, hydrothorax, pneumothorax, tumor, severe limitation of lung mobility in widespread adhesive process in the pleura and severe obesity (Pickwickian syndrome), as well as paralysis of the respiratory muscles, including dysfunction of the diaphragm (central respiratory failure, dermatomyositis, poliomyelitis ). At the same time, the Tiffeneau test and pneumotachometry indicators are unchanged.

The consequence of the discrepancy between lung ventilation and tissue metabolism in respiratory failure is a violation of the gas composition of the blood, manifested by hypercapnia, when PCO2 _is more than 50 mm Hg (the norm is up to 40 mm Hg) and hypoxemia - a decrease in PO2 to 75 mm Hg (the norm is up to 100 mm Hg).

Most often, hypoxemia (usually without hypercapnia) occurs with a restrictive type of respiratory failure, in contrast to situations where there is severe hypoventilation, causing hypoxemia and hypercapnia.

Hypoxemia and hypercapnia are especially dangerous for brain and heart tissue, as they cause significant and even irreversible changes in the function of these organs - up to and including deep cerebral coma and terminal cardiac arrhythmias.

The degree of respiratory failure is usually judged by the severity of the main clinical signs, such as dyspnea, cyanosis, tachycardia. An important criterion for the degree of respiratory failure is the effect of physical exertion on them, which primarily applies to dyspnea that occurs initially (degree I respiratory failure) only with physical exertion; degree II - the appearance of dyspnea with minor physical exertion; at degree III, dyspnea bothers the patient even at rest. Tachycardia increases synchronously with dyspnea. The gas composition of the blood changes at degree II, but especially at degree III respiratory failure, when it remains changed even at rest.

It is extremely important to be able to distinguish between the main types of respiratory failure, especially in its early stages, when influencing the mechanisms of obstruction or restriction development can prevent the progression of functional disorders.

Adult respiratory distress syndrome is the most common cause of acute respiratory failure with severe hypoxemia in a person with previously normal lungs due to rapid accumulation of fluid in the lung tissue at normal pulmonary capillary pressure and sharply increasing permeability of the alveolar-capillary membranes. This condition is caused by the membrane-damaging effects of toxins and other agents (medicines, especially narcotics, toxic products formed during uremia), heroin, aspirated gastric contents, water (drowning), excessive formation of oxidants, trauma, sepsis caused by gram-negative bacteria, fat embolism, acute pancreatitis, inhalation of smoky or hot air, CNS trauma, and, apparently, direct action of a virus on the alveolar membrane. As a result, lung compliance and gas exchange are impaired.

Acute respiratory failure develops very quickly. Dyspnea appears and rapidly increases. Additional muscles are involved in the work, a picture of non-cardiogenic pulmonary edema develops, a lot of different-sized moist rales are heard. Radiologically, a picture of interstitial and alveolar pulmonary edema is revealed (diffuse infiltrative changes in the form of "white switching off" of the pulmonary fields). Signs of respiratory failure with hypoxemia and then hypercapnia increase, fatal heart failure intensifies, disseminated intravascular coagulation (DIC syndrome) and infection may join in, which makes the prognosis very grave.

In clinical practice, it is often necessary to isolate and evaluate the activity of bronchopulmonary infection, which accompanies acute and chronic bronchitis, bronchiectasis, lung abscesses, pneumonia. Some of these diseases have a chronic course, but with periodic exacerbations.

Signs of bronchopulmonary infection and its exacerbations are an increase in temperature (sometimes only moderate subfebrile), the appearance or intensification of cough, especially with sputum, the dynamics of the auscultatory picture in the lungs, especially the appearance of wet ringing rales. Attention is paid to changes in the hemogram (leukocytosis over 8.0-10 ⁹ /l) with neutrophilia, an increase in ESR. Leukopenia and neutropenia are more often detected in viral infections.

It is more difficult to assess changes in the radiographic picture, especially with a long-term course of the underlying disease.

It is especially important to detect active bronchopulmonary infection in patients with bronchial asthma (with pronounced obstructive syndrome), exacerbations of which are sometimes associated with exacerbation of chronic bronchitis or pneumonia. In this case, special attention is paid to an increase in temperature, the appearance of a section of moist ringing wheezing in the lungs, and changes in the blood.

When assessing the dynamics of bronchopulmonary infection signs, attention should be paid to the amount and nature of the secreted sputum, especially to the abundant secretion of purulent sputum. Its significant reduction, along with the dynamics of other signs, allows us to discuss the issue of discontinuing antibiotics.

It is always important to have data on the nature of the bacterial flora (sputum culture) and its sensitivity to antibiotics.

Thus, diseases of the respiratory system manifest themselves in a wide variety of symptoms and syndromes. They are identified through a thorough clinical examination, including a detailed analysis of complaints, course characteristics, as well as examination, palpation, percussion and auscultation data. When used skillfully, these methods can provide information whose importance is difficult to overestimate. It is very important to try to combine the detected signs into syndromes based on the common mechanisms of occurrence. First of all, these syndromes are a complex of symptoms identified as a result of a traditional examination of the patient. Of course, appropriate additional methods (X-ray, radionuclide, etc.) are necessary to confirm the detected signs, clarify, and detail the mechanisms of their development, although sometimes special methods can be the only ones for identifying the described changes, for example, with small sizes or deep localization of compaction.

The identification of syndromes is an important stage of the diagnostic process, ending with the determination of the nosological form of the disease.