Main Clinical Syndromes

Syndrome of focal consolidation of pulmonary tissue. The syndrome of focal consolidation of lung tissue is caused by filling of the alveoli with the inflammatory fluid and fibrin (in pneumonia), blood (in lung infarction), growing connective tissue in the lung (pneumosclerosis, carnification) in long-standing pneumonia, or developing tumour. The common complaint of the patient is dyspnoea. Examination of the patient reveals thoracic lag­ging of the affected side during respiration; vocal fremitus is intensified in the consolidated area; the percussion sound over the consolidation site is slightly or absolutely dull; auscultation reveals bronchial respiration, exag­gerated bronchophony and (in the presence of liquid secretion in fine bron­chi) resonant (consonating) rales. X-ray examination shows the focus of consolidation as an area of increased density in the lung tissue, its size and contours depending on the character and stage of the disease, and some other factors.

Special Part

Chapter 5. Respiratory System

Cavity in the lung. Cavity in the lung is formed in abscess or tuber­culosis (cavern) or during degradation of the lung tumour. An empty large cavity is communicated with the bronchus and surrounded by a ring of in­flamed tissue. Examination of the chest reveals unilateral thoracic lagging and intensified vocal fremitus. Percussion reveals dulled tympany or (if the cavity is large and peripheral) tympany with a metallic tinkling. Ausculta­tion reveals amphoric breathing, intensified bronchophony, and often medium and large resonant vesicle rales. X-ray examination proves the presence of the cavity in the lung.

Fluid in the pleural cavity. The syndrome of accumulation of pleural fluid occurs in hydrothorax (accumulation of non-inflammatory effusion, i.e. transudate, for example in cardiac failure), or in pleurisy with effusion (inflammation of the pleura). The syndrome is characterized by dyspnoea due to respiratory insufficiency caused by lung compression and decreased respiratory surface, asymmetry of the chest (enlargement of the side where pleural effusion is accumulated) and unilateral thoracic lagging during respiration. Vocal fremitus is markedly weakened over the area of the pleural effusion, or it may be undeterminable; percussion reveals a dulled sound or absolute dullness; in auscultation respiration and bronchophony are markedly weakened or absent. X-ray examination reveals an area of in­creased density in the area of accumulation of the pleural fluid, which is usually at the bottom of the chest (often bilateral in hydrothorax). Its up­per border is quite distinct. If transudate is accumulated in the pleural cavi­ty its border is more horizontal, while in the presence of pleural effusion, the border is scant, to coincide with the Damoiseau's curve as determined by percussion (see " Pleurisy with Effusion").

Air accumulation in the pleural cavity. Air is accumulated in the pleural cavity when the bronchi are communicated with the pleural cavity (in subpleural tuberculosis cavern or abscess), in injury to the chest, or in ar­tificial pneumothorax (injection of air into the pleural cavity for medical purposes in the presence of large caverns in the lungs). Asymmetry of the chest found in this syndrome is due to the enlarged side where air is ac­cumulated; the affected side of the chest cannot take part in the respiratory act. Vocal fremitus is markedly weaker or absent altogether over the site of air accumulation; percussion reveals tympany. Breathing sounds and bron­chophony are either weak or absent and are not conducted to the chest sur­face to be detected by auscultation. X-ray examination reveals a light pulmonary field without pulmonary pattern; a shadow of the collapsed lung can be seen toward the root.

External respiratory dysfunction. The function of the external respiratory apparatus is to supply the body with oxygen and to remove car­bon dioxide formed by exchange reactions. This function is realized firstly

by ventilation, i.e. gas exchange between the outer and alveolar air. This ensures the required oxygen and carbon dioxide pressure in the alveoli (an important factor is intrapulmonary distribution of the inspired air). Secondly, this function is realized by diffusion of carbon dioxide and ox­ygen through the walls of the alveoli and lung capillaries (oxygen is sup­plied from the alveoli to the blood and carbon dioxide is diffused from the blood to the alveoli). Many acute and chronic diseases of the bronchi and the lungs cause respiratory insufficiency (Wintrich, 1854). The degree of morphological changes in the lungs does not always correspond to the degree of their dysfunction.

Respiratory insufficiency is now defined as the condition with abnor­mal gas composition of the blood, or this abnormality is compensated for by intense work of the external respiratory apparatus and higher load on the heart. This decreases functional abilities of the body. It should be noted that the external respiratory function is closely connected with the blood circulatory function: the heart work is intensified during external respiratory insufficiency, which is an important compensatory element of the heart function.

Respiratory insufficiency is manifested clinically by dyspnoea and cyanosis; at later stages, when cardiac failure joins the process, oedema oc­curs.

The patient with respiratory insufficiency employs the same compen­satory reserves as a healthy person does during heavy exercise. But the compensatory mechanisms of a sick person are actuated much earlier and at loads under which a healthy person would feel no discomfort (e.g. dyspnoea and tachypnoea can develop in a patient with lung emphysema even during slow walking).

Among the first signs of respiratory insufficiency are inadequate changes in ventilation (rapid and deep breathing) at comparatively light loads for a healthy individual; the minute volume increases. In certain cases (bronchial asthma, lung emphysema, etc.) respiratory insufficiency is compensated by intensified work of the respiratory muscles, i.e. by the altered respiratory mechanics. In other words, in patients with pathology of the respiratory system, the external respiratory function is maintained at the required level by mobilizing compensatory mechanisms (i.e. by efforts greater than required for healthy persons), and by minimizing the respiratory reserves: the maximum lung ventilation decreases, the coeffi­cient of oxygen consumption drops, etc.

Various mechanisms are involved gradually to compensate for pro­gressive respiratory insufficiency depending on its degree. At the early stages of respiratory insufficiency the external respiratory function at rest *s realized in normal way. The compensatory mechanisms are only actuated

H-1556

Special Part

Chapter 5. Respiratory System

during exercise in a sick person. In other words, only reserves of the exter­nal respiratory apparatus are decreased at this stage. As insufficiency fur­ther progresses, tachypnoea, tachycardia, and signs of intensified work of the respiratory muscles (during both inspiration and expiration), with in­volvement of accessory muscles, develop during light exercise and even at rest. At the later stages of respiratory insufficiency, when the body com­pensatory reserves are exhausted, arterial hypoxaemia and hypercapnia develop. In addition to the growing vivid arterial hypoxaemia, signs of la­tent oxygen deficit also develop; underoxidized products (lactic acid, etc.) are accumulated in the blood and tissues.

Still at later stages, right ventricular incompetence joins pulmonary in­sufficiency because of the developing hypertension in the lesser circulation, which is attended by increased load on the right ventricle, and also because of dystrophic changes in the myocardium occurring as a result of its cons­tant overload and insufficient oxygen supply. Hypertension in the vessels of the lesser circulation in diffuse affections of the lungs arises by reflex mechanisms in response to insufficient lung ventilation and alveolar hypoxia— the Euler-Liliestrand reflex (this reflex mechanism is an impor­tant adaptation means in focal lung affections; it limits blood supply to in­sufficiently ventilated alveoli). Further, in chronic inflammatory diseases of the lungs due to cicatricial and sclerotic changes in the lungs (and due to affections in the lung vessels) blood passage through the lesser circulation becomes even more difficult. Increased load on the myocardium of the right ventricle stimulates gradual development of its insufficiency to cause congestion in the greater circulation (pulmonary heart).

Depending on the cause and mechanism of developing respiratory in­sufficiency, three types of disordered lung ventilation are distinguished: obstructive, restrictive and mixed (combined).

The obstructive type is characterized by difficult passage of air through the bronchi (because of bronchitis, bronchospasm, contraction or com­pression of the trachea or large bronchi, e.g. by a tumour, etc.). Spirography shows marked decrease in the MLV and PVC, the VC being decreased insignificantly. Obstruction of the air passage increases the load on the respiratory muscles. The ability of the respiratory apparatus to per­form additional functional load decreases (fast inspiration, and especially expiration, and also rapid breathing become impossible).

The restrictive type of ventilation disorder occurs in limited ability of the lungs to expand and to collapse, i.e. in pneumosclerosis, hydro- and pneumothorax, massive pleural adhesions, kyphoscoliosis, ossification of the costal cartilages, limited mobility of the ribs, etc. These conditions are in the first instance attended by a limited depth of the maximum possible inspiration. In other words, the vital capacity of the lungs decreases

(together with the maximum lung ventilation), but the dynamics of the respiratory act is not affected: no obstacles to the rate of normal breathing (and whenever necessary, to significant acceleration of respiration) are im­posed.

The mixed, or combined type includes the signs of the two previous disorders, often with prevalence of one of them; this type of disorder oc­curs in long-standing diseases of the lungs and the heart.

External respiratory dysfunction occurs also when the anatomical dead space increases (in the presence of large cavities inside the lung, caverns, abscesses, and also in multiple large bronchiectases). Similar to this type is the respiratory insufficiency due to circulatory disorders (e.g. in throm-boembolism, etc.) during which part of the lung is excluded from gas ex­change, while its ventilation is to a certain degree maintained. Finally, respiratory insufficiency arises during uneven distribution of air in the lungs (distribution disorders), when a part of the lung is not ventilated (in pneumonia, atelectasis), with preservation of blood circulation. Part of venous blood is not oxygenated before it enters pulmonary veins and the left chambers of the heart. Similar to this type of respiratory insufficiency (with regard to pathogenesis) is the so-called vascular bypass or shunting (from right to left), during which part of the venous blood from the pulmonary artery system enters directly the pulmonary vein (bypassing the capillaries) to mix with oxygenated arterial blood. Oxygenation of blood in the lungs is thus upset but hypercapnia may be absent due to compensatory intensification of ventilation in the intact parts of the lung. This is partial respiratory insufficiency (as distinct from total insufficiency where hypox­aemia and hypercapnia are present).

Respiratory insufficiency is characterized by upset gas exchange through the alveolar-capillary membrane of the lungs. It occurs when this membrane is thickened to interfere with normal gas diffusion through it (the so-called pneumonoses, alveolar-capillary block). It is not accom­panied by hypercapnia either since the rate of CO₂ diffusion is 20 times higher than that of oxygen. This form of respiratory insufficiency is, in the first instance, characterized by arterial hypoxaemia and cyanosis. Lung ventilation is intensified.

Respiratory insufficiency associated with toxic inhibition of the respiratory centre, anaemia, or oxygen deficit in the inhaled air, is not con­nected directly with the pathology of the lungs.

Acute and chronic respiratory insufficiency are differentiated. The former occurs in attacks of bronchial asthma.

Three degrees and three stages of respiratory insufficiency are also distinguished. The degrees of respiratory insufficiency reflect the gravity of the disease at a given moment. The first degree of respiratory insufficiency

Special Part

Chapter 5. Respiratory System

(dyspnoea, in the first instance) becomes evident only at moderate or significant physical load. Dyspnoea develops during light exercise in the se­cond degree of insufficiency; the compensatory mechanisms are involved when the patient is at rest and functional diagnosis can reveal some devia­tions from the normal indices. The third degree is characterized by dyspnoea at rest and cyanosis as a manifestation of arterial hypoxaemia; deviations from the normal indices during functional pulmonary tests are significant.

Stages of respiratory insufficiency in chronic diseases of the lungs reflect the changes occurring during the progress of the disease. Stages of latent pulmonary, pronounced pulmonary, and cardiopulmonary insuffi­ciency are normally differentiated.

Treatment. The treatment of respiratory insufficiency includes (1) treatment of the main disease upon which the insufficiency depends (pneumonia, pleurisy with effusion, chronic inflammations in the bronchi and the pulmonary tissue, etc.); (2) removal of bronchospasm and im­provement of lung ventilation (giving broncholytics, remedial exercises, etc.); (3) oxygen therapy; (4) pulmonary heart is treated by cardiac glycosides and diuretics; (5) phlebotomy is indicated in the presence of reflex erythrocytosis and congestion in the greater circulation.