Pathological anatomy. The increase lung emphysema is due to the high content of the air in their respiratory Department, i.e. distal to the terminal bronchioles. The nature of the flow are acute and chronic emphysema lungs, on the localization of foci, diffuse, bilateral, and unilateral, lobes, in relation to acinus - panacinar (indiscriminate total swelling of all elements of acinus) and selective (with primary swelling proximal or distal departments of acinus). To the electoral emphysema is centrilobular characterized by predominant stretching respiratory bronchioles of the first and second order against unstretched of the alveoli. Pathogenetic features distinguish obstructive, senile, compensatory emphysema lung lobes and emphysema of the lungs in newborns.
The most prevalent chronic bilateral obstructive paracinema emphysema (synonym: substantial, vesicular, hypertrophic). Light increased in volume, fuzzy, after opening the pleural cavities not zadayutsya, front edges rounded, come one after the other, can cover the mediastinum, on a cut have a porous view, pale, especially upper sections. Predominantly in the upper shares under the pleura is often seen large bubbles from a few millimeters to 1 cm and more in diameter (bubble, or bullous, emphysema light). During feeling light crunch, the surface of the cut looks rather dry. Pale dry tissues of the lungs caused by reduced blood supply due to narrow capillaries, held in sharply stretched the walls of the alveoli. The bronchi and bronchioles diffuse expanded and clearance is determined by the naked eye, even in subpleural zone, while in norm and in acute swelling light gleams large bronchi are defined only in the root zone. It is exactly this sign along with multiple sclerosis interstitial tissue, giving it the appearance krupneishii whitish network (Fig. 1), distinguishes chronic emphysema lungs from acute swelling of the lungs due to agonistic processes.
Interstitial sclerosis while emphysema is caused by the violation of circulation, and chronic bronchitis and bronchiolitis, which are the most important trigger point determining the development of emphysema lungs, leading to inadequate ventilation delay of air in respiratory parts. Exhalation is broken due to excessive accumulation of mucus or weakening of muscle function-elastic apparatus bronchial tree when it inflammation or sclerosis.
Inflammation of the bronchi with emphysema often wears catarrhal or catarrhal-purulent character, but is not accompanied by suppuration and destruction of the wall. The greatest changes are small bronchi and bronchioles, the walls of their permeated inflammatory infiltrates, often sclerotic (fibrous). Smooth muscle bundles respiratory bronchioles are able dystrophy, multiple sclerosis, lose their contractility, so that the intervals between them representing the basis of the alveoli, as the lumen of the bronchioles, expand, and the alveoli flattened. This changes the ratio between the areas of the departments conducting the air, and actually respiratory. Vozdukhoplavania area respiratory bronchioles is much greater than the sum of the squares of the alveoli, related to the bronchioles, while the norm is much smaller (figure 2). This leads to the reduction of the area of gas exchange. Cross cut respiratory bronchiole turns into a vial stretched walls and is not typical of norms scalloped or zigzag borders. These bubbles and give a slice of light porous.
The formation of bubbles caused by breaks of the alveoli and merge them is not of such great significance, as it was supposed earlier. The change of oxygen tension in flattened the alveoli along with the blockade of capillaries to blood flow through their prirastajte leads to the development of hypertension in the pulmonary circulation. The consequence of this is the expansion gaps major branches of the pulmonary artery, the thickness of their walls due to hypertrophy, and sclerosis of the middle layer and the development of atherosclerosis intima.
The most important sign of hypertension in the pulmonary circulation during emphysema is hypertrophy of the right ventricle of the heart. Older people may mistakenly put the postmortem diagnosis of chronic obstructive pulmonary emphysema when combined atonal acute swelling of the lungs with hypertrophy of the right ventricle due to postinfarction cardiosclerosis left ventricle of the heart. For differentiation of these processes is necessary to consider the above interstitial pneumosclerosis and bronchi, typical for chronic emphysema lungs. You must also not limited to measuring the thickness of the wall of the right ventricle of the heart, to determine isolated the weight of the walls of the heart chambers (G. I. Ilyin), allowing to analyze the ratio of hypertrophy of the right and left ventricles of the heart. With postinfarction cardiosclerosis weight of the left ventricle above the norm, while in case of chronic emphysema it normal or below normal; when this occurs anatomical programme.
For postmortem diagnosis of chronic pulmonary emphysema must also be taken into account barrel nature of the chest, stupid epigastric angle, low standing of the dome of the diaphragm (V, VI rib instead IV on the right and V to the left, typical of normal), ossification of the first four pairs of rib cartilage. However, none of these signs may not be decisive, since the low standing of the diaphragm may be associated with the accumulation of fluid in the pleural cavity, acute swelling and oedema of the lungs, and other changes may be age norm (for example, ossification of the first pair rib cartilage for people 50-60 years).
Senile emphysema observed changes similar to those described, but pronounced age brutalization of elastic fibers of light and there are no signs of hypertension pulmonary, including hypertrophy of the right ventricle of the heart.
Compensatory emphysema is the outcome of compensatory hypertrophy of light that occurs after surgery pneumo - and lobectomy and differs from obstructive emphysema enrichment alveolar capillaries, absence of chronic bronchitis.
Lobes pulmonary emphysema newborns is more common in boys, localized predominantly in the upper lobe of the left lung, which disproportionately pererastayut, pale. The mediastinal shift in the healthy side that can cause respiratory and cardiovascular failure. The rest of the lobe of the lung look atelectatic. Assume that the basis of pathogenesis lobes of emphysema is the dysfunction of lobar bronchus, which often show symptoms of hypoplasia. It is not excluded vicar origin in congenital atelectasis other shares.
Complication any of emphysema can be gap bubbles, air penetration in interstitial lung tissue and the development of so-called interstitial emphysema (accumulation and movement of air bubbles in the lymph and tissue cracks interstice lungs). In the course of connective tissue layers are visible chain from air bubbles most intensively expressed in the forward-top of our lungs. Interstitial emphysema can also develop on the background of unchanged lung tissue as the result of a sudden increase in pressure in the respiratory tract with a strong cough, laryngospasm. Most strongly interstitial emphysema is expressed in children. Outcomes: resorption, development of purulent lymphangitis lung breakthrough bubbles and spontaneous pneumothorax (see), which usually goes into mediastinal emphysema.

Fig. 1. Diffuse the bronchi and bronchioles and sclerosis of interstice chronic emphysema.
Fig. 2. The scheme of the bronchial tubes in normal and emphysema (vozdukhoplavania part shaded): above - normal bronchiole, below - emphysema.