Morphological study of the lungs, bronchi and diaphragm after autopsy. Histological examination revealed lymphoid infiltration of the interstitial lung tissue. The lymphoid infiltration of the bronchi of all calibers was diagnosed. The foci of tumor infiltrates were determined in the peribronchial tissue. Marked dilation and congestion of blood vessels, the lumens of many vessels were filled with lymphocytes with the formation of leucostasis. Hemorrhages in the intestine and respiratory tissue were observed. Multiple atelectasis of the pulmonary tissue alternated with areas of emphysematous enlargement of the alveoli. There were abnormalities and sclerosis of interalveolar septa, peribronchial, perivascular, interstitial sclerosis. The mucous membrane of the bronchi over a considerable distance was thinned, sclerosed,the preserved epithelium is partially metaplaced into a stratified flat. The diaphragm thickness is 3.7 mm. Myocytes have prevailedmedium sized. However, there was a marked increase in myocytes of large and small sizes (15.2 and 39.1%), a significant growth of the stroma around the vessels, in the intermuscular space, and large areas of lipomatosis. Lymphoid infiltration of the diaphragm and lymphocytic stasis in small vessels was revealed.

After analyzing and comparing data from studies of regional ventilation and pulmonary blood flow with X-ray and morphological studies of the bronchopulmonary system in CLL patients, it was concluded that the functional disorders of the respiratory system are directly dependent on the morphological changes in the lungs, bronchi and diaphragm in these patients in different stages of tumor progression. In the process of tumor progression of hemoblastosis, lymphoid infiltration of the lungs and bronchi appears, in the lungs pneumosclerosis, localized emphysema, is noted. As a result, there is a morphological change in the alveoli and a violation of their functional ability. There is a significant violation of endobronchial microhemocirculation, one of the reasons for which is high leukocytosis,contributing to the formation of leukostasis in the vessels of the bronchopulmonary system. Disorders of microhemocirculation are progressing with the development of anemic syndrome. As a result, trophic tissue suffers. The metabolism in cells of a mucous membrane of a bronchial tube is broken. Thinning, hardening of the mucous membrane occurs. Against this background, due to pronounced immunodeficiency, an inflammatory process joins. In 60% of patients with progressive CLL, there is a latent course of chronic non-structural bronchitis. Excursion of the diaphragm is reduced due to its compression by significantly enlarged liver and spleen and specific leukemic lesions. The hemodynamics of a small circle of blood circulation is broken. All of the above leads to impaired general and regional ventilation and lung perfusion.In addition to the above, the progression of impaired lung ventilation in the terminal stage of CLL is facilitated by the sarcoma of the lymph nodes of the mediastinum with the development of compression syndrome, hemorrhage into the lung tissue and bronchi due to the development of thrombocytopenia.

Decreases in regional ventilation and pulmonary blood flow account for a decrease in pO2 during tumor progression of CLL. Severe and protracted obstructive processes in the bronchi, restrictive processes in the lungs, impaired function of the diaphragm and hemodynamics of the ICC, pathology of the microvasculature, contribute to the development of hypoxemia and pulmonary hypertension. Therefore, in the process of tumor progression of CLL, the pressure in the system of the pulmonary artery increases.