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• W1991473141 abstract "Knowledge about the relationship of right ventricular hypertrophy to intrinsic lung disease depends upon detailed quantitative assessment of both organs. There is considerable overlap in the thickness measurement of normal and abnormal right ventricles measured in the anterior wall of the pulmonary conus. A measurement of 6 mm. or greater in this area is a reliable guide to the existence but not the severity of RVH. The mass of the free wall of the right ventricle in relation to that of the left ventricle and interventricular septum (LV+S/RV) provides a tool with considerable merit in the recognition and quantitation of chronic cor pulmonale. Pulmonary hypertension secondary to intrinsic lung disease is induced by a variety of anatomic and functional alterations determined and conditioned by the nature of the pulmonary disease. Assignment of a primary role to one or another factor does not yet seem justified, particularly in a complex disorder such as pulmonary emphysema. Here, although physiologic data are abundant, quantitative morphologic study of the lung has not yet received wide usage. Three principal mechanisms contribute to increased PVR secondary to intrinsic lung disease. Hypoxia, resulting from impaired ventilation or impairment of diffusion, may induce a functional and partially reversible increase in PVR through a mechanism as yet undetermined. Through distortion and obliteration of small blood vessels, parenchymal destruction produces an irreversible increase in PVR which may be either latent appearing only during stress, or manifest at rest. Finally, secondary hypertensive vascular changes may so restrict the vascular bed that perfusion is decreased to a degree incompatible with life. Abnormal vascular communications have been demonstrated in a variety of situations, but their hemodynamic significance is uncertain. Thus far, histologic examination of the lungs in chronic emphysema has shown only minor evidence of either hypoxic or secondary hypertensive vascular changes. On the other hand, there is evidence, as yet only partially evaluated, that restriction of the vascular bed by parenchymal changes combines with loss of respiratory surface to form the basis for pulmonary hypertension in panlobular emphysema. In contrast, the severity of the ventilatory disturbance may be more important than loss of either vascular bed or respiratory surface in central lobular emphysema. Development of new methods for postmortem measurement of the pulmonary vascular bed in relation to disturbance of respiratory volume and surface area may help resolve these issues not only in chronic emphysema, but also in the broad spectrum of intrinsic pulmonary disease with which significant pulmonary hypertension may be associated." @default.
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• W1991473141 date "1966-11-01" @default.
• W1991473141 modified "2023-09-26" @default.
• W1991473141 title "The anatomy of chronic cor pulmonale secondary to intrinsic lung disease" @default.
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• W1991473141 doi "https://doi.org/10.1016/s0033-0620(66)80025-7" @default.
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