The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases. The role and importance of club cells (Clara cells) in the pathogenesis of some respiratory diseases. Rokicki W, Rokicki M, Wojtacha J, Dżeljijli A. Elastin in lung development and disease pathogenesis. A unique cellular organization of human distal airways and its disarray in chronic obstructive pulmonary disease. The comparison of the lengths and diameters of main bronchi measured from two-dimensional and three-dimensional images in the same patients. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V'A/Q' ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.Lee JW, Son JS, Choi JW, Han YJ, Lee JR. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V'A/Q') heterogeneity has been the most important pathophysiological mechanism. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure.
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