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- W2123227952 abstract "An elevated physiological dead space, calculated from measurements of arterial CO 2 and mixed expired CO 2 , 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. 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. 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. 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." @default.
- W2123227952 created "2016-06-24" @default.
- W2123227952 creator A5091400200 @default.
- W2123227952 date "2014-11-13" @default.
- W2123227952 modified "2023-10-16" @default.
- W2123227952 title "Dead space: the physiology of wasted ventilation" @default.
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- W2123227952 doi "https://doi.org/10.1183/09031936.00137614" @default.
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