![]() ![]() 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. Philadelphia: Wolters Kluwer, p.116.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. We can apply these assumptions to the ideal gas law ( PV = nRT) to derive an equation for the physiological dead space:īoron, W. ![]() The volume of the alveoli (V A) that participated in gas exchange, together with the physiological dead space (V D), will equal the volume of the expired air: V A+V D=V E.The molar amount of CO 2 produced in the alveoli ( n A CO 2) will be the same amount that is expired ( n E CO 2).The subject breathes in normal room air, and respiration (production of CO 2) happens everywhere, except in the volume occupied by the dead spaces. Physiological dead space is the sum of the anatomical dead space and the alveolar dead space. In the ideal healthy adult, this is zero. However, it is quick enough that it can be approximated (averaged out) as an abrupt transition.Īlveolar dead space includes those parts of the respiratory zone that do not participate in gas exchange. Note that in practice, O 2 is replaced by N 2 more gradually, as a sigmoid curve. When the gas is expired, the pure O 2 is expired first. ![]()
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