alveolar dead space) contain a gas mixture which is. Alveoli which are ventilated but not perfused (i.e. If there was no alveolar dead space, end-tidal CO 2 would be identical to alveolar CO 2. 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. In summary: Normal PaCO 2 -EtCO 2 difference is 2-5 mmHg ( Satoh et al, 2015) This is due to alveolar dead space, which is small in healthy adults. 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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