9, 10 Yet, there is a marked paucity of regional ventilation and perfusion data to support either changes in the Q ˙ or redistribution of V ˙ as the primary determinant of increased alveolar dead-space during early lung injury. 3, 5– 7 Thus, it has been speculated that such abnormalities would be the main contributor to larger dead-space in ARDS by generating either regions of complete alveolar dead-space, 3, 8 or a dead-space effect. Perfusion abnormalities, including the disruption of lung microcirculation, are key features of experimental and clinical lung injury. However, dead-space effects are also present in alveolar units with increased (but not infinite) V ˙ / Q ˙, due either to regional increased V ˙ or reduced Q ˙. 5, 6 Such regions of alveolar dead-space are at the extreme end of the V ˙ / Q ˙ distribution where V ˙ / Q ˙~∞. The alveolar dead-space reflects by definition alveolar units with ventilation ( V ˙) but without perfusion ( Q ˙), which could be caused for instance by capillary collapse (West zone 1 4) or thromboembolism. The anatomical dead-space is the luminal airway volume and approximately constant. In reality, physiological dead-space has two components: anatomical and alveolar. In clinical investigations, physiological dead-space is commonly estimated with the Bohr–Enghoff equation, 1– 3 in which all ventilation inefficiencies are lumped into a single compartment of ventilation without perfusion. 1– 3 However, the mechanisms underlying such early dead-space changes are still incompletely quantified and understood. Physiological dead-space increases shortly after ARDS onset (~11 ± 7 hours) and this increase is associated with mortality. Pulmonary physiological dead-space is a measure of wasted alveolar ventilation, ie, the component of lung ventilation that does not contribute to CO 2 elimination.
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