![]() ![]() Microthrombosis, endothelial swelling, and damage, 3, 7, 11 and abnormal vasoactivity secondary to lung injury 12, 13 could produce marked local hypoperfusion or even vascular occlusion, while interstitial edema and lung derecruitment would cause the redistribution of V ˙ in large regions of the lungs. Furthermore, it is unclear if this phenomenon occurs throughout the lung, or if changes are regional. 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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