alveolar dead space vs physiologic dead space

In this early ARDS model, increases in alveolar dead-space occur within 20 hours due to the regional redistribution of perfusion and not ventilation. The increased alveolar dead-space derived mostly from areas with intermediate V ˙ / Q ˙ (0.5≤ V ˙ / Q ˙ ≤10), not areas of nearly 'complete' dead-space ( V ˙ / Q ˙ >10). 031), while the spatial distribution of ventilation did not change, resulting in increased V ˙ / Q ˙ in non-dependent regions. This was mediated by perfusion redistribution away from non-dependent regions (-5.9%, P =. 031), mainly in non-dependent regions (+0.03, P =. Maps of voxel-level lung ventilation, perfusion, V ˙ / Q ˙, CO 2 partial pressures, and alveolar dead-space fraction were estimated from positron emission tomography at baseline and 20 hours.Īlveolar dead-space fraction increased during the 20 hours (+0.05, P =.

We hypothesized that: increased dead-space results from the spatial redistribution of pulmonary perfusion, not ventilation such redistribution is not related to thromboembolism (ie, areas with perfusion = 0 and infinite ventilation-perfusion ratio, V ˙ / Q ˙ ), but rather to moderate shifts of perfusion increasing V ˙ / Q ˙ in non-dependent regions.įive healthy anesthetized sheep received protective ventilation for 20 hours, while endotoxin was continuously infused.

We aimed to investigate the physiological mechanism and spatial distribution of increased physiological dead-space, an early marker of ARDS mortality, in the initial stages of ARDS.

Alveolar dead space vs physiologic dead space