ArticleActa anaesthesiologica Scandinavica2021
Physiological mechanism and spatial distribution of increased alveolar dead-space in early ARDS: An experimental study.
Article in Acta anaesthesiologica Scandinavica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Imaging in animal models: bridging experimental findings and human pathophysiology.Critical care (London, England) · 2025Review
- Intraoperative Factors Associated With Mechanical Ventilation Duration Following Aortic Surgery.Journal of cardiothoracic and vascular anesthesia · 2025Observational
- Imaging the pulmonary vasculature in acute respiratory distress syndrome.Nitric oxide : biology and chemistry · 2024Review
- Lung functional imaging.Breathe (Sheffield, England) · 2023Article
- Worsening of lung perfusion to tissue density distributions during early acute lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Effects of airway pressure release ventilation on lung physiology assessed by electrical impedance tomography in patients with early moderate-to-severe ARDS.Critical care (London, England) · 2023Article
- The end-tidal alveolar dead space fraction for risk stratification during the first week of invasive mechanical ventilation: an observational cohort study.Critical care (London, England) · 2023Observational
- Alveolar dead space fraction is not associated with early RV systolic dysfunction in pediatric ARDS.Pediatric pulmonology · 2023Article
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6 authors.
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Abstract
backgroundWe 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. 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,
methodsFive healthy anesthetized sheep received protective ventilation for 20 hours, while endotoxin was continuously infused. Maps of voxel-level lung ventilation, perfusion,
resultsAlveolar dead-space fraction increased during the 20 hours (+0.05, P = .031), mainly in non-dependent regions (+0.03, P = .031). This was mediated by perfusion redistribution away from non-dependent regions (-5.9%, P = .031), while the spatial distribution of ventilation did not change, resulting in increased
conclusionsIn this early ARDS model, increases in alveolar dead-space occur within 20 hours due to the regional redistribution of perfusion and not ventilation. This moderate redistribution suggests changes in the interplay between active and passive perfusion redistribution mechanisms (including hypoxic vasoconstriction and gravitational effects), not the appearance of thromboembolism. Hence, the association between mortality and increased dead-space possibly arises from the former, reflecting gas-exchange inefficiency due to perfusion heterogeneity. Such heterogeneity results from the injury and exhaustion of compensatory mechanisms for perfusion redistribution.
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