Abstract:
BACKGROUND: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. 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. METHODS:Five healthy anesthetized sheep received protective ventilation for 20 hours, while endotoxin was continuously infused. Maps of voxel-level lung ventilation, perfusion, V ˙ / Q ˙ , CO2 partial pressures, and alveolar dead-space fraction were estimated from positron emission tomography at baseline and 20 hours. RESULTS:Alveolar 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 V ˙ / Q ˙ in non-dependent regions. 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). CONCLUSIONS:In 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.
journal_name
Acta Anaesthesiol Scandjournal_title
Acta anaesthesiologica Scandinavicaauthors
Beda A,Winkler T,Wellman TJ,De Prost N,Tucci M,Vidal Melo MFdoi
10.1111/aas.13702subject
Has Abstractpub_date
2021-01-01 00:00:00pages
100-108issue
1eissn
0001-5172issn
1399-6576journal_volume
65pub_type
杂志文章abstract:BACKGROUND:Ketamine (K) has been reported to produce bronchodilation in patients suffering from asthma. Although most researchers have used indirect measurements to study the effect of K in vivo, the reliability of these indirect methods are controversial. We have developed a new technique to measure the bronchial cros...
journal_title:Acta anaesthesiologica Scandinavica
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journal_title:Acta anaesthesiologica Scandinavica
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journal_title:Acta anaesthesiologica Scandinavica
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journal_title:Acta anaesthesiologica Scandinavica
pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:Acta anaesthesiologica Scandinavica
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journal_title:Acta anaesthesiologica Scandinavica
pub_type: 临床试验,杂志文章,随机对照试验
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journal_title:Acta anaesthesiologica Scandinavica
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pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:2002-03-01 00:00:00
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pub_type: 杂志文章
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更新日期:2018-11-01 00:00:00