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Impairment of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome
European Respiratory Review ( IF 7.5 ) Pub Date : 2021-09-15 , DOI: 10.1183/16000617.0059-2021
Mareike Gierhardt 1, 2, 3, 4 , Oleg Pak 1, 2 , Dieter Walmrath 1 , Werner Seeger 1, 2, 3, 5 , Friedrich Grimminger 1, 2 , Hossein A Ghofrani 1, 2, 6 , Norbert Weissmann 1, 2 , Matthias Hecker 1, 7 , Natascha Sommer 1, 2, 7
Affiliation  

Acute respiratory distress syndrome (ARDS) is a serious complication of severe systemic or local pulmonary inflammation, such as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. ARDS is characterised by diffuse alveolar damage that leads to protein-rich pulmonary oedema, local alveolar hypoventilation and atelectasis. Inadequate perfusion of these areas is the main cause of hypoxaemia in ARDS. High perfusion in relation to ventilation (V/Q<1) and shunting (V/Q=0) is not only caused by impaired hypoxic pulmonary vasoconstriction but also redistribution of perfusion from obstructed lung vessels. Rebalancing the pulmonary vascular tone is a therapeutic challenge. Previous clinical trials on inhaled vasodilators (nitric oxide and prostacyclin) to enhance perfusion to high V/Q areas showed beneficial effects on hypoxaemia but not on mortality. However, specific patient populations with pulmonary hypertension may profit from treatment with inhaled vasodilators. Novel treatment targets to decrease perfusion in low V/Q areas include epoxyeicosatrienoic acids and specific leukotriene receptors. Still, lung protective ventilation and prone positioning are the best available standard of care. This review focuses on disturbed perfusion in ARDS and aims to provide basic scientists and clinicians with an overview of the vascular alterations and mechanisms of V/Q mismatch, current therapeutic strategies, and experimental approaches.



中文翻译:

急性呼吸窘迫综合征缺氧性肺血管收缩受损

急性呼吸窘迫综合征 (ARDS) 是严重全身或局部肺部炎症的严重并发症,例如由严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染引起。ARDS 的特征是弥漫性肺泡损伤,导致富含蛋白质的肺水肿、局部肺泡通气不足和肺不张。这些区域的灌注不足是 ARDS 低氧血症的主要原因。与通气 (V/Q<1) 和分流 (V/Q=0) 相关的高灌注不仅是由缺氧性肺血管收缩受损引起的,而且是由阻塞的肺血管重新分配灌注引起的。重新平衡肺血管张力是一项治疗挑战。先前关于吸入血管扩张剂(一氧化氮和前列环素)以增强高 V/Q 区域灌注的临床试验显示对低氧血症有益,但对死亡率没有影响。然而,特定的肺动脉高压患者群体可能会受益于吸入性血管扩张剂的治疗。减少低 V/Q 区域灌注的新治疗目标包括环氧二十碳三烯酸和特定的白三烯受体。尽管如此,肺保护性通气和俯卧位仍然是目前最好的护理标准。本综述侧重于 ARDS 中的灌注紊乱,旨在为基础科学家和临床医生提供 V/Q 不匹配的血管改变和机制、当前治疗策略和实验方法的概述。特定的肺动脉高压患者群体可能会受益于吸入性血管扩张剂的治疗。减少低 V/Q 区域灌注的新治疗目标包括环氧二十碳三烯酸和特定的白三烯受体。尽管如此,肺保护性通气和俯卧位仍然是目前最好的护理标准。本综述侧重于 ARDS 中的灌注紊乱,旨在为基础科学家和临床医生提供 V/Q 不匹配的血管改变和机制、当前治疗策略和实验方法的概述。特定的肺动脉高压患者群体可能会受益于吸入性血管扩张剂的治疗。减少低 V/Q 区域灌注的新治疗目标包括环氧二十碳三烯酸和特定的白三烯受体。尽管如此,肺保护性通气和俯卧位仍然是目前最好的护理标准。本综述侧重于 ARDS 中的灌注紊乱,旨在为基础科学家和临床医生提供 V/Q 不匹配的血管改变和机制、当前治疗策略和实验方法的概述。肺保护性通气和俯卧位是目前最好的护理标准。本综述侧重于 ARDS 中的灌注紊乱,旨在为基础科学家和临床医生提供 V/Q 不匹配的血管改变和机制、当前治疗策略和实验方法的概述。肺保护性通气和俯卧位是目前最好的护理标准。本综述侧重于 ARDS 中的灌注紊乱,旨在为基础科学家和临床医生提供 V/Q 不匹配的血管改变和机制、当前治疗策略和实验方法的概述。

更新日期:2021-09-15
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