The Pathophysiology and Dangers of Silent Hypoxemia in COVID-19 Lung Injury.
The Pathophysiology and Dangers of Silent Hypoxemia in COVID-19 Lung Injury.
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DOI：
10.1513/annalsats.202011-1376cme
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发表时间：
2021-07
影响因子：
8.3
通讯作者：
Swenson ER
中科院分区：
文献类型：
--
作者：
Swenson KE;Ruoss SJ;Swenson ER
正在进行的冠状病毒病(新冠肺炎)大流行在许多层面上都是史无前例的，尤其是在理解这些新的危重患者的病理生理学方面面临挑战。一种被广泛报道的现象是，深度低氧血症患者的呼吸困难与放射学异常的程度和肺顺应性的改变不成比例。这种明显独特的表现，有时被称为“幸福性低氧血症或缺氧”，但更好地描述为“静止性低氧血症”，这使得人们推测新冠肺炎肺损伤和其他原因引起的急性呼吸窘迫综合征之间存在潜在的病理生理差异。我们探讨了新冠肺炎的三个显著特征，它们可能与无症状性低氧血症的发生有关，包括肺顺应性、肺血管对低氧的反应以及神经系统对低氧的感知和反应的差异。在已知的呼吸生理学和神经生物学原理的背景下，我们讨论了这些特殊的发现是由于病毒的直接作用，还是同样可信的，属于典型的ARDS病理生理学和健康人广泛的缺氧性呼吸和肺血管反应以及呼吸困难感觉的范围。虽然我们通过更具侵入性和纵向研究来确认这些表型的能力有限，但新冠肺炎患者的肺损伤类型与其他原因引起的急性呼吸窘迫综合征之间的比较被这场大流行的范围和严重性所笼罩，这可能是描述“新的”表型的基础。然而，考虑到新冠肺炎肺损伤的病理生理学中任何独特之处的不确定性，目前还没有令人信服的病理生理学原因来支持这些患者不同于ARDS公认的治疗标准的治疗方法。
The ongoing coronavirus disease (COVID-19) pandemic has been unprecedented on many levels, not least of which are the challenges in understanding the pathophysiology of these new critically ill patients. One widely reported phenomenon is that of a profoundly hypoxemic patient with minimal to no dyspnea out of proportion to the extent of radiographic abnormality and change in lung compliance. This apparently unique presentation, sometimes called “happy hypoxemia or hypoxia” but better described as “silent hypoxemia,” has led to the speculation of underlying pathophysiological differences between COVID-19 lung injury and acute respiratory distress syndrome (ARDS) from other causes. We explore three proposed distinctive features of COVID-19 that likely bear on the genesis of silent hypoxemia, including differences in lung compliance, pulmonary vascular responses to hypoxia, and nervous system sensing and response to hypoxemia. In the context of known principles of respiratory physiology and neurobiology, we discuss whether these particular findings are due to direct viral effects or, equally plausible, are within the spectrum of typical ARDS pathophysiology and the wide range of hypoxic ventilatory and pulmonary vascular responses and dyspnea perception in healthy people. Comparisons between lung injury patterns in COVID-19 and other causes of ARDS are clouded by the extent and severity of this pandemic, which may underlie the description of “new” phenotypes, although our ability to confirm these phenotypes by more invasive and longitudinal studies is limited. However, given the uncertainty about anything unique in the pathophysiology of COVID-19 lung injury, there are no compelling pathophysiological reasons at present to support a therapeutic approach for these patients that is different from the proven standards of care in ARDS.