Donina Zh A
Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
J Evol Biochem Physiol. 2022;58(1):73-80. doi: 10.1134/S0022093022010070. Epub 2022 Mar 5.
The global pandemic of a new coronavirus disease (COVID-19) has posed challenges to public health specialists around the world associated with diagnosis, intensive study of epidemiological and clinical features of the coronavirus infection, development of preventive approaches, therapeutic strategies and rehabilitation measures. However, despite the successes achieved in the study of COVID-19 pathogenesis, many aspects that aggravate the severity of the disease and cause high mortality of patients remain unclear. The main clinical manifestation of the new variant of SARS-CoV-2 virus infection is pneumonia with massive parenchymal lesions of lung tissue, diffuse alveolar damage, thrombotic manifestations, disruption of ventilation-perfusion relationships, etc. However, symptoms in patients hospitalized with COVID pneumonia show a broad diversity: the majority has minimal manifestations, others develop severe respiratory failure complicated by acute respiratory distress syndrome (ARDS) with rapidly progressing hypoxemia that leads to high mortality. Numerous clinical data publications report that some COVID pneumonia patients without subjective signs of severe respiratory failure (dyspnea, "air hunger") have an extremely low saturation level. As a result, there arises a paradoxical condition (called "silent hypoxia" or even "happy hypoxia") contradicting the very basics of physiology, as it essentially represents a severe life-incompatible hypoxemia which lacks respiratory discomfort. All this raises numerous questions among professionals and has already ignited a discussion in scientific publications concerned with the pathogenesis of COVID-19. Respiratory failure is a complex clinical problem, many aspects of which remain controversial. However, according to the majority of authors, one of the first objective indicators of the clinical sign of respiratory failure are hypoxemia-associated changes in external respiration. This review addresses some possible causes of hypoxemia in COVID-19.
新型冠状病毒病(COVID-19)的全球大流行给世界各地的公共卫生专家带来了挑战,涉及冠状病毒感染的诊断、流行病学和临床特征的深入研究、预防方法、治疗策略及康复措施的制定。然而,尽管在COVID-19发病机制的研究中取得了一些成果,但许多加剧疾病严重程度并导致患者高死亡率的方面仍不清楚。新型严重急性呼吸综合征冠状病毒2(SARS-CoV-2)病毒感染的主要临床表现是肺炎,伴有肺组织的大量实质性病变、弥漫性肺泡损伤、血栓形成表现、通气-灌注关系破坏等。然而,因COVID肺炎住院的患者症状表现多样:大多数患者症状轻微,其他患者则发展为严重呼吸衰竭,并伴有急性呼吸窘迫综合征(ARDS),伴有迅速进展的低氧血症,导致高死亡率。众多临床数据出版物报告称,一些没有严重呼吸衰竭主观症状(呼吸困难、“气促”)的COVID肺炎患者血氧饱和度极低。结果,出现了一种与生理学基本原理相悖的矛盾情况(称为“沉默性低氧血症”甚至“快乐性低氧血症”),因为它本质上代表了一种严重的、与生命不相容的低氧血症,却没有呼吸不适。所有这些都在专业人士中引发了诸多问题,并且已经在有关COVID-19发病机制的科学出版物中引发了讨论。呼吸衰竭是一个复杂的临床问题,其许多方面仍存在争议。然而,根据大多数作者的观点,呼吸衰竭临床体征的首要客观指标之一是与低氧血症相关的外呼吸变化。本综述探讨了COVID-19中低氧血症可能的一些原因。