Silent hypoxaemia in COVID-19 patients.
Silent hypoxaemia in COVID-19 patients.
复制标题
DOI：
10.1113/jp280769
复制
发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Malhotra A
中科院分区：
文献类型：
--
作者：
Simonson TS;Baker TL;Banzett RB;Bishop T;Dempsey JA;Feldman JL;Guyenet PG;Hodson EJ;Mitchell GS;Moya EA;Nokes BT;Orr JE;Owens RL;Poulin M;Rawling JM;Schmickl CN;Watters JJ;Younes M;Malhotra A
由于感染SARS-CoV-2而导致的新冠肺炎的临床表现具有很大的多样性，大多数患者都有轻微的症状，也有一些人发展为严重的呼吸衰竭。这种差异的原因尚不清楚，但迫切需要调查。一些新冠肺炎患者被贴上了“快乐低氧”的标签，据报道，在这种情况下，患者没有呼吸困难的主诉和明显的呼吸窘迫迹象。根据正在进行的辩论，我们强调了可能导致静止性低氧血症表现差异的关键呼吸和神经成分，并确定了后续研究的优先事项。空气饥饿的起源。在导致空气饥饿的机制的工作模型中，脑干呼吸中心向前脑发送投射(必然放电)，引起呼吸不适的程度与必然放电的大小成比例。这些脑干呼吸中心还发送下行投射，驱动呼吸运动神经元和呼吸肌活动以产生通风。脑干中心的输入包括化学感受器输入、运动和来自运动皮质的自愿输入。来自肺伸展感受器的传入反馈调节不同性质的呼吸困难感觉。慢慢适应的肺伸展感受器对空气饥饿有抑制作用。肺C纤维受体与空气饥饿有关，但精确的神经投射并不是很清楚。当相应的放电达到某一阈值时，或当通风不能满足需求时，就会发生呼吸困难。引起呼吸困难的输入用蓝色箭头表示；抑制呼吸困难的输入用蓝色圆圈表示。黑色箭头表示呼吸的动态平衡调节。
The clinical presentation of COVID-19 due to infection with SARS-CoV-2 is highly variable with the majority of patients having mild symptoms while others develop severe respiratory failure. The reason for this variability is unclear but is in critical need of investigation. Some COVID-19 patients have been labelled with ‘happy hypoxia’, in which patient complaints of dyspnoea and observable signs of respiratory distress are reported to be absent. Based on ongoing debate, we highlight key respiratory and neurological components that could underlie variation in the presentation of silent hypoxaemia and define priorities for subsequent investigation. Genesis of air hunger. In a working model of mechanisms giving rise to air hunger, brainstem respiratory centres send projections (corollary discharge) to the forebrain, giving rise to breathing discomfort in proportion to the magnitude of corollary discharge. These brainstem respiratory centres also send descending projections, driving respiratory motor neurons and respiratory muscle activity to generate ventilation. Inputs to the brainstem centres include chemoreceptor inputs, exercise and voluntary inputs from the motor cortex. Afferent feedback from lung stretch receptors modulates different qualities of dyspnoeic sensation. Slowly adapting lung stretch receptors are inhibitory to air hunger. Pulmonary C-fibre receptors contribute to air hunger, but precise neural projections are not well understood. Whenever corollary discharge reaches a certain threshold, or when ventilation fails to meet demand, dyspnoea ensues. Inputs contributing to dyspnoea are indicated by blue arrows; inputs that inhibit dyspnoea are indicated with blue circles. Black arrows indicate homeostatic regulation of breathing.