2021
DOI: 10.1186/s12931-021-01614-1
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Conceptions of the pathophysiology of happy hypoxemia in COVID-19

Abstract: In their letter-to-the-editor entitled “Misconceptions of pathophysiology of happy hypoxemia and implications for management of COVID-19”, Tobin et al. (Respir Res 21:249, 2020) debated our views on happy hypoxemia in COVID-19 (Respir Res 21:198, 2020). We thank the authors for their interesting comments and alternative viewpoints, and we would like to clarify several important aspects raised.

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Cited by 31 publications
(30 citation statements)
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References 30 publications
(36 reference statements)
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“… 38 The pathophysiological cause of silent hypoxaemia is unclear, but it may be due to intrapulmonary shunting, loss of lung perfusion regulation, endothelial injury and impaired diffusion capacity. 39 , 40 These patients require close monitoring. Desaturation may be transient but is often prolonged or associated with rapid respiratory decompensation.…”
Section: Methodsmentioning
confidence: 99%
“… 38 The pathophysiological cause of silent hypoxaemia is unclear, but it may be due to intrapulmonary shunting, loss of lung perfusion regulation, endothelial injury and impaired diffusion capacity. 39 , 40 These patients require close monitoring. Desaturation may be transient but is often prolonged or associated with rapid respiratory decompensation.…”
Section: Methodsmentioning
confidence: 99%
“…That means damaged alveolar epithelial cells and the pulmonary endothelial cell can activate platelets and induce intravascular microthrombi formation [58] , [71] . The above changes appear to contribute to impaired hypoxemic vasoconstriction and the clinical phenotype of happy hypoxemia [72] . SARS-CoV-2 infection-specific inflammatory cytokine and growth factor dysregulation SARS-CoV-2 induces the production and release of inflammatory mediators including cytokines and chemokines.…”
Section: Sars-cov-2 Induced Inflammation and Coagulopathymentioning
confidence: 99%
“…That means damaged alveolar epithelial cells and the pulmonary endothelial cell can activate platelets and induce intravascular microthrombi formation [58] , [71] . The above changes appear to contribute to impaired hypoxemic vasoconstriction and the clinical phenotype of happy hypoxemia [72] .…”
Section: Sars-cov-2 Induced Inflammation and Coagulopathymentioning
confidence: 99%
“…Damaged respiratory epithelial cells and pulmonary endothelial dysfunction activate platelets and formation of intravascular microthrombi ( Connors and Levy, 2020 ; Del Turco et al, 2020 ). These pathophysiological changes will contribute to impaired hypoxemic vasoconstriction and the clinical phenotype of “happy hypoxemia” in COVID-19 patients ( Dhont et al, 2021 ). If the immune system doesn’t gain control, endothelial dysfunction and coagulation defects might spread systemically causing vasculitis, disseminated intravascular coagulopathy (DIC) and immunothrombosis ( Engelmann and Massberg, 2013 ; Jackson et al, 2019 ).…”
Section: Respiratory Immunologymentioning
confidence: 99%