Possible Role of Corollary Discharge in Lack of Dyspnea in Patients With COVID-19 Disease

Vito, Eduardo L De

doi:10.3389/fphys.2021.719166

Cited by 3 publications

(4 citation statements)

References 32 publications

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“…In the Wuhan cohort, 62.4% of severe COVID-19 cases and 46.3% of those who were eventually intubated and ventilated exhibiting sinus tachypnea (increase in normal breathing rate) and higher inflammatory marker levels, or who died, did not present dyspnea [ 25 , 26 , 27 ]. Similar observations of shortness of breath have also been reported by other clinicians who suggested the possibility of SARS-CoV-2-induced ACE2 positive neuronal cells death in areas devoted to the sensory perception of dyspnea, or that the cytokine storm associated with the Ang II-AT1R pathway leads to indirect toxic effects on the corticolimbic network [ 28 , 29 ].…”

Section: Clinical Evidence Of ‘Silent Hypoxia’supporting

confidence: 81%

Unraveling the Underlying Molecular Mechanism of ‘Silent Hypoxia’ in COVID-19 Patients Suggests a Central Role for Angiotensin II Modulation of the AT1R-Hypoxia-Inducible Factor Signaling Pathway

Devaux

Lagier

2023

JCM

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A few days after being infected with SARS-CoV-2, a fraction of people remain asymptomatic but suffer from a decrease in arterial oxygen saturation in the absence of apparent dyspnea. In light of our clinical investigation on the modulation of molecules belonging to the renin angiotensin system (RAS) in COVID-19 patients, we propose a model that explains ‘silent hypoxia’. The RAS imbalance caused by SARS-CoV-2 results in an accumulation of angiotensin 2 (Ang II), which activates the angiotensin 2 type 1 receptor (AT1R) and triggers a harmful cascade of intracellular signals leading to the nuclear translocation of the hypoxia-inducible factor (HIF)-1α. HIF-1α transactivates many genes including the angiotensin-converting enzyme 1 (ACE1), while at the same time, ACE2 is downregulated. A growing number of cells is maintained in a hypoxic condition that is self-sustained by the presence of the virus and the ACE1/ACE2 ratio imbalance. This is associated with a progressive worsening of the patient’s biological parameters including decreased oxygen saturation, without further clinical manifestations. When too many cells activate the Ang II-AT1R-HIF-1α axis, there is a ‘hypoxic spillover’, which marks the tipping point between ‘silent’ and symptomatic hypoxia in the patient. Immediate ventilation is required to prevent the ‘hypoxic spillover’.

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Section: Clinical Evidence Of ‘Silent Hypoxia’supporting

confidence: 81%

Unraveling the Underlying Molecular Mechanism of ‘Silent Hypoxia’ in COVID-19 Patients Suggests a Central Role for Angiotensin II Modulation of the AT1R-Hypoxia-Inducible Factor Signaling Pathway

Devaux

Lagier

2023

JCM

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“…Classical ARDS commonly occurs within 1 week after a predisposing cause, yet researchers have reported that the median time from symptoms onset to CARDS is longer than that of classical ARDS, manifesting within a period of 9.0-12.0 days (1,17,22-24) (Figure 1). Similar to the classical ARDS, the clinical manifestations of CARDS usually include fever, dry cough, cyanosis of the mouth and lips, and respiratory distress which cannot be adjusted by normal oxygen therapy (25,26). A distinguishing feature of COVID-19 disease is that a lack of dyspnea is recognized in the most critical cases (26), the major reason for which is the direct neurotoxic impact of the virus and a general response caused within the infectious context (27).…”

Section: Clinical Manifestationmentioning

confidence: 99%

“…Similar to the classical ARDS, the clinical manifestations of CARDS usually include fever, dry cough, cyanosis of the mouth and lips, and respiratory distress which cannot be adjusted by normal oxygen therapy ( 25 , 26 ). A distinguishing feature of COVID-19 disease is that a lack of dyspnea is recognized in the most critical cases ( 26 ), the major reason for which is the direct neurotoxic impact of the virus and a general response caused within the infectious context ( 27 ). There are two mechanisms associated with it: one is the direct invasion of SARS-CoV-2 into ACE2-expressing brain cells in the limbic system (especially in the insula), and the second is the indirect toxic effect on the cortical network, which plays a major role in expressing the sensation of dyspnea, through cytokine storm ( 28 ).…”

Section: Clinical Manifestationunclassified

A narrative review of COVID-19-related acute respiratory distress syndrome (CARDS): “typical” or “atypical” ARDS?

Pu¹,

Zhai²,

Zhou³

et al. 2022

Ann Transl Med

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Background and Objective: The coronavirus disease of 2019 (COVID-19) is highly infectious and mainly involves the respiratory system, with some patients rapidly progress to acute respiratory distress syndrome (ARDS), which is the leading cause of death in COVID-19 patients. Hence, fully understanding the features of COVID-19-related ARDS (CARDS) and early management of this disease would improve the prognosis and reduce the mortality of severe COVID-19. With the development of recent studies which have focused on CARDS, whether CARDS is "typical" or "atypical" ARDS has become a hotly debated topic. Methods:We searched for relevant literature from 1999 to 2021 published in PubMed by using the following keywords and their combinations: "COVID-19", "CARDS", "ARDS", "pathophysiological mechanism", "clinical manifestations", "prognosis", and "clinical trials". Then, we analyzed, compared and highlighted the differences between classic ARDS and CARDS from all of the aspects above.

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“…Its onset of symptoms seems to be prolonged at 8–12 days compared to 7 days in classical ARDS [ 4 ]. Besides the classical symptoms of ARDS such as fever, cyanosis, and respiratory distress, which cannot be adjusted by normal oxygen therapy, it often shows an atypical lack of dyspnea, which might be explained by the neurotoxic characteristics of the virus [ 9 ]. Such as in classical causes of ARDS, age seems to be a major risk factor for developing ARDS with COVID-19.…”

Section: Introductionmentioning

confidence: 99%

Same but Different? Comparing the Epidemiology, Treatments and Outcomes of COVID-19 and Non-COVID-19 ARDS Cases in Germany Using a Sample of Claims Data from 2021 and 2019

Bernauer,

Alebrand,

Heurich

2023

Viruses

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Background: Acute respiratory distress syndrome (ARDS) is a severe lung condition that can be caused by a variety of underlying illnesses. Due to SARS-CoV-2, the number of cases with ARDS has increased worldwide, making it essential to compare this form of acute respiratory failure with classical causes of ARDS. While there have been several studies investigating the differences between COVID-19 and non-COVID-19 ARDS in early stages of the pandemic, little is known about the differences in later phases, especially in Germany. Aim: The aim of this study is to characterize and compare the comorbidities, treatments, adverse events, and outcomes of COVID-19-associated ARDS and non-COVID-29 ARDS using a representative sample of German health claims data from the years 2019 and 2021. Methods: We compare percentages and median values of the quantities of interest from the COVID-19 and non-COVID-19 ARDS group, with p-values calculated after conducting Pearson’s chi-squared test or the Wilcoxon rank sum test. We also run logistic regressions to access the effect of comorbidities on mortality for COVID-19 ARDS and non-COVID-19 ARDS. Results: Despite many similarities, we find that that there are some remarkable differences between COVID-19 and non-COVID-19 ARDS cases in Germany. Most importantly, COVID-19 ARDS cases display fewer comorbidities and adverse events, and are more often treated with non-invasive ventilation and nasal high-flow therapy. Conclusions: This study highlights the importance of comprehending the contrasting epidemiological features and clinical outcomes of COVID-19 and non-COVID-19 ARDS. This understanding can aid in clinical decision making and guide future research initiatives aimed at enhancing the management of patients afflicted with this severe condition.

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Possible Role of Corollary Discharge in Lack of Dyspnea in Patients With COVID-19 Disease

Cited by 3 publications

References 32 publications

Unraveling the Underlying Molecular Mechanism of ‘Silent Hypoxia’ in COVID-19 Patients Suggests a Central Role for Angiotensin II Modulation of the AT1R-Hypoxia-Inducible Factor Signaling Pathway

Unraveling the Underlying Molecular Mechanism of ‘Silent Hypoxia’ in COVID-19 Patients Suggests a Central Role for Angiotensin II Modulation of the AT1R-Hypoxia-Inducible Factor Signaling Pathway

A narrative review of COVID-19-related acute respiratory distress syndrome (CARDS): “typical” or “atypical” ARDS?

Same but Different? Comparing the Epidemiology, Treatments and Outcomes of COVID-19 and Non-COVID-19 ARDS Cases in Germany Using a Sample of Claims Data from 2021 and 2019

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