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Alveolar hyperoxia and exacerbation of lung injury in critically Ill SARS-CoV-2 pneumonia

Alveolar hyperoxia and exacerbation of lung injury in critically Ill SARS-CoV-2 pneumonia
Alveolar hyperoxia and exacerbation of lung injury in critically Ill SARS-CoV-2 pneumonia

Acute hypoxic respiratory failure (AHRF) is a prominent feature of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) critical illness. The severity of gas exchange impairment correlates with worse prognosis, and AHRF requiring mechanical ventilation is associated with substantial mortality. Persistent impaired gas exchange leading to hypoxemia often warrants the prolonged administration of a high fraction of inspired oxygen (FiO2). In SARS-CoV-2 AHRF, systemic vasculopathy with lung microthrombosis and microangiopathy further exacerbates poor gas exchange due to alveolar inflammation and oedema. Capillary congestion with microthrombosis is a common autopsy finding in the lungs of patients who die with coronavirus disease 2019 (COVID-19)-associated acute respiratory distress syndrome. The need for a high FiO2 to normalise arterial hypoxemia and tissue hypoxia can result in alveolar hyperoxia. This in turn can lead to local alveolar oxidative stress with associated inflammation, alveolar epithelial cell apoptosis, surfactant dysfunction, pulmonary vascular abnormalities, resorption atelectasis, and impairment of innate immunity predisposing to secondary bacterial infections. While oxygen is a life-saving treatment, alveolar hyperoxia may exacerbate pre-existing lung injury. In this review, we provide a summary of oxygen toxicity mechanisms, evaluating the consequences of alveolar hyperoxia in COVID-19 and propose established and potential exploratory treatment pathways to minimise alveolar hyperoxia.

COVID-19, Critical Illness, Humans, Hyperoxia/complications, Hypoxia, Inflammation, Lung Injury, Oxygen, Respiratory Distress Syndrome, SARS-CoV-2, hyperoxia, intensive care, oxygen therapy, lung injury
2076-3271
Dushianthan, Ahilanandan
013692a2-cf26-4278-80bd-9d8fcdb17751
Bracegirdle, Luke
a23d4bd0-eab9-4d0b-a2bc-fc02b5130511
Cusack, Rebecca
dfb1595f-2792-4f76-ac6d-da027cf40146
Cumpstey, Andrew F.
050a389c-f550-4453-a80a-f1a6e57db923
Postle, Anthony D
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Grocott, Michael P.W.
1e87b741-513e-4a22-be13-0f7bb344e8c2
Dushianthan, Ahilanandan
013692a2-cf26-4278-80bd-9d8fcdb17751
Bracegirdle, Luke
a23d4bd0-eab9-4d0b-a2bc-fc02b5130511
Cusack, Rebecca
dfb1595f-2792-4f76-ac6d-da027cf40146
Cumpstey, Andrew F.
050a389c-f550-4453-a80a-f1a6e57db923
Postle, Anthony D
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Grocott, Michael P.W.
1e87b741-513e-4a22-be13-0f7bb344e8c2

Dushianthan, Ahilanandan, Bracegirdle, Luke, Cusack, Rebecca, Cumpstey, Andrew F., Postle, Anthony D and Grocott, Michael P.W. (2023) Alveolar hyperoxia and exacerbation of lung injury in critically Ill SARS-CoV-2 pneumonia. Medical Sciences, 11 (4), [70]. (doi:10.3390/medsci11040070).

Record type: Review

Abstract

Acute hypoxic respiratory failure (AHRF) is a prominent feature of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) critical illness. The severity of gas exchange impairment correlates with worse prognosis, and AHRF requiring mechanical ventilation is associated with substantial mortality. Persistent impaired gas exchange leading to hypoxemia often warrants the prolonged administration of a high fraction of inspired oxygen (FiO2). In SARS-CoV-2 AHRF, systemic vasculopathy with lung microthrombosis and microangiopathy further exacerbates poor gas exchange due to alveolar inflammation and oedema. Capillary congestion with microthrombosis is a common autopsy finding in the lungs of patients who die with coronavirus disease 2019 (COVID-19)-associated acute respiratory distress syndrome. The need for a high FiO2 to normalise arterial hypoxemia and tissue hypoxia can result in alveolar hyperoxia. This in turn can lead to local alveolar oxidative stress with associated inflammation, alveolar epithelial cell apoptosis, surfactant dysfunction, pulmonary vascular abnormalities, resorption atelectasis, and impairment of innate immunity predisposing to secondary bacterial infections. While oxygen is a life-saving treatment, alveolar hyperoxia may exacerbate pre-existing lung injury. In this review, we provide a summary of oxygen toxicity mechanisms, evaluating the consequences of alveolar hyperoxia in COVID-19 and propose established and potential exploratory treatment pathways to minimise alveolar hyperoxia.

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medsci-11-00070-v2 (1) - Version of Record
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Accepted/In Press date: 30 October 2023
Published date: 1 November 2023
Keywords: COVID-19, Critical Illness, Humans, Hyperoxia/complications, Hypoxia, Inflammation, Lung Injury, Oxygen, Respiratory Distress Syndrome, SARS-CoV-2, hyperoxia, intensive care, oxygen therapy, lung injury

Identifiers

Local EPrints ID: 486046
URI: http://eprints.soton.ac.uk/id/eprint/486046
ISSN: 2076-3271
PURE UUID: 880f6c47-91ea-4b3d-bce5-d856299ff8c6
ORCID for Ahilanandan Dushianthan: ORCID iD orcid.org/0000-0002-0165-3359
ORCID for Rebecca Cusack: ORCID iD orcid.org/0000-0003-2863-2870
ORCID for Andrew F. Cumpstey: ORCID iD orcid.org/0000-0001-6257-207X
ORCID for Anthony D Postle: ORCID iD orcid.org/0000-0001-7361-0756
ORCID for Michael P.W. Grocott: ORCID iD orcid.org/0000-0002-9484-7581

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Date deposited: 08 Jan 2024 17:33
Last modified: 30 Nov 2024 02:59

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Contributors

Author: Ahilanandan Dushianthan ORCID iD
Author: Luke Bracegirdle
Author: Rebecca Cusack ORCID iD
Author: Andrew F. Cumpstey ORCID iD

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