COVID-19 pneumonia : pathophysiology and management
Copyright ©The authors 2021..
Coronavirus disease 2019 (COVID-19) pneumonia is an evolving disease. We will focus on the development of its pathophysiologic characteristics over time, and how these time-related changes determine modifications in treatment. In the emergency department: the peculiar characteristic is the coexistence, in a significant fraction of patients, of severe hypoxaemia, near-normal lung computed tomography imaging, lung gas volume and respiratory mechanics. Despite high respiratory drive, dyspnoea and respiratory rate are often normal. The underlying mechanism is primarily altered lung perfusion. The anatomical prerequisites for PEEP (positive end-expiratory pressure) to work (lung oedema, atelectasis, and therefore recruitability) are lacking. In the high-dependency unit: the disease starts to worsen either because of its natural evolution or additional patient self-inflicted lung injury (P-SILI). Oedema and atelectasis may develop, increasing recruitability. Noninvasive supports are indicated if they result in a reversal of hypoxaemia and a decreased inspiratory effort. Otherwise, mechanical ventilation should be considered to avert P-SILI. In the intensive care unit: the primary characteristic of the advance of unresolved COVID-19 disease is a progressive shift from oedema or atelectasis to less reversible structural lung alterations to lung fibrosis. These later characteristics are associated with notable impairment of respiratory mechanics, increased arterial carbon dioxide tension (P aCO2 ), decreased recruitability and lack of response to PEEP and prone positioning.
| Errataetall: |
CommentIn: Eur Respir Rev. 2022 Jun 28;31(164):. - PMID 35768129 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:30 |
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| Enthalten in: |
European respiratory review : an official journal of the European Respiratory Society - 30(2021), 162 vom: 31. Dez. |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Gattinoni, Luciano [VerfasserIn] |
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| Anmerkungen: |
Date Completed 27.10.2021 Date Revised 08.08.2022 published: Electronic-Print CommentIn: Eur Respir Rev. 2022 Jun 28;31(164):. - PMID 35768129 Citation Status MEDLINE |
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| doi: |
10.1183/16000617.0138-2021 |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM332110230 |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright ©The authors 2021. | ||
| 520 | |a Coronavirus disease 2019 (COVID-19) pneumonia is an evolving disease. We will focus on the development of its pathophysiologic characteristics over time, and how these time-related changes determine modifications in treatment. In the emergency department: the peculiar characteristic is the coexistence, in a significant fraction of patients, of severe hypoxaemia, near-normal lung computed tomography imaging, lung gas volume and respiratory mechanics. Despite high respiratory drive, dyspnoea and respiratory rate are often normal. The underlying mechanism is primarily altered lung perfusion. The anatomical prerequisites for PEEP (positive end-expiratory pressure) to work (lung oedema, atelectasis, and therefore recruitability) are lacking. In the high-dependency unit: the disease starts to worsen either because of its natural evolution or additional patient self-inflicted lung injury (P-SILI). Oedema and atelectasis may develop, increasing recruitability. Noninvasive supports are indicated if they result in a reversal of hypoxaemia and a decreased inspiratory effort. Otherwise, mechanical ventilation should be considered to avert P-SILI. In the intensive care unit: the primary characteristic of the advance of unresolved COVID-19 disease is a progressive shift from oedema or atelectasis to less reversible structural lung alterations to lung fibrosis. These later characteristics are associated with notable impairment of respiratory mechanics, increased arterial carbon dioxide tension (P aCO2 ), decreased recruitability and lack of response to PEEP and prone positioning | ||
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| 700 | 1 | |a Steinberg, Irene |e verfasserin |4 aut | |
| 700 | 1 | |a Busana, Mattia |e verfasserin |4 aut | |
| 700 | 1 | |a Palermo, Paola |e verfasserin |4 aut | |
| 700 | 1 | |a Lazzari, Stefano |e verfasserin |4 aut | |
| 700 | 1 | |a Romitti, Federica |e verfasserin |4 aut | |
| 700 | 1 | |a Quintel, Michael |e verfasserin |4 aut | |
| 700 | 1 | |a Meissner, Konrad |e verfasserin |4 aut | |
| 700 | 1 | |a Marini, John J |e verfasserin |4 aut | |
| 700 | 1 | |a Chiumello, Davide |e verfasserin |4 aut | |
| 700 | 1 | |a Camporota, Luigi |e verfasserin |4 aut | |
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