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Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery
BACKGROUND: Pathological evidence suggests that coronavirus disease 2019 (COVID-19) pulmonary infection involves both alveolar damage (causing shunt) and diffuse microvascular thrombus formation (causing alveolar dead space). We propose that measuring respiratory gas exchange enables detection and q...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
European Respiratory Society
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515481/ https://www.ncbi.nlm.nih.gov/pubmed/36137595 http://dx.doi.org/10.1183/13993003.01117-2022 |
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author | Harbut, Piotr Prisk, G. Kim Lindwall, Robert Hamzei, Sarah Palmgren, Jenny Farrow, Catherine E. Hedenstierna, Goran Amis, Terence C. Malhotra, Atul Wagner, Peter D. Kairaitis, Kristina |
author_facet | Harbut, Piotr Prisk, G. Kim Lindwall, Robert Hamzei, Sarah Palmgren, Jenny Farrow, Catherine E. Hedenstierna, Goran Amis, Terence C. Malhotra, Atul Wagner, Peter D. Kairaitis, Kristina |
author_sort | Harbut, Piotr |
collection | PubMed |
description | BACKGROUND: Pathological evidence suggests that coronavirus disease 2019 (COVID-19) pulmonary infection involves both alveolar damage (causing shunt) and diffuse microvascular thrombus formation (causing alveolar dead space). We propose that measuring respiratory gas exchange enables detection and quantification of these abnormalities. We aimed to measure shunt and alveolar dead space in moderate COVID-19 during acute illness and recovery. METHODS: We studied 30 patients (22 males; mean±sd age 49.9±13.5 years) 3–15 days from symptom onset and again during recovery, 55±10 days later (n=17). Arterial blood (breathing ambient air) was collected while exhaled oxygen and carbon dioxide concentrations were measured, yielding alveolar–arterial differences for each gas (P(A−aO(2)) and P(a−ACO(2)), respectively) from which shunt and alveolar dead space were computed. RESULTS: For acute COVID-19 patients, group mean (range) for P(A−aO(2)) was 41.4 (−3.5–69.3) mmHg and for P(a−ACO(2)) was 6.0 (−2.3–13.4) mmHg. Both shunt (% cardiac output) at 10.4% (0–22.0%) and alveolar dead space (% tidal volume) at 14.9% (0–32.3%) were elevated (normal: <5% and <10%, respectively), but not correlated (p=0.27). At recovery, shunt was 2.4% (0–6.1%) and alveolar dead space was 8.5% (0–22.4%) (both p<0.05 versus acute). Shunt was marginally elevated for two patients; however, five patients (30%) had elevated alveolar dead space. CONCLUSIONS: We speculate impaired pulmonary gas exchange in early COVID-19 pneumonitis arises from two concurrent, independent and variable processes (alveolar filling and pulmonary vascular obstruction). For most patients these resolve within weeks; however, high alveolar dead space in ∼30% of recovered patients suggests persistent pulmonary vascular pathology. |
format | Online Article Text |
id | pubmed-9515481 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | European Respiratory Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-95154812022-11-14 Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery Harbut, Piotr Prisk, G. Kim Lindwall, Robert Hamzei, Sarah Palmgren, Jenny Farrow, Catherine E. Hedenstierna, Goran Amis, Terence C. Malhotra, Atul Wagner, Peter D. Kairaitis, Kristina Eur Respir J Original Research Articles BACKGROUND: Pathological evidence suggests that coronavirus disease 2019 (COVID-19) pulmonary infection involves both alveolar damage (causing shunt) and diffuse microvascular thrombus formation (causing alveolar dead space). We propose that measuring respiratory gas exchange enables detection and quantification of these abnormalities. We aimed to measure shunt and alveolar dead space in moderate COVID-19 during acute illness and recovery. METHODS: We studied 30 patients (22 males; mean±sd age 49.9±13.5 years) 3–15 days from symptom onset and again during recovery, 55±10 days later (n=17). Arterial blood (breathing ambient air) was collected while exhaled oxygen and carbon dioxide concentrations were measured, yielding alveolar–arterial differences for each gas (P(A−aO(2)) and P(a−ACO(2)), respectively) from which shunt and alveolar dead space were computed. RESULTS: For acute COVID-19 patients, group mean (range) for P(A−aO(2)) was 41.4 (−3.5–69.3) mmHg and for P(a−ACO(2)) was 6.0 (−2.3–13.4) mmHg. Both shunt (% cardiac output) at 10.4% (0–22.0%) and alveolar dead space (% tidal volume) at 14.9% (0–32.3%) were elevated (normal: <5% and <10%, respectively), but not correlated (p=0.27). At recovery, shunt was 2.4% (0–6.1%) and alveolar dead space was 8.5% (0–22.4%) (both p<0.05 versus acute). Shunt was marginally elevated for two patients; however, five patients (30%) had elevated alveolar dead space. CONCLUSIONS: We speculate impaired pulmonary gas exchange in early COVID-19 pneumonitis arises from two concurrent, independent and variable processes (alveolar filling and pulmonary vascular obstruction). For most patients these resolve within weeks; however, high alveolar dead space in ∼30% of recovered patients suggests persistent pulmonary vascular pathology. European Respiratory Society 2023-01-26 /pmc/articles/PMC9515481/ /pubmed/36137595 http://dx.doi.org/10.1183/13993003.01117-2022 Text en Copyright ©The authors 2023. https://creativecommons.org/licenses/by-nc/4.0/This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions@ersnet.org (mailto:permissions@ersnet.org) |
spellingShingle | Original Research Articles Harbut, Piotr Prisk, G. Kim Lindwall, Robert Hamzei, Sarah Palmgren, Jenny Farrow, Catherine E. Hedenstierna, Goran Amis, Terence C. Malhotra, Atul Wagner, Peter D. Kairaitis, Kristina Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title | Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title_full | Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title_fullStr | Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title_full_unstemmed | Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title_short | Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery |
title_sort | intrapulmonary shunt and alveolar dead space in a cohort of patients with acute covid-19 pneumonitis and early recovery |
topic | Original Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515481/ https://www.ncbi.nlm.nih.gov/pubmed/36137595 http://dx.doi.org/10.1183/13993003.01117-2022 |
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