RT Journal Article
SR Electronic
T1 Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 2201117
DO 10.1183/13993003.01117-2022
VO 61
IS 1
A1 Piotr Harbut
A1 G. Kim Prisk
A1 Robert Lindwall
A1 Sarah Hamzei
A1 Jenny Palmgren
A1 Catherine E. Farrow
A1 Goran Hedenstierna
A1 Terence C. Amis
A1 Atul Malhotra
A1 Peter D. Wagner
A1 Kristina Kairaitis
YR 2023
UL http://erj.ersjournals.com/content/61/1/2201117.abstract
AB 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 (PA−aO2 and Pa−ACO2, respectively) from which shunt and alveolar dead space were computed.Results For acute COVID-19 patients, group mean (range) for PA−aO2 was 41.4 (−3.5–69.3) mmHg and for Pa−ACO2 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.Hypoxaemia in COVID-19 is due to a variable combination of intrapulmonary shunt and increased dead space, likely from both airspace and vascular pathology. Increased dead space present up to 2 months later suggests persistent pulmonary vascular pathology. https://bit.ly/3ROtboc