Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery

Abstract

BackgroundPathological 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.MethodsWe studied 30 patients (22 males; mean±sdage 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−aO2andPa−ACO2, respectively) from which shunt and alveolar dead space were computed.ResultsFor acute COVID-19 patients, group mean (range) forPA−aO2was 41.4 (−3.5–69.3) mmHg and forPa−ACO2was 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<0.05versusacute). Shunt was marginally elevated for two patients; however, five patients (30%) had elevated alveolar dead space.ConclusionsWe 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.