ABSTRACT
Introduction/Aim: We previously reported impaired pulmonary gas exchange in acute COVID-19 patients resulting from both increased intrapulmonary shunt (SH) and increased alveolar dead space (AD) 1 . The present study quantifies gas exchange in recovered patients. Method(s): Unvaccinated patients diagnosed with acute COVID-19 infection (March-December 2020) were studied 15 to 403 days post first SARS-CoV-2 positive PCR test. Demographic, anthropometric, acute disease severity and comorbidity data were collected. Breathing room air, steady-state exhaled gas concentrations were measured simultaneously with arterial blood gases. Alveolar CO 2 and O 2 (P A CO 2 and P A O 2 ;mid-exhaled volume) determined;AaPO2, aAPCO2, SH% and AD% calculated. 2 Results: We studied 59 patients (33 males, Age: 52[38-61] years, BMI: 28.8[25.3-33.6] kg/m 2 ;median[IQR]). Co-morbibities included asthma (n = 2), cardiovascular disease (n = 3), hypertension (n = 12), and diabetes (n = 9);14 subjects smoked;44 had experienced mild-moderate COVID-19 (NIH category 1-2), 15 severe-critical disease (NIH category 3-5). PaCO 2 was 39.4[35.6-41.1] mmHg, PaO 2 92.1[87.1-98.2] mmHg;P A CO 2 32.8[28.6-35.3] mmHg, P A O 2 112.9[109.4-117.0] mmHg, AaPO 2 18.8[12.6-26.8] mmHg, aAPCO 2 5.9[4.3-8.0] mmHg, SH 4.3 [2.1-5.9]% and AD 16.6 [12.6-24.4]%. 14% of patients had normal SH (<5%) and AD (<10%);1% abnormal SH and normal AD;36% both abnormal SH and AD;49% normal shunt and abnormal AD. Previous severe-critical disease was a strong independent predictor for increased SH (OR 14.8[2.28-96], [95% CI], p < 0.01), increasing age weakly predicted increased AD (OR 1.18[1.01, 1.37], p < 0.04). Time since infection, BMI and comorbidities were not significant predictors (all p > 0.11). Conclusion(s): Prior COVID-19 was associated with increased intrapulmonary shunt and/or increased alveolar dead space in 86% of this cohort up to ~13 months post infection, with those with more severe acute disease, and older patients, at greater risk. Increased intrapulmonary shunt suggests persistent alveolar damage, while increased alveolar dead space may indicate persistent pulmonary vascular occlusion.