Intrapulmonary Shunt and Alveolar Dead Space in a Cohort of Patients with Acute COVID-19 Pneumonitis and Early Recovery.

BACKGROUND: Pathological evidence suggests that COVID-19 pulmonary infection involves both alveolar damage (causing shunt) and diffuse micro-vascular 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 deadspace in moderate COVID-19 during acute illness and recovery. METHODS: We studied 30 patients (22 males, 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 O2 and CO2 concentrations were measured, yielding alveolar-arterial differences for each gas (AaPO2, aAPCO2) from which shunt and alveolar dead space were computed. MEASUREMENTS AND MAIN RESULTS: For acute COVID-19 patients, group mean (range) for AaPO2 was 41.4 (-3.5 to 69.3) mmHg; aAPCO2 was 6.0 (-2.3 to 13.4) mmHg. Both shunt (% cardiac output) at 10.4 (0 to 22.0)%, and alveolar dead space (% tidal volume) at 14.9 (0 to 32.3)% were elevated (normal: <5% and <10%, respectively), but not correlated (p=0.27). At recovery, shunt was 2.4 (0 to 6.1)% and alveolar dead space was 8.5 (0 to 22.4)% (both p<0.05 versus acute); shunt was marginally elevated for 2 patients, however, 5 (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.