Despite the fervent scientific effort, a state-of-the art assessment of the different causes of hypoxemia (shunt, ventilation-perfusion mismatch and diffusion limitation) in COVID-19 ARDS is currently lacking. In this study we aimed to understand what is the relative contribution of the different mechanisms of hypoxemia in this disease and what is their relationship with the distribution of tissue and blood within the lung.


We prospectively enrolled 10 patients with COVID-19 ARDS, intubated for <7 days. We performed the Multiple Inert Gas Elimination Technique (MIGET) and a Dual-Energy Computed Tomography (DECT), which was quantitatively analyzed both for the tissue and blood volume. We also recorded variables related to the respiratory mechanics and invasive hemodynamics (PiCCO).


The population (51±15 years, PaO2/FiO2 172±86 mmHg) had a mortality of 50%. MIGET showed a shunt of 25±16% and a deadspace of 53±11%. The ventilation and perfusion were mismatched (LogSD, Q 0.86±0.33). Unexpectedly, we also found evidence of diffusion limitation/post-pulmonary shunting (Predicted PaO2= 1.6*measured PaO2 - 37.5 mmHg). In the well-aerated regions, the blood volume was in excess compared to the tissue, while the opposite happened in the atelectasis. Shunt was proportional to the blood volume of the atelectasis (R 2=0.70, p=0.003). VA/QT mismatch was correlated with the blood volume of the poorly-aerated tissue (R 2=0.54, p=0.016). The overperfusion coefficient was related to PaO2/FiO2 (R 2=0.66, p=0.002), excess tissue mass (R 2=0.84, p<0.001) and to EtCO2/PaCO2 (R 2=0.63, p=0.004).


These data support the hypothesis of a highly multifactorial genesis of hypoxemia. Evidence from autoptic studies (i.e., opening of Intrapulmonary Bronchopulmonary Anastomosis) may explain the unexpected post-pulmonary shunting. The hyperperfusion might be related to the disease severity.

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