Fig. 2

a, b Prominent hypoperfusion in the well-aerated lung and hyperperfusion in areas of injured lung. Seventy-eight-year-old male patient, RT-PCR-confirmed COVID-19, 10 days since symptom onset, with hypoxemia, (PaO₂/FiO₂) 206, d-dimer 1600 ng/mL progressively increasing. There are extensive foci of consolidation and ground-glass opacities, associated with septal thickening, with a predominantly posterior and subpleural bilateral distribution, which correlate with the areas of hyperemia and iodine pooling in subtraction CT iodine maps (black arrows). There are areas of markedly decreased perfusion in both lungs, which correlate with the apparently healthy lung parenchyma in conventional chest CT images (white arrows). Bilateral pleural effusion. This could be explained by an increased blockage of ACE2 receptors in the lung endothelium, leading to increased local levels of angiotensin II, which leads to vasoconstriction and ventilation/perfusion mismatch. This patient was managed with invasive mechanical ventilation, with highly compliant lung parenchyma, in accordance with the type 1 or L phenotype described by Gattinoni et al.