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Editorial
. 2020 Jul 6;24(1):395.
doi: 10.1186/s13054-020-03125-9.

COVID-19: a hypothesis regarding the ventilation-perfusion mismatch

Mario G Santamarina  1   2 , Dominique Boisier  3 , Roberto Contreras  4 , Martiniano Baque  5 , Mariano Volpacchio  6 , Ignacio Beddings  7
Affiliations
Editorial

COVID-19: a hypothesis regarding the ventilation-perfusion mismatch

Mario G Santamarina et al. Crit Care. .
No abstract available

Keywords: Angiotensin II; Angiotensin converting enzyme 2; COVID-19; Coronavirus; Vasoconstriction; Vasoplegia; Ventilation-perfusion ratio.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
a, b Slight hypoperfusion in the well-aerated lung, hyperemia, and small zones of hypoperfusion in the areas of injured lung. Fifty-nine-year-old male patient, RT-PCR-confirmed COVID-19, 11 days since symptom onset, without hypoxemia, (PaO2/FiO2) 538, d-dimer 340 ng/mL. There are isolated foci of ground-glass opacities associated with septal thickening, with a predominantly subpleural distribution, which correlate with areas of hyperemia (middle lobe) and small zones of hypoperfusion (lower right lobe) in subtraction CT iodine maps (large black arrows). There is an evident area of hypoperfusion in the middle lobe and lower right lobe (white arrows) that correlates with the apparently normal lung parenchyma in conventional chest CT images. The conventional CT image also shows pulmonary arterial vascular dilatation in the periphery of the ground-glass opacity in the middle lobe (small black arrow). These slight perfusion abnormalities do not impact the PaFi ratio. The ground-glass opacity in the lower right lobe shows slight peripheral hypoperfusion, probably due to compensatory vasoconstriction, an expected regulatory mechanism when vasoplegia is not fully established
Fig. 2
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.
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