We believe that a severe V/Q mismatch underlies the pathophysiology of moderate to severe COVID-19 cases, in which downregulation of ACE2 secondary to viral endocytosis plays a key role. There is low V/Q ratio in areas of injured lung parenchyma with ground-glass opacities or consolidation, secondary to loss of compensatory hypoxic pulmonary vasoconstriction (vasoplegia) and increased blood flow, which result in high perfusion to the areas of non-aerated lung, but there is also high V/Q ratio in areas of apparently healthy lung secondary to prominent vasoconstriction.

We hypothesize that hypoperfusion of apparently healthy areas could be a consequence of vasoconstriction due to accumulation of angiotensin II, caused by decreased availability of ACE2, and that these changes in vascular resistance lead to a shunt or steal of vascular flow towards areas of non-aerated hyperperfused lung in moderate to severe COVID-19 cases.

The improved oxygenation in prone position that has been described in patients with COVID-19 could be explained mainly through vascular redistribution towards the areas of apparently healthy lung with a high V/Q ratio, rather than alveolar recruitment.

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