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Abstract
The coronavirus disease 2019 (COVID-19) causes acute respiratory failure (ARF) altering the pulmonary microvasculature with simultaneous vasoconstriction and thrombosis in ventilated areas, hyperperfusion [1] and neo-angiogenesis in gasless regions [2]. The progressive derangement of the lung vasculature and parenchyma worsens the shunt fraction and deadspace, and consequently hypoxaemia and hypercapnia.
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